What is the anatomical location of colon cancer vs. rectal cancer?A:
Colon Cancer: From the cecum to the sigmoid colon.
Rectal Cancer: Last 15 cm of the GI tract, ending at the anal verge.
What is the most common histological type of colon and rectal cancer?
Adenocarcinoma for both.
What are the common symptoms of colon cancer?
Change in bowel habits (diarrhea/constipation).
Occult blood in stool (right-sided) or rectal bleeding (left-sided).
Abdominal pain, iron-deficiency anemia, unintentional weight loss.
What are the common symptoms of rectal cancer?
Rectal bleeding (bright red blood).
Tenesmus (feeling of incomplete evacuation).
Painful defecation and pelvic pain in advanced stages.
: How do right-sided colon cancers typically present?
Occult bleeding → iron-deficiency anemia.
Vague abdominal pain.
Late obstruction (exophytic growth).
How do left-sided colon cancers typically present?
Narrow stools ("pencil-thin").
Gross rectal bleeding or hematochezia.
Early obstruction (circumferential growth).
What is the hallmark symptom of rectal cancer?
: Tenesmus and rectal bleeding.
What is the gold standard diagnostic test for colon and rectal cancer?
: Colonoscopy with biopsy.
in rectal cancer : typical apple core lesion.
Which tumor marker is used to monitor colon and rectal cancer?
Carcinoembryonic Antigen (CEA).
What is the primary treatment for early-stage colon cancer?
: Surgery (colectomy with lymphadenectomy).
What are common screening methods for colon cancer?A:
Colonoscopy every 10 years. after age 45
Fecal immunochemical test (FIT) annually.
CT colonography every 5 years.
Complications of colon cancer
peritoneal carcinomas
bowel obstruction
bowel perforation
prolonged bleeding
What are the key local complications of colon cancer?
Bowel Obstruction
Common in left-sided tumors (circumferential growth).
Symptoms: Abdominal distension, constipation, vomiting.
Perforation
Tumor necrosis weakens the bowel wall.
Leads to peritonitis, fecal contamination, and sepsis.
Bleeding
Chronic occult bleeding → iron-deficiency anemia.
Rarely, massive hematochezia (severe acute bleeding).
Fistula Formation
Tumor invasion creates abnormal connections (e.g., colovesical fistula).
Symptoms: Pneumaturia in colovesical fistula.
Abscess Formation
Secondary to tumor perforation or necrosis.
Presents with localized pain and fever.
What are the goals of surgery in non-complicated colon cancer?
Achieve R0 resection (complete removal with clear margins).
Perform adequate lymphadenectomy (removal of ≥12 lymph nodes).
What are the surgical procedures for non-complicated colon cancer?
Segmental Colectomy
Removes tumor and regional lymph nodes.
Types:
Right Hemicolectomy: For cecum and ascending colon tumors.
Left Hemicolectomy: For descending colon tumors.
Sigmoid Colectomy: For sigmoid colon tumors.
How is bowel obstruction due to colon cancer managed surgically?
Stable patient: Perform colectomy with primary anastomosis.
Unstable patient: Create a diverting stoma (e.g., colostomy).
Definitive resection is performed later in a staged approach.
How is perforation due to colon cancer managed surgically?
Emergency surgery to prevent peritonitis and sepsis.
Options:
Hartmann’s Procedure: Resect tumor, end colostomy, and leave rectal stump.
Reconnect bowel in a second-stage surgery.
Primary anastomosis is avoided in unstable patients
How is severe bleeding in colon cancer treated?
Perform segmental resection of the affected colon.
Preoperative embolization may stabilize bleeding in selected cases.
What are the types of intestinal polyp?
Pedunculated
Sessile- broad based polyp without stalk
Clinical symptomts of intestinal polyp?
hematochezia (bright red stools, also seen in left sided colon cancer + rectal cancer)
change in bowel habits, mucous in stool
palapable rectal polyp
Treatment for intestinal polyp
Colonoscopy + polpyectomy
<1cm —> cold snare polypectomy
>1cm —> hot snare (especially if pedunculated)
High risk:
snare polpyectomy
if more than 2cm —> endoscopic mural resection
Famililal adenamtous polpyosis syndrome
Clinical Criteria:
Presence of >100 colorectal adenomatous polyps.
Genetic Testing:
Confirmatory testing for APC mutation. (autosomal dominant)
Associated Syndromes
Turcot Syndrome:
FAP + central nervous system tumors (e.g., medulloblastoma).
Diverticulitis
Inflammation or infection of diverticula. Most commonly in the sigmoid colon
Left lower quadrant pain
Types of diverticulitis
Uncomplicated: no infection, abscess, perforation
Complicated: abscess, fistula, perforation, obstruction
perforation —> peritonitis
clinical features of diverticulitis
left lower quadrant pain
fever (if infection)
alterted bowel habits (constipation, diarrhea)
nausea + vomitting
SIGNS:
LLQ tenderness on palpation
guarding or rebound tenderness ( peritonitis)
Diagnostic features of diverticulitis
Lab:
leukocytosis
elevated CRP
Imaging:
CT with contrast
if signs suggestive of divierticulitis, avoid colonoscopy
Complications of diverticulitis
Bleeding (painless hematochezia + signs of anemia)
Diveriticulitis
CHronic inflammation (treat like Chrohn’s disease)
Abscess
NPO + antibiotics + emergency surgery
Management of diverticulitis v
Uncomplicated:
clear liquid diet
oral antibiotics ( ciproflaxcin + metrondiazole)
Complicated:
hospitalization
percutaneous drainage for abscess >3cm
Emergency surgery:
in perforation or peritonitis (if hemodynamically stable —> laparoscopic or open colectomy & primary anastomosis)
Hartmann’s procedure (also done in colon cancer)
What is ileus?
Ileus is a condition characterized by intestinal hypomotility (reduced or absent bowel movement) It often affects the small or large bowel.
What are the types of ileus?
Paralytic Ileus: Complete lack of bowel motility. due to muscle not moving
Mechanical Ileus: Functional obstruction caused by a physical blockage.
Key causes of mechanical ileus
Small bowel:
hernias
intussception
adhesions
Large bowel:
volvulus
cancer
Key causes of functional ileus
paralytic ileus
dilated cecum (colonic pseudoobstruction)
Symptoms in ileus
C- Colicky pain, cramping
A- abdominal distention
V- vomitting
O- Obstipation
Abdominal pain (colicky or dull).
Abdominal distension (bloating).
Nausea and vomiting.
Constipation or inability to pass gas.
Absence of bowel sounds (hypoactive or absent) presnet in functional ileus, mechanical ileus has bowel sounds
Causes of ileus
post surgical
hypokalemia
due to pain medication (opoids)
peritonitis
Diagnosis of Ileus
Clinical Diagnosis: History of surgery, medications, or infections.
Abdominal X-ray: Gas-filled loops of bowel, no transition zone.
presence of transition zone —> mechanical ileus
CT scan: More detailed, shows underlying cause.
Lab tests: Check electrolyte abnormalities (e.g., low potassium).
Management of Ileus
Supportive care:
NPO (nil per os): No oral intake.
IV fluids: Correct dehydration and electrolyte imbalances.
Electrolyte correction: Especially for potassium, magnesium.
Treat underlying causes: Discontinue offending medications, treat infections.
Surgical intervention: Rare, for complications like peritonitis or bowel ischemia. (laparotomy)
What is a fistula?
A fistula is an abnormal connection or passage that forms between two organs, vessels, or between an organ and the skin. It can be caused by inflammation, infection, injury, or surgical complications.
Types of Fistulas
Enterocutaneous Fistula: Between the intestine and skin.
Colovesical Fistula: Between the colon and bladder (e.g., in diverticulitis).
Colovaginal Fistula: Between the colon and vagina.
Arteriovenous Fistula: Abnormal connection between an artery and vein.
Tracheoesophageal Fistula: Between the trachea and esophagus, often congenital in infants.
Rectovaginal Fistula: Between the rectum and vagina, often caused by trauma or childbirth.
Causes of Fistulas
nflammatory Bowel Disease (IBD): e.g., Crohn’s disease.
Diverticulitis (leading to colovesical fistula).
Trauma or injury: Surgery, accidents, or childbirth.
Infections or abscesses: Infections may create a passage between two organs.
Cancer: Tumor growth may create abnormal passages.
Radiation therapy: Can lead to tissue necrosis and fistula formation.
Clinical Features of Fistulas
Persistent discharge
Abdominal pain or discomfort
Infections or abscesses
Recurrent urinary or gastrointestinal symptoms:
Diagnosis of Fistulas
Clinical Examination: Look for abnormal discharges or symptoms suggestive of abnormal connections.
CT scan: Excellent for detecting abdominal or pelvic fistulas, especially in inflammatory diseases like Crohn's.
Fistulography: Special imaging for evaluating fistulas, especially in the gastrointestinal system.
Colonoscopy/Endoscopy: To visualize fistulas in the GI tract.
Cystoscopy: For diagnosing colovesical fistulas (via visualization of the bladder).
MRI: Useful in evaluating complex or deep fistulas, especially rectovaginal fistulas.
Common Fistula Locations and Symptoms
Colovesical Fistula:
Symptoms: Pneumaturia (passing gas in urine), recurrent urinary tract infections, fecaluria (stool in urine).
Cause: Diverticulitis or Crohn’s disease.
Enterocutaneous Fistula:
Symptoms: Foul-smelling drainage from the skin, weight loss, malnutrition, abdominal pain.
Cause: Surgery, inflammatory bowel disease, cancer.
Colovaginal Fistula:
Symptoms: Passage of gas or stool through the vagina, vaginal discharge.
Cause: Trauma, childbirth, diverticulitis, or cancer.
Rectovaginal Fistula:
Symptoms: Stool or gas passing through the vagina, vaginal discomfort.
Cause: Childbirth trauma, surgery, radiation.
Arteriovenous Fistula:
Symptoms: Abnormal pulsatile mass, heart failure symptoms, bruits over the fistula site.
Cause: Trauma, surgery, or congenital.
How are fistulas treated?
Conservative Management:
Nutritional support (especially in enterocutaneous fistulas).
Antibiotics: To prevent or treat infections.
Drainage: If there is abscess formation.
Medication: Somatostatin to decrease fluid secretion
Surgical Treatment:
Fistula repair surgery: Often required, especially for complex fistulas (e.g., colovaginal or colovesical).
lysis of adhesions
resection of diseases bowel and connecting healthy parts
Stoma: In some cases (e.g., diverticulitis with a colovesical fistula).
Medical Management:
Biological therapy: For fistulas caused by Crohn’s disease (e.g., infliximab).
Radiation therapy: In some cases for radiation-induced fistulas.
When is a fistulotomy done?
Is a common treatment for anal fistulas, which are abnormal connections between the anal canal and the skin around the anus.
Not done for all cases, cannot be done in complex fistula/ it is the opening of a fistula allowing it to drain and heal with time + use of sitz baths, wound care and antibiotics.
What are the key features of acute paraproctitis?
Paraprocritis —> inflammation and infection of tissues surrounding the anal canal and rectum
A sudden infection of the pararectal spaces, often caused by bacterial infection (e.g., E. coli or Staphylococcus).
Cause: Anorectal abscess (which often leads to paraproctitis if not drained)
Symptoms of acute paraprocritis
Severe perianal pain: Localized to the anal or rectal region.
Swelling and redness: Around the anus, may be associated with an abscess.
Fever: Often present with systemic signs of infection.
Tenderness: On palpation, especially in the perianal area.
Abscess formation: May develop if infection is not treated promptly.
Difficulty sitting or walking due to pain.
Painful defecation.
Diagnosis of acute paraprocritis
Clinical examination
Imaging
ultrasound or CT scan
Treatment of acute paraprocritis
Incision and drainage of abscesses to relieve pressure.
Antibiotics: Broad-spectrum antibiotics for infection control.
Pain management: Analgesics for symptom relief.
sitz bath
stool softeners
What are the key features of chronic paraproctitis?
A long-standing infection or inflammation of the pararectal spaces, often due to incomplete healing of an acute abscess or a recurrent issue.
Cause: Chronic anal fistulas often develop as a result of chronic paraproctitis, with persistent drainage or an abscess that does not resolve properly.
Symptoms of chronic paraprocitis
Recurrent or persistent anal drainage: May be mucopurulent or serous.
Fistula formation: Abnormal connection between the anal canal and skin, causing leakage of stool or pus.
Faint perianal swelling: May occur without the severe acute symptoms seen in acute paraproctitis.
Intermittent pain or discomfort: Often less severe than in acute paraproctitis, but can worsen with defecation.
Chronic itching: Due to prolonged drainage or irritation of the skin.
Absence of systemic symptoms: Unlike acute paraproctitis, fever is not common in chronic paraproctitis.
Diagnosis of chronic paraprocritis
DRE
transrectal ultrasound or endoscopy
MRI or CT
Treatment of Chronic Paraprocitis
Surgical intervention: Surgical drainage of abscess and repair of any fistula (e.g., fistulotomy, fistulectomy, or seton placement for complex fistulas).
Antibiotics: Not typically required unless there's a secondary infection.
Management of fistulas: If a fistula is present, surgical treatment is needed to prevent recurrence.
Pain management: If there's any discomfort, analgesics can be used.
What is a hemorrhoid
Hemorrhoids are swollen veins in the lower rectum or anus that can be internal or external. They are common and can be classified based on severity. The treatment options depend on the type (internal or external) and severity (grade 1 to 4).
Internal hemorroids
Located above the dentate line
covered by mucosa
classficiation:
I no prolapse, may cause internal bleeding
II prolapse, during straining
III Prolapse required manual reduction
IV irreducible prolapse
Diagnosis of hemorroids
DGE
proctoscopy or ansocopy
flexible sigmoidoscopy or colonoscopy
Treatment for hemorroids (lifetsylye)
Lifestyle:
high fiber
increased fluid
daily exercise
avoid fatty, spicy food
treatment for hemorroids (stage II-III)
Rubber Band Ligation:
The most common treatment for internal hemorrhoids.
A small rubber band is placed at the base of the hemorrhoid, cutting off blood supply. The hemorrhoid shrinks and falls off in 1–2 weeks.
Effective for grade 1 and 2 hemorrhoids.
Sclerotherapy:
An injection of a sclerosing solution into the hemorrhoid to shrink it.
Used for smaller hemorrhoids and can be combined with rubber band ligation.
Infrared Coagulation:
A laser or infrared light is used to coagulate the blood vessels in internal hemorrhoids.
Used for grade 1 or 2 hemorrhoids.
Surgical treatement of hemmorhoid
hemorrhoidectomy (surgical removal of hemorrhoids)
Stapled Hemorrhoidopexy
A circular stapling device is used to remove a portion of the hemorrhoidal tissue and fix the prolapsed hemorrhoids back into place.
Doppler guided hemorrhoidal artery ligation
A Doppler probe is used to identify and ligate the arteries supplying blood to the hemorrhoids, reducing their size.
What is the recommended approach to managing asthma in adults and adolescents (12+ years)?
Use the "Assess, Adjust, Review" cycle:
Assess: Symptom control, modifiable risk factors, comorbidities, inhaler technique, adherence, patient preferences, and goals.
Adjust: Treat modifiable risks, consider non-pharmacological strategies, adjust medications, provide education and skills training.
Review: Check symptoms, exacerbations, side effects, lung function, and patient satisfaction.
What is the preferred reliever for asthma management in Track 1?
As-needed low-dose ICS-formoterol.
What is the alternative reliever in Track 2, and when is it used?
As-needed short-acting beta₂-agonist (SABA), used if adherence to inhaled corticosteroids (ICS) is ensured.
What is bronchial asthma?
Asthma is a heterogeneous disease characterized by chronic inflammation. It involves respiratory symptoms such as:
Wheeze
Shortness of breath
Chest tightness
Cough
These symptoms vary over time and intensity and are associated with variable expiratory airflow limitation.
What are the main steps in diagnosing asthma?
History: Allergens, triggers, and symptom patterns.
Symptoms: Wheezing, cough, chest tightness, shortness of breath, worse at night or early morning.
Provocation: Symptoms triggered by exercise, laughter, allergens, cold air, or viral infections.
Examination: Expiratory wheezing on auscultation.
Variability tests: Confirm with lung function tests and response to bronchodilators.
How is the diagnosis of asthma confirmed?
Spirometry: FEV1 < 80% and FEV1/FVC < 75%.
Bronchodilator test: FEV1 improvement > 12% and > 200 mL.
Peak flow variability > 10% over 2 weeks.
Positive bronchial challenge test (methacholine/exercise).
Significant improvement in lung function after 4 weeks of ICS treatment.
Testing for triggers: Skin prick tests, GERD evaluation.
What are the common symptoms of asthma?
Wheezing
Dyspnea (shortness of breath)
Symptoms worse at night or early morning (e.g., "night asthma").
How is asthma classified based on phenotype and control levels?
Phenotypes:
Allergic asthma
Late-onset asthma
Persistent airflow limitation asthma
Asthma with obesity
Control Levels:
Well-controlled: Symptoms < 4–5 days/week.
Partially controlled: Moderate symptoms most days.
Uncontrolled: Severe daily symptoms with poor lung function.
How is asthma severity assessed?
Mild: Symptoms < 4–5 days/week, controlled with Step 1 or 2 treatment (low-dose ICS + formoterol).
Moderate: Symptoms most days or nighttime awakenings, controlled with Step 3 (low-maintenance ICS + formoterol).
Severe: Daily symptoms, poor lung function, requires Step 4 or 5 (medium/high-dose ICS + formoterol or add-on therapies).
What is pneumonia, and how is it classified?
By acquisition:
CAP: Community-acquired pneumonia (Typical & Atypical).
HAP: Hospital-acquired pneumonia (early >48h, late 7–10 days after discharge).
VAP: Ventilator-associated pneumonia (>48h after intubation).
HCAP: Healthcare-associated pneumonia (from healthcare facilities/nursing homes).
By radiology:
Lobar: Dense alveolar infiltration in 1–2 lobes.
Interstitial: Bilateral diffuse reticular and micronodular changes.
Bronchopneumonia: Bilateral patchy infiltrates; may cause cavitation.
Thromboembolic: Due to emboli.
By etiology:
Viral: Influenza, COVID-19.
Bacterial: Typical (e.g., S. pneumoniae, H. influenzae), Atypical (e.g., Mycoplasma, Legionella).
Fungal: Pneumocystis jiroveci, Aspergillus.
Clinical Manifestations of Pneumonia
Typical:
Dyspnea, tachypnea, productive cough, fever (>4 days), crackles, pleuritic chest pain, dull percussion, fremitus pectoralis.
Atypical:
Non-productive cough, sore throat, fatigue, myalgia, slow onset.
Severity Assessment of Pneumonia
CURB-65 criteria:
Confusion.
Urea >7 mmol/L.
Respiratory rate ≥30 breaths/min.
Blood pressure <90 mmHg systolic or ≤60 mmHg diastolic.
Age ≥65. Score Interpretation:
0–1: Outpatient.
2: Consider inpatient.
≥3: Inpatient or ICU.
What are the diagnostic investigations for pneumonia?
Clinical Symptoms: Dyspnea, tachypnea, cough, fever, crackles.
Laboratory:
CRP >100 mg/L, CBC, inflammatory markers, pulse oximetry, blood gases.
Urea, glucose, electrolytes, liver tests.
Chest X-ray (AP, LL views).
CT scan if X-ray is inconclusive.
Microbiological Tests:
Blood & sputum cultures.
Bronchoscopy (FBS with brushing).
Urine antigen tests (Legionella, S. pneumoniae).
PCR for bacterial/viral DNA from sputum or nasal swabs.
How is community-acquired pneumonia (CAP) treated outpatient?A:
Antibiotics:
Amoxicillin 500 mg–1 g PO
± macrolide(azithromycin) or doxycycline. (if allergic to penicillin)
Short course (5 days), follow guidelines.
Symptomatic Therapy:
Mucolytics, hydration, rest.
Paracetamol for pleuritic pain.
ive hear amoxiclav is better for smokers
How is community-acquired pneumonia (CAP) treated inpatient?
Empiric Antibiotics (moderate/severe):
Amoxicillin ± macrolide (azithromycin) or doxycycline.
Broad-spectrum beta-lactamase inhibitors for severe cases (e.g., co-amoxiclav).
Duration: 7–10 days (depending on pathogen and severity).
Supportive Care: Hydration, oxygen, nutrition, mucolytics.
What are the discharge criteria and post-discharge advice for pneumonia?
Discharge Criteria (last 24h):
Temp <37.5°C.
RR <24,
HR <100,
SpO₂ >90%,
stable BP, normal mental status, oral intake.
Define and classify hospital-acquired pneumonia (HAP).
Pneumonia caused by hospital-acquired pathogens, developing ≥48h after admission.
Classification:
Early: >48h after admission.
Late: 7–10 days post-discharge.
VAP: >48h post-intubation.
All pneumonia patients should…?
All cases of pneumonia should have a repeat chest X-ray at 6 weeks after clinical resolution to ensure that the consolidation has resolved and there is no underlying secondary abnormalities (e.g. a lung tumour).
What is acute appendicitis?
Acute appendicitis is the inflammation of the appendix, typically presenting with
right lower quadrant abdominal pain,
fever
leukocytosis.
It may progress to complications such as abscess, perforation, or peritonitis.
What are the steps in the initial management of suspected appendicitis?
Keep NPO (nothing by mouth).
Start IV fluids, analgesia, and antiemetics.
Assess likelihood of appendicitis based on:
Patient demographics (age, sex).
Clinical features of appendicitis.
Initial lab studies (e.g., CBC, CRP).
will show neutrophilis leukocytosis
Appendicitis risk scores (e.g., Alvarado, AIR).
What is the management for moderate likelihood of appendicitis?
Perform confirmatory imaging (e.g., abdominal ultrasound or CT abdomen).
If imaging confirms appendicitis: Proceed with treatment.
If imaging is inconclusive: Reassess clinical findings and likelihood.
What is the management for high likelihood of appendicitis?
What is the management for high likelihood of appendicitis? A:
Urgent surgical consultation for admission and treatment.
Start empiric antibiotic therapy. ( cefazolin + metrondiazole)
Proceed with:
Laparoscopic appendectomy for uncomplicated cases (within 24 hours).
Emergency appendectomy for complicated cases with systemic manifestations (e.g., sepsis).
What diagnostic tools are used for acute appendicitis?
Lab studies:
CBC: Leukocytosis with left shift.
CRP: Elevated (>10 mg/L).
Urinalysis: Mild pyuria/hematuria (if present).
β-hCG: Rule out ectopic pregnancy in women.
CT abdomen (nonpregnant adults): Most accurate initial imaging.
Ultrasound (pregnant adults, children): First-line imaging.
MRI (pregnancy/contraindication to CT): If ultrasound is inconclusive.
Findings: Distended appendix (>6 mm), periappendiceal fat stranding, target sign, appendiceal fecalith.
How is complicated appendicitis different from uncomplicated appendicitis?
Uncomplicated: Inflammation confined to the appendix, no systemic signs of infection.
Complicated: Includes appendiceal phlegmon, abscess, perforation, or generalized peritonitis.
When is nonoperative management used for appendicitis?
Recommended for complicated appendicitis with appendiceal phlegmon or abscess.
Considered for early uncomplicated appendicitis in select cases after consultation with a surgeon.
Parenteral antibiotics for 2–3 days, then oral antibiotics for 7 days (uncomplicated cases).
3–5 days for complicated cases.
Cefazolin + Metronidazole.
signs associated with acute appendicits
Differential diagnosis of acute appendicits
gastroenteritis
ectopic pregnancy
diverticulitis
IBD
complications of acute appendicits
Early
Late
Post op ileus
Abscess formation
Plegmon
intraabdominal abscess
Peritonitis
Sepsis
if there is a periappendicular infiltration and abscess
if <4cm broad spectrum antibiotics —> appendectomy
if >4cm:
antibiotic therapy + image guided percutaneous drainage + cultures from aspirate
Perforated Gastric and Duodenal Ulcers
Clinical features
Sudden, severe abdominal pain: Diffuse pain with rigidity (due to peritonitis).
Signs of systemic inflammation: Fever, tachycardia, tachypnea, hypotension (from fluid loss).
Pneumoperitoneum: Air under the diaphragm seen on imaging.
Referred shoulder pain: From phrenic nerve irritation.
Diagnosis of gastric and duodenal ulcers that are perforated
Patient history: Look for history of ulcers and sudden onset of pain.
First-line imaging:
X-ray (abdomen & chest): Detects free air (extraluminal gas).
Most useful test: CT scan for detailed evaluation.
Surgical Treatment for perforated gastric or dudodenal ulcer
Open or laparoscopic surgery is standard.
Ulcer bed management:
Sewing over the ulcer.
Graham patch: Omentum is fixed over the ulcer if sewing is challenging.
Stomach ulcers: Ulcer resection preferred due to higher cancer risk.
Complicated cases:
Subtotal gastrectomy (75% stomach removal):
Reconstruction via Billroth II (preferred) or Roux-en-Y.
Damage control procedures for septic patients:
Pyloric exclusion + gastrojejunal anastomosis.
Bleeding Gastric and Duodenal Ulcers
clinical features
Symptoms of blood loss:
Weakness, dizziness, sweating, palpitations, collapse.
Hematemesis: Vomiting blood (bright red or coffee-ground appearance).
Melena: Black, tarry stools (common with duodenal ulcers).
