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Final FA review > 2/22 > Flashcards

2/22 Flashcards

1
Q

Congenital long QT syndromes

-problem w/what?

A

-disorder of myocardial repolarization, typically due to ion channel defects.

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2
Q

QT interval

A
  • mechanical contraction of ventricles.
  • QRS wave til end of T wave (repol).
  • long QT interval predisposes to Torsades
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3
Q

Romano-Ward syndrome

A
  • congenital long QT
  • auto dom.
  • pure cardiac phenotype, no deafness
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4
Q

Jervell and Lange Neilson syndrome

A
  • congenital long QT
  • auto recessive
  • sensorineural deafness
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5
Q

What is neg. feedback on renin?

A
  • angio2, aldo.

- you can also have low renin (not just by neg feedback) but by high renal perfusion and low Cl- at the macula densa!)

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6
Q

What is the most common side effect of epleronone and spironolactone?

A
  • gynecomastia.

- more so w/spironolactone

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7
Q

What causes type 4 renal tubular acidosis

A

-hypoaldosteronism.

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8
Q

1-Familial hyperchylomicronemia

  • protein defect?
  • whats happening?
  • major manifestations?
A
  • LPL or apoC2
  • TGs can’t be broken down and taken out of chylos & VLDL.
  • acute pancreatitis, eruptive skin xanthomas, hepatosplenomegaly.
  • lipemia retinalis = milky appearing retinal vasculature
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9
Q

2a-familial hypercholesterolemia

  • protein defect?
  • whats happening?
  • major manifestations?
A
  • LDL receptor, apoB100
  • LDL = full of cholesterol, gets trapped in blood cuz can’t be taken up by liver.
  • premature CAD, corneal arcus, tendon xanthomas, xanthelasmas.
  • xanthoma of achilles tendon
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10
Q

4-hypertriglyceridemia

  • problem?
  • manifestation?
A
  • hepatic overprod. of VLDL.

- pancreatitis

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11
Q

Ligand for LDL receptor?

A

apoB-100

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12
Q

familial hyperchylomicronemia

-are they are risk for premature CAD?

A
  • no
  • their LDL and HDL levels are fine.
  • CAD risk main indicator is HDL levels.
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13
Q

What types of drugs have a low volume of distribution?

A
  • large/charged molecules

- plasma protein bound

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14
Q

Whats the average total body water?

A

41 liters

  • plasma volume = 3 L
  • interstitial = 11 L
  • so about 14 L out of 41 L is extracellular fluid.
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15
Q

Lichtenburg figures

A

-fern-leaf pattern cutaneous marks following a lightning strike. lol.

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16
Q

U wave

  • what is it?
  • what can it point to?
A
  • electrical activity of papillary muscles.

- hypokalemia, bradycardia

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17
Q

midline of EKG

A
  • cells are depolarized

- no more current flowing

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18
Q

which interval = systole?

A

QT interval

-so vent repolarization is also part of systole.

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19
Q

Which drugs can slow down AV node? and how?

-can prevent atrial tachys from getting to ventricles.

A
  • Ca channel blockers: slow phase 0 of AV node.
  • beta blockers: blocking beta-1
  • digialis: inc. vagal activity, inhibition conduction thru AV node.
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20
Q

Heart block

-which segment is elongated?

A
  • AV nodal block aka junctional block.

- PR segment

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21
Q

2nd deg. heart block: Mobitz 1

*Wenckebach

A

Progressive elongation of PR interval until one P wave not followed by QRS, then cycle repeats.
*usually asymptomatic.

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22
Q

2nd deg. heart block: Mobitz 2

A

PR interval is stable, but at some point, a P wave is not followed by QRS.

  • often found as 2:1 Heart Block
  • often treated w/pacemaker
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23
Q

Causes of torsades de pointe

-treatment?

