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UWORLD QuestionQuestions > Cardio > Flashcards

Cardio Flashcards

1
Q

AV fistula will cause what changes to TPR, CO, and venous return?

A

Deacrease TPR
Increase CO
Increase VR

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2
Q

Cardiac Abnormalities of Turner’s (3)

A

Coarctation of Aorta
Bicuspid Aortic Valve
Aortic Dissection in Adulthood

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3
Q

Name 3 Appetite Suppressants, and what can they cause

A

Secondary pulmonary hypertension

Fenfluramine, dexfluramine, Phentermine

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4
Q

First Line Atrial fibrillation? (2 types)

Second line?

A

CCB (diltiazem), Cardioselective B-Blockers

Digoxin

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5
Q

2 Mechanism of Digoxin?

A

1- Increase Contractility (block Na-K-ATPase on cardiac myocytes=> Incr. intracellular Ca2+)
2-Decr AV nodal conduction (Incr. Parasympathetic Tone)

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6
Q

What is a Blowing Holosystolic murmur best heard over Apex?

A

MVRegurg.

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7
Q

Janeway lesions are seen in what disease? What are they?

A

Bacterial Endocarditis.

-Microemboli fragments of infected intracardiac vegetations to cutaneous blood vessels

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8
Q

Describe pulsus paradoxus and what is it associated with (4)

A

decrease in systolic Blood pressure (10mmHg) w/ inspiration
IN acute cardiac tamponade, constrictive pericarditis, severe obstructive lung disease (ASTHMA) and restrictive cardiomyopathy

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9
Q

what receptor is activated for control of an Asthma exacerbation

A

b2 agonist => bronchial smooth m relaxation (via increased intracellular cAMP)

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10
Q

S4 (hypertesion related) is due to?

A

increased stiffness of left ventricular wall

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11
Q

Nitroglycerin dilates what portion of circulatory system? how does this treat angina

A

VENODILATES=> decr. preload

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12
Q

(which valve problems)
1-Aortic valve calcification?
2-Aortic Vlave infecive endocarditis?
3- Rheumatic aortic heart Disease

A

Aortic Stenosis
Aortic Regurg.
Combined Sten + regurg

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13
Q

Lidocaine (Class, specific for, replaced by)?

A

Class IB antiarrythmic
Ischemic myocardium (it binds rapidly deporalizing/depolarzed cells)
Amiodarone

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14
Q

Dystrophic Calcification

A

hallmark of preceding cell injury and necrosis- can occur after trauma.

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15
Q

Does coarctation of aorta cause cyanosis?

A

No. Not unless severe, if so pt dies without corrective surgery

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16
Q

What usually causes acute rheumatic fever? Timing?

A

Group A Strep. 10d-6weeks before hand.

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17
Q

What cells are typically found in rheumatic fever?

A

Aschoff giant cells within myocardium

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18
Q

More common myocarditis- bacterial or viral?

A

Bacterial-GAS rheumatic carditis

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19
Q

Sodium channel binding strength of class 1? (Prioritize class 1A1B1C)

A

1C>1A>1B. 1C most “use dependence”

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20
Q

Myocyte contraction begins with depolarization of which type of channel?

A

Voltage-dependent ca2+channel

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21
Q

How is calcium efflux prior to myocyte relaxation achieved?

A

Use of Ca2+-ATPase and Na+/Ca2+ exchange mechanism. Active process!

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22
Q

Does prolongation of phase 3 of the cardiac action potential increase the QT Interval?

A

Yes, prolong thre QT Interval of the EKG.

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23
Q

What portion of the EKG do b-blockers affect?
How about the cardiac conduction curve?
Do they change QRS complex?

A

Prolong the PR interval, decrease SA/AV Nodal activity.
Decrease phase four slope (not as prominent as PR changes).
No.

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24
Q

What is the major factor for forward (thru aortic valve) : regurgitant (back thru mitral valve) volume ratio?

A

LV Afterload. Increase in Afterload decreases ratio, decrease in Afterload increases the ratio.

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25
Q

What type of myopathy will amyloidosis cause?

What type of dysfunction will be seen?

A

Restrictive cardiomyopathy

Diastolic dysfunction.

