What are the vasomotor symptoms associated with menopause?
Hot flashes, night sweats, palpitations, and sleep disturbances.
What are the urogenital symptoms caused by estrogen deficiency in menopause?
Vaginal dryness, dyspareunia, urinary frequency, urgency, and recurrent urinary infections.
What are the psychological symptoms linked to menopause?
Irritability, mood swings, fatigue, decreased libido, and memory loss.
How does menopause affect skeletal and soft tissue?
Causes osteoporosis, joint pain, thinning skin, loss of elasticity, brittle nails, and reduced breast size.
What are the indications for Hormone Replacement Therapy (HRT)?
Relief of menopausal symptoms, prevention/treatment of osteoporosis, and management of premature ovarian insufficiency.
What are the absolute contraindications to HRT?
Undiagnosed vaginal bleeding, breast/endometrial cancer, history of DVT/PE, and active liver disease.
What are the common side effects of HRT?
Breast tenderness, bloating, nausea, mood swings, abnormal uterine bleeding, increased risk of VTE and breast cancer.
What tests should be conducted before initiating HRT?
Mammography, lipid profile, glucose tolerance tests, and endometrial evaluation in certain cases.
What is the purpose of adding progestin to HRT in women with an intact uterus?
To prevent the development of endometrial hyperplasia or malignancy caused by unopposed estrogen.
How is estrogen delivered in HRT, and when is transdermal preferred?
Orally or via transdermal patch/gel; transdermal is preferred in cases of impaired liver function or hypertriglyceridemia.
What are the risks of estrogen monotherapy in HRT?
Increased risk of endometrial hyperplasia and endometrial cancer.
What lifestyle factors should be managed alongside HRT for optimal outcomes in menopause?
Regular exercise, calcium and vitamin D supplementation, smoking cessation, and maintaining a healthy weight.
What is the definition of primary amenorrhea?
Absence of menarche at: 1. 15 years of age with normal secondary sexual characteristics. 2. 13 years of age without secondary sexual characteristics.
What is the definition of secondary amenorrhea?
Absence of menses for: 1. >3 months in individuals with previously regular cycles. 2. >6 months in individuals with irregular cycles.
What are the causes of primary amenorrhea due to constitutional delay?
- Normal puberty, but adrenarche and gonadarche occur late. - Hormonal levels: ↓ GnRH, ↓ FSH, ↓ Estrogen (prepubertal levels).
What are the causes of primary amenorrhea due to hypogonadotropic hypogonadism?
- Deficient GnRH release due to: Kallmann syndrome (anosmia, hypogonadism), Prader-Willi syndrome, Eating disorders, stress, competitive sports, CNS tumors (e.g., craniopharyngioma). - Hormonal levels: ↓ GnRH, normal/↓ FSH, ↓ Estrogen.
What are the causes of primary amenorrhea due to hypergonadotropic hypogonadism?
- Ovarian failure despite GnRH release (e.g., Turner syndrome). - Hormonal levels: ↑ GnRH, ↑ FSH, ↓ Estrogen.
What are the causes of primary amenorrhea due to anatomical anomalies?
- Outflow tract obstruction with otherwise normal puberty: MĂĽllerian agenesis, Imperforate hymen, Vaginal atresia, Transverse vaginal septum. - Hormonal levels: Normal GnRH, FSH, and Estrogen.
What are the main causes of secondary amenorrhea?
1. Pregnancy (most common). 2. Ovarian disorders (e.g., PCOS, premature ovarian failure). 3. Medications (antipsychotics, contraceptives). 4. Endocrine disorders (e.g., hypothyroidism, Cushing syndrome). 5. Functional hypothalamic amenorrhea (e.g., stress, exercise, eating disorders). 6. Anatomical causes (e.g., Asherman syndrome).
What are the initial diagnostic steps for amenorrhea?
1. Pregnancy test. 2. Evaluate secondary sexual characteristics. 3. Assess for anatomical anomalies (e.g., pelvic ultrasound). 4. Hormonal levels: FSH, LH, Prolactin, TSH, Estradiol.
What is the role of a progestin withdrawal test in amenorrhea?
- Induces withdrawal bleeding if estrogen is present. - No bleeding: Suggests estrogen deficiency or an anatomical problem.
What are the diagnostic steps if secondary amenorrhea with galactorrhea is present?
1. Measure prolactin and TSH levels. 2. Perform a brain MRI to rule out a pituitary adenoma.
What are the main features of functional hypothalamic amenorrhea?
1. Caused by stress, excessive exercise, or eating disorders. 2. ↓ GnRH pulsatility → ↓ FSH and LH → ↓ Estrogen → Anovulation. 3. Associated with the female athlete triad: calorie deficit, low bone density, amenorrhea.
What is the treatment for hyperprolactinemia-induced amenorrhea?
Dopamine agonists (e.g., bromocriptine, cabergoline).
What is the treatment approach for functional hypothalamic amenorrhea?
1. Lifestyle modifications: reduce stress, increase calorie intake, achieve BMI >19. 2. GnRH or gonadotropin therapy for ovulation induction.
What are the diagnostic criteria for primary ovarian insufficiency?
1. ↑ FSH levels (>30–40 mIU/mL) on two separate occasions. 2. ↓ Estradiol levels (<50 pg/mL). 3. >3 months of menstrual irregularities in women under 40 years old.
