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STEP Review > 4-21 > Flashcards

4-21 Flashcards

1
Q

Nitric oxide is made from which amino acid

A

Arginine + O2

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2
Q

How does NO cause smooth muscle relaxation

A

Activates guanylyl cyclase, increase formation of cGMP, activates protein kinase G, reduces cytosolic calcium levels = relaxation

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3
Q

Fatigue and exertional dyspnea 3 weeks after tooth extraction

A

Bacterial endocarditis from Strep viridans

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4
Q

Culture-negative endocarditis organisms

A

HACEK (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)

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5
Q

Persistent fever w/ tricuspid vegetations/regurg

A

Bacterial endocarditis from S. aureus in IV drug users

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6
Q

Strep bovis

A

Bacterial endocarditis in previously normal heart valves, associated with underlying colon cancer

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7
Q

Decrease in systolic blood pressure >10mmHg with inspiration

A

Pulsus paradoxus (seen in cardiac tamponade, constrictive pericarditis, severe obstructive lung disease, restrictive cardiomyopathy)

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8
Q

Loss of cardiomyoctye contractility occurs within ___ after onset of total ischemia

A

60 seconds (>30 minutes of ischemia = irreversible damage)

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9
Q

Digoxin activity on AV node

A

Decreases nodal conduction by increasing parasympathetic tone via action on vagus nerve (used to treat atrial fibrillation)

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10
Q

Major criteria for acute rheumatic fever

A

JONES - joints (migratory polyarthritis), heart (pancarditis), subcutaneous nodules, erythema marginatum, sydenham chorea

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11
Q

Most common cause of death during acute phase of acute rheumatic fever

A

Myocarditis (Aschoff bodies with Anitschkow “caterpillar” cells and fibrinoid material)

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12
Q

Elevated ASO or antiDNase B titer 2-3 weeks post pharyngitis in children

A

Acute rheumatic fever

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13
Q

Mechanism that group A beta-hemolytic strep causes disease

A

M protein, exhibits molecular mimicry by resembling our own proteins

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14
Q

Complications of Aortic Stenosis

A

Concentric LV hypertrophy, angina/syncope w/ exercise (limited blood flow across valve), Microangiopathic hemolytic anemia (RBCs damaged while crossing valve)

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15
Q

Systolic ejection click w/ crescendo-decrescendo murmur

A

Aortic stenosis

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16
Q

If have fusion of aortic valve commisssures and coexisting mitral stenosis, will this be rheumatic disease or just “wear and tear”

A

Rheumatic disease (since involves mainly mitral valve)

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17
Q

“wear and tear” valvular disease

A

Aortic stenosis (late adulthood >60 years old)

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18
Q

Early blowing diastolic murmur

A

Aortic regurgitation

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19
Q

Most common cause of aortic regurgitation

A

Isolated aortic root dilation (can also be caused by syphilitic anuerysm, aortic dissection or valvular dmg/infectious endocarditis)

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20
Q

Hyperdynamic circulation describes the pathophysiology of which heart disorder

A

Aortic regurgitation (systolic pressure increases, diastolic pressure decreases, so overall pulse pressure increases)

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21
Q

Ehlers-Danlos and Marfan syndrome may be associated with which heart valve abnormality

A

Mitral valve prolapse (since myxoid degeneration, “gel-like” of mitral valve making it floppy)

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22
Q

Mid-systolic click, followed by regurg murmur

A

Mitral valve prolapse

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23
Q

Opening snap followed by diastolic rumble

A

Mitral stenosis

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24
Q

Phases of cardiac cycle

A

Systolic (ejection), Diastolic (filling)

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25
Q

Most common valve disorders with acute vs. chronic rheumatic disease

A

Acute=Mitral valve prolapse, Chronic = mitral stenosis

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26
Q

Bounding water hammer pulses, head bobbing

A

Aortic regurgitation

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27
Q

Holosystolic blowing murmur

A

Mitral regurgitation

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28
Q

Clinical features of mitral stenosis

A

Pulmonary congestion (edema, alveolar hemorrhage), pulmonary htn/R. CHF, atrial fibrillation/risk for mural thrombi = volume overload of Left atrium

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29
Q

What does expiration do to the heart?