A
  • drugs, dec. K, dec. Mg

- Tx: magnesium sulfate

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24
Q

Drugs that can cause torsades

A 
Sotalol, Risperidone (antipsychotics), Macrolides
Chloroquine, Protease inhibitors (-navir), Quinidine (class Ia; also class III), Thiazides
*Some Risky Meds Can Prolong QT
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25
Q

Afib: describe tracing

A

-irregularly irregular
-no discrete P waves (atrial depol)
-

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26
Q

Atrial flutter: describe tracing

A
  • A rapid succession of identical, back-to-back atrial depolarization waves.
  • Sawtooth appearance.
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27
Q

Vfib: describe tracing

A

-no identifiable waves

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28
Q

3rd degree heart block (complete)

-what infection can result in this?

A
  • no AV conduction. atria and ventricles independent of each other.
  • atria are faster than ventricles.
  • lyme diseaes can lead to complete heart block.
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29
Q

B-type (brain) natriuretic peptide

-where is it released from?

A
  • Released from ventricular myocytes in response to inc. tension.
  • longer half life than ANP.
  • good negative predictive value for diagnosing heart failure.
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30
Q

recombinant form of BNP?

A

neseritide

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31
Q

aortic arch baroreceptor

-what does it respond to?

A
  • only respond to increases in BP.

- inc. in BP = inc. firing of vagus to solitary nucleus = increased inhibition of sympathetics.

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32
Q

carotid sinus baroreceptor

-what does it respond to?

A

-responds to both increases and decreases in BP.

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33
Q

Cushing reaction triad

A

-increased BP, resp. depression, and dec. heart rate.

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34
Q

Periph. chemoreceptors

-stimulated by what?

A
  • dec. pH
  • inc. pCO2
  • dec. pO2
  • so only stimulated when you need to breath more.
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35
Q

Which organ extracts the most O2 from its blood supply?

A
  • Heart. Extracts ~80% O2 from its blood source.

- so inc. O2 demand met by inc. coronary blood flow, not by extracting more O2.

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36
Q

Heart: local vasodilatory metabolites?

A
  • adenosine
  • CO2
  • NO
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37
Q

Skeletal muscle: local vasodilatory metabolites?

A
  • lactate
  • H
  • K
  • adenosine
  • CO2
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38
Q

Filtration constant Kf

-determined by what?

A

capillary permeability

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39
Q

Jv = ?

A 
Jv = net fluid flow
Jv = Kf*Pnet
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40
Q

Whats one disease that inc. oncotic pressure of interstitum?

A

lymphatic blockage

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41
Q

What are the 5 right-left congenital cardiac shunts?

A 
1-truncus artiosus
2-transposition of great vessels
3-tricuspid atresia
4-tetralogy of fallot
5-total anomalous pulm. venous return
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42
Q

Cause of truncus arteriosus?

A

Abnormal neural crest cell migration

43
Q

Which maternal disease predisposed to transposition of great vessels?

A

maternal DM.

44
Q

Cause of transposition of great vessels?

A

Abnormal neural crest cell migration leading to problems w/septation.
*heart will be dome shaped & enlarged.

45
Q

Tricuspid atresia

-what does it require to be viable?

A

Both ASD and VSD.

-need a way to get to that RV.

46
Q

Boot shaped heart on CXR

A

Tetralogy of fallot

-due to RV hypertrophy

47
Q

Tet spells

A

In Tetralogy of fallot

  • Suddenly develop deep blue skin, nails and lips after crying, feeding, having a bowel movement, or kicking his or her legs upon awakening. Caused by a rapid drop in the amount of oxygen in the blood.
  • Toddlers or older children may instinctively squat when they are short of breath. Squatting increases blood flow to the lungs by inc. systemic resistance/pressure which inc pressure in RV so blood shunted thru stenotic pulm art.
48
Q

Total anomalous pulmonary venous return (TAPVR)

A

-Pulm. veins drain into right heart circulation; associated with ASD and sometimes PDA to allow for right-to-left shunting to maintain CO.

49
Q

Dilated coronary sinus, think what?

A

Pulm HTN.

