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PANCE Flashcards

1
Q

What do you give in narrow complex tachycardia and terminates 90% of SVTs?

A

adenosine

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2
Q

first line treatment in symptomatic sinus bradycardia

A

atropine

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3
Q

treatment for sick sinus syndrome

A

permanent pacemaker (PPM) with automatic implantable cardioverter defribillator (AICD)

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4
Q

management for A-flutter

A

vagal, CCB, b-blocker, DCC if unstable

radiofrequency ablation definitive tx*

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5
Q

what is included in the CHADS2 criteria?

A 
congestive heart failure
hypertension
age >75
diabetes mellitus
stroke, tia, thrombus (2 points)

high risk>2 –> warfarin
moderate: 1 –> warfarin or asa

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6
Q

what is wandering atrial pacemaker (WAP)? and what is Multifocal atrial tachycardia (MAT)?

A

WAP: HR <100 and >3 P wave morphologies

MAT if HR >100

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7
Q

what is MAT (multifocal atrial tachycardia) associated with?

A

severe COPD

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8
Q

what is a delta wave (slurred QRS upstrokc, wide QRS >0.12 sec) and short PRI associated with?

A

wolff-parkinson-white

-accessory pathway (Kent bundle) “pre-excites ventricle”

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9
Q

what is the treatment for WPW?

A

vagal maneuvers

antiarrhythmics (procainamide**, amiodorone)

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10
Q

what is torsades mc due to?

A

hypomagnesemia

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11
Q

ST elevation CONCAVE precordial leads
PR depressions seen in same leads with the ST elevations
NO reciprocal changes

A

EKG findings of acute pericarditis

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12
Q

what should you be cautious of using in an inferior (R-sided) MI?

A

nitroglycerin and morphine

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13
Q

why should you be cautious of using nitroglycerin and morphine in an inferior MI?

A

because they decrease preload and the R side is more dependent on preload (and stroke volume)

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14
Q

what is hyperadlosteronism associated with?

A

increased BP and hypokalemia

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15
Q

what is the most useful noninvasive test in evaluating patients with suspected coronary artery disease

A

stress test

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16
Q

risk factors for coronary artery disease

A

DM, hypoerlipidemia, smoking, HTN, males, age >65, family h/o CAD

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17
Q

EKG findings of CAD

A

ST depression* with exertion, T wave inversion, poor R wayve progression +/- normal (50%)

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18
Q

gold standard for cAD

A

coronary angiography

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19
Q

contraindication to pharmacologic stress testing

A

bronchospastic disease

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20
Q

contraindications for using nitroglycerin

A

SBP <90, RV infarction, use of viagra (sildenafil)

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21
Q

progression of an EKG in acute coronary syndrome

A

hyperacute (peaked ) T waves–> ST elevations –> Q waves –> T wave inversions

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22
Q

when does troponin peak and return to baseline?

A

peakes 12-24 hr, returns to baseline 7-10 days (appears 4-8 h)

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23
Q

side effect of enoxaparin (lovenox)

A

thrombocytopenia (obtain CBC prior to use)

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24
Q

what is clopidogrel?

A

plavix (ADP inhibitor) –> useful in initial tx of ACS in patients with ASA allergy

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25
Q

what is the MOA of betabolockers?

A

lowers myocardial O2 consumption, antiarrythmic effects

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26
Q

when are beta blockers contraindicated?

A

severe bradycardia (HR <50), hypotension, decompensated CHF, 2nd/3rd degree geart block, cardiogenic shock, cocain induced MI, severe asthma, COPD

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27
Q

when are beta blockers contraindicated in acute MI?

A

cocaine induced MI : use benzodiazepines bc b-blockers cause unopposed alpha vasoconstriction

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28
Q

what should yo ugive in a r ventricular (ninferior walle0 MI?

A

IV fluids for preload (cautious with IV nitrates and morphine use)

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29
Q

MC arrhythmia in MI

A

ventricular fibrillation

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30
Q

post MI pericarditis associated with fever and pulmonary infilltrates

A

dressler’s syndrome

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31
Q

chest pain usually at rest, not usually due to exertion

A

prinzmetal’s angina (coronary spasm –> transient ST elevations usually without MI)

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32
Q

diagnosis of pritzmetal’s angina

A

ECG shows transient ST elevations (symptoms and ST elevations rapidly resolve with CCB and nitro)

treatment: CCB

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33
Q

pathophys of cocaine induced MI

A

coronary artery spasm

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34
Q

absolute contraindications for thrombolytic use in ACS

A

any prior ICH, non-hemorrhagic stroke within 6 months or closed head/facial trauma within 3 months, intracranial neoplams, aneurysm, AVM, active internal bleeding, suspected aortic dissection

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35
Q

most common causes of L sided heart failure

A

coronary artery disease and hypertension

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36
Q

most common cause of r-sided heart failure

A

left sided heart failure

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37
Q

difference between systolic and diastolic HF

A

systolic: decreased EF associated with S3 gallop
diastolic: normal/increased EF associated with S4 gallop

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38
Q

MC symptom of L sided heart failure

A

dyspnea. initially exertional –> orthopnea and paroxysmal nocturnal dyspnea

pulmonary congestion/edema: rales, rhonchi, chronic nonproductive cough (commonly missed) esp with pink frothy sputum (surfactant)

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39
Q

MC cause of transudative pleural effusion

A

CHF

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40
Q

deeper faster breathing with gradual decrease and periods of apnea

A

cheyne stroke’s breathing (CHF PE)

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41
Q

clinical manifestions of R sided heart failure

A

peripheral edema, JVD, GI/hepatic congestion

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42
Q

most useful test to diagnose Heart failure

A

echo

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43
Q

most important determinant in heart failure prognosis

A

ejection fraction (normal 55-60)

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44
Q

unless contraindicated, what two drugs should every patient with Heart failure be on?

