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Family Med 1 EOR Exam > Cardio > Flashcards

Cardio Flashcards

1
Q

How does dilated cardiomyopathy present?

A

CHF

systolic dysfunction dominates (heart gets progressively weak, dialted and does not contract well)

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2
Q

What are common causes of dilated cariomyopathy?

A
  • POST-INFECTION (myocarditis)
  • excess alcohol
  • post-partum
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3
Q

What murmur so you expect to hear with dilated cardiomyopathy?

A

mitral regurg (valve leaflets unable to close adequately because of stretched LV)

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4
Q

How do you treat dilated cardiomyopathy?

A
  • BETA-BLOCKERS
  • afterload reduction: ACEI/ARB
  • preload reduction: diuretics, nitrates
  • anticoag
  • cardiac transplant
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5
Q

What is a common cause of sudden death in young athletes?

A

Hypertrophic cardiomyopathy

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6
Q

How do you get hypertrophic cardiomyopathy?

A

genetically transmitted (autosomal dominant with high penetrance)

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7
Q

What is the pathophysiology behind hypertrophic cardiomyopathy?

A
  • causes STIFF ventricle
  • DIASTOLIC DYSFUNCTION (small LV cavity)
  • marked increase in left ventricular mass, especially SEPTUM
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8
Q

What are PE finding in someone with hypertrophic cardiomyopathy?

A

-brisk carotid pulse (often bisferiens– double impulse due to ventricle contarcting and then getting pass obstruction)

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9
Q

What is the murmur of hypertrophic cardiomyopathy?

A

-loud, harsh aortic outfloe (cresendo-decresendo) heard at LSB

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10
Q

How do you make the murmur of hypertrophic cardiomyopathy louder?

A

with LESS BLOOD- standing, valsalva

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11
Q

How do you make the murmur of hypertrophic carduimyopathy less?

A

with MORE BLOOD (more blood causes the heart to be less obstructed)

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12
Q

What is treatment for hypertrophic cardiomyopathy?

A
  • essential to minimize physical exertion
  • CORNERSTONE: B-blockers
  • NON-dihydropyridine CCB
  • surgery to reduce septal muscle (alcohol ablation)
  • dual chamber pacemaker
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13
Q

What is hallmark of restrictive/infiltrative cardiomyoapthies?

A

ventricular wall excessively rigid impede diastolic filling– HALLMARK diastolic function

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14
Q

What is Tako-tsubo cardiomyopathy?

A

MIMICS STEMI

assocaited with significant stressful event– causes outpouring of catecholamines

ABSENCE OF CAD

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15
Q

What do you expect to see on echo with dx of tako-tsubo?

A

apex resembles fishing pot– apical and inferior ballooning

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16
Q

Patient presents with tachycaria, fever, muffled heart sounds and had a prodromal viral syndrome

A

myocarditis

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17
Q

What are most common pathogens of myocarditis?

A
  • Coxsacki B virus

- HIV

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18
Q

What do you want to avoid with myocarditis?

A

NSAIDS (may increase myocardial damage)

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19
Q

Patient presents with intense, SHARP chest pain that is worse with lying down and better with leaning forward.

A scratching, grating, high-pitched sound is heard on auscultation

A

acute pericarditis

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20
Q

What are common etiologies of acute pericarditis?

A
  • neoplastic disease
  • early post-MI
  • uremia
  • Coxsackie B virus (MOST COMMON)
  • autoimmune (RA, SLE)
  • drug-induced (hydralazine, isoniazid, penicillin)
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21
Q

What does the EKG of someone with acute pericarditis look like?

A

Diffuse ST-segment elevation in all leads except aVR and V1

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22
Q

How do you treat acute pericarditis?

A
  • NSAIDS
  • avoid anticoags

sxs resolve in 2-4 weeks

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23
Q

Patient presents with hypotension, elevation of systemic venous pressure, quiet heart sounds and pulsus paradoxus

A

cardiac tamponade

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24
Q

What is Becks Triad?

A
  • hypotension
  • elevation of systemic venous pressure
  • quiet heart sounds

related to cardaic tamponade

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25
Q

What is pulsus paradoxus?

A

slight drop in systolic BP with inspiration (due to inspirationcausing marked decrease in LV volume)

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26
Q

How do you tx cardiac tamponade?

A
  • pericardiocentesis

- surgery if recurrent

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27
Q

What is pathogenesis behind endocarditis?

A

Bacteremia with virulent organism

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28
Q

What is most common pathogen behind endocarditis?

