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Cardiology part 7 Flashcards

1
Q

Endocardial Cushion Defect

A

x

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2
Q

association

A

x

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3
Q

what is the most common disease associated with endocardial cushion defect?

A

down syndrome

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4
Q

syx

A

x

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5
Q

what are the syx of endocardial cushion defect?

A

SOB, face turns blue during feeding and when crying

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6
Q

PE

A

x

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7
Q

what are the physical exam findings of endocardial cushion defect?

A

harsh holosystolic murmur heard best over the lower left sternal border

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8
Q

what murmur do you hear on auscultation?

A

harsh holosystolic murmur heard best over the lower left sternal border

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9
Q

dx

A

x

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10
Q

what is the diagnostic test for endocardial cushion defect?

A

Echocardiography

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11
Q

what would CXR show ?

A

degree of cardiomegaly and pulmonary marking

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12
Q

what test is reserved for cases of endocardial cushion defect in which the size of the shunt is uncertain, lab data and clinical findings are equivocal, or when pulmonary vascular disease is suspected?

A

cardiac catheterization

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13
Q

Down Syndrome

A

x

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14
Q

complications

A

x

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15
Q

what are other malformations of down syndrome?

A

duodenal atresia, hirschsprung’s disease, atlanto-axial instability, and hypothyroidism

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16
Q

what are patients with Down Syndrome at increased risk of developing?

A

acute leukemia, alzheimer like dementia, autism, ADHD, depressive disorder, and seizure disorder

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17
Q

Benign Prostatic Hyperplasia (BPH)

A

x

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18
Q

treatment

A

x

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19
Q

which medication can worsent prostate sympotoms and induce bronchoconstriction?

A

metoprolol

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20
Q

what are three classes of meds to treat BPH?

A
  • alpha adrenergic antagonists (terazosin, tamsulosin);
  • 5 alpha reductase inhibitors (finasteride, dutasteride);
  • Antimuscarinics (tolterodine)
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21
Q

alpha adrenergic antagonists (terazosin, tamsulosin);

A

x

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22
Q

MOA

A

x

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23
Q

how do these drugs work?

A

-relax smooth muscle in bladder neck, prostate capsule and prostatic urethra

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24
Q

what is it’s purpose in regards to BPH?

A

work against dynamic componenet of bladder outlet obstruction, usually within days to weeks

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25
Q

side effects

A

x

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26
Q

what are the side effects of alpha adrenergic antagonists?

A

orthostatic hypotension, dizziness

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27
Q

5 alpha reductase inhibitors (eg finasteride, dutasteride)

A

x

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28
Q

MOA

A

x

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29
Q

how do these drugs work?

A

inhibit conversion of testosterone to DHT in the prostate

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30
Q

what is it’s purpose in regards to BPH?

A

reduce the prostate gland size (volume) to improve fixed component of bladder outlet obstruction

symptom improvement can take up to 6-12 months

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31
Q

what are the side effects of 5 alpha reductase inhibitors (eg finasteride, dutasteride)?

A

decreased libido, erectile dysfunction

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32
Q

Antimuscarinics (eg tolterodine)

A

x

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33
Q

MOA

A

x

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34
Q

what is it’s purpose in treatment?

A

may be useful in men with overactive bladder, urinary frequency, urgency and incontinence

sometimes combined with one of the therapies listed above

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35
Q

trx

A

x

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36
Q

what patient population do antimuscarinics serve?

A

usually restricted to men with low post void residual volme

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37
Q

Pulmonary Embolism (PE)

A

x

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38
Q

trx

A

x

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39
Q

when are IV thrombolytics indicated?

A

hypotension (SBP<90mm Hg) or shock

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40
Q

Ischemic Cardiomyopathy

A

x

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41
Q

syx

A

x

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42
Q

what are syx of cardiomyopathy?

A

SOB, DOE,

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43
Q

dx

A

x

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44
Q

what would echo show?

A

demonstrates LV systolic (rather than only diastolic) dysfunction

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45
Q

what is the test to order for evaluating PE if patient cannot undergo CT pulm Angio due to renal insufficiency?

A

V/Q perfusion scan

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46
Q

trx

A

x

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47
Q

what is the optimal medical therapy for ischemic cardiomyopathy?

A

ACEi, BBlocker, loop diuretic, and aldosterone antagonist

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48
Q

classifications of NYHA heart failure

A

x

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49
Q

what is Class I NYHA heart failure?

A

No symptomatic limitation of physical activity

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50
Q

what is Class II NYHA Heart failure?

