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Congenital heart defects Flashcards

1
Q

22q11

A

truncus, tetralogy

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2
Q

Down’s

A

ASD/VSD/endocardial cushion defect

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3
Q

Turner

A

Coarctation of the aorta (infantile, pre-ductal)

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4
Q

Marfan’s

A

Aortic insufficiency/dissection.

  • -Weak connective tissue (fibrillin)
  • -So aorta dilates and the media of the vessel splits because of weakness in the wall!
  • -WEAK VESSELS
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5
Q

Diabetic mom

A

Transposition of Great vessels

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6
Q

Bulbus cordis

A

Smooth L and R ventricles

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7
Q

Primitive atria

A

Trabeculated L and R atria

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8
Q

Left horn of sinus venosus

A

coronary sinus

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9
Q

Right horn of sinus venosus

A

Smooth part of right atrium

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10
Q

Right common cardinal vein and right anterior cardinal vein

A

SVC

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11
Q

Smooth L and R ventricles

A

Bulbus cordis

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12
Q

Trabeculated L and R atria

A

Primitive atria

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13
Q

Coronary sinus

A

L horn of sinus venosus

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14
Q

Smooth part of right atrium

A

R horn of sinus venosus

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15
Q

SVC

A

R common cardinal and R anterior cardinal veins

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16
Q

erythopoiesis occurs in yolk sac during which weeks?

A

3-10 weeks

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17
Q

Erythropoiesis of the liver?

A

6 weeks-birth

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18
Q

Eryropoiesis of the spleen?

A

15-30 weeks

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19
Q

Erythropoiesis of the bone marrow?

A

22 weeks to adult

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20
Q

Major source of RBC at 25 weeks

A

Liver

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21
Q

Major source of RBCs at birth

A

Bone marrow

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22
Q

Major source of RBC at 7 weeks

A

Yolk sac

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23
Q

Which organs make RBCs at 25 weeks?

A

Liver, spleen and bone

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24
Q

Which organs make RBCs at 32 weeks?

A

Liver and bone

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25
Q

Ductus venosum

A

ligamentum venosum

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26
Q

Umbilical vein

A

ligamentum teres

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27
Q

Umbilical arteries

A

medial umbilical ligaments

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28
Q

Allantois

A

MEDIAN umbilical ligament

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29
Q

what conditions have pulsus paradoxus as a finding?

A

cardiac tamponade
pericarditis
asthma
sleep apnes

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30
Q

What are the sx of a cardiac tamponade?

A
  1. mechanism: blood accumulates in pericardial sac

signs/symptoms: pulsus paradoxus (systolic blood pressure decreases > 10 mmHg during inspiration)

signs/symptoms: triad of hypotension, increased JVP, muffled heart sounds

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31
Q

Causes of serous pericardidits

A

Autoimmune disorder

Viral pericarditis

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32
Q

What else can cause an aortic dissection aside from marfans?

A

bicuspid aortic valve and hypertension

–Presents as sudden chest pain radiating to the back

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33
Q

What are the class IA antiarrythmics?

A

Disopyramide
Quinidine
Procainamide

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34
Q

How do class IA antiarrythmics work?

A

INCREASE AP duration and increase QT interval

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35
Q

What do you use Class IA for?

A

re-entrant/ectopic supraventricular tachycardia

Ventricular tachycardia

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36
Q

What are the side effects in general of class IA?

A

thrombocytopenia, Torsades from long QT

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37
Q

What is the side effect of quinidine?

A

headache/tinnitus

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38
Q

What is the side effect of procainamide?

A

SLE syndrome

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39
Q

What is the side effect of disopyramide?

A

heart failure

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40
Q

What are the class IB antiarrhythmics?

A

Lidocaine
Mexiletine
Tocainamide

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41
Q

How do class IB work?

A

Decrease AP duration

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42
Q

When do you use class IB?

A

Post MI Ventricular Arrhythmias

Also in DIGOXIN toxicity

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43
Q

What is the side effect of class IB?

A

CNS stimulation/depression

CV depression

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44
Q

What are the class IC drugs?

A

Propafenone

Flecainide

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45
Q

How does class IC work?

A

No effect on AP duration

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46
Q

When do you use class IC?

A

As a last resort for ventricular tachycardias–>VF and SVT

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47
Q

When is class IC contraindicated?

A

post-MI or pts with structural heart disease

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48
Q

Toxicity of class IC?

A

Proarrhythmic

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49
Q

What are the class II antiarrhythmics?

A

Beta blockers

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50
Q

How do beta blockers work as an antiarrhytmic?

A

Decrease SA and AV nodal activity by decreasing cAMP and Ca currents

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51
Q

When would you use a beta blocker?

A

Vtach
SVT
ALSO Afib and Aflutter

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52
Q

What are the side effects of beta blockers?

A
  1. Impotence
  2. sedation/fatigue
  3. Metoprolol causes dyslipidemia
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53
Q

Who is contraindicated for a beta blocker?

A
  1. ASTHMATICS–do not use a nonselective beta blocker
  2. Also, MASKS hypoglycemia signs! Be careful with DIABETICS
  3. Propranolol worsens prinzmetal’s angina
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54
Q

What are the class III antiarrhythmics?

A

K+ channel blockers

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55
Q

How do class III drugs work?

A

Increase AP duration and QT and ERP

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56
Q

When do you use Class III

A

As a last resort

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57
Q

What are the toxicities of class III?

A

Sotalol: torsades
Ibutilide: torsades
Amiodarone: pulmonary fibrosis, Thyroid issues, hepatotoxicity, photodermatitis

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58
Q

What do you need to get labs on before giving amiodarone?

A

LFTs and PFTs and TFTs!!

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59
Q

Name the class III antiarrhythmics

A

Amiodarone
Ibutilide
Dofetilide
Sotalol

AIDS MNEMONIC

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60
Q

What are the class IV drugs?

A

calcium channel blockers verapamil and diltiazem

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61
Q

When do you use class IV drug?

A

SVT (nodal arrhtymias)

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62
Q

What are the side effects of class IV drugs?

A

Constipation, flushing, edema, CV effects

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63
Q

What are other antiarrhythmics?

A

Adenosine

Mg2+

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64
Q

What is the drug of choice in SVT?

A

Adenosine

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65
Q

How does adenosine work?

A

Increase K efflux out of cell, hyperpolarizing it and decreasing calcium influx

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66
Q

What are adenosine side effects

A

flushing, hypotension, chest pain.

effects blocked by theophylline and caffeine

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67
Q

When do you use mg?

A

torsade de pointes and digoxin toxicity

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68
Q

How can you treat digoxin toxicity?

A

Magnesium or Class IB antiarrhythmics (Lidocaine, tocainamide, Mexiletine)

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69
Q

What do veno/vasodilators do to preload and afterload?

A

Venodilators decrease preload

Vasodilators decrease afterload

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70
Q

Does viscosity of blood increase or decrease in anemia?

A

Decreases

–Fewer RBCs, more water in the blood

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71
Q

JVP A wave

A

atrial contraction

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72
Q

JVP c wave

A

RV contraction

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73
Q

JVP x descent

A

atrial relaxation

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74
Q

JVP v wave

A

Increased right atrial pressure with filling

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75
Q

JVP y descent

A

Flow of blood from RA to RV

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76
Q

When do you see wide splitting?

A

Pulmonic stenosis

RBBB

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77
Q

When do you see paradoxical splitting?

A

Aortic stenosis

LBBB

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78
Q

Which sound comes first in physiologically split S2?

A

A2 then P2 (aortic then pulmonic)

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79
Q

Most murmurs increase with hand grip. What are the exceptions?

A

AS and HOCM

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80
Q

Most murmurs decrease with valsalva (decrease venous return). What are the exceptions?

A

MVP and HOCM murmurs increase

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81
Q

What will rapid squatting do? Which murmurs are affected?

A

Rapid squatting increases venous return. After some time, afterload increases too
–MVP and HOCM murmurs decrease

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82
Q

How do you increase MVP and HOCM murmurs?

A

Valsalva

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83
Q

How do you decrease MVP and HOCM murmurs?

A

Squatting

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84
Q

What do you hear at the aortic area?

A

Aortic stenosis

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85
Q

What do you hear at the left sternal border?

A

Aortic regurg
pulmonic regurg
HOCM

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86
Q

What do you hear at the pulmonic area?

A

Pulmonic stenosus, PDA

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87
Q

What do you hear at the tricuspid area?

A

VSD, ASD, Tricuspid regurg/stenosis

88
Q

What do you hear at the mitral area?

A

Mitral regurg and stenosis

89
Q

You hear a holosystolic high pitched murmur at the apex which radiates to the axilla

A

Mitral regurg

90
Q

Holosystolic high pitched murmur at tricuspid area extending to right sternal border

A

tricuspid regurg

91
Q

Symptoms of aortic stenosis

A

SAD: syncope, angina, dyspnea on exertion

92
Q

Holosystolic harsh sounding murmur at tricuspid area

A

VSD

93
Q

Midsystolic click folowed by crescendo murmur. Heard best over apex

A

MVP

94
Q

Blowing diastolic decrescendo murmur

A

Aortic regurg

95
Q

What are the other signs of aortic regurg?

A

bounding pulses and head bobbing

96
Q

You hear an opening snap in diastole followed by a rumbling diastolic murmur

A

Mitral stenosis

97
Q

What is a common cause of PDA?

A

congenital rubella

98
Q

What are the causes of sensorineural deafness with congenital torsades?

A

Jervell and lange-nielsen syndrome

99
Q

How does ANP work its magic?

A

Decreases Na resorption
Constricts efferent renal arterioles
Dilates afferent arterioles

100
Q

What’s the difference between peripheral and central chemoreceptors?

A

Peripheral receptors respond to O2 < 60, but central chemoreceptors do not

101
Q

What factors are important for autoreguation of the heart?

A

Adenosine
NO
CO2 all dilate the heart’s vessels.

102
Q

You see a cyanotic baby with a boot shaped heart

A

tetralogy of fallot

103
Q

How do pts with Tetralogy of fallot alleviate their symptoms?

A

By squatting to increase PVR and decrease Right to Left shunting (cyanosis)

104
Q

What causes adult type coarcatation of aorta?

A

Bicuspid aortic valve. Will present with HTN in upper extremities, weak pulses, and notching of the ribs.

105
Q

Pipestem arteries

A

Monckeberg arteriosclerosis

106
Q

onion skinning arteriolosclerosis

A

Malignant hypertension

107
Q

How does PDA present as?

A

Cyanosis in the lower extremities

108
Q

EKG shows I and aVL Q waves

A

Lateral wall infarction

109
Q

When are you at greatest risk for ventricular aneurysm formation?

A

1 week post MI

110
Q

When ar eyou at greatest risk for ventricular free wall rupture?

A

3-14 days

111
Q

What are the causes of dilated cardiomyopathy?

A 
ABCCCD
Alcohol
Beriberi
Coxsackie B
Chronic cocaine
Chagas
Doxorubicin
112
Q

How do you treat dilated vs hypertrophic cardiomyopathy?

A

Dilated: ACE, diuretics, transplant
Hypertrophic: Beta blocker, NON DIHYDROPYRIDINE calcium channel blocker

113
Q

You see endomyocardial fibrosis with a prominent eosinophilic infiltrate

A

Loffler’s syndrome, a type of restrictive cardiomyopathy

114
Q

What are the main causes of restrictive (fibrotic) cardiomyopathy?

A

sarcoidosis, hemachromatosis, loffler’s,

115
Q

Which drugs reduce mortality in CHF?

A

Beta blocker, ACEI, and spironolactone. Sometimes hydralazine

everything else is symptomatic, including other diuretics.

116
Q

Nutmeg liver:

A

Right heart failure resulting in hepatomegaly

117
Q

What are the symptoms of rheumatic fever?

A 
Fever
Erythema marginatum
Valvular damage
ESR
Red-hot joints
Subcutaneous nodules
Sydenham's chorea
118
Q

Which valves are most often affected in rheumatic fever?

A

Mitral>aortic»tricuspid (high pressure valves)

119
Q

Histological findings of rheumatic fever

A

Schoff bodies and anitschkow’s cells with ASO titer elevation.

120
Q

What type of hypersensitivity is rheumatic fever?

A

Type II hypersensitivity with antibodies to M protein

121
Q

Symptoms of pericarditis

A

Sharp pleuritic pain relieved by sitting up and leaning forward with a friction rub. Widespread ST elevation

122
Q

What are the symptoms of cardiac tamponade

A

Hypotension, diminished heart sounds, friction rub

PULSUS PARADOXUS

123
Q

treebark aorta and calcifications of the aortic root

A

syphilitic heart disease

124
Q

Kussmaul’s sign

A

Increase in JVP on inspiration instead of a decrease. Seen in constrictive pericarditis, cardiac tamponade

125
Q

What is the most common heart tumor?

A

A metastasis
In children: rhabdomyoma
In adult: myxoma

126
Q

Resistance equals to

A

Delta P/Q (flow)

=(8n x l)/(pi*r^4)

127
Q

Strawberry hemangioma

A

benign capillary hemangioma of infancy that regresses at age 5-8

128
Q

Cherry hemangioma

A

Benign capillary hemangioma of the elderly that does not regress

129
Q

cystic hygroma

A

cavernous lymphangioma of neck

130
Q

What is cystic hygroma associated with?

A

Turner syndrome

131
Q

Pyogenic granuloma

A

Polypoid capillary hemangioma that ulcerates and bleeds. Associated with trauma/pregnancy

132
Q

Glomus tumor

A

Benign painful red-blue tumor under finger nails. FROM SMOOTH MUSCLE CELLS!!

133
Q

bacillary angiomatosis

A

Benign capillary skin papules caused by cartonella henselae

134
Q

What pts often get bacillary angiomatosis?

A

AIDS pts

135
Q

Angiosarcoma

A

Blood vessel malignancy

136
Q

What is angiosarcoma associated w/

A

breast cancer and hodgkins pts getting chemo

137
Q

Lymphangiosarcoma

A

Lymphatic malignancy associated with persistent lymphedema

138
Q

Sturge weber

A

port wine stain
Intracerebral AVM (leptomeningeal angiomatosis)
Seizures
early glaucoma

139
Q

Why don’t we use dihydropyridines (end in -dine) to treat angina?

A

do not treat angina because their powerful systemic vasodilator and pressure lowering effects can lead to reflex cardiac stimulation= increase myocardial oxygen demand.

140
Q

Which are the non dihydropyridine CCBs to treat angina? they have stronger selectivity for the heart muscle

A

verapamil»diltiazem
(V for ventricle)

Less of a systemic vasodilatory effect. These work more strongly on the HEART

141
Q

First line anti-HTN therapy for diabetics

A

ACEI or ARBS, then everything else.

142
Q

Which CCBs work stronger on the vascular smooth muscle?

A

amlodipine=nifedipine > diltiazem>verapamil

143
Q

How does hydralazine work?

A

Increase cGMP=smooth muscle relaxation. Vasodilation of arterioles more than veins

144
Q

Uses of hydralazine?

A

severe HTN, CHF

145
Q

In which population is hydralazine first line?

A

Pregnancy! with methyldopa

146
Q

What is hydralazine frequently prescribed with?

A

Beta blocker to prevent reflex tachycardia

147
Q

Nitroprusside

A

Direct release of CO causing increase in cGMP. Mostly a vasodilator

148
Q

toxicity of nitroprusside?

A

cyanide toxicity

149
Q

Fenoldopam

A

Dopamine D1 agonist used for vasodilation to treat malignant hypertension

150
Q

How does nitroglycerin work?

A

Dilates veins&raquo_space; arteries, decreasing preload

151
Q

What are the problems with using nitrates?

A

Increase in contractility and heart rate from reflex response

152
Q

How do you solve the problem with nitrates?

A

Co-prescribe with beta blockers

153
Q

Side effects of HMG-CoA reductase

A

Hepatotoxicity and rhabdomyolysis

154
Q

effect of niacin

A

LDL decrease
HDL increase
–minor effect on triglycerides

155
Q

How does niacin work?

A

Inhibits lipolysis in adipose tissue

Reduces VLDL secretion

156
Q

Side effects of niacin?

A

flushing
Hyperglycemia
hyperuricemia

157
Q

How do you prevent flushing from niacin?

A

Give aspirin

158
Q

What are the effects of bile acid resins?

A

Decrease LDL

159
Q

How does ezetimibe work?

A

Decreases cholesterol reabsorption at the small intestine brush border

160
Q

What are the side effects of ezetimibe?

A

LFTs increase

diarrhea

161
Q

What are the side effects of fibrates?

A

myositis, hepatotoxicity, gallstones

162
Q

How do fibrates work?

A

upregulate LPL to increase triglyceride clearance

163
Q

What are the side effects of cardiac glycosides?

A

cholinergic toxicity + blurry yellow vision
EKG changes, with arrhythmias
Hyperkalemia

164
Q

Who is at risk for digoxin toxicity?

A

Renal failure
Hypokalemia
Quinidine

165
Q

What is the antidote for digoxin tox?

A 
Normalize K
Lidocaine
Cardiac pacer
Anti-dig Fab
Mg2+
166
Q

Treatment for malignant hypertension

A

Nitroprusside or fenoldopam which are both VASOdilators

167
Q

Does prinzmetal’s angina cause ST elevation or depression?

A

elevation

168
Q

You see wavy bands on biopsy of a pt’s heart: How long has it been since infarct?

A

4-12 hours

169
Q

You see a hyperemic border to a yellow section of heart. How long has it been since MI?

A

3-14 days

170
Q

You see contraction bands on a heart. How long has it been?

A

12-24 hours

171
Q

The infarcted heart tissue looks yellow

A

1-7 days (from WBC migration)

172
Q

What are the four modifiable risk factors for atherosclerosis?

A
  1. HTN
  2. Hypercholesterolemia
  3. Smoking
  4. Diabetes
173
Q

Who do you see kaposi’s sarcoma in?

A

Elderly european males
transplant pts
Aids pts

174
Q

Do kaposi’s lesions blanch?

A

No, a tumor of endothelial cells, not vascular lesions

175
Q

Angiosarcoma of the liver is associated with

A

PVC exposure

176
Q

Major side effect of ACE inhibitors

A

angioedema, with swelling of face can cause difficulty breathing.

  • ->From increased bradykinin levels
  • ->ACE usually breaks down bradykinin
177
Q

Which drugs reduce VLDL?

A

fibrates and nicotinic acid

178
Q

Venous return fxn of

A

peripheral resistance
blood volume
–>starling curve stays the same if the above do

179
Q

CO fxn of

A

SV x HR

180
Q

Abrupt standing maneuver is similar to

A

valsalva-ing (decrease Venous Return)

181
Q

passive leg raise maneuver is similar to

A

Squatting (increase preload)

182
Q

Severity of mitral regurg determined by

A

S3

183
Q

Most common cause of cor pulmonale

A

COPD

In 20-40 year old woman, can also be idiopathic pulmonary hypertension

184
Q

Common cause of sudden cardiac death in a young healthy person

A

Wolff Parkinson White syndrome

185
Q

Worrisome complication after coronary angioplasty

A

Embolization

  • ->Renalfailure
  • ->Livedo reticularis
186
Q

Causes of restrictive cardiomyopathy

A

sarcoidosis
amyloidosis
hemochromatosis
radiation therapy

187
Q

amylnitrite

A

vasodilation that decreases PVR–> should reduce most murmurs

188
Q

Systolic ejection murmur accentuated by standing

A

Hypertrophic obstructive cardiomyopathy

standing decreases VR, should decrease most murmurs EXCEPT MVP and HOCM

189
Q

Late diastolic decrescendo murmur decreased by amyl nitrite

A

aortic regurg

190
Q

Late diastolic murmur eliminated by atrial fibrillation

A

mitral/tricuspid stenosis

191
Q

Buerger’s disease

A

Smokers < 35 presenting with claudication with cold sensitivity and ulcerations.

192
Q

Granulomatous inflammation of the media

A

temporal arterities

193
Q

The five cyanotic heart disease are caused by a problem with

A

neural crest cell migration

194
Q

digoxin effect on Afib

A

increases parasympathetic tone, decreasing AV nodal conduction

195
Q

Amaurosis fugax

A

transient monocular vision loss from an embolus to the ophthalmic artery lasting a few seconds

196
Q

Which classes of antiarrhythmic class I have strong/weak sodium channel binding strength?

A

1C>1A>1B. Thus, 1C can promote arrhythmias. High use dependence, which means slow dissociation allows blocking effect to accumulate with time.

1B dissociates from sodium quickly, less likely for this effect to occur

197
Q

Sx henoch-schonlein

A

henoch-schonlein

GI pain, bleeding
IgA nephropathy
palpable purpura
Joint pain

198
Q

Coronary sinus lies within

A

atrioventricular groove

199
Q

Myocardial hibernation

A

Persistent low flow causes chronic reversible loss of contractile functioning

200
Q

Myocardial stunning

A

Brief ischemia causing a short trem reversible loss in contractility

201
Q

Signs of digoxin toxicity

A

Arrhythmias!!

-color vision alterations, GI sx and Neuro Sx

202
Q

Cause of varicose veins

A

impairment of venous valves and reflux of venous blood. Causes superficial venous thrombosis. Most commonly will cause ulcers over the medial malleolus

203
Q

What does a HOCM murmur sound like

A

systolic ejection murmur

204
Q

Most common site of injury of aorta in MVA

A

Aortic arch. heart and aorta decerate at different rates

205
Q

DiGeorge heart abnormality

A

Tetralogy of fallot

Interrupted aortic arch (extreme coarctation dx at birth)

206
Q

Friederich ataxia heart abnormality

A

HOCM

207
Q

Marfan heart abnormality

A

mitral valve prolapse

cystic medial necrosis

208
Q

Tuberous sclerosus heart abnormalities

A

rhabdomyomas causing valvular obstruction

209
Q

Turner syndrome heart abnormalities

A

bicuspid aortic valve

coarctation

210
Q

weight loss, fatigue
-mid diastolic rumble at apex
pedunculated mass

A

atrial myxoma, most common cardiac neoplasm

211
Q

myxoma histology

A

scattered cells in a mucopolysaccharide stroma

212
Q

QRS interval prelongation

A

bundle branch block

213
Q

absent P waves

A

atrial fibrillation

214
Q

Only P waves

A

Atrial flutter

215
Q

Class 1C mechanism antiarrhyth

A

Inhibit sodium channels in phase 0

  • -prolong QRS
  • -Use dependence–effect stronger with increased heart rate
216
Q

Class III antiarrhythmic mechanism

A

Blocks k repolarization, prolonging QT interval.

–Effect stronger at SLOWER heart rates

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