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DIT STEP 2 > CARDIOLOGY > Flashcards

CARDIOLOGY Flashcards

1
Q

In 70% of patients, the posterior descending artery derives from what?

A

Right coronary artery.

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2
Q

In 70% of patients, the posterior descending artery derives from what?

A

Right coronary artery.

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3
Q

Coronary arteries fill during which stage of cardiac cycle?

A

Diastole. Therefore, conditions or drugs that reduce disastolic filling allow less coronary perfusion.

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4
Q

LAD supplies?

A

Anterior wall of LV. Septal branch of LAD supplies anterior 2/3 of IV septum.

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5
Q

Circumflex branch supplies?

A

LA, lateral wall of LV, posterior wall of LV

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6
Q

PDA supplies?

A

Inferior wall of LV, posterior 1/3 of IV septum

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7
Q

Marginal branch supplies?

A

RA, RV

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8
Q

SA, AV nodal branches supply

A

SA and AV nodes. Duh.

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9
Q

Acidosis causes what effect on SV?

A

Decreases.

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10
Q

Hypoxia causes what effect on SV?

A

Decreases.

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11
Q

CO increases during exercise initially due to? Later due to?

A

Increasing SV, THEN increasing HR.

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12
Q

MAP = ?

A

CO x TPR aka diastolic arterial pressure + 1/3 pulse pressure

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13
Q

Pulse pressure = ?

A

SBP - DBP

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14
Q

Vitamins that apparently help prevent CAD

A

Vitamins E and C as well as beta carotene

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15
Q

STrongest predictor for stroke?

A

HTN

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16
Q

HDL > 60 cancels how many risks?

A

1

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17
Q

HMG-CoA reductase inhibitors site of action

A

Liver

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18
Q

Ezetimibe MOA

A

Cholesterol absorption inhibitor.

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19
Q

Ezetimibe ONLY affects which cholesterol?

A

LDL

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20
Q

Fibric acids site of action

A

Blood, as they stimulate lipoprotein lipase

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21
Q

Fibric acids greatest effect on? Least effect on/

A

Greatest effect on triglycerides. Then LDL, then HDL.

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22
Q

Bile acid sequestrates have no effect on ?

A

HDL. May or may not actually RAISE triglycerides.

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23
Q

Niacin site of action

A

Liver

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24
Q

Niacin has the least effect on which lipid?

A

Triglycerides.

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25
Q

Niacin has been shown to exacerbate which disease?

A

Gout

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26
Q

Niacin has what effect on insulin?

A

Insulin resistance.

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27
Q

Increased LFTs can be seen in which classes of lipid lowering anents?

A

Statins, cholesterol absorption inhibitors, fibric acids, and niacin.

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28
Q

Nitroglycerin may also reduce effects of which 2 cause of chest pain?

A

GERD, esophageal spasm.

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29
Q

Electrolytes to keep an eye on during treatment of unstable angina

A

Potassium to keep K+ levels >4 mEq/L. Magnesium to keep levels >2 mEq/L.

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30
Q

When os CABG considered?

A

Left am stenosis >50%, 3 vessel disease, or history of CAD and DM.

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31
Q

2 vessels most commonly used in CABG

A

Saphenous vein and internal mammary artery

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32
Q

ST elevation in V2-V4 indicates which artery is occluded?

A

LAD. Anterior area of infarct.

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33
Q

ST elevation in V1-V3 indicates which artery is occluded?

A

LAD. Septal area of infarct.

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34
Q

ST elevation in II, III, and aVF indicates which artery is occluded?

A

either posterior descending or marginal branch. Inferior area of infarct.

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35
Q

ST elevation in I, aVL, V4-V6 indicates which artery is occluded?

A

LAD or circumflex. Lateral area of infarct.

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36
Q

ST elevation in V1 and V2 indicates which artery is occluded?

A

PDA. Posterior area of infarct.

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37
Q

Greatest risk of sudden cardiac death is how long post-MI?

A

First few hours from tach, fib, or cariogenic shock.

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38
Q

Which types of heart block get ventricular pacemaker?

A

Mobitz II or complete/third-degree block

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39
Q

PDA supplies?

A

Inferior wall of LV, posterior 1/3 of IV septum

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40
Q

Marginal branch supplies?

A

RA, RV

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41
Q

CO increases during exercise initially due to? Later due to?

A

Increasing SV, THEN increasing HR.

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42
Q

Vitamins that apparently help prevent CAD

A

Vitamins E and C as well as beta carotene

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43
Q

2 vessels most commonly used in CABG

A

Saphenous vein and internal mammary artery

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44
Q

Greatest risk of ventricular wall rupture is how many days post-MI?

A

4-8 days.

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45
Q

PR interval in first degree heart block

A

> 0.2 sec

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46
Q

Second degree heart block Type I is caused by?

