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intro to biomedical sciences IBMS > Atherosclerosis thrombosis and embolism > Flashcards

Atherosclerosis thrombosis and embolism Flashcards

we will cover atherosclerosis thrombosis and emboli types of risk factors development treatment prevention ischaemia and infarction shock

1
Q

how many people die each year from a hospital acquired venousthrombo embolism

A

32000

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2
Q

describe the physiology of blood vessels and endothelial cells

A

inner layer: intima
middle media
outer- adventitia

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3
Q

what is the difference between the media in a vein and an artery

A

the media in the artery is much bigger diameter

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4
Q

what is the origin of endothelial cells

A

mesodermal origin

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5
Q

what are endothelial cells found

A

interior surface of blood vessels and the lymphatics and on the inside of the heart( called the endocardium)

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6
Q

what are endothelial cells called inside the heart

A

endocardium

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7
Q

what is the function of the endothelial cells

A

semi selective barrier function- allows WBC to move out to the area of infection (diapedesis)

  • angiogenesis
  • mediator of coagulation
  • blood pressure control
  • fluid filtration
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8
Q

what happens with prolonged inflammation to the endothelial cells

A

increased permeability and tissue swelling

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9
Q

what clotting factors do endothelial cells mediate

A

von willibrands factor- stabilises factor VIII which binds to collagen linking platelets
heparan sulphate- inactivates clotting cascade

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10
Q

what does heparan sulphate control

A

inactivates clotting cascade

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11
Q

which diseases is endothelial cell dysfunction

A

many diseases
septic shock
hypertension
behcets

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12
Q

how else can endothelial cell dysfunction arise

A

tobacco and air pollution

trans fat consumption

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13
Q

how can endothelial cell dysfunction improve

A

smoking cessation
weight loss
improved diet
exercise

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14
Q

what is a atheroma

A

is an accumulation of intracellular and extracellular lipid in the intima of large and medium sized arteries

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15
Q

what is atherosclerosis

A

the thickening and hardening of arterial walls as a consequence of atheroma

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16
Q

why do atheromas form

A

due to chronic endothelial cell damage- in the arteries as BP is higher

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17
Q

how does an atheroma develop 11 steps

A
  1. chronic endothelial cell dysfuction
    2 endothelial dysfunction
    3 entrance of LDL in intimia
    4 lipid engulfed by macrophages
    5 flat yellow(fatty streak) early atheroma
    6 accumulation of lipids- in macrophages and smooth muscle wall
    7 raised yellow lipid plaque
    8 extracellular lipid deposits and collagen deposition and calcification
    9 fibrous cap over the lipid core(fibroatheroma)
    10 ulceration of plaque
    11 predisposition to thrombus formation- advanced complicated plaque
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18
Q

what are the risk factors for atheroma

A 
high LDL/low HDL 
hypertension
diabetes 
sedentary lifestyle
obesity
smoking
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19
Q

what are the two forms of prevention for the formation of atherosclerosis

A

primary- risk factor modification

secondary- includes regulation medications such as aspirin and the prevention of the recurrence of events

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20
Q

when do early atheromas start forming

A

in your early 20s-30s

progressive

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21
Q

which medications can be used to stabilise the plaques and prevent rupture

A

statins

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22
Q

what medication can be used if the atheroma was to rupture

A

antithrombotic agents

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23
Q

which sites can be affected

A

aorta-
coronary artery
iliac and popliteal arteries
internal carotid arteries

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24
Q

iwhat happens if the aorta is affected by atheroma

A

weakening of the aorta can cause aortic aneurysm and then risk of rupturing

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25
Q

what happens if the coronary artery is affected by atheroma

A

narrowing of the artery lumen-reduced blood flow and ischaemia
thrombus formation over plaque-occlusion of the lumen causing MI

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26
Q

what happens if the iliac and popliteal arteries are affected by atheroma

A

narrowing of the artery lumen

reduced blood flow leading to ischaemia

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27
Q

what happens if the internal carotid arteries are affected by atheroma

A

emboli travels p the the brain causing ischaemia (if transient) or infraction( TIA/stroke)

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28
Q

what is a thrombus

A

a structured solid mass or plug of blood constituents formed within the heart or blood vessels during life

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29
Q

what is thrombosis

A

the process of thrombus formation-

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30
Q

what can thombosis be considered as

A

the inappropriate activation of the normal haemostatic process

31
Q

where can thrombosis occur

A

in the CVD anywhere

32
Q

what are the types of thrombus

A

arterial
cardiac
venous

33
Q

where do arterial thrombus occur

A

at sites of endothelial injury or turbulence

usually occlusive lesions

34
Q

when are the common sites of arterial thrombus

A

coronary arteries
cerebral arteries
femoral arteries

35
Q

what is a cardiac thrombus also known as

A

mural thrombi

36
Q

where can cardiac thrombus occur

A

over areas of endomyocardial injury

37
Q

what else can cardiac thrombus occur with

A

arrhythmia and cadiomyopathy

38
Q

where can venous thrombus occur

A

at sites of vascular stasis- in the veins of the lower limbs(DVT)