A

increases return to the left atrium

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30
Q

What does squatting do to the heart?

A

increases systemic resistance so decreases ventricular emptying

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31
Q

Most common overall cause of endocarditis

A

Bacterial infection with strep viridans (low-virulence organism, so requires previously damaged valves)

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32
Q

Endocarditis does/does not destroy the valve?

A

Does NOT! Only creates small vegetations that can trap bacteria floating in blood stream

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33
Q

high-virulence organism infecting normal tricuspid valve

A

Staph. Aureus (causes large vegetations, destroys valve) - common in IV drug users

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34
Q

Staph epidermidis

A

Associated with endocarditis of prosthetic valves

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35
Q

TEE is a good diagnostic tool in_

A

Bacterial endocarditis (can detect lesions on valves)

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36
Q

Clinical features of bacterial endocarditis

A

“Bacteria FROM JANE” - Fever, Roth spots, Osler’s nodes, Murmur, Janeway lesions (erythematous on palms/soles), Anemia of chronic disease, Nail-bed splinter hemorrhages, Emboli

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37
Q

Pt with lupus that has a heart murmur, most likely caused by what?

A

Libman-Sacks endocarditis (non-bacterial), causes sterile vegetations on both sides of mitral valve, resulting in mitral regurg

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38
Q

Pt with sterile vegetations along lines of mitral valve closure

A

Nonbacterial thrombotic endocarditis, associated with a hypercoagulable state OR underlying adenocarcinoma

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39
Q

Pt has mitral regurg heard on auscultation w/o history of bacterial infection, what other clinical problems could they potentially encounter?

A

Underlying adenocarcinoma (this is Non-bacterial thrombotic endocarditis), hypercoagulation state

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40
Q

Most common causes of dilated cardiomyopathy

A

Genetic (autosomal dominant), Myocarditis from Coxsackie A/B infection, alcohol abuse, drugs/doxorubicin/cocaine, pregnancy

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41
Q

Pt has arrhythmia, mitral & tricuspid regurg, with decreased systolic function

A

Dilated cardiomyopathy (all 4 chambers affected)

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42
Q

Most common cause of dilated cardiomyopathy

A

Idiopathic, then myocarditis from coxsackie infection

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43
Q

Pt experiences syncope with exercise, decreased cardiac output from diastolic dysfunction; what will you see on biopsy of heart itssue? Will his son be affected with this?

A

Hypertrophic cardiomyopathy (thickened left ventricle) decreases compliance so can’t fill properly; will see myofiber disarray; Yes his son will get it since it is autosomal dominant mutation in sarcomere proteins

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44
Q

Child with low-voltage EKG and diminished QRS amplitude

A

Restrictive cardiomyopathy, caused by ENDOCARDIAL FIBROELASTOSIS

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45
Q

Loeffler syndrome

A

Endomyocardial fibrosis with eosinophilic infiltrate that causes reduced compliance of ventricle/restricts filling during diastole (Restrictive cardiomyopathy)

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46
Q

Causes of restrictive cardiomyopathy

A

Amyloidosis, sarcoidosis, hemochromatosis, endocardial ribroelastosis (kids), Loeffler syndrome (eosinophils)

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47
Q

Child with tuberous sclerosis can develop which cardiac tumor

A

Rhabdomyoma (benign hamartoma of cardiac muscle) in ventricle

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48
Q

Most common primary cardiac tumor in adults

A

Myxoma (gelatinous appearance)

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49
Q

Pt diagnosed with a myxoma, where is this commonly located and what adverse events may ensue secondary to this?

A

Pedunculated mass in left atrium can cause syncope due to mitral valve obstruction

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50
Q

Congenital failure of neural crest migration can result in which cardiac abnormalities

A

Tetralogy of Fallot (skewed aorticopulmonary septum), Transposition of great vessels (failure to spiral), persitent truncus arteriosus (partial AP septum development)

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51
Q

Left and right horns of sinus venosus develop into which structures in the adult heart

A

Left horn = Coronary sinus, right horn = smooth part of Right atrium

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52
Q

The superior vena cava develops from which embryonic structures?