Diagnosis of bleeding ulcer
nitial evaluation:
History and clinical signs.
Lab tests: CBC, hemoglobin, CMP (for blood loss).
Definitive test:
FGS (esophagogastroduodenoscopy) to visualize the bleed and treat.
Treatment for bleeding ulcer
Endoscopic Approach (Based on Forrest Classification)
Forrest 1a, 1b, 2a:
1a = active spurting, IB= active bleeding , 2a = non bleeding visible ulcer
Hemoclip + epinephrine injection or cauterization.
Forrest 2b ( adherent clot)
Remove the clot and cauterize any visible bleed.
Forrest 2c, 3:
2c = flast spot in ulcer base, III = clean base ulcer
Conservative management, rarely requiring surgery.
urgical Options
Gastric ulcers:
Partial gastrectomy + Billroth I/II reconstruction (due to cancer risk).
Duodenal ulcers:
Suturing over the bleed (or pyloroduodenotomy if proximal).
Stenosing Gastric and Duodenal Ulcers (Pyloric Stenosis)
Compensated stenosis: Feeling of tightness in the stomach region.
Decompensated stenosis:
Vomiting old food, weight loss, and dehydration.
Postprandial non-bilious vomiting.
Succussion splash: Splashing sound on auscultation (due to retained gastric contents).
Lab findings:
Increased HCO3 (from vomiting), decreased Cl and K.
X-ray with barium swallow or CT scan:
Enlarged stomach, no peristalsis, delayed barium passage, pyloric stricture.
EGD for confirmation.
Symptomatic Management:
Nasogastric suction, electrolyte replacement, parenteral nutrition.
Definitive Treatment:
Endoscopic balloon dilation (first-line for mild stenosis).
Surgery (severe or refractory cases):
Gastrojejunostomy or pyloroplasty
What defines acute kidney injury (AKI) in children?
Increase in serum creatinine > 0.3 mg/dL within 48 hours.
Increase in serum creatinine to > 1.5× baseline within 7 days.
Decreased urine output to < 0.5 mL/kg/h for > 6 hours.
What are the main categories of AKI causes in children?
Prerenal (most common):
Dehydration
Congestive heart failure (CHF)
Liver failure
Renal:
Hemolytic Uremic Syndrome (HUS) (most common renal cause):
Associated with EHEC infection
Classic triad: AKI, hemolytic anemia, thrombocytopenia
Glomerulonephritis (e.g., post-streptococcal)
Acute tubular necrosis
Congenital abnormalities of the kidney and urinary tract
Postrenal (less common):
Obstruction (e.g., stones, congenital anomalies).
What are the clinical symptoms of AKI in children?
Oliguria or anuria
Edema
Hypertension
Electrolyte imbalances:
Hyperkalemia
Hyponatremia
Uremic symptoms (nausea, lethargy)
Metabolic acidosis
What are the key diagnostic steps for AKI in children?
Laboratory Tests:
Serum creatinine, BUN, CBC
Electrolytes
Urinalysis
Renal ultrasound (to check for obstruction or anomalies)
GFR assessment
How is AKI treated in children?
Treat underlying cause.
Indications for renal replacement therapy (RRT):
Acidosis
Electrolyte imbalance (e.g., severe hyperkalemia)
Intoxications
Overload (fluid)
Uremia
What is Hemolytic Uremic Syndrome (HUS)?
A condition caused by thrombosis in small blood vessels, leading to:
Hemolytic anemia
Thrombocytopenia (low platelet count)
Acute kidney injury (AKI)
Triggered by Shiga toxin from E. coli (EHEC) or Shigella.
What are the key clinical features of HUS?
Gastroenteritis symptoms: diarrhea, often bloody.
After 5 days:
↓ Urine output (oliguria)
Hematuria
Abdominal pain
Lethargy or irritability
Confusion
How is HUS managed in children?
Supportive treatment (self-limiting condition).
Avoid antibiotics! (can worsen toxin release).
Dialysis if indicated for severe cases.
What are the key lab findings in HUS?
Hemolytic anemia (schistocytes on blood smear).
Thrombocytopenia (low platelets).
AKI indicators:
Elevated creatinine
Proteinuria, hematuria
Decreased urine output.
Stool testing for Shiga toxin (culture or PCR).
What is acute epiglottitis?
A rare, life-threatening inflammation of the epiglottis and surrounding structures (supraglottic laryngitis), most common in children aged 2–5 years.
What is the most common cause of acute epiglottitis?
Haemophilus influenzae type B (Hib).
Q: Name other pathogens that cause acute epiglottitis. A:
Streptococcus pneumoniae
Group A Streptococcus (GAS)
Staphylococcus aureus, including MRSA
What are the hallmark symptoms of acute epiglottitis?
Inspiratory stridor
Drooling
Tripod positioning
Dysphagia
Muffled (hot potato) voice
Fever, irritability, lethargy, and severe sore throat.
What causes airway obstruction in acute epiglottitis?
inflammation and swelling of the epiglottis and surrounding tissues.
What imaging finding is characteristic of acute epiglottitis?
Thumb sign on lateral neck X-ray.
What tests are used to confirm the diagnosis?
Clinical evaluation.
X-ray (Thumb sign).
Blood culture.
CBC.
Swab of the epiglottis (in a controlled environment).
Name three differential diagnoses for acute epiglottitis.
Croup (subglottic laryngitis): Gradual onset, barking cough, steeple sign on X-ray.
Anaphylaxis: Rapid onset, associated with hives, wheezing, and hypotension.
Foreign body aspiration: Sudden onset, asymmetrical breath sounds.
What is the first priority in treating acute epiglottitis?
Which antibiotics are used empirically for acute epiglottitis?
What medication is used to reduce inflammation?
Airway management to prevent obstruction ( can do intubation, if fails —> tracheostomy)
IV Ceftriaxone or Cefotaxime.
IV Prednisolone.
supportive:
Inhaled adrenaline to reduce airway swelling.
Humidified oxygen.
IV fluids for hydration.
Analgesics and antipyretics for pain and fever.
How can acute epiglottitis be prevented?
Hib vaccination as part of routine childhood immunization.
What are the exam buzzwords for acute epiglottitis?
Drooling, inspiratory stridor, tripod positioning.
Thumb sign on X-ray.
IV Ceftriaxone + Prednisolone.
Prevention with Hib vaccination.
Acute Gastroenteritis in children
Definition
Sudden onset of diarrhea (≥3 loose/watery stools in 24 hours) and/or vomiting, often with fever.
Usually self-limiting and resolves in 1 week.
Dehydration is the biggest concern.
Etiology of gastroenteritis in children
Viral (most common, ~80%)
Rotavirus (first sign is vomiting).
Norovirus.
Adenovirus.
Enterovirus.
2. Bacterial (<20%)
Salmonella, Shigella, Campylobacter, E. coli (bloody diarrhea).
3. Parasitic
Giardia lamblia, Entamoeba histolytica.
Symptoms of gastroenteritis in children
Symptoms
Diarrhea:
Watery, non-bloody (viral).
Bloody (bacterial).
Vomiting:
Common in viral gastroenteritis, first sign in Rotavirus.
Fever.
Dehydration Signs:
Increased thirst.
Sunken eyes.
Dry mucosa.
Reduced urine output.
Lethargy, irritability.
Severe dehydration:
Tachycardia, tachypnea, sunken fontanel (infants).
Severe lethargy or altered mental state.
Red Flags of gastroenterirts in children
Severe abdominal pain.
Persistent diarrhea (>7 days).
Blood in stool.
Vomiting without diarrhea.
Treatemtn of Gastroenteririts in children
Treatment
1. Rehydration (mainstay):
Oral Rehydration Therapy (ORT) (preferred).
IV fluids for moderate/severe dehydration or if oral fluids are not tolerated.
2. Antiemetics:
Ondansetron for vomiting.
3. Probiotics:
Lactobacillus can reduce duration of diarrhea.
4. Antibiotics:
Usually not needed.
Indicated only in bacterial infections with systemic involvement (e.g., Shigella, cholera, or sepsis).
Prevention: Rotavirus vaccination (routine childhood immunization).
Diagnosis of Gastroenteritis in children
Clinical diagnosis: Assess dehydration severity.
Stool analysis (if red flags):
Culture, PCR, or antigen test for pathogens.
Blood analysis (if severe dehydration):
Electrolytes, CRP, glucose.
How does asthma in children differ from asthma in adults?
Triggers: Viral infections are more common in children; allergens and smoking in adults.
Presentation: Episodic symptoms in children; persistent in adults.
Diagnosis: Spirometry is difficult in children <5 years.
Medication: Weight-based dosing in children.
Prognosis: Many children outgrow symptoms; asthma in adults is often lifelong.
What are the common asthma triggers in children?
Viral infections (most common).
Allergens (dust, pollen, mold, pets).
Exercise.
Environmental pollutants (smoke, air pollution).
How is asthma diagnosed in children?
Children >6 years: Spirometry with reversibility testing (FEV1 increase ≥12% and 200 mL after bronchodilator).
Children <5 years: Clinical history, signs of recurrent wheezing, and response to treatment.
What are the GINA treatment steps for children <5 years with asthma?
Step 1: Low-dose ICS + SABA as needed.
Step 2: Daily low-dose ICS + SABA as needed.
Step 3: Moderate-dose ICS or low-dose ICS + Leukotrine receptor antagonist LTRA.
Step 4: Referral to a specialist.
What are the GINA treatment steps for children 6–11 years with asthma?
Step 1: Low-dose ICS-formoterol as needed.
Step 2: Daily low-dose ICS + as-needed SABA.
Step 3: Low-dose ICS-LABA (MART).
Step 4: Medium-dose ICS-LABA ± LTRA or tiotropium.
Step 5: Referral to a specialist; consider biologics.
What are the criteria for well-controlled asthma?
Symptoms ≤2 days/week.
No nighttime symptoms.
No activity limitation.
SABA use ≤2 times/week.
What are the key components of non-pharmacological asthma management in children?
Trigger avoidance (allergens, smoke, viral infections).
Education (inhaler technique, asthma action plan).
Vaccination (influenza, pneumococcal).
Encourage physical activity with proper control.
Definition of Atopic Dermatitis in Children
Chronic inflammatory skin condition commonly seen in children, often associated with
allergic rhinitis and bronchial asthma (collectively referred to as atopy).
Infants (0-2 years):
Common Areas Affected:
Face, scalp, extensor surfaces (arms/legs).
Symptoms:
Cradle cap (yellowish, scaly plaques on the scalp).
Weeping, erythematous plaques with excoriation, possibly superinfected with S. aureus.
Sparing of the diaper area.
Childhood/Adolescence (2 years - adolescence):
Common Areas Affected: Flexor surfaces (elbows, knees).
Dry, scaly, hyperpigmented plaques.
Lichenification (skin thickening from chronic scratching).
Excoriation marks from itching.
Diagnostic features of atopic dermatitis in children
Anamnesis: Ask about symptoms, family history of atopic diseases (asthma, rhinitis, eczema).
Atopy Score: Used to assess the likelihood of an atopic condition.
IgE Levels: Often elevated in atopic dermatitis.
Prick Test: Identifies common environmental and food allergens.
Provocation Test: Controlled exposure to allerg
Treatmnet for atopic dermatitis
Avoid Triggers: Identify and avoid allergens, irritants (e.g., soaps, fragrances).
Emollients: Regular application of thick creams or ointments to maintain the skin barrier.
Bathing: Short, lukewarm baths with mild, fragrance-free products.
Pharmacologic Treatment:
Antihistamines: For pruritus (itching).
Topical Corticosteroids:
First-line treatment during flare-ups.
Use mild steroids on the face (e.g., hydrocortisone).
Topical Calcineurin Inhibitors (e.g., Tacrolimus, Pimecrolimus):
Used for sensitive areas (face, eyelids).
Antibiotics: For secondary infections (e.g., Staphylococcus aureus), often with mupirocin or oral cephalexin.
Skin Care: Regular use of emollients, avoid harsh soaps, and allergens.
Vaccination: Ensure proper vaccination, especially influenza and pneumococcal vaccines, to reduce the risk of infections, as children with atopic dermatitis may have weakened skin barriers.
Definition of bronchiolitis in children
Acute viral infection of the lower respiratory tract, characterized by inflammation and obstruction of the small airways (bronchioles).
Most Common Age: Affects infants and young children,
especially those under 2 years.
Most common etiology of bronchiolitis in children
Respiratory Syncytial Virus
Key Symptoms of Bronchiolitis in children
Initial Symptoms (Prodrome):
Runny nose (rhinorrhea).
Cough (typically dry, becoming more productive).
Mild fever.
Wheezing (often noticeable on expiration).
Progressive Symptoms:
Dyspnea (difficulty breathing).
Tachypnea (rapid breathing, often > 60 breaths per minute).
Nasal flaring and intercostal retractions (signs of respiratory distress).
Grunting (in severe cases).
Cyanosis (in severe cases due to oxygen desaturation).
Physical Exam Findings of bronchiolitis in children
Wheezing: High-pitched sound during exhalation.
Crackles: Fine rales or crackling sounds may be heard.
Respiratory Distress:
Tachypnea.
Nasal flaring.
Intercostal and subcostal retractions.
Use of accessory muscles for breathing.
Grunting (especially in severe cases)
Diagnosis of bronchiolitis in children
Clinical Diagnosis: Based primarily on history and physical examination (often no need for specific tests).
can do nasopharyngeal swab to check for RSV
Treatment of bronchiolitis in children
Supportive Care:
Oxygen therapy if hypoxic (low oxygen levels).
Hydration (oral or intravenous).
Nasal suctioning to clear secretions, especially in infants.
Bronchodilators and corticosteroids not recommended in children <2 years
Administration of respiratory syncytial virus vaccine to pregnant individuals minimizes the risk of bronchiolitis in young infants.
Differential diagnosis of bronchiolitis in children
Obstructive bronchitis
Asthma
CKD in children
CKD is defined as persistent kidney damage or decreased kidney function (glomerular filtration rate [GFR] < 60 mL/min/1.73 m²) lasting 3 months or more.
causes of CKD in children
Congenital Causes:
Polycystic kidney disease (PKD). mainly autosomal recessive
Congenital anomalies of the urinary tract (e.g., posterior urethral valves, vesicoureteral reflux).
Congenital nephrotic syndrome (e.g., Finnish-type nephrotic syndrome).
Renal dysplasia.
Acquired Causes:
Glomerulonephritis (e.g., post-streptococcal, IgA nephropathy).
Hemolytic uremic syndrome (HUS).
Systemic diseases (e.g., lupus nephritis).
Chronic pyelonephritis.
Hypertension (often secondary to other conditions).
Risk factors for developing CKD in children
Family history of kidney disease.
Congenital kidney abnormalities.
Low birth weight.
Urinary tract infections (UTIs) or recurrent UTIs.
Hypertension.
Diabetes (Type 1 or 2).
Immunologic diseases (e.g., lupus).
Symptoms of CKD in children
Growth failure (poor growth and failure to thrive).
Edema (puffiness, especially around the eyes or legs).
Anemia (fatigue, pallor).
Proteinuria (frothy urine).
Uremic symptoms: nausea, vomiting, anorexia.
Bone pain (due to secondary hyperparathyroidism).
Polyuria or oliguria (in advanced stages).
Developmental delay in children.
: Diagnostic Approach to CKD in Children
Growth patterns
Urinary habits
Family history
Serum creatinine and estimated GFR (eGFR) for assessing kidney function.
Urinalysis: To check for proteinuria, hematuria, and casts.
Urine protein-to-creatinine ratio (important for diagnosing glomerular disease).
Electrolytes: To assess for abnormalities like hyperkalemia or metabolic acidosis.
CBC: To evaluate for anemia.
Albumin: To detect nephrotic syndrome (if applicable).
Ultrasound: To evaluate kidney size, structure, and signs of obstruction or cysts.
Staging of CKD (based on GFR)
Treatment of CKD in children
Control blood pressure: Antihypertensive medications (e.g., ACE inhibitors, ARBs).
Manage proteinuria: ACE inhibitors or ARBs to reduce protein loss.
Erythropoiesis-stimulating agents: To treat anemia (e.g., epoetin alfa).
Vitamin D supplementation: To manage bone mineral disorders.
Phosphate binders: To control hyperphosphatemia.
Electrolyte management: Correct imbalances like hyperkalemia and metabolic acidosis.
Dietary Management:
Low-protein diet may be recommended in advanced stages.
Sodium, potassium, and fluid restrictions in advanced disease.
Renal Replacement Therapy (RRT):
Dialysis (hemodialysis or peritoneal dialysis) is required in end-stage renal disease (ESRD).
Kidney transplantation: Considered for children with ESRD and appropriate donor availability.
COVID 19 in children
caused by the SARS-CoV-2 virus, affects children differently than adults. Most children experience mild or asymptomatic infections,
Epidemiology and Transmission of COVID 19 in children
COVID-19 is less common in children compared to adults, with the majority of cases being mild or asymptomatic.
Transmission: Primarily transmitted through respiratory droplets and aerosols, and can spread via contact with contaminated surfaces.
Risk Factors: Children with underlying chronic health conditions (e.g., asthma, obesity, immunocompromised states) are at higher risk of severe disease.
Symptoms of COVID-19 in Children
MIld to moderate
Severe
Cough.
Fatigue.
Sore throat.
Headache.
Myalgia (muscle aches).
Gastrointestinal symptoms (e.g., diarrhea, nausea, vomiting).
Loss of taste or smell (less common in children compared to adults).
Rash (in some cases).
Difficulty breathing.
Persistent chest pain.
Bluish lips or face.
Severe fatigue.
Confusion or altered mental state.
what is a rare complication of Vocid 19 only seen in children
Multisystem Inflammatory Syndrome in Children (MIS-C)
Symptoms of MIS-C:
Abdominal pain.
Rash (often non-specific).
Conjunctivitis (red eyes).
Swollen hands and feet.
Diarrhea and/or vomiting.
Cranial nerve involvement (e.g., facial weakness).
Shock (in severe cases).
Laboratory Findings:
Elevated inflammatory markers (e.g., CRP, ESR).
Elevated D-dimer.
Low lymphocyte count.
Positive or recent history of SARS-CoV-2 infection.
Treatment:
Intravenous immunoglobulin (IVIG).
Corticosteroids.
Aspirin (for anti-inflammatory and anticoagulation effects).
Supportive care (e.g., oxygen, fluids).
Diagnosis of COVID-19 in Children
PCR (Polymerase Chain Reaction): The gold standard for diagnosing active COVID-19 infection.
Antigen tests: Less sensitive than PCR, but can provide rapid results.
Serology tests: To detect past infection by identifying antibodies (IgM, IgG).
Mild Cases:
Home care with rest, hydration, and over-the-counter medications (e.g., acetaminophen) to manage symptoms.
Monitoring for worsening symptoms (e.g., difficulty breathing).
Severe Cases:
Hospitalization for oxygen therapy, IV fluids, and other supportive measures.
Mechanical ventilation or intubation may be required for severe respiratory distress.
Antiviral treatment (e.g., Remdesivir) and monoclonal antibodies may be considered for high-risk cases.
The Pfizer-BioNTech COVID-19 vaccine is recommended for all children in the US ≥ 5 years of age
Type 1 Diabetes (T1DM):
Usual features and symptoms
Usually thin or normal weight.
Symptoms appear suddenly:
Weight loss without trying.
Polydipsia (excessive thirst), polyuria (frequent urination), polyphagia (excessive hunger).
Fatigue, irritability, blurred vision, frequent infections.
Complication of diabetes type 1
Ketoacidosis: High glucose → Body breaks fat → Ketones → Acidosis.
Positive urine/serum ketones, low pH.
Type 2 Diabetes (T2DM):
usual look
Often overweight.
May be asymptomatic for years.
Common initial signs: Numbness, tingling, fatigue, infections.
Complications:
Atherosclerosis (e.g., CAD, stroke).
Long-term: Retinopathy, nephropathy, neuropathy.
Compensation Goals for diabetes
premeal
post meal
Hba1C
Before bed
Cholestrol
BP
Blood Sugar (Glycemia):
Pre-meal (fasting): 3.9–7.2 mmol/L (70–130 mg/dL).
Post-meal: <10 mmol/L (<180 mg/dL).
HbA1c: 6.0–6.5% (higher if life expectancy is shorter).
Before bed: 6.0–7.0 mmol/L.
Other Goals:
Cholesterol: <5.2 mmol/L.
Blood Pressure: <140/90 mmHg.
Microalbuminuria: Monitor yearly for kidney function.
Follow up and management for diabetes
Monitoring:
Blood pressure, cholesterol, weight, and blood sugar.
Urine microalbumin yearly (Type 1 = 5 years after onset; Type 2 = at diagnosis).
Eye exams (Type 1 = 5 years after onset; Type 2 = at diagnosis).
Vaccination:
Pneumococcal every 5 years; flu annually.
Foot care:
Annual exams, self-care, and proper footwear.
Psychological care:
Screen for depression or cognitive issues.
Non- pharmocological therapy for diabetes
Type 1 DM:
Carb counting: 1 Bread Unit (BU) = 12g carbs = 1 unit of insulin.
Example: 1 potato or 2 tablespoons of rice = 1 BU.
Glycemic index:
Low GI (<55) = Slow blood sugar rise.
High GI (>70) = Fast spikes.
Type 2 DM:
Lifestyle changes:
Stop smoking.
Physical activity.
Balanced diet:
Carbs: 45-60%, Protein: 15-20%, Fats: <35%.
Biguanides (metformin)
: What is the mechanism of action (MOA) of metformin?
Reduces liver glucose production, increases peripheral insulin sensitivity, and reduces intestinal glucose absorption.
Worries about Metformin
Metformin should be used after meal
Due to GI side effects, makes osmotic gradient in intestine atleast 5-7% cannot take metoformin
Should be titrated, so not usually done for outpatient clinic. In clinic it is usally increased in a matter of 3 days if there is gastrointestinal side effects.
Mean therapeutical dosage is 2grams (1000 morning, 1000 evening)
Metformin goes through urine in unchanged form
GFR < 30 mL/min/1.73 m²: Metformin is absolutely
o If iv contrast, should stop metformin one day before!
Metformin can increase lactate, works on mitochondria, if body builder and stuff cannot use (lactic acidosis). If sedentary lifestyle 2000mg
What are the main benefits of metformin?
High efficacy in lowering blood sugar.
Minimal risk of hypoglycemia (when used alone).
May cause slight weight loss.
Low cost.
What are the common side effects of metformin?
Gastrointestinal upset (nausea, diarrhea).
Vitamin B12 deficiency with long-term use.
Rare but serious: Lactic acidosis.
When is metformin contraindicated?
Severe kidney disease (eGFR <30 mL/min).
Use with caution if eGFR is 30–45 mL/min.
Severe liver disease, alcoholism, or history of lactic acidosis.
What is the mechanism of action of sulfonylureas and name examples
glimepiride, gliclazide
Stimulates insulin secretion from pancreatic beta cells by closing ATP-sensitive potassium channels.
What are the common side effects of sulfonylureas?
Weight gain.
Hypoglycemia (especially with missed meals or overdose).
May lose efficacy over time (beta-cell burnout).
When are sulfonylureas contraindicated?
Severe kidney or liver dysfunction.
Meglitinides (Glinides)
What is the MOA of meglitinides and examples?
repaglinide, nateglinide
Similar to sulfonylureas, they stimulate insulin release but have a shorter duration of action.
What are the advantages of meglitinides over sulfonylureas?
Reduced risk of hypoglycemia.
Useful for controlling postprandial glucose.
What are the side effects of meglitinides?
Hypoglycemia (less frequent than sulfonylureas).
Thiazolidinediones (TZDs)
What is the MOA of thiazolidinediones and examples
pioglitazone, rosiglitazone
: Improves insulin sensitivity in muscle and fat tissue by binding to PPAR-γ receptors.
What are the benefits of TZDs?
No hypoglycemia (when used alone).
Improves lipid profile (increases HDL).
Long-lasting glucose-lowering effect.
What are the side effects of TZDs?
Fluid retention (risk of heart failure).
Risk of bone fractures.
Bladder cance
When are TZDs contraindicated?
Heart failure (NYHA Class III/IV).
Active bladder cancer or history of it.
SGLT2 Inhibitors
What is the MOA of SGLT2 inhibitors and examples
Empagliflozin, canagliflozin)
Inhibit sodium-glucose co-transporter 2 in the kidneys, causing increased glucose excretion in urine.
What are the benefits of SGLT2 inhibitors?
Weight loss.
Blood pressure reduction.
Cardiovascular and renal protective effects.
What are the side effects of SGLT2 inhibitors?
Genital infections (e.g., yeast infections).
Increased risk of UTIs.
Dehydration (orthostatic hypotension).
Risk of diabetic ketoacidosis.
When are SGLT2 inhibitors contraindicated?
Frequent urinary tract infections.
GLP-1 Receptor Agonists
MOA and examples
exenatide
Enhances insulin secretion.
Suppresses glucagon secretion.
Slows gastric emptying (increases satiety).
What are the benefits of GLP-1 receptor agonists?
Effective weight loss.
Low risk of hypoglycemia.
Cardiovascular benefits.
What are the side effects of GLP-1 receptor agonists?
Nausea, vomiting, diarrhea.
Rare risk of pancreatitis.
Gallbladder issues.
DPP-4 Inhibitors - MOA and examples
sitagliptin, linagliptin
Inhibits DPP-4 enzyme, increasing levels of GLP-1 and GIP → Increases insulin secretion and suppresses glucagon after meals.
