Cardio Flashcards

1
Q

atherosclerosis definition

A

atheromatous deposits in the intima of arteries and inner layer fibrosis

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2
Q

characteristics of atherosclerosis

A

intimal thickening
narrowing of lumen
lipid accumulation

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3
Q

3 components of athersoclerotic plaque

A

ECM - collagen, elastin, proteoglycans
cells - smooth muscle cells, macrophages, T lymphocytes
lipids - both intra and extracellular

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4
Q

modifiable risk factors

A

t2dm, hypertension, smoking, hypercholesterol

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5
Q

non-modifiable

A

age, sex, family history,

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6
Q

factors that make a plaque VULNERABLE (4)

A
  1. high amounts of lipid/foam cells
  2. thin fibrous cap
  3. decreased amount of smooth muscle cells
  4. large clusters of inflamm cells
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7
Q

most common sites of atherosclerosis

A

infrarenal abdominal aorta, abdo aorta&raquo_space;> thoracic.

coronarys, popliteal, circle of willis

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8
Q

where along a blood vessel is atherosclerosis most likely to form?

A

ostia (origins) of major branches as there will be increased turbulent flow - oscillatory shear stress - atherogenic

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9
Q

an occlusive intracoronoary thrombus overlying a disrupted atherosclerotic plaque, leading to myocardial ischaemia

A

MI

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10
Q

pathogenesis of MI

A

atherosclerotic plaque rupture –> platelet activation –> thrombosis –> vasospasm

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11
Q

how long must ischaemia last before irreversible damage?

A

20-40min

myocyte death

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12
Q

mechanical complications of MI

A
  1. contractile dysfunction - cardiogenic shock
  2. ventricular dysfunction - cardiogenic shock
  3. LV infarct and papillary muscle damage - mitral regurg
  4. cardiac rupture - R>L shunts, haemopericardium
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13
Q

> 4 weeks post MI with persistent ST elevation

A

ventricular aneurysm

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14
Q

how many patients develop arrythmia post MI

A

90%

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15
Q

arrythmia causing death in <24hr post MI

A

VF

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16
Q

chest pain, fevers, and effusion weeks after MI

A

Dressler’s syndrome

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17
Q

histological findings 6hrs post MI

A

normal

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18
Q

Most commonly affected vessel in MI

A

LAD 50%
RCA 40%
LC 10-20%

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19
Q

evolution of MI (cells)

A

no more atherogenic food

neutrophils, macrophages, angioblasts, fibroblasts

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20
Q

6-12 hours post MI - histology

A

oedema and necrosis. homogenous

21
Q

1-4 days post MI

A

PMN infiltration

22
Q

5-10 days

A

macrophages - clear up debris

23
Q

1-2 weeks

A

granulation, angiogenesis, collagen deposition

24
Q

weeks-months

A

cellularising, scarring, strenthening. myofibroblasts

25
Q

Reperfusion injury in MI is caused by:

A

oxidative stress, CA overload and inflammation
can cause arrythmia and stunned myocardium
reversible

26
Q

complication of mural thrombus

A

can embolise

bowel ischaemia is common

27
Q

liver histology seen with Right sided heart failure

A

nutmeg liver - cirrhosis

28
Q

signs of RVH systemically

A

engorgement of systemic vasculature
peripheral oedema
ascites
facial engorgement

29
Q

signs of LVH

A

breathless, orthopnoea, PND, wheeze, fatigue, pulmonary oedema.

30
Q

common cause of RVH

A

2ry to LVH

can also be caused by chronic massive pulmonary hypertension

31
Q

histology of heart failure

A

replacement of myocardium with fibrotic tissue

32
Q

3 types of cardiomyopathy

A
  1. too thick - hypertrophic
  2. too thin - dilated
  3. too stiff - restricted
33
Q

large heart with loss of myocytes

A

dilated cardiomyopathy

34
Q

normal sized heart with large atria

A

restrictive cardiomyopathy

35
Q

large hypertrophic left ventricle

A

hypertrophic cardiomyopathy

36
Q

main problem in restrictive cardiomyopathy

A

reduced ventricular compliance leading to restricted filling of the heart

37
Q

causes of restrictive CM

A
  1. idiopathic

2. 2ry to myocardial disease - amyloid, sarcoid

38
Q

causes of HOCM

A

50% AD genetic disorder in B myosin chains

39
Q

causes of DCM

A

idiopathic, infective , toxic, hormonal, genetics

40
Q

which valve is usually implicated in Rheumatic fever

A

mitral

41
Q

causative organism of Rheumatic

A

Lancefield group a strep

42
Q

pathogenesis of rheumatic heart disease

A

antigenic mimicry leading to GAS-abs crossreacting with myosin protein on cardiac tissue

43
Q

Histological findings in Rheumatic fever heart disease

A
vegetations
Aschoff bodies (small giant cell granulomas)
Anitschkov myocytes (regenrating myocytes)
44
Q

Rx of RhF

A

BenPen

45
Q

large irregular masses on valve cusps, extending into chordae.

A

Infective endocarditis.

46
Q

small bland vegetations formed of thrombi. associated with DIC/hypercoagulable states

A

non-bacteral thrombotic endocarditis

47
Q

small, warty vegetations ‘verrucae’ along lines of valve closure leaflets

A

Rheumatic valve disease

48
Q

small, sterile warty vegetations which are platelet rich. associated with SLE and APL

A

Libman-Sacks