A

Right common cardinal vein and right anterior cardinal vein

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53
Q

Eisenmenger’s syndrome

A

Late reverse of an initial L to R shunt, becoming a R to L shunt, due to onset of pulmonary hypertension (RV builds up more pressure than left side of heart, so blood wants to flow into LV towards lower pressure)

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54
Q

Membranous septal defect causes _

A

Left to right shunt

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55
Q

Pathogenesis of patent foramen ovale

A

Failure of septum primum and secundum to fuse after birth

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56
Q

List the locations of fetal erythropoiesis during development

A

“Young Livers Synthesize Blood” - yolk sac (3-10wks), liver (6wk-birth), spleen (15-30 wks), bone marrow (22wks-adult)

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57
Q

alpha2beta2 hemoglobin seen in fetal or adult blood?

A

Adult (fetal is alpha2gamma2)

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58
Q

Median umbilical ligament is formed from which embryonic structure

A

allantois

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59
Q

medial umbilical ligaments formed from which embryonic structure

A

Umbilical arteries

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60
Q

ligamentum teres from which embryonic structure

A

umbilical vein

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61
Q

Asymptomatic prolonged PR interval

A

First degree AV block, PR>200msec

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62
Q

Progressive lengthening of PR interval until a beat is dropped

A

Mobitz type I Wenckebach, 2nd degree AV block

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63
Q

Completely erratic rhythm with no identifiable waves

A

Ventricular fibrillation (fatal)

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64
Q

“sawtooth appearance” of waves

A

Atrial flutter

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65
Q

Chaotic and erratic EKG with no discrete P waves in btwn irregularly spaced QRS complexes

A

Atrial fibrillation

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66
Q

Atria and ventricles beat independently of each other

A

Complete 3rd degree AV block

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67
Q

Which disease can result in a 3rd degree AV block

A

Lyme disease

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68
Q

Dropped QRS complex not preceded by a change in length of PR interval

A

Mobitz type II, 2nd degree AV block -> progress to 3rd degree

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69
Q

Congenital cardiac abnormality with a wide, fixed split S2

A

ASD, due to high blood volume passing into RA and RV

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70
Q

Most common cause of early cyanosis

A

Tetralogy of Fallot

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71
Q

Most common congenital cardiac anomaly

A

VSD

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72
Q

Kid that learns to squat in order to relieve cyanotic sx

A

Increases peripheral vascular resistance (afterload) and decreases blood flowing across shunt from RtoL

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73
Q

Hypertension in upper extremities with hypotension in lower extremities seen in adult pt, what is the most common assoicated valvular condition

A

Bicuspid aortic valve (pt has adult/postductal type coarctation of aorta)

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74
Q

Child with hypotension of lower extremities

A

Infantile type coarctation of aorta, associated with Turner syndrome

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75
Q

If congenital transposition of great vessels is seen, what is the most common cause (clinical)

A

Diabetic mother

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76
Q

22q11 syndromes cause which congenital cardiac abnormalities

A

Truncus arteriosus, tetralogy of Fallot

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77
Q

Pulsus paradoxus w/ distant heart sounds and increased JVD w/ hypotension

A

Cardiac tamponade

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78
Q

What is pulsus paradoxus

A

decrease in amplitude of systolic BP by >10mmHg during inspiration

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82
Q

Limiting factor to facilitated diffusion

A

Carrier proteins present and saturation

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83
Q

Mandibular hypoplasia, facial abrnormalities due to failure of neural crest migration of 1st branchial arch

A

Treacher-Collins syndrome

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84
Q

What does the 3rd aortic arch develop into in the adult human?

