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Board questions > Kaplan guy - cardio > Flashcards

Kaplan guy - cardio Flashcards

1
Q

chest pain on exertion relieved with rest or nitro

A

stable angina

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2
Q

what four things do you think of with sudden onset of chest/trunk pain?

A

MI

PE

pneumothorax

ectopic

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3
Q

What are causes of stable angina?

A
  • CAD
  • aortic stenosis
  • hypertrophic obstructive cardiomyopathy
  • aortic regurgitation
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4
Q

What is the only cause of stable angina without a murmur?

A

CAD

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5
Q

What stable angina pt should you not give nitro to?

Why?

A

hypertrophic obstructive cardiomyopathy

the heart is thickened below the level of the aortic valve, resulting in decreased cardiac output. if we give nitro, a vasodilator we could worsen the output

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6
Q

Both restrictive cardiomyopathy and constrictive pericarditis present with what major ssx?

A

Kussmaul sign: JVD on deep breath

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7
Q

What does S3 sound like?

A

rhythmic, melodious “I’m relaxed”

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8
Q

What does S4 gallop sound like?

A

abrupt “A stiff heart”

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9
Q

Chest pain radiating to the back, tearing pain

A

aortic dissection

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10
Q

What is the pathophysiology behind JVD and the Kussmaul sign specifically?

A

the heart muscle is not compliant upon filling; as the pt takes a deep breath, the entire chest is filled with a negative pressure, including the heart, but the heart can’t accomodate the blood trying to come in

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11
Q

Pt is having chest pain that gets worse with changing position, dx?

A

pericarditis

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12
Q

What are two different types of pericarditis and when would they occur?

A
  • fibrinous pericarditis can happen almost immediately after MI
  • autoimmune pericarditis/Dressler syndrome will be after 1 week s/p MI
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13
Q

What causes pleuritis?

A

fibrinous exudate from injury to the lung surface

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14
Q

What kind of things would increase afterload in a cardiac pt?

A

handgrip, HTN, squatting

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15
Q

What things would decrease the preload in cardiac pts?

A

valsalva, nitrates, standing, fluid depletion

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16
Q

How can we increase preload in cardiac pts?

A

fluid overload, squatting, leg raising, inspiration

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17
Q

How can we decrease afterload in cardiac pts?

A

vasodilators, ACE inhibitors

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18
Q

What type of cell starts acute inflammation process?

How does this work?

A

macrophages

  • use toll-like receptors to find things that don’t belong
  • sends message to nucleus with NF-kappaB
  • to DNA to produce cytokines
    • TNF
    • IL-1
    • IL-6
    • IL-8
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19
Q

What do cytokines created s/p macrophage activation do?

A
  • TNF
    • increase temp and cause apoptosis by activating caspases causing cachexia
  • IL-1
    • increase temp and degranulate mast cells (doesn’t need IgE involved)
  • IL-6
    • stimulates hepcidin
  • IL-8
    • chemoattractant for neutrophils
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20
Q

What is hepcidin?

A
  • hormone regulating iron absorption
  • produced by the liver based on iron stored there
  • increased Fe will cause increased hepcidin in order to keep iron in liver
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21
Q

What will too much IL-6 cause? Why?

A

anemia of chronic disease

stimualtes hepcidin which will sequester iron in the liver

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22
Q

In diastolic heart failure, what is the issue? What would my EF be?

A

poor filling capacity

normal EF >60%

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23
Q

If I have systolic heart failure, what is the issue and what will my EF be?

A

pump failure

low EF <45%

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24
Q

When are hemosiderin laden macrophages found? what else are they called? What stain is used to show these cells?

A
  • blood gets into alveoli, macrophages break them down, and are filled with iron
  • heart failure cells
  • prussian blue stain
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25
Q

What is the clinical symptom of hemosiderin laden macrophages?

A

flecks of blood in sputum

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26
Q

What drugs have no direct affect on preload or afterload?

A

beta blockers

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27
Q

What are four classic ssx of CHF?

A
  • hemosiderin laden macrophages
  • Kerley B lines on CXR at the lung margins
  • Interstitial and perivascular edema
  • fluid in alveolar space with widening of alveolar septum
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28
Q

What is my first line drug for systolic CHF?

