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cardio Flashcards

1
Q

normal murmur in children and pregnant women

A

s3

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2
Q

murmur ass. with increased filling pressures (HF, mitral reurg) and dilated ventricles, restrictive cardiomyopathy

A

s3

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3
Q

murmur with ventricular hypertrophy

A

s4

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4
Q

which wave of JVP is absent in afib

A

a wave (atrial contraction). x wave (a, c, x goes down) absent in tricuspid regurg

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5
Q

pulmonic stenosis, RBBB

A

wide split

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6
Q

ASD (left to right shunt). regardless of breath

A

fixed split

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7
Q

sortic stenosis, LBBB, paradoxical split. on inspiration, p2 and a2 are closer so inspiration paradoxically eliminates the split

A

paradoxical split

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8
Q

Continuous murmur at left infraclavicular region

A

PDA

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9
Q

systolic murmur at LSB

A

Hypertrophic Cardiomyopathy

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10
Q

baroreceptor firing rate

A

mimics BP. So ANS is checking out the baroreceptor, when the baroreceptor firing rate decreases the ANS knows the BP is also decreased

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11
Q

lack of aorticopulmonary septum formation (problem of neural crest cells)

A

Truncus arteriosus

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12
Q

separation of systemic and pulmonic circulation, not compatible with life without shunt

A

Transposition of great vessels

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13
Q

failure of aorticopulmonary septum to spiral

A

transpotion of great vessels

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14
Q

displacement of the infundibular septum

A

tetrology of fallot

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15
Q

tetrology of fallot

A
  1. Pulmonary stenosis (prognostic)
  2. RVH
  3. Overriding aorta
  4. VSD
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16
Q

why do you squat during tet spell

A

Increases systemic vascular resistance, which decreases the normal R–>L shunt and improves cyanosis (get more blood to go to lungs)

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17
Q

frequency of l-r shunts

A

VSD> ASD>PDA: blue kids use VAP’s

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18
Q

congenital heart disease: babies/kids cyanosis

A

R->L Shunts = 5 T’s. Blue babies drink from TiTTies

L->R Shunts = VSD>ASD>PDA. Blue kids hit the VAP

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19
Q

ASD vs PFO

both can cause paradoxical emboli (venous to systemic)

A

ASD: Septa are missing tissue (i.e. ostium primum defect)
Patent Foramen Ovale: failure of ostium primum and secundum to fuse

PFO is a problem of fusion

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20
Q

PFO is a _______ __ ________

A

PFO is a problem of fusion

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21
Q

PDA can be caused by (2)

A

Congenital Rubella
Neonatal Respiratory Distress Syndrome (surfactant deficiency–>alveolar collapse–>low 02)(risk increased with prematurity, maternal diabetes, c-section)

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22
Q

PDA/eseinmenger clinical manifestation

A

Lower Extremity cyanosis

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23
Q

Turner syndrome cardiac manifestations

A

Bicuspid aortic valve

coarctation of the aorta

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24
Q

HTN in upper extremities, delayed pulse in LE (brachial-femoral delay)

A

Coarctation of the aorta

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25
Q

notched appearance on CXR

A

Coarctation of the aorta

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26
Q

maternal diabetes cardiac manifestation

A

Transposition of the great vessels

indirectly to PDA because ass. with NRDS

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27
Q

Fetal alcohol syndrome congenital defects

A

All 3 VAP
Tetralogy of fallot

So it took mom 4 drinks and a VAP to give her baby FAS. Tetra + VAP

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28
Q

Marfan syndrome cardiac manifestations

A

MVP
Thoracic Aortic Aneurysm
Cystic medial necrosis of aorta: Aortic regurg and Aortic dissection

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29
Q

ebstein anomaly

A

lithium exposure (Bipolar patient)

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30
Q

22q11 (aka DiGeorge)

A

Tetralogy of Fallot, Truncus Arteriosus, Transposition of great vessels

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31
Q

string of beads appearance, HTN in 20-30 year old caucasian chick

A

Fibromuscular dysplasia

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32
Q

which organ is spared in Polyarteritis nodosa

A

LUNGS BETA. No PAN in the PULM

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33
Q

Hypertensive emergency

A

get acute end-organ damage: Papilledema, Encephalopathy, retinal hemorrhages, etc

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34
Q

HTN predisposes to:

A

afib, CAD, LVH, aortic dissection/aneurysm, CKD

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35
Q

Hyperlipidemia sings (3)

A

Xanthoma
Tendinous xanthoma (achilles)
Corneal arcus

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36
Q

thickening of wall via smooth muscle hyperplasia

A

Onion skin apperance –> Hyperplastic arteriolosclerosis

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37
Q

3 types of arteriosclerosis

A

Atherosclerosis (Intima of medium/large. cholesterol plaques)
Arteriolosclerosis (small arterioles.hyaline/hyperplastic)
Monckeberg (Media)

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38
Q

vascular stiffening without obstruction (intima not involved)

A

Monckeberg (medial calcific sclerosis)

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39
Q

Arteriosclerosis caused by buildup of cholesterol plaques

A

Atherosclerosis

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40
Q

who is most likely to get atherosclerosis

A

Men and Postmenopausal women

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41
Q

first step of atherosclerosis

A

Endothelial cell dysfunction.

increased endothelial cell permeability = LDL cholesterol into intima = phagocytosis by MQ = foam cell and VSMC from media to intima (these are all “initial step”)

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42
Q

what promotes migration of smooth muscles from media to intima and SMC proliferation?

A

PDGF and FGF

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43
Q

Obliterative endarteritis of the vaso vasorum

A

Tertiary Syphilis

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44
Q

diastolic decrescendo murmur

A

Aortic Regurg.

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45
Q

Aortic Regurg + mediastinal widening

A

Aortic Aneurysm

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46
Q

intimal tear vs intimal streak

A

tear: Aortic dissection
streak: atherosclerosis

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47
Q

Presentation of aortic aneurysm

A

lower back/abdominal pain. Abdominal AA presents as pulsatile abdominal mass

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48
Q

pathology: AAA vs Thoracic AA

A

Abdominal: transmural inflam
Thoracic: cystic medial degeneration

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49
Q

unequal BP in arms + severe pain

A

Aortic dissection (intimal tear)

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50
Q

CXR of aortic dissection

A

mediastinal widerning

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51
Q

arteries involved in atherosclerosis

A

ABDOMINAL Aorta> coronary artery>popliteal artery>carotid

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52
Q

marfan and ehlers danlos

A

cystic medial necrosis (media)

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53
Q

known triggers of Prinzmetal angina

A

Tobacco, cocaine, triptans

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54
Q

tx of prinzmetal

A

Ca channel blocker, nitrate, smoking cessation

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55
Q

t-wave inversion but no cardiac biomarker elevation

A

Unstable angina (nstemi would show increase biomarkers)

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56
Q

coronary steal

A

administation of dypridamole or adenosine aka vasodilators will make existing ischemia worse, helps detect ischemic coronary artery perfusion

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57
Q

common occluded coronary arteries (MI)

A

LAD> RCA>circumflex

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58
Q

MI presentation

A 
diaphoresis
nausea/vomiting
severe retrosternal pain
crushing pain in left arm/jaw
shortness of breath 
fatigue
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59
Q

postinfarction fibrinous pericarditis

A

1-3 days post MI

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60
Q

Dressler syndrome

A

autoimmune polyserositis aka fibrinous pericarditis. Weeks post MI

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61
Q

risk of free wall rupture –>tamponade

or papillary muscle rupture –> mitral regurg

A

3-14 days. macrophages are eating away at the tissue and cause weakness

62
Q

troponin and CK-MB

A

Troponin goes on a long trip…elevated a week/10 days, but is specific

CK-MB good for reinfarcation because back to normal after 48 hours. CK-MB is normal after 1-2 days.

63
Q

V1-V6

A

LAD (anterior)

64
Q

I, aVL

A

LCX (lateral)

65
Q

II, III, aVF

A

RCA (inFerior)

66
Q

which ions buildup intracellular post-MI?

A

Na and Ca. Ischemia = decreased ATP/anaerobic metab = decreased Na/K pump and SR Ca ATPase = increase Na and Ca intracellulary

67
Q

for a stemi, _______therapy is most important

A

Reperfusion therapy

percuratenous coronary intervention >fibrinolysis

68
Q

most common cardiomyopathy

69
Q

cardiomyopathy with systolic dysfunction

70
Q

conditions that cause DCM

A 
Alcohol
Beriberi (wet)
Coxsackie B myocarditis
Cocaine
Chagas 
Doxorubicin
Sarcoidosis 
Hemochromatosis and peripartum

ABCCCD’S

71
Q

sudden death in young athlete

72
Q

cardiomyopathy ass. with Friedreich ataxia

73
Q

VSD vs ASD murmur

A 
VSD = holosystolic
ASD = FIXED SPLITTING
74
Q

diastolic dysf(x)

75
Q

sarcoidosis

A

+systolic dysfunction = DCM

+diastolic dysfunction = RCM

76
Q

Endomyocardial fibrosis with a prominent eosinophilic infiltrate

A

Loffler syndrome (restrictive cardiomyopathy)

77
Q

Endocarditis

A

Culture neg = coxiella, bartonella, HACEK (H flu, Actinobacillus, Cardiobacterium, Eikenella, Kingella)

78
Q

Aschoff bodies

A

Rheumatic fever (granuloma with giant cells)

79
Q

Anitschkow cells

A

RF (enlarged macrogphages with ovoid, wavy, rod lke nucleus)

80
Q

equilibriation of diastolic pressure in all 4 chambers of heart

A

Cardiac tamponade

81
Q

Beck triad: hypotension, distended neck veins, distant heart sounds

A

cardiac tamponade

82
Q

define pulsus paradoxus

A

decrease in systolic BP by at least 10 mmHg during inspiration

83
Q

conditions associated with pulsus paradoxus

A

Asthma, cardiac tamponade, OSA, pericarditis, croup

84
Q

most frequent cardiac tumor in children

A

rhabdomyoma –> ass. with tuberous sclerosis

85
Q

Kussmaul sign

A

increase in JVP on inspiration instead of normal decrease. impaired flow through RV. restrictive cardiomyopathy/tumor

86
Q

Define diastolic HF

A

normal ejection fraction AND LV-EDV in the setting of increased LV-EDP

87
Q

erythrocytosis

A

Relative (dehydration; normal rbc mass) vs absolute (increased rbc mass)

Primary (low EPO) vs secondary (high EPO i.e. high altitude)

88
Q

path of Malignant Hypertension

A

Hyperplastic arteriolosclerosis + Fibrinoid Necrosis (localized destruction of vascular wall with circumferential ring of pink)

89
Q

Define hyaline arteriolosclerosis

A

deposition of eosinophilic hyaline material (PAS +) in the intima and media of small vessels

90
Q

insoluble pigment of aging

A

Lipofuscin: seen in heart/liver of aging people. yellow brown polypeptide. result of free radical injury and lipid peroxidation.

91
Q

meds causing orthostatic hypotension

A

alpha1 antagonists (zosins i.e. used for BPH), diuretic

92
Q

pulsatile mass with thrill on palpation; bruit on ausc.

A

av fistula

93
Q

mitral stenosis most likely cause

A

Rheumatic fever (99% of cases)

94
Q

Does BNP contribute to worsening HF?

A

No, it is released to alleviate HF by causing vasodilation, diuresis/natriuerisis, and dec. BP

95
Q

what physiological response can exacerbate HF?

A

SNS/RAAS: increased afterload (excessive vasoconstriction), excess fluid retention, deleterious cardiac remodeling (from increased preload and afterload,

96
Q

features of constrictive pericarditis

A

increased JVP
Kussmaul sign
Pulsus Paradoxus
Pericardial knock

97
Q

Define Kussmaul sign

A

Normally, inspiration causes JVP to drop

Kussmaul = paradoxical rise in JVP during inspiration

–>due to RV is volume-restricted (constrictive pericarditis) is unable to accomodate the inspiratory increase in venous return

98
Q

thick fibrous tissue in the pericardial space (restricting)

A

Pericarditis

99
Q

Causes of Pericarditis

A 
Idiopathic (usually viral)
Coxsackie virus
Autoimmune (SLE, Rheumatoid arthritis)
Uremia
Acute STEMI (post-infarction pericarditis day 1-3) or Dressler
Radiation
100
Q

Sharp pain, aggravated by inspiration. relieved by sitting forward

A

Pericarditis

101
Q

sudden deceleration of incoming blood as ventricle reaches its elastic limit

102
Q

sharper sound heard earlier in diastole than an S3

A

pericardial knock (ventricular compliance reduced due to external force)

103
Q

vfib in 20-30 year old

104
Q

severe MR

A

presence of an S3 (worst prognostic marker)

105
Q

blunting of costophrenic angle

A

acute decompensated heart failure

106
Q

Diuretics vs ACE-I: Which reduces mortality

A

ACE-I my niggAAA. ACE-I and ARB in all HF pt to increase survival
Diuretics only provide symptomatic relief.

107
Q

pain in the jaw after eating/chewing

A

Jaw Claudication –> Giant Cell aka Temporal Arteritis

108
Q

weak UE pulses (+arthritis, myalgias)

A

Takasayu Arteritis

109
Q

Granulomatous thickening of Aortic Arch

A

Takasayu Arteritis

110
Q

Vasculitis with granulomatous inflammation

A

Temporal(giant cell) Arteritis (age >50) and Takasayu (female

111
Q

segmental transumural inflammation with __________ = __________ (vascultis)

A

with Fibrinoid Necrosis = Polyarteritis nodosa

112
Q

Hepatitis B seropositivity + vasculitis

A

Polyarteritis nodosa

113
Q

3 clinical sx (constitutional) of SLE

A

Fever, weight loss, fatigue

114
Q

serositis (pleurisy, pericarditis, peritonitis)

A

ass. with SLE

115
Q

severe chest pain that radiates to the shoulders/neck. increases on inspiration

A

Pericarditis

116
Q

half life of a drug

A

(Volume of distribution x 0.7)/ Clearance

117
Q

maintenance dose

A

Steady-state plasma conc x Clearance (and tally up units)

decreased in renal/liver failure pt

118
Q

loading dose

A

Volume of distribution x Steady-state plasma conc

unchanged in liver/renal failure pt

119
Q

when you see a pt taking a sildenafil etc PDE inhibitor for Erectile dysfunction, what do you have to avoid?

A

Nitrates.

If you see nitrates in the question, think PDE inhibitor. keep them linked, they do NOT get prescribed together.

120
Q

severe chest pain that doesn’t respond to aspirin or nitroglycerin

121
Q

first ECG signs of transmural MI

A

First sign = PEAKED T WAVE. (due to hyperkalemia)

ST elevation follows w/in minutes to hours

122
Q

widened/prolonged QRS interval tx

A

Sodium Bicarbonate.

i.e. TCA OD can look like anticholinergic toxicity + QRS widening/arrythmia

123
Q

dont confuse Widened Pulse Pressure with Pulsus Paradoxus

A

Widened: Aortic Regurg

Pulsus Paradoxus: Cardiac tamponade etc. A fall in systolic BP upon inspiration

124
Q

Angiosarcoma i.e. lymphangiosarcoma

A

ass. with radiation/mastectomy

Hepatic angiosarcoma specifically ass. with arsenic/vinyl chloride

125
Q

what are the 4 T’s of DiGeorge syndrome:

A

Thymic aplasia
Tetralogy of Fallot
Truncus arteriosus
Transposition of the great vessels

126
Q

congenital AV septal defect

A

Down syndrome

127
Q

loud S1, opening snap + late diastolic rumble

A

Mitral stenosis (99% of the time caused by RF)

128
Q

Complications of Mitral stenosis

A

can lead to RA enlargement –> afib or mural thrombi

129
Q

Patient with a known DVT develops a stroke or MI (“cerebrovascular event”) is suspicious for?

A

Paradoxical emboli basically…so probably has an ASD or a PFO.

–>ASD murmur = fixed s2 (does not change with respiration)

130
Q

Ejection murmur that increases with standing
vs
Ejection murmur that decreases with standing

A

So standing = decreased venous return

So in HCM, increased preload actually helps push away the septum from LVOT –> So STANDING INCREASES EJECTION MURMUR OF HCM

131
Q

Stabbing/sharp chest pain thats worse with inspiration

A

Pulmonary/Pleuritic
Pericarditis: worse when lying flat
PE/Pneumothorax: Resp distress/hypoxia

132
Q

2 histological features of HCM

A
  1. Massive hypertrophy of septal region

2. Myofiber disarray (wavepool like)

133
Q

Is nonbacterial endocarditis solely due to SLE/antiphospholipid?

A

NO. These two do cause it, but its really primarily associated with Advanced MALIGNANCY, or hypercoaguble state or lupus

134
Q

Culture negative bacterial endocarditis

A

Coxiella, Bartonella, or HACEK

Haemophilus 
Actinobacillus 
Cardiobacterium
Eikenella 
Kingella
135
Q

Post MI: Pericardial Inflammation overlying the necrotic segment of myocardium
vs
Pericardial inflam due to autoimmune rxn to necrotic tissue

A

Early onset fibrinous pericarditis
(first few days afterwards, and resolved within few more days with aspirin therapy)

Dresslers (a week-month later. also responds to nsaids/steroids)

136
Q

Pericardial inflammation due to viral infection

A

Viral pericarditis POST URI usually

137
Q

Rheumatic fever effect on Mitral valve

A

Initially, MR (younger patient, 20-30s)

Older, MS (middle aged)

138
Q

Heart contractility: effects of sodium and of digitalis?

A

Increased contractility with decreased Na+ (extracellulary) –> decreased activity of Na/Ca exchanger

Digitalis blocks Na/K pump = increased intracellular (thus decreased extracellular Na) = decreased Na/ Ca exchanger = Increased Ca intracelular
(so both Na and Ca higher inside)

139
Q

Effects of low O2/high CO2 (hypoxia and hypercapnia) on Contractility? also, acidosis

A

these all decrease Contractility (and thus SV)

140
Q

Nitroglycerin

A

VENOdilator = decrease prEload

141
Q

ACE-I and ARB

A

Decrease both Preload and Afterload

142
Q

Fever + New Murmur

A

INFECTIOUS ENDOCARDITIS

143
Q

Predisposes to IE

A

Valvular abnormalities: RF, MVP, Prosthetic valve, congenital heart disease

Bacteremia: IVDU, Dental procedure

144
Q

Staph aureus, Strep viridans, Staph epidermidis and IE

(these bugs will adhere to platelet-fibrin deposits on the abnormal valve)

(vs Rheumatic Fever is from Strep Pyo aka GAS duh)

A

Staph Aureus: ACUTE endocarditis –> large vegetations on previously normal valves, Rapid onset

Strep Virdans: SUBACUTE –> small vegetations on diseased/congenitally abnormal valves. Post-dental procedure. Gradual onset

Staph epidermidis: Prosthetic valves

145
Q

IE (FROMJANE)

A 
FEVER
Roth Spots (round white on retina)
Osler nodes (OUCH, painful)
Murmur (New)
Janeway lesions (J-entle. palms/soles, microemboli)
Anemia
Nail-bed hemorrhage (SPLINTER)
Emboli
146
Q

Early and late conseq of RF

A

Early: Mitral Regurg
Late: Mitral Stenosis

147
Q

Aschof bodies

A

RF: Granuloma with giant cells. contain anitschkow cells (macrophage with ovoid/wavy nucleus)

148
Q

What type of hypersensitivity is RF?

A

Type 2 (Immune mediated): Antibodies to M protein cross-react with self antigen

149
Q

Is Rheumatic Fever a direct effect of bacteria?

A

NO, its IMMUNE MEDIATED BRUH

150
Q

Tx/prophylaxis for Rheumatic Fever

A

PENICILLIN PENICILLIN PENICILLIN
PENICILLIN PENICILLIN
PeNiCiLLiN

151
Q

JONES (RF)

A 
Joints (mgratory polyarthritis)
O - Endocarditis
Nodules in skin 
Erythema marginatum 
Sydenhams chorea

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