What are the treatment goals for premature ovarian failure?
1. Hormone replacement therapy to prevent osteoporosis. 2. Ovulation induction if pregnancy is desired. 3. Address underlying causes if identified.
What is PCOS, and what are its main characteristics?
PCOS is a common endocrine disorder in women characterized by hyperandrogenism (hirsutism, acne), ovulatory dysfunction (irregular menses), and polycystic ovaries.
What is the prevalence of PCOS?
Affects 6–12% of women of reproductive age in the US.
What is the pathophysiology of PCOS?
Insulin resistance leads to hyperinsulinemia, increasing androgen production. Excess androgens disrupt follicle maturation, causing anovulation. Increased LH/FSH ratio and unopposed estrogen contribute to hyperplasia and carcinoma risks.
What are the clinical features of PCOS?
Menstrual irregularities, hyperandrogenism (hirsutism, acne), metabolic syndrome, infertility, obesity, skin conditions (acanthosis nigricans), and psychiatric symptoms (depression, anxiety).
How is PCOS diagnosed?
Using Rotterdam Criteria: 2 out of 3 - (1) Oligo-/anovulation, (2) Hyperandrogenism (clinical or biochemical), (3) Polycystic ovaries on ultrasound. Exclude other endocrinological conditions.
What are the common laboratory findings in PCOS?
Increased testosterone, LH:FSH ratio > 2:1, decreased SHBG, elevated androstenedione, and exclusion of thyroid dysfunction or congenital adrenal hyperplasia.
How is PCOS managed for patients not planning to conceive?
Lifestyle modifications (weight loss, healthy diet), combined oral contraceptives (regulate cycles, treat hyperandrogenism), metformin (improves insulin sensitivity), and antiandrogens (for hirsutism, alopecia).
How is PCOS managed for patients planning to conceive?
Letrozole (first-line for ovulation induction), clomiphene citrate, exogenous gonadotropins, laparoscopic ovarian drilling, and IVF if other treatments fail.
What are the long-term health risks associated with PCOS?
Metabolic syndrome, cardiovascular disease, endometrial cancer, and infertility.
What is the pathologic appearance of PCOS on microscopy?
Ovarian hypertrophy with thick capsule, stromal hyperplasia and fibrosis, multiple small cystic follicles, hyperluteinized theca cells, and decreased granulosa cells.
What are the main differential diagnoses for PCOS?
Non-classic congenital adrenal hyperplasia (↑ 17-hydroxyprogesterone), androgen-secreting tumors (↑ DHEA-S > 700 µg/dL), Cushing syndrome (↑ cortisol levels), hypothyroidism (↑ TSH), and hyperprolactinemia (↑ prolactin).
What is the definition of Abnormal Uterine Bleeding (AUB)?
Irregular uterine bleeding in nonpregnant individuals of reproductive age, with abnormalities in frequency, duration, regularity, or volume.
What are the FIGO classifications for AUB based on bleeding characteristics?
Frequency: Infrequent (>38 days), Frequent (<24 days). Duration: Prolonged (>8 days). Volume: Heavy menstrual bleeding. Intermenstrual bleeding: Random or cyclic bleeding between cycles.
What is the PALM-COEIN classification of AUB?
PALM: Polyp, Adenomyosis, Leiomyoma, Malignancy/Hyperplasia. COEIN: Coagulopathy, Ovulatory dysfunction, Endometrial dysfunction, Iatrogenic, Not otherwise classified.
What are the common causes of ovulatory dysfunction in AUB?
PCOS, thyroid disorders, hyperprolactinemia, obesity, perimenopause, Cushing syndrome, eating disorders.
What are the first steps in diagnosing AUB?
1. Rule out pregnancy with β-hCG test. 2. Perform clinical history and gynecological examination. 3. Obtain CBC, coagulation tests, and thyroid function tests.
What imaging modality is first-line for evaluating AUB?
Pelvic ultrasound (preferably transvaginal ultrasound) to assess endometrial thickness and structural abnormalities.
When is an endometrial biopsy indicated for AUB?
1. Women ≥45 years with AUB. 2. Women <45 years with persistent bleeding despite treatment, obesity, PCOS, or unopposed estrogen exposure.
What are the laboratory tests used in AUB evaluation?
β-hCG, CBC, ferritin, platelet count, PT/PTT, thyroid function tests, and prolactin levels.
What is the treatment for acute AUB in unstable patients?
1. High-dose IV conjugated estrogen. 2. Immediate hemodynamic stabilization. 3. Intrauterine tamponade or surgical intervention if refractory.
What is the first-line pharmacologic treatment for chronic AUB?
Hormonal Therapy: Combined oral contraceptives, progestin-only therapy, or levonorgestrel IUD. Nonhormonal Therapy: NSAIDs or tranexamic acid during bleeding episodes.
What surgical options are available for AUB?
1. Hysteroscopy: Polypectomy or myomectomy (fertility-sparing). 2. Dilation and Curettage (D&C). 3. Endometrial Ablation: Non-fertility-preserving. 4. Hysterectomy: Definitive treatment for refractory AUB.
What are the risk factors for endometrial hyperplasia or cancer in AUB?
Obesity, unopposed estrogen, PCOS, tamoxifen therapy, Lynch syndrome, diabetes mellitus.
How do you differentiate structural from nonstructural causes of AUB?
