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Review / Wrong Answers > 6/17 UWorld > Flashcards

6/17 UWorld Flashcards

1
Q

Uses of Magnesium as an anti-arrhythmic

A

Useful for the treatment of certain arrhythmias (e.g. torsades)

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2
Q

Describe effects of hyper and hypokalemia on EKG

A
  • Hyperkalemia = high, peaked T wave
  • Hypokalemia = flat T wave with possible U wave
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3
Q

Describe the MOA of Adenosine as an anti-arrhythmic

A

Increases K+ out of cells, hyperpolarizing the cell

Decreases Ca2+ into cells, decreasing AV node conduction

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4
Q

Uses of Adenosine as an anti-arrhythmic

A
  • First-line agent for acute treatment of supraventricular arrhythmias
    • = illuminated top of neon heart with #1 ribbon
  • Coronary dilation (mediated by A2 receptors)
    • = dilated coronary crown
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5
Q

Adverse effects of Adenosine

A
  • High-grade AV block
    • = hat blocking heart of swing dancer
  • Shortness of breath, chest pain, major flushing, and sense of impending doom
    • = flushed dancer clutching chest
  • Hypotension (due to vasodilation) and HA
    • = fainting dancer
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6
Q

What ECG leads will have an abnormal QRS deflection in L axis deviation?

A

Negative (-) deflection of QRS in lead aVF and II

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7
Q

What ECG leads will have an abnormal QRS deflection in R axis deviation?

A

Positive (+) deflction of QRS in lead III

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8
Q

What is the normal length of QRS complex

A

Normally < 120 msec (e.g. 3 boxes)

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9
Q

Rank the parts of the conduction pathway from fastest to slowest

A

Purkinje > atria > ventricles > AV node

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10
Q

Causes of L axis deviation

A

Inferior wall MI

L anterior fascicular block

LV hypertrophy

LBBB

High diaphragm

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11
Q

What arrhythmia is this:

  • ECG:
    • Chaotic and erratic baseline with no discrete P waves in between irregularly spaced QRS complexes
    • Irregularly irregular (spacing between R waves are inconsistent)
    • Absent P waves
A

Atrial fibrillation

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12
Q

Describe EKG of atrial flutter

A
  • Identical, back-to-back atrial depolarizations = consecutive P waves
  • Sawtooth pattern
  • Regular
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13
Q

EKG of ventricular tachycardia

A
  • Defined as 3 or more successive ventricular (QRS) complexes
  • May be non-sustained (< 30 s) or sustained (> 30 s)
  • Rhythm is usually regular
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14
Q

Describe Torsades de Pointes, its predisposing condition, and its feared complication

A
  • Type of ventricular tachycardia characterized by shifting sinusoidal waveforms on ECG
    • Amplitude going back and forth between tall and short
  • Can progress to ventricular fibrillation
  • Long QT intervals predispose to Torsades de Pointes
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15
Q

Treatment of Torsades de pointes

A

Magnesium

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16
Q

Describe first degree AV block

A

Prolonged PR interval > 200 msec (5 blocks)

Recall that PR interval is time between atrial and ventricular depolarization (hence, AV block)

Asymptomatic

No treatment needed

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17
Q

Describe Mobitz type I AV block

A

Type II AV block

Progressive lengthening of PR interval until a beat is “dropped”

P wave not followed by a QRS complex

Usually asymptomatic

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18
Q

Describe Mobtiz type II AV block

A

“Dropped” beats without a warning

Not preceded by change in length of PR interval

May progress to third degree block

Treated with pacemaker

19
Q

Describe 3rd degree AV block

A
  • Atria and ventricles beat independently of each other
    • No correlation between P waves and QRS complex
  • Atrial rate > ventricular rate
  • Usually treated with pacemaker
  • Associated with Lyme disease
20
Q

What is a Cushing reaction, and what is it in response to?