A

ACE inhibitor

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29
Q

When are S3 and S4 gallops best heard?

A

at the end of expiration

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30
Q

What is my first line drug for diastolic CHF?

A

beta blocker

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31
Q

When would I hear an S4 gallop?

A

“a stiff heart” with diastolic CHF, heart is still strong, but unable to fill well

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32
Q

What is the renin-angiotensin system?

A
  • renal blood flow is reduced and stimulates renin release
  • renin converts angiotensinogen to AT 1
  • AT 1 is converted to AT II by ACE (angiotensin converting enzyme)
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33
Q

What is AT II and where does it work?

A

potent vasoconstrictor (efferent kidney) and stimulates aldosterone

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34
Q

What does aldosterone do once stimulated by AT II?

A

stimulates Na+ and water retention along with K+ excretion in order to raise BP and keep electrolytes even

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35
Q

What does an ACE-I do? What is an example of one?

What are some possible AEs?

A
  • enalapril
  • decreases peripheral resistance, decreasing afterload by inhibiting the conversion of AT I to AT II
  • by decreasing the amount of AT II present, there is less vasoconstriction and aldosterone is inhibited as well
  • with aldosterone inhibited, K+ may not be excreted as well causing hyperkalemia
  • these also increase bradykinin by decreasing the degradation of it; bradykinin causes cough
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36
Q

Where does bradykinin come from and what does it do?

A
  • phospholipids
    • arachadonic acid
      • PGs and bradykinin (inflammatory mediators)

causes vasodilation at the afferent arterioles of the kidney

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37
Q

With classic CHF, what three drug classes should you give?

A
  1. ACE-I
  2. beta-blocker
  3. diuretic
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38
Q

Where would I find beta-1 adrenergic receptors and what do they do here?

A
  • heart
    • rate, contractility, conduction
  • kidney
    • stimulates renin production leading to vasoconstriction
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39
Q

What are three fairly common beta-1 selective blocking drugs?

What are they used for?

On the physiologic level, what is their MOA?

A
  • metoprolol, acebutolol, atenolol
  • control HR and force of contraction
  • Beta-1 are Gs - so they get inhibited, reducing the production of cAMP by the heart, reducing contractility due to decreased amount of calcium
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40
Q

What are some indications for beta-blockers?

A

angina, MI, HTN, arrythmia (tachy), CHF (diastolic and systolic)

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41
Q

What is the small vessel pathology of DM?

Why would giving an ACE-I help?

A

hyaline arteriolosclerosis - narrowing of arterioles, compromising the blood supply to tissues

this drug would protect the kidney from microproteinuria because DM causes decreased GFR causing dilation of teh efferent arteriole; the drug would cause aff>eff and increase pressure in the kidneys, raising GFR

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42
Q

Where does furosemide work and what is its MOA?

A

thin ascending loop of henle

blocks Na/K/2Cl transporter

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43
Q

What numbers does the Na-K pump send back and forth?

How does this leave the cell, charge wise?

How does the lumen in the kidney respond?

A

for every 3 Na out, 2 K in,

leaving the cell with a slightly negative charge

K+ will still flow out of channels into the lumen, leaving Cl- in the cell; the lumen becomes positive because of Mg2+, Ca2+, and K+ being there. The positive ions then are mostly absorbed back into the body, leaving the lumen

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44
Q

All diuretics compete with what?

Therefore, what disease state contraindicates the use of diuretics, specifically HCTZ?

A
  • excretion of uric acid
  • gout
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45
Q

What electrolyte imbalances will you seen with use of furosemide?

A
  • hypercalciuria
  • hypocalcemia
  • hypomagnecemia
  • hypokalemia
  • hyperuricemia
46
Q

S4 gallop is caused by…

A

LVH

47
Q

a non-occlusive thrombus over an atherosclerotic plaque will cause what?

A

unstable angina

48
Q

spasm of a coronary artery

A

Prinzmetal angina

49
Q

How would you calculate Mean Arterial Pressure?

A

= (SBP + 2(DBP))/3

50
Q

what drug inhibits Na channels, blocking depolarization and can be used for angina?

