Hemodinamic disorders

- active process

- dilatation of arterioles and increased blod inflow

- hyperemic tissues are redder than normal due to inflow of oxigenated blood

Examples -> blushing, exercise, inflammation

- passive process

- impaired venous outflow

-it can occure sistematically or locally

- congested tissues are cyanotic (bluish) due to accumulation of

deoxigenated hemoglobin

Examples -> heart failure, venous obstruction

nutmeg liver (seen in gross examination)

central areas are slightly depressed due to pericentral hepatocite necrosis

the uncongested zones are tan, sometimes fatty

• inflammatory

• hydrostatic

• oncotic

• obstructive

• hpervolemic

inflamation-increased vascular permeability

-general congestive heart failure, constrictive pericarditis

- local-deep venous thrombosis, external pressure

nephrotic syndrome, liver cirrhosis, protein malnutrition

lymphatic obstruction by tumor cells parasites chronic inflammation, surgery or irradiation

primary hyperaldosteronism (adrenal hyperplasia, adrenal adenoma)

combi of hydrostatic and hypervolemic

leads to pulmonary congestion, edema and pleural effusion

leads to chronic congestion of liver and spleen, ascites, congestion and edema of lower extremities

most commonly due to left-sided heart failure

massive edema of lower extremity caused by parasitic infection by wucheria nabcrofti

severe generalised edema with profound swelling of subcutaneous tissues and accumulation of fluid in body cavities (hydrotorax, hydropericardium, ascites)

the cancer cells block the dermal lymphatics and produce a “peau d’orange” appearance of the breast skin.

• Hematemesis

• Hemoptysis

• Hematuria

• Hematochezia

• Hemotorax

• Hemopericardium

• Hemoperitoneum

• Hemartrosis

blood clot formation in intact vessel

1. endothelial injury

2. stasis or turbulent blood flow

3. hypercoagulability of the blood

- downregulated expression of

thrombomodulin - sustained activation of thrombin

- activation of platelets and induction of inflammation

- downregulation of anticoagulants (prote C, tissue factor protein inhibitor)

- secretion of plasminogen activator inhibitors (PAI)- lower fibrinolysis

Factor V mutation (2-15%)

-mutation alters an amnio-acid and makes it resistant to proteolysis by protein C

-heterozygotes 5-fold increased risk and homozygotes 50-fold increased risk for venous thrombosis

Prothrombin mutation (1-2%)

-single nucleotide substitution (G-A) in the prothrombine results inincreased prothrombine transcription

-3-fold increased risk for venous thrombosis

• Immobilization

• Myocardial infarction

• Atrial fibrilation

• Tissue injury (burns, surgery)

• Cancer

• Pregnancy

myocardial infarction, arrhytmias, dilated cardiomyopathy, endomyocardial injury, myocarditis, catheter trauma

infective- bacterial or fungal infection

sterile-hypercoagulable states

atherosclerosis, vasculitis, trauma

stasis-immobilisation, hypercoagulable states (burns, pregnancy, cancer)

thrombus: clot adherent to cell wall, laminated

p.m. clot: not adherent to vessel wall. plasma and rbc seperate

Embolus- detached intravascular solid, liqiud or gaseous mass that is carried by the blood from its point of origin to a distant site resulting in partial or complete vascular obstruction.

1) Thromboemboli: fragments of thrombi

2) Liquid emboli: fat, amniotic fluid

3) Gaseous emboli: air injection, decompression sickness

4) Solid particle emboli: cholesterol crystals, tumor cells,

bone marrow

originate in veins, are carried by venous circulation to the lungs and cause pulmonary embolism

originate in the left heart, aorta or major arteries and cause infarcts in many organs (brain, kidneys, spleen, intestines, legs)

originate in the deep leg veins but move through a foramen ovale or ventricular septal defect (VSD), causing symptoms similar to those of arterial emboli

mostly originates from deep veins

large embolus lodge at bifurcation -> sudden death

medium sized -> pul. hemmorage/infarction

smal sized in small end ateriolar -> infarction

=> multiple emboly cause hypertension and RVF

soft tissue crush / long bone fracture -> fat & bm into circulation

• 1-3 days after injury

• pulmonary insufficiency

• neurologic symptoms

• anemia, thrombocytopenia

• diffuse petechial rash

● Patogenesis: occlusion of pulmonary and cerebral microvasculature by fat

globules followed by platelet and RBC aggregation

amniotic fluid in maternal circulation

mortality rate 80% but rare

clinical symptoms: dyspnea, cyanosis, hypotensive shock, coma, DIK

Patogenesis: mechanical obstruction of pulmonary vessels and activation of coagulation system by release of thrombogenic substances from amniotic fluid- disseminated intravascular coagulation (DIC)

can obstruct blood flow -> ischemia

decompression sicknes

caused by arterial occlusion in solid organs with end- arterial circulation such as the heart, spleen, or kidney.

caused by:

• venous occlusion (ovarian or testical torsion)

• loose, spongy tissues where blood can permeate infarcted zones (lung)

• organs with a dual blood supply (lung, intestines)

• myocardial infarction

• arrhytmia

• pulmonary embolism

• cardiac tamponade

• hemorrhage

• fluid loss (vomiting, diarea, burns)

• gram-positive septicemia

• gram-negative sepsis

• IgE mediated hypersensitivity

1. initial nonprogressive phase

2. progressive phase

3. irreversible phase

vital organ perfusion is maintained due to activation of compensatory mechanisms :

- tachycardia

- peripheral vasoconstriction (cool, pale skin)

- renal fluid retention (activation of renin-angiotensin-aldosteron axis)

tissue hypoperfusion and hypoxia resulting in anaerobic glycolises, metabolic acidosis and decreased vasomotor response

-dilatation of arterioles and peripheral pooling of the blood

-vital organs began to fail

severe cellular and tissue injury, survival is not possible even if underlying cause is corrected

- worsening of myocardial contractile function

- progressive renal failure

blood engorged alveolar capillaries and variable degrees of alveolar septal edema and intraalveolar hemorrage

the septa become thiken and fibrotic

alveolar spaces contain numerous macrophages laden with hemosiderin (heart failue cells) derived from phagocytosed red cells

vegetations

widespread throbosis in microcorculation may be sudden

consumes platelets and coagulation proteins

may coexixst with exessive clotting and bleeding

intracardial mural thrombi -> 2/3 LV infarcts

75% lower extreities

10% CNS