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Gen Path #1 > Disorders of blood fluidity > Flashcards

Disorders of blood fluidity Flashcards

1
Q

Thrombosis

A

-formation of an inappropriate clot of fibrin and/or platelets along with other blood elements on the wall of a blood or lymphatic vessel or heart

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2
Q

Virchow’s triad

A

-causes of thrombosis
1.endothelial injury
2.abnormal blood flow
3.hypercoagulation (rare)

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3
Q

Endothelial injury

A

-exposed basement membrane results in stimulation of clot synthesis
>problem when it has the ability to block a blood vessel
occurs in heart and arteries

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4
Q

Alterations in blood flow

A

-Two types: stasis or turbulence
-disrupted laminar flow resulting in platelet contact with endothelium. Slowed blood results in greater chance of blood clots.

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5
Q

Hypercoagulability

A

-homeostasis poor and leans towards clot formation
>Antithrombin III is at low levels means less anticoagulant
-occurs in pregnancy. Women prepare to lose blood so get in hypercoagulable state

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6
Q

Arterial thrombus

A

-endothelial injury
-part where it is stuck to wall due to injury is white and form because parts of clot near wall are mostly platelets and fibrin; low RBCs
-part attached to white is gelatinous and red areas in which the RBCs get trapped

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7
Q

Venous thrombus

A

-slow blood flow
-RBCs are trapped within mixture of platelets and fibrin
-soft, gelatinous and red

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8
Q

Venous thrombus and post-mortem clots

A

-both are soft, red, gelatinous, but genuine thrombus will be attached to the vessel wall

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9
Q

Vegetative valvular endocarditis

A

-thrombosis of cardiac valves
-endothelial injury superimposed by bacterial colonization
-grey yellow, firm and friable

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10
Q

Significance of thrombosis to animal

A

-thrombosis of large vessels
>infarction
>source of thromboemboli
-vegetative valvular endocarditis
>source of thromboemboli (usually septic)
>heart failure
-DIC localized or systemic
>always significant clinically, linked to many conditions

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11
Q

Propagation of thrombus

A

-accumulate more platelets and fibrin= occlusion

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12
Q

Embolization

A

-dislodgement of thrombi resulting in vascular obstruction by emboli

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13
Q

Dissolution

A

-recent thrombi may be removed by fibrinolysis

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14
Q

Organisation

A

-fibrin is replaced by vascularized fibrous tissue
-endothelial cells slide over organized thrombus
-incorporation of residual thrombotic tissue in subendothelial layer

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15
Q

Recanalization

A

-In growth of angioblasts and fibroblasts with neutrophils and macrophages
-capillaries anastomose to create channels reestablishing blood flow

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16
Q

Disseminated intravascular coagulation (DIC) causes

A

**widespread microvascular thrombosis, and depletion of platelets and coagulation factors= bleeding
-septic
-injury to endothelium
-protein losing nephropathy
-uremia
-disseminated metastatic neoplasia

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17
Q

Postmortem clotting

A

-occurs within several hours in normal animal
-when it does not occur, coagulation issues are most likely present (anticoagulate toxicities)

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18
Q

Chicken fat clot

A

-occurs when RBCs sediment quickly resulting in bottom red mass and upper pale yellow mass

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19
Q

Horse clots

A

-will appear more like chicken fat clot
-due to rouleax formation

20
Q

Embolism

A

-embolus is detached intravascular mass that is carried to a site distant from its point of origin and it obstructs partially or completely vessels

21
Q

Ischemic necrosis

A

-no collateral blood supply

22
Q

What do emboli consist of?

A

-portions of thrombi
-bacteria
-parasites (ex. heartworm)
-fat (eg. Broken major bone, bone marrow emboli)
-cartilage
-neoplastic cells
-air
-Hair

23
Q

Vegetative valvular endocarditis

A

-thrombus on the heart valves
-bits of this thrombus break off and shoot through circulatory system and can block anywhere

24
Q

Embolic pneumonia

A

-Septic embolism
>bacteria emboli causing intermittent areas of inflammation

25
Q

Dyspneic cat: sudden severe pain and hind leg paresis

A

-Large heart, hypertrophy of left ventricle from left atrial thrombosis
-pooling back in lungs=dyspneic
-embolism=pain and high leg paresis
>cell swelling and pale

26
Q

Acute coagulation necrosis

A

-embolism
-will see cell swelling and pale

27
Q

Saddle thromboembolism

A

-clot
-pain, lack of pulse,
-cats

28
Q

Infarction

A

-an area of ischemic necrosis in which all components of the affected tissue have undergone necrosis
-Caused by occlusion of either the arterial supply or venous drainage

29
Q

Determinants of infarction

A

-nature of vascular supply
-vulnerability of hypoxia
-oxygen content of blood- cardiovascular function (Low oxygen environment, then tissues already predisposed to infarction)
-rate of development of occlusion (body can adapt if occlusion develops over a long time)

30
Q

Resistance to infarction

A

-Areas of dual blood supply (lungs, liver)
-Anastomoses and collateral blood supply (intestines)

31
Q

Renal circulation and infarctions

A

-end-arterial supply (single way in, single way out) making them more prone to infarction

32
Q

Vulnerability to hypoxia

A

-Neurons: irreversible injury after 3-4 mins of ischemia
-myocardial cells: irreversible injury after 20-30 mins of ischemia
-fibroblasts within the myocardium remain variable after many hours of ischemia

33
Q

Morphology of infarction

A

-White-pale infarcts (red in lungs, skin, spleen)
>arterial occlusions in solid organs
>turgid/firm and swollen due to cellular swelling and necrosis
>increased local pressure due to cell swelling
>temporary prevention of blood seepage from the adjacent tissue (pallor)

34
Q

Renal infarct

A

1.initially white due to pressure build up, surrounded by hyperemia, cells die (acute)
2. Becomes red from seepage of blood from nearby tissues
3.Turn white again. Due to fibrosis and scarring. Also get contration. (chronic)

35
Q

Outcome of infarction

A

-scarring/fibrosis
-sloughing
-sequestrum

36
Q

Shock

A

-cardiovascular collapse
-many causes but predictable course
-hypotension (low blood pressure) = impaired perfusion and hypoxia

37
Q

Causes of shock

A

-Cardiogenic (heart failure)
>blood not pumping effectively, oxygen supply too low
-Hypovolemic (hemorrhage, fluid loss)
>blood pressure drops, circulating blood volume drops
-Blood maldistribution (sepsis, neurogenic, anaphylaxis, electrocution)

38
Q

Anaphylaxis

A

-systemic activation of mast cells by IgE
-location of effects varies between species based on mast cell location and granule mediators

39
Q

Dog shock organ

A

liver

40
Q

Cats, horses, pigs shock organ

A

-lungs and intestines

41
Q

Cattle and sheep shock organ

A

lungs

42
Q

Animals with shock

A

-reduced blood pressure
-increased heart rate
-increased resp rate
-reduced urine output
-reduced body temperature

43
Q

Heat stroke

A

-vasodilation results in reduced blood pressure

44
Q

Fear

A

-sympathetic nervous system, opens up vasculature, reduces blood pressure

45
Q

Burns

A

-fluid loss increase leading to hypovolemic shock

46
Q

Ventricular fibrillation

A

-poor contraction= cardiogenic

Gen Path #1 (12 decks)

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