A

ranolazine

51
Q

What is the MOA of nitrates?

A

stimulate guanylate cyclase, increasing cGMP, dephosphorylating myosin, creating dilation of blood vessels

52
Q

What converts phospholipids into arachidonic acid?

A

PL A2 (phospholipase A2)

53
Q

If ASA is inhibiting the COX pathway, what happens?

A

arachidonic acid gets shunted to LOX side

Leukotrienes produced

  • B4 - chemoattractant
  • C4, D4, E4 - smooth muscle contraction
54
Q

What can be used to prevent clot formation over rupture of atherosclerotic plaque?

A

acetyl-salicyclic acid

55
Q

Pt has fluid overload, what three systems could be involved and how would you decide which was the one actually involved?

A
  • cardiac
    • S3 or S4 gallop
  • renal failure
    • protein in urine or elevated BUN or creatinine
  • liver disease
    • jaundice, caput medusa, ascites
56
Q

What is the best way to hear S3/S4?

A
  • bell of stethoscope
  • laying on L side
  • at end of exertion
57
Q

What kind of murmur sounds like a sweeping broom?

Where is it best heard?

A

systolic murmur

best heard at base

58
Q

Where is the murmur for HCM best heard? What is special about this murmur?

A

best heard in aortic area

murmur increases/gets worse with less blood (valsalva)

59
Q

Both HCM and Aortic stenosis have what kind of murmur?

A

systolic murmur

60
Q

What kind of murmur sounds like a washing machine?

A

diastolic murmur

61
Q

If a murmur worsens with inspiration, where is it located?

A

R side

62
Q

What are the three murmurs of aortic regurgitation?

A
  • L sternal border hear aortic regurg
  • Austin-Flint murmur hear anterior mitral valve with regurg
  • Aortic flow murmur at base
63
Q

Autosomal dominant mutation in cardiac sarcomeric protein gene; muscle fibers in disarray; prominent in septum; obstruction of outflow tract

dx?

A

hypertrophic obstructive cardiomyopathy

64
Q

When do you always need to get an ABG?

why?

A

When RR >24

represents an acid-base disturbance

65
Q

Quickest way to determine rate on EKG?

A

QRS complexes x 6

66
Q

leads II, III, and aVF

A

inferior wall

67
Q

V2, V3, V4

A

anterior wall

68
Q

v5, V6

A

lateral

69
Q

v1

A

septal

70
Q

If both I and aVF are positive, what is the axis?

A

normal

71
Q

I is negative on EKG

A

R axis

72
Q

aVF is negative on EKG

A

L axis

73
Q

1-4 hours s/p MI, what will you see on heart autopsy?

A

normal heart

74
Q

4-12 hours s/p MI, what will you see on heart autopsy?

A

swelling of muscle fibers

75
Q

When might rupture of structures occur after an MI?

A

3-10 days as macrophages are phagocytizing dead cells

76
Q

2?-14 days s/p MI, what will you see on heart autopsy?

A

granulation tissue and neovascularization

77
Q

When would you see contraction bands and karyolyis on heart autopsy s/p MI?

What is this from?

A

<1 day old MI

as heart is reperfused, calcium causes contraction bands

78
Q

How long does it take neutrophils to show up?

How long will they be present, say after an MI?

A

about 24 hours

1-3 days s/p you will see coagulative necrosis and neutrophilic infiltration

79
Q

What are three steps of ischemia and what parts are reversible?

A
  1. cell swells
    • without O2, decrease ATP, Na-K pump stops, increasing Na, increasing water
    • reversible
  2. decrease protein production from RER
    • reversible
  3. Ca-ATP pump stops
    • increase Ca2+ in cell, activating proteases and endonucleases, leaking into blood
    • irreversible
80
Q

What murmur acts similarly to HCM? Why is this unique?

A

mitral valve prolapse

murmur will decrease with more blood (ie handgrip)

81
Q

After a pt suffers an MI, I will never give what medication?

A

anti-arrhythmia prophylactically

any rx you give has a greater risk of causing arrhythmia than the post MI pt alone

82
Q

valve leaflets are too big for annulus causing…

what will I hear?

A

mitral prolapse

closing ‘click’ from valve leaflets

83
Q

What is the MC cardiomyopathy?