50
Q

Frequency of left to right shunts:

A

VSD > ASD > PDA.

51
Q

Common cause of VSD?

A

Fetal alcohol syndrome

52
Q

Marked distinction btwn foramen ovale and ASD.

A
  • ASD = septum is missing tissue.

- PFO = tissue is not fused properly.

53
Q

ASD: usually occurs in septum primum or secundum?

A

-secundum.

54
Q

which L=>R shunt can result in differential cyanosis?

A

PDA b/c ductus is AFTER the major aortic branches, so upper extremities will not be receiving deoxy blood!

55
Q

Common cause of PDA?

A

congenital rubella

56
Q

Infantile coarctation

  • proximal or distal to ductus artiosus?
  • proximal or distal to aortic major branches?
A
  • proximal to ductus arteriosus.

- distal to aortic major branches (so is adult type).

57
Q

22q11 syndromes

-lead to which cardiac abnormalities?

A
  • truncus arteriosus

- tetralogy of fallot

58
Q

Turners

-leads to preductal or postductal coarctation?

A

-obviously preductal cuz you’re born with it.

59
Q

Mönckeberg (medial calcific sclerosis)

  • calcification in which layer of artery?
  • which arts are most likely to be affected?
A
  • media.
  • no intima involvement.
  • seen in radial & ulnar arts.
  • “pipestem” arteries on x-ray
60
Q

Statistical power

A

(1 - beta)

  • probability of finding a true relationship
  • beta = probability of missing a relationship when one actually exists.
61
Q

stats: beta

A
  • probability of committing a type 2 error.

- ie. a study finding that aspirin does not impact platelet function when in fact it does.

62
Q

type 1 error

A
  • finding a significant difference when one doesn’t actually exist.
  • alpha = max probability of committing a type 1 error that a researcher is willing to accept. Usually .05.
  • alpha comparable to p-value.
63
Q

ACE inhibitors can dec. GFR and inc. creatinine.

-can precipitate acute renal failure.

A
  • no AT2 = no constriction of efferent areriole = dec. GFR (dec. filtration fraction).
  • especially in pts w/bilat renal art. stenosis.
64
Q

Avoid ACE inhibitors in which pts?

A
  • bilat renal art stenosis.

- they need their efferent arteriole constricted to get as much filtration fraction/GFR as possible.

65
Q

Mnemonic for P450 inducers

A

Chronic alcoholic mona steals phen phen and never refuses greasy carbs.

66
Q

Mnemonic for P450 inhibitors

A

MAGIC RACKS in GQ

67
Q

Mnemonic for P450 substrates

A

Always Always Always Always think before starting others.

*4 always.

68
Q

CHF

-mixed venous O2 content. Inc or Dec?

A
  • dec.
  • less arterial blood delivered to tissues (due to vasoconstriction & dec. perfusion pressure), so whatever blood is delivered, more O2 sucked out of it.
69
Q

Pulm edema

-affect on lung compliance?

A

-dec lung compliance.

70
Q

presystolic gallop

A

S4

  • unlike S3, S4 is always pathological, even in kids.
  • happens during atrial contraction into a stiff/non compliant ventricle. So late diastole, right before systole.
71
Q

protodiastolic gallop

A

S3

72
Q

Carotid sinus

  • in which carotid
  • proximal or distal to bifurcation?
A

-internal carotid, right after bifurcation of common carotid.

73
Q

Cherry hemangioma

  • in old or young people?
  • does it regress?
A
  • old people
  • does NOT regress

*usually much smaller than strawberry hemangiomas.

74
Q

Which drug can lead to ebstein’s anomaly?

A

Lithium

75
Q

Lysyl oxidase

  • cross links collagen or elastin?
  • fucked up in what disease?
A
  • both

- ehlers danlos

76
Q

Migratory thrombophlebitis

-should make you think what?

A

Cancer

-hypercoag = common paraneoplastic syndrome seen in adenocarcinomas of pancreas, colon, or lung.

