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Flashcards in 2/22 Deck (104)
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1
Q
Congenital long QT syndromes
-problem w/what?
A
-disorder of myocardial repolarization, typically due to ion channel defects.
2
Q
QT interval
A
-mechanical contraction of ventricles.
-QRS wave til end of T wave (repol).
-long QT interval predisposes to Torsades
3
Q
Romano-Ward syndrome
A
-congenital long QT
-auto dom.
-pure cardiac phenotype, no deafness
4
Q
Jervell and Lange Neilson syndrome
A
-congenital long QT
-auto recessive
-sensorineural deafness
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!)
6
Q
What is the most common side effect of epleronone and spironolactone?
A
-gynecomastia.
-more so w/spironolactone
7
Q
What causes type 4 renal tubular acidosis
A
-hypoaldosteronism.
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
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
10
Q
4-hypertriglyceridemia
-problem?
-manifestation?
A
-hepatic overprod. of VLDL.
-pancreatitis
11
Q
Ligand for LDL receptor?
A
apoB-100
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.
13
Q
What types of drugs have a low volume of distribution?
A
-large/charged molecules
-plasma protein bound
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.
15
Q
Lichtenburg figures
A
-fern-leaf pattern cutaneous marks following a lightning strike. lol.
16
Q
U wave
-what is it?
-what can it point to?
A
-electrical activity of papillary muscles.
-hypokalemia, bradycardia
17
Q
midline of EKG
A
-cells are depolarized
-no more current flowing
18
Q
which interval = systole?
A
QT interval
-so vent repolarization is also part of systole.
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.
20
Q
Heart block
-which segment is elongated?
A
-AV nodal block aka junctional block.
-PR segment
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.
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
23
Q
Causes of torsades de pointe
-treatment?
A
-drugs, dec. K, dec. Mg
-Tx: magnesium sulfate
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
25
Q
Afib: describe tracing
A
-irregularly irregular
-no discrete P waves (atrial depol)
-
26
Q
Atrial flutter: describe tracing
A
-A rapid succession of identical, back-to-back atrial depolarization waves.
*Sawtooth appearance.
27
Q
Vfib: describe tracing
A
-no identifiable waves
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.
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.
30
Q
recombinant form of BNP?
A
neseritide
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.
32
Q
carotid sinus baroreceptor
-what does it respond to?
A
-responds to both increases and decreases in BP.
33
Q
Cushing reaction triad
A
-increased BP, resp. depression, and dec. heart rate.
34
Q
Periph. chemoreceptors
-stimulated by what?
A
-dec. pH
-inc. pCO2
-dec. pO2
*so only stimulated when you need to breath more.
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.
36
Q
Heart: local vasodilatory metabolites?
A
-adenosine
-CO2
-NO
37
Q
Skeletal muscle: local vasodilatory metabolites?
A
-lactate
-H
-K
-adenosine
-CO2
38
Q
Filtration constant Kf
-determined by what?
A
capillary permeability
39
Q
Jv = ?
A
Jv = net fluid flow
Jv = Kf*Pnet
40
Q
Whats one disease that inc. oncotic pressure of interstitum?
A
lymphatic blockage
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
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.