A

Common carotid artery and proximal part of the internal carotid arteries

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85
Q

What does the 4th aortic arch form in an adult

A

On the right forms proximal part of R. subclavian artery/on left forms the aortic arch

86
Q

What does the 6th aortic arch develop into in an adult

A

On right proximal part of pulmonary arteries, on left the ductus arteriosus

87
Q

Good way to remember aortic arch derivatives

A

1st is maximal (maxillary artery), second is stapedial, 3rd/C is 3rd letter of alphabet (carotid), 4th for 4 limbs/systemic (subclavian and aortic arch), 6th (none)

88
Q

Baby found to have 22q11 deletion, what cardiac defects will it most likely have

A

This is DiGeorge syndrome, associated with Tetralogy of Fallot and an interrupted aortic arch (also see hypocalcemic tetany and T-cell deficiency)

89
Q

Pt found to have his heart on the Right side of his body with recurrent sinusitis, what disorder does he most likely have?

A

Kartagener syndrome (situs inversus, immotile cilia w/ autosomal recessive pattern of inheritance)

90
Q

What are the boundaries of the femoral triangle

A

Inguinal ligament superiorly, sartorius muscle laterally, adductor longus muscle medially

91
Q

Longest vein in the body, can be used for coronary bypass grafting

A

Great saphenous veina (courses along medial aspect of lower leg and thigh)

92
Q

If pt has a baker’s cyst, what nerves and vessels can be compromised?

A

Popliteal artery and vein, Tibial nerve

93
Q

Child with throat pain and difficulty breathing, no prior vaccination history, what kind of Ab’s would increase his/her chance of survival

A

Pt has C. diphtheriae (since no DPT vaccine), exotoxin deactivates EF-2 elongation factor, inhibiting protein synthesis -> cardiac and neural toxicity (heart failure, paralysis, coma)

94
Q

Prazosin, terazosin, doxazosin, tamsulosin activity on heart

A

Alpha-1 selective blockers, can be used in pts with HTN and diabetes because blocks smooth m. vasoconstriction

95
Q

2 most common important S/E of digoxin toxicity

A

AV block and Vtach (also hyperkalemia)

96
Q

Drugs that cause rash on face and trunk, multiple joint pain, and very high ANA titers

A

(Drug-induced SLE) Hydralazine (direct vasodilator), Procainamide (class IA antiarrhythmic/Na+ channel blocker), Isoniazid = HIP drugs

97
Q

MOA of a drug that can be used in severe HTN or CHF, can cause S/E of excess fluid retention, compensatory tachycardia, and lupus-like syndrome

A

(Hydralazine) Is a selective direct vasodilator that increases cGMP to cause smooth muscle relaxation

98
Q

Drug that can cause increase in cardiac contractility and decreased vascular resistance

A

Isoproterenol (Beta-agonist/sympathomimetic) - acts on Beta 1 receptors in heart to increase contractility, acts on Beta-2 in smooth muscle to vasodilate/decrease vascular resistance

99
Q

If a pt has CHF and a previous MI w/ evidence of cardiomegaly, which drug would be best to control long-term HTN

A

ACE-I’s because inhibit the chronic effects of AngII-mediated ventricular hypertrophy and remodeling

100
Q

Drugs used to provide symptomatic relief of pulmonary edema and acute CHF tx

A

Diuretics

101
Q

Dobutamine MOA and uses

A

Sympathomimetic, mainly at Beta-1 receptors; causes increased inotropic effect (increase contractility/CO), positive chronotropic effect (increase HR/myocardial O2 consumption) -> used for acute heart failure associated with cardiogenic shock

102
Q

Nitroglycerin vs. Dobutamine on myocardial oxygen consumption

A

Nitroglycerine DECREASES this, vs. Dobutamine INCREASES this (since causes increased myocontractility)

103
Q

Reflex effects seen with nitroglycerin administration

A

Causes venous pooling, baroreceptors will sense this as low BP and reflex tachycardia will occur

104
Q

Primary indication for digoxin administration

A

Chronic heart failure with LV systolic dysfunction and atrial fibrillation (since slows conduction through AV node)

