Lecture 13- Heart Disease Flashcards

1
Q

describe atherosclerosis

A

o Monocytes adhere to endothelial surface proteins (adhesion molecules)–>monocytes migrate into intima, accumulate cholesterol, form foam cells –> release growth factors–>triggers proliferation of SMC–>lipid accumulates
o Plaque develops over decades, acute complications occur suddenly i.e. rupture of plaque (don’t know what triggers this to happen)

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2
Q

long term management of atherosclerosis and effects

A

lowering of LDL-C by statins (HMG CoA reductase inhibitors)
- reduces lipid content in plaque, inflammation and thrombosis
- relative risk reduction about 24%
lowering BP, quit smoking, control diabetes

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3
Q

Compare CHD event rates in secondary and primary prevention trials

A

secondary
- stronger the statin, the lower the mortality rate drops compared to the placebo
- event rate is so high- statin saves lives
primary
- event rate is less compared to secondary
- when event rate is already really low, then taking statin to reduce risk is not really worth it
- only worth it with other risk factors combined with elevated LDL

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4
Q

examples of acute coronary syndromes

A
  • heart attack
  • MI- death of myocardium
  • unstable angina- presence of chest pain without myocardial damage
  • sudden onset of chest pain
  • myocardial damage (troponin, CK in blood)
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5
Q

definition difference between secondary and primary prevention trials

A

secondary- had an attack then put the patient on statins

primary- high LDL cholesterol but not yet had heart attack

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6
Q

what is a culprit lesion?

A

often mild plaque–>little calcification

may expand outwards in days/weeks

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7
Q

pathology of acute MI with reference to occlusive coronary thrombi

A

thrombus forms on ruptured atheromatous plaque- suddenly occludes or severely narrows artery

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8
Q

why do plaques rupture?

A

controversial

  • macrophages may be responsible for decreased collagen synthesis, increased collagen breakdown by MMPs, production of procoagulants so induce thrombosis when plaque ruptures
  • remember- one localised plaque ruptures, not multiple
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9
Q

ways to manage acute coronary syndromes

A
recognition- patient, ambulance, medical
urgent reperfusion
- thrombolysis- IV
- stent (percutaneous coronary intervention) into artery to open it wide then give drugs to reduce thrombolysis 
- anticoagulants, antiplatelet agents 
-lipid lowering
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10
Q

most heart valve disease is ?

A

degenerative

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11
Q

valvular heart disease used be a consequence of ?

A

rheumatic fever

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12
Q

what is rheumatic fever?

A

immune response to strep pyogenes, antibody cross-reactivity-
Type II hypersensitivity

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13
Q

age group common for rheumatic fever?

A

children 6-15 yrs

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14
Q

clinical features of rheumatic fever?

A

heart murmur–>valvular damage especially to mitral valve

- fever, arthritis, rash, skin nodules

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15
Q

methods for RhF prevention

A

penicillin and public health

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16
Q

RhF is a disease of?

A

poverty and poor housing- lower socioeconomic communities

17
Q

what is rheumatic heart disease? what happens in it?

A

repeated attacks of RhF that worsen heart disease

  • valve thickening, narrowing
  • progression to heart failure
  • over long time course 5-10years
18
Q

3 forms of cardiomyopathy

A

hypertrophic
restrictive
dilated

19
Q

what occurs in hypertrophic cardiomyopathy?

A

increased left ventricular wall thickness- especially of septum and outflow obstruction
-cellular hypertrophy–>stiff ventricle–>ventricular arrhythmias–>sudden death

20
Q

genetic basis for hypertrophic cardiomyopathy

A
  • AD
  • mutation in genes for sarcomere protein (e.g. beta cardiac myosin heavy chain)
  • 2000 mutations in 11 genes
  • heterogenous phenotype (partially correlated to mutation, same mutation may cause different phenotypes)
21
Q

causes of dilated cardiomyopathy

A

multiple causes
mostly idiopathic
some genetic (sarcomere proteins, desmosomes, cytoskeleton, connections between cells)

22
Q

what is bradycardia?

A

an arrhythmia

- sinus node dysfunction, atrio-ventricular node block

23
Q

what is tachycardia?

A

an arrhythmia

- automatic focus, re-entry, channelopathies

24
Q

other arrhythmias

A

atrial flutter, atrial fibrillation, AV nodal re-entry tachycardia, ventricular tachycardia