A

S. aureus

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29
Q

What part of the heart is most commonly affected by endocarditis?

A

Mitral and aortic valves

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30
Q

What are clinical findings of endocarditis? (4)

A
  1. febrile illness
  2. regurg murmur
  3. Infectious emboli (palate/conjunctiva petechiae, subungal splinter h
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31
Q

How do you diagnosis endocarditis?

A

Dukes criteria (blood culture essential!)

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32
Q

What imaging technique is best used to diagnosis endocarditis?

A

trans-esophageal (TEE)

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33
Q

What finding is pathonomonic on US of endocarditis?

A

VEGETATION

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34
Q

What are the major duke critiera?

A
  • 2 or more pos BC
  • vegetation on echo
  • new regurg murmur
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35
Q

What are the minor duke criteria?

A
  • predisposing condition (valve abn, IVDU)
  • fever
  • vascular phenomenon (systemic emboli, organ infarction, cutaneous hemorrhage, petechiae)
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36
Q

What are oslor nodes?

A

painful red reaised lesions on fingers/toes that can be seen with endocarditis

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37
Q

What are Janeway lesions?

A

painless red lesion son palms or soles seen with endocarditis

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38
Q

What are Roth spots?

A

exudative lesions in the retina seen on fundoscopic seen with endocarditis

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39
Q

How do you treat endocarditis?

A

-should be based on organism ID by blood cultures

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40
Q

What is the clinical definition of orthostasis/postural hypotension?

A

-greater than 20mmHg drop in systolic BP or 10mmHG drop in diastolic BP

41
Q

What are common causes of orthostasis?

A
  • reduced CO
  • dysrhythmias
  • low blood volume
  • medications
42
Q

What are common precipatory factors of PACs?

A
  • ETOH
  • tobacco
  • caffeine
  • adrenergic stimulation
43
Q

What is “holiday heart”?

A

afib caused by stress, stimulatnts, ETOH, surgery

44
Q

When should someone with afib be started on anticoags?

A

If they have been in afib for over 72 hrs

45
Q

What is different between afib and aflutter?

A

aflutter is ALWAYS PRESENT

46
Q

How do you treat aflutter?

A

cardioversion only tx

47
Q

What arrhythmia is caused by a re-entry in AV node?

48
Q

What does PSVT look like on EKG?

A

narrow QRS, regular tachy, 150-220bpm

49
Q

What should you think about in someone with something that looks like afib but is greater than 200bpm?

A

WPW syndrome

50
Q

What is considered vtach?

A

3 or more PVCs over 100bpm and sustained for over 30 seconds

51
Q

What is the pathology of HF?

A

progressive weakening of myocardium

52
Q

What are some common etiologies of HF?

A
  • CHD
  • cardiomyopathies
  • viral myocarditis
  • valvular disease
  • congenital heart disease
  • long-standing, uncontrolled HTN
53
Q

What is the classification of HF?

A

I- no limitation of physical activity
II- slight limitation of physical activity (exertion causes sxs)
III- marked limitation of physical activity (walking, dressing causes sxs)
IV- symptomatic at rest or minimal acitivty

54
Q

What is systolic heart failure defined as?

A

contraction abnormality

Inadequate delivery of O2 to tissues and associated sxs

55
Q

What are causes of systolic HF?

A
  • large MI
  • dilated cardiomyopathy
  • chronic AR, MR
56
Q

What is diastolic HF defined as?

A

impaired ventricular filling

-elevation of ventricular filling pressures and associated sxs

57
Q

What are common causes of diastolic HF?

A
  • LVH
  • hypertrophic cardiomyopathy
  • restrictive cardiomyopathy
58
Q

What could cause acute onset HF?

59
Q

What are the 2 compensatory mechanisms of HF?

A
  1. activation of adrenergic nervous system

2. renin-angiotensin-aldosterone system

60
Q

What does activation of adrenergic nervous system do?

A
  • redistribution of CO to vital organs (brain, myocardium) and reduced flow to skin and muslces
  • increased levels of NE (increased HR, contractility, SVR)
  • Bad becauses INCREASES afterload (increased SVR), increased O2 demand
  • long-term elevation of catecholamines leads to progressive myocardial damage and fibrosis
61
Q

What does activation of the renin-angiotensin system do?

A
  • Na and water (causes increased fluid and increased SVR)
  • helps maintain CO via staling mechanism
  • bad because volume overload and increased afterload
62
Q

What are clinical features of HF?