105
Q

Nitroprusside MOA

A

Arterial and venous vasodilation to decrease afterload AND preload

106
Q

Nesiritide MOA

A

Synthetic brain natriuretic peptide, can be used to decrease afterload by dilating arteries and veins, improving hemodynamics (stimulating diuresis)

107
Q

If a pt is experiencing CHF but has bilateral renal artery stenosis, which class of drugs would you NOT give

A

ACE-I’s

108
Q

What are the different classes of drugs that can be used to treat HTN

A

Diuretics, Beta-blockers, ACE-I’s, Angiotensin receptor blockers, direct renin inhibitors, CCBs, alpha-blockers (alpha1), other (clonidine, minoxidil/hydralazine, methyldopa, sodium nitroprusside)

109
Q

Which diuretic has an additional benefit of diminishing cardiac remodeling that occurs in heart failure

A

Spironolactone (K+-sparing diuretic & Aldosterone receptor antagonist)

110
Q

How do beta-blockers help in the treatment of HTN

A

Decrease CO (block Beta-1 receptors in heart), decrease peripheral resistance (decrease beta-1 renin release & decrease AngII vasoconstriction)

111
Q

Withdrawal syndrome may occur with which drugs in treatment of HTN

A

Beta-blockers, Alpha-2 agonist

112
Q

1st dose phenomenon is seen in which drugs

A

Apha-1 selective blockers (Prazosin, terazosin, doxazosin)

113
Q

Good drugs to use in a pt with concomitant HTN and diabetes

A

ACE-I’s or ARB’s

114
Q

For CCBs, which drugs have more vascular affects vs. cardiac effects

A

-dipines’ (Amlodipin, nifedipine) vs. verapamil and diltiazem that have more cardiac effects (decrease HR, contractility)

115
Q

Is Losartan/valsartan beneficial in an african-american pt

A

No, they are less responsive to ARB’s/ACE-I’s and more responsive to CCBs and diuretics

116
Q

“-dipines”

A

CCBs

117
Q

Which HTN drugs are contraindicated in pregnancy

A

Anything that affects Renal function (ACE-Is/ARBs, diuretics)

118
Q

“-zosins”

A

Alpha-1 selective blockers

119
Q

Selective HTN drug that is useful when pts have renal disease

A

Clonidine & Methyldopa (Alpha-2 selective agonist, centrally-acting), does not have activity on renal blood flow or GFR

120
Q

Monotherapy for pregnancy-induced HTN

A

Hydralazine (direct vasodilator by inhbiting IP3-induced Ca+2 release from SR in smooth muscle cells, so muscle does not contract/constrict) and stimulates endothelium to make NO

121
Q

Which anti-hypertensive drug can also be used to treat malepattern baldness

A

Minoxidil (S/E causes hypertrichosis)

122
Q

MOA of minoxidil

A

Used to treat HTN as a direct vasodilator (decreases the amount of intracellular Ca+2 available for smooth muscle contraction by opening K+ channels)

123
Q

Immediate continuous IV infusion of which drug is used to treat Hypertensive emergencies

A

Sodium nitroprusside, since causes prompt vasodilation of both arteries and veins (so will also decrease cardiac preload)

124
Q

How is fenoldopam a better alternative in hypertensive emergencies

A

It is a peripheral D1 agonist, so lowers BP while increasing renal perfusion (since it relaxes renal vascular smooth muscle)

125
Q

Which anti-hypertensive agent can precipitate a hypertensive crisis following abrupt cessation of therapy

A

Clonidine (Alpha-2 agonist, that could potentially cause rebound hypertension)

126
Q

Cyanide toxicity is seen with which anti-hypertensive drug

A

Nitroprusside

127
Q

Which drug is safe to use in pregnancy that is often given w/ a beta-blocker, but can cause compensatory tachycardia and lupus-like syndrome

A

Hydralazine

128
Q

Describe MOA of labetalol and important use

A

Mixed Alpha/beta antagonist that is used in malignant HTN tx

129
Q

How do nitrates work to cause vasodilation

A

Conversion into NO at vascular smooth muscle cell membrane, NO stimulates guanylate cyclase (converts GTP -> cGMP), increased cGMP decreases intracellular Ca+2/myosin dephosphorylation, causing muscle relaxation

130
Q

If a pt has an allergic rxn to aspirin, what is the next best alternative drug and MOA

A

Clopidogrel, irreversibly blocks plt surface ADP receptors (necessary for plt activation/aggregation/fibrin binding)

131
Q

Synergistic effects of 2 drugs used in tx of thromboembolic disease

A

Aspirin and clopidogrel (different MOA’s)

132
Q

Which nitrate compound has the highest bioavailability if given orally?

