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Step 1 Miscellanous > Cardio SketchyPharm > Flashcards

Cardio SketchyPharm Flashcards

1
Q

What is one of the earliest lab values which indicates poor prognosis of digoxin toxicity?

A

Hyperkalemia -> elevated blood K+ levels due to too much blockade of Na/K ATPase

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2
Q

What does digoxin do to the ST segments with longterm use?

A

Concave ST segments - think of the taSTy scoop of ice cream

-> does not indicate toxicity, just longterm use

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3
Q

What are some common causes of digoxin toxicity?

A
  1. Hypokalemia - permissive effect on Na/K ATPase binding, usually loop diuretics or vomiting / diarrhea
  2. Renal insufficiency
  3. Drugs which inhibit tubular clearance of digoxin - i.e. verapamil, amiodarone, quinidine
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4
Q

What is the mechanism of action of milrinone?

A

You’re one in a million - Don’t phoster disinterest in the cAMPaign

Increases cAMP via being a PDE inhibitor. Causes:

  1. Vasodilation - think of the big red ears
  2. Increased contractility - increasing cAMP in a non-beta receptor dependent method - think of the poster flexing.
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5
Q

What is the mechanism of action of nesiritide?

A

Don’t BuMP the GruMP - It’s NECessary to turn the Tide

Increases cGMP via mimicking BNP
Decreases afterload and preload - think of the blue pants and red ears of the elephant
Also improves diuresis - think of stomping on those peanuts

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6
Q

What is the mechanism of action of ATII in the proximal tubule of the kidney?

A

Stimulates the Na/H exchanger, promoting contraction alkalosis
-> think of the guy watching the pro kart TV in sketchy

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7
Q

What lab value is expected to bump by about 30% after starting an ACE inhibitor?

A

Creatinine - think creatinine credit card

-> due to loss of AT2 constriction of the efferent arteriole and thus loss of GFR

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8
Q

Why do ACE inhibitors improve mortality in heart failure and post MI?

A
  1. They reduce AT2-mediated cardiac remodelling
  2. They reduce preload by reducing AT2’s affect at proximal tubule + aldosterone at distal tubule
  3. They reduce afterload by reducing AT2-mediated vasoconstriction
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9
Q

Why are ACE inhibitors contraindicated in pregnancy?

A

Increased risk of fetal hypotension, anuria, and renal failure

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10
Q

How does verapamil differ from diltiazem?

A

Note that verapamil (very vanilla) is farthest to the right in the sketch -> most cardioselective (non-DHP effect), and least smooth muscle effect (DHP)

Diltiazem is still quite cardioselective but acts a little more like the dihydropyridines in its L-type calcium channel blockade in smooth muscle (blood vessels)

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11
Q

What is the mechanism of amlodipine? Why is it preferred over other CCBs for the treatment of hypertension?

A

It is a dihydropyridine (all ‘dippins) calcium channel blocker which increases vasodilation via L-type calcium channel blockade in blood vessels
-> reduces afterload and stimulates coronary artery vasodilation

Preferred because it has a long halflife -> will not trigger reflex tachycardia as easily

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12
Q

When are nifedipine, nicardipine, and clevidipine used?

A

Nifedipine - a CCB known to be safe in pregnancy
Nicardipine - Nice card - rapid action and safe in hypertensive emergency
Clevidipine - Clover - rapid action and safe in hypertensive emergency

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13
Q

What CCB is contraindicated in patients with unstable angina or post-MI and why?

A

Nifedipine - think of the pregnant lady cutting through the heart-shaped apple
-> due to reflex tachycardia triggered by vasodilation, which increases myocardial oxygen consumption

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14
Q

Why do CCBs cause peripheral edema?

A

Arteriolar vasodilation increases the capillary hydrostatic filtering pressure -> more fluid into interstitium

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15
Q

What are the contraindications of CCBs in general?

A
  1. Concomitant use of beta blockers or another rate control agent -> additive heart blockade
  2. Heart failure - think of the guy with the heart failure balloon outside -> due to decreased cardiac inotropy (bad, that’s why we use digoxin), as well as reflex sympathetic activation
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16
Q

What is one classic side effect of verapamil other than constipation? What other drugs have this?

A

Gingival hypertrophy - think of the guy blowing gum

Also seen with phenytoin and cyclosporine (but not tacrolimus)

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17
Q

What are the first line treatments for primary (essential) hypertension and when should you consider using dual therapy?

A

Think of the black elderly guy in the pool holding ice cream for optimal treatment

  • > HCTZ / CCBs i.e. amlodipine
  • > casino is nearby - ACE inhibitors / ARBs also used

Considered using dual therapy if >20 mmHg over the target.

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18
Q

What are the values which indicate hypertensive emergency?

A

Think of the 180 degree arch over 12 inch ruler = 180/120

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19
Q

What are the beta blockers used in hypertensive emergency? Their mechanisms?

A

IV metoprolol or esmolol - selective beta1 blockade

IV labetalol - combined alpha1 and nonselective beta blockade
-> think of the pregnant labeta organist

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20
Q

What antihypertensive medications are safe in pregnancy?

A

Hydralazine, methyldopa (alpha-2 agonist), labetalol, nifedipine

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21
Q

What is the mechanism of action of most agents used in hypertensive emergency?