A

InTRAnodal or His bundle conduction defect, , drug effects (.eg., B-blockers, digoxin, CCB) or increased vagal tone.

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47
Q

Second degree heart block Type II is caused by?

A

InFRAnodal conduction problem (bundle of His, parking fibers).

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48
Q

Which types of heart block get ventricular pacemaker?

A

Mobitz II or complete/third-degree block

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49
Q

Narrow QRS not associated with p waves, rate of 60

A

3rd degree block (junctional rhythm)

50
Q

Wide QRS not associated with p waves, rate >40 but

A

accelerated ventricular rhythm

51
Q

Narrow QRS not associated with p waves, rate >100

A

junctional tachycardia

52
Q

Wide QRS, not associated with p waves, rate 20-40

A

ventricular rhythm

53
Q

Wide QRS, not associated with p waves, rate >100

A

ventricular tachycardia

54
Q

Narrow QRS not associated with p waves, rate >60 but

A

accelerated junctional rhythm

55
Q

Difference between wandering pacemaker and Multifocal atrial tacky?

A

> 3 diff p wave morphologies but wandering pacemaker is ventric rate of 100.

56
Q

Treatment for PACs?

A

None

57
Q

Drug of choice in PSVT?

A

IV adenosine

58
Q

Scenarios you’d see Kussmaul’s sign

A

Increased JVD with inspiration is seen in right ventricular infarct, massive PE, constrictive pericarditis, restrictive cardiomyopathy, and rarely, cardiac tamponade.

59
Q

When might a subclinical mitral stenosis from rheumatic heart disease become clinically apparent?

A

Volume overload state, such as pregnancy.

60
Q

Diastolic murmur heard best in left lower sternum that increases with inspiration

A

Tricuspid stenosis

61
Q

Late diastolic murmur with an opening snap (no change with inspiration)

A

Mitral stenosis

62
Q

Systolic murmur heard best in the second right IC space

A

Pulmonic stenosis

63
Q

Systolic murmur heard best in the second left IC space

A

Aortic stenosis

64
Q

Late systolic murmur best heard at the apex

A

MVP

65
Q

Diastolic murmur with a widened pulse pressure

A

AR

66
Q

Holosystolic murmur that is louder wit inspiration at the left lower sternum

A

Tricispid regurg

67
Q

Holosystolic murmur heard at the apex and radiates to the axilla

A

MR

68
Q

When do PVCs become concerning for development of other ventricular arrhythmias?

A

> 3 PVC/min

69
Q

Anti-arrhythmic commonly used in Vtach?

A

Lidocaine or tocainamide, type IB.

70
Q

Causes of sytstolic dysfunction

A

Caused by decreased contractility, increased preload, increased after load, HR abnormalities, or high output conditions such as anemia, hyperthyroidism

71
Q

Causes of diastolic dysfuntion

A

Hypertrophy or restrictive cardiomyopathy.

72
Q

Chronic constrictive pericarditis is most commonly caused by?

A

Radiation, heart surgery

73
Q

Pathophys of Brugada Syndrome

A

Mutation in the gene that encodes for sodium ion channel in the cell membranes of the myocytes. Loss-of-function mutations in this gene lead to a loss of the action potential dome of some epicardial areas of the right ventricle. This results in transmural and epicardial dispersion of repolarization. The transmural dispersion underlies ST-segment elevation and the development of a vulnerable window across the ventricular wall, whereas the epicardial dispersion of repolarization facilitates the development of phase 2 reentry, which generates a phase 2 reentrant extrasystole that captures the vulnerable window to precipitate ventricular tachycardia and/or fibrillation that often results in sudden cardiac death.

74
Q

Genetics of Brugada syndrome

A

AD, more common in males and higher prevalence in Asians

75
Q

ECG of Brugada syndrome

A

Persistent ST elevations in V1-V3 with right BBB with or without terminal S waves. Prolongation of PR interval is also sometimes seen.

76
Q

Why is there an elevated pulse pressure in aortic regurg:

A

Due to insufficiency of aorta, blood flows back into LA, lowering DBP. This widens the pulse pressure.

77
Q

Treatment of AR

A

Decrease after load with a vasodilator like an ACE-I or CCB like nifedipine.

78
Q

High levels of what are associated with 3x risk of atherosclerosis

A

Homocysteine

79
Q

Unique symptoms of inferior wall MI

A

Bradycardia, diarrhea, lightheadedness.

Inferior wall MI is caused by infarction of posterior descending artery. The supply of PDA is posterior (duh) heart, and when this is irritated, it irritates the surrounding structures which happen to include the left vagus nerve. This is why you see vagal sx.

80
Q

Pt is in vtach and pulseless

A

Non-synchronized CVN / defibrillation

Arrhythmia + no pulse.

81
Q

Pt has PEA or asystole

A

Give 1 mg of IV epi during CPR.