A

Isosorbide mononitrate, an active metabolite of isosorbide dinitrate (must be swallowed, Nitroglycerin has the most rapid onset of action but is given sublingually)

133
Q

Cinchonism can be caused by which drug

A

Quinidine (Class IA antiarrhythmic) , headache, dizziness with tinnitus

134
Q

Class IA antiarrhythmic drugs

A

Quinidine, Procainamide, Disopyramide

135
Q

Which antiarrhythmic can cause systemic sx that mimic an autoimmune disorder

A

Procainamide (lupus-like syndrome)

136
Q

___ enhances digoxin toxicity

A

Quinidine

137
Q

Best antiarrhythmic drugs to use in case of chronic ventricular arrhythmias if pt has previous hx of MI

A

Class IB = Best (Lidocaine, Mexiletine, Tocainide); preferntially affects ischemic Purkinje/ventricular tissue

138
Q

Flecainide and Propafenone are contraindicated in_

A

pts with structural abnormalities (post-MI, any type of heart conditions) - usually only used as a last resort in refractory cases

139
Q

Can you use lidocaine IV to treat a supraventricular arrhythmia?

A

NO! it is ineffective

140
Q

Tocainide

A

Class IB

141
Q

Disopyramide

A

Class IA

142
Q

Propafenone

A

Class IC

143
Q

Mexiletine

A

Class IB

144
Q

Quinidine

A

Class IA

145
Q

Activity of Class IA drugs

A

slow rate of AP rise/increase threshold, prolong AP duration, & prolong ERP (shift curve to right and out)

146
Q

Activity of Class IB drugs

A

Decrease AP duration, shorten repolarization (therefore not effective in SVA or Atrial arrhythmias!) -curve is shifted left/in

147
Q

Activity of Class IC drugs

A

Slow rate of AP rise/increase threshold, but don’t affect AP duration (curve is pretty close to normal curve)

148
Q

Activity of Class II drugs

A

Beta-blockers that block phase 4 depolarization of abnormal pacemakers, decrease SA/AV node activity by decreasing cAMP/Ca+2 currents = increase PR interval (used to treat atrial fib/flutter and SVT)

149
Q

Which short-acting Class II drug is used in surgery or emergency situations

A

Esmolol

150
Q

Dyslipidemia in a pt on a anti-arrhythmic drug

A

Metoprolol

151
Q

Exacerbation of vasospasm in a pt on an antiarrhythmic drug

A

Propranolol

152
Q

Activity of Class III drugs

A

K+ channel blockers, diminish outward current during repolarization - prolong AP and ERP (AIDS-Amiodarone, Ibutilide, Dofetilide, Sotalol)

153
Q

Sotalol

A

Class III drug

154
Q

Ibutilide

A

Class III drug

155
Q

Dofetilide

A

Class III drug

156
Q

Amiodarone

A

Class III drug

157
Q

2 major classes of antiarrhythmics that prolong the QT interval

A

Class IA and Class III

158
Q

Drug class used to prevent nodal arrhythmias, SVT

A

Class IV-Ca+2 channel blockers

159
Q

Pt with sinus node depression, flushing and constipation, most likely on which drug

A

Class IV -CCC (Verapamil, diltiazem) - other effects seen from vasodilation

160
Q

Adenosine MOA as antiarrhythmic

A

At higher doses it increases K+ current outward, hyperpolarizing the cell; Used to abolish SVT