What are the advantages of DPP-4 inhibitors?
Oral, well-tolerated.
No weight gain.
Low hypoglycemia risk.
Combination therapy in diabetes
Metformin + SGLT2 inhibitors.
Metformin + GLP-1 receptor agonists.
Avoid combining sulfonylureas and meglitinides (same MOA → Hypoglycemia).
Caution with SGLT2 inhibitors + diuretics (dehydration risk).
What is the mechanism behind ketoacidosis in T1DM?
Lack of insulin leads to glucose not being used by cells.
Lipids are broken down via beta-oxidation, increasing acetyl-CoA and ketone body production.
Ketones lower blood pH, causing metabolic acidosis (evident by Kussmaul breathing).
What causes fruity breath in ketoacidosis?
: Elevated ketone bodies, particularly acetone.
Why does Kussmaul breathing occur in ketoacidosis?
Acidosis stimulates peripheral chemoreceptors, causing deep, rapid breathing to expel CO2 and reduce acidity.
What electrolyte imbalance is common in ketoacidosis?
Hyperkalemia (potassium moves out of cells due to lack of insulin).
Q: What is insulin resistance?
A reduced ability of insulin to stimulate glucose uptake and utilization in muscle, adipose tissue, and liver.
How does obesity contribute to insulin resistance?
Visceral fat releases inflammatory cytokines (e.g., TNF-α, IL-6) and free fatty acids, impairing insulin signaling.
Central obesity increases cardiovascular risk via pro-inflammatory states.
What is the role of inflammation in insulin resistance?
Chronic low-grade inflammation disrupts insulin signaling pathways, mediated by cytokines like TNF-α.
Why is visceral fat more metabolically active than peripheral fat?
: It releases more free fatty acids and inflammatory molecules, increasing insulin resistance.
What is the lower limit of fasting plasma glucose in diabetics to define hypoglycemia?
Below 3.9 mmol/L.
What are the neurogenic symptoms of hypoglycemia?A:
Tremor, pallor, tachycardia, sweating.
Anxiety and hunger (sympathetic activity).
What are neuroglycopenic symptoms of hypoglycemia?
Confusion, agitation, drowsiness, or coma.
Seizures or focal neurological deficits in severe cases.
How is hypoglycemia treated in a conscious patient?
Oral glucose: 15-20g of fast-acting carbohydrates like candy or juice.
How is hypoglycemia treated in a non conscious patient?
- In hospital: 25 g of 50% glucose IV (dextrose) and regular serum glucose monitoring.
- If oral and IV not avaliable: 0.5-1.0 mg glucagon IM or SC
What is visceral obesity, and why is it more harmful?
Fat around the abdomen and organs, associated with:
Higher inflammatory cytokines.
Increased free fatty acids → insulin resistance.
Greater risk of cardiovascular disease.
What is peripheral obesity?
Subcutaneous fat in areas like thighs and hips, releasing fewer free fatty acids and cytokines, with lower metabolic risk.
Why is foot care essential in diabetics?
: What does routine foot care involve?
To prevent ulcers, infections, and amputations due to neuropathy and poor circulation.
Daily inspection and cleaning.
Wearing well-fitting shoes.
Annual professional exams.
“apple type obesity” refers to the pattern of fat accumulation around abdomen and visceral organs.
Associated with higher risk of obesity
risk of cardiovascular diseases
This means more free fatty acid and inflamatory moleculres into the bloodstream, increased insulin resistance, hypertension, high cholestrol and atherosclerosis. All these likelyhood of cardiovascular diseases.
Hypogonadism is common in men with central obesity and can contribute to further fat accumulation in the abdominal area.
Coeliac Disease in Children:
Pathophysiology
Trigger: Gluten ingestion leads to an immune response that damages the intestinal mucosa.
These autoantibodies target the epithelial cells of the small intestine, leading to inflammation. These antibodies relate to disease activity and will rise with more active disease and may disappear with effective management.
The inflammation affects?
Inflammation affects the small bowel, particularly the jejunum. The surface of the small intestine is covered in projections called villi, which increase the surface area and help with nutrient absorption. Coeliac disease causes atrophy of the intestinal villi, resulting in malabsorption.
What are the antibodies associated
Anti-tissue transglutaminase antibodies (anti-TTG)
Anti-endomysial antibodies (anti-EMA)
Mechanism
Gluten peptides, especially gliadin, are deamidated by tissue transglutaminase (tTG).
These peptides bind to HLA-DQ2 or HLA-DQ8 molecules on antigen-presenting cells, activating T-cells.
Results in villous atrophy, crypt hyperplasia, and chronic inflammation of the sm
Presentation
Coeliac disease is often asymptomatic and is under-diagnosed, so have a low threshold for testing for coeliac disease in patients where it is suspected.
Presenting symptoms can include:
Failure to thrive in young children (short stature)
Diarrhoea
Bloating
Fatigue
Weight loss
Mouth ulcers
Dermatitis herpetiformis is an itchy, blistering skin rash, typically on the abdomen, caused by coeliac disease.
Anaemia occurs secondary to malabsorption and deficiency of iron, B12 or folate.
Rarely coeliac disease can present with neurological symptoms:
Peripheral neuropathy
Cerebellar ataxia
Epilepsy
Diagnosis
The patient must continue eating gluten while being investigated. Antibodies and histology may be normal if the patient is gluten-free.
The first-line blood tests are:
Total immunoglobulin A levels (to exclude IgA deficiency)
Anti-endomysial antibodies (anti-EMA) are a second-line option where there is doubt (e.g., a borderline result).
HLA testing: HLA- DQ2/ DQ8
Patients with a positive antibody test are referred to a gastroenterologist to confirm the diagnosis by endoscopy and jejunal biopsy. Typical biopsy findings are:
Crypt hyperplasia
Villous atrophy
Management and complications
A lifelong gluten-free diet should completely resolve the symptoms. Dietician input may be helpful. Relapse will occur upon consuming gluten. Coeliac antibodies may help monitor the disease.
Nutritional deficiencies
Anaemia
Osteoporosis
Hyposplenism (with immunodeficiency, particularly to encapsulated bacteria such as Streptococcus pneumoniae)
Ulcerative jejunitis
Enteropathy-associated T-cell lymphoma (EATL)
Non-Hodgkin lymphoma
Small bowel adenocarcinoma
Croup in children
Croup (Laryngotracheobronchitis)
A viral respiratory infection causing inflammation of the larynx, trachea, and bronchi, leading to airway narrowing and the classic barking cough.
common age affected in croup
children aged 6 months to 3 years (peak at 2 years).
etiology of croup
Viral infection (most common):
Parainfluenza virus (Type 1 & 3): Primary cause.
Others:
Respiratory Syncytial Virus (RSV).
Influenza A & B.
Rarer causes: Measles virus.
Pathophysiology of croup
Viral infection → inflammation and edema of the subglottic region of the airway → narrowing.
Subglottic region is the narrowest part of the pediatric airway, making children more susceptible.
Results in stridor (due to turbulent airflow), barking cough, and respiratory distress.
Symptoms of croup
Prodromal symptoms (early stage):
Non-barking cough.
Coryza (runny nose, congestion).
Low-grade fever.
Acute Symptoms:
Barking cough: Seal-like, worse at night.
Hoarse voice.
Inspiratory stridor (high-pitched sound on inspiration). (same found in acute laryngitis)
Respiratory distress:
Chest retractions (intercostal, subcostal, and suprasternal).
Fever: May or may not be present.
Symptoms often worsen with agitation or crying, so calm the child.
Diagnosis of croup
Clinical Diagnosis:
Based on symptoms: barking cough, stridor, and respiratory distress.
(clinical diagnosis, same done for acute laryngitis, if needed Xray)
Not routinely needed but can help in severe or atypical cases.
Neck X-ray:
Classic finding: Steeple sign (narrowing of the subglottic trachea).
Differential DIagnosis of croup
Epiglottitis
bacterial trachitis
foreign body aspiration
anaphylacis
management of croup
Mild Croup:
Antipyretics: Paracetamol or ibuprofen for fever.
Humidified air: May help soothe inflamed airway.
Moderate Croup:
Corticosteroids:
Oral dexamethasone (0.15–0.6 mg/kg, max 10 mg) is the first-line treatment.
Reduces airway swelling and duration of symptoms.
Onset: Within 1–2 hours.
Consider nebulized budesonide in certain cases.
Severe Croup:
Nebulized adrenaline (epinephrine):
For significant respiratory distress or stridor at rest.
Provides temporary airway relief (vasoconstriction reduces edema).
Always follow with corticosteroids (to prevent rebound symptoms).
Oxygen therapy: For hypoxemia (SpO₂ < 92%).
Intubation: Rare, but consider if respiratory failure develops.
Cystic Fibrosis (paed)
is an autosomal recessive genetic disorder caused by mutations in the CFTR gene (Cystic Fibrosis Transmembrane Conductance Regulator).
Pathogenesis of cystic fibrosis (paed)
Dysfunctino of chloride and sodium ion transport, thick sticky secretions in multiple organs.
Due to chloride not being able to go into mucus, water from mucus goes inside the cell drying up the mucous and reducing ability of airway clearance.
Key consequences of cystic fibrosis (paed)
Thick pancreatic and biliary secretions that cause blockage of the ducts, resulting in a lack of digestive enzymes such as pancreatic lipase in the digestive tract
Low volume thick airway secretions that reduce airway clearance, resulting in bacterial colonisation and susceptibility to airway infections
Congenital bilateral absence of the vas deferens in males. Patients generally have healthy sperm, but the sperm have no way of getting from the testes to the ejaculate, resulting in male infertility
Presentation in new born of cystic fibrosis
Cystic fibrosis is screened for at birth with the newborn bloodspot test.
Meconium ileus is often the first sign of cystic fibrosis. The first stool that a baby passes is called meconium.
This is usually black and should be passed within 24 hours of birth. In about 20% of
babies with CF, the meconium is thick and sticky, causing it to get stuck and obstruct the bowel. This is called meconium ileus, and is practically pathognomonic for cystic fibrosis. This presents as not passing meconium within 24 hours, abdominal distention and vomiting.
If cystic fibrosis is not diagnosed shortly after birth it can present later in childhood with typical signs and symptoms, recurrent lower respiratory tract infections, failure to thrive or pancreatitis.
Symptoms of cystic fibrosis
Chronic cough
Thick sputum production
Recurrent respiratory tract infections
Loose, greasy stools (steatorrhoea) due to a lack of fat digesting lipase enzymes
Abdominal pain and bloating
Parents may report the child tastes particularly salty when they kiss them, due to the concentrated salt in the sweat
Poor weight and height gain (failure to thrive)
finger clubbing
Diagnosis of cystic fibrosis (paed)
Newborn blood spot testing is performed on all children shortly after birth and picks up most cases
The sweat test is the gold standard for diagnosis
Genetic testing for CFTR gene can be performed during pregnancy by amniocentesis or chorionic villous sampling, or as a blood test after birth
Sweat Test
The sweat test is the key investigation to remember for cystic fibrosis. It is the gold standard for confirming the diagnosis. A patch of skin is chosen for the test, typically on the arm or leg. Pilocarpine is applied to the skin on this patch. Electrodes are placed either side of the patch and a small current is passed between the electrodes. This causes the skin to sweat. The sweat is absorbed with lab issued gauze or filter paper and sent to the lab for testing for the chloride concentration. The diagnostic chloride concentration for cystic fibrosis is more than 60mmol/l.
Management of cystic fibrosis (paed)
Airway clearance:
Chest physiotherapy: Postural drainage, percussion.
Mucolytics:
Dornase alfa (DNase): Breaks down mucus.
Hypertonic saline: Improves mucus clearance.
Bronchodilators: Albuterol for wheezing.
Oral, IV, or inhaled for infections (e.g., tobramycin for Pseudomonas).
Prophylactic antibiotics in some cases.
Anti-inflammatory therapies:
Azithromycin (chronic use for inflammation and infection suppression).
Lung transplant in advanced disease.
Pancreatic enzyme replacement therapy (PERT):
Improves digestion of fats and proteins.
High-calorie, high-protein diet:
Supplementation with fat-soluble vitamins (A, D, E, K).
Treat meconium ileus with enemas or surgery if needed.
Ursodeoxycholic acid for liver disease.
Adequate hydration and electrolyte replacement during hot weather or exercise.
Complications of cystic fibrosis (paed)
Respiratory:
Chronic respiratory failure.
Pulmonary hypertension → Cor pulmonale.
Bronchiectasis.
Gastrointestinal:
Pancreatitis.
Biliary cirrhosis.
Intestinal obstruction (distal intestinal obstructive syndrome).
Endocrine:
CF-related diabetes mellitus (CFRD).
Reproductive:
Male infertility.
What is Congenital Heart Disease (CHD)?
What are the causes of CHD?
Structural or functional abnormalities of the heart or great vessels present at birth, affecting 0.8–1% of live births.
Genetic Factors (10–15%)
Chromosomal abnormalities: Down Syndrome, Turner Syndrome, DiGeorge Syndrome.
Single-gene mutations: Noonan Syndrome, Marfan Syndrome.
Environmental Factors:
Maternal illnesses: Diabetes mellitus, rubella, phenylketonuria.
Drug/toxin exposure: Alcohol, lithium, antiepileptics, smokin
How is Congenital heart disease classified
Acyanotic CHD (Left-to-right shunt)
Cyanotic CHD (Right-to-left shunt)
Obstructive Lesions
What defects are classified as Acyanotic CHD?
Atrial Septal Defect (ASD)
Ventricular Septal Defect (VSD)
Patent Ductus Arteriosus (PDA)
Atrioventricular Septal Defect (AVSD)
What are the clinical features of Acyanotic CHD?
Symptoms: Breathlessness, fatigue, frequent respiratory infections, poor growth, failure to thrive.
What defects are classified as Cyanotic CHD?
Truncus Arteriosus
Transposition of the Great Arteries
Tricuspid Atresia
Tetralogy of Fallor
Total Anamalous Pulmonary Venous Return
What are the clinical features of Cyanotic CHD?
Cyanosis, clubbing, growth failure, "Tet spells" (hypercyanotic episodes in TOF).
Murmur:
Tetrology of fallot : Harsh systolic ejection murmur (pulmonary stenosis).
What is a "Tet spell," and how is it managed?
Tet Spell: Sudden cyanosis triggered by exertion/crying in TOF.
Management: Knee-chest position, oxygen, beta-blockers.
What defects are classified as Obstructive CHD?
what are the symptoms?
Coarctation of the Aorta (CoA)
Pulmonary Stenosis (PS)
Aortic Stenosis (AS)
Infants: Heart failure, shock.
Older children: Hypertension (upper limbs), weak/absent femoral pulses, claudication.
What is the diagnostic workup for congenital heart disease?
Clinical Examination: Cyanosis, murmurs, clubbing, failure to thrive.
Pulse Oximetry: Detects hypoxemia.
Chest X-ray:
Tetrology of fallot : Boot-shaped heart.
Transposition of great arteries : Egg on a string.
Echocardiography: Gold standard.
ECG: Chamber enlargement/hypertrophy.
Cardiac Catheterization: Measures pressures, confirms diagnosis.
What are the general management principles for CHD?
Correct hemodynamic instability with oxygen, fluids, inotropes.
Prostaglandin E1 (PGE1): Maintains ductal patency in duct-dependent lesions (TOF, TGA, CoA).
diureitcs and ace inhibitors: to mange heart failure with large left to right shunts
Bb blockers for infants with tetrology of fallor to reduce frequency of tet spells
Corrective surgery
Heart transplant if no other treatment is viable
Dehydration in paed
Defintion
Dehydration refers to a deficit in total body water, occurring when fluid losses exceed intake. It is one of the most common pediatric conditions, especially in younger children due to higher water turnover and metabolic rates.
Dehydration in Pediatrics
Types of Dehydration
Isotonic (Isonatremic):
Most common in children (~80% of cases).
Equal loss of water and sodium.
Sodium: 135–145 mmol/L.
Causes: Acute diarrhea, vomiting.
Hypotonic (Hyponatremic):
Greater sodium loss than water.
Sodium: <135 mmol/L.
Causes: Prolonged diarrhea, inappropriate replacement with hypotonic fluids (e.g., water, dilute ORS).
Hypertonic (Hypernatremic):
Greater water loss than sodium.
Sodium: >145 mmol/L.
Causes: High fever, severe vomiting/diarrhea, improper rehydration with hypertonic fluids (e.g., soda, salt solutions).
Common Causes of Dehydration in Pediatrics
Gastrointestinal Losses: (gastroenteritis) Diarrhea, vomiting.
Increased Insensible Losses: Fever, burns, sweating.
Decreased Intake: Illness, difficulty feeding.
Renal Losses: Diuretics, diabetes insipidus, osmotic diuresis (e.g., DKA).
Assessment of Dehydration in paed
Fluid management in dehdration
>80 kg = 2700 ml/kg
for fluid requirement in children
Fluid repeacement strategy for children (ORT)
Mild Dehydration:
Oral Rehydration Therapy (ORT):
Use ORS (oral rehydration solution) containing sodium, glucose, potassium, chloride, and water.
Dose: 50 mL/kg over 4–6 hours, plus ongoing losses.
Example: A 10 kg child → 10×50=500 mL over 4–6 hours10 \times 50 = 500 \, \text{mL over 4–6 hours}10×50=500mL over 4–6 hours.
Moderate Dehydration:
ORT or IV Fluids:
Start with ORS if tolerated, else use IV fluids.
Dose: 100 mL/kg over 4–6 hours, plus maintenance and ongoing losses.
Severe Dehydration:
IV Fluid Resuscitation:
Resuscitation Bolus:
Use Normal Saline (0.9% NaCl) or Ringer’s Lactate.
Dose: 10–20 mL/kg IV over 30–60 minutes, repeat as necessary.
Deficit Correction:
Replace deficit over 24–48 hours with isotonic fluids.
Maintenance Fluids:
Add to ongoing therapy as per Holliday-Segar formula.
What is developmental delay?
A condition where a child does not reach developmental milestones at the expected time compared to peers.
What are the types of developmental delays?
Gross Motor Delay
Fine Motor Delay
Speech and Language Delay
Social and Emotional Delay
Cognitive Delay
Name two common causes of developmental delay.
Genetic conditions (e.g., Down syndrome) and prematurity.
What are warning signs of developmental delay in infants (0-12 months)?
Lack of smiling or eye contact.
Not rolling over, sitting, or crawling at expected ages.
t what age should a child say single words to avoid concern for delay?
By 16 months.
What are some specialized tests for diagnosing developmental delay?
Genetic testing (e.g., karyotyping).
Brain imaging (e.g., MRI, CT scan).
Metabolic screening.
Name two therapies used in the management of developmental delay.
List two environmental causes of developmental delay.
Speech Therapy
Physical Therapy
Neglect and lack of stimulation.
Febrile Convulsions in Pediatrics
Febrile convulsions (FC) are seizures occurring in children
aged 6 months to 5 years, associated with fever (≥38°C)
without evidence of intracranial infection or another identifiable cause of seizures.
Classification of febrile convulsions
SImple
Complex
generalized tonic clonic seizure
focal features (affection on one side of the body)
Duration <15 minutes
duration >15 minutes
occurs once in 24 hours period
recurs within 24 hours
no postictal neurological deficits
postictal neurological abnormalities
clinical presentation of febrile convulsions
Fever >38°C.
Seizure activity:
Simple: Generalized tonic-clonic movements.
Complex: Focal movements or prolonged seizure.
Postictal drowsiness in some cases.
differential diagnosis of febrile convlusions in paed
Meningitis/Encephalitis: Rule out with lumbar puncture if suspected.
Epilepsy: Recurrent afebrile seizures.
Metabolic Disorders: Hypoglycemia, hyponatremia
Diagnosis of febrile convulsions
History and Examination:
Detailed history of fever and seizure episode.
Family history of febrile convulsions/epilepsy.
Physical exam to assess fever source.
Investigations:
Blood Tests: Rarely required, only if metabolic cause suspected.
Lumbar Puncture:
Indicated if signs of meningitis/encephalitis.
Strongly considered in infants <12 months.
Neuroimaging (CT/MRI): Indicated for focal/complex seizures or abnormal neurological exam.
EEG: Not routinely recommended for simple febrile seizures.
Management of febrile convulsions
During the Seizure:
Place the child in a safe position (on their side to avoid aspiration).
Do not restrain movements or put anything in the mouth.
Monitor duration of the seizure.
Post-Seizure Care:
Treat the fever: Antipyretics (e.g., paracetamol, ibuprofen).
Address the underlying cause of fever (e.g., viral or bacterial infection).
Hospitalization for prolonged, complex, or recurrent seizures.
Medications:
Abortive Therapy (if seizure lasts >5 minutes):
Diazepam (rectal) or lorazepam (IV).
Midazolam (intranasal or buccal).
What is the primary cause of Type 1 Diabetes Mellitus (T1DM) in the pediatric population?
Autoimmune destruction of pancreatic beta cells, leading to absolute insulin deficiency.
How is Type 1 Diabetes Mellitus diagnosed in the pediatric population?
Blood Glucose: Random ≥11.1 mmol/L (≥200 mg/dL) with symptoms or fasting ≥7.0 mmol/L (≥126 mg/dL).
HbA1c: ≥6.5%.
Autoantibodies: GAD65, IA-2, ZnT8.
C-Peptide: Low or absent.
What is the cornerstone of treatment for T1DM in the pediatric population?
Insulin therapy (basal-bolus or insulin pump), blood glucose monitoring, carbohydrate counting, and regular physical activity.
What are the primary causes of Type 2 Diabetes Mellitus (T2DM) in the pediatric population?
Insulin resistance due to obesity and inactivity.
Progressive beta-cell dysfunction over time.
Genetic predisposition and hormonal changes during puberty.
How does T2DM differ from T1DM in clinical presentation in the pediatric population?
T2DM has a slower onset, often with mild polyuria, polydipsia, and fatigue.
Associated with overweight/obesity and acanthosis nigricans.
What are the key management strategies for T2DM in the pediatric population?
Lifestyle modifications: Diet and exercise for weight loss.
Medications: Metformin, GLP-1 receptor agonists, or insulin if necessary.
Blood glucose and HbA1c monitoring.
What is Diabetic Ketoacidosis (DKA), and why does it occur in the pediatric population?
A life-threatening complication of diabetes caused by severe insulin deficiency, leading to hyperglycemia, ketosis, and metabolic acidosis.
What are the most common causes of DKA in the pediatric population?
Newly diagnosed T1DM.
Missed insulin doses.
Severe infections or stress.
What are the hallmark clinical features of DKA in the pediatric population?
Early Symptoms: Polyuria, polydipsia, weight loss, fatigue.
Severe Symptoms: Abdominal pain, nausea, vomiting, Kussmaul breathing, fruity breath, and dehydration.
What is the initial treatment of DKA in the pediatric population?
Fluids: Isotonic saline (10–20 mL/kg over 1–2 hours).
Insulin: Low-dose IV insulin (0.05–0.1 units/kg/hour).
Electrolytes: Potassium supplementation once urine output is confirmed.
What is the most common life-threatening complication of DKA in the pediatric population?
Cerebral edema,
key differences in diabetes comparing adults and children
Cerebral Edema Risk: Much higher in children with DKA due to brain sensitivity and fluid shifts.
Comorbidities: Adults often have pre-existing conditions like cardiovascular disease, making management more complex.
Fluid Management: More cautious in children to avoid cerebral edema; more aggressive in adults to address larger fluid deficits.
Diabetes Type Prevalence: T1DM dominates in children, while T2DM is more common in adults.
What are the two main categories of lower urinary tract symptoms
Irritative Symptoms (Storage LUTS):
Urinary frequency, urgency, urge incontinence, nocturia, dysuria.
Obstructive Symptoms (Voiding LUTS):
Hesitancy, straining to urinate, poor/intermittent stream, terminal dribbling, incomplete voiding, acute urinary retention.
What symptoms can BPH cause?
LUTS (both storage and voiding symptoms).
Gross hematuria (possible in advanced cases).
hat are the findings on a digital rectal exam (DRE) in BPH?
Symmetrically enlarged, smooth, firm, nontender prostate with a rubbery or elastic texture.
What tools and assessments help diagnose BPH?
History and physical examination.
Voiding diary (tracks frequency and volume).
Symptom severity scores (e.g., IPSS, DAN-PSS-1).
Labs: PSA (optional, especially if cancer is suspected).
Imaging: US, TRUS (if complications or biopsy is needed).
What are important PSA thresholds in BPH evaluation?
PSA >1.5 ng/mL: Suggests prostate volume >40 mL.
PSA >4 ng/mL: Increases risk of prostate cancer.
What causes LUTS in BPH?
Bladder outlet obstruction (BOO) due to prostatic enlargement or overactive bladder (OAB).
What is the first-line drug treatment for LUTS in BPH?
Alpha-1 blockers (e.g., tamsulosin, doxazosin).
Relaxes smooth muscle in the bladder neck and prostate.
Used when prostate is small (PSA <1.5 ng/mL).
Key Side Effect: Orthostatic hypotension, especially in elderly.
What drugs reduce prostate size in BPH?
5-alpha reductase inhibitors (5-ARIs): Finasteride, dutasteride.
Inhibits conversion of testosterone to DHT, reducing growth.
Effective for large prostates.