39
Q

what can be the outcomes of thrombus formation if the patient survives the immediate effects of occlusion

A

are propagation
embolism
dissolution-broken down
organisation/recanalisation- organise or reattach

40
Q

what are some hypercoagulable conditions

A

primary( genetic

secondary environmental

41
Q

what are some primary hypercoagulable conditions

A

protein C or S deficiency
antithrombin III
factor V mutations
prothrombin mutation

42
Q

what are some secondary hypercoagulable decisions

A

stasis- prolonged bed rest
smoking
oral contraceptives

43
Q

why can antithrombin III deficiency occur if it is secondary

A

liver damage

44
Q

what does protein c do

A

vitamin K dependant glycoprotein
inactivates factor Va and VIIIa
deficiency increases the risk of clotting

45
Q

describe protein S

A

vitamin K dependant glycoprotein
cofactors works with C
helps to inactivate V and VIIIa

46
Q

describe antithrombin III

A

glycoprotein produced in the liver
AKA antithrombin
can inherit deficiency
can acquire deficiency- due to liver failure

47
Q

what does antithrombin activate

A 
factor 9 
factor 10
factor 11
12
2
7
48
Q

what are factor V mutations also known as

A

leiden disease

49
Q

how can oral contraceptive increase the risk of atheroscleorosis

A

increase in circulating fibrogen

50
Q

how do we clinically prevent thrombosis

A

aspirin
heparin
warfarin
thrombolysis

51
Q

how is aspirin used

A
  • used for primary and secondary prevention of CVA and MI, and for treatment of MI
52
Q

how is heparin used to prevent thrombosis

A

to prevent post op DVT

53
Q

how is warfarin used to prevent thrombosis

A

prevents thrombi in patients with AF and prosthetic heart valves

54
Q

what are the main drugs used in thrombolysis

A

streptokinase and tissue-type plasminogen activator (TPA)

55
Q

how do streptokinase and TPA work

A

body’s natural fibrinolytic system to break down thrombus, and minimise myocardial damage.

56
Q

what are some new therapeutics which can be used

A

Rivaroxaban/apixaban/betrixaban- oral anticoagulant

clopidogrel- anti platelet

57
Q

what is virchows triad

A

factors predisposing to thrombosis
changes in blood constritiency
changes in vessel wall
changes in pattern of blood flow

58
Q

what can change blood constituents

A

OCP
risks eg obesity
personal history
social history

59
Q

what can include changes in vessel wall

A

atheroma
trauma
inflammation
neoplasia

60
Q

what is an embolus

A

an abnormal mass of material( gas or solid)which is carried in the bloodstream- impacting a vessel whose calibre is too small to let the embolus through

61
Q

describe pulmonary embolism

A

Embolus originating from detached piece of thrombus sitting in a deep vein of the leg.- Travels via venous system to the right heart, then out through pulmonary artery.- Lodges in pulmonary arterial tree (location depends on size of embolus

62
Q

describe systemic embolism

A

Embolus originating from detached piece of mural thrombus, or left heart valvular vegetation.- Travels via aorta into systemic arterial circulation.- Can lodge in arteries leading to lower limbs, brain, kidneys or gut.

63
Q

what is a paradoxical embolism

A

Embolism that originates in systemic veins and enters systemic arterial circulation.

64
Q

what is ischaemia

A

Impaired vascular perfusion of an area of tissue, thus depriving it of vital nutrients, especially oxygen”

65
Q

what is infarction

A

Death (necrosis) of an area of tissue due to ischaemia

66
Q

what is shock

A

’is a life-threateningmedicalcondition of low bloodperfusionto tissues resulting in cellular injury and inadequate tissue function’

67
Q

what are the four types of shock

A

cardiogenic
obstructive
hypovolaemic
distributive

68
Q

what is the patheay for shock

A

inadequate perfusion
cell hypoxia
energy deficit
lactic acid production

69
Q

what are the symptoms of cardiogenic shock

A

Distended jugular veins due to increased venous pressure
Weak or absent pulse
Arrhythmia (most frequently tachycardia)
Reduced blood pressure

70
Q

what are the symptoms of obstructive shock

A

Cardiac Tamponade
Pulmonary Embolism
Aortic Stenosis

71
Q

what are the symptoms of hypovolaemic shock

A 
Rapid, weak thready pulse
Tachycardia
Cool, clammy skin – vasoconstriction
Hypothermia
Thirst and xerostomia
Cold, mottled skin
72
Q

symptoms of distributive shock

A

SIRS (Systemic Inflammatory Response Syndrome) – High resp rate, body temp >36 deg celsius, tachycardia and WBC count between 4000-12000

73
Q

what is the treatment of shock

A

ABCDE
oxygen and bolus of fluid- saline and RBC later
vasopressors if hypotension not improved with fluids

74
Q

what is a cardiac tamponade

A

fluid around the pericardium- heart cannot contract as well cus of fluid

intro to biomedical sciences IBMS (35 decks)

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