Structural causes are identifiable on imaging (e.g., polyps, leiomyomas), while nonstructural causes involve hormonal, coagulopathic, or iatrogenic issues.
What is the role of the PALM-COEIN system in diagnosing AUB?
It classifies AUB into structural (PALM) and nonstructural (COEIN) causes, guiding targeted evaluation and management.
What is Pelvic Inflammatory Disease (PID)?
PID is a bacterial infection of the female reproductive organs that spreads beyond the cervix to the uterus (endometritis), fallopian tubes (salpingitis), ovaries (oophoritis), and surrounding pelvic structures. It can also involve the pelvic peritoneum (peritonitis).
What are the most common pathogens causing PID?
The most common pathogens are Chlamydia trachomatis and Neisseria gonorrhoeae. Less common pathogens include E. coli, Ureaplasma, Mycoplasma, and anaerobes.
What are the main risk factors for PID?
- Multiple sexual partners \n- Unprotected sex \n- History of prior STIs or PID \n- Use of intrauterine devices (IUDs), especially within the first 3 weeks of placement \n- Vaginal dysbiosis.
What are the hallmark symptoms of PID?
- Bilateral lower abdominal pain \n- Abnormal vaginal discharge (yellow/green, mucopurulent) \n- Fever (>38.3°C/101°F) \n- Pain during sex (dyspareunia) \n- Irregular bleeding (e.g., menorrhagia or metrorrhagia) \n- Painful urination (dysuria) or urgency.
What is cervical motion tenderness, and why is it significant in PID?
Cervical motion tenderness refers to severe pain elicited by manipulation or movement of the cervix during a bimanual pelvic examination. It is a key diagnostic criterion for PID.
What are the minimum diagnostic criteria for PID?
Presence of any of the following in a sexually active female with pelvic/lower abdominal pain and no alternative explanation: \n- Cervical motion tenderness \n- Uterine tenderness \n- Adnexal tenderness.
What additional supportive findings strengthen a PID diagnosis?
- Oral temperature > 38.3°C (101°F) \n- Mucopurulent cervical discharge \n- Cervical friability \n- Abundant WBCs on vaginal secretion microscopy \n- Elevated ESR or CRP \n- Confirmed cervical infection with N. gonorrhoeae or C. trachomatis.
What tests should be done to rule out other conditions when PID is suspected?
- Pregnancy test (to rule out ectopic pregnancy) \n- Cervical swabs for N. gonorrhoeae and C. trachomatis \n- Wet mount microscopy for WBCs, trichomoniasis, or bacterial vaginosis \n- Blood tests: CBC, CRP, ESR, HIV testing, RPR for syphilis.
When should imaging be performed in suspected PID?
Imaging is indicated if the diagnosis is unclear, symptoms persist after treatment, or there is concern for complications (e.g., tubo-ovarian abscess). Transvaginal ultrasound is typically used.
What are the potential complications of untreated PID?
- Infertility: due to fallopian tube scarring. \n- Chronic pelvic pain: from adhesions. \n- Ectopic pregnancy: increased risk due to tubal damage. \n- Tubo-ovarian abscess: can rupture, causing sepsis.
What is the initial antibiotic regimen for outpatient treatment of PID?
- IM ceftriaxone (single dose) \n- Oral doxycycline (14 days) \n- Oral metronidazole (14 days).
When should a patient with PID be admitted for inpatient treatment?
Indications for admission: \n- Concern for a surgical emergency (e.g., differential diagnosis of acute abdomen) \n- Severe illness (e.g., fever >38.5°C, nausea, vomiting) \n- Tubo-ovarian abscess \n- Pregnancy \n- Inability to tolerate or adhere to oral therapy.
What is the preferred inpatient antibiotic regimen for severe PID?
- IV cefotetan or cefoxitin + IV/oral doxycycline. \n- If penicillin-allergic: IV clindamycin + IV gentamicin.
How should sexual partners of a PID patient be managed?
- Test and presumptively treat partners for chlamydia and gonorrhea. \n- Instruct patients and partners to abstain from sex until treatment is completed for all. \n- Educate on STI prevention.
What are the surgical indications for PID?
Surgery may be required for: \n- Drainage of a tubo-ovarian abscess if unresponsive to antibiotics. \n- Removal of an IUD if no improvement after 72 hours of treatment.
What are the differential diagnoses for PID?
- Ectopic pregnancy: rule out with pregnancy test. \n- Appendicitis: localized RLQ pain, fever. \n- Ovarian torsion: sudden, severe pain, adnexal mass on imaging. \n- Ruptured ovarian cyst: acute onset pain without fever. \n- Urinary tract infection: dysuria without pelvic tenderness.
How is PID prevented?
- Practice safe sex (use condoms). \n- Limit the number of sexual partners. \n- Regular STI screening. \n- Timely treatment of STIs in both patient and partners. \n- Careful monitoring during and after IUD placement (higher PID risk in the first 3 weeks post-insertion).
What is pelvic floor dysfunction?
Pelvic floor dysfunction is the inability to relax and coordinate pelvic floor muscles correctly to urinate and/or have bowel movements.
What are the clinical features of pelvic floor dysfunction?
Urinary incontinence, urgency, and/or dysuria
Fecal incontinence
Dyssynergic defecation
Dyspareunia
Lower back or pelvic pain
Feeling of pressure on the pelvic region or rectum
Pelvic muscle spasms
What diagnostic methods are used for pelvic floor dysfunction?