161
Q

Pt with FLUSHING, HYPOTENSION, CHEST PAIN that gets better with drinking coffee (or giving theophylline), most likely on which anti-arrhythmic

A

Adenosine (increases K+ efflux/out of cells), hyperpolarizing the cell

162
Q

If have digoxin toxicity or torsades pointes, can give this

A

Mg+2

163
Q

Which antiarrhythmic can predispose a pt to digoxin toxicity

A

Quinidine

164
Q

Production of a bidirectional block is useful in tx of

A

Reentrant arrhythmias; class I drugs prevent this

165
Q

Muffled heart sounds, elevated JVP, profound hypotension

A

Pericardial tamponade

166
Q

QRS prolongation that has little effect on QT interval duration, which phase does this correspond to on a myocyte action potential figure?

A

Phase 0 (depolarization occurs when rapid movement of sodium in the myocyte)

167
Q

Pulsus paradoxus

A

Pericardial pressure >10mmHg, seen in cardiac tamponade; can progresses to collapse of atria (death from cardiogenic shock)

168
Q

Palpate radial pulse and it disappears during inspiration

A

Pulsus paradoxus

169
Q

Pulsus parvus et tardus

A

Pulse of low magnitude with delayed peak, seen in aortic stenosis

171
Q

Repeated episodes of palpitations that start and stop abruptly in a young adult pt

A

Wolff-Parkinson-White pre-excitation syndrome

172
Q

Triad of WPW on EKG

A

Shortened PR interval <.12 seconds, wide QRS complex, early upslope delta wave immediately preceding QRS

173
Q

Head bobbing

A

Seen in Aortic Regurgitation, sign of widened pulse pressure (increased peak systolic pressure relative to end-diastolic pressure)

174
Q

If stable angina in a pt, what percentage coronary occlusion by atherosclerotic plaque would you start to see sx

A

> 75%

175
Q

Most likely cause of fatigue and new onset murmur in a young adult

A

Bacterial endocarditis, can progress to acute diffuse proliferative glomerulonephritis

176
Q

Pt given glucagon to treat overdose of a drug, how does this make pts condition better

A

Pt probably took Metoprolol which can cause dyslipidemia; glucagon serves to decrease cAMP and Ca+2 currents in cardiac myocytes

177
Q

Drugs that can result in torsades de pointes

A

(Those which prolong the QT interval) Class IA antiarrhythmics (Quinidine, Procainamide, Disopyramide) and Class III (Amiodarone, Ibutilide, Dofetilide, Sotalol)

178
Q

Drug given to abolish supraventricular tachycardia

A

Adenosine

179
Q

Pt recently put on new antiarrhythmic, notices blue-grey skin lesions and constipation; HR is bradycardic; labs reveal hypothyroidism; what is MOA of drug

A

(Amiodarone toxicity) Class III, K+ channel blocker that alters lipid membrane

180
Q

2 classes of drugs that are better at treating atrial arrhythmias

A

Class II beta blockers & Class IV CCBs since they both decrease conduction velocity/increase PR interval

181
Q

Drug that has no effect on AP duration, used only in pts without structural abnormalities

A

Propafenone, Flecainide (Class IC), contraindicated in post-MI pts

182
Q

Which drugs preferentially affects ischemic or depolarized cardiac tissue

A

Class IB, Lidocaine, Mexilitine, Tocainide

183
Q

Which antiarrhythmic drugs can cause bradycardia, heart block, CHF

A

Class II beta blockers (-olol’s), Class III K+ channel blocker Amiodarone, Class IV CCBs (verapamil, diltiazem)

184
Q

Drug that can be used for A-fib and CHF begins to cause T-wave inversion on EKG, nausea, vomiting, diarrhea, blurry yellow vision; what is the MOA

A

Inhibition of Na+/K+ ATPase and stimulation of vagus nerve (increase intracellular Ca+2 and decrease HR)

185
Q

Antiarrhythmic drug preferentially used in post-MI pts, can also be used to reverse toxicity of which other drug

A

Digoxin (this drug is Lidocaine)