Side Effects: Sexual dysfunction, gynecomastia.
What is the role of antimuscarinics (e.g., tolterodine, oxybutynin) in BPH?
Treats overactive bladder symptoms by relaxing the detrusor muscle.
When is combination therapy used for BPH?
severe symptoms or inadequate relief by singular agent
Alpha-blocker + 5-ARI: For bladder outlet obstruction with severe symptoms.
Alpha-blocker + antimuscarinic: For Bladder outlet obstruction + overactive bladder symptoms.
What is the gold standard surgical treatment for BPH?
Transurethral Resection of the Prostate (TURP):
Removes hyperplastic prostatic tissue using a resectoscope.
Risks: TURP syndrome (fluid overload), bleeding.
What are alternative surgical options for large prostates (>60g)?
Open/laparoscopic prostatectomy.
Laser enucleation (holmium/thulium).
What are early symptoms of prostate cancer?
Asymptomatic in early stages.
May present with LUTS: Frequency, weak stream.
Hematuria or incontinence if bladder invasion occurs.
What symptoms suggest advanced prostate cancer?
Bone pain (metastasis).
Neurological deficits.
Weight loss and fatigue
How is prostate cancer diagnosed?
What imaging is used for staging prostate cancer?
PSA: Elevated (>4 ng/mL), but values can vary. PSA/PsA ratio not increased
DRE: Nodules, asymmetry, loss of sulcus.
Biopsy (TRUS-guided): Gleason grading (2–10).
CT/MRI: For local and lymph node spread.
Bone scan (technetium-99): To detect bone metastases.
: What is the Gleason grading system
Score 2–6: Low risk.
Score 7: Intermediate risk.
Score 8–10: High risk.
used for prostate cancer
What are treatment options for localized prostate cancer?
Active surveillance (low-risk).
Radical prostatectomy (curative).
Radiation therapy (curative alternative).
What are options for advanced/metastatic prostate cancer?
Androgen Deprivation Therapy (ADT):
LHRH agonists (goserelin).
Orchiectomy (irreversible).
Chemotherapy: Docetaxel for metastatic disease.
Palliative Radiation: For bone metastases.
What are novel therapies for prostate cancer? (other approaches)
Brachytherapy: Radioactive seeds implanted in the prostate.
Cryotherapy: Freezing tissue to induce necrosis.
High-Intensity Focused Ultrasound (HIFU): For low-risk cases.
What is androgen deprivation therapy, and how does it work?
Suppresses androgen production or blocks androgen receptors to slow prostate cancer progression.
How do BPH and prostate cancer differ in presentation?
BPH: Symmetric enlargement, no hard nodules.
Cancer: Hard nodules, asymmetry, elevated PSA, or systemic symptoms in advanced stages.
How does PSA help differentiate between BPH and prostate cancer?
BPH: PSA <1.5 ng/mL typically.
Cancer: PSA >4 ng/mL, with a lower free PSA ratio (<25%
What is a hydrocele?
Painless accumulation of fluid in the tunica vaginalis around one or both testicles.
What are the types and causes of hydrocele?
Idiopathic: Most common.
Congenital:
Communicating: Failure of processus vaginalis closure.
Non-communicating: No connection to peritoneal cavity.
Acquired:
Trauma, tumor, torsion, infection.
Lymphatic filariasis: Wuchereria bancrofti.
How is hydrocele diagnosed?
Clinical exam: Fluctuating, painless scrotal swelling.
Transillumination Test: Scrotum shines under light.
Ultrasound: Hypoechoic fluid confirms diagnosis.
What are the treatment options for hydrocele?
Congenital Hydrocele: Resolves by 6 months; no intervention.
Surgery Indications:
No resolution by 1 year.
Discomfort, compromised scrotal skin, suspected pathology, or infertility concerns.
Techniques:
Hydrocelectomy.
Percutaneous aspiration + sclerosing agent (for adults).
What are the clinical features of testicular torsion?
Abrupt, severe testicular/lower abdominal pain.
Swollen, tender testis.
Absent cremasteric reflex.
Negative Prehn sign (lifting scrotum doesn’t relieve pain).
How is testicular torsion diagnosed?
Clinical diagnosis primarily.
Ultrasound:
Whirlpool Sign: Twisted spermatic cord.
Reduced blood flow.
Heterogeneous parenchyma: Suggests necrosis.
What is the treatment for testicular torsion?
Emergency Surgery (within 6 hours):
Detorsion and orchidopexy (fixation) of both testicles.
Orchiectomy if necrosis.
Manual detorsion may be attempted but requires follow-up surgery.
What are the types of urinary stones and their causes?
Calcium Oxalate (75%): Hypercalciuria, hyperoxaluria, hypocitraturia.
Uric Acid (10%): Gout, hyperuricemia, high protein diet.
Struvite: UTI with urease-producing bacteria (e.g., Proteus).
Calcium Phosphate: Alkaline urine, hyperparathyroidism.
Cystine/Xanthine: Rare, inherited.
What are the symptoms of renal colic?
Severe, colicky unilateral flank pain.
Hematuria, nausea, vomiting.
Dysuria, urgency, frequency.
Fever and chills (if infected).
How is renal colic diagnosed?
Clinical symptoms + labs (CBC, BMP, b-hCG, urinalysis).
Imaging: CT abdomen/pelvis without contrast is the gold standard.
Ultrasound for pregnant patients.
what is renal colic
a specific type of pain caused by urinary stones or other urinary tract disorders.
What is the treatment for renal colic?
Symptomatic: NSAIDs (first-line), opioids if severe pain.
Specific Treatment for Stones:
<10 mm: Medical expulsive therapy (alpha-blockers like tamsulosin).
10–20 mm: Ureterorenoscopy or ESWL.
20 mm or complex stones: Percutaneous nephrolithotomy this is last resort
What is phimosis, and what are its causes?
Tight foreskin that cannot be retracted over the glans.
Causes: Post-infectious, congenital, scarring, poor hygiene, skin conditions.
How is phimosis treated?
Conservative: Steroid creams (e.g., betamethasone) + stretching exercises.
Surgical: Preputioplasty or circumcision.
What is paraphimosis, and how is it treated?
Retracted foreskin that cannot return to its normal position.
Manual reduction with pain control.
If reduction fails: Dorsal slit or circumcision.
What are the symptoms of urinary bladder cancer?
Early: Painless gross hematuria.
Later: Dysuria, frequency, urgency, suprapubic pain.
Advanced: Palpable mass, perineal pain, BOO symptoms.
How is urinary bladder cancer diagnosed?
Three Whales:
Urine cytology.
Fibrocystoscopy.
CT urography (gold standard).
Imaging: CT/MR urography, renal US.
Cystoscopy with biopsy (if lesions are seen).
What are the treatment options for urinary bladder cancer?
Non-invasive tumors:
TURBT (resection) + intravesical BCG (this BCG vaccine is a weakened tubculous bacterium stimulating immune system to attack residual cancer cells) or chemotherapy.
Regular follow-ups every 3 months.
Invasive tumors (non-metastatic):
Radical cystectomy + neoadjuvant chemotherapy.
Bladder preservation: Transuretheral resection of bladder tumor + chemo + radiation.
Metastatic: Cisplatin-based palliative chemotherapy.
What is the difference between incontinent and continent urinary diversions after cystectomy?
Incontinent: Urine is diverted to a bag (e.g., Bricker operation).
Continent:
Ureterosigmoidostomy: Urine passes through the anal sphincter.
Orthotopic bladder substitution: New bladder formed from intestines.
What is pediatric glomerulonephritis?
Inflammation of the glomeruli in children, leading to symptoms such as hematuria, proteinuria, edema, and altered renal function. It can be caused by primary renal diseases or secondary to systemic conditions.
How is pediatric glomerulonephritis classified based on presentation?
Acute Glomerulonephritis (AGN): Sudden onset of hematuria, edema, and hypertension.
Chronic Glomerulonephritis (CGN): Gradual progression to renal dysfunction over months or years.
Rapidly Progressive Glomerulonephritis (RPGN): Severe renal dysfunction progressing over weeks with crescents on biopsy.
What are the primary and secondary causes of pediatric glomerulonephritis?
Primary Causes:
Minimal Change Disease (MCD),
IgA Nephropathy,
Membranoproliferative Glomerulonephritis (MPGN).
Secondary Causes:
Post-Streptococcal Glomerulonephritis (PSGN): Common after streptococcal infections.
Henoch-Schönlein Purpura (HSP): A vasculitis with IgA deposition.
Lupus Nephritis: Associated with systemic lupus erythematosus (SLE).
ANCA-Associated Vasculitis: Autoimmune small vessel vasculitis.
What is the pathophysiology of pediatric glomerulonephritis?
Immune Complex Deposition: Triggers inflammation, complement activation, and glomerular injury (e.g., PSGN, SLE).
Autoantibodies: Target glomerular components (e.g., Goodpasture syndrome, lupus nephritis).
Direct Injury: Caused by infections, toxins, or systemic conditions.
What are the clinical features of pediatric nephritic syndrome?
Hematuria: Cola-colored urine. (esp post streptococcal)
Proteinuria: Mild to moderate (<3.5 g/day).
Edema: Periorbital, worse in the morning.
Hypertension: Due to sodium and fluid retention.
Oliguria: Reduced urine output.
Systemic Symptoms: Fever, malaise in cases with infections
What is the hallmark presentation of pediatric nephrotic syndrome compared to nephritic syndrome?
Feature
Nephritic Syndrome
Nephrotic Syndrome
Proteinuria
Mild to moderate (<3.5 g/day).
Severe (>3.5 g/day).
Common (cola-colored urine).
Rare or absent.
Periorbital, mild to moderate.
Severe, generalized (anasarca).
Other Signs
Hypertension, RBC casts.
Hypoalbuminemia, hyperlipidemia.
What are the key features of Post-Streptococcal Glomerulonephritis (PSGN) in pediatrics?
Etiology: Group A beta-hemolytic streptococcal infection (pharyngitis/impetigo).
Symptoms: Cola-colored urine, periorbital edema, hypertension, oliguria.
Diagnosis:
Labs: Low C3, normal C4, positive ASO titer.
Urinalysis: RBC casts.
Treatment: Supportive care (fluid management, antihypertensives, diuretics).
How does IgA nephropathy (Berger Disease) present in pediatric patients?
Etiology: IgA deposition in glomeruli after mucosal infections.
Symptoms: Gross hematuria following a URI; persistent microscopic hematuria between episodes.
Diagnosis: Normal complement levels, biopsy shows mesangial IgA deposits.
Treatment: BP control with ACE inhibitors/ARBs; corticosteroids for severe proteinuria.
What distinguishes Henoch-Schönlein Purpura (HSP) from other pediatric glomerulonephritis causes?
Systemic Symptoms: Palpable purpuric rash (lower extremities), abdominal pain, arthralgia.
Renal Symptoms: Hematuria, proteinuria, nephritic or nephrotic syndrome.
Diagnosis: Clinical (IgA deposition on biopsy if needed).
Treatment: Supportive care; steroids for severe renal involvement.
What are the renal manifestations of lupus nephritis in children?
Symptoms: Hematuria, proteinuria, systemic lupus features (malar rash, arthritis, fever).
Diagnosis: Positive ANA, anti-dsDNA, low C3/C4. Biopsy confirms immune complex deposition.
Treatment: Immunosuppression with corticosteroids, mycophenolate, or cyclophosphamide.
What laboratory findings differentiate pediatric glomerulonephritis causes?
Condition
Complement Levels
Autoantibodies
Other Findings
PSGN
Low C3, normal C4.
None.
Positive ASO titer.
IgA Nephropathy
Normal.
IgA deposition on biopsy.
HSP
Purpuric rash, systemic symptoms.
Lupus Nephritis
Low C3 and C4.
ANA, anti-dsDNA.
Systemic lupus signs (rash, fever).
What diagnostic tools are critical for pediatric glomerulonephritis?
Urinalysis: RBC casts, proteinuria.
Blood Tests: Renal function (BUN, creatinine), complement levels (C3/C4), autoantibodies (ANA, ANCA).
Imaging: Renal ultrasound to rule out obstruction.
Renal Biopsy: Definitive for uncertain or severe cases
What are the treatment principles for pediatric glomerulonephritis?
Fluid and electrolyte management.
Blood pressure control (ACE inhibitors/ARBs).
Diuretics for edema.
Specific Therapy:
Corticosteroids (IgA nephropathy, lupus nephritis).
Immunosuppressants (cyclophosphamide, mycophenolate).
Plasmapheresis for RPGN or ANCA vasculitis.
Infections: Antibiotics if infections are present (e.g., strep throat).
Dialysis: For severe AKI or CKD.
What are key biopsy findings in pediatric glomerulonephritis?
PSGN: Subepithelial humps (immune complex deposits).
IgA Nephropathy: Mesangial IgA deposits.
Lupus Nephritis: Full-house immune deposits.
MPGN: Tram-track appearance.
What is Henoch-Schönlein Purpura (HSP) in pediatric patients?
HSP, also known as IgA vasculitis, is the most common small-vessel vasculitis in children. It is characterized by IgA deposition in small vessels, causing inflammation of the skin, joints, GI tract, and kidneys.
What are the common triggers of HSP in children?Henoch-Schönlein Purpura (HSP)
Infections: Group A streptococci, Mycoplasma, Parvovirus B19, EBV.
Drugs: Antibiotics (e.g., penicillin), vaccinations.
Environmental Factors: Seasonal (commonly winter and spring).
What is the pathophysiology of HSP in pediatrics?
HSP is caused by IgA1 immune complex deposition in small vessel walls, triggering inflammation. It primarily affects the skin, joints, GI tract, and kidneys.
What are the hallmark clinical features of pediatric HSP?
Skin: Palpable purpura on buttocks and lower limbs.
GI Tract: Colicky abdominal pain, GI bleeding (melena, hematochezia).
Joints: Arthralgia or arthritis (knees, ankles).
Kidneys: Hematuria, proteinuria, nephritic or nephrotic syndrome.
What are the serious complications of HSP in pediatric patients?
Intussusception: GI complication due to bowel edema.
Chronic Kidney Disease (CKD): Persistent glomerulonephritis.
Hypertension: Associated with nephritis.
How is HSP diagnosed in pediatric patients?
Clinical Diagnosis: Palpable purpura + one of the following:
Arthritis/arthralgia.
Renal involvement (hematuria, proteinuria).
Labs:
Normal platelet count (distinguishes from ITP).
Elevated ESR, CRP.
Hematuria, proteinuria, or RBC casts on urinalysis.
Abdominal US for intussusception.
Biopsy is confirmatory finding
What are the treatment options for HSP in pediatric patients?
Supportive Care: Mainstay for most cases.
Adequate hydration.
NSAIDs for arthralgia (if no renal involvement).
Corticosteroids: Indicated for severe abdominal pain, GI bleeding, or nephritis.
Dose: Prednisone 1–2 mg/kg/day, tapered over 1–2 weeks.
Renal Management:
ACE inhibitors or ARBs for proteinuria.
Immunosuppressants (e.g., mycophenolate) for severe nephritis.
Intussusception: Surgical intervention required.
Differential diagnosis for Henoch Schonlein Purpura
Purpura without thrombocytopenia:
o Acute hemorrhagic edema of infancy, hypersensitivity vasculitis. •
Arthritis/Arthralgia:
o Juvenile idiopathic arthritis, lupus, septic arthritis.
Abdominal Pain:
o Appendicitis, intussusception, or other causes of acute abdomen.
Kidney Disease:
o IgA nephropathy, lupus nephritis.
What is hypoglycemia in the pediatric population?
Low blood glucose levels insufficient to meet metabolic demands:
Neonates: <2.6 mmol/L (<47 mg/dL).
Infants and children: <3.0 mmol/L (<54 mg/dL).
What are the most common causes of hypoglycemia in paediatric neonates?
ransient Causes:
Prematurity or low birth weight.
Maternal diabetes (infant hyperinsulinism).
Persistent Causes:
Congenital hyperinsulinism.
Endocrine deficiencies (e.g., cortisol or growth hormone deficiency).
What are the most common causes of hypoglycemia in older paediatric children?
Fasting Hypoglycemia:
Prolonged fasting, starvation.
Glycogen storage diseases.
Hyperinsulinemia:
Excess exogenous insulin or sulfonylureas.
Insulinoma.
Endocrine Disorders:
Adrenal insufficiency, growth hormone deficiency.
Metabolic Disorders:
Fatty acid oxidation defects, gluconeogenesis disorders.
What are the symptoms of hypoglycemia in paediatric patients?
Autonomic Symptoms:
Sweating, pallor, tachycardia, tremors, irritability, hunger.
Neuroglycopenic Symptoms:
Confusion, dizziness, lethargy, seizures, coma (severe).
How is hypoglycemia diagnosed in the pediatric population?
Critical Sample: Taken during hypoglycemia:
Blood glucose, insulin, ketones, lactate, cortisol, growth hormone, free fatty acids.
Urinalysis: Ketones.
Genetic Testing: If a metabolic disorder is suspected.
What is the immediate management of hypoglycemia in pediatric patients?
Mild Hypoglycemia: Oral glucose (sugary drink or glucose gel).
Severe Hypoglycemia:
IV Dextrose: 2–4 mL/kg of 10% dextrose (D10W) bolus, followed by infusion.
Glucagon: 0.03–0.1 mg/kg IM/SC if IV access unavailable.
What is hypothyroidism in the paediatric population?
Hypothyroidism in paediatrics is a condition where there is insufficient production of thyroid hormones (T3 and T4), leading to impaired growth, development, and metabolism. It can be congenital or acquired.
What are the two main types of hypothyroidism in paediatric patients?
Congenital Hypothyroidism (CH):
Present at birth; most common preventable cause of intellectual disability.
Acquired Hypothyroidism:
Develops later in childhood or adolescence, often due to Hashimoto's thyroiditis.
What are the common causes of congenital hypothyroidism in the paediatric population?
Thyroid Dysgenesis (85%):
Ectopic thyroid gland, agenesis, or hypoplasia.
thyoid gland absent or very little
Thyroid Dyshormonogenesis (15%):
Genetic defects in thyroid hormone synthesis.
Transient CH:
Maternal iodine deficiency/excess or TSH-receptor blocking antibodies.
What are the common causes of acquired hypothyroidism in paediatrics?
Autoimmune Thyroiditis (Hashimoto's): Most common in children and adolescents.
Iodine Deficiency/Excess.
Post-Treatment Causes: After thyroidectomy or radioactive iodine therapy.
Central Hypothyroidism: Pituitary or hypothalamic dysfunction.
What are the clinical features of congenital hypothyroidism in the paediatric population?
Prolonged neonatal jaundice.
Feeding difficulties, poor sucking, lethargy.
Hypotonia (floppy baby).
Coarse facial features (macroglossia, large fontanelles).
Umbilical hernia.
Developmental delay if untreated.
How is hypothyroidism diagnosed in the paediatric population?
Newborn Screening: Elevated TSH or low T4.
Primary Hypothyroidism:
High TSH, low Free T4.
Central Hypothyroidism:
Low TSH and low Free T4.
Autoimmune Hypothyroidism:
Positive anti-thyroid peroxidase (TPO) or anti-thyroglobulin antibodies.
Bone Age X-Ray: Delayed skeletal maturation.
What imaging is used for diagnosing hypothyroidism in paediatric patients?
Ultrasound: Identifies thyroid dysgenesis or nodules.
Scintigraphy: Locates ectopic thyroid tissue or assesses thyroid function.
What is the treatment for hypothyroidism in the paediatric population?
Levothyroxine: First-line treatment.
Dose: 10–15 mcg/kg/day in neonates, adjusted based on TSH and Free T4 levels.
Lifelong Therapy: For permanent hypothyroidism.
Dietary Management: Ensure iodine sufficiency if deficient.
What are the key clinical signs of congenital hypothyroidism in neonates?
Large anterior and posterior fontanelles.
Macroglossia.
Prolonged jaundice.
Poor feeding and lethargy.
Definition of JIA
JIA is the most common childhood rheumatologic condition, characterized by arthritis before age 16, lasting ≥6 weeks, and excluding other causes.
Classification of JIA
what are the classifications
systemic arthritis
oligoarthritis
polyarthritis
psoriatic arthritis
enthesitis related
undifferentiated
Systemic arthritis
Fever >2 weeks with daily spikes (>38.5°C).
Salmon-pink rash, arthritis, lymphadenopathy, organomegaly, or serositis.
Associated with macrophage activation syndrome (MAS).
≤4 joints in the first 6 months.
Persistent (remains ≤4 joints) or Extended (>4 joints later).
ANA-positive: High risk of anterior uveitis.
Classification of jia
≥5 joints in the first 6 months.
RF-positive: Severe, mimics adult RA.
RF-negative: Milder course.
JIA
psoriatic
arthritis with psoriasis or dactylitis, nail pitting, or family history of psoriasis.
Systemic JIA (sJIA) Highlights
Clinical Features: Fever, rash, arthritis, lymphadenopathy, hepatosplenomegaly, serositis.
MAS: Life-threatening complication with pancytopenia, fever, hyperferritinemia.
Labs: Elevated WBC, CRP/ESR, hyperferritinemia, negative ANA/RF.
Treatment: NSAIDs, biologics (IL-1/IL-6 inhibitors), steroids for severe cases.
Oligoarticular JIA Highlights
Presentation: Large joints (knees, ankles), asymmetrical.
Complications: Uveitis, leg-length discrepancy.
Treatment: Intra-articular steroids, NSAIDs, methotrexate for severe cases.
Polyarticular JIA Highlights
RF-Positive: Severe, resembles adult RA.
RF-Negative: Milder, affects small and large joints.
Labs: Elevated ESR, anemia, ANA.
Treatment: NSAIDs, methotrexate, biologics for refractory cases.
Treatment of JIA
First-Line:
NSAIDs for symptom control.
Intra-articular steroids for oligoarticular disease.
DMARDs:
Methotrexate: First-line for polyarticular or extended disease.
Biologics:
Anti-TNF (e.g., etanercept) for refractory arthritis or axial disease.
IL-1/IL-6 inhibitors for systemic JIA.
Complications Management:
Uveitis: Topical steroids or TNF inhibitors.
MAS: High-dose steroids, IL-1 inhibitors.
What is Inflammatory Bowel Disease (IBD) in paediatrics?
A chronic inflammatory condition of the GI tract that includes:
Crohn's Disease (CD): Transmural inflammation, can affect any part of the GI tract.
Ulcerative Colitis (UC): Mucosal inflammation, confined to the colon and rectum.
What is the peak age of onset for IBD in paediatrics?
Typically between 12–15 years, but can occur in infants or young children.
What are the key differences between Crohn’s Disease (CD) and Ulcerative Colitis (UC) in paediatrics? `
Crohn's Disease (CD)
Ulcerative Colitis (UC)
Location
Any part of GI tract (mouth to anus).
Colon and rectum only.
Inflammation
Transmural (full thickness).
Mucosal (limited to surface).
Pattern
Skip lesions (discontinuous).
Continuous from rectum upward.
Diarrhoea (± blood), weight loss.
Bloody diarrhoea, urgency.
What are the extraintestinal manifestations of paediatric IBD?
Musculoskeletal: Arthritis, sacroiliitis.
Skin: Erythema nodosum, pyoderma gangrenosum.
Eyes: Uveitis, episcleritis.
Hepatobiliary: Primary sclerosing cholangitis (PSC), fatty liver.
What are the complications of Crohn’s Disease in paediatrics?
Strictures → Obstruction.
Fistulas → Abnormal connections (e.g., enterovesical).
Malabsorption: Iron, B12, and fat-soluble vitamins.
What are the complications of Ulcerative Colitis in paediatrics?
Toxic Megacolon: Life-threatening colonic dilation.
Colorectal Cancer: Increased risk with disease duration
How is IBD diagnosed in paediatric patients?
Clinical History: Chronic diarrhoea, abdominal pain, growth failure.
Lab Tests: Elevated CRP/ESR, anaemia, faecal calprotectin.
Endoscopy:
CD: Cobblestoning, skip lesions.
UC: Diffuse erythema, mucosal friability.
Imaging: MRI enterography for small bowel CD.
What is the role of serological markers in diagnosing paediatric IBD?
p-ANCA: Positive in UC.
ASCA: Positive in CD.
What are the first-line medications for treating paediatric UC and CD?
Medication
Use in Paediatrics
5-ASA Aminosalicylic acids. (e.g., Mesalamine)
Mild UC.
Corticosteroids
Moderate-severe flares (short-term).
Immunomodulators
Maintenance (e.g., azathioprine).
Biologics
Severe disease (e.g., anti-TNF).
What are the surgical indications for IBD in paediatric patients?
Crohn’s Disease: Complications like strictures or fistulas.
Ulcerative Colitis: Total colectomy for severe or refractory disease.
What lab markers help monitor paediatric IBD activity?
Inflammatory Markers: CRP, ESR.
Stool Markers: Faecal calprotectin.
Nutritional Status: Albumin, vitamin D, B12.
Intestinal Infections:
Management
Rehydration and Nutrition
Oral Rehydration Solution (ORS):
First-line treatment for dehydration.
• Early Feeding:
Initiate within 12 hours of rehydration. o Use foods like:
Complex carbohydrates: Rice, wheat, potatoes, bread, cereals. ▪ Lean meats.
Yogurts.
Fruits and vegetables.
Probiotics and Adjunctive Therapies
Probiotics:
Adjunct to ORS; reduces duration and severity of diarrhea.