82
Q

NYHA Class I CHF

A

HF with no limitations on physical activity and no symptoms, even with exertion

83
Q

NYHA Class II CHF

A

Slight limitations on physical activity and symptoms of heart failure with physical activity.

84
Q

NHA Class III CHF

A

Symptoms such as angina, SOB and palpitations qitth physical exertion

85
Q

NYHA Class IV heart failure

A

sx of heart failure even at rest

86
Q

what is Heyde’s syndrome

A

Combo of calcific aortic stenosis and GI bleeding due to colonic angiodysplasia. It is thought that aortic stenosis causes type 2 von willebrand syndrome which results in inefficient hemostasis in high flow areas. This results in bleeding from angiodysplastic lesions.

87
Q

Medical treatment of PAD

A

Cilostazol to improve flow to LE and decrease claudication. CONTRAINDICATED IN HEART FAILURE.

88
Q

Second line medical treatment of PAD

A

Pentoxifylline, also contraindicated in CHF. Ginko biloba. Thats fun.

89
Q

When are compressing stockings effective in post op prevention of DVT?

A

In low risk post op general surgery or neurosurgery pts.

90
Q

Where is the rash in Kawasakis

A

Truncal

91
Q

Tx of Kawasakis

A

IVIG and high dose ASA. Echo in acute phase and 6-8 weeks later.

92
Q

When is anticoag considered in superficial thrombophlebitis

A

In lower extremity or extension into femoral vein

93
Q

Tx of small VSD

A

Monitor/reassurance. 40% close by 3 years and 75% close by 10 yrs

94
Q

Tx of large VSD

A

Monitor nutirtion and weight gain due to higher risk of FTT
Treat CHF with ACE, diuretics, digoxin
Influenza vaccine and winter pavlivizumab if younger than 2 for RSV prevention

95
Q

When are large VSD surgically repaired

A

Medical management fails

Signs of pHTN at

96
Q

When is endocarditis ppx indicated in VSD patients

A

If it was surgically repaired

97
Q

Common defect in pts with abstains anomal

A

PFO with R – > L shunt. Also can have dilated RA giving increased risk of SVT and WPW

98
Q

Tx of Abstains anomaly

A

PGE
Digoxin
Diuresis
PRopranolol for SVT

99
Q

Next step in management of congenital heart disease with early cyanosis

A

PGE (keep it open!!!!)

100
Q

6 week old infant presents to meds ER for irritability and is found to have signs of left sided heart failure. An EKG is interpreted as a left sided MI. What is most likely dx?

A

Anomalous origin of Left coronary artery (from pulm rather than aorta)

101
Q

What class of meds is indicated in pts wit ha hereditary prolongation of QT interval in order to prevent v fib

A

Beta blockers

102
Q

Weak pulses in upper extremities – which vasculitis?

A

Takayasu

103
Q

Which vasculitis has necrotizing granulomas of lung and necrotizing GN

A

WEgeners

104
Q

Which vasculitis has necrotizing immune complex inflammation of visceral and renal vessels

A

Poly arteritis nodosa

105
Q

Which vasculitis is the most common

A

Temporal arteritis

106
Q

Which vasculitis is associated with Hep B

A

Polyarteritis nodosa

107
Q

Which vasculitis a/w perf of nasal septum

A

Wegeners

108
Q

Defects that comprise ToF

A

Overriding aorta
Pulm stenosis
VSD
RVH

109
Q

What are classic findings of HSP?

A 
Recent uri
Abdominal pain
Arthritis
Renal disease
LE purpura
110
Q

Persistent ST elevations in anterior leads 5 weeks after an MI

A

Ventricular aneurysm

111
Q

Tx of Prinzmetal angina

A

CCB, nitrates.

112
Q

Contraindicated in prinzmetals angina

A

Beta blockers (non selective) because of unopposed alpha receptor vasoconstriction which can worsen sx cause death.

113
Q

When should you consider 2 drug therapy in hypertension

A

When BP is more than 20/10 mmHg above goal.

114
Q

Goal BP in pts >60

A
115
Q

Combo therapy of choice in htn

A

ACE/ARB in concert with long acting dihydropyridine CCB.

ACE/ARB + diuretic can also be used but may be less beneficial.

116
Q

Initial mono therapy for HTN in blacks

A

Thiazide or long acting CCB

117
Q

Initial mono therapy in pts who have diabetic nephropathy or non diabetic CKD and proteinuria with HTN

A

ACE or ARB

118
Q

Initial mono therapy in pt with ischemic heart disease or CHF with decreased EF along with HTN

A

Beta blocker

119
Q

Goal BP in pts with diabetes or CKD without proteinuria

A
120
Q

Define proteinuria

A

> 500-1000 mg/day

121
Q

HbA1C diagnostic of DM

A

> 6.5%

122
Q

Goal HbA1C for diabetics

A

DIT STEP 2 (17 decks)

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