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26
Q

What are causes of restrictive caardiomyopathies? At least 3

A

Amyloidosis
Sarcoidosis
Metastatic cancer
Products of inborn metabolic errors

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27
Q

How do b-blockers decrease blood pressure?

A

B1 receptors on renal juxtaglomerular cells blocks renin release which does not allow angiotensinogen to become angiotensin 1.
=>no AT 2, no Aldosterone release, no increase blood pressure.

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28
Q

Can b-blockers blunt circulating catecholamines?

A

No. They have no direct effect.

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29
Q

Combination of which 2 cardio drugs can cause Negative chronotropic effects? What are these effects?

A

Virapamil/diltiazem & bBlockers (metoprolol)

Severe bradycardia and hypotension.

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30
Q

Symptoms of acute mitral valve regurg v chronic MVR

A

Acute- pulmonary hypertension & pulmonary edema

Chronic- atrial fibrillation and mural thromboembolism

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31
Q

When is LV free wall rupture post-transmural MI most likely to occur?
What is “protective” against this?

A

3-7days after the onset of an MI

Previous MI, LV hypertrophy

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32
Q

What does strep. Viridians/ mutans require to form and endocarditis infection?

Is there another organism that can adhere to INTACT endothelium?

A

Preexisting endothelial damage leading to fibrin and platlet deposition/ aggregation.

Yes, staph. Aureus

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33
Q

Most serious complication of kawasakis?

A

Coronary artery aneurysms

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34
Q

Symptoms of kawasakis?

A 
Persistent fever
Bilateral conjunctivitis
Lymphadenopathy
Strawberry tongue/mouth
Peripheral rash that moves to trunk 
Peripheral edema and desquamation of fingertips.
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35
Q

Diastolic dysfunction seen in heart failure causes what changes to ventricular diastolic compliance and contractile performance?
What does this cause heart to do (technical terms)?
What is seen on PV curves?

A

Decrease compliance.

No change/ normal performance.

LEDP must increase to keep LEDV normal and EF is preserved as contractility does not change.
Bottom line of PV curve is elevated.

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36
Q

Brain/Atrial Natriuretic peptide des what to vasculature and water concentration and BloodPressure. Where is each sensed (brain/atrial)?

A

VasoDilates
Diuresis/Natriuresis
Decreasing Blood Pressure
ventricle/ Atrium

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37
Q

Increased Renal sympathetic nerve activity does what? What is are the cardiac effects? When might this be seen?

A

activates Renin-angiotensin-Ald system
Incr. BP
Heart Failure

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38
Q

When does fibrous/serofibrous pericarditis occur after a transmural Thrombosis? how often? SYMPTOMS?

A

2-4 days following thrombosis
10-20% of patients
Sharp/Pleuritic

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39
Q

what is Dressler’s syndrome?
time frame?
features?
% ?

A

Autoimmune polyserositis from exposed antigens post-MI => diffuse inflammation
1week-few month
Fever, pleuritis, leukocytosis, pericardial friction rub, Xray with pleural effusion

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40
Q

How long after total ischemia is cardiac contractility lost?
At which time-point does reversible contractile dysfuntion become IRREVERSIBLE?

A

60 Sec/ 1 Min

~ >30 Min

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41
Q

Where is decreased femoral:brachial BP ratio seen?

A

Congenital coarctation of aorta

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41
Q

what is direction blood flow in TOF @ the VSD? where is O2 drop seen?

A

usually R-> Left due to pulmonic stenosis.

O2 drop in LV

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41
Q

where do atherosclerotic plaques first develop in humans? (prioritize)

A

Large elastic arteries

Abdominal aorta>coronary aorta> poplitieal arteries>internal carotids> circle of willis

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41
Q

CO equation (Not HR x SV)

A

CO= O2 consumption/ Ateriovenous O2 difference

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41
Q

what is the most common congenital heart disease?

A

VSD

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41
Q

What kind of VSD would cause increase in RV SpO2, with no corresponding increase in RA? what murmur accompanies this?

A

a small VSD,

Holosystolic murmur heard best over left mid-sternal border

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41
Q

When is precordial continuous machine like murmur during systole/diastole seen?
Where is O2 change seen and what is it?

A

Patent Ductus Arteriosus

Pulmonary Artery SpO2 increase

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41
Q

bifid carotid pulse with brisk upstroke seen when?