Zinc Supplementation:
Supports bowel nutrition and function.
What is Kawasaki Disease (KD) in the paediatric population?
A medium-sized vessel vasculitis affecting children <5 years.
What are the clinical features of Kawasaki Disease?
What are the phases of Kawasaki Disease in paediatrics?
Acute Phase (0–2 weeks):
Fever, rash, conjunctivitis, oral changes, extremity swelling.
Subacute Phase (2–6 weeks):
Skin peeling (desquamation), risk of coronary aneurysms.
Convalescent Phase (6–8 weeks):
Resolution of symptoms, lab markers normalize.
What are the complications of Kawasaki Disease in paediatrics?
Coronary Artery Aneurysms (CAA): Risk in untreated cases (~25%).
Myocarditis/Pericarditis.
Toxic Shock-Like Syndrome.
How is Kawasaki Disease diagnosed in paediatrics?
Clinical Diagnosis: Fever + 4/5 features.
Thrombocytosis (late phase).
Sterile pyuria.
Echocardiography: Detect coronary artery abnormalities.
What is the treatment for Kawasaki Disease in paediatrics?
Intravenous Immunoglobulin (IVIG):
Dose: 2 g/kg single infusion.
Reduces coronary artery complications.
Aspirin:
High-dose (anti-inflammatory) during fever.
Low-dose (antiplatelet) after fever subsides.
Refractory KD: Second IVIG, corticosteroids, or infliximab.
What are the main liver biochemical tests used in paediatric hepatitis?
Liver Enzymes:
ALT: Liver-specific marker.
AST: Found in liver, heart, and muscles.
ALP: Elevated in cholestasis or biliary obstruction.
GGT: Suggests hepatobiliary disease.
What history and physical signs are important for diagnosing paediatric hepatitis?
Travel, IV drug use, contaminated food/water.
Drug or toxin exposure (e.g., acetaminophen).
Physical Signs:
Jaundice, hepatomegaly.
Spider nevi, palmar erythema (chronic liver disease).
Tender liver (acute hepatitis).
What laboratory patterns indicate the type of liver injury?
Hepatocellular: Elevated ALT > ALP (e.g., viral hepatitis).
Cholestatic: Elevated ALP > ALT (e.g., biliary obstruction).
Isolated Hyperbilirubinemia: Elevated bilirubin with normal ALT/ALP.
What are the key causes of hepatitis in paediatrics?
Infectious: HAV, HBV, HCV, EBV, CMV.
Toxic/Drug-Induced: Acetaminophen, herbal remedies.
Autoimmune Hepatitis: Common in teenagers.
Metabolic: Wilson disease, alpha-1 antitrypsin deficiency.
How is viral hepatitis diagnosed in paediatrics? Hep A
Hepatitis A (HAV):
Anti-HAV IgM: Acute infection.
Anti-HAV IgG: Past infection/vaccination.
How is viral hepatitis diagnosed in paediatrics? Hep B
Hepatitis B (HBV):
HBsAg: Active infection.
Anti-HBs: Immunity.
Anti-HBc IgM: Recent infection.
How is viral hepatitis diagnosed in paediatrics? Hep C
HCV RNA PCR: Active infection.
Anti-HCV antibodies: Exposure.
What imaging and advanced tests are used for paediatric hepatitis?
Ultrasound: Assess liver size, texture, and biliary obstruction.
MRI/MRCP: Evaluate biliary or vascular issues.
Liver Biopsy: For autoimmune or unclear cases.
How is hepatitis A treated and prevented in paediatrics?
Treatment: Self-limiting; supportive care only.
Prevention:
Universal vaccination (2 doses at 12–23 months).
Hygiene (avoid contaminated food/water).
How is hepatitis B treated and prevented in paediatrics?
Antivirals (e.g., tenofovir) for chronic cases with high ALT or fibrosis.
Universal infant vaccination.
Postexposure prophylaxis (vaccine + HBIG) for infants of HBV-positive mothers.
How is hepatitis C treated in paediatrics?
Children ≥3 years: Direct-acting antivirals (DAAs) like sofosbuvir-velpatasvir.
Children <3 years: Monitor for spontaneous clearance; treat when eligible.
What are the complications of chronic hepatitis in paediatrics?
Cirrhosis: Progression in untreated cases.
Hepatocellular Carcinoma (HCC): Associated with HBV/HCV.
Growth Failure: Due to chronic disease and malnutrition.
Indications and Choice of Operative Approach for Adrenal Operations
Primary Hyperaldosteronism
Conn syndrome,
hypertension, hypokalemia, and suppressed plasma renin levels.
Excess aldosterone production by the adrenal glands is caused by low renin levels.
Aldosterone helps regulate blood pressure by controlling sodium and potassium levels in the body.
Indication:
adrenal vein sampling confirming aldosteroma
unilateral adrenal mass >1cm, normal contralateral adrenal mass and patients <40 years
preferred surgery: laparoscopic adrenalectomy
Indications for Adrenal Surgery
Cushing Syndrome
ACTH-independent disease: Adrenalectomy.
during surgery perioperative and postoperative steroids are recommended. Hydrocortisone 100mg every 8hr for 24 hr.
ACTH-detectable: Pituitary microsurgery may be considered instead. Transphenoidal pituatory microsurgery
Adrenocortical Carcinoma:
rare, at time of finding usually has already spread.
Surgery= radical resection with open surgery
Pheochromocytoma
Pheochromocytoma is a rare tumor of the adrenal medulla
Surgery:
Preoperative:
alpha-blockade to control blood pressure.
Laparascopic apprach can be attempted only if local invasion is not seen. Open resection should be done if larger than 6cm
DDifferent Approaches to adrenal surgery
Flashcard 3: Surgical Approaches for Adrenal Surgery
Open Surgery:
Used for large tumors (>8 cm), suspected malignancy, or local invasion.
Laparoscopic Surgery:
For smaller, benign tumors (<7 cm).
Advantages: Minimally invasive, shorter recovery time.
Posterior Retroperitoneoscopic Adrenalectomy:
Best suited for tumors <7 cm; avoids abdominal cavity entry.
Diagnostics in Primary Hyperparathyroidism (pHPT)
condition characterized by excess secretion of parathyroid hormone (PTH) causing hypercalcemia.
Elevated serum calcium (>10.5 mg/dL).
Increased or inappropriately normal PTH levels (>25 pg/mL).
DXA for bone mineral density
abdominal noncontrast CT/ US —> kindey stones or nephrocalcinosis
parathyroid imaging is not often necessaey
PET/CT, US
Surgical Approaches for Primary Hyperparathyroidism (pHPT)
Focused Parathyroidectomy: Single gland removal via small incision if imaging confirms adenoma.
Bilateral Neck Exploration: For inconclusive imaging or suspected multiple gland involvement.
Subtotal Parathyroidectomy: Removal of 3½ of 4th glands in hyperplasia cases.
Intraoperative Monitoring in pHPT
Real-time assessment of PTH levels during surgery to confirm the removal of hyperactive tissue.
Key Monitoring:
Miami Criterion: PTH levels drop by 50% within 10 minutes of excision.
Purpose: Confirms success and reduces reoperation risk.
INTRAOPERATIVE MONITORING OF PTH
guides surgeon when to stop operation
helps to confirm that there is no residual functioning parathyroid gland
Blood is drawn from a peripheral vein, arterial line, anterior jugular vein, or internal jugular vein at specific time points before and during the operation based on the protocol followed (check before removal and after removal).
The PTH level is expected to drop after the pathologic gland(s) are excised due to the short half-life of PTH (3–5 minutes)
Diagnostics in Thyroid Cancer
Lab Tests:
TSH: Normal or mildly elevated.
Tumor Markers: Calcitonin and CEA for medullary carcinoma.
thyroid ultrasound: solid/ hypoechoic irregular margins. Microcalcification, taller than wide.
thyroid scintigraphy: required if multinodular thyroid to identify which nodules need fine- needle aspiration cytology,
cold - more likely to be cancer
Surgical Approaches in Thyroid Cancer
Total Thyroidectomy: Tumors >4 cm, bilateral disease, or aggressive histology.
Hemithyroidectomy: For small (<4 cm), low-risk, localized tumors.
Adjuvant Therapy in Thyroid Cancer
Radioactive Iodine Ablation (RAIA): For high-risk or metastatic cases.
TSH Suppression Therapy: High-dose levothyroxine to suppress tumor regrowth.
Surgical principles of thyroid surgery
Transverse, 2 cm above the sternal notch.
Structures to Preserve:
Recurrent laryngeal nerve.
Parathyroid glands.
Intraoperative Neuromonitoring: Monitors recurrent laryngeal nerve function.
electrical stimulator probes are used to deliver electrical
current to the vagus nerve or RLN, which leads to an electromyographic signal at the vocal cord detected by contact electrodes embedded on the surface of the endotracheal tube
Postoperative Hematoma and Hypoparathyroidism
Hematoma: Accumulation of blood causing swelling post-surgery.
Hypoparathyroidism: Long-term reduction in PTH levels.
Management:
Hematoma: Immediate surgical drainage if causing airway compromise.
Hypoparathyroidism: Oral calcium and Vitamin D supplements to maintain serum calcium levels.
Complications of thyroid surgery
Hypocalcemia: Tingling, muscle cramps;
treated with calcium and Vitamin D.
Nerve Injury:
Unilateral recurrent laryngeal nerve damage: Hoarseness.
Bilateral injury: Airway obstruction, may require tracheostomy.
Classification of inguinal hernia
Indirect inguinal hernia
direct inguinal hernia
Indirect Inguinal Hernia
Definition: .
Location:
Coverings:
Population:
Definition: Congenital, due to incomplete closure of processus vaginalis.
Location: Passes through external & internal ring; outside Hesselbach’s triangle.
Coverings: Surrounded by external spermatic fascia, cremasteric muscle fibers, and internal spermatic fascia.
Population: Common in male infants.
Direct Inguinal Hernia
Definition:
Definition: Acquired, caused by weakening of the transversalis fascia.
Location: Herniates through the external ring; within Hesselbach’s triangle.
Coverings: Only external spermatic fascia.
Population: Common in elderly men.
Diagnosis of Inguinal Hernias and imaging
linical Symptoms:
Mass in the inguinal region.
Increases with coughing, decreases when lying down.
May be reducible.
Used if diagnosis is unclear or for surgical planning.
Differentiates between direct and indirect hernias.
Complications of hernia
Incarcerated: Irreducible mass, normal skin.
Obstructed: Nausea, vomiting, abdominal distention.
Strangulated: Severe pain, erythematous, warm, tender skin around scrotum.
Treatment Methods
Inguinal hernia
Conservative:
Only for non-complicated
involves observation
Surgical management:
Hernioplasty. (mesh repair)
open repair:
mesh placed between transversalis fascia and external oblique
recommended for complicated hernias
laproscopic repair
transabdominal preperitoneal repair ( mash placed after cutting and resewing the peritoneum)
total extraperitoneal repar (mesh placed without opening peritoneum)
Herniorrhaphy (non- mesh repair)
uses autologous tissue
older technique, high risk
sutures posterior wall of inguinal canal
Incarcerated hernia
Irreducible hernia where the contents of the hernia sac cannot be returned to the abdominal cavity.
May progress to strangulation, obstruction, or bowel ischemia.
Types of Incarcerated hernia
Elastic Incarceration:
Increased intra-abdominal pressure → intestine slips through a temporarily enlarged hernia orifice → hernia gets stuck due to contraction of hernia orifice.
Fecal Incarceration:
Herniation caused by fecal matter or gas causing obstruction.
Retrograde Incarceration:
Only part of the bowel loop protrudes; the rest remains in the abdominal cavity.
Richter's Incarceration:
Only a portion of the bowel circumference becomes incarcerated.
Clinical features of incarcerated hernia
Sudden Onset Symptoms:
Pain at the hernia site.
Tenderness and irreducibility.
Signs of Bowel Dysfunction:
Bowel obstruction: nausea, vomiting, abdominal distension.
Signs of Peritonitis (if strangulated):
Abdominal rigidity.
Fever, hemodynamic instability.
Local Signs:
Redness, tenderness, and inability to reduce hernia.
Diagnostics of incarcerated hernia
Diagnostics
Physical Examination:
Irreducible, painful hernia mass suggests incarceration.
Chronic cases may present with minimal tenderness.
Ultrasound (US):
First-line for inguinal and femoral hernias.
CT Scan:
Used for abdominal hernias to evaluate bowel viability, strangulation, or obstruction.
Treatment of incarcerated hernia (viable vs non viable)
Viable Bowel (No ischemia):
Action: Reduce the hernia and repair the defect.
Surgical Approach: Depends on hernia type (see below).
Non-Viable Bowel (Ischemic or necrotic):
Action: Resect the damaged bowel (30-40 cm proximal and 15-20 cm distal to the affected area).
Perform anastomosis or create a stoma if needed.
Surgical treatment of hernia
Inguinal and Femoral Hernias
Early incarceration (No ischemia):
Mesh can be used for repair unless there's significant contamination.
Complicated cases (e.g., strangulated or ischemic):
Avoid mesh due to infection risk. Repair the defect directly.
Open Repair (Preferred for complicated hernias):
Lichtenstein Repair: Use mesh to strengthen the posterior wall of the inguinal canal.
Laparoscopic Repair (Preferred for bilateral/recurrent hernias):
TAPP (Transabdominal Preperitoneal Repair): Place the mesh between peritoneum and fascia after cutting and resealing the peritoneum.
TEP (Total Extraperitoneal Repair): Place the mesh without entering the peritoneal cavity.
if it is an abdominal hernia
Epigastric Hernias:
Small incision with interrupted sutures or mesh repair.
Umbilical Hernias (>4 cm):
Laparoscopic Repair: Preferred to assess bowel viability and repair defect.
Open Repair: For smaller hernias.
Incisional hernia
Hernia occurring at the site of a previous surgical incision
Most frequently occurs after midline incisions.
Clinical Features of incisional hernia
Asymptomatic Presentation:
Some hernias are discovered incidentally.
Typical Symptoms:
Reducible mass at the site of previous incision.
Irreducible in complicated cases.
Large hernias → skin changes like erythema or ulceration.
Discomfort:
Patients may experience abdominal pain or pressure.
Strangulation, obstruction, or bowel ischemia in severe cases.
Diagnostics of incisional hernia
History of previous abdominal surgery is key.
Look for palpable mass or protrusion at the incision site.
Can be challenging in obese patients.
CT Scan is recommended:
Essential for hernias >10 cm.
Treatment of incisional hernia
expectant Management:
Suitable for minor/asymptomatic cases.
Observation is preferred in patients unfit for surgery.
Operative Management:
General Principles:
Repair is mandatory in strangulated or obstructed hernias.
Elective repair is avoided in high-risk patients (e.g., obese, diabetic) unless symptomatic.
surgical repair of incisional hernia
Small Hernias (<1 cm):
Can be repaired using sutures +/- small mesh.
Medium Hernias (1–10 cm):
Repair with mesh placement:
Often performed laparoscopically.
Large Hernias (>10 cm):
Requires advanced techniques:
Mesh underlay technique (most common, laparoscopic or open).
Alternative: Inlay or component separation techniques.
Flank Incisional Hernias:
Managed as flank/lumbar hernias.
Use intraperitoneal mesh in smaller hernias.
For larger hernias, open surgery with preperitoneal/retromuscular mesh.
Femoral hernias
what is it
Intra-abdominal contents herniate through the femoral canal via the femoral ring.
Non-complicated Femoral Hernia
Globular swelling in the groin.
Location: Inferior to inguinal ligament, lateral to pubic tubercle, and medial to femoral vein.
Valsalva maneuver (e.g., coughing) increases size.
May cause non-specific groin pain.
Complicated Femoral Hernia:
Signs of incarceration: Irreducibility.
Signs of strangulation: Warmth, tenderness, severe pain, and swelling.
Diagnostic of femoral hernia
Clinical Findings:
Palpable mass and reducibility.
Groin Ultrasound (US) for difficult palpation, especially in obese patients.
Treatment for femoral hernia
General Recommendations:
Surgery is advised for all femoral hernias due to the high risk of complications.
Non-complicated Cases:
Elective repair with mesh hernioplasty (tension-free repair via TEP or TAPP).
Posterior approach (preferred for better access and avoiding inguinal canal dissection).
omplicated Cases:
Clean cases: Use synthetic mesh.
Clean-contaminated cases: Use large-bore mesh.
Contaminated cases (e.g., bowel perforation): No mesh (risk of infection).
Alternative Technique:
Plug and Patch Repair:
Plug inserted into the hernia orifice and fixed with an onlay patch.
Umbilical hernias
Due to delayed closure of the umbilical ring after midgut herniation.
90% close spontaneously.
Develops adjacent to the umbilicus, pushing it into a crescent shape.
Treatment of umbilical hernia
Congenital Cases:
Leave untreated unless:
Age >5 years.
Hernia persists >3 years and is large (cosmetic repair recommended).
Acquired Cases:
Surgical repair based on size:
<1–2 cm: Sutures (Mayo Procedure - open repair).
2 cm: Mesh repair (laparoscopic or open methods, e.g., v-patch).
Suitable for asymptomatic small hernias or poor surgical candidates (use hernia belt).
What is Acute Malnutrition? (Pediatrics)
Acute Malnutrition: Rapid loss of body weight due to insufficient nutrition or disease.
Severe Acute Malnutrition (SAM):
Criteria: Mid upper circumference <11.5 cm, Weight for height <-3, or bilateral pitting edema.
<11.5 cm
Subtypes:
Marasmus: Wasting with loss of muscle and fat; no edema.
Kwashiorkor: Edema, shiny skin, and hair changes.
Moderate Acute Malnutrition (MAM):
Criteria: MUAC 11.5–12.4 cm or WHZ -2 to -3.
What defines chronic malnutrition, and what does it indicate?
Height-for-age Z-score < -2.
Long-term nutritional inadequacies, poor growth, and cognitive development.
What are the key tools and methods to diagnose pediatric malnutrition?
Anthropometric Measures:
Weight-for-height (wasting), height-for-age (stunting), MUAC.
Bilateral pitting edema for Kwashiorkor.
Growth Charts: WHO/CDC charts for Z-score classification.
Mid upper circumference : Quick, field-ready assessment tool.
How is Moderate Acute Malnutrition (MAM) managed in children?
Outpatient Supplementary Feeding:
Use RUSF (Ready-to-Use Supplementary Food).
Nutrition Education:
Promote appropriate foods for developmental stages.
Discharge Criteria:
MUAC >12.5 cm or WHZ >-2.
How is uncomplicated Severe Acute Malnutrition (SAM) managed?
Community-Based Management:
Use RUTF (Ready-to-Use Therapeutic Food).
Empiric antibiotics (e.g., amoxicillin for 7 days).
Follow-Up:
Weekly/biweekly monitoring for weight gain.
What routine supplementation is provided for malnourished children?
Vitamin A: For immune support.
Zinc: Helps with diarrhea and skin issues.
Iron: For anemia.
Vitamin D: Addresses rickets.
Define enteral nutrition and list its benefits. for malnutrition
Definition: Nutrition provided via the gastrointestinal tract (e.g., nasogastric or gastrostomy tubes).
Benefits:
Lower cost than parenteral nutrition.
Maintains gut integrity.
Fewer complications than IV feeding.
What are the types of enteral feeding methods?
Short-Term: Nasogastric or orogastric tubes (<3 months).
Long-Term: Gastrostomy tubes for prolonged feeding.
Feeding Methods:
Bolus Feeding: Mimics normal meals.
Continuous Feeding: For feeding intolerance, slow infusion via a pump.
What is the causative agent of measles?
Measles virus, a paramyxovirus of the genus Morbillivirus.
How is measles transmitted?
Via airborne droplets or direct contact with nasal/throat secretions.
What is the incubation period for measles?
: 7–14 days (asymptomatic phase).
What is the clinical triad of the prodromal phase in measles?
Coryza (nasal congestion and discharge)
Conjunctivitis (red, watery eyes with photophobia).
What are Koplik spots, and when do they appear?
Small bluish-white lesions on an erythematous base on the buccal mucosa, appearing during the prodrome phase. They are pathognomonic for measles.
Describe the rash associated with measles.
Starts behind the ears and spreads to the face, trunk, and extremities.
Maculopapular, erythematous rash.
Fades in the same order it appears, leaving desquamation.
What are the common complications of measles?
Otitis media (most common).
Pneumonia (leading cause of mortality).
Diarrhea (causing dehydration).
Encephalitis (acute or SSPE).
Vitamin A deficiency exacerbation.
What laboratory findings are diagnostic of measles?
Positive IgM antibodies to measles virus.
RT-PCR detects measles RNA.
Leukopenia in CBC.
What is the role of Vitamin A in measles treatment?
Reduces morbidity and mortality.
Dosage:
<6 months: 50,000 IU/day for 2 days.
6–12 months: 100,000 IU/day for 2 days.
>12 months: 200,000 IU/day for 2 days.
How is measles prevented?
MMR vaccine:
First dose at 12–15 months.
Second dose at 4–6 years.
Post-Exposure Prophylaxis (PEP):
MMR vaccine within 72 hours.
Immune globulin within 6 days for high-risk contacts.
What are the hallmark signs for clinical identification of measles in pediatric cases?
Classic prodrome: Fever, cough, coryza, conjunctivitis.
Presence of Koplik spots.
Rash progression from behind the ears to the rest of the body.
History of unvaccinated status or exposure to a confirmed case.
What is mumps, and what virus causes it?
Mumps is a viral illness caused by the mumps virus, a paramyxovirus. It primarily affects the parotid glands and can involve multiple systems.
What age group and transmission method are associated with mumps?
Age group: Most common in children aged 5–9 years.
Transmission: Spread via droplet and direct contact with infected saliva.
What are the classic symptoms of mumps?
Prodromal symptoms:
Malaise.
Myalgia.
Parotitis:
Swelling and tenderness of one or both parotid glands.
Pain worsens with chewing or sour foods.
Bilateral swelling occurs in 70% of cases.
What does the face of a mumps patient typically look like?
A "hamster-like" facial swelling due to enlarged parotid glands, often obscuring the angle of the jaw
Name the key complications of mumps.
Orchitis: Testicular swelling and pain, more common in postpubertal males.
Aseptic Meningitis: Headache, photophobia, and vomiting.
Pancreatitis: Abdominal pain and elevated amylase.
Hearing Loss: Sensorineural, may be unilateral or bilateral
How is mumps diagnosed?
Clinical diagnosis: Based on parotid swelling and prodromal symptoms.
Confirmatory tests:
Serology: Positive mumps IgM or a fourfold rise in IgG titers.
RT-PCR: Detects mumps RNA, especially in vaccinated cases.
How is mumps differentiated from bacterial parotitis?
Mumps: Gradual onset, bilateral swelling, normal overlying skin.
Bacterial parotitis: Unilateral swelling, erythema, and purulent discharge.
What is the treatment for mumps?
Analgesics (acetaminophen, ibuprofen).
Warm or cold compresses.
Hydration and soft diet.
Isolation: For 5 days after symptom onset to prevent transmission.
How is mumps prevented?
First dose: 12–15 months.
Second dose: 4–6 years.
Vaccine efficacy:
One dose: ~78%.
Two doses: ~88%.
What is Pertussis?
Pertussis, also known as whooping cough, is a highly contagious bacterial infection caused by Bordetella pertussis.
What are the key epidemiological features of pertussis?
Most severe in infants <6 months.
Spread via droplets (coughing or sneezing).
Incubation period: 7–10 days (range: 4–21 days).
Vaccine-preventable but outbreaks occur due to waning immunity.
What are the clinical stages of pertussis?
Catarrhal Phase (1–2 weeks):
Mild upper respiratory symptoms (rhinorrhea, sneezing, low-grade fever).
Highly contagious stage.
Paroxysmal Phase (2–8 weeks):
Severe paroxysmal coughing fits followed by inspiratory "whoop."
Post-tussive vomiting and cyanosis.
Infants: Apnea instead of a whoop.
Convalescent Phase (Weeks to months):
Gradual recovery; coughing fits decrease in frequency/severity.
What are the clinical features of pertussis?
Classic triad:
Paroxysmal cough.
Inspiratory "whoop."
Post-tussive vomiting.
Infants: May present with apnea, cyanosis, and feeding difficulties.
Signs of respiratory distress in severe cases.
How is pertussis diagnosed?
Clinical diagnosis: Based on characteristic cough and history of exposure.
PCR: Preferred for rapid diagnosis.
Culture: Gold standard but takes longer; useful in early stages.
Serology: Detects antibodies in later stages.
What conditions mimic pertussis?
Viral bronchiolitis: No paroxysmal cough or whoop.
Croup: Barking cough and stridor instead of whoop.
Foreign body aspiration: Sudden onset, no fever or systemic signs.
What is the treatment for pertussis?
Oxygen for hypoxia.
Monitor for apnea in infants.
First-line: Azithromycin (macrolide).
Start during catarrhal phase to reduce severity and transmission.
Hospitalization:
For infants <6 months or severe complications (e.g., apnea, pneumonia).
What are the common complications of pertussis?
Infants:
Apnea.
Secondary bacterial pneumonia (most common cause of death).
Seizures.
Hypoxic encephalopathy.
Older children/adults:
Rib fractures from severe coughing.
Syncope.
How is pertussis prevented?
DTaP: Given in childhood (5 doses by age 6 years).
Tdap: Booster at 11–12 years and during each pregnancy.
