Circulatory Disorder: DIC, Infarction, Shock

Question 1

Describe disseminated intravascular coagulation. (DIC)

Answer 1

-systemic reaction
-thrombo hemorrhagic disorder
-generalized activation of blood coagulation system
-not a primary disease
-signs of tissue hypoxia, infarction, hemorrhage seen

Fibrin thrombi DIC

Question 2

Describe what the diffuse endothelial damage is due to.

Answer 2

-extensive tissue injury
-neoplasia
-systemic immunologic reactions -> anaphylaxis
-sepsis -> severe systemic infection

Question 3

Describe the DIC 3 stages.

Answer 3

1. First stage
   -inc blood coagulation in microvessels > fibrin clots (fibrinoembolism)
2. Second stage
   -dec thrombocytes, fibrinogen, prothrombin in blood -> consumption coagulopathy -> bleeding diathesis & hemorrhagic syndrome
3. Third stage
   -fibrinolysis activation -> hemorrhagic syndrome more severe

Question 4

Describe infarction.

Answer 4

-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

Question 5

Describe the factors that influence the development of an infarct.

Microscopically = focal area of coagulationn necrosis

Answer 5

1. Nature of vascular supply
2. Rate of development of occulsion
3. Vulnerability of affected tissue/organ to hypoxia
4. Oxygen content of blood at time of infarction

Question 6

Describe red infarcts.

Intestinal volvulus

Answer 6

-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

Question 7

Describe pale infarcts.

Answer 7

-w/o blood
-solid organs
-red zone in periphery
-arterial infarcts initially hemorrhagic but become pale as the area of coagulation necrosis becomes evident

Question 8

Describe infarct repair VS septic infarct.

Answer 8

1. Repair:
   -scar tissue replace parenchyma
   -parenchymal loss + fibrous tissue contraction = depression/indent of surface
2. Septic:
   -from septic (bacterial infected) thromboembolus
   -necrotic tissue by opportunistic bacteria

Repair

Question 9

Describe venous obstruction/infarction.

Answer 9

-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

Question 10

Describe pulmonary arterial thrombosis/thromboembolism (PTE) causes.

Answer 10

-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)

Question 11

Describe shock.

Answer 11

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)

Question 12

Describe the pathogenesis of shock.

Answer 12

-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

Question 13

Describe the 3 different types of shock.

Answer 13

1. Cardiogenic shock
2. Hypovolemic shock
3. Vasculogenic shock

Question 14

Describe cardiogenic shock.

Answer 14

-failure of heart to maintain normal CO
-results from:
1. Reduced cardiac filling
-ex = cardiac tamponade
2. Reduced cardiac emptying
-ex = pulmonary embolism

Question 15

Describe hypovolemic shock.

Answer 15

-dec circ blood vol
-result from:
>blood loss from hemorrhage
>fluid loss (dehydration)
—vomit, diarrhea, burns

Question 16

Describe vasculogenic shock.

Answer 16

-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

Question 17

Describe the pathogenesis of septic shock.

Answer 17

-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 *

Question 18

Describe the clinical signs & lesions of shock.

Answer 18

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

Question 19

Describe the stages of shock.

Answer 19