Clinical features and physical examination
Pelvic ultrasound
Urodynamic studies
Anorectal manometry
What are the treatment options for pelvic floor dysfunction?
- Pelvic floor muscle training (e.g., Kegel exercises) and physical therapy \n- Biofeedback and electrical stimulation (probes or electrodes to stimulate pelvic floor muscles) \n- Stool softeners and muscle relaxants
What is the pathogen for bacterial vaginosis?
Gardnerella vaginalis
What is the characteristic discharge in bacterial vaginosis?
Gray/milky with a fishy odor
What is the vaginal pH in bacterial vaginosis?
> 4.5
What is the microscopy finding in bacterial vaginosis?
Clue cells
What is the treatment for bacterial vaginosis?
Metronidazole
What is the pathogen for trichomoniasis?
Trichomonas vaginalis
What is the characteristic discharge in trichomoniasis?
Frothy, yellow-green, foul-smelling
What is the microscopy finding in trichomoniasis?
Flagellated protozoa
What is the treatment for trichomoniasis?
Metronidazole; treat sexual partner(s)
What is the pathogen for vaginal yeast infection?
Candida albicans
What is the characteristic discharge in vaginal yeast infection?
White, crumbly, thick (cottage cheese-like), odorless
What is the vaginal pH in vaginal yeast infection?
4–4.5
What is the microscopy finding in vaginal yeast infection?
Pseudohyphae
What is the treatment for vaginal yeast infection?
Topical azoles or nystatin; oral fluconazole in nonpregnant adults
What is the pathogen for gonorrhea?
Neisseria gonorrhoeae
What is the characteristic discharge in gonorrhea?
Purulent, creamy
What is the microscopy finding in gonorrhea?
Gram-negative, intracellular diplococci
What is the treatment for gonorrhea?
Ceftriaxone (IV/IM); treat sexual partner(s)
What is the pathogen for chlamydia infections?
Chlamydia trachomatis serotype D–K
What is the characteristic discharge in chlamydia infections?
Purulent, bloody
What is the microscopy finding in chlamydia infections?
Intracellular organisms that Gram stain poorly
What is the treatment for chlamydia infections?
Azithromycin or Doxycycline in nonpregnant patients; treat sexual partner(s)
What is an ectopic pregnancy?
Ectopic pregnancy occurs when a fertilized egg implants outside the uterus, most commonly in the fallopian tubes (95%). Rare sites include the ovary, cervix, and abdomen.
What are the risk factors for ectopic pregnancy?
- Anatomic alterations: PID, tubal surgeries, endometriosis, previous ectopic pregnancy, ruptured appendix. - Nonanatomic: Smoking, age > 35, IVF or assisted reproductive technologies, IUD use.
How does an ectopic pregnancy present in uncomplicated cases?
- Lower abdominal pain (unilateral or bilateral). - Vaginal bleeding or spotting. - Amenorrhea (missed period). - Symptoms of pregnancy (nausea, breast tenderness, frequent urination).
What are the signs of a ruptured ectopic pregnancy?
- Acute abdomen: sudden, severe abdominal or pelvic pain. - Shock signs: hypotension, tachycardia, fainting, pallor. - Peritoneal signs: guarding, rebound tenderness.
How is ectopic pregnancy diagnosed?
1. Pregnancy test: Serum β-hCG. 2. Transvaginal ultrasound: Identify pregnancy location. 3. Laparoscopy if unstable or diagnosis is unclear.
What is the significance of β-hCG levels in ectopic pregnancy?
β-hCG > 1,500–3,000 IU/L: A gestational sac should be visible on ultrasound. - If not, suspect ectopic pregnancy. - Rising, plateauing, or declining β-hCG levels help differentiate ectopic from normal or failing pregnancies.
What imaging findings suggest ectopic pregnancy?
Empty uterine cavity with thickened endometrial lining. - Tubal ring sign (echogenic ring in the fallopian tube). - Free fluid in the pouch of Douglas (suggests bleeding).
What is the management approach for stable patients with ectopic pregnancy?
- Medical management: Methotrexate for stable, unruptured cases (β-hCG ≤ 5,000 IU/L, mass < 3.5 cm). - Expectant management: In asymptomatic patients with declining β-hCG levels and no ectopic mass on ultrasound.
When is surgical management indicated for ectopic pregnancy?
- Hemodynamic instability. - Signs of rupture (severe pelvic pain, peritonitis). - Failed medical therapy.
What surgical procedures are used for ectopic pregnancy?
- Salpingostomy: Removal of ectopic pregnancy while preserving the tube (for unruptured cases).
- Salpingectomy: Removal of the entire fallopian tube (preferred for rupture or severe damage).
When is methotrexate contraindicated?
- Ruptured ectopic pregnancy. - Intrauterine pregnancy. - Breastfeeding. - Methotrexate allergy.
What supportive care is needed for ectopic pregnancy?
Pain management.
- Rh immunoglobulin for Rh-negative patients with bleeding.
- Prenatal and contraceptive counseling after treatment.
What is the role of serial β-hCG measurements?
- Helps differentiate ectopic from normal pregnancies.
- Normal IUP: β-hCG increases by >33–49% in 48 hours.