77
Q

Metalloproteinases in atheroma

-more of these = more or less risk of rupture?

A
  • more risk of rupture

- released by macros

78
Q

Common locations for atherosclerosis

A

Abdominal aorta > coronary artery > popliteal

artery > carotid artery

79
Q

Can HTN cause cystic medial degeneration?

-what does that predispose to?

A
  • yes.

- aneurysm, dissection.

80
Q

Stable angina: EKG?

A

-ST depression or nothing.

81
Q

Prinzmetal: EKG?

A

-transient ST elevation

82
Q

Triggers of prinzmetal angina

A

-triptans (vasoconstrictors for migrains), cocaine, tobacco.

83
Q

Unstable/crescendo angina: EKG?

A

-ST depression

84
Q

Can you give prinzmetal pts beta-blockers?

A

do NOT given prinzmetal pts beta-blockers. This will block the vasodilatory effects of beta-2 and make matters worse.
-The coronary vessel dilation is a balance between alpha-1 (constriction) and beta-2 (dilation).

85
Q

Coronary steal syndrome

A

Distal to coronary stenosis, vessels are maximally dilated at baseline. Administration of vasodilators (e.g., dipyridamole, regadenoson) dilates normal vessels and shunts blood toward well-perfused areas => dec. flow and ischemia in the poststenotic region. Principle behind pharmacologic stress tests.

86
Q

How many minutes of ischemia in heart before necrosis?

A

-20 min

87
Q

Most common 3 spots for occlusion of coronary.

A 
#1 = LAD
#2 = Right coronary art
#3 = Left circumflex
88
Q

How long after MI do neutrophils arrive?

A

24 hrs.

89
Q

Is fibrinous pericarditis seen w/subendocardial infarction?

A

-no, only w/transmural infarct do you get fibrinous pericarditis.

90
Q

Q waves

-seen w/STEMIs or NSTEMIs?

A

-seen w/STEMIs (transmural infarcts)

91
Q 
Anterior wall (LAD)
-Q waves in which leads?
A

V1–V4

92
Q

Anteroseptal (LAD)

-Q waves in which leads?

A

V1–V2

93
Q

Anterolateral (LAD or LCX)

-Q waves in which leads?

A

V4–V6

94
Q 
Lateral wall (LCX)
-Q waves in which leads?
A

I, aVL

95
Q 
InFerior wall (RCA)
-Q waves in which leads?
A

II, III, aVF

96
Q

What type of pericarditis does Dressler syndrome lead to?

A

fibrinous

97
Q

Irreversible cell damage changes

A
  • nuclear pyknosis, karyorrhexis, karyolysis
  • plasma membrane damage
  • lysosomal rupture
  • mito permeability/vacuolization
98
Q

Which aortic arch is PDA from?

A

sixth aortic arch

99
Q

PDA

-Sxs

A
  • palpable thrill over left infraclavicular region due to turbulent flow thru PDA.
  • wide pulse pressure (inc. volume in LV = higher systolic, and dec. diastolic cuz some fluid leaving aorta going back into pulm art).
  • volume overloads LV, can lead to Sxs of heart failure like failure to thrive & respiratory distress.
100
Q

Which calcium channel blocker is the most cardioselective?

A

verapamil

-can lead to gingival hyperplasia.

101
Q

mnemonic for dilated cardiomyopathy causes:

A

ABCCCD

  • alcohol
  • (wet) beriberi
  • cocaine
  • coxsackie B
  • chagas
  • doxorubicin

-also hemochromatosis & pregnancy.

102
Q

Which trinucleotide repeat is associated w/hypertrophic cardiomyopathy?

A

Friedrich ataxia (GAA)

103
Q

Löffler syndrome

A

Endomyocardial fibrosis with a prominent eosinophilic infiltrate.
-causes restrictive cardiomyopathy.

104
Q

Restrictive/infiltrative cardiomyopathy

-result in systolic or diastolic dysfunction?

A

-diastolic.

Final FA review (52 decks)

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