A

slight limitation of physical activity (eg dyspnea with climbing stairs)

ordinary activity causes fatigue, palpitations, or dyspnea

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51
Q

what is Class III NYHA Heart failure?

A

marked limitation of physical activity (eg dyspnea with house chores)

less than ordinary activity causes fatigue, palpitations, or dyspnea

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52
Q

what is Class IV NYHA heart failure?

A

inability to perform physical activity without significant discomfort

can have symptoms at rest

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53
Q

managmeent

A

x

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54
Q

in select patients in this group, cardiac resynchronization therapy w biventricular pacing is recommended why?

A

improve excercise tolerance and NYHA functional class, and reduce the rate of recurrent hospitilzation and overall mortality

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55
Q

Management of Heart Failure

A

x

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56
Q

do CCBs (amlodipine, felodipine) have any mortality benefit or syx benefit to CHF patients?

A

nope

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57
Q

in increasing order of therapy for all NYHA class CHF, what is the first class of therapy?

A

ACEi or ARB

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58
Q

in which patients are ACEi and ARBs contraindicated?

A

those with hypotension, renal failure, or hyperkalemia

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59
Q

in increasing order of therapy for all NYHA class CHF, what is the next class of therapy if ACEi or ARB don’t work?

A

Diuretic therapy (occassionally can use metolazone , which is a thiazide diuretic, if inadequate response to loop diuretics)

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60
Q

in increasing order of therapy for all NYHA class CHF, what is the next class of therapy if EF <=40% and euvolemic after diuresis?

A

beta blockers

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61
Q

in increasing order of therapy for all NYHA class CHF, what is the next class of therapy if EF < 30% and stable renal function and potassium?

A

Spironolactone

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62
Q

in increasing order of therapy for all NYHA class CHF, what is the next class of therapy if EF <= 30% ?

A

Defibrillators

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63
Q

in increasing order of therapy for NYHA class II and III and IV CHF, what is the next class of therapy after ACEi, diuretics, beta blockers, and spiranolactone……when the patient is African American?

A

isosorbide dinitrie + hydralazine

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64
Q

in increasing order of therapy for NYHA class II and III and IV CHF, what is the next class of therapy after ACEi, diuretics, beta blockers, and spiranolactone……when the patient is symptomatic with spiranolactone?

A

digoxin

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65
Q

in increasing order of therapy for NYHA class II and III and IV CHF, what is the next class of therapy after ACEi, diuretics, beta blockers, and spiranolactone……when the QRS>150ms?

A

cardiac resynchronization

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66
Q

in increasing order of therapy for NYHA class III and IV CHF, what is the last resort for CHF management?

A

Transplant/Ventricular Assist Device Evaluation

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67
Q

Mitral Stenosis (MS)

A

x

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68
Q

cause

A

x

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69
Q

most common cause of Mitral Stenosis?

A

Rheumatic Heart Disease

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70
Q

syx

A

x

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71
Q

what are common symptoms of Mitral Stenosis?

A

dyspnea (70% of patients), fatigue, atrial fibrillation, and thromboembolism (eg stroke), PND

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72
Q

what are rarer symptoms of Mitral Stenosis?

A

hemoptysis (from pulm edema or pulm apoplexy) and hoarseness (due to compression of recurrent laryngeal nerve by enlarged left atrium-ortner syndrome)

73
Q

complicaitons

74
Q

which patient population with mitral stenosis is at risk of afib and pulm edema ?

A

pregnant women (due to physiologic hypervolemia and increased left atrial and pulmonary venous pressure)

76
Q

what are physical exam fidnings of mitral stenosis?

A
  • mitral facies (pinkish purple patches on cheeks)
  • Loud S1, loud P2 if pulmonary HTN
  • opening snap (high frequency early diastolic sound)
  • mid-diastolic rumble (best heard at cardiac apex)
77
Q

what is the classic murmur of Mitral Stenosis?

78
Q

where is the best location to hear the murmur?

A

with the bell of the stethoscope at the cardiac apex

79
Q

what is the best position for position for patients to hear the murmur?

A

fifth intercostal space (between the 5th and 6th ribs) at the left mid clavicular line. Often helpful if the patients exhales and lies in left lateral decubitus position

81
Q

what do you see on CxR for mitral stenosis?

A

pulm blood flow redistribution to upper lobes, elevation of the left mainstem bronchus, dilated pulmonary vessels, left atrial enlargement with a flattening of the left heart border

82
Q

what do you see on EKG for mitral stenosis?

A

P mitrale: broad and notched P waves, atrial tachyarrhythmias, RVH (tall R waves in V1 and V2)

83
Q

what do you see on transthoracic echocardiogram?