Describe pathogenesis

A

Triad of hypertension, bradycardia, and respiratory depression in response to increased intracranial pressure

  • Increased ICP = pressure constricts arterioles in brain = cerebral ischemia = sympathetic response increases peripheral vasoconstriction, thus increasing BP = aortic baroreceptors sense increased BP = respond with reflex bradycardia and respiratory depression
21
Q

What is the difference betwen hypertensive urgency and hypertensive emergency

A
  • Hypertensive urgency:
    • BP > 180/20
    • With no evidence of end organ damage
  • Hypertensive emergency:
    • BP > 180/120
    • With evidence of end organ damage:
      • Encephalopathy, stroke, retinal hemorrhage, papilledema, MI, HF, aortic dissection, kidney injury, microangiopathic hemolytic anemia, eclampsia
22
Q

Difference in location and treatment of Stanford Type A vs. Type B aortic dissection

A
  • Stanford Type A
    • Involves ascending aortas
    • Rx = surgery
  • Stanford Type B
    • Confined to descending aorta, distal to L subclavian
    • Rx = medically: beta-blockers then vasodilators
23
Q

Treatment of atrial fibrillation/flutter

A

Anticoagulation (to remove clots) – Heparin, Enoxaparin, Coumadin (Warfarin)

Rate control – Digoxin, Beta-blockers (Class II), Calcium channel blockers (Class IV)

Rhythm control – Amiodarone or Sotalol (Class IV), Flecainide (Class IC)

24
Q

What drugs prolong the QT interval, and therefore predispose to Torsades de pointes?

A
  • Drugs that prolong QT interval – ABDCE
    • AntiArrhythmics (IA, III)
    • AntiBiotics (e.g. macrolides, chloroquine)
    • Anti”C”ychotics (e.g. Haloperidol)
    • AntiDepressants (e.g. TCAs)
    • AntiEmetics (e.g. ondansetron)
25
Q

Difference between baroreceptors and chemoreceptors

A
  • Baroreceptors - respond to blood pressure (hyper- /hypotension)
    • Located in aortic arch and carotid sinus
  • Chemoreceptros - respond to pO2, pCO2, and pH
    • Peripheral
    • Central - does not response to pO2
26
Q

What are the treatment options for primary (essential) HTN?

And which do elderly/black respond best to?

A

Thiazide diuretics

Dihydropyridine CCBs - best for elderly/black

ACEI / ARBs

27
Q

What is the MOA of Labetalol treating hypertensive emergency

A
  • Labetalol is an alpha and beta antagonist
    • = alpha and beta buttons on organ
  • Beta-blockers lower BP by directly decreased HR and contractility
  • Alpha-1 antagonists lead to vasodilation
28
Q

Which type of CCBs are used for treating HTN emergency, and what is their MOA

A

Dihydropyridines CCBs cause arteriolar dilation which reduces systemic resistance (e.g. afterload)

(vs. non-DP for anti-arrhythmia)

29
Q

Describe the MOA of Hydralazine

A
  • Mechanism of action:
    • Direct arteriolar vasodilator with little or no effect on venous circulation
      • = dilated red hose
30
Q

Describe the main adverse effect of Hydralazine and what can be done to minimize the effect

A
  • Can cause hypotension
    • = pregnant lady fainting
  • Hydralazine induced reflex tachycardia can worsen angina
    • = anvil anchoring hydroboat
  • Because of worsening angina, a beta-blocker is co-administered
    • = beta-1 bugler leaving to get on hydro boat and pushing over the reflex tachycardia hammer doc
31
Q

What drugs cause drug-induced lupus

A

SHIPP-E

S – sulfa drugs

H – Hydralazine

I – Isoniazid

P – Procainamide

P – Phenytoin

E – Etanercept

32
Q

MOA of Nitroglycerin vs. Nitroprusside

A
  • Nitroglycerine - mostly venous dilator
    • Sublingual
    • Used in combo with hydralazine (arteriolar dilator) to treat heart failure - mortality benefit
  • Nitroprusside
    • Venous and arteriolar dilation
33
Q