A
  • dyspnea (due to elevation of pulmonary venous pressure)
  • orthopnea (redistribution of fluid from abdomen and lower extermities into chest)
  • paroxsymal nocturnal dyspnea (attacks of SOB, cough, wheexing awakening patient from sleep)
  • unexplained weight gain
63
Q

What are things you can see on xray with HF?

A
  • cardiomegaly
  • Kerley B lines
  • pleural effusions
64
Q

What is the best tool used to dx HF?

65
Q

What are medications that decrease preload?

A
  • diuretics

- nitrates

66
Q

What are medications that decrease afterload?

A

-vasodilators (AE)/ARB)

67
Q

What are medications that improve contractility of heart muslce?

A
  • digoxin

- sympathomimetics

68
Q

What are medications that help prevent cardiac remodeling?

A
  • ACEI
  • BB
  • spironolactone
69
Q

What is the max amount of Na someone with HF should have daily?

70
Q

What does HTN majorly predispose people for?

71
Q

What is secondary HTN?

A

renal, endocrine, congenital etiologies

72
Q

What are retinal changes that can be seen in someone with uncontrolled HTN?

A
  • narrowing of arterioles
  • AV nicking
  • silver/copper wired
  • hemorrhages or exudates
  • papilledema
73
Q

What is the general first-line DOC for HTN?

74
Q

What do you need to watch for when you prescribe thiazides?

A

HYPOKALEMIA!

75
Q

If someone has HTN and angina, what would be a good medication to put them on?

76
Q

What should all DM and CKD patients be on?

77
Q

What are the 2 pathologies behind renal vascular HTN?

A
  1. fibromuscular hyperplasia

2. Atherosclerosis

78
Q

What are eruptive xanthomas?

A

red papules on butt seen with extreme high levels of triglycerides

79
Q

What are tendinous xanthomas?

A

very high LDL causes nodules on tendones

80
Q

What is xanthelasma?

A

yellow plaques in skin around eyes

81
Q

What is hypertriglyceridermia associated with?

A
  • obesity
  • DMT2
  • metabolic syndrome
82
Q

How do you treat hypertrigly?

A
  • fibric acid

- niacin

83
Q

What are the 4 groups of people that should be treated with statins?

A
  1. individuals with clinical ASCVD (h/o MI, angina, revascularization, stroke, PAD)
  2. LDL over 190
  3. 40-75yo w/DM and LDL 70-189
  4. 40-75yo w/o clinical ASCVD/DM with LDL 70-189 and have an increase risk over 7.5
84
Q

What does the risk score calculator of ASCVD NOT include?

A

family history

85
Q

What are the 9 factors to input into ASCVD risk calculator?

A
  • age
  • sex
  • race
  • total cholesterol
  • HDL
  • BP
  • BP treatment status
  • DM
  • current smoking status
86
Q

How much does high intensity statin therapy lower LDL by?

A

Over 50 percent

87
Q

How much does moderate intensity statin therapy lower LDL by?

A

30-50 percent

88
Q

What do you see on EKG in someone with angina?

A
  • normal in between episodes

- during episodes– ST depression, T-wave changes

89
Q

What is most useful non-invasive test for dx angina?

A

stress test

90
Q

What is the gold standard for dx angina?

A

coronary angiography

91
Q

How do you tx angina?

A
  • eliminate aggravating factors
  • acute attacks– nitro
  • BB– prevent angina by decreased MVO2 (decrease HR)
  • long-acting nitrates
  • CCB (decrease MVO2, decrease afterload)
92
Q

Who should be put on ASA?

A

ALL PATIENTS WITH CHD/PAD, CAROTID DISEASE!

93
Q

Patient presents with chest pain that happens in the morning at rest?

A

Prinzmetals angina

94
Q

What is prinzemetals angina?

A

ischemia as a result of vasospasm

95
Q

What causes prinzmetals angina?

A

Cold, stress, meds (ergot), drugs (cocaine)

96
Q

What is definition of unstable angina?

A

angina at rest or with minimal activity lasting over 10 min

97
Q

What does EKG of unstable angina look like?

A

ST depression, TW inversion

NO ELEVATION OF CARDIAC MARKERS/enzymes

98
Q

How do you treat unstable angina?

A
  • hospitalize
  • anticoag and antiplatelet therapy (heparin, ASA)
  • nitraites, BB, CCB to decrease O2 demand

Family Med 1 EOR Exam (3 decks)

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