- Ectopic or failing pregnancy: Plateauing or falling β-hCG levels.
What are the complications of untreated ectopic pregnancy?
- Tubal rupture leading to hemoperitoneum or shock.
- Infertility (due to tubal scarring).
- Increased risk of ectopic pregnancy recurrence.
Red Flags for Ruptured Ectopic Pregnancy:
Severe, sudden abdominal pain.
Signs of shock: hypotension, tachycardia, pallor, fainting.
Acute abdomen (rigidity, guarding, or rebound tenderness).
Peritoneal irritation or free fluid on ultrasound.
What is primary dysmenorrhea?
Recurrent lower abdominal pain shortly before or during menstruation in the absence of pathologic findings that could account for the symptoms.
When does primary dysmenorrhea typically manifest?
During adolescence, typically within three years of menarche.
What is the pathophysiology of primary dysmenorrhea?
Increased endometrial prostaglandin (PGF2 alpha) production leads to vasoconstriction/ischemia and stronger, sustained uterine contractions to prevent blood loss.
What are the clinical features of primary dysmenorrhea?
Spasmodic, crampy pain in the lower abdominal/pelvic midline, radiating to the back or thighs.
- Typically occurs during the first 1–3 days of menstruation.
- Accompanying symptoms: headaches, diarrhea, fatigue, nausea, flushing.
- Normal pelvic examination.
How is primary dysmenorrhea diagnosed?
It is a diagnosis of exclusion. Rule out conditions that cause secondary dysmenorrhea.
How is primary dysmenorrhea treated?
- Symptomatic treatment: NSAIDs, topical heat.
- Hormonal contraceptives: combined oral contraceptive pill, IUD with progestogen.
What are some uterine causes of secondary dysmenorrhea?
- Pelvic inflammatory disease (PID)
- Intrauterine device (IUD)
- Adenomyosis
- Fibroids (intracavitary or intramural)
- Cervical polyps
What are some extrauterine causes of secondary dysmenorrhea?
- Endometriosis
- Adhesions
- Functional ovarian cysts
- Inflammatory bowel disease
What is preeclampsia?
Preeclampsia is new-onset gestational hypertension (≥ 140/90 mmHg) after 20 weeks of gestation with either proteinuria or end-organ dysfunction.
What is HELLP syndrome?
A severe form of preeclampsia characterized by Hemolysis, Elevated Liver enzymes, and Low Platelets. It may occur without hypertension or proteinuria.
What are the key risk factors for preeclampsia?
- Nulliparity \n- Advanced maternal age (> 35 years) \n- Obesity \n- Family history of preeclampsia \n- Chronic hypertension \n- Diabetes mellitus \n- Renal disease \n- Multiple gestation \n- History of preeclampsia.
What is the pathophysiology of preeclampsia?
Abnormal trophoblastic invasion leads to poor placental perfusion. Release of antiangiogenic factors causes widespread endothelial dysfunction, resulting in hypertension, proteinuria, and end-organ damage.
What are the clinical features of mild preeclampsia?
- BP ≥ 140/90 but < 160/110 mmHg \n- Proteinuria: ≥ 300 mg/24 hours or urine protein/creatinine ratio ≥ 0.3
What are the clinical features of severe preeclampsia?
- BP ≥ 160/110 mmHg \n- Severe proteinuria (> 5 g/24 hours, but not mandatory) \n- End-organ dysfunction (e.g., CNS changes, liver involvement, renal impairment, thrombocytopenia, pulmonary edema).
What are common maternal complications of preeclampsia?
- Eclampsia (seizures) \n- Placental abruption \n- HELLP syndrome \n- Acute renal failure \n- Disseminated intravascular coagulation (DIC).
What are common fetal complications of preeclampsia?
- Intrauterine growth restriction (IUGR) \n- Preterm birth \n- Stillbirth \n- Placental insufficiency.
What are the diagnostic criteria for preeclampsia?
- BP ≥ 140/90 mmHg on two occasions after 20 weeks of gestation \n- Proteinuria: ≥ 300 mg/24 hours or protein/creatinine ratio ≥ 0.3, or dipstick ≥ 1+.
What additional labs are done for preeclampsia?
- CBC (platelet count) \n- CMP (AST, ALT, creatinine) \n- LDH (hemolysis marker)
What medications are used for BP control in preeclampsia?
- Acute control: Labetalol, hydralazine, or nifedipine \n- Chronic management: Methyldopa, labetalol, or long-acting nifedipine.
What medication is used for seizure prophylaxis in preeclampsia?
Magnesium sulfate. Monitor for toxicity (loss of reflexes, respiratory depression); treat toxicity with calcium gluconate.
When is delivery indicated in preeclampsia?
- Immediate delivery if ≥ 37 weeks \n- If < 37 weeks: Deliver if severe preeclampsia, complications (e.g., HELLP), or fetal compromise.
What is superimposed preeclampsia?
Preeclampsia occurring in a patient with preexisting chronic hypertension.
What are key differentials for preeclampsia?
- Gestational hypertension \n- Chronic hypertension \n- Gestational trophoblastic disease (onset < 20 weeks)
What is the follow-up for preeclampsia postpartum?
Monitor BP and symptoms postpartum (preeclampsia may persist or worsen). Screen for long-term cardiovascular risks.
Plan B
(Levonorgestrel): Progestin-based emergency pill.