A

Arteriolar vasodilators -> direct drop in BP

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22
Q

What is the mechanism of hydralazine and when is its use contraindicated? Why can it cause fluid retention?

A

Direct arterial vasodilator which reduces afterload / BP. -> minimal effects on preload

Contraindicated in CAD / MI due to reflex tachycardia -> generally administered with a betablocker

Can cause fluid retention via sympathetic activation of RAA system in response

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23
Q

What is the usage of hydralazine in heart failure?

A

Can be used in combination with nitrates for a mortality benefit -> results in both preload / afterload reduction

Think of the mortality flag and the throwing of dynamite out of the hydralazine boat (nitrates).

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24
Q

What is the mechanism of action of sodium nitroprusside and its toxicity?

A

Metabolized to nitric oxide which increases the cGMP (grump) and leads to BOTH arterial and venous vasodilation

Toxicity - cyanide poisoning -> lactic acidosis and altered mental status

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25
Q

What is the signalling used by D1/D2 receptors?

A

D1 - Gs - increases cAMP

D2 - Gi - decreases cAMP

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26
Q

What is the mechanism of action of fenoldopam?

A

fenolDOPAm - D1 agonist. Much like beta2 receptors, it increases cAMP which causes vessel dilation.

It is particularly useful because D1 receptors are expressed on renal / splanchnic arteries -> permits vasodilation of these vascular beds in hypertensive emergency.

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27
Q

Why is fenoldopam particularly useful in hypertensive emergency?

A

Dilates coronary arteries - think of the old lady’s crown
Dilates renal arteries - only BP medication to lower BP and improve renal perfusion
-> improved blood flow to renal arteries also improves natriuresis -> think of the lady holding the peanuts

28
Q

Why do class 1A antiarrhythmics prolong the QT?

A

They have some potassium channel blocking effects in addition to their Na+ blockade

  • > prolong the phase 3 action potential and thus the QT interval
  • > think of the prom queen throwing aside that potassium curtain
29
Q

What are the side effects of quinidine?

A

Cinchonism - Headache, tinnitus
Thrombocytopenia - broken plates
Prolonged QT

30
Q

Are class 1A antiarrhythmics good in heart failure? Why or why not?

A

No - they can exacerbate heart failure - think of the heart balloon with a dart thru it in the prom king’s room

Due to negative inotropic effect of 1A antiarrhythmics

31
Q

What are the three class 1B antiarrhythmics? What do they do to the AP duration overall?

A

Lidocaine (you lied), Mexilitine, Phenytoin

Shorten the action potential by reducing Na+ current upstroke -> think of the girl pulling in the curtain.

32
Q

What are the side effects of concern for 1B antiarrhythmics?

A

CNS stimulation / depression - paresthesias / tremor. This is easy to remember since phenytoin is in class

33
Q

Why are 1B antiarrhythmics only used for ventricular arrhythmias?

A

Since they have such weak Na+ channel binding, only ventricular or ischemic cardiac tissue is highly affected

34
Q

What effect do 1C antiarrhythmics have on the ERP? What are they used for?

A

Significantly prolong ERP in AV node, but no effect in Purkinje / ventricular system (think of the curtain not being touched in the room with the propafenone purple phone)

Used for SVTs, usually AFib, in patients with no history of ischemic or structural heart disease (healthy hearts only please).

35
Q

What is the specific mechanism of SA / AV nodal conduction decrease by beta-blockers?

A

Blockade of Beta1 channels decreases cAMP, which decreases Ca+2 currents in the SA / AV nodes which are normally triggered towards the ends of phase 4 by the I-funny channels (Na/K channel). This prolongs phase 4 slow diastolic depolarization and prolongs the time before the phase 0 Ca+2-mediated upstroke occurs.

36
Q

How does amiodarone share features of all four classes of antiarrhythics?

A

1 - Blocks inactivated Na+ channels
2 - Weak beta-blocker activity
3 - Blocks potassium channels -> prolongs repolarization
4 - Weak calcium channel blocker

37
Q

What neurologic side effects can amiodarone cause?

A

Tremor, ataxia, peripheral neuropathy, sleep disturbances

  • > due to brain accumulation
  • > think of the skull tracing on the mariachi bands’ hats
  • > also consider these may be caused by hypo/ hyperthyroidism
38
Q

What side effects can amiodarone have on the skin / heart?

A

Heart - heart block, heart failure with prolonged use

Skin - gray-blue skin discoloration

39
Q

What does activating A1 receptors on the heart do?

A

Think of banana flying out of cup - increases outward potassium current
Think of calcium falling down -> decreases calcium inflow

  • > hyperpolarizes cell, a parasympathetic like effect
  • > reason why adenosine can be used as an antiarrhythmic.
40
Q

What does stimulation of A2 receptors do?

A

Coronary vasodilation - think of the crown on the adenosine guy.

41
Q

What is the specific mechanism of nitrates?

A

Increasing cGMP -> decreased intracellular calcium -> calcium-calmodulin complex can no longer increase the activity of myosin light chain kinase -> myosin dephosphorylation predominates.

-> dephosphorylation of myosin light chain (snipping off of locks) -> decreases myosin / actin interaction -> smooth muscle relaxation

42
Q

How do M3 receptors cause smooth muscle contraction?

A

Gq -> stimulation of IP3 