DTaP:
D: Diphtheria
T: Tetanus
aP: Acellular Pertussis
Tdap:
d: Diphtheria (lower dose compared to DTaP)
These vaccines protect against diphtheria, tetanus, and pertussis (whooping cough).
Defintiion of obestiy
Obesity: BMI ≥95th percentile for age and sex.
Overweight: BMI between 85th–94th percentiles.
What is the first critical respiratory adaptation for a newborn?
The first breath helps clear lung fluid and establish normal breathing patterns.
Respiratory rate: 30–60 breaths/minute.
Periodic breathing is normal but should not cause cyanosis or bradycardia ( is concerna if pauses longer than 20 seconds)
What changes occur in the cardiovascular system after birth?
Closure of fetal circulatory shunts:
Ductus arteriosus: Functionally closes within hours; anatomically within days.
Foramen ovale: Closes due to left atrial pressure > right atrial pressure.
Ductus venosus: Closes as placental blood flow ceases.
Pulse rate: 120–160 bpm, varying with activity.
What thermoregulation challenges do newborns face?
imited thermoregulation due to:
Large surface area-to-body mass ratio.
Thin skin and minimal fat insulation.
Heat production relies on metabolizing brown fat (non-shivering thermogenesis).
Interventions: Skin-to-skin contact, warm environment
What are the key metabolic adaptations in newborns?
Transition to feeding: Shift from placental nutrition to breastfeeding/formula.
Energy reliance: Glycogen stores initially, frequent feeding needed.
Weight loss: 5–10% of birth weight lost in the first week, regained by two weeks.
What causes physiological jaundice in newborns?
Increased red blood cell turnover and immature liver enzymes.
Leads to transient hyperbilirubinemia, resolving within 1–2 weeks.
Important to monitor bilirubin levels to prevent complications (e.g., kernicterus)
How do newborns acquire immunity?
Passive immunity:
Maternal antibodies (IgG) cross the placenta.
Breast milk provides IgA for mucosal protection.
Active immunity: Develops as the newborn encounters antigens.
What are the common symptoms of meningitis in infants?
Fever, irritability, poor feeding, vomiting, diarrhea.
Bulging fontanelle (increased intracranial pressure).
Nuchal rigidity (may be subtle in infants).
Seizures (especially with parechovirus).
What are the symptoms of meningitis in older children?
Fever, headache, nausea, vomiting, stiff neck, photophobia.
Rash (e.g., enteroviruses), conjunctivitis.
Neurologic signs: altered mental status, focal deficits, seizures
Viral vs. Bacterial Meningitis: CSF Findings
Viral Meningitis:
WBC: 10–500 cells/μL (mononuclear predominance).
Glucose: Normal or slightly low.
Protein: Normal to mildly elevated.
Bacterial Meningitis:
WBC >1000 cells/μL (neutrophilic predominance).
Glucose: Low.
Protein: High.
What are the age-specific common pathogens causing bacterial meningitis?
<3 months: Group B Streptococcus, E. coli, S. pneumoniae, N. meningitidis.
>3 months: S. pneumoniae, N. meningitidis.
What empiric antibiotics are used for bacterial meningitis?
Children: Ceftriaxone or cefotaxime + vancomycin.
Which vaccines help prevent bacterial meningitis?
Pneumococcal vaccine (S. pneumoniae).
Haemophilus influenzae type B (Hib) vaccine.
Meningococcal vaccine (N. meningitidis).
How is viral meningitis managed?
Supportive care: Hydration, antipyretics.
Avoid aspirin in children (risk of Reye syndrome).
Acyclovir for suspected HSV.
Antiviral Therapy:
HSV: IV acyclovir.
Paed: Types of Lymphoma
Hodgkin Lymphoma (HL): Reed-Sternberg cells, peaks at 15–19 years.
Non-Hodgkin Lymphoma (NHL): High-grade, aggressive subtypes, more common in males and older children.
Paed: Clinical Features of Hodgkin Lymphoma
Painless lymphadenopathy (cervical/supraclavicular).
B Symptoms: Fever >38°C, night sweats, weight loss >10% in 6 months.
Mediastinal mass: Found in up to 75%.
Rare: Pruritus, alcohol-induced pain.
Paed: Diagnosis of Hodgkin Lymphoma
Excisional Biopsy: Identifies Reed-Sternberg cells (gold standard).
Paed: Treatment of Hodgkin Lymphoma
Risk-Adapted Therapy:
Low-Risk: ABVE-PC ± low-dose radiation.
Intermediate/High-Risk: Escalated regimens ± radiation.
Relapsed/Refractory: ICE + stem cell transplant.
Paed: Clinical Features of Non-Hodgkin Lymphoma
Rapidly enlarging, nontender lymphadenopathy.
Compression symptoms: Respiratory distress, facial swelling, acute abdominal pain.
Oncologic Emergencies: Mediastinal mass, tumor lysis syndrome, CNS involvement.
Subtypes of Non-Hodgkin Lymphoma
Lymphoblastic Lymphoma (LBL): T-cell dominant, mediastinal masses common.
Burkitt Lymphoma (BL): Abdominal masses, associated with EBV.
Diffuse Large B-Cell Lymphoma (DLBCL): Rapidly growing masses.
Anaplastic Large Cell Lymphoma (ALCL): CD30+, may involve skin/CNS.
🌧️ Paed: Viral Pneumonia - Management
Hydration.
Antipyretics for fever.
Oxygen if needed.
💊 Paed: Bacterial Pneumonia - Treatment
Outpatient:
First-line: Amoxicillin or Cefdinir.
Inpatient:
Ampicillin or Ceftriaxone.
Add Vancomycin if MRSA suspected.
ICU care, oxygen/ventilation.
Broad-spectrum antibiotics
When is CABG preferred over PCI for stable CAD?
Proximal LAD stenosis.
Left main stenosis >50%.
SYNTAX score >23.
Multi-vessel disease or impaired LV function.
What are indications for myocardial revascularization in NSTEMI?
CABG: 2+ vessel disease. often preffered
PCI: 1-vessel disease, non-proximal LAD.if not important arteries
What method is preferred in STEMI
CABG is recommended for left main stenosis, proximal LAD stenosis, or SYNTAX score >23.
What are the main methods for myocardial revascularization?
CABG:
Grafts: Arterial (e.g., mammary, radial) or venous (e.g., saphenous).
Methods: Off-pump (heart beating) or on-pump (cardiopulmonary machine).
PCI:
Stents: Bare-metal or drug-eluting.
Minimally invasive via femoral artery.
if drug electing stent —> dont forget to use dual antiplatelet therapy for 1 month
what grafts are used for CABG
a. thoracica interna
not suitable for obese patients
< 75 —> both mammary glands
> 75 —> mammary + radial artery
a. radialis
calcium channel blockers needed forever
Venous grafts
v. saphena magna
What are the complications of CABG
My Graft Drains Vital Arteries Poorly":
myocardial infarction
graft occlusion
decreased cardiac output
vasodilatory shock
arrythmias
pericardiits
What are the complications of PCI
Risky Catheters Puncture Narrow Hearts Easily"
reanastomosis
coronary artery dissection
perforation
no reflow
hemodynamic collapse
entrapped equipemnt
What are the options for heart valve replacement in adults?
Approaches: Open surgery, percutaneous (via femoral artery).
Types of valves:
Mechanical: Lasts indefinitely but requires lifelong warfarin anticoagulation.
Biological: Lasts 10–15 years; no lifelong anticoagulation. Suitable for elderly, dialysis patients, childbearing-age women, IV drug users, or those with compliance issues.
What are the types of aortic valve replacement procedures and their indications?
urgical Aortic Valve Replacement (SAVR):
Indicated for:
Life expectancy >10 years.
Endocarditis.
Aortic thrombus.
Anatomy unsuited for TAVI.
Transcatheter Aortic Valve Implantation (TAVI):
Indicated for older patients or those unfit for open surgery.
Not suitable for severely calcified valves or infective endocarditis (IE).
Mitral Valve Replacement or Repair
What procedures are available for mitral valve conditions?
Mitral Stenosis:
Percutaneous Mitral Commissurotomy (high restenosis rates).
Open surgery (for severe calcifications or prior surgery).
Mitral Regurgitation:
Annuloplasty.
Chorda repair.
MITRACLIP (minimally invasive via femoral vein).
What are the surgical options for tricuspid valve disorders?
Tricuspid Regurgitation:
Suturing (e.g., Kay or De Vega procedures).
Annuloplasty using a semi-rigid ring.
Tricuspid Stenosis:
Valve replacement (bioprosthetic/mechanical).
Percutaneous balloon commissurotomy (under investigation).
What mechanical circulatory support devices are used for heart failure?
Intra-Aortic Balloon Pump:
Improves myocardial perfusion and reduces oxygen demand.
Inserted via the femoral artery to the thoracic aorta.
Impella Heart Pump:
Pulls blood from the left ventricle and expels into the ascending aorta.
Inserted via catheterization through the femoral artery.
What is ECMO, and what are its types?
Veno-Arterial ECMO: Supports both heart and lungs; blood bypasses these organs for oxygenation.
Veno-Venous ECMO: Supports only the lungs; blood is oxygenated and returned to the venous system.
What are the indications and contraindications for heart transplant?
Indications:
Cardiogenic shock requiring continuous support.
Persistent NYHA IV symptoms refractory to treatment.
Severe CAD or life-threatening arrhythmias.
Contraindications:
Life expectancy <2 years.
Irreversible pulmonary HT.
Active substance abuse or inability to comply with immunosuppression.
What anticoagulation therapy is required after heart valve replacement?
Mechanical Valves: Lifelong warfarin therapy.
Biological Valves: No lifelong anticoagulation unless atrial fibrillation or another risk factor is present.
What are the common symptoms of peptic ulcer disease in children?
Epigastric pain (most common).
Nausea/vomiting (may include hematemesis).
Melena (black, tarry stools).
Poor appetite and weight loss.
Irritability in younger children.
⚠️ What are the alarm symptoms in pediatric PUD?
Severe or sudden abdominal pain (indicates perforation).
Hematemesis or melena (suggests bleeding).
Unexplained weight loss.
Anemia or signs of systemic illness.
🧪 What tests are used for diagnosing H. pylori in children?
Non-invasive Tests:
Urea breath test (preferred).
Stool antigen test.
Invasive Test:
Endoscopic biopsy for histology and culture.
🔬 What does endoscopy reveal in pediatric PUD?
Visible ulcers in the stomach or duodenum.
Inflammation or bleeding sites.
Allows biopsy for:
H. pylori detection.
Rule out malignancy (rare in children).
🔍 What are the common lab findings in pediatric PUD?
CBC: May show anemia (microcytic or normocytic).
Stool Occult Blood Test: Positive in bleeding ulcers.
Inflammatory Markers: Usually normal unless there’s a secondary condition.
Abdominal Ultrasound: Excludes other causes of abdominal pain (e.g., gallstones).
CT Scan: Used in suspected complications like perforation or obstruction.
💡 What are the common symptoms of gastritis in children?
Epigastric pain or burning sensation.
Loss of appetite.
Bloating or early satiety.
Hematemesis (if erosive gastritis).
⚠️ What are alarm symptoms in pediatric gastritis?
Vomiting blood (hematemesis).
Severe or persistent abdominal pain.
🧪 What tests are used for diagnosing gastritis?
Urea breath test (for H. pylori).
Stool antigen test (H. pylori).
Invasive Tests:
Upper gastrointestinal endoscopy with biopsy.
🔍 What lab findings may support a gastritis diagnosis?
CBC: Anemia (due to chronic blood loss).
Stool Occult Blood Test: Positive if there’s GI bleeding.
Serum Gastrin Levels: Elevated in autoimmune gastritis.
Electrolytes: Abnormal in severe vomiting or dehydration.
📌 What are the causes of gastritis in children?
Infectious:
H. pylori (most common).
Viral infections (e.g., rotavirus, CMV).
Chemical:
NSAIDs, aspirin, corticosteroids.
Autoimmune:
Associated with pernicious anemia.
Allergic:
Eosinophilic gastritis linked to food allergies.
🩻 How is H. pylori-associated gastritis diagnosed?
Gold Standard: Endoscopic biopsy with histology and urease testing.
What is the definition of precocious puberty in children?
Precocious puberty is the onset of secondary sexual characteristics before age 8 in girls and age 9 in boys, occurring earlier than the population norm.
What three key questions should be asked when evaluating precocious puberty?
Is the child too young for this pubertal milestone?
What is causing the early development (central or peripheral)?
Is therapy needed, and what therapy is appropriate?
What are the common causes of central precocious puberty?
diopathic (most common in girls).
Brain abnormalities such as tumors or infections.
Genetic mutations affecting puberty regulation.
What causes peripheral precocious puberty?
Hormone-producing ovarian or testicular tumors.
Adrenal gland disorders like congenital adrenal hyperplasia.
Exogenous hormone exposure.
What are the key diagnostic steps for precocious puberty?
History and physical examination to assess onset and progression.
Laboratory tests including hormone levels.
Imaging: Bone age X-ray, brain MRI, and pelvic ultrasound.
Extensive anamnesis
- Physical examination
- Labs: LH, FSH, Estradiol, Testosterone, other serum androgen levels: e.g. 17-OH progesterone, DHEAS, androstendione, GnRH (LHRH) test (basal and post-GnRH LH, and FSH levels)
- Tanner scale: puberty staging
- Check for abdominal and genital masses
- Urine: steroid profile (sex/adrenal steroids)
- Pelvic US (ovarian morphology; testicular masses)
- Abdominal US, e.g. adrenal glands
- MRI scan brain
What is the main treatment for central precocious puberty?
GnRH agonists, which suppress the hypothalamic-pituitary-gonadal axis to delay further progression.
buserelin, goserelin
Peripheral precocious puberty
- Tumor producing excessive hormone → surgical removal
- CAH → cortisol replacement
- Ovarian cysts → no intervention is necessary (spontaneous resolution is common)
How is peripheral precocious puberty treated?
By addressing the underlying cause, such as removing tumors or using hormone-blocking medications like aromatase inhibitors.
What defines delayed puberty in children?
: Delayed puberty is the absence of secondary sexual characteristics by age 13 in girls and age 14 in boys.
What causes primary hypogonadism in delayed puberty?
Turner syndrome in girls. Missing or damaged X chromosome.
Klinefelter syndrome in boys. Extra X chromosome (XXY).
Underdeveloped gonads or gonadal failure.
What are common causes of secondary hypogonadism in delayed puberty?
Brain-related issues such as hypothalamic or pituitary disorders.
Chronic illnesses like malnutrition or hypothyroidism.
Genetic conditions such as Kallmann syndrome.
Diagnostic approach to delayed puberty
Growth History: Height and weight changes.
Signs of Chronic Illness: Fatigue, delayed growth.
Tanner Staging: Assess sexual development stages.
LH/FSH, Estradiol/Testosterone: Determines hypogonadism type.
Thyroid Function: Rules out hypothyroidism.
Prolactin Levels: High levels can suppress puberty.
Bone Age X-ray: Delayed in CDGP.
MRI Brain: Looks for structural issues in the hypothalamus or pituitary.
What are the treatment options for delayed puberty?
Observation for mild delays or constitutional delay.
Hormonal therapy: Testosterone in boys or estradiol in girls.
Treating underlying conditions like chronic illness or hypothyroidism
Defintion of rickets
Rickets is a disorder caused by impaired bone mineralization at the growth plates in children, leading to skeletal deformities.
It is most commonly due to vitamin D deficiency but can also result from calcium or phosphate abnormalities.’
What are the main causes of rickets in children?
Nutritional Rickets: Vitamin D or calcium deficiency.
Vitamin D-Dependent Rickets:
Type 1: Deficiency in activating enzyme for vitamin D.
Type 2: Resistance to active vitamin D.
Hypophosphatemic Rickets: Renal phosphate wasting (e.g., X-linked hypophosphatemia).
Chronic Kidney Disease: Impaired vitamin D metabolism.
What increases the risk of developing rickets?
Environmental: Lack of sunlight, darker skin tones.
Dietary: Inadequate intake of vitamin D or calcium, exclusive breastfeeding without supplementation.
Health Conditions: Prematurity, malabsorption syndromes (e.g., celiac disease), chronic illnesses.
How does rickets develop physiologically?
Vitamin D deficiency reduces calcium and phosphate absorption.
Hypocalcemia triggers increased parathyroid hormone (PTH), causing bone resorption( osteoclasts break down the tissue in the bones and release the minerals) and phosphate wasting.
Impaired bone mineralization leads to skeletal deformities and growth plate widening
What are the clinical features of rickets in children?
General: Irritability, poor growth, muscle weakness.
Skeletal Deformities: Bowed legs, knock knees, craniotabes, rachitic rosary.
Neurological: Tetany, seizures (due to hypocalcemia).
Dental: Delayed tooth eruption, enamel hypoplasia.
How is rickets diagnosed?
History & Exam: Nutritional history, skeletal deformities, growth patterns.
Low vitamin D, hypocalcemia, hypophosphatemia.
Elevated alkaline phosphatase and parathyroid hormone.
Imaging: X-rays show widened growth plates, frayed metaphyses, bowing of long bones.
Management of Nutritional Rickets Q: How is nutritional rickets treated
Vitamin D: High-dose therapy (2,000–5,000 IU daily for 6–12 weeks), then maintenance (400–1,000 IU daily).
Calcium: 1,000–1,500 mg/day.
Encourage sunlight exposure and a diet rich in vitamin D and calcium.
How can rickets be prevented?
Vitamin D Supplementation:
Infants: 400 IU/day from birth.
Older children: 400–600 IU/day.
Encourage safe sun exposure (15–30 mins, 2–3 times weekly).
Diet: Include dairy, fish, and fortified foods.
At-risk groups may need higher supplementation.
Definition of Reactive Arthritis in Pediatrics
Q: What is reactive arthritis in children?
Reactive arthritis is an autoimmune condition triggered by an infection elsewhere in the body,
typically involving the joints, eyes, and urogenital system.
It occurs after infections like gastrointestinal or genitourinary infections.
What are common infections that trigger reactive arthritis in children?
Gastrointestinal Infections: Salmonella, Shigella, Campylobacter, Yersinia.
Genitourinary Infections: Chlamydia trachomatis.
Respiratory Infections: Mycoplasma pneumoniae, Streptococcus species.
What is the pathophysiology of reactive arthritis?
Triggered by infections outside the joints.
Cross-reactive immune response leads to inflammation in synovial joints. (typical for all seronegative arthritis)
Genetic predisposition (HLA-B27 positivity increases risk).
What are the key clinical features of reactive arthritis in children?
Joint Symptoms:
Asymmetric oligoarthritis (affecting 1–4 joints).
Commonly involves lower extremities (knees, ankles).
Extra-articular Features:
Eyes: Conjunctivitis, uveitis.
Skin: Keratoderma blennorrhagicum, (to differentiate for psoratic arthritis)
ureterarthritis, cervitis
Mucous Membranes: Oral ulcers.
findger: dactylitis
spinal cord: sacroiliac joint
Systemic Symptoms: Fever, fatigue, weight loss.
How is reactive arthritis diagnosed in children?
History of preceding infection within 1–4 weeks.
Clinical signs: Joint swelling, redness, warmth, limited mobility.
Laboratory: Elevated ESR/CRP, leukocytosis.
Imaging: X-rays or MRI may show periarticular swelling, effusions.
HLA-B27 testing if suspected genetic predisposition.
What conditions need to be ruled out in pediatric reactive arthritis?
Septic arthritis.
Juvenile idiopathic arthritis (JIA).
Post-streptococcal arthritis.
Lyme arthritis.
How is reactive arthritis treated in children?
Supportive Care: Rest, physical therapy.
NSAIDs: First-line for pain and inflammation (e.g., ibuprofen, naproxen).
Corticosteroids: For severe cases or when NSAIDs fail (intra-articular or systemic).
DMARDs: Methotrexate for chronic or refractory arthritis.
Antibiotics: Only for active infections (e.g., Chlamydia).
What is rubella
A contagious viral illness caused by the rubella virus
severe congential anomalies
if contracted during pregnancy (congenital rubella syndrome)
What are the main modes of rubella transmission?
Airborne droplets from respiratory secretions.
Transplacental transmission during pregnancy.
Infectious period: 7 days before and after rash onset.
How does rubella present in neonates (congenital rubella syndrome)?
Sensorineural hearing loss (most common).
Congenital heart defects: Patent ductus arteriosus, pulmonary stenosis.
Ocular anomalies: Cataracts, glaucoma.
Neurological impairments: Intellectual disability, microcephaly.
Blueberry muffin rash, hepatosplenomegaly, thrombocytopenia.
Stages of rubella
Prodromal Phase (1–5 days):
Low-grade fever, malaise.
Lymphadenopathy: Cervical, posterior auricular, suboccipital nodes.
Mild upper respiratory symptoms.
Exanthem Phase (2–3 days):
Maculopapular rash:
Begins on the face, spreads caudally to trunk/extremities, spares palms/soles.
Fades in about 3 days.
Forchheimer spots: Red spots on the soft palate.
Mild nonexudative conjunctivitis.
Polyarthritis (common in older children/adolescents).
What are the complications of rubella in children?
Arthritis: Particularly in adolescent females.
Thrombocytopenic purpura.
How is rubella diagnosed in pediatric cases?
Rubella-specific IgM serology:
Preferred test; detectable 4 days after rash onset.
Real-Time RT-PCR:
Detects viral RNA in throat swab, nasopharyngeal aspirates, or urine.
Best within first 3 days of rash onset.
Congenital Rubella Syndrome:
Persistent IgG antibodies beyond 6 months indicate CRS.
How is rubella managed in children?
No specific antiviral therapy.
Antipyretics for fever (e.g., paracetamol).
Rest.
Isolation for 7 days post-rash onset to prevent spread.
How is rubella prevented?
accination (MMR):
Live attenuated vaccine combining measles, mumps, and rubella.
Doses:
Contraindications: Pregnancy, immunocompromised individuals.
Pregnancy considerations:
Ensure vaccination prior to conception.
Post-exposure prophylaxis with immunoglobulin for pregnant women.
When should rubella be suspected?
Unvaccinated children with:
Maculopapular rash spreading cephalocaudally.
Posterior auricular, cervical, and suboccipital lymphadenopathy.
Forchheimer spots or mild systemic symptoms.
What causes scarlet fever, and how is it transmitted?
Causative Agent: Group A Streptococcus (Streptococcus pyogenes) producing pyrogenic exotoxins.
Transmission: Respiratory droplets or direct contact with infected individuals or contaminated surfaces.
What is the incubation period for scarlet fever?
Incubation Period: Approximately 1–4 days after exposure to the bacteria.
Initial Symptoms (Prodromal Phase)Q: What are the initial symptoms of scarlet fever in children?
Sudden onset of fever (often over 38.5°C or 101.3°F).
Sore throat and difficulty swallowing.
Headache, nausea, and abdominal pain.
Possible vomiting.
Characteristics of the Rash (Exanthem)Q: Describe the rash associated with scarlet fever.
Appears 12–48 hours after fever onset.
Diffuse, finely papular, erythematous rash with a "sandpaper-like" texture.
Begins on the chest and spreads to the trunk, extremities, and face.
Spares the palms and soles.
Rash blanches on pressure.
Fades in 3–5 days, followed by peeling (desquamation), especially on hands and feet.
What are Pastia's lines, and how are they related to scarlet fever?
Pastia's Lines: Linear petechial streaks found in the skin folds (e.g., armpits, elbow creases).
They result from capillary fragility and are a characteristic sign of scarlet fever.
What are the key oral findings in scarlet fever?
Pharynx: Reddened (erythematous) with possible exudate.
Strawberry Tongue:
Initially, a white coating with prominent red papillae ("white strawberry tongue").
Later, the white coating peels off, leaving a red, raw tongue ("red strawberry tongue").
What distinctive facial features are seen in scarlet fever?
Flushed cheeks with a notable pale area around the mouth (circumoral pallor).
Which lymph nodes are commonly enlarged in scarlet fever?
Tender, enlarged anterior cervical lymph nodes (in the neck).
What tests are used to confirm a diagnosis of scarlet fever?
Throat Swab and Culture:
Gold standard to identify Group A Streptococcus.
Rapid Antigen Detection Test (RADT):
Quick results; highly specific but less sensitive than culture.
What laboratory findings might support a diagnosis of scarlet fever?
Complete Blood Count (CBC): May show leukocytosis with neutrophilia.
Elevated Inflammatory Markers: Such as ESR (erythrocyte sedimentation rate) and CRP (C-reactive protein).
Antistreptolysin O (ASO) Titers: May rise but are more useful for retrospective diagnosis.
What conditions should be considered in the differential diagnosis of scarlet fever?
Viral Exanthems: Measles, rubella, fifth disease.
Kawasaki Disease: Similar rash but with additional features like conjunctivitis and swollen hands/feet.
Staphylococcal Scalded Skin Syndrome: Diffuse redness and peeling skin.
Drug Reactions: Such as allergic reactions causing rash.
What are potential complications of scarlet fever?
Suppurative Complications:
Otitis Media: Middle ear infection.
Sinusitis: Infection of the sinuses.
Peritonsillar Abscess: Collection of pus beside the tonsil.
Nonsuppurative Complications:
Acute Rheumatic Fever: Can affect the heart, joints, skin, and brain.
Post-streptococcal Glomerulonephritis: Kidney inflammation leading to hematuria.