Non-hormonal Methods
protection
Copper IUD:
contraindications for oral contraception
History of thromboembolism
Migraines with aura
Uncontrolled hypertension
Smoking in women > 35 years
Breast cancer
What causes constipation, GERD, and varicose veins during pregnancy?
Progesterone and relaxin decrease smooth muscle tone, causing constipation, GERD (relaxed esophageal sphincter), and varicose veins/hemorrhoids (relaxed blood vessels and uterine pressure reducing venous return).
What are the key respiratory changes during pregnancy?
Increased oxygen demand, tidal volume, and physiological dyspnea due to progesterone. Decreased total lung capacity, residual volume, and expiratory reserve volume; estrogen causes nasal congestion and nosebleeds.
How does circulation change during pregnancy?
Peripheral vasodilation decreases blood pressure mid-pregnancy; heart rate increases by 20 bpm, cardiac output increases by 40%, and mild cardiac hypertrophy occurs.
What are hematologic changes during pregnancy?
Plasma volume increases, causing dilutional anemia; RBC, WBC, and platelets increase; fibrinogen and coagulation factors increase, enhancing clotting and creating a hypercoagulable state.
What are common skin changes during pregnancy?
Hyperpigmentation (e.g., linea nigra, melasma, darkened nipples/areola), stretch marks (striae gravidarum), palmar erythema, and spider naevi due to increased prolactin and skin stretching.
Key Antenatal Visit
Important Takeaways
First Visit (<12+0 weeks)
Confirm pregnancy, complete blood count (Rh, ABO, Hb, ferritin, iron, folate), screen for infections (HBV, HCV, HIV, syphilis), urinalysis for UTI/proteinuria, PAP smear, BP, BMI, and ultrasound for gestational dating.
First Trimester Visit (11+0-13+6 weeks)
Nuchal translucency (risk of chromosomal anomalies), crown-rump length (CRL), PAPP-A + hCG (chromosomal screening), Doppler fetal heart rate (from week 12), and assess preeclampsia risk (start aspirin 150 mg if high risk).
OGTT (24–28 weeks)
Perform 75g oral glucose tolerance test (OGTT) for gestational diabetes. High-risk groups include high BMI, rapid weight gain, maternal age >35, previous macrosomia, or family history of DM.
36–37 Weeks Visit
Screen for Group B Streptococcus (GBS). If positive, administer ampicillin prophylaxis during labor to prevent neonatal infections. Offer external cephalic version for breech presentation.
Post-Term (41+3 weeks)
Induce labor if not spontaneously initiated to prevent complications.
How is GDM Diagnosed?
creening depends on risk factors:
High-risk women (e.g., past GDM, obesity): Fasting glucose at booking. If normal, do OGTT at 16–18 weeks.
Normal-risk women: Perform a 75g Oral Glucose Tolerance Test (OGTT) between 24–28 weeks.
OGTT criteria for GDM diagnosis:
Fasting glucose: ≥5.1 mmol/L.
1-hour post-load glucose: ≥10 mmol/L.
2-hour post-load glucose: ≥8.5 mmol/L.
What are the Impacts of GDM?
mother
For the Mother:
During Pregnancy:
Hypertension and preeclampsia.
Premature delivery.
During Labor:
Induced labor or cesarean section.
Perineal trauma or assisted vaginal delivery.
Postpartum:
Higher risk of type 2 diabetes (DM2) or cardiovascular disease.
Postpartum hemorrhage or infection.
baby
For the Baby:
Before birth:
Macrosomia (big baby) leading to delivery trauma (e.g., shoulder dystocia).
Increased risk of stillbirth or polyhydramnios.
After birth:
Neonatal hypoglycemia and respiratory distress.
Hyperbilirubinemia and NICU admission.
Long-term risk of obesity, diabetes, and heart disease.
First-Trimester Key Markers:
PAPPA: Low in trisomies.
β-hCG:
High in Down syndrome.
Low in trisomy 18 and 13.
Nuchal Translucency (NT): Enlarged in Down syndrome and trisomy 18.
Second-Trimester Key Markers:
AFP: Elevated in neural tube defects or abdominal wall defects.
Quad screen abnormalities suggest chromosomal anomalies.
Diagnostic Tests to Confirm Abnormalities:
Chorionic Villus Sampling (CVS): Done early (10–13 weeks).
Amniocentesis: Done later (15–20 weeks).
cffDNA (NIPT): Non-invasive, detects chromosomal and inherited conditions.
First Stage of Labor
Definition: Onset of labor until complete cervical dilation (10 cm). Phases:
Latent Phase
Characteristics: Mild, irregular contractions; gradual cervical dilation (< 1 cm/hour).
Duration:
Primipara: < 20 hours
Multipara: < 14 hours
Active Phase
Characteristics: Regular, stronger contractions; rapid cervical dilation (1–4 cm/hour).
Primipara: ≥ 1.2 cm/hour
Multipara: ≥ 1.5 cm/hour
Clinical Features:
Cervical effacement and dilation.
Bloody show: Blood-tinged mucous discharge.
Spontaneous rupture of membranes (SROM): Watery discharge from amniotic sac rupture.
Management:
Pain relief: Analgesia upon request.
Fetal heart rate monitoring.
Assess fetal position via Leopold's maneuvers or ultrasound.