MOA of Fenoldopam

A
  • Sketchy = old lady Pam
  • Mechanism of actionSelective dopamine 1 receptor agonist
    • = old lady propelling from a single rope
  • Results in a rise in cAMP
    • = camping tent
  • cAMP causes vasodilation in arteries
    • = dilated red sleeves
  • Can also cause coronary vasodilation
    • = dilated coronary crown
  • Dilation of renal arteries, increasing renal perfusion
    • = kidney shaped thing attached to rope
  • Dopamine also leads to increased Na+ and water excretion
    • = salty peanuts falling into water = natriuresis
34
Q

Describe the 2 type of arteriolosclerosis

A
  • Hyaline
    • Caused by protein leaking into vessel wall, producing vascular thickening
    • Consequence of benign HTN or diabetes
    • Protein seen as pink hyaline on microscopy
  • Hyperplastic
    • Thickening of vessel wall caused by hyperplasia of smooth muscle
    • “Onion skin” on microscopy (too many muscle layers)
    • Consequence of severe HTN
35
Q

Rank affected arteries of atherosclerosis in order

A
  • Abdominal aorta > coronary artery > popliteal artery > carotid artery
36
Q

Describe the pathogenesis of atherosclerosis

A

Endothelial damage = lipids leak into intima = macrophage oxidize and consume lipids = result in foam cell = fatty streak (collection of macrophages with lipids within them) = smooth muscle cell migration (involves PDGF and FGF), proliferation, and extracellular matrix deposition à fibrous plaque = complex atheroma

37
Q

What does it mean to have a R dominant heart

A

Posterior descending/interventricular artery arises from RCA

This occurs in 80% of population

38
Q

Treatment of prinzmetal angina

A

Dihydropyridine CCBs

39
Q
A
40
Q

Adverse effects of Bile acid resins

A
  • Increase in serum triglyceridesIncreased endogenous production of cholesterol will also cause increase in hepatic production TAG and VLDL
    • = lobster pushing out VLDL (hypertriglyceridemia)
    • So should not be used in hypercholesterol patients who also have hypertriglycerides
  • Cholesterol gall stones (liver is throwing too much cholesterol into biliary tract
    • = sea gull standing on stones
  • GI upset (constipation and bloating)
    • = lobster clamping GI pipe
  • Steatorrhea (can lead to reduced absorption of fat soluble vitamins, ADEK)
    • = DEcK-A
  • Bile-acid binding resins decrease statin absorption (Must be given 4 hours apart)
    • = lobster clashing with statin pirate
41
Q

Adverse effects of Ezetimibe

A
  • Increase in transaminases – Increased LFTs
    • =raised LFT flag
  • Diarrhea/steatorrhea
    • = oily water coming from eel in water
42
Q

MOA of fibrates

A
  • Decreases serum VLDL (35-50% and decreased triglycerides by activating PPAR-alpha at liver and peripheral tissues
    • = news PPAR of light house attendant, being used as a signal
  • When activated, PPAR-alpha upregulates LPL at extra-hepatic sites
  • This means increased hydrolysis of chylomicron and VLDL TG’s at peripheral tissues – aka decreased serum TGs
    • = Jellyfish taking down VLDL ship
    • = trident passengers escaping from ships that were trapped by jellyfish
  • Less VLDLs means less conversion into LDLs (very mild effect )
    • = jelly fish sinking LDL ship
  • Elevate HDLsFibrates activate the synthesis of Apolipoproteins A1 and A2 by hepatocytes, which are necessary for production of nascent HDLs
    • = jelly fish raising HDL submarine
43
Q

Adverse effects of fibrates

A
  • Myopathy
    • = bit chicken leg
    • Risk is even more elevated when combined with statins
  • Increased risk for cholesterol gallstones= sea gull balancing on stones
    • Inhibition of cholesterol 7a-hydroxylase, which catalyzes the rate limiting step in the synthesis of bile acids
    • Reduced bile acid production results in decreased cholesterol solubility in bile
    • Leads to increased formation of cholesterol stones
44
Q

What are the 2 dyslipidemia drugs that cause cholesterol stones

A

Bile acid resins

Fibrates

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