Why are antibiotics prescribed for scarlet fever, and which ones are commonly used?
Purpose: Eliminate the bacteria, reduce symptom duration, prevent complications, and minimize transmission.
Common Antibiotics:
Penicillin V (first-line treatment).
Amoxicillin.
Erythromycin or azithromycin for penicillin-allergic patients.
Main causes of sespsis in neonates and children
Neonates: Group B Streptococcus, Escherichia coli.
Infants/children: Streptococcus pneumoniae, Neisseria meningitidis, and Staphylococcus aureus.
clinical presentation of sepsis
Fever or hypothermia.
Tachycardia and tachypnea (early signs of systemic inflammation).
Hypotension and poor perfusion (cold extremities, prolonged capillary refill, mottling).
Altered mental status due to multi-organ dysfunction.
Signs of coagulopathy: Petechiae or purpura.
Laboratory Findings of sepsis
Sepsis:
Elevated inflammatory markers: C-reactive protein (CRP), procalcitonin.
Blood cultures: May show the causative organism.
Elevated lactate levels: Indicate tissue hypoperfusion.
Coagulation profile: Possible disseminated intravascular coagulation (DIC).
complications of sepsis
Multi-organ failure (e.g., acute respiratory distress syndrome, acute kidney injury).
Death due to overwhelming infection.
what is procalcitonin
PCT is a precursor of the hormone calcitonin, produced by various tissues during bacterial infections.
why are lactate levels important in terms of sepsis
sepsis causes tissue hypoperfusion (low oxygen delivery to tissues) due to systemic inflammation, vasodilation and hypotension.
This make cells shift from aerobic to anaerobic metabolism.
what is the most severe complication in sespsis
Disseminated intravascular coagulation
what is it ?
includes test like prothrombin time (PT), APTT, fibrinogen levels and D-dimer.
there is a consumption of clotting factors and platelets which increases bleeding risk.
DIC in sepsis:
a severe complication where microvascular thrombi form throughout the body, impairing blood flow and consuming clotting factors resulting in bleeding and organ dysfunction.
lab findings:
prolonged Pt and aPTT
low fibrinogen ( consumed in clot formation)
elevated D dimer ( this indicates there is a clot breakdown)
thrombocytopenia (low platelets)
What is thrombocytopenia?
Definition: Platelet count <150,000/μL.
Severe: <50,000/μL (risk of bleeding).
Critical: <20,000/μL (spontaneous hemorrhage risk)
What are the most common causes of thrombocytopenia in neonates?
Neonatal Alloimmune Thrombocytopenia (NAIT).
Congenital infections (TORCH: Toxoplasmosis, Rubella, CMV, Herpes simplex).
Sepsis or DIC.
: What are the common causes of thrombocytopenia in infants and young children?
Immune Thrombocytopenia (ITP) – post-viral.
Hemolytic Uremic Syndrome (HUS) – following diarrheal illness (E. coli O157:H7).
Congenital syndromes (e.g., Wiskott-Aldrich Syndrome).
What are the key diagnostic steps in thrombocytopenia?
History:
Recent infections, medications, family history of bleeding disorders.
Physical Exam:
Bleeding signs: Petechiae, purpura, mucosal bleeding.
Systemic signs: Hepatosplenomegaly, lymphadenopathy.
Complete Blood Count (CBC): Platelet count, other cytopenias.
Peripheral smear: Assess for morphology (giant platelets, schistocytes).
Coagulation panel: For DIC assessment.
What does the CBC and peripheral smear indicate in thrombocytopenia?
Isolated thrombocytopenia: Suggests ITP.
Pancytopenia: Suggests bone marrow failure (e.g., leukemia, aplastic anemia).
Schistocytes: Seen in DIC, HUS, or TTP.
What are the hallmark features of Immune Thrombocytopenia (ITP)?
Isolated thrombocytopenia.
Preceding viral illness.
Petechiae, purpura, mucosal bleeding.
Normal coagulation panel.
What is the significance of a prolonged PT/aPTT in thrombocytopenia?
Suggests DIC or severe liver dysfunction.
How can you distinguish
Immune Thrombocytopenia (ITP)
Disseminated Intravascular Coagulation (DIC)
Hemolytic Uremic Syndrome (HUS),
Thrombotic Thrombocytopenic Purpura (TTP)?
Immune Thrombocytopenia (ITP):
Isolated low platelet count (thrombocytopenia) with normal coagulation tests.
Commonly occurs after a viral illness.
Disseminated Intravascular Coagulation (DIC):
Low platelet count (thrombocytopenia) combined with prolonged Prothrombin Time (PT) and Activated Partial Thromboplastin Time (aPTT).
Peripheral blood smear shows fragmented red blood cells (schistocytes).
Hemolytic Uremic Syndrome (HUS) / Thrombotic Thrombocytopenic Purpura (TTP):
Triad of thrombocytopenia, destruction of red blood cells (hemolytic anemia), and kidney dysfunction (renal involvement).
What is thyrotoxicosis?
A clinical syndrome caused by elevated levels of thyroid hormones (T3 and/or T4) leading to a hypermetabolic state.
What are the primary causes of thyrotoxicosis?
Primary Hyperthyroidism: Graves' disease, toxic multinodular goiter, toxic adenoma.
Secondary Hyperthyroidism: TSH-secreting adenoma.
Thyroid Destruction: Subacute thyroiditis, postpartum thyroiditis.
Exogenous: Overuse of thyroid hormone supplements
What are the hallmark symptoms of thyrotoxicosis?
Weight loss despite normal appetite.
Palpitations, tachycardia.
Heat intolerance, sweating.
Tremors, restlessness, and irritability.
Goiter (in Graves’ disease).
Exophthalmos (Graves’ disease).
How is thyrotoxicosis diagnosed?
Suppressed TSH (<0.1 mIU/L) in primary cases.
Elevated Free T3/T4 levels.
Autoantibodies: TSI (specific for Graves’ disease).
Radioactive Iodine Uptake (RAIU): Differentiates Graves’ disease (high uptake) from thyroiditis (low uptake).
What are the complications of thyrotoxicosis?
Thyroid storm (life-threatening).
Atrial fibrillation.
Heart failure.
Osteoporosis with chronic untreated cases.
What is a thyroid storm?
A life-threatening exacerbation of thyrotoxicosis characterized by fever, tachycardia, delirium, vomiting, and potential organ failure.
How is thyroid storm managed?
Beta-blockers (e.g., propranolol) for symptom control.
High-dose PTU or methimazole.
Iodine solutions to inhibit hormone release.
Corticosteroids to reduce T4 to T3 conversion.
Supportive care: Cooling, fluids, electrolytes.
What are the treatment options for thyrotoxicosis?
Beta-blockers for symptomatic relief.
Antithyroid drugs: Methimazole (preferred), PTU (in pregnancy or thyroid storm).
Radioactive Iodine Therapy (RAI): Definitive treatment, leads to hypothyroidism.
Surgery (Thyroidectomy): For large goiters, malignancy suspicion, or contraindications to RAI.
What are the features of Graves' disease-specific thyrotoxicosis?
Diffuse goiter.
Exophthalmos (eye bulging).
Pretibial myxedema.
Positive thyroid-stimulating immunoglobulin (TSI).
How is exophthalmos in Graves' disease treated?
Mild: Artificial tears, sunglasses.
Moderate to severe: Corticosteroids, orbital decompression surgery.
Sandpaper-like rash, strawberry tongue, fever, pharyngitis.
Pastia’s lines (rash accentuated in skin folds).
Scarlet Fever
Group A Streptococcus (GAS).
Mild fever, pinpoint maculopapular rash spreading cephalocaudally.
Posterior auricular and suboccipital lymphadenopathy.
Rubella (German Measles)
Paroxysmal cough with inspiratory "whoop."
Catarrhal, paroxysmal, and convalescent phases.
Whooping Cough
Fever, malaise, parotid gland swelling (bilateral or unilateral).
Orchitis or oophoritis in adolescents.
Mumps
High fever, cough, coryza, conjunctivitis (3 Cs).
Koplik spots (bluish-white spots on buccal mucosa).
Maculopapular rash starts on face, spreads cephalocaudally.
Measles
Key Features: Fever >5 days + 4 of the following:
Conjunctivitis, rash, extremity changes, cervical lymphadenopathy, mucous membrane changes (strawberry tongue).
Kawasaki Disease
Key Features:
Palpable purpura (without thrombocytopenia), arthritis, abdominal pain, hematuria.
Henoch-Schönlein Purpura (HSP
"Barking" cough, hoarseness, inspiratory stridor.
Worse at night; may improve with cool air or steam.
Diagnosis: Clinical; X-ray shows "steeple sign."
Wheezing, nasal flaring, tachypnea, retractions.
Occurs primarily in children <2 years.
Bronchiolitis
Itchy, red, scaly patches (commonly on flexural surfaces in children).
Exacerbated by allergens, stress, or irritants.
Atopic Dermatitis
Vomiting, diarrhea (watery, bloody if bacterial).
Dehydration signs: dry mucous membranes, sunken eyes, poor skin turgor.
Acute Gastroenteritis
Rapid onset fever, severe sore throat, stridor.
Drooling and difficulty swallowing.
Child appears toxic and sits in a "tripod position" for easier breathing.
Acute Epiglottitis
Varicella (Chickenpox)
Highly contagious viral illness caused by Varicella-Zoster Virus (VZV), a member of the herpesvirus family
Age Group Affected for chicken pox
transmission
Primarily affects children under 10 years but can occur at any age.
Transmission:
Direct contact with vesicular fluid.
Virus enters respiratory tract and multiplies in regional lymph nodes.
Spreads hematogenously to skin, causing vesicular lesions.
Latency: VZV remains dormant in dorsal root ganglia.
Reactivation (Shingles): May occur later in life, especially in immunocompromised states.
Clinical features of chicken pox
Prodromal Phase (1–2 days before rash):
Fever, malaise, headache, sore throat.
Exanthem Phase:
Classic Rash Progression: "Crops" of lesions at different stages.
Macules → Papules → Vesicles → Pustules → Crusts.
Lesions are pruritic.
Distribution: Starts on face and trunk → spreads to extremities. Centripetal distribution (more on trunk than extremities).
Spares palms and soles.
Systemic Symptoms:
Low-grade fever, irritability.
complications of chicken pox
Skin and Soft Tissue:
Secondary bacterial infections (impetigo, cellulitis).
Neurological:
Cerebellar ataxia.
Encephalitis.
Reye syndrome (if aspirin is used).
Pulmonary:
Varicella pneumonia (rare in children but serious in adults).
Other:
Hepatitis, nephritis, thrombocytopenia.
Diagnosis of varicella
Based on rash and prodromal symptoms.
Laboratory Testing (if needed):
Tzanck Smear: Multinucleated giant cells (non-specific).
PCR for VZV DNA: Gold standard for confirmation.
Direct Fluorescent Antibody (DFA): Rapid diagnosis.
Serology for VZV IgM/IgG (for immune status).
Differential Diagnosis for chicken pox
Measles (rash with Koplik spots, high fever).
Rubella (faster rash progression, no vesicles).
Hand-Foot-Mouth Disease (vesicles on palms, soles, and mouth).
Insect bites (isolated lesions).
Management of chicken pox
Symptom Relief:
Antipyretics: Paracetamol (avoid aspirin due to Reye syndrome risk).
Pruritus: Calamine lotion, antihistamines.
Hydration: Adequate oral fluids.
Immunocompromised children.
Severe disease.
Adolescents >12 years.
Drug of Choice:
Acyclovir (within 24 hours of rash onset). Dosage: 20 mg/kg/dose, 4 times daily for 5 days.
Hospitalization Indications:
Complications like encephalitis, pneumonia, or disseminated varicella.
Prevention of chicken pox
Varicella Vaccine:
Live Attenuated Vaccine:
Administered as part of routine immunization.
Schedule:
1st dose: 12–15 months.
2nd dose: 4–6 years.
95% effective in preventing severe varicella.
Post-Exposure Prophylaxis:
Unvaccinated individuals exposed to varicella:
Varicella vaccine within 3–5 days of exposure.
Varicella-Zoster Immune Globulin (VZIG): High-risk individuals (e.g., immunocompromised, neonates)
What is a urinary tract infection (UTI)?
UTI is an infection involving any part of the urinary system, most commonly caused by bacteria, particularly Escherichia coli.
What are key risk factors for UTIs in children?
Female gender (shorter urethra).
Uncircumcised males.
Vesicoureteral reflux (VUR).
Constipation.
Poor hygiene.
Structural abnormalities of the urinary tract.
What are the most common pathogens causing UTIs in children?
Escherichia coli (>80%).
Klebsiella pneumoniae.
Proteus mirabilis.
Enterococcus species.
What are common UTI symptoms in infants?
Poor feeding.
Vomiting.
Irritability.
Failure to thrive.
What are common UTI symptoms in older children?
Dysuria (painful urination).
Frequency and urgency.
Abdominal or flank pain.
Hematuria (blood in urine).
Foul-smelling urine.
How is a UTI diagnosed in children?
Urinalysis:
Leukocyte esterase (+).
Nitrites (+).
Pyuria (WBCs >5/hpf).
Urine Culture:
Definitive diagnosis: Colony count ≥100,000 CFU/mL.
What are the methods for urine collection in children?
Clean-catch midstream (preferred).
Catheterization (if clean catch is not possible).
Suprapubic aspiration (for infants).
What is the empiric antibiotic therapy for UTIs in children?
Uncomplicated UTIs: Oral antibiotics (amoxicillin-clavulanate, cefixime).
Pyelonephritis: IV antibiotics (ceftriaxone, gentamicin).
3–5 days for uncomplicated cystitis.
7–10 days for febrile UTIs or pyelonephritis.
tension pneumothorax
What is a pneumothorax?
Pneumothorax is the presence of air in the pleural space, causing partial or complete lung collapse.
What are the types of pneumothorax?
Spontaneous Pneumothorax:
Primary: No underlying lung disease.
Secondary: Associated with lung diseases like COPD or cystic fibrosis.
Traumatic Pneumothorax:
Caused by blunt or penetrating chest trauma or medical procedures.
Tension Pneumothorax:
Life-threatening; air is trapped, causing mediastinal shift and hemodynamic compromise.
What are the risk factors for pneumothorax?
Smoking.
Genetic predisposition (e.g., Marfan syndrome).
Underlying lung diseases (e.g., COPD, asthma).
High-altitude flying or deep-sea diving.
Medical procedures (e.g., central line placement, mechanical ventilation).
What is the pathophysiology of tension pneumothorax?
Air enters the pleural space during inspiration but cannot exit.
Intrathoracic pressure increases, compressing the heart, great vessels, and contralateral lung.
Leads to mediastinal shift, decreased venous return, and hemodynamic instability.
Sudden, sharp chest pain (often unilateral).
Dyspnea (shortness of breath).
Reduced or absent breath sounds on the affected side.
Hyperresonance on percussion.
Asymmetrical chest movement.
Subcutaneous emphysema (crepitus).
pneumothorax
Severe dyspnea.
Tracheal deviation away from the affected side.
Hypotension, distended neck veins, cyanosis (late sign).
Tension Pneumothorax Specific:
How is pneumothorax diagnosed?
Visible visceral pleural line.
Absence of lung markings beyond the pleural line.
Mediastinal shift in tension pneumothorax.
More sensitive; used if X-ray findings are inconclusive.
What is the treatment for pneumothorax?
Stable Pneumothorax:
Observation for small pneumothorax (<2 cm).
Needle aspiration for moderate pneumothorax.
Chest tube placement for larger pneumothoraces.
Tension Pneumothorax (Emergency): treatment
Immediate needle thoracostomy (2nd intercostal space, midclavicular line).
Followed by chest tube insertion.
Recurrent or Persistent Pneumothorax: treatment
Pleurodesis (chemical or surgical).
Video-assisted thoracoscopic surgery (VATS).
What are the complications of pneumothorax?
Respiratory failure.
Recurrence (common in spontaneous pneumothorax).
Persistent air leak.
Tension pneumothorax → hemodynamic instability and death if untreated.
The safe triangle is a designated anatomical area on the lateral chest wall used for the insertion of chest tubes (thoracostomy). It minimizes the risk of injury to vital structures, such as nerves, vessels, and organs.
Boundaries of the Safe Triangle
Anterior Border:
Lateral edge of the pectoralis major muscle.
Posterior Border:
Anterior edge of the latissimus dorsi muscle.
Inferior Border:
Line parallel to the 5th intercostal space or the level of the nipple.
Superior Border:
Base of the axilla.
What are the primary causes of diaphragmatic relaxation?
Trauma (direct to diaphragm, phrenic nerve, or C3-C5 compression).
Neurological diseases (ALS, MS, Myasthenia Gravis, Duchenne Muscular Dystrophy).
Infections (West Nile, polio, Lyme disease).
Autoimmune diseases (sarcoidosis, amyloidosis).
Cancerous processes, congenital anomalies, chronic cough.
What is the gold standard diagnostic test for diaphragmatic relaxation?
: Fluoroscopy.
How does fluoroscopy aid in diagnosing diaphragmatic relaxation?
It provides dynamic imaging to assess diaphragmatic movement during respiration.
What are other imaging modalities for diagnosing diaphragmatic relaxation?
Ultrasound: Measures diaphragm thickness during inspiration and expiration.
X-ray: Shows initial signs but is not confirmatory.
CT Scan: Useful for structural evaluation and detecting tumors.
What do pulmonary function tests reveal in diaphragmatic relaxation? A:
Reduced Forced Vital Capacity (FVC), especially in the supine position.
What are the primary treatment options for diaphragmatic relaxation?
Treat underlying cause (e.g., antivirals for infections, immunosuppressants for autoimmune diseases).
Physiotherapy to strengthen respiratory muscles.
Surgical options like laparoscopic diaphragmatic plication or phrenic nerve pacing.
When is phrenic nerve pacing indicated, and how does it work?
Indicated for patients with phrenic nerve dysfunction causing diaphragmatic paralysis.
Works by laparoscopically placing electrodes at the diaphragm's motor units to stimulate contractions.
What systemic diseases can cause diaphragmatic relaxation?
ALS, MS, myasthenia gravis,
What is mediastinitis?
Mediastinitis is an inflammation of the mediastinum, often caused by infection, trauma, or surgical complications. It can be acute (e.g., post-surgical, esophageal perforation) or chronic (e.g., granulomatous infections or fibrosing mediastinitis).
What are the key causes of acute mediastinitis?
Postoperative complications (e.g., median sternotomy).
Esophageal perforation (spontaneous, iatrogenic, or traumatic).
Spread from odontogenic or cervical infections.
Respiratory infections or lung abscesses.
Severe chest pain (retrosternal, radiating to neck/back).
Dyspnea, fever, chills, and systemic toxicity (sepsis).
Subcutaneous emphysema ( infiltration of air underneath the dermal layers of skin) (if esophageal perforation).
Dysphagia, odynophagia, and tachycardia.
acute mediastinitis
Dyspnea, wheezing (due to airway compression).
Superior vena cava syndrome (facial swelling, cyanosis).
Chest pain or recurrent respiratory infections.
chronic mediastinitis
What diagnostic tests are used for mediastinitis?
Lab tests: Elevated CRP, ESR, leukocytosis, blood cultures.
Chest X-ray: Widened mediastinum, pneumomediastinum.
CT scan (gold standard): Detects fluid, gas, or abscesses.
Esophagogram (contrast swallow): For esophageal perforation.
Other: Bronchoscopy, esophagoscopy, or biopsy for chronic cases
What are complications of mediastinitis?
Sepsis and septic shock.
Airway obstruction.
Cardiac tamponade.
Superior vena cava syndrome.
Spread to adjacent structures like pleura or lungs.
How is acute mediastinitis managed?
Emergency surgery: Debridement, abscess drainage, esophageal repair.
Broad-spectrum antibiotics: Vancomycin + piperacillin-tazobactam (adjust based on cultures).
ICU care: Respiratory and hemodynamic support.
Nutritional support via enteral or parenteral feeding.
Hamman sign
crunching or crackling sound heard over the precordium, synchronous with the heartbeat. It indicates the presence of air in the mediastinum (
Where is a lung abscess located compared to a pleural abscess?
A lung abscess is within the lung parenchyma, while a pleural abscess is in the pleural space.
What imaging findings are characteristic of a lung abscess?
Thick-walled cavity with air-fluid levels within the lung, often surrounded by consolidation.
What are the key imaging features of a pleural abscess
EMPYEMA
Homogeneous pleural opacity, possible loculations or septations on ultrasound or CT, with a sharp pleural border.
What are common symptoms of a lung abscess?
Fever, productive cough with foul-smelling sputum, localized chest pain, and sometimes night sweats.
Q: What symptoms typically present with a pleural abscess
Fever, pleuritic chest pain, dyspnea, and absent or reduced breath sounds over the effusion.
What diagnostic test confirms a pleural abscess?
Thoracentesis:
pleural fluid analysis showing
pH <7.2,
glucose <60 mg/dL,
and high LDH.
= EXUDATIVE
What role does a CT scan play in diagnosing lung abscess vs. pleural abscess?
For lung abscess, shows thick-walled cavities.
For pleural abscess, shows fluid collections with smooth pleural margins.
What laboratory test is specific for lung abscess?
Sputum culture or bronchoscopy samples to identify the causative organisms (often mixed anaerobes).
How does auscultation differ between lung and pleural abscess?
Lung abscess: Crackles or bronchial breath sounds.
Pleural abscess: Absent or reduced breath sounds over the effusion.
Treatment of lung abscess
broad- spectrum a/b
ampicillin- sulbactam or clindamycin
if MRSA —> vancomycin
Pleural abscess
stage I
Exudative Phase
Pathophysiology:
Inflammatory response leads to accumulation of sterile fluid in the pleural space.
Protein and inflammatory cells begin to enter the pleural fluid.
Clinical Features:
Mild pleuritic chest pain.
Dyspnea may be present.
Diagnostic Findings:
Pleural fluid is clear or slightly cloudy.
pH >7.2, glucose >60 mg/dL, and normal LDH levels.
Antibiotics alone may be sufficient if identified early.
Pleural Abscess
Stage II
Fibrinopurulent Phase
Bacterial invasion of the pleural space.
Increased fibrin deposition and loculated pus formation.
More pronounced chest pain and dyspnea.
High fever and systemic signs of infection.
Pleural fluid becomes turbid or frankly purulent.
pH <7.2, glucose <60 mg/dL, elevated LDH.
Ultrasound shows loculated pleural fluid collections.
Drainage via thoracentesis or chest tube insertion.
Broad-spectrum antibiotics covering common pathogens
Step III of pleural abscess
Organization Phase (Chronic Phase)
Fibroblast proliferation leads to the formation of a thick, inelastic pleural peel.
The peel can encase the lung, leading to trapped lung or pleural fibrosis.
Persistent symptoms of infection and respiratory compromise.
Reduced lung expansion causing chronic dyspnea.
CT shows thickened pleura and entrapped lung tissue.
Loculated or multiloculated fluid with a thick pleural rind.
Surgical intervention such as decortication or video-assisted thoracoscopic surgery (VATS).
treatment of pleural abscess
Empiric therapy covering common pathogens (streptococci, Staphylococcus aureus, anaerobes, Gram-negative bacteria).
Examples:
Amoxicillin-clavulanate.
Piperacillin-tazobactam.
Ceftriaxone + Metronidazole (to cover anaerobes).
MRSA coverage if suspected: Add vancomycin or linezolid.
Duration:
At least 2–6 weeks, depending on clinical response.
Transition from IV to oral antibiotics when improvement is observed.
Thoracentesis (Needle Aspiration):
Performed for diagnostic purposes and initial treatment in early stages (exudative phase).
Not sufficient for thick or loculated pus.
Chest Tube Insertion:
Indication: Fibrinopurulent phase with frank pus or loculations.
Technique:
Ultrasound or CT-guided placement to ensure proper positioning.
Fluid drainage may require irrigation with saline or fibrinolytics (e.g., streptokinase or tissue plasminogen activator [tPA]) to break loculations.
Video-Assisted Thoracoscopic Surgery (VATS):
Loculated empyema not resolving with chest tube drainage.
Organized phase (chronic empyema).
Minimally invasive and effective for drainage and pleural debridement.
Open Thoracotomy with Decortication:
Advanced organization phase with thick pleural peel (trapped lung).
Restores lung expansion by removing fibrous tissue.
Oxygen Therapy:
For patients with respiratory compromise.
Nutritional Support:
To address catabolic state due to infection.
Pain Management:
Adequate analgesia to facilitate deep breathing and prevent atelectasis.
Monitor for Complications:
Persistent infection or recurrent empyema.
Development of chronic pleural fibrosis or bronchopleural fistula.
Follow-Up Imaging:
Chest X-ray or CT scan to confirm resolution.
Stage
Antibiotics, thoracentesis (if fluid significant).
Antibiotics, chest tube drainage ± fibrinolytics.
Organization Phase
Antibiotics, VATS, or open thoracotomy with decortication.
What are the main types of lung cancer, and how are they classified?
Non-Small Cell Lung Cancer (NSCLC):
Adenocarcinoma: Peripheral, non-smokers, good prognosis.
Squamous Cell Carcinoma: Central, smokers.
Large Cell Carcinoma: Peripheral, poor prognosis, early metastasis.
Small Cell Lung Cancer (SCLC):
Central, smokers only, aggressive, paraneoplastic syndromes common.
Pulmonary: Cough, hemoptysis, dyspnea, chest pain.