What often occurs with it?

A

dilated cardiomyopathy

mitral regurgitation

84
Q

What are common causes of dilated cardiomyopathy?

A

alcohol

doxorubicin

cocaine

coxsackie B, enterovirus

Chagas disease

pregnancy

85
Q

What will exercise and chronic AV fistula do to CO and VR?

A

both CO and VR will increase in this scenario

86
Q

If I am concerned for a possible reinfarct s/p MI, what should I do?

A

recheck enzymes

troponin lasts 10days while CPK-MB only lasts 3 days

87
Q

Pt is having chest pain within 1 week of her MI and the pain is worse when laying down. What are we suspecting?

A

fibrinous pericarditis

88
Q

About 3-4 days s/p MI of inferior lateral wall infarct and now the pt has a sudden onset of CHF, what am I concerned for?

A

papillary muscle rupture

89
Q

What injury could occur 4-8 weeks s/p MI?

A

ventricular aneurysm

90
Q

What type of hypersensitivity reaction is Dressler syndrome?

When does it occur?

A

type II HS rxn - autoimmune

1-8 weeks s/p MI

91
Q

How do you tx dilated cardiomyopathy?

A

transplant

92
Q

What four things can have liquefactive necrosis?

A

pancreas, brain, abscess, wet gangrene

93
Q

Where would I be most likely to find fat necrosis?

A

breast tissue, calcium deposit

94
Q

What arrhythmia might mitral regurgitation precipitate?

A

ventricular fibrillation

95
Q

In what heart disease would I see myxomatous degeneration (mucous)?

Specifically what genetic disease might have this?

A

mitral valve prolapse

marfan syndrome

96
Q

What heart defect might you see in Turner syndrome?

A

bicuspid aortic valve

97
Q

age related wear and tear of the heart and cells in valves resemble osteoblasts - deposition of calcium salts

A

degenerative calcific aortic valve stenosis

98
Q

What are the major Jones criteria for Rheumatic fever

A
  • migratory polyarthritis - joint inflammation
  • pancarditis
  • nodules (subcutaneous)
  • erythema marginatum
  • sydenham chorea
99
Q

Subacute infective endocarditis usually affects what side of the heart? What bacterial pathogen is usually associated?

A

L side of heart

Strep viridans

100
Q

What are systemic symptoms of subacute infective endocarditis?

A
  • roth spots in retina
  • Janeway lesions (nonpainful)
  • osler nodes (painful)
  • splinter hemorrhages
101
Q

defect in the arterial septum at the level of the tricuspid and mitral valves

What is this associated with?

A

ostium primum

Down Syndrome

102
Q

People with a ventral septal defect are at higher risk for …

A

infective endocarditis

103
Q

headache and nosebleed, weakness on exertion and leg pain, legs feel cool and under developed (claudication)

no cyanosis or clubbing

notching of the ribe

A

coarctation of the aorta

104
Q

preductal coarctation of the aorta if it is preductal will be associated with what findings?

A

Turner syndrome

PDA

right ventricular hypertrophy

weak pulses and cyanosis

105
Q

coarctation of the aorta postductal

A

HTN in UE

hypotension in LE

notching ribs

intracerebral hemorrhage

dissecting aortic aneurysm

106
Q

overriding aorta, VSD, pulmonary stenosis, right ventricular hypertrophy in an infant

How can the cyanosis be relieved?

A

Tetralogy of Fallot

relieved by squatting

107
Q

machine like murmur in an infant

cyanosis and clubbing of toes and not fingers

A

patent ductus arteriosis

108
Q

To keep PDA open give…

To close PDA give…

A

Prostaglandin E2

indomethacin

109
Q

What does vasoconstriction and increased platelet aggregation and is blocked by NSAIDs?

A

TXA2

110
Q

What does vasodilation and decreased platelet aggregation?

A

PGI2, PGE2, PGD2

111
Q

aortic regurgitation, s3 heart sound, eccentric sarcomere added in series

A

eccentric hypertrophy

112
Q

aortic stenosis, S4 heart sound, concentric sarcomere added in parallel

A

concentric hypertrophy

Board questions (24 decks)

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