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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
Difference between baroreceptors and chemoreceptors
* 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
What are the treatment options for primary (essential) HTN? And which do elderly/black respond best to?
Thiazide diuretics Dihydropyridine CCBs - best for elderly/black ACEI / ARBs
27
What is the MOA of Labetalol treating hypertensive emergency
* 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
Which type of CCBs are used for treating HTN emergency, and what is their MOA
Dihydropyridines CCBs cause arteriolar dilation which reduces systemic resistance (e.g. afterload) (vs. non-DP for anti-arrhythmia)
29
Describe the MOA of Hydralazine
* Mechanism of action: * Direct arteriolar vasodilator with little or no effect on venous circulation * = dilated red hose
30
Describe the main adverse effect of Hydralazine and what can be done to minimize the effect
* 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
What drugs cause drug-induced lupus
SHIPP-E S – sulfa drugs H – Hydralazine I – Isoniazid P – Procainamide P – Phenytoin E – Etanercept
32
MOA of Nitroglycerin vs. Nitroprusside
* Nitroglycerine - mostly venous dilator * Sublingual * Used in combo with hydralazine (arteriolar dilator) to treat heart failure - mortality benefit * Nitroprusside * Venous and arteriolar dilation
33
MOA of Fenoldopam
* 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
Describe the 2 type of arteriolosclerosis
* 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
Rank affected arteries of atherosclerosis in order
* Abdominal aorta \> coronary artery \> popliteal artery \> carotid artery
36
Describe the pathogenesis of atherosclerosis
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
What does it mean to have a R dominant heart
Posterior descending/interventricular artery arises from RCA This occurs in 80% of population
38
Treatment of prinzmetal angina
Dihydropyridine CCBs
39
40
Adverse effects of Bile acid resins
* 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
Adverse effects of Ezetimibe
* Increase in transaminases – Increased LFTs * =raised LFT flag * Diarrhea/steatorrhea * = oily water coming from eel in water
42
MOA of fibrates
* 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
Adverse effects of fibrates
* 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
What are the 2 dyslipidemia drugs that cause cholesterol stones
Bile acid resins Fibrates

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