Extrapulmonary:
Hoarseness (recurrent laryngeal nerve compression).
Paraneoplastic syndromes (Cushing's, Lambert-Eaton syndrome).
lung cancer
What is the diagnostic approach for lung cancer?
X-ray (initial test).
CT (for suspected cases or metastasis evaluation).
PET-CT (detects metastases).
Biopsy:
Bronchoscopy for central lesions.
CT-guided needle aspiration for peripheral lesions.
Thoracocentesis for pleural effusion.
How is the malignancy risk of solitary pulmonary nodules assessed?
Risk factors: Age >40, smoking, family history, carcinogen exposure.
Use predictive models to estimate malignancy likelihood
What are the follow-up guidelines for solid pulmonary nodules based on size?
8mm: CT at 3, 6, and 12 months; biopsy if suspicious.
6–8mm: CT at 6–12 months; recheck at 18–24 months if needed.
<6mm: No routine follow-up unless risk factors.
Subsolid nodule >6mm: CT at 3–6 months, then periodically.
How are solitary pulmonary nodules treated?
High-risk or >30mm: Surgical excision.
Suspicious or growing nodules: Biopsy or removal.
Low-risk: Observation with periodic imaging.
What is the most common etiology of acute pancreatitis?
Biliary pancreatitis (40% caused by gallstones).
Alcohol consumption (20%).
Idiopathic causes.
What are the severity grades of acute pancreatitis according to the revised Atlanta classification?
Mild: No organ failure or local/systemic complications.
Moderate: Transient organ failure (<48 hours) and/or local or systemic complications.
Severe: Persistent organ failure (>48 hours).
What are the diagnostic criteria for acute pancreatitis?
Characteristic abdominal pain.
Increased pancreatic enzymes (lipase/amylase >3x normal).
Imaging findings (CT/MRI): Edema, pancreatic enlargement, necrosis, or collections.
What are the key laboratory findings in acute pancreatitis?
Elevated lipase and amylase (>3x upper limit).
Increased BUN and creatinine (indicating severity).
Elevated CRP and procalcitonin (inflammatory markers).
ALT >150 U/L and elevated AST, GGT, bilirubin, ALP (biliary pancreatitis).
Increased LDH (necrotizing pancreatitis).
Triglycerides >1,000 mg/dL (triglyceride-induced pancreatitis).
What imaging modalities are used in acute pancreatitis, and when are they indicated?
Ultrasound: Identifies biliary causes but limited for pancreas visualization (~20%).
CT with contrast: Gold standard for confirming diagnosis and assessing severity:
Pancreatic edema or necrosis.
Fluid collections.
Walled-off necrosis (>4 weeks after onset).
MRI/MRCP: Useful for suspected biliary pancreatitis.
ERCP: Not diagnostic; used only for therapeutic purposes (e.g., biliary stones).
How is necrotizing pancreatitis identified on imaging?
Non-enhancing areas of pancreatic parenchyma on CT with contrast.
Air within necrotic tissue suggests infection.
What is the primary treatment for acute pancreatitis?
IV Fluids:
Crystalloids (Ringer’s lactate or normal saline).
Goal: Urine output >0.5-1 mL/kg/h.
NSAIDs or opioids.
Severe cases may require patient-controlled analgesia or epidural.
Nutrition:
Early oral feeding if tolerated.
Enteral or parenteral nutrition if oral feeding is not possible.
How is biliary pancreatitis treated?
Therapeutic ERCP: Within 24 hours for:
Cholangitis.
Persistent bile duct obstruction.
Cholecystectomy: Performed after recovery to prevent recurrence.
What are the surgical indications for acute pancreatitis?
Gallstone pancreatitis: Elective cholecystectomy after recovery.
Infected necrosis: Pancreatic debridement if unresponsive to antibiotics.
Necrosectomy: Reserved for walled-off necrosis or non-resolving infection.
What is the role of imaging in managing complications of acute pancreatitis?
CT with contrast:
Identifies collections, necrosis, and infection.
Ultrasound: Useful for fluid drainage guidance.
Endoscopic ultrasound (EUS): Assesses pancreatic and bile ducts.
How are hypertriglyceridemia-induced pancreatitis and alcohol-related pancreatitis managed?
Hypertriglyceridemia:
Insulin.
Plasmapheresis or hemofiltration in severe cases.
Long-term triglyceride-lowering therapy.
Alcohol-related pancreatitis:
Thiamine, magnesium, and pyridoxine supplementation.
Alcohol cessation programs.
What are the systemic complications of acute pancreatitis?
Organ failure (respiratory, renal, or circulatory).
Sepsis: Often due to infected necrosis.
ARDS (acute respiratory distress syndrome).
SIRS (systemic inflammatory response syndrome).
Define mastitis and distinguish between lactational and non-lactational mastitis.
Mastitis is inflammation of breast tissue that may or may not involve infection.
Lactational Mastitis: Occurs during breastfeeding due to poor milk drainage, often within the first 3 months postpartum.
Non-lactational Mastitis: Includes periductal mastitis (chronic, seen in young smokers) and idiopathic granulomatous mastitis (rare, unknown cause, more common in the Middle East).
What are the symptoms of lactational mastitis?
Symptoms include:
Pain, redness, and swelling in the breast.
Malaise, flu-like symptoms, and fever.
Localized warmth and tenderness.
What are the symptoms of periductal and granulomatous mastitis?
Periductal Mastitis:
Pus drainage from the areola (duct rupture).
Abscess formation.
Granulomatous Mastitis:
Solitary or multiple tender masses.
Abscesses, ulceration, nipple retraction, peau d’orange, axillary adenopathy (may mimic cancer).
How is lactational mastitis treated?
Symptomatic Care:
NSAIDs, cold compress for pain/swelling.
Encourage complete breast emptying (e.g., breastfeeding or pumping).
For fever/symptoms persisting >12–24 hours.
Examples: Dicloxacillin, cephalexin (target S. aureus).
Abscess Management:
Ultrasound-guided fine-needle aspiration (FNA) or drainage + antibiotics.
How is periductal mastitis treated?
antibiotics + Drainage (50% resolve):
Examples: Amoxicillin-clavulanate, dicloxacillin, or cephalexin (5–7 days or up to 14 days).
Surgery (50% cases with repeated episodes):
Excision of diseased ducts, often through the 6 o’clock position of the nipple.
What is the treatment for granulomatous mastitis?
Usually resolves on its own within 5–20 months.
Abscesses: Manage with antibiotics + drainage.
What are the clinical features of early-stage breast cancer?
Single, nontender, firm mass, often in the upper outer quadrant.
Poorly defined margins.
What are the clinical features of locally advanced breast cancer?
Breast asymmetry.
Skin changes: Retractions, dimpling, peau d’orange.
Nipple changes: Inversion, bloody discharge.
What are the signs of progressive breast cancer?
What is the diagnostic approach for breast cancer?
Clinical assessment: Age, family history, palpation of lumps and lymph nodes.
Women <30 years: Start with ultrasound.
Women ≥30 years: Start with mammography, followed by ultrasound if needed.
What are the biopsy methods used for breast lesions?
Fine Needle Aspiration (FNA): For lesions not suspected to be malignant.
Core Needle Biopsy (CNB): Preferred to distinguish invasive from non-invasive cancer.
Surgical Biopsy: Used when CNB is inconclusive
What hormone receptors are tested in breast cancer diagnosis?
PR: Progesterone receptor.
ER: Estrogen receptor.
HER2/neu: Human epidermal growth factor receptor 2.
What imaging studies are used for metastasis evaluation in breast cancer?
Chest X-ray and CT scan.
Brain MRI.
PET-CT (especially in advanced or inflammatory cases).
What are the main types of breast surgery for breast cancer?
Simple mastectomy: Removes breast tissue; axillary lymph nodes untouched.
Skin/nipple-sparing mastectomy: Allows immediate reconstruction.
Radical mastectomy: Removes breast tissue and all axillary lymph nodes.
What are the clinical features of peritoneal adhesions?
Gastrointestinal symptoms: Meteorism, irregular bowel movements, changes in stool form.
Chronic pain: Especially in the lower abdomen.
Other symptoms: Digestive problems, infertility, dyspareunia (in women).
Severe cases: Signs of intestinal obstruction.
What are the common risk factors for peritoneal adhesions?
History of abdominal surgeries.
Abdominal or pelvic inflammatory conditions.
Radiation therapy.
What diagnostic methods are used for peritoneal adhesions?
Patient History: Previous surgeries, inflammation, or radiation therapy.
CT Scan: Identifies signs like "fat bridging" or "whirl sign," (same as testicular torsion) which are nonspecific.
Can also rule out obstruction.
Definitive Diagnosis: Direct visualization via laparoscopy or laparotomy.
When is surgical treatment indicated for peritoneal adhesions?
Persistent bothersome lower abdominal pain.
Infertility associated with adhesions.
Intestinal obstruction development.
What are the surgical treatment options for peritoneal adhesions?
Adhesiolysis: Cutting or electrocauterizing adhesions, typically laparoscopic in elective cases.
Cut around the adhesion midpoint to avoid intestinal damage.
Obstruction Management:
Open Adhesiolysis for obstruction.
Necrotized bowel: Requires nasogastric decompression and resection.
What are the signs of intestinal obstruction caused by peritoneal adhesions?
Abdominal distension (meteorism).
Severe pain.
Failure to pass stool or gas.
What is primary peritonitis?
Generalized bacterial peritoneal infection without loss of peritoneal barrier function.
Causes: Liver cirrhosis, peritoneal dialysis.
What is secondary peritonitis?
Peritonitis due to loss of peritoneal barrier function, typically caused by infections.
Most common form.
What is tertiary peritonitis?
Recurrent infection following primary or secondary peritonitis.
What are the principles of antibiotic treatment for peritonitis?
Mild to moderate severity:
Combination: Ceftriaxone + metronidazole.
Monotherapy: Piperacillin-tazobactam or meropenem.
Hospital-acquired infection: Consider Pseudomonas aeruginosa, ESBL, and MRSA coverage.
What are the goals of surgery in peritonitis management?
Drain infectious components.
Eliminate further contamination (e.g., resection of perforated viscera).
Restore anatomy and physiology.
What are the main surgical approaches in peritonitis?
One-stage surgery:
Resection and closure of perforated viscera.
Complete resection of infected components and necrotic debridement.
Step-up approach:
On-demand re-laparotomy or programmed laparotomy every 36–48 hours.
Abdomen left open (e.g., VAC device).
Percutaneous drainage when appropriate.
When is the abdomen left open during peritonitis surgery?
If achieving source control is not possible (e.g., severe contamination).
Presence of "shock bowel" with excessive bowel edema.
Q: When should the abdomen be closed? A:
As early as possible to prevent complications like fistulae or hernia.
Fascia closure criteria: Adequate source control, controlled sepsis, and manageable intra-abdominal pressure.
Early closure: 4–7 days post-initial laparotomy.
Late closure: After 7+ days.
What are the types of pancreatic tumors?
Exocrine Tumors:
Cystic Neoplasms:
Serous: Benign, resect if >4cm or symptomatic.
Mucinous: Mucin-producing, risk of malignancy, requires curative resection.
Intraductal Papillary Mucinous Neoplasm (IPMN): Malignant potential, partial/total pancreatectomy.
Adenocarcinoma: Most common and aggressive.
Endocrine Tumors:
Pancreatic Neuroendocrine Tumors (NETs): Localized or metastatic, treated with partial resection or enucleation.
What is the Whipple procedure, and when is it used?
Whipple Procedure (Pancreaticoduodenectomy):
Used for tumors in the head of the pancreas.
Removes the head of the pancreas, duodenum, part of the stomach, and bile duct.
Reconstruction:
Pancreaticojejunostomy: Reconnects the pancreas to the small intestine.
Hepaticojejunostomy: Reroutes bile to the small intestine.
What is the treatment for tumors in the body or tail of the pancreas?
Distal Pancreatectomy + Splenectomy: Removes the tumor and spleen.
What are the palliative surgical options for pancreatic tumors?
Biliary Obstruction:
ERCP + Stent (minimally invasive).
Surgical bypass: Roux-en-Y hepaticojejunostomy.
Gastric Outlet Obstruction:
Endoscopic stenting.
Double bypass: Hepaticojejunostomy + gastrojejunostomy.
How are pancreatic neuroendocrine tumors treated?
Localized:
Partial resection or enucleation (preserves pancreas).
Metastatic:
Radical resection with regional lymphadenectomy.
How is pancreatic cancer diagnosed?
CT scan: Identifies tumor size and spread.
MRI/MRCP: Evaluates biliary involvement.
FNA: Fine needle aspiration for benign lesions.
CNB: Core needle biopsy for suspected malignancy.
Tumor Markers:
CA 19-9: Commonly elevated in pancreatic cancer.
What is acute mesenteric ischemia?
It is a sudden reduction in arterial or venous blood flow to the small intestine, potentially leading to bowel ischemia or infarction.
What are the primary types of acute mesenteric ischemia?
Acute mesenteric arterial embolism.
Acute mesenteric arterial thrombosis.
Non-occlusive mesenteric ischemia (NOMI).
Mesenteric venous thrombosis (MVT).
What is the main cause of acute mesenteric arterial embolism?
Atrial fibrillation is the most common cause, along with heart valve diseases, recent heart attack, or surgeries involving the aorta.
What is the key diagnostic tool for mesenteric ischemia?
: CT angiography is the gold standard for diagnosing mesenteric ischemia, as it visualizes blood flow disruptions and clots.
Blood Tests for Mesenteric Ischemia
Elevated Lactate Levels
Indicates tissue hypoperfusion and anaerobic metabolism.
Higher levels are associated with advanced ischemia or infarction.
Leukocytosis
Increased white blood cell (WBC) count due to systemic inflammation or sepsis.
Elevated C-reactive protein (CRP)
A marker of inflammation, though non-specific.
Elevated D-Dimer
Suggests clot formation and breakdown; useful in identifying thrombotic causes.
Metabolic Acidosis
Reflects lactic acid buildup from ischemic tissue.
Increased Serum Amylase/Lipase
Can be elevated, mimicking pancreatitis.
Elevated Creatinine and Blood Urea Nitrogen (BUN)
May indicate dehydration, shock, or renal dysfunction from systemic effects.
Electrolyte Imbalance
May include hyperkalemia due to tissue necrosis.
What is the definition of polytrauma?
Polytrauma refers to severe traumatic injuries affecting two or more body regions or organ systems, with at least one injury or the cumulative effect of all injuries being life-threatening (Injury Severity Score ≥16).
What are the goals of the primary survey in trauma?
A: Airway and cervical spine protection.
B: Breathing and ventilation assessment.
C: Circulation and hemorrhage control.
D: Disability assessment (neurological evaluation).
E: Exposure and environmental control.
What is included in the airway assessment during the primary survey?
Check for airway obstruction (e.g., blood, foreign objects).
Stabilize the cervical spine if trauma is suspected.
Use adjuncts like oropharyngeal airways or intubation if needed.
What is the goal of circulation assessment in the primary survey?
Control hemorrhage.
Restore adequate perfusion using IV fluids or blood transfusion.
Monitor signs of shock: tachycardia, hypotension, cold clammy skin.
What does the secondary survey involve?
Detailed head-to-toe assessment to identify injuries missed in the primary survey.
Collect AMPLE history: Allergies, Medications, Past illnesses, Last meal, Events leading to trauma.
Imaging and diagnostic tests as needed.
What should be included in the physical examination during the secondary survey?
Head/Face: Palpate for deformities, check pupils, and use an otoscope for hemotympanum.
Neck: Palpate for tenderness or subcutaneous emphysema.
Chest: Inspect and auscultate for signs of hemothorax or pneumothorax.
Abdomen: Check for bruising, tenderness, and rigidity.
Rectum/Genitourinary: Perform a rectal exam if bowel or pelvic injury is suspected.
Musculoskeletal: Inspect for fractures or deformities.
Neurological: Perform a full neurologic examination, including GCS.
Skin: Look for lacerations or abrasions.
What imaging studies are typically used in polytrauma?
X-rays: Initial imaging for fractures or chest injuries.
CT Scan: Comprehensive imaging for head, neck, chest, and abdomen (if stable).
FAST (Focused Assessment with Sonography for Trauma): Quick ultrasound to assess free fluid in the abdomen, pelvis, and pericardium.
What is the primary goal of damage control surgery (DCS)?
Arrest hemorrhage.
Limit contamination (e.g., spilling of gastrointestinal contents).
Maintain blood flow to vital organs and extremities.
Prioritize life-threatening injuries to head, neck, chest, and abdomen over extremities.
What are the principles of DCS?
Laparotomy: Most commonly used surgical approach.
Operation time: Keep under 90 minutes to minimize patient deterioration.
Abdomen left open: Reduces risk of compartment syndrome; similar for thoracotomy in tamponade or pleural hemorrhage.
Temporary vascular shunts: Maintain blood flow if definitive repair is delayed.
Temporary abdominal closure: Use negative pressure dressings.
What are the 4 phases of damage control surgery?
Phase 0 (Pre-surgery): Rapid transport and triage.
Phase 1 (Surgery):
Limit contamination.
Maintain vital organ perfusion.
Phase 2 (ICU resuscitation): Restore fluids, prevent hypothermia.
Phase 3 (Definitive repair): Staged repairs of injuries once patient stabilizes.
Phase 4 (Closure): Delayed wound or abdominal closure after recovery.
What are the surgical principles during laparotomy in DCS?
Packing and exploration:
Pack all quadrants to identify damaged organs.
Control hemorrhage:
Resect non-essential organs (e.g., spleen).
Pack vital organs (e.g., liver).
Ligate non-essential intra-abdominal vessels.
Control contamination:
Seal or resect damaged intestines or gallbladder.
Staple gastric injuries quickly.
Repair small bowel injuries and resect severely damaged segments.
Leave bowel in discontinuity for later repair.
How is contamination limited during DCS?
Quickly seal or staple gastrointestinal injuries.
Temporarily resect or isolate damaged organs.
Avoid anastomosis during initial surgery; bowel repairs are deferred.
What are the principles for vascular injury management in DCS?
Use vascular shunts to maintain blood flow temporarily.
Definitive vascular repairs are delayed until the patient is stabilized.
Ligate non-essential vessels if necessary.
What are the resuscitation goals in the ICU (Phase 2 of DCS)?
Restore adequate fluid balance.
Maintain normothermia.
Monitor and stabilize vital organ function.
When is the abdomen closed in DCS (Phase 4)?
Once source control is achieved.
Severe sepsis and intra-abdominal pressure are managed.
Typically closed within 4-7 days, if possible.
What is the first-line diagnostic tool for liver trauma in unstable patients?
FAST (Focused Assessment with Sonography for Trauma).
Detects fluid or blood around the liver or in the hepatorenal space.
Negative FAST does not rule out liver trauma.
What is the gold standard diagnostic tool for liver trauma?
CT Scan with Contrast.
Confirms liver trauma and determines the grade of injury.
Used for stable patients
What are the signs of liver trauma on a CT scan?
Subcapsular hematoma.
Intraperitoneal fluid.
Liver parenchymal lacerations.
Vascular involvement in severe grades.
What are the treatment principles for liver trauma?
Stabilize the patient using ABCDE approach.
Management depends on:
Hemodynamic status.
Injury grade.
Presence of other injuries.
Stable patients: Conservative treatment.
Unstable patients: Surgery or interventional radiology.
What are the indications for surgical treatment of liver trauma?
Ongoing uncontrolled bleeding despite conservative measures.
Hemodynamic instability (BP <90 mmHg, HR >120 bpm).
Grade III or higher liver injuries (e.g., large hematomas, vascular involvement).
Gunshot wounds.
Peritonitis.
What are the grades of liver injury that require surgical intervention?
Subcapsular hematoma >50% of liver surface.
Ruptured subcapsular or parenchymal hematoma.
Intraparenchymal hematoma >10 cm.
Vascular injury or active bleeding within the liver.
What clinical sign is associated with spleen trauma?
Kehr sign – Left shoulder pain that worsens on inspiration.
What is the first imaging tool used for spleen trauma in unstable patients?
3: What is the gold standard diagnostic tool for spleen trauma?
Findings: Black rim around the spleen indicating fluid accumulation.
CT of the abdomen with contrast.
What are the general principles of spleen trauma treatment?
tabilize the patient with ABCDE approach.
Determine management based on:
Hemodynamic stability.
Presence of other injuries or comorbidities.
Choose between conservative or surgical treatment.
What is included in conservative management of spleen trauma?
Observation and monitoring.
General care:
NPO (nil per os).
Trauma prophylaxis (e.g., DVT prophylaxis).
Fluids and blood transfusions if necessary.
Splenic embolization: For stable patients with:
Active contrast extravasation.
Splenic pseudoaneurysm.
Large volume hemoperitoneum.
What are the surgical options for spleen trauma?
Splenorraphy (splenic salvage): Repair of the spleen.
Splenectomy: Removal of the spleen when salvage is not possible.
How is blunt trauma of the pancreas classified?
Grade I-II:
Contusion or superficial laceration without ductal injury.
Grade III:
Parenchymal laceration >3 cm in depth or with ductal injury.
Grade IV-V:
High-grade injuries involving major ductal damage or extensive destruction of pancreatic head.
What is the approach for conservative management of pancreatic trauma?
indicated for Grade I-II injuries with hemodynamic stability and no ductal injury.
Includes:
Gastrointestinal decompression (e.g., nasogastric tube for duodenal hematoma).
Nutritional support (e.g., nasojejunal tube or surgical jejunostomy).
Close monitoring of clinical and biochemical parameters.
When is surgery required in pancreatic trauma?
Hemodynamically unstable patients.
High-grade injuries (Grade IV-V).
Associated injuries (e.g., duodenal or vascular injuries).
Surgery types:
Damage control surgery: Packing to control bleeding, wide drainage, and no reconstructive procedures during initial phase.
Definitive surgery: Resection, often delayed until patient stabilization.
What surgical options are available for specific grades of pancreatic trauma?
Grade III (Distal injuries):
Distal pancreatectomy.
Grade IV-V (Proximal injuries):
Resection of the pancreatic head.
Reconstruction delayed until stabilization.
Liver Trauma
Spleen Trauma
Pancreatic Trauma
Etiology
Blunt trauma, penetrating injuries, or iatrogenic causes (e.g., surgeries).
Blunt abdominal trauma or penetrating injuries.
Blunt abdominal trauma (handlebar injury, direct blow) or penetrating trauma.
Clinical Features
- Right upper quadrant pain. - Referred shoulder pain. - Abdominal distension.
- Left upper quadrant pain. - Kehr’s sign (left shoulder pain). - Abdominal distension.
- Epigastric pain. - Nausea, vomiting. - Possible back pain.
- FAST scan for unstable patients. - CT with contrast for stable patients. - LFT abnormalities.
- FAST scan for unstable patients. - CT with contrast for stable patients. - Possible anemia.
- CT with contrast: evaluates parenchymal damage. - Amylase/lipase elevation in ductal injury.
Imaging Features
- Subcapsular hematoma, parenchymal lacerations, active bleeding on CT.
- Subcapsular hematoma, active bleeding, lacerations, or vascular injury on CT.
- Contusions, lacerations, or ductal injury seen on contrast CT or MRI.
Grading
- Grade I–VI: Based on laceration depth, hematoma size, and vascular injury severity.
- Grade I–V: Includes subcapsular hematomas, lacerations, and parenchymal or vascular injuries.
- Grade I–V: Based on depth of injury and ductal involvement.
Conservative Management
- Hemodynamically stable patients. - Observation and monitoring. - Embolization if active bleeding.
- Hemodynamically stable patients. - Observation and monitoring. - Embolization for ongoing bleeding.
- For Grade I–II injuries: Observation and supportive care (e.g., fluids, NPO).
Surgical Indications
- Hemodynamic instability. - Persistent bleeding. - Grade IV–VI injuries.
- Hemodynamic instability. - Persistent bleeding. - Grade III+ injuries with significant damage.
- Ductal injury or Grade III–V injuries. - Uncontrolled bleeding or associated duodenal injury.
Surgical Procedures
- Damage control surgery. - Packing or hepatorrhaphy. - Lobectomy in severe cases.
- Splenectomy for irreparable damage. - Splenorrhaphy for repairable cases.
- Damage control surgery: packing, drainage. - Distal pancreatectomy or resection for severe injuries.
Post-Surgical Concerns
- Risk of bile leak. - Risk of sepsis or abscess formation.
- Risk of overwhelming post-splenectomy infection (OPSI). - Requires vaccination.
- Risk of pancreatic fistula. - Requires drainage for fluid collections.
deep vein thrombosis - definition
formation of a blood clot (thrombus) within the deep vein, mostly in the lower limbs.
It is a significant medical condition due to its potential complications such as pulmonary embolism.
DVT develops due to Virchow’s Triad
what are the components
risk factors of DVT
prolonged immbolization
surgery
malignancy
symptoms of DVT
swelling, pain
tenderness
redness
warmth of the affected limb
scoring system used to assess DVT
Wells score
what is the first imagine modality in diagnosing DVT
compression ultrasound
what lab tests are done in order to rule out DVT in low- risk
D- dimer test
what is the golden standard for DVT
venography (rarely done due to invasiveness)
what are two classes of anticoagulants used to treatmet DVT
direct oral anticoagulants and vitamin K
eg. warfarin
complciations of DVT
pulmonary embolism
post-thrombotic syndrome
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