Regular cervical and fetal descent checks.
Amniotomy during active phase (if safe).
Second Stage of Labor
Definition: From full cervical dilation (10 cm) to delivery of the baby. Duration:
Primipara: < 3 hours
Multipara: < 2 hours
Strong, regular uterine contractions.
Crowning: Appearance of fetal head at the vaginal opening.
Warm compresses and perineal massage for comfort.
Encourage safe, comfortable maternal positioning.
Episiotomy only if indicated (e.g., shoulder dystocia, assisted delivery).
Delay cord clamping (~1 minute) or milk the cord.
Third Stage of Labor
Definition: From delivery of the baby to placenta expulsion. Duration: ~30 minutes
Uterine contractions expel the placenta.
Signs of placental separation:
Cord lengthening
Gush of vaginal blood (~300 mL loss)
Uterine fundal rebound (uterus becomes spherical).
Fundal massage: Stimulates uterine contraction to minimize bleeding.
Active management:
Oxytocin: Administered after cord cutting to enhance uterine contraction.
Controlled cord traction: Assists placental separation (Brandt-Andrews maneuver).
Examine placenta for completeness (cord, membranes, 3 vessels).
Fourth Stage of Labor
Definition: Immediate postpartum period (~2 hours post-delivery).
Key Steps:
Examine placenta for completeness.
Repair any obstetric lacerations.
Monitor closely for:
Postpartum hemorrhage.
Preeclampsia symptoms (e.g., elevated BP, seizures).
What is the postpartum period?
The 6-8 week period after birth when the body recovers from pregnancy and childbirth.
What are common findings in the first 24 hours postpartum?
Low-grade fever, shivering, and leukocytosis, which do not necessarily indicate an infection.
What is uterine involution?
The process where the uterus contracts and returns to its pre-pregnancy size by the 6th–8th week postpartum.
What are afterpains?
Painful uterine cramps caused by postpartum uterine contractions, more common in multiparous women.
What is lochia?
Postpartum vaginal discharge from uterine lesions, cervical mucus, and other components during healing.
How much weight is typically lost after delivery?
- Immediately after delivery: ~6 kg (13 lbs) from baby, amniotic fluid, and placenta.
- Additional weight loss: ~2–7 kg (5–15 lbs) due to lochia and uterine involution.
When can contraception be initiated postpartum?
After 4 weeks, all methods can be used depending on personal preference and breastfeeding status.
What contraception is suitable for breastfeeding women?
- Progestin-only pills, implants, or injections.
What contraception methods should be avoided in breastfeeding women initially?
Combined hormonal contraceptives (estrogen + progestin) in the first 6 weeks due to the risk of reduced milk supply.
What are the main causes of first trimester bleeding?
Obstetric causes: ectopic pregnancy, miscarriage (threatened, inevitable, complete, incomplete), implantation bleeding, placenta previa, gestational trophoblastic disease. Non-obstetric causes: infections, trauma, malignancy, uterine abnormalities (polyps, fibroids).
What are the clinical signs of first trimester bleeding?
Vaginal bleeding of varying severity, abdominal cramping/pain, general weakness, nausea. Severe cases: tachycardia, hypotension, anemia, tachypnea, dyspnea, and syncope.
What is the role of diagnostics in first trimester bleeding?
- Anamnesis and physical/vaginal/speculum examination.
- Transvaginal ultrasound (TVUS).
- Beta-hCG levels to evaluate pregnancy status and rule out ectopic pregnancy or miscarriage.
What are the stages of lactation?
- Stage I (Secretory Initiation): During pregnancy, glands differentiate but prolactin action is blocked by high estrogen/progesterone levels. Colostrum may be expressed.
- Stage II (Secretory Activation): After delivery, decrease in estrogen/progesterone allows prolactin to act, oxytocin causes milk ejection (galactokinesis).
What are the benefits of breastfeeding?
- Bonding between mother and child.
- Decreases risk of infant allergies, respiratory and GI infections.
- Faster uterine involution.
- Early maternal weight loss.
- Prolongs postpartum anovulation.
What are TORCH infections and their impact on pregnancy?
TORCH: Toxoplasmosis, Others (syphilis, listeria, varicella, parvovirus B19), Rubella, Cytomegalovirus, Herpes.
Impact: congenital defects, growth restriction, preterm birth, spontaneous abortion, lifelong morbidity (e.g., hearing/vision loss).
How is HIV vertical transmission prevented?
- Low viral load (<1000 copies/ml): Any delivery mode is acceptable.
- High viral load (>1000 copies/ml): Planned c-section at 38 weeks, IV zidovudine during labor.
- Infant prophylaxis: Zidovudine for low risk, combination therapy for high risk.
What are the major causes of second/third trimester bleeding?
Placenta previa, placental abruption, uterine rupture, vasa previa.
Non-obstetric: cervical/vaginal lesions, cervical trauma, "bloody show" before labor.
What are the risk factors and prevention for postpartum hemorrhage (PPH)?
Risk Factors: Uterine atony, retained placenta, trauma, coagulation disorders.
Prevention: Antenatal risk assessment (e.g., anemia), active management of the third stage of labor (e.g., oxytocin administration), bimanual uterine massage, controlled cord traction, careful monitoring postpartum
What are the types of hypertensive disorders during pregnancy?
- Gestational hypertension: BP >140/90 after 20 weeks without proteinuria.
