Disorders of haemostasis - embolism, DIC, shock

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40 Terms

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Non thrombus causes of embolism

Bacterial, parasites, fat droplets (fractures), bubbles, bone marrow, cartilage, foreign bodies, tumour fragments (metastases)

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<p>What happens in bacterial emboli (bacterial endocarditis)  </p>

What happens in bacterial emboli (bacterial endocarditis)

Bacterial embolus in pulmonary + systemic circulation → embolic metastatic diseases (glomerulonephritis, pneumonia, hepatitis)

<p>Bacterial embolus in pulmonary + systemic circulation → embolic metastatic diseases (glomerulonephritis, pneumonia, hepatitis)</p>
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<p>Tyzzers disease </p>

Tyzzers disease

Enterocolitis → organisms enter hepatic portal vein

<p>Enterocolitis → organisms enter hepatic portal vein </p>
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<p>Dirofilaria immitis </p>

Dirofilaria immitis

Heart worm in RV + pulmonary artery → systemic circulation

<p>Heart worm in RV + pulmonary artery → systemic circulation </p>
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<p>What can happen after fractures </p>

What can happen after fractures

Fat embolism

<p>Fat embolism </p>
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<p>Common site of fibro-cartilaginous embolism </p>

Common site of fibro-cartilaginous embolism

Spinal cord

<p>Spinal cord </p>
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<p>Term for tumour cell embolus production </p>

Term for tumour cell embolus production

Metastasis

<p>Metastasis </p>
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<p>Squamous cell carcinoma is what (common in white cats)</p>

Squamous cell carcinoma is what (common in white cats)

Neoplasm of keratinocytes

<p>Neoplasm of keratinocytes </p>
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DIC stands for

Disseminated intravascular coagulation

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DIC def

Acute/subacute/chronic thrombo-haemorrhagic disorder occurring as secondary complication in variety of diseases

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steps of DIC

Activation of coagulation cascade in whole body → formation of micro thrombi throughout microcirculation → consumption of platelets, fibrin, coagulation factors, activation of fibrinolysis

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CS of DIC

Tissue hypoxia, infarction, haemorrhagic disorder (consumption coagulopathy)

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<p>Major underlying mechanisms of DIC (causes)</p>

Major underlying mechanisms of DIC (causes)

Release of tissue factor, thromboplastic substances into circulation

Widespread injury to endothelial cells → coagulation cascade

<p>Release of tissue factor, thromboplastic substances into circulation </p><p>Widespread injury to endothelial cells → coagulation cascade </p>
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<p>Pathogenesis of DIC- causes </p>

Pathogenesis of DIC- causes

Massive tissue destruction, sepsis, endothelial injury

<p>Massive tissue destruction, sepsis, endothelial injury </p>
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<p>Pathogenesis of DIC- Effects </p>

Pathogenesis of DIC- Effects

Fibrinolysis, ischaemic tissue damage, consumption of clotting factors + platelets, bleeding

<p>Fibrinolysis, ischaemic tissue damage, consumption of clotting factors + platelets, bleeding </p>
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Pathogenesis of DIC- Commonly associated with

Severe systemic infections (from direct endothelium injury, immune complex deposition), septic shock, neoplasm, extensive trauma/burns, extensive surgery

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<p>Pathogenesis of DIC- How does sepsis (gram -) leads to DIC</p>

Pathogenesis of DIC- How does sepsis (gram -) leads to DIC

Bacterial endotoxins → monocytes release tissue factor + pro inflammatory cytokines → endothelial cells increase expression of tissue factor, decrease expression of thrombomodulin → activate clotting cascade, inhibit clotting control

<p>Bacterial endotoxins → monocytes release tissue factor + pro inflammatory cytokines → endothelial cells increase expression of tissue factor, decrease expression of thrombomodulin → activate clotting cascade, inhibit clotting control </p>
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<p>Pathogenesis of DIC- How does sepsis (gram +) leads to DIC</p>

Pathogenesis of DIC- How does sepsis (gram +) leads to DIC

Bacterial lysis → release cell wall components → monocytes produce cytokines + SIRS + DIC

Neutrophils adhere to endothelium → release proteases + O radicals → capillary dmamage → haemorrhage → shock

<p>Bacterial lysis → release cell wall components → monocytes produce cytokines + SIRS + DIC </p><p>Neutrophils adhere to endothelium → release proteases + O radicals → capillary dmamage → haemorrhage → shock </p>
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<p>Viral diseases associated with DIC - pigs </p>

Viral diseases associated with DIC - pigs

Classical Swine fever

By endothelial alterations → petechia

<p>Classical Swine fever</p><p>By endothelial alterations → petechia </p>
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Viral diseases associated with DIC - Dog

Infectious canine hepatitis

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<p>Viral diseases associated with DIC - Rabbit </p>

Viral diseases associated with DIC - Rabbit

Rabbit haemorrhagic diease

Hepatocyte necrosis

<p>Rabbit haemorrhagic diease</p><p>Hepatocyte necrosis </p>
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Viral diseases associated with DIC - Sheep

Blue tongue

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Viral diseases associated with DIC - Mink

Aleutian disease

Immune complex deposition in BV wall → complement + coagulation cascade

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Viral diseases associated with DIC - Deer

epizootic haemorrhagic disease

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Shock - def + causes

Culmination in systemic hypoperfusion due to reduced CO, reduced effective circulating blood vol

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Causes of shock

Severe haemorrhage, microbial sepsis, extensive trauma/burns, large infarction, massive pulmonary embolism

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Effects of shock

Hypotension → impaired perfusion → cellular hypoxia

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Types of shock

Cardiogenic, hypovolaemic, septic, neurogenic, anaphylactic

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Types of shock - cardiogenic

Failure of myocardial pump

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Types of shock - hypovolaemic

Loss of blood/ plasma

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Types of shock - septic

Systemic microbial infection

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Types of shock - neurogenic

Depression of vasomotor centre

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Types of shock - anaphylactic

Generalised IgE mediated hypersensitivity

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Stages of shock

Non progressive, progressive, irreversible

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Pathogenesis of septic shock - type of bacteria

Endotoxin (LPS) producing gram -

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<p>Pathogenesis of septic shock - With low LPS</p>

Pathogenesis of septic shock - With low LPS

Activation of monocytes, endothelial cells, complement → cascade → local acute inflammation + bacterial clearance

<p>Activation of monocytes, endothelial cells, complement → cascade → local acute inflammation + bacterial clearance </p>
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<p>Pathogenesis of septic shock - With mod LPS</p>

Pathogenesis of septic shock - With mod LPS

Cytokine induced effectors (NO + PAF) → fever, acute phase reactants, endothelial injury, DIC

<p>Cytokine induced effectors (NO + PAF) → fever, acute phase reactants, endothelial injury, DIC</p>
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<p>Pathogenesis of septic shock - With high LPS</p>

Pathogenesis of septic shock - With high LPS

Systemic vasodilation, reduced cardiac contractility, DIC → MOSF, SIRS

<p>Systemic vasodilation, reduced cardiac contractility, DIC → MOSF, SIRS</p>
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what does MOSF stand for

Multi organ system failure

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Pathogenesis of septic shock in gram + bacteria

Cytokine production (monocytes), SIRS, DIC

Neutrophils adhering to endothelium, release of proteases, O radicals → shock