186
Q

Pt recently started on a drug and is found to have high levels of cyanide; what is the MOA of this drug

A

Cyanide toxicity from administration of Nitroprusside, used to treat Malignant hypertensive emergencies; MOA is to increase cGMP via direct release of NO (smooth muscle relaxation)

187
Q

Pt recently started on hydralazine and now experiences rapid HR, what other drug could be used concomitantly to prevent this

A

Beta blocker (prevents reflex tachycardia)

188
Q

Prolongation of QT interval upon administration of a drug, but does NOT predispose to torsades de pointes

A

Amiodarone

189
Q

Asthmatic pt recently started on additional drug for HTN, starts having more frequent asthma attacks; which drug is he most likely on

A

Beta blocker, can cause exacerbation of asthma, impotence

190
Q

Most common digoxin S/E

A

N/V, diarrhea, blurry yellow vision, AV block, arrhythmia, ST scooping/T-wave inversion, SHORTENED QT INTERVAL, prolonged PR interval, HYPERKALEMIA

191
Q

Male pt w/ erectile dysfunction (that is being treated) takes several tablets to relieve an episode of chest pain. Good or bad idea?

A

BAD idea, Nitroglycerin (nitrate, vasodilator, increases cGMP conc.) plus Sildenafil/Tadalafil for ED (Phosphodiesterase inhibitor, increases cGMP conc.) will cause profound HYPOTENSION due to extreme vasodilation

192
Q

Major complication of Doxorubicin

A

Dilated cardiomyopathy (better to use Dexrazoxane, decreases formation of free radicals)

193
Q

Reflex tachycardia can be seen with administration of which cardiac drugs

A

Nitrates and Hydralazine (direct vasodilators)

194
Q

Non-antiarrhythmic agents that can cause QT prolongation and precipitate torsades

A

Phenothiazines & tricyclic antidepressants

195
Q

What should be monitored when pt is started on warfarin/coumadin for loong-term anticoagulation

A

Prothrombin time (PT)

196
Q

Which drugs significantly decrease heart failure progression as well as all-cause mortality in patients with CHF

A

Beta-blockers, particularly CARVEDILOL (should NOT be given in pts with unstable heart failure!)

197
Q

Pt given esmolol infusion, which portion of EKG does it exert its greatest effects

A

Slows AV conduction, therefore prolongs the PR interval

198
Q

Activity of cAMP in myocytes

A

Increases the conductance of calcium channels in the sarcoplasmic reticulum, more calcium allowed to enter cytoplasm and increase force of contraction

199
Q

Milrinone

A

Phosphodiesterase isoenzyme 3 inhibitor that can increase cardiac contractility (positive inotropic agent)

200
Q

Site of action of K+-sparing diuretics

A

Collecting duct of renal tubule

201
Q

Main side effects of Niacin

A

Cutaneous flushing, warmth, itching that is mediated by Prostaglandin (may be prevented co-administration with aspirin)

202
Q

Most common S/E of statins

A

hepatotoxicity, myopathy, rhabdomyolysis

203
Q

Which statin is drug of choice if pt is on erythromycin

A

Pravastatin (Erythromycin inhibits cytochrome P450, which metabolizes most statins)

204
Q

Risk of myopathy with statin use in increased when used in combination with which other drugs

A

Fibrates (gemfibrozil increases the concentration of statins, fenofibrate causes compouding risk for myopathy)

205
Q

Which statin has the highest associated risk of myopathy

A

Simvastatin

206
Q

Statin MOA

A

Inhibits HMG-CoA reductase (necessary for cholesterol synthesis), causing up-regulation of hepatocyte LDL receptors

207
Q

First-dose hypotension can be an adverse effect in pts initiating a drug with which predisposing risk factors

A

(ACE-I’s) Hyponatremia, hypovolemia secondary to diuretics, low baseline BP, high renin/aldosterone levels, renal impairment, heart failure

208
Q

Which drugs are particularly useful for the tx of both HTN and BPH

A

Alpha-1 selective blockers (Prazosin, Terazosin)

STEP Review (2 decks)

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