A

MV thickening/calcification/decreased mobility, coexisiting MR

84
Q

Noonan Syndrome

86
Q

what are the physical exam findings of noonan syndrome?

A

short stature, facial dysmorphism, spectrum of congenital heart defects

87
Q

epid

88
Q

what is the epid of Noonan Syndrome?

A

autosomal dominant disorder

89
Q

Restrictive Cardiomyopathy

91
Q

what are the physical exam findings of restrictive cardiomyopathy?

A

JVD, bibasilar crackles, pulmonary vascular congestion, biatrial enlargement, and pulmonary artery HTN

92
Q

Peripartum Cardiomyopathy (PPCM)

93
Q

risks

94
Q

what are risk factors for cardiomyopathy?

A

maternal age >30, mulitple gestation, preE or eclampsia

96
Q

what would echo show?

97
Q

what is important to rule out when dx peripartum cardiomyopathy?

A

no other cause of heart failure

98
Q

onsest

99
Q

what is the onset of peripartum cardiomyopathy?

A

36 weeks gestation- 5months postpartum

100
Q

management

101
Q

what is the best management of peripartum cardiomyopathy?

A
  • deliver based on maternal hemodynamic stability
  • standard systolic heart failure regimen
  • thromboembolism prophylaxis
102
Q

regardless of of PPCM rsolution, patients are evaluated with serial echocardiograms for how long?

103
Q

after delivery, what happens to those with PPCM?

A

some patients will have spontaneous resolution of ventricular dysfunction and can discontinue their medication regimen

104
Q

recurrence risk

105
Q

what is the recurrence risk of peripartum cardiomyopathy?

A

if LVEF < 20% at diagnosis or persistent LV Systolic dysfucntion

106
Q

Patent Ducturs Arteriosus (PDA)

107
Q

PE

108
Q

what does the characteristic murmur sound like for PDA?

A

continuous murmur that is heard best in the left infraclavicular area

109
Q

pathophys

110
Q

what is the pathophys of PDA?

A

abnormal connection between aorta and pulmonary artery

111
Q

Atrial Fibrillation

112
Q

management

113
Q

what is the preferred antiarryhtmic in patients with Afib with no CAD or structural heart disease?

A

flecainide, propafenone

114
Q

what is the preferred antiarryhtmic in patients with Afib with LV hypertrophy?

A

drondedarone, amiodarone

115
Q

what is the preferred antiarryhtmic in patients with Afib with CAD without heart failure?

A

sotalol, dronedarone

116
Q

what is the preferred antiarryhtmic in patients with Afib with CHF?

A

amiodarone, dofetilide

117
Q

what is the preferred antiarryhtmic in patients with Afib with recurrent AF symptoms refractory to medication?

A

radiofrequency ablation

118
Q

what is the preferred rate control agent in some patients with AF and RVR, especially those with low or borderline blood pressure CHF due to LV systolic dysfunction?

119
Q

what is an option for adjunctive therapy in those who continue to have Afib RVR despite beta blockers and CCB?

120
Q

what are three components of Afib trx?

A

anticoagulation, rate control, or rhythm control

121
Q

what is a good anticoag?

A

rivaroxaban

122
Q

what is a good rate control agent?

A

AV nodal blocker (Beta Blocker, CCB)

123
Q

what is a good rate control goal for beta blocker or CCB?

A

goal <=110bpm

124
Q

in most cases, rate control is preferred over rhythm control , however what situations are rhythm control better?

A
  • inability to maintain adequate heart rate control with rate control agents
  • persistence of symptomatic episodes (eg heart failure exacerbation) on rate control agents
125
Q

if HD unstable patient with Afib require what?

A

emergency cardioversion

126
Q

if HD stable patient with Afib, what meds can you use?

A

beta blockers, diltizaem, digoxin

127
Q

prevention of stroke in Afib

128
Q

antiocagulation in (non valvular) afib

129
Q

what is the scoring we use for anticoagulation therapy in Afib?

A

CHA2DS2-VASc Score

130
Q

what is the scoring criteria for CHA2DS2VASc?

A 
C-congestive heart failure: 1
H-HTN: 1
A2-Age: 2
D-Diabetes Mellitus: 1
S2- Stroke/TIA/Thromboembolism: 2
V-Vascular Disease (prior MI, PAD, or aortic plaque); 1
A-Age 65-74: 1
Sc-Sex Category (ie female): 1

Max score : 9

131
Q

if chadsvasc score is 0, what is the stroke risk and what is the anticoag therapy?

A

low, and no anticoag therapy

132
Q

if chadsvasc score is 1, what is the stroke risk and what is the anticoag therapy?

