CVD Flashcards

1
Q

What are the two main dangerous consequ3nces of atheromatous plaque

A

stenosis

rupture

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2
Q

What is a fatty streak made up of

A

lipid filled foamy macrophages

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3
Q

when does coronary artery stenosis cause angina

A

when demand > supply

over 70% occlusion

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4
Q

what are features of vulnerable plaques

A

lots of foam cells / lipids
thin fibrous cap
few smooth muscle cells
clusters of inflammarory cells

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5
Q

why can emotion cause sugdeen death

A

because adrenaline causes vasoconstriction> increased physical stress withhin the plaque > stenosis / rupture

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6
Q

Explain angina

A

Transient ischaemia that does NOT produce myocyte necrosis

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7
Q

Explain stable angina

A

comes on with exertion, relieved by rest

NO plaque disruption

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8
Q

Explain prinzmetal angina

A

due to coronary artery spams

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9
Q

explain unstable angina

A

more frequent, longer lasting pain
onset at rest / after less exertion
due to disruption of plaque

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10
Q

when do histologycal changes start to occur following MI

A

after 6h

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11
Q

what is the most common valve affected in rheumatic heart disease

A

mitral

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12
Q

what changes occur in rheumatic heart disease

A

thickened valve leaflets
valve commissures fuse
thickened, shortened chordae tendinae
valves look like BUTTONHOLES (thhick, tight, sclerosed)

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13
Q

what are the 3 key components of an athorsclerotic plaque

A

Cells (smooth muscle, macrophages, leukocytes)
ECM (incl collagen)
Fluid (intracell and extracellular)

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14
Q

Which part of the aorta is affected most from atherosclerosis

A

Abdominal aorta

more than thoracic aorta

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15
Q

Which locations of vessels are affected more by atherosclerosis and wgy

A
Near origins (ostia) of major branches 
As turbulent blood flow has low / oscillatory shear stress, which is atherogenic 

While high laminar flow is protectivew

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16
Q

List some modifiable RF for heart disease

A

T2DM
HTN
Hypercholesteraemia
Smoking

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17
Q

List some non-modifiable RF for atherosclerosis

A

gender (male)
increasing age
FH

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18
Q

What are some categories of complications of MI

A

Mechanical
Arrhythmia
Pericardial

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19
Q

What are mechanical complications of MI

A
  • loss of muscle > contractile dysfunction > cardiogenic shock
  • ventricular dysfunction > congestive HF
  • LV infarct > papillary muscle dysfunction/necrosis > mitral regurg
  • ruptureof ventricular wall, septum, papillary muscle
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20
Q

What does rupture of papillary muscle cause

A

Mitral regurg

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21
Q

What type of arrhythmia commonly develops post MI

A

VF (in the first 24hours) - sudden death

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22
Q

What can occur to the pericardium post MI

A

Pericarditis
Pericardial effusion
Dressler syndrome

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23
Q

Explain the evolution of MI - under 6h

A

Normal by histology, with CK-MB also normal

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24
Q

Explain the evolution of MI - 6h-24h

A

loss of nuclei, homogeneous cytoplasm, necrotic cell death

25
Q

Explain the evolution of MI - 1-4 days

A

infiltration of polymorphs then macrophages (to clean up debris)

26
Q

Explain the evolution of MI - 5-10 days

A

Removal of debris

27
Q

Explain the evolution of MI - 1-2 weeks

A

granulation tissue
new blood vessels
myofibroblasts
collagen synthesis

28
Q

How does fluid overload occur from cardiac damage

A

Cardiac damage > decreased cardiac output > activation of RAS > salt and water retention (to maintain perfusion) > eventually overloaded

29
Q

Explain LV failure presentation

A

pooling of blood into pulmonary circulaton > dyspnoea, orthoponeoa, PND, wheeze, fatigue

30
Q

Explain why RV failure may occur

A

often secondary to LVF OR from chronic severe pulmonary HTN

31
Q

Explain presentation of RV failure

A

engorgenment of systemic and venous system > peripheral oedema, ascites, fascial engorgement

32
Q

explain hypertrophic cardiomyopathy

A

heart is thick walled, heavy, hypercontra cting

33
Q

what is the inheritance of HCM

A

Autosomal DOMINANCE

common mutation in beta-MHC gene

34
Q

what is hypertrophic obstructive cardiomyopathy

A

septal hypertrophy

causes outflow tract obstruction

35
Q

what is a consequence of HOCM

A

DCM

36
Q

what age does rheumatic fever peak at

A

5-15

37
Q

what are symptoms of rheumatic fever

A

heart: pancardiitis
Joints: arthritis, synovitis
Skin: erythema marginatum, subcut nodules
CNS: encepalopathy, Sydenham’s chorea

38
Q

What infection does RhF occur after

A

Strep throat (group A streP)

39
Q

what do you need for diagnosis of RHF

A

group A strep infection + 2 major crit or 1major+2minor

40
Q

What are Jones major criteria for RHF

A
CASES 
Carditis 
Arthritis 
Sydenham's chorea 
Erythema marginatum 
Subcut nodules
41
Q

what are Jones minor criteria

A
fever 
raised ESR/CRP 
migratory arthralgia 
prolonged PR interval 
prior RhF 
Malaise 
tachycardiA
42
Q

What do you see on histology of RhF

A

AVA

Aschoff bodies (small giant-cell granulomas) 
V - beady fibrous vegetations (verrucae) 
Anitschkov myocytes (regenerating myocytes)
43
Q

How do you manage RhF

A

Benzylpen

44
Q

What is the pathology behind cardiac damage in RhF

A

Antigenic outcry - cross reaction of anti-strep antibodies with heart tissue

45
Q

describe the vegetations you see in RhF

A

small warty vegetations (verrucae)

46
Q

describe the vegetations you see in IE

A

large, irregular masses on valve cusps, extending into the chordae

47
Q

describe the vegetations you see in non-bacterial thrombotic endocarditis

A

small, bland vegetations attached to lines of closure

formed by thrombiu

48
Q

describe the vegetations you see in Libman sacks

A

small warty vegetations

STERILE and platelet-rich

49
Q

what are causative organisms for acute. IE

A

Staph aureus

Strep pyogenes

50
Q

What are causative organisms for chronic IE

A

Strep viridans

Staph epidermis

51
Q

What valves are usually involved in IE

A

mitral/aortic

52
Q

what valves are involved in drug users IE

A

tricuspid

53
Q

what criteria can you use for IE

A

Duke criteria

54
Q

Explain how many Duke criteria you need for IE diagnosis

A

2 major
1 major+3minor
5 minor

55
Q

what are the two major duke criteria

A

+ve culture (typical organisms) OR 2 positive cultures 12h apart

vegetation/abscess on echo or new regurg murmur

56
Q

what antibiotic do you give for subacure IE

A

benzylpen + gent

57
Q

what antibiotic do you give for acute IE

A

fluclox for MSSA

rifamèicin + vanc + gent for MRSA

58
Q

What is the triad with Young’s syndrome

A

BAR

Bronchiectasis
Azoospermia
Rhinosinusitis

59
Q

explain Dressler syndrome

A

autoimmune complication of MI

occurs 4 weeks after the episode

Features: chest pain, fever, pericardial rub