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Cardiovascular FA > MTB and important from FA 2 > Flashcards

MTB and important from FA 2 Flashcards

1
Q

cardiac sound S3 in normal in

A

children and pregnant

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2
Q

auscultation of the heart - Aortic area (what we hear)

A

systolic murmur (aortic stenosis, flow murmur eg. physiologic murmur, aortic valve sclerosis)

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3
Q

auscultation of the heart - left sternal border (what we hear)

A
  1. diastolic murmur: aortic regurgitation, pulmonic regurgitation
  2. systolic murmur hypertrophic cardiomyopathy
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4
Q

auscultation of the heart - Pulmonic area (what we hear)

A

systolic ejection murmur: pulmonic stenosis, flow murmur (eg physiologic murmur)

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5
Q

auscultation of the heart - mitral valve (what we hear)

A
  1. holosystolic murmur: mitral regurgitation

2. diastolic murmur: mitral stenosis

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6
Q

auscultation of the heart - tricuspid valve (what we hear)

A
  1. holosystolic murmur: tricuspid regurgitation, ventricular septal defect
  2. diastolic murmur: tricuspid stenosis, ASD
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7
Q

ASD auscultation

A

ASD commonly present with a pulmonary flow murmur (increased flow through pulmonary valve) and a diastolic rumble (increased flow across tricuspid). Blood flow across the actual ASD does not cause murmur (no significant P gradient). The murmur later progress to a louder diastolic murmur of pulmonic regurgitation from dilaton of the pulmonary arterey

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8
Q

auscultation of the heart - aortic regurgitation mumur

A

high-pitched early long diastolic decrescendo murmur.

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9
Q

auscultation of the heart - mitral stenosis mumur

A

follows opening snap. Delayed rumbling diastolic murmur

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10
Q

auscultation of the heart - aortic stenosis mumur

A

crescendo - decrescendo systolic ejection murmur

ejection click MAY be present

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11
Q

aortic stenosis pulse

A

pulsus parvus et tardus: weak with delayed peak

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12
Q

aortic stenosis is often related to

A
  1. age related calcification
  2. early onset calcification of bicuspid aortic valve
  3. rarely - Rheumatic heart disease (mitral valve is also involved)
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13
Q

MVP murmur

A

late systolic crescendo murmur with midsystolic click.

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14
Q

acute pericarditis - presentation

A

sharp chest pain, aggravated by inspiration and lying supine, relieved by sitting up and leaning forward

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15
Q

acute pericarditis - ECG

A
  1. ST-segmented
    and/or
  2. PR depression
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16
Q

cardiac tamponade - clinical examination

A
  1. Beck’s triad (hypotension, distended neck veins, distant heart sounds)
  2. increased HR
  3. pulsus paradoxus
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17
Q

most frequent primary cardiac tumor in children

A

Rhabdomyomas

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18
Q

kussmual sign - definition / may be seen in

A
  • increasing in JVP on inspiration instead of normal decreasing
    1. constrictive pericarditis
    2. restrictive cardiomyopathy
    3. right atrial or ventricular tumors
    4. severe right ventricular failure
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19
Q

BNP blood test

A
  1. used for diagnosis of heart failure

2. very good negative predictive value

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20
Q

hypertrophic cardiomyopathy - clinical examination findings

A
  1. S4
  2. Systolic murmur (left sternal border) (loudest with valsava, standing up)
  3. maybe mitral regurgitation due to impaired mitral valve closure
  4. paradoxical splitting
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21
Q

hypertrophic cardiomyopathy - treatment

A
  1. cessation of high intensity athletics
  2. non-didydropyridines Ca2+ channel blockers
  3. β-blockers
  4. Implantable Cardioverter Defibrillator (ICD) if patient is high risk
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22
Q

hypertrophic cardiomyopathy - pulse

A

quick rise arterial pulse

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23
Q

restrictive/infiltrative cardiomyopathy - major causes

A
  1. sarcoidosis
  2. amyloidosis
  3. postradiation fibrosis
  4. endocardial fibroelastosis
  5. Loeffler syndrome
  6. hemochromatosis
  7. scleroderma
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24
Q

Loeffler syndrome

A

endomyocardial fibrosis with prominent eosinophilic infiltrate

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25
Q

endocardial fibroelastosis

A

thick fibroelastic tissue in endocardium of young children

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26
Q

restrictive cardiomyopathy - type of dysfunction

A

diastolic

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27
Q

hyperlipidemia signs

A
  1. xanthomas
  2. tendinous xanthoma
  3. corneal arcus
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28
Q

lipid-lowering agents groups

A
  1. HMG-CoA reductase inhibitors (statins)
  2. Bile acid resins
  3. Ezetimibe
  4. Fibrates
  5. Niacin
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29
Q

statins side effect

A

hepatotoxicity (increased LFTs)

myopathy (especially when used with fibrates or niacin)

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30
Q

bile acid resins drugs

A

cholestyramine
colestipol
colesevelam

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31
Q

bile acid resins mechanism of action

A

prevent intestinal reabsorption of bile acids SO the liver must use cholesterol to make more

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32
Q

bile acid resins side effects

A
  1. GI upset

2. decreased reabsorption of other drugs and fat-soluble vitamins

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33
Q

Ezetimibe mechanism of action

A

prevent cholesterol absorption at small intestine brush border

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34
Q

Ezetimibe side effects

A
  1. increased LFT (rare)

2. diarrhea

35
Q

Fibrates drugs

A

-FIBRATES
clofibrate, bezafibrate, fefenofibrate
AND GEMFIBROZIL

36
Q

fibrates mechanism of action

A
  1. upregulate LPL –> increased TG clearance

2. Activates PPAR-α to induce HDL synthesis

37
Q

fibrates side effecrs

A
  1. myopathy (increased risk with statins)

2. cholesterol gallstones

38
Q

niacin mechanism of action

A
  1. inhibits lypolyisis (hormone sensitive lipase) in addipose tissue
  2. reduces hepatic VLDL synthesis
39
Q

3 agents able to stabilize the atherosclerotic plaques

A
  1. Beta blocker
  2. ACE inhibitor
  3. statins
40
Q

increased of TG leves - agent

A

bile acid resins (SLIGHTLY)

41
Q

LDL levels calculation

A

LDL ch = TOTAL ch - HDL - (TG/5) (no if tg more than 400)

42
Q

niacin side effects

A
  1. hyperglycemia
  2. Hyperuricemia
  3. Red, flashed face, which is decreased by NSAID or long term use
43
Q

MI: complications at 0-4hr

A
  1. arrhythmia
  2. HF
  3. cardiogenic shock
44
Q

MI: complications at 4-24hr

A
  1. arrhythmia
  2. HF
  3. cardiogenic shock
45
Q

MI: complications at 1-3 days

A

postinffraction fibrinous pericaridtis

46
Q

MI: complications at 3-14 days

A
  1. Free wall rupture: a. tamponade
    b. papillary muscle rupture (mitral regurgitation)
    c. interventricular septal rupture ( leads to shunt) due to macrophage-mediated structural degradation
  2. LV pseudoaneurysm (risk of rupture)
47
Q

MI: complications at 2weeks to several months

A
  1. Dressler syndrome
  2. HF
  3. True ventricular aneurysm (RISK OF MURAL THROMBUS)
48
Q

Diagnosis of MI - ECG localization of STEMI and vessel - ANTEROSEPTAL

A

LAD

V1-2

49
Q

Diagnosis of MI - ECG localization of STEMI and vessel -

ANTEROAPICAL

A

DISTAL LAD

V3-4

50
Q

Diagnosis of MI - ECG localization of STEMI and vessel -

ANTEROLATERAL

A

LAD or LCX

V5-6

51
Q

Diagnosis of MI - ECG localization of STEMI and vessel -

LATERAL

A

LCX

I, aVL

52
Q

Diagnosis of MI - ECG localization of STEMI and vessel -

INFERIOR

A

RCA

II, III, aVF

53
Q

Myocardial infraction complication - Interventricular septal rupture, papillary muscle rupture, ventricular pseudoaneurysm, ventricular free wall rupture - time

A

Interventricular septal rupture –> 2-3 d
papillary muscle rupture –> 3-7 d
ventricular pseudoaneurysm –> 3-14 d
ventricular free wall rupture –> 5-14 d

54
Q

Diagnosis of MI - ECG localization of STEMI and vessel -

posterior

A

PDA

V7-V9, ST depression in V1-V3 with tall R waves

55
Q

causes of sabacute endocarditis

A

viridans streptococci (low virulence)

56
Q

MCC of endocariditis in drug users

A
  1. S aureus
  2. Candida
  3. pseudomons
57
Q

Olser nodes vs Janeway lesions

A

Osler: tender raised lesions on finger or toe pads

Janeway lesions: small painless erythematous lesions on palm or sole

58
Q

culture negative infective endocarditis

A
  1. Coxiella burnetti
  2. Bartonella
  3. HACEK
  4. prior treatment with antibiotics
59
Q

rheumatic fever - major criteria

A
  1. migratory polyarthritis
  2. carditis
  3. Nodules on skin (subcotaneous)
  4. Erythema marginatum
  5. Sydenham chorea
60
Q

systemic inflammatory response syndrome

A

> =2:

  1. fever/hypothermia
  2. tachycardia
  3. tachypnea
  4. leukocytosis/leukopenia
61
Q

Ischemic heart disease manifestations - types

A
  1. angina (stable, unstable, variant)
  2. Coronary steal syndrome
  3. MI
  4. sudden cardiac death
  5. Chronic ischemic heart disease
62
Q

Sudden cardiac death: definition

A

death from cardiac causes within 1 hour of onset of symptoms most commonly sue to lethal arrhythmia (eg ventricular fibrillation)

63
Q

antiarrhytmics Class IA drugs

A
  1. Quinidine
  2. Procainamide
  3. Disopyramide
64
Q

antiarrhytmics Class IA - clinical use

A

Both atrial and ventricular arrhythmias

esp re-entrant (eg WPW), ectopic SVT (eg atrial fibrillation) and VT

65
Q

antiarrhytmics Class IA - toxicity

A
  1. Cinchonism (headache, tinnitus, psychosis) - quinidine
  2. reversble SLE-like syndrome - procainamide
  3. heart failure - disopyramide
  4. thrombocytopenia
  5. torsades de pointes due to increased QT interval
66
Q

antiarrhytmics Class IB -drugs

A
  1. Lidocaine
  2. Mexiletine
  3. phenytoin
67
Q

antiarrhytmics Class IB - clinical use

A
  1. acute ventricular arrhythmias (esp post MI)

2. digitalis-induced arrhythmias

68
Q

antiarrhytmics Class IB - toxicity

A
  1. CNS stimulation/depression

2. cardiovascular depression

69
Q

antiarrhytmics Class IC - drugs

A
  1. Flecainide

2. Propafenone

70
Q

antiarrhytmics Class IC - toxicity

A

proarrhythmic (esp in post-MI)

71
Q

antiarrhytmics Class IC - contraindicated

A
  1. ischemic heart disease (post-MI)

2. stractural ischemic heart disease

72
Q

antiarrhytmics Class IC - clinical use

A
  1. SVT (including atrial fibrillation)

2. Only last resort in refractory VT

73
Q

treat β-blockers overdose

A

saline, atropine, glucagon

74
Q

anthiarrhythmics class II - clinical use

A

SVT (ventricular rate control for atrial fibrillation and flutter)

75
Q

anthiarrhythmics class II - toxicity

A
  1. impotence 2. exacerbation of COPD/athma
  2. cardiovascular effects (bradycardia, AV block, HF)
  3. CNS effects (sedation, sleep alterations) 5. may mas hypoglycemia signs 6. dyslipidemia (metoprolol)
  4. exacerbate vasospasm in prinzmetal (propranolol)
76
Q

anthiarrhythmics class III - drugs

A
  1. Amiodarone
  2. Ibutilide
  3. Dofetilide
  4. Sotalol
77
Q

anthiarrhythmics class III - clinical use

A
  1. atrial fibrillation
  2. atrial flutter
  3. ventricular tachycardia (amiodarone, soloatol)
78
Q

solatol toxicity

A
  1. torsades de pointes

2. excessive β blockage

79
Q

ibutilide toxicity

A

torsades de pointes

80
Q

amiodarone toxicity

A
  1. pulmonary fibrosis 2. hypo/hyperthyroidism
  2. hepatotoxicity 4. act as hapten 5. neurological defects 6. comstipation 7. cardiovascular effects (bradycardia, heart block, HF)
81
Q

antiarrhythmics IV - drugs

A

verapamil, diltiazem

82
Q

other antiarrhythmics drugs

A
  1. adenosine

2. Mg2+

83
Q

Mg2+ as antiarrhythmic

A

effective in torsades de pointes and digoxin toxicity

84
Q

adenosine as antiarrhythmic - clinical use

A

drug of choice in diagnosing/abolishing SVT

Cardiovascular FA (8 decks)

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