A

intermediate, none or oral anticoagulant

133
Q

if chadsvasc score is >=2, what is the stroke risk and what is the anticoag therapy?

A

high, oral anticoagulant (warfarin, rivaroxaban, dabigatraban, apixaban)

134
Q

syx

135
Q

what are the syx of Afib RVR exacerbating systolic heart failure?

A

dizziness, palpitations, SOB, and LE edema

136
Q

side effects of antiarrythmics

137
Q

what are side effects of flecainide?

A

increased risk of arrythmias and death (so avoid in patients iwth structural or coronary heart disease)

138
Q

Acute Aortic Dissection

139
Q

syx

140
Q

what are symptoms of acute aortic dissection?

A

2 hour hx of sharp, stabbing CP under sternum, radiating to upper back and shoulders

141
Q

PE

142
Q

what are physical exam fidnings of aortic dissection?

A

> 20mm Hg difference in SBP between arms

143
Q

Dx

144
Q

what would an EKG show?

A

normal or nonspecicif ST and T wave changes (eg T wave inversion in leads V5 and V6)

145
Q

what would CXR show?

A

mediastinal widening

146
Q

what are definitive diagnostic tests for aortic dissection?

A

CTA or TEE

147
Q

complications

148
Q

what are the complications of ascending aortic dissection?

A

aortic regurg, ACS (RCA occlusion), cardiac tamponade (hemopericardium), stroke (carotid artery occlusion), horner syndrome (SG compression), vocal cord paralysis (recurrent LN compression)

149
Q

what are the complications of descending aortic dissection?

A

hemothorax or hemoperitneum, renal injury (renal artery occlusion), mesenteric ischemia (eg SMA occlusion), LE ischemia, LE paraplegia (spinal cord ischemia)

150
Q

Ascending Aortic Dissection

151
Q

Trx

152
Q

what is the treatment of ascending aortic dissection?

A

IV beta blockers (labetalol, propanolol, or esmolol) to slow HR<60, lowering blood pressure, reducing left ventricular contractility.

153
Q

in addiitonal to medication therapy, what other intervention is needed for ascending aortic dissection?

A

emergency surgical repair

154
Q

Guidelines for Statin Therapy

155
Q

what are the indications for statin therapy?

A

clinically significant ASCVD

156
Q

what is meant by clinically significant ASCVD?

A

Acute Coronary Syndrome, Stable Angina, Arterial revascularizatoin (eg CABG), Stroke, TIA, PAD

157
Q

what is the recommended therapy for clinically significant ASCVD?

A

age <=75y.o. : High intensity statin

age >75y.o.: Moderate intesity statin

158
Q

If LDL >=190mg/dL, what do you do?

A

give high intensity statin

159
Q

if age 40-75 y.o. with DM, what do you do?

A

assess ASCVD risk

160
Q

if age 40-75 y.o. with DM, and ASCVD risk >= 7.5%, what do you do?

A

high intensity statin

161
Q

if age 40-75 y.o. with DM, and ASCVD risk >= 7.5%, what do you do?

A

moderate-intensity statin

162
Q

if 10 year ASCVD risk >=7.5%, what do you give?

A

mod to high intensity statin

163
Q

Statin Types

164
Q

what are the high intensity statins?

A

atorvastatin 40-80 mg, rosuvastatin 20-40 mg

165
Q

what are the moderate intensity statins?

A

moderate-intensity statins include atorvastatin 10-20 mg, rosuvastatin 5-10 mg, simvastatin 20-40 mg, pravastatin 40-80 mg, lovastatin 40 mg.

166
Q

Hypertriglyceridemia

167
Q

dx

168
Q

what is considered high triglycerides?

A

> 500-1000mg/dL

169
Q

trx

170
Q

what role does niacin play?

A

lowers LDL and raises HDL

171
Q

patients with moderate hypertriglyceridemia would benefit from?

A

statin therapy

172
Q

if >880mg/dL Triglycerides, what is good management?

A
  • fibrate therapy (or fish oil or niacin if fibrates not tolerated) to lower risk of pancreatitis.
  • once TG are lowered, add statin therapy
173
Q

what is mild hypertriglyceridemia and do you need to treat?

A

150-500mg/dL, and no need to treat

174
Q

Fibrates and Niacin have favorable effects on lipids but no found to improve cardiovascular outcomes or mortality in patients with known ASCVD. T or F

175
Q

Orlistat

176
Q

trx

177
Q

what is orlistat used for?

A

treatment of obesity

178
Q

MOA

179
Q

what is the mechanism of orlistat?

A

intestinal lipase inhibitor

Cardiology (7 decks)

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