A

hypertrophic obstructive cardiomyopathy

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41
Q

Most common cardiac primary tumor of heart?
Histological findings of this tumor?
Releases which Interlukin causing what symptoms

A

Myxomas
pedunculated mass, composed of scattered cells within a mucopolysaccaride stroma
IL-6=> constitutional (fevers, weight loss)

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41
Q

when is fixed wide splitting of S2 seen?

A

Atrial Septal Defect pts.

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41
Q

Heart sound of Mitral Stenosis?

A

Opening Snap @ beg. of diastole with low pitched diastolic rumble murmur heard best at apex

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41
Q

When is precordial continuous machine like murmur during systole/diastole seen?
Where is O2 change seen and what is it?

A

Patent Ductus Arteriosus

Pulmonary Artery SpO2 increase

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41
Q

Toxicities of Digoxin?
Treatments?
What to avoid?

A

Hyperkalemia (HYPOKALEMIA increases susceptibility to digoxin toxicity), Vfib/Vtach from AVnodal block ( incr. parasympathetics)

Management of Hyperkalemia w/ insulin etc, Digoxin specific Ab to bind dig in tissue/vascular space

Ca-gluconate

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41
Q

Ventricular Action Potential Phases correspond to what on EKG? exclude Phase 1

A

Phase 0- QRS
Phase 2- QT interval (+ phase 0- aka after QRS )
Phase 3- T wave (L&R V repolarization)
Phase 4- PR Interval (not exactly but changes can effect this interval)
pg 6-9 of becker physio

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41
Q

QT interval prolongation can be due to?

A

mutations to K+ currents through channel proteins.

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41
Q

second most common endocarditis organism in IV Drug users (1=Aureus)

A

P. Aeruginosa.

41
Q

what drug is used to prevent doxirubicin cardiomyopathy?

A

Dexrazoxane= iron chelating agent that decreases formation of oxygen free radicals

41
Q

What are Antracyclines and what are they associated with?

Name 4 or what they end in?

A

chemotherapeutic agents assoc. with cardiotox.

Daunorubicin, doxorubicin, epirubicin, idarubicin

41
Q

Process of doxirubicin toxicity?

A

(early) sweling of sarcoplasmic reticulum => loss of cardiomyocytes “myofibrillar dropout” => CHF symptoms

41
Q

Heart sound of Mitral Stenosis?

A

Opening Snap @ beg. of diastole with low pitched diastolic rumble murmur heard best at apex

41
Q

where do atherosclerotic plaques first develop in humans? (prioritize)

A

Large elastic arteries

Abdominal aorta>coronary aorta> poplitieal arteries>internal carotids> circle of willis

41
Q

Artery assoc. with ST seg Elevation in leads II, III, aVF and sinus node dysfunction

A

Right Coronary Artery

41
Q

what is the long term Rx of hypertension w/ CHF.

A

ACE inhibitors & B-blockers

41
Q

Most common cardiac primary tumor of heart?
Histological findings of this tumor?
Releases which Interlukin causing what symptoms

A

Myxomas
pedunculated mass, composed of scattered cells within a mucopolysaccaride stroma
IL-6=> constitutional (fevers, weight loss)

41
Q

Congenital Bicuspid Aorta will lead to what disorder and at what age?

A

Aortic Stenosis in patients 60’s

41
Q

CO equation (Not HR x SV)

A

CO= O2 consumption/ Ateriovenous O2 difference

67
Q

What is Non-Bacterial Thrombotic Endocarditis due to? another name?
What is it associated with?
what does this MOA resemble?

A

result of hypercoaguable state leading to vegetations of bland thrombus without inflammation or valve damage; MARANTIC ENDOCARDITIS.

Cancers- mucinous adenocarcinoma of pancreas, adenocarcinoma of lung

Tumor assoc. release of procoagulants IN migratory thrombophebitis= Trousseau Syndrome.

68
Q

Most common cause of death due to MI? when does this usually occur?

A 
Heart Failure (Ventricular Failure) 
2-10 days during in hospital phase
69
Q

What is the most common cause of death due to MI during pre-hospital phase? MOA?

A

Ventricular Fibrillation

Acute plaque change=> Acute myocardial ischemia => electrical instability=> lethal arrhythmia

70
Q

What finding confirms the severity of Mitral Valve Regurgitation?

A

s3 gallop = indicates high regurgitant volume (MVR)

71
Q

90% are cardiomyopathies are what type?
what percentage of these cardiomyopathies account for SCD?
Name 3

A

Dilated Cardiomyopathy
10-15%
Rheumatic Fever, SLE, polymositis

72
Q

Name 4-5 Restrictive Cardiomyopathies

A 
idiopathic/ Idiopathic Myocardial fibrosis
endomyocardial fibrosis
endocardial fibroelastosis
amyloidosis
hemochromatosis
73
Q

Amyloidosis of the cardiac atria is done by which type? (name the others if possible)-thyroid, pancreas, brain, pituitary, systemic)

A

Atrial Natriuretic peptide
Thryroid: calcitonin
pancreatic islets: islet amyloid protein (amylin)
Cerebrum/Cerebral blood vessels: B-amyloid
Pituitary: Prolactin
systemic: Immune globin light chains!!!

74
Q

Mechanism of ANP (Atrial Natriuretic Peptide) ?

Where + how it acts on each organ system (3) ?

A

ANP binds to NP-receptor on cell membranes
Activating guanylate cyclase and forming cyclicGMP

1) Kidney-dilates afferent arteriole=> INCR. GFR & excr. of sodium and water; DECR. Na+ reabsorption in Prox. Tubule/CT and inhibits renin secretion!
2) Adrenal Gland- restrics ALD secr=> sodium and water excretion by kidneys
3) Blood Vessels- Vasodilates & incr. capillary permeability

75
Q

What maintenance is necessary for Nitrates and why?

A

Nitrate-free period every day is necessary to AVOID TOLERANCE to the drug.

76
Q

What is the interaction between Nitrates & PDE inhibitors? main side effect?

A

Nitrates convert to NO with production of cGMP as second messenger (Incr. dilation).
PDE inhibitors block cGMP metabolism within cells.

HYPOTENSION

77
Q

Use dependence explanation examples with Class 1 C and Class III anti-arrhythmics

A

Basically think of as direct (strong UD) v Indirect (reverse UD) correlation.

Class 1C are sodium channel blockers with Strong UD by prolonging QRS duration to greater extent at higher heart rates

Class III block repolarizing potassium currents = reverse UD (slower the HR the more the QT interval is prolonged)

78
Q

which nitrate is 100% bioavailable when given orally

A

Isosorbide mononitrate

79
Q

When given orally what type of metabolism do NO and Isosorbide Dinitrate

A

First Pass metabolism in the liver

80
Q

How is sodium Nitroprusside delivered?

A

IV

81
Q 
What drugs (name 2) reduce the rate of spontaneous depolarization in cardiac pacemaker cells? 
(decrease rate of atrial contraction)
A

Acetylcholine and Adenosine.

82
Q

Golden yellow or brownish cytoplasmic granules could contain what 2 things? How can Prussian blue stain differentiate the 2?

A

Either Lipofuscin or Hemosiderin.

Prussian blue turns blue-black in presence of Iron (hemosiderin)

83
Q

How is Hemosiderin in alveolar macrophages indicitive of Left sided heart failure

A

indicates chronic elevation of pulmonary capillary hydrostatic pressure => LHF

84
Q

Common causes of MVP?

A

sporadic myxomatous degeneration
Marfan sydrome
Ehlers-Danlos syndrome

85
Q

Which bug is Cat+ Coagulase -

A

S. Epidermidis, S. Saprophitycus

86
Q

DOC for S. Epidermidis

A

Vancomycin

87
Q

What side effect in utero is seen by children of mothers taking lithium?

A

Ebsteins Anomaly- apical (apex) placement of Right heart Valves (tricuspid) => decreased volume of R. ventricle, atrialazation of R. Ventricle

88
Q

What could occur if a pregnant female with bipolar disorder continues her drug regimen?

A

Lithium=> Epsteins anomaly in utero

89
Q

What might cause EDV to increase?

An increase in EDV does what to preload?

A

Fluid overload:

  • renal failure
  • CHF
  • Fluid infusion

Increases

90
Q

Murmur of Aortic Regurgitation?

What physiologic finding is associated with this?

A

Bounding “Water-hammer” carotid pulsations (and femoral) accompanied with Head Bobbing

WIDE PULSE PRESSURE
PP= peakSysArtPr-EndDiast arterial Pressure

91
Q

When is pulvus et Tardus seen?

A

Aortic Stenosis

92
Q

Carcinoid syndrome Cardiac Complications?

How can you detect this

A

Right sided endoardial fibrosis. leading to pulmonic stenosis or restrictive cardiomyopathy.

Plasma serotonin or Urinary excretion of 5-HT (serotonin) metabolite = 5-Hydroxyindoleactetic acid

93
Q

Pacemaker cells Action potential phase descriptions:
Phase 4
Phase 0
Phase 3

A

P4- Sodium INFLUX
P0- Calcium INFLUX
P3- Potassium EFFLUX (outward current)

94
Q

What is coronary steal and what can it lead to?

A

Bloodflow in ischemic areas is reduced due to arteriolar vasodilation in nonischemic areas

Hypoperfusion/worsening of ischemia

95
Q

use aPTT to monitor what?

A

unfractionated heparin

96
Q 
microscopic changes after MI?
0-4hr
4-12 hr
12-24 hr
1-5 day
5-10days
10-14 days
2Wk-2Mo
A

0-4 =No change

4-12 =early coagulation necrosis, wavy fibers

12-24 =coagulation necrosis + Marginal Contraction band necrosis

1-5d =nuetrophilic infiltrate

5-10d= macrophage phagocytosis of dead cells

10-14d= granulation tissue and neovascularization

2-2mo= coagulation necrosis/scarformation

97
Q

Dobutamine effects:

A

Increase HR, contractility, conduction velocity, myocardial oxygen consumption.

98
Q

Does NO yield a increase or decreased HR?

A

Increased (reflex tachy)

99
Q

Left ventricular outflow obstruction in hypertrophic cariomyopathy is usually created by what 2 things?

A

IVS

Mitral Valve Cusps

100
Q

Pericardial tamponade triad?

name a cause of this

A

muffled heart sounds
elevated Jugular venous Pressure
HYPOTENSION

Ventr. Free wall rupture 3-7d post-MI.

101
Q

Prinzmetal variant angina presentation=
Detecton?
Treatment?

A

episodic transient anginal chest pain in night hours with Holter monitor readings of ST-seg elevation

Ergonovine; ergot alkaloid=> coronary smasm => chest pain

Treatment: Nitrates/CCBs

102
Q

Decrease Plaque stability traits:

A

Thin fibrous cap
Rich lipid core
active inlammation in atheroma

103
Q

Treatment for B-Blocker overdose?

MOA?

A

Glucagon; increases intracellular cAMP=> incr release of intracellular calcium during muscle contraction

104
Q

5 age related changes to the heart?

A

Decr. apex to base dimensions
sigmoid shaped IVS
myocyte atrophy with interstitial fibrosis
accumulation of cytoplasmic lipofuscin pigment.

105
Q

What effect does chronic anemia have on CO?

A

increases… also partial increase in venous return due to decreased blood viscosity

106
Q

where is the ductus arteriousus derived from?

A

6th aortic arch

107
Q

Sinus venosus forms what in adults?

A

smooth part of R atrium = sinus venarum

108
Q

Bulbis cordis in adults?

A

smooth portions of L&R ventricles just before aortic and pulmonary arteries

109
Q

primitive atria in adults?

A

rough portion of R&L atriums

110
Q

what keeps a PDA open? closed?

A

PGE2

Indomethacin

111
Q

In reperfusion injury what enzyme leaks across a damaged Cell Membrane?

A

creatine kinase surge

112
Q

which hypolipemic agent increases blood trigylceride levels

A

Bile acid-binding resins- Cholestyramine

113
Q

What are first-line treatment drugs (name 2 ) for hypertriglyceridemia?

A

Fibric Acid derivivatives:

Gemfibrozil
fenofibrate

114
Q

What is the MOA of Ezetimibe?

use with what?

A

selectively inhibits the intestinal absorption of cholesterol from diet/bile acid.
REDUCING LDL.

use with statins

115
Q

Niacin does what to HDL LDL and TRIGs

A

Primarily Decreases Triglycerides
ALSO INCR. HDL
mild LDL decrease

116
Q 
Side effects of Statin Therapy?
which other class of drugs share these effects
A

Hepatotoxicity
Myopathy (incr. creat. kinases)

Fibrates and Statins

117
Q

What type of drug and which one specifically reduces overall mortality to CHF?

A

B-blockers

Carvedilol

118
Q

What type of drug is Cilostazol?

What is it superior to for treatment of?

A

Phosphodiesterase inhibitor in pts with intermittent claudication

better than aspirin for Peripheral arterial disease.

119
Q

When is Calcium gluconate indicated?

A

Severe Hypocalcemia

120
Q

What type of drug is phentolamine?

When might it be used?

A

a1 blocker

prevent tissue necrosis via Vasodilation ( EX: due to NE extravasastion/ vasoconstriction to infusion site)

121
Q

What are the effects (using which receptors) of epinephrine on HR, SBP, DBP at low and high doses?

A

incr. HR (b1)
INCR. SBP (b1 + a1)
low dose = Decr. DBP (b2 > a1)
high dose= Incr. DBP (a1 > b2)

122
Q

What could a mismatched V/Q defect of a perfusion defect not matched by ventilation defect indicate?

A

Blood flow is occluded to that segment of the lung

123
Q

A matched V/Q defect (ventilation defect matches perfusion defect/ vice versa) indicates what?

A

lung collapse or consolidation.

124
Q

cutaneous strawberry type capillary hemangiomas are benign or malignant tumors in babies?
How are they treated?

A

Benign

Increase with age before eventually regressing by age 7

125
Q

Receptors a1, a2, b1, b2
Change induced by Stimulation (IP3, cAMP, DAG)
clinical effect

A

a1- ^ IP3 - peripheral vasoConstriction
a2- v CAMP - v Release of NE & Insulin
b1- ^ cAMP - Increased contractility
b2- ^ cAMP - Bronchodilation, VasoDilation

126
Q

Best indicator of MitralStenosis severity?

A

Time from s2 to Opening snap. Shorter the interval the longer the stenosis.

127
Q

When would lymphangiosarcoma been seen? why?

A

typically 10 years post mastectomy

due to chronic dilation of lymphatic channels

128
Q

Dopamine
Low Dose
Med Dose
High Dose

A

low- stim D1 => vasodilate renal vasculature.

med- b1 agonist => increase cardiac contractility

high- a1 agonism=> decr. cardiac output with vasoconstriction (and increased afterload)

129
Q

(3) a1-blockers are used for treatment of what 2 diseases together in older males? MOA of a1block in treatments?

A

BPH
Hypertension

Decrease TPR via arteriolar/venous sm. m relaxation

Relax sm. m of bladder neck/ prostate

130
Q

First line in CAD/HYpertension + CHF?

A

cardioselective. b-Blockers

131
Q

essential hypertension is first treated with?

A

Hydrochlorothiazide.

132
Q

how does cholestyramine effect hepatic cholesterol synthesis and how?

A

INCREASES.

Binds bile acids in GI tract interfering with enterohepatic circulation of bile acids and resulting in the excretion of bile acids. Cholesterol is then sequestered for new bile acid production from liver.

133
Q

Describe orthostatic hypotension mechanics?

A

systolic BP decr. of >20 or diastolic >10 from lying to standing up

less blood goes back to heart, decr. BP, Baroreceptor compensation => sympathetic increase to raise vascular resistance via a1 receptors!!!!

a1 receptor blockers cause Orthostatic hypotension because peripheral vasoconstriction is NOT maintained during hypoperfusion of standing up.

134
Q

cystic medial degeneration can lead to ?
what can cause this?
which disease is this seen in?

A

Aortic dissection, anuerysms (large arteries)

Myxomatous Degeneration

Marfans

135
Q

how does basal vascular tone change in response to:

1-Nitric oxide
2-Alpha adrenergic stim
3-beta adrenergic stim

A

Vasodilate

VasoConstrict

Vasodilate

136
Q

what increases cardiac perfusion?

A

hypoxemia

adenosine acculumation

137
Q

LCX a. occlusion leads to ischemia where (anatomically) and with wich ST elevations ?

A

Transmural left ventricular wall ischemia

V5-V6

138
Q

LAD a occlusion leads to ischemia where antatomically and in which leads?

A

anteroseptal transmural ischemia

V1-V4

UWORLD QuestionQuestions (12 decks)

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