Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

SD2 > Pathology- Thrombosis, Embolism, Infarction > Flashcards

Pathology- Thrombosis, Embolism, Infarction Flashcards

1
Q

what is ischaemia?

A

insufficient blood supply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is infarction?

A

death of tissue as a result of ischaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is thrombosis

A

the formation of a blood clot inside a blood vessel, obstructing the flow of blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is embolism

A

the blockage of an artery by an embolus (foreign body e.g. blood clot (mass of coagulant), air bubble etc)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is atheroma also known as

A

atherosclerosis, hardening of the arteries, coronary heart disease, ischaemic heart disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

atheroma is the principle cause of death and disability in the western world true or false

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the aetiology of atheroma

A

smoking, hypertension, hyperlipidemia, diabetes, age (older), sex (males), genetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what causes primary endothelial injury

A

smoking, hypertension, hyperlipidemia, immune factors, toxins, viruses, turbulent blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what does increased LDL and reduced HDL - or - increased V-CAM, IL-1 or TNF expression lead to

A

accumulation of lipids and macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what causes the migration of smooth muscle cells

A

PDGF (platelet derived growth factor), FGF (fibroblast growth factor), TGF beta (transforming growth factor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are foam cells

A

dead macrophages containing consumed LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what surrounds the fatty streak

A

fibrous cap (collagen fibres) and damaged endothelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what happens to atheromatous plaques over time

A

progress and become complicated

fatty streak- fibrofatty plaque- complicated plaque (with overlying thrombus)

further loss of luminal potency and arterial wall weakness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

under what circumstances (3) is atheromatous narrowing of an artery likely to produce critical disease

A

it is the only artery supply a tissue/organ

small artery diameter

overall blood flow is reduced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are the complications of atheroma

A

stenosis, thrombosis, aneurysm, dissection, embolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is stenosis and what does it lead to

A

narrowing of the arterial lumen,

reduced elasticity,

reduced flow in systole,

tissue ischaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are the clinical effects of cardiac ischaemia

A

reduced exercise tolerance

angina

unstable angina

myocardial infarction

cardiac failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

describe cardiac fibrosis and what it causes

A

loss of cardiac myocytes- replacement by fibrous tissue

loss of contractility, reduced elasticity and filling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

can arterial stenosis affect any artery

A

yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what can arterial stenosis in carotid arteries cause

A

TIA, stroke and vascular dementia (reduction in cognitive skills due to reduction in blood flow to brain)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what can arterial stenosis cause when in the renal arteries

A

hypertension and renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what can arterial stenosis cause when in the peripheral arteries

A

claudication (cramping in lower leg due to insufficient blood supply) and foot/leg ischaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what does superadded

A

to add in a way that compounds the effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are the clinical effects of thrombosis

A 
infarctions; 
myocardial 
cerebral 
renal 
intestinal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is an aneurysm

A

Abnormal and persistent dilatation of an artery due to a weakness in its wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what are the types of aneurysm

A 
mycotic (fungus)
atherosclerotic
dissecting
congenital
arteriovenous
traumatic 
syphillitic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

where is the most common site for an aneurysm

A

abdominal aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what are the complications of an aneurysm

A

rupture, thrombosis, embolism, pressure erosion of adjacent structures, infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is an arterial dissection

A

splitting within the media by flowing blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what are the risk factors for arterial dissection

A

middle age +/- atheroma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is a false lumen

A

filling of blood inbetween tunica intima and media

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what can artial dissection cause

A

sudden collapse, high mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what conditions are associated with aortic dissection

A

atheroma, hypertension, trauma, coarctation, marfan’s, pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what are the usual consequences caused by embolis

A

cerebral infarct

renal infarct and renal failure

lower limb infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

describe the structure of athero-embolism

A

cholesterol clefts within embolic material

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

where sites are preferred for thrombosis formation

A

VIRCHOWS TRIAS

sited of endothelial injury

turbulent blood flow

hypercoaguable blood

37
Q

how is a thrombus formed

A

intravascular coagulation which requires;

  • platelet activation
  • fibrin production via coagulation cascade
38
Q

is the formation of t thrombus an active or passive process

A

active

39
Q

what is the difference between activated and inactivation platelets

A

activated platelets (more sticky) attract and aggregate with other platelets.

also aggregate with fibrin

40
Q

what is the start and end point of the coagulation cascade

A

start platelets

end fibrin

41
Q

what happens to collagen when the endothelium is lost

A

exposed and binds to glycoprotein Ia/IIb and von Willebrands factor (vWF) (surface receptors) on platelets activating them

42
Q

what event during platelet activation allows them to bind

A

increase in intergrins (transmembrane receptors that facilitate cell-extracellular matrix (ECM) adhesion)

43
Q

what binds fibrinogen on platelets

A

glycoprotein IIb/IIIa

44
Q

what do activated platelets release

A

granules to attract other platelets (vWF, platelet activating factors (PAF), thromboxane A2 (TXA2), ADP

45
Q

why is it called the coagulation cascade

A

One factor activates another and so on like a domino effect

46
Q

what does the domino affect of the coagulation cascade allow

A

Sequences provide lots of opportunities for checks and balances – areas to inhibit or stimulate

47
Q

what is the common pathway both the intrinsic and extrinsic pathways of the coagulation pathways

A

converting fibrinogen to fibrin to cross linked fibren

48
Q

what is the coagulation cascade dependant on

A

calcium dependant

49
Q

what initiates the extrinsic coagulation pathway

A

tissue injury

50
Q

what does the intrinsic pathway start with

A

hageman factor (FXII) and kalikrien

51
Q

what is Prothrombin Time (PT)

A

blood test measuring how long it takes blood to clot (intrinsic pathway)

52
Q

what joins together yo make the common pathway of the extrinsic coagulation pathway

A

tissue factor (TF) binds with factor VII

53
Q

what is the blood test used to characterise blood coagulation in the extrinsic pathway

A

Activated Partial Thromboplastin Time (APTT)

54
Q

what factors activate fibrinogen and turn it into fibrin

A

II and XIII

55
Q

what is required to make factors II, VII, IX and X

A

vitamin K

56
Q

what is vitamin K

A

fat soluble vitamin, stored in the liver

57
Q

what factors are missing in liver disease

A

II, VII, IX and X

58
Q

what does warfarin stop the production of

A

factors II, VII, IX and X

59
Q

describe hypercoagulable blood

A

extra thick

60
Q

in a normal arterial system why is there not coagulation

A

as high flow system so pro-coagulant materials washed along before being able to do anything

61
Q

what is needed for thrombosis to occur in arterial systems

A

underlying atherosclerosis

62
Q

what is atherosclerosis

A

formation of plaques etc. at sites of endothelial damage

63
Q

why is there increased endothelial damage at branched arteries

A

as turbulent flow where arteries branch

64
Q

what are common resulting conditions of atherosclerosis

A

cerebral infarction, carotid atheroma-emboli (TIA or cerebral infarcts), myocardial infarction (cardiac failure), aortic aneurysm, peripheral vascular disease, gangreen

65
Q

what are complications of atherosclerosis

A

thrombosis, exercised induced angina, stable angina, plaque rupture

66
Q

what is unstable angina

A

when coronary arteries have been occluded due to thrombus

67
Q

what is primary vasculitis

A

autoimmune disease characterised by inflammation directed at vessel walls (immune system attacks own vessels)

68
Q

name 4 branching arteries

A

coronary arteries, above bifurcation of aorta, origin and division of carotid arteries, renal arteries, superior mesenteric artery

69
Q

why do branching vessels pose such a risk- give 2 examples

A

as vessels distal to branches are susceptible to embolism and infarction

stroke, small bowel infarction

70
Q

what does turbulence cause

A

endothelial cell injury

stasis

71
Q

what is margination

A

increased contact of platelets etc with vessel walls

72
Q

what is stasis

A

when blood flow slows down

73
Q

where does blood flow slow down (stasis)

A

deep venous system, faulty valves, venous insufficiency

74
Q

what causes hypercoaguability

A

dehydration, polycythemia (number of cells), leukaemias (increase white blood cells)

75
Q

what degrades clots

A

plasmin

76
Q

what are three anti clotting proteins

A

protein C, protein S and antithrombin III

77
Q

what factors do proteins C and S degrade

A

factor V and VIII

78
Q

what factors do antithrombin III degrade

A

II, IX and X

79
Q

what is factor V leiden

A

a variant (mutated form) of human factor V which causes an increase in blood clotting (hypercoagulability) (inherited disorder)

80
Q

what other deficiencies can lead to hypercoaguability

A

protein C deficiency, protein S deficiency, antithrombin III deficiency

81
Q

what are components involved in anti thrombotic mechanisms

A

plasmin, protein C and S, antithrombin III

also heparin

82
Q

what is heparin

A

anticoagulant drug

83
Q

what are secondary causes of hypercoagulability

A 
Prolonged immobility
Significant tissue injury – burns, RTA
Antiphospholipid syndrome – autoimmune
Myocardial infarction
Atrial fibrillation (irregular cardiac rhythm)
cancer 
therapt
marantic endocarditis
84
Q

how does cancer cause hypercoagulability

A

Activate coagulation cascade through tumour produced TF, mucin, inflammatory cytokines

85
Q

how does therapy cause hypercoagulability

A

many chemotherapeutic agents injure endothelium and increase risk of thrombosis

86
Q

what are more low risk secondary causes of hypercoagulability

A

the pill, smoking, renal disease, cardiomyopathy

87
Q

what is an embolism

A

Dislodge thrombus – travels around the vascular system until it gets stuck

88
Q

what can cause an embolism (the thrombus)

A

clot, air, septic, amniotic fluid, tumour, fat

89
Q

how do cells die from hypoxia

A

lack of ATP, increase calcium,leads to breakdown of membranes, cytoskeleton and DNA plus releases pro death factors

SD2 (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions