pathology 8 - disorders of the circulation 2 Flashcards

0
Q

in an intrinsic pathway defect what will be increased?

A

APTT. (activated pro-thrombin type) as it is not being converted to thrombin.

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1
Q

In factor VII deficiency what will happen to prothrombin? PT. and which pathway does this assess?

A

it will be increased - extrinsic factor defect. as not being converted to thrombin.

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2
Q

in thrombocytopaenia what test will you use?

A

low platelets present in the blood as not being produced/destructed. causes low ability for clotting.

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3
Q

with multpile defects which tests would you use?

A

prothrombin and APTT would both be increased.

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4
Q

DIC - stands for? what is it? which tests would you use and what would be the results?

A

disseminated intravascular coagulation - endothelial damage - activates the coagulation cascade all the time. hypercoagubility. widespread clotting disease. massive cosumption of coagulation factors and platelets leads to haeorrhagic diathesis (reduce clotting and tendecny to haemorrhage and bleed. you could use all the tests. PT - increase, APTT - increase, d-dimer increase (FDP)platelets decrease, fibrinogen decrease.

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5
Q

in thrombosis - what is it? what is a thromboembolus?

A

thrombus is a solid mass of fibrin, platelets and other blood elements within a vessel/heart. thromboembolus - may be free within the wall.

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6
Q

explain virchows triad? 3 factors that predispose to thrombus formation.

A
  1. endothelial injury - cells damaged alter anti-thrombotic effects- exposed collagen and BM.
  2. abnormal blood flow - blood is normally laminar (plasma peripheral and cell central) if turbulent then can et mixed and so stasis of blood - platelets and clotting factor are not washed away. eg. aneurysms.
  3. hypercoagulability - altered haemostatic proteins.
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7
Q

significance of a thrombus depends on?

A

size, location, rate of formation.
small - removed by thrombolysis
rapid formation - no time for collateral blood flow to increase and compensate for reduction of perfusion eg. kidney.

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8
Q

initially a thrombus is mural? may become?

A

mural - attached to vessel wall.

occlusive - moved.

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9
Q

thrombi can be high, medium or low pressure. ? what are the characteristics?

A

low pressure = no platelets just fibrin. red soft and conforms to vessel shape. often at damaged sites
medium = laminated, soft and nodular, platelets and fibrin rbcs and wbcs, variable flow, damaged arterial walls, valves
high = pale or white, friable or firm, few rbcs, fast and pulsatile flow, walls of arteries and arterioles.

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10
Q

endotheial injury is part of virchows triad that predisposes to thrombi formation. what can cause it?

A
virus - herpes
bacteria - salmonella
parasites - strongylus vulgaris
DIC
Iv injection. (venepuncture)
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11
Q

what is the difference between a thrombus and a coagulum?

A

thrombus - antemortem - granular, dry, dull, firm/friable, white/cream or red, laminated, ovoid/flattened, attached to vessel wall/chordae tendinae.

post mortem coagulum - smooth moist, elastic, gelatinous, homogenous, dark red/chicken fat clot, comforms to vessel shape/heart chamber, no adherant but may be trapped on chordae tendinae.

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12
Q

types of thrombus? (4)

A
  1. aterial - secondary to aterioschlerosis. fibrous thickening of wall of artery , verminous (strongylus vulgaris) aorto-iliac (saddle), pulmonary - may cause sudden death.
  2. cardiac - usually valvular, may be mural, eg. infection of valves/stenosis (narrowing) hypertrophy. if disseminate from right - pulmonary, from left - systemic (kidney)
  3. venous - fairly common. thin walled so easily traumatised. + slow flow rates. can be due to excessive venepuncture.
  4. capillary thrombosis - microthrombi, DIC. disseminated intravenous coagulation.
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13
Q

what are the fates of a thrombus? (3)

A
  1. dissolution - removed by fibrinolysis.
  2. propagation/embolisation - move around body as bit flake off.
  3. organisation and recanalisation - scar tissue and may get lumen of the vessel back (flow reestablished.)
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14
Q

embolism - what is it?

A

solid/gaseous mass carried by the bloodstream from its origin to a distant site in the circulation. embolus typically stops when it arrives at a bv that is too small. can cause blockage of a major vessel eg. pulmonary artery. blocked small vesssls cause infarction. or may have same fate as a thrombus.

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15
Q

types of emboli? (6) omphalophlebitis? saddle thrombus? how do heartworms lodge?

A
  1. thromboembolism - common. fragmenst to thrombi detach and move around. e.g. bacterial endocarditis of heart valves. multifocal abcesses in other organs such as kidney or lung. may lodge at aorto-iliac bifurcation (saddle) thrombus. omphalophlebitis - in young lambs etc.- bacterial contamination of umbilicus leads to infection of navel and emboli may go to liver etc.
  2. gas emboli - if air injected into vein/artery.
  3. fat embolism - adipocytes from the bone marrow may be released into the circulation from a bone fracture.
  4. tumour cells - maligant neoplasms - metastisise. erode veins/lymphatics. then grow into secondary tumours wherethey lodge.
  5. parasites - heartworms in dogs may embolise in pulmonary trunk when they die following anthelmintic treatment. sronglye larvae in horses. /fluke larvae.
  6. foreign bodies - metal etc. skin hair - following wounds/venepuncture.
16
Q

what is ischaemia? 3 causes?

A

failure or marked reduction in blood supply yo organ/tissue.

  1. ateriospasm - trauma/drugs
  2. compression of vessel - ligature/torsion
  3. thromboembolism - vascular obstruction eg. frost bite, wire.
17
Q

determining factors if ischaemia is a problem?

A
  1. degree of occlusion - total/incomplete
  2. speed of occlusion - sudden/gradual
  3. collateral circulation - kidney has none
  4. vulnerability of tissue affected - eg. neurones need O2!!!
18
Q

What are the sequelae to ischaemia?

A
  1. complete/sudden blockage - necrosis unless a collateral blood supply - infarction!
  2. incomplete/gradual - cellular hypoxia, compensation can occur. may lead to atrophy and washing away.
19
Q

what is infarction?

A

segmental/localised area of ischaemic necrosis due to lack of blood supply and O2. hypoxia. kidney often affected as no collateral blood supply.