Circulatory Disorder: DIC, Infarction, Shock Flashcards
Describe disseminated intravascular coagulation. (DIC)
-systemic reaction
-thrombo hemorrhagic disorder
-generalized activation of blood coagulation system
-not a primary disease
-signs of tissue hypoxia, infarction, hemorrhage seen
Describe what the diffuse endothelial damage is due to.
-extensive tissue injury
-neoplasia
-systemic immunologic reactions -> anaphylaxis
-sepsis -> severe systemic infection
Describe the DIC 3 stages.
- First stage
-inc blood coagulation in microvessels > fibrin clots (fibrinoembolism) - Second stage
-dec thrombocytes, fibrinogen, prothrombin in blood -> consumption coagulopathy -> bleeding diathesis & hemorrhagic syndrome - Third stage
-fibrinolysis activation -> hemorrhagic syndrome more severe
Describe infarction.
-local area of ischemic necrosis in tissue/organ caused by occlusion of arterial supply or venous drainage
-due to: thrombosis, embolism, vascular occulsion from twisting of vessel
-renal infarction common
-gross appearance:
>wedge shaped
>early = ill defined & red
>later = pale
Describe the factors that influence the development of an infarct.
- Nature of vascular supply
- Rate of development of occulsion
- Vulnerability of affected tissue/organ to hypoxia
- Oxygen content of blood at time of infarction
Describe red infarcts.
-blood
-acute w damaged vessels & hemorrhage
-organs w dual blood supply
-venous infarcts intensely hemorrhagic as blood backs up into the affected tissue behind the obstruction
Describe pale infarcts.
-w/o blood
-solid organs
-red zone in periphery
-arterial infarcts initially hemorrhagic but become pale as the area of coagulation necrosis becomes evident
Describe infarct repair VS septic infarct.
- Repair:
-scar tissue replace parenchyma
-parenchymal loss + fibrous tissue contraction = depression/indent of surface - Septic:
-from septic (bacterial infected) thromboembolus
-necrotic tissue by opportunistic bacteria
Describe venous obstruction/infarction.
-complete venous obstruction leads to venous infarction
-due to twisting of vessels -> shock/death
-obstruction of portal vein or vena cava
-etiology in dogs: severe heartworm inf & tumor invasion
-etiology in ruminants: rupture of hepatic abscesses into cd vena cava
-blockage of cd vena cava -> acute R heart failure *
-outcome:
>acute = sudden death
>chronic = possible collateral circ from azygous vein
Describe pulmonary arterial thrombosis/thromboembolism (PTE) causes.
-occulsion of blood vessel by embolus thats broken away from thrombus & travels until stuck
>pneumonia
>parasites (ex. Heartworm)
>hypercoagulability
—nephrotic syndrome
—hyperadrenocorticism
—exogenous steroids
>liver abscess rupture into vena cava
—thromboembolism into lung
*result depends on size of artery blocked:
-small vessel or incomplete -> subclinical
-complete & large artery -> death
(May cause pulmonary infarction)
Describe shock.
Cardiovascular collapse
-acute reduction of effective circulating blood volume
-inadequate perfusion of cells & tissues
-caused by:
>reduced CO or reduced effective circulating blood volume
-end result:
>hypotension, impaired tissue perfusion, cell hypoxia
may lead to DIC & multi organ system failure
(Brain & heart are very sus to tissue hypoxia)
Describe the pathogenesis of shock.
-perfusion of brain & heart maintained at expense of blood supply to viscera & skin
-impaired tissue perfusion -> anaerobic glycolysis
-lactic acidosis -> lysosomal damage & widespread cell injury
Describe the 3 different types of shock.
- Cardiogenic shock
- Hypovolemic shock
- Vasculogenic shock
Describe cardiogenic shock.
-failure of heart to maintain normal CO
-results from:
1. Reduced cardiac filling
-ex = cardiac tamponade
2. Reduced cardiac emptying
-ex = pulmonary embolism
Describe hypovolemic shock.
-dec circ blood vol
-result from:
>blood loss from hemorrhage
>fluid loss (dehydration)
—vomit, diarrhea, burns
Describe vasculogenic shock.
-maldistribution -> dec in peripheral vascular resistance & resultant pooling of blood in peripheral tissue
-results from vasodilation
1. Anaphylactic = type I HS (release vasoactive amines)
2. Neurogenic = neurological injury leading to loss of vascular tone & peripheral pooling of blood
3. Septic = release of chem mediators associated w inflam
Describe the pathogenesis of septic shock.
-caused by endotoxin producing gram neg bacilli = endotoxic shock (ex. Mastitis)
1. Endotoxins released from the bacteria
2. Activate/injury of endothelial cells by LPS
3. Activate complement + activate WBCs to release cytokines
4. Coagulation activation (DIC) & complement activation
>cytokine induced secondary effectors (NO & PAF)
>systemic TNF & IL1 -> fever, acute phase response
>endothelial cell injury -> triggers coagulation cascade
5. Microcirculation thrombosis & vasodilation -> tissue ischemia *
Describe the clinical signs & lesions of shock.
CS: lethargy, reduced mentation, subnormal temp, irregular breathing, low BP, tachycardia, weak pulse, pallor, anuria
Lesions:
-pulmonary congestion & edema
-hepatic congestion
-heart - hemorrhage & necrosis
-brain - neuronal cell death
-kidneys - acute tubular necrosis
blood vessel - endothelial damage (thrombosis/DIC)
-adrenal glands - hemorrhage
GIT - congestion & hemorrhage
-skeletal muscle - pallor
Describe the stages of shock.