- Chronic hypertension: Diagnosed before 20 weeks or pre-pregnancy.
- Preeclampsia: Gestational HTN + proteinuria or end-organ dysfunction.
- Eclampsia: Severe preeclampsia with seizures.
What is the treatment approach for epilepsy during pregnancy?
High-risk pregnancy; ensure adequate folic acid supplementation (1–4 mg/day).
- Safest AED: Lamotrigine.
- Adjust AED dose for increased renal clearance during pregnancy.
- Post-pregnancy: Taper pregnancy-level AED doses, discuss contraceptive options.
What are the FDA pregnancy medication safety categories?
- A: Safe in pregnancy (e.g., folic acid).
- B: No harm in animals or limited human data (e.g., metformin).
- C: Harm in animals, unclear in humans; benefits may outweigh risks (e.g., gabapentin).
- D: Harmful, but benefits may outweigh risks (e.g., losartan).
- X: Contraindicated in pregnancy (e.g., statins).
Why is valproate contraindicated in pregnancy?
Causes neural tube defects (e.g., spina bifida), intrauterine growth restriction, and increased autism risk. Should be avoided in women of childbearing age unless no alternatives are available.
How is magnesium sulfate used in preeclampsia management?
Given for seizure prophylaxis in severe preeclampsia. Monitor for magnesium toxicity (e.g., muscle weakness, respiratory depression), and provide calcium gluconate for reversal if needed.
What are the risk factors for DVT/PE during pregnancy?
Previous DVT, thrombophilia, antiphospholipid syndrome, lupus, sickle cell disease, acute respiratory infections, maternal age >35, gestational diabetes, smoking, obesity, prior stroke, hypertension, and cancers.
What are prophylaxis options for DVT during pregnancy/postpartum?
Mechanical: Compression stockings.
Medical: LMWH (e.g., enoxaparin 40 mg SC daily) or UFH in renal impairment.
Antepartum prophylaxis: Start in high-risk patients preconception or by 28 weeks. Continue until delivery.
Postpartum prophylaxis: Continue for 6 weeks–3 months.
What are the main causes of premature delivery?
Genetic factors, infections, cervical surgery, uterine malformations, chronic medical disorders (DM, HT), assisted reproduction, short cervix, smoking, alcohol use, stress, poor prenatal care, history of preterm birth, spontaneous abortion, and short interpregnancy interval.
How is premature labor managed?
- High-risk patients may benefit from progesterone supplements or cervical cerclage.
- If labor starts: corticosteroids for lung maturation (betamethasone), tocolytics (e.g., magnesium sulfate) to delay labor for 48 hours, and antibiotics for GBS prophylaxis.
- Magnesium sulfate for neuroprotection if <32 weeks gestation.
What are short- and long-term complications of cesarean delivery?
Short-term: Fever (endometritis), wound infections, hemorrhage, surgical injury, ileus, psychiatric complications.
Long-term: Placenta previa/accreta, uterine rupture, scar pain, adhesions, bowel obstruction, infertility, unexplained stillbirths, preterm births, and fetal complications like allergies and infections.
What are the indications for cesarean delivery?
Maternal indications: Placenta previa, uterine rupture, severe HT, maternal skeletal deformities.
Fetal indications: Fetal distress (e.g., pathological CTG, acidosis), malpresentation, macrosomia, and multiple pregnancy with significant weight difference.
What are the risk factors for postpartum endometritis?
Cesarean delivery, prolonged labor, multiple cervical exams, retained products of conception, meconium-stained amniotic fluid, and low socioeconomic status.
How is postpartum endometritis managed?
Empiric antibiotics (IV clindamycin + gentamicin), removal of retained products of conception by curettage.
What is neonatal asphyxia?
Birth asphyxia caused by oxygen deprivation during labor, leading to hypoxemia, hypercapnia, and acidemia. Associated with low Apgar scores (<3 at 5 minutes) and umbilical cord arterial pH <7.2.
What are the principles of newborn resuscitation?
1. Warmth and drying to prevent hypothermia.
2. Clear airways if necessary (suction mouth before nose).
3. Provide positive pressure ventilation for apnea or HR <100 bpm.
4. If HR <60 bpm, initiate chest compressions (3:1 ratio with ventilation).
5. Administer epinephrine if HR remains <60 bpm.
6. Continue resuscitation for up to 15 minutes if there is no improvement.
What are the steps in neonatal resuscitation?
- Initial evaluation: Warm the baby, dry with warm towels, assess breathing/HR.
- Airway clearance: Suction mouth and nose.
- Positive pressure ventilation: 40-60 breaths/min for apnea or HR <100 bpm.
- Chest compressions: If HR <60 bpm, 3 compressions to 1 ventilation.
- Medications: Epinephrine 0.01–0.03 mg/kg via IV or endotracheal route every 3–5 minutes if HR <60 bpm.
What are causes of bleeding in the second half of pregnancy
Placenta previa, placental abruption, uterine rupture, vasa previa. Non-obstetric causes: vaginal/cervical lesions, trauma.
How is postpartum hemorrhage (PPH) prevented?
Active management of the third stage of labor: administration of oxytocin, controlled cord traction, and uterine massage. Assess antenatal risk factors (e.g., anemia), avoid unnecessary episiotomies, and maintain proper monitoring postpartum.
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