A

ACEI (decreases mortality, hospitalizations, and directly reverses the pathology by decreasing renin and sympathetic stimulation) and diuretic

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45
Q

MOA of ACEI in HF

A

decrease preload/afterload, decrease aldosterone production

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46
Q

side effects of ACEI

A

1st dose hypotension
azotemia/renal insufficiency
hyperkalemia
cough (often dry) and angioedema due to increased bradykinin**

47
Q

contraindications to ACE

A

pregnancy

hypotension

48
Q

ending for ACEI

A

“-pril”

49
Q

what do beta blockers do for HF patients?

A

decrease mortality, increase EF and reduce ventricular size

50
Q

drug that is most effective tx for symptoms of mild-moderate HF

A

diuretics

51
Q

side effects of diuretics

A

hypOkalemia/calcemia/natremia, hyperglycemia, hyperuricemia

52
Q

side effects of K sparking diuretics

A

hyperkalemia, gynecomastia

53
Q

digoxin toxicity

A

digitalis effect on ECG: downsloping sagging ST segment, junctional rhythms, hypokalemia worsens toxicity**

54
Q

what is treatment for patients with HF and an EF <35%

A

implantable cardioverter defibrillator

55
Q

most common etiology of pericarditis

A

viral (enteroviruses: coxsackie and echovirus)

56
Q

pericarditis 2-5 days s/p MI

A

dressler’s syndrome

57
Q

EKG of pericarditis

A

diffuse ST elevations in precordial leads and associated PR depressions

58
Q

treatment of pericarditis

A

aspirin or NSAIDs x 7-14 days + colchicine

59
Q

exg with low voltage QRS complexes

A

large pleural effusion or tamponade

60
Q

treatment of pericardial effusion

A

observation if small and no evidence of tamponade, treat underlying cause

+/- pericardiocentesis if tamponade, large effusion. pericardial window drainage if recurrent

61
Q

pericardial effusion causing significant pressure on heart –> restriction of cardiac ventricular filling –> decreased CO

A

pericardial tamponade

62
Q

what is beck’s triad

A

distant (muffled) heart sounds
elevated JVP
systemic hypotension

63
Q

what will an echo show in pericardial tamponade?

A

diastolic collapse of cardiac chambers

64
Q

treatment of pericardial tamponade

A

pericardiocentesis

65
Q

most common etiologies of myocarditis

A

enterovirus (esp coxsacki B) mc cause and echovirus

bacterial: rickettsial (lyme dz, rocky mountain spotted fever, Q fever)

66
Q

clinical manifestation of myocarditis

A

viral prodrome (fever, myalgias, malaise) x several days –> HF symptoms** (dyspnea @ rest, exercise intolerance, syncope, tachypnea, tachycardia) impaired systolic function

67
Q

classic diagnostic study findings of myocarditis

A

cardiomegaly (dilated cardiomypathy)

68
Q

gold standard in diagnosing myocarditis

A

endomyocardial biopsy

69
Q

most common causes of dilated cardiomyopathy

A

idiopathic (50%): (viral probably the origin of idiopathic)
viral myocarditis : enterovirus MC
toxic: alcohol abuse, cocaine, anthracyclies (doxorubicin)** –> chemo drug

70
Q

diagnostic studies for dilated cardiomyopathy

A

echocardiogram: left ventricular dilation **, large ventricular chamber, decreased ejection fraction, regional LV hypokinesis

71
Q

apical left ventricular balooning following an event that causes a catecholamine surge (emotional stress, “broken heart syndrome”, surgery)

A

takotsubo cardiomypoathy

72
Q

most common cause of restrictive cardiomyopathy

A

amyloidosis , followed by sarcoidosis

73
Q

treament of HCMP

A

focus on early detection, medical managment, surgical and/or ICK placement**, counseling to avoid dehydration and extreme exertion/exercise very important !!

beta blockers (cautious use of digoxin, nitrates and diuretics)
myomectomy
alcohol septal ablation

74
Q

when is rheumatic fever MC and in who?

A

children 5-15 y, 2-3 weeks p symptomatic or asymptomatic strep pharyngitis

75
Q

criteria for rheumatic fever

A

jones criteria

Major:
migratory polyarthritis (2 or more joints)
active carditis
syndenhajm’s chorea
subcutaneous nodules (rare, seen over joints)
erythema margitanum (macular, erythematous, non-pruritic anular rash with rounded, sharply demarkated edges)

minor:
fever( 101-104)
arthralgias
increase in acute phase reactants (ESR, CRP, leukocytosis)

PLUS: supporting evidence of a recent group A streptococcal infection

76
Q

treatment of rheumatic fever

A

penicillin G drug of choice (or erythromycin if PCN allergic)
anti-inflammatory: ASA (2-6 weeks with taper)

77
Q

CXR that shows “egg on a string”

A

transposition of the great vessels

78
Q

what is carvallo’s sign?

A

increased murmur intensity with inspiration –> sign of tricuspid regurgitation

79
Q

blowing holosystolic murmur @ apex with radiation to the axilla

A

mitral regurgitation

80
Q

management of hypertensive emergency

A

decrease BP (MAP) by 10% first hour and an additional 15% next 2-3 hours using IV agents** -sodium nitroprusside

(different than hypertensive urgency- no end-organ damage- decrease by 25% 24-48 hours using PO agents)

81
Q

what are the lipid guidelines for statin use?

A
  • type 1 or 2 patients with DM between 40-75 years old
  • people >21 with LDL levels greater than or equal to 190 Mg/dL
  • people with cardiovascular disease
82
Q

MC bacteria of subacute bacterial endocarditis

A

strep viridans - oral flora source of infection

83
Q

MC bacteria of acute bacterial endocarditis and IVDA

A

staph aureus

84
Q

clinical manifestations of endocarditis

A

fever (80-90%)

janeway lesions (painless erythematous macules on palms/soles)

osler nodes

roth spots, petechiae

splinter hemorrhages

85
Q

diagnostic studies in suspected bacterial endocarditis

A

blood cultures (3 sets @ least 1 hour apart)

EKG (prone to arrythmias)

echo

labs: CBC - leukocytosis, anemia, elevated ESR/RF

86
Q

criteria for endocarditis

A

duke criteria

87
Q

treatment for infective endocarditis

A

Native valve acute bacterial endocarditis:
nafcillin + gentamicin x 4-6 weeks
vancomycin (if MRSA suspected or PCN allergic)

88
Q

intermittent claudication(brought on by exercise and relieved with rest) is MC presentation of what?

A

PAD

89
Q

diagnosis of PAD

A

ankle-brachial index (ABI), arteriography is gold standard (only done if revasulcarization is planned)

90
Q

treatments of PAD

A 
platelet inhibitos (cilostazole**)
ASA
Clopidogrel (plavix)
91
Q

MC place for AAA

A

infrarenally

92
Q

MC risk foactors for AAA development

A

atherosclerosis, age >60, smoking, males, caucasians

93
Q

initial imaging study for patients with suspected AAA

A

abdominal ultrasound

94
Q

test of choice for thoracic aneurysms

A

CT scan

95
Q

drug that reduces shearing forces in AAA

A

beta blockers

96
Q

most important predisposing factor of aortic dissection

A

hypertension, follwed by age (55-60 y)

97
Q

variation in pulse (>20 MMHG difference) between R and L arm is indication of what?

A

aortic disection

98
Q

diagnostic test for aortic dissection

A

CT scan test of choice
MRI angiography is gold standard
TEE if patient unstable
CXR shows widening of mediastinum

99
Q

giant cell arteritis/temporal arteritis is same clinical spectrum as what?

A

polymyalgia rheumatica

100
Q

clinical manifestations of giant cell arteritis

A

headache (unlateral, temporal, lancinating)

jaw claudication with mastication

acute vision distrubances : amaurosis fugax

101
Q

diagnosis of giant cell arteritis

A

ESR > 100, elevated CRP

102
Q

treatment of giant cell arteritis

A

high dose corticosteroids** (40-60 mg/day x 6 weeks)

-if suspected, start prednisone rather than wait for testing

103
Q

headache, scalp tenderness, jaw claudication, fevers, visual loss

A

giant cell arteritis

104
Q

nonatherosclerotic inflammatory disease of small and medium arteries and veins, strongly associated with tobacco, MC in young men 20-45

A

buerger disease

105
Q

suspect in young smokers/tobacco users with distal extremity ischemia, ischemic digit ulcers and digital gangrene

A

buerger disease

106
Q

beurger disease is also known as what?

A

thromboantiitis obliterans

107
Q

what is trousseau’s sign?

A

migratory thrombophlebitis usually associated with malignancy or vasculitis

108
Q

most specific sign of DVT

A

unilateral swelling/edema of lower extremity

109
Q

treatment of DVT

A

heparin, LMWH –> warfarin x 3-6 months

110
Q

skin findings of DVT

A

stasis dermatitis

111
Q

skin findings of PAD

A

livedo reticularis

112
Q

venous stasis ulcers are usually found where?

A

medial malleolus

113
Q

treatment of cardiogenic shock

A

smaller amounts of fluid **only shock in which large amounts of fluids aren’t given)

inotropic support - dobutamine, epi, balloon pump

114
Q

pathophys of cardiogenic shock

A

decreased CO, increased pulmonary capillary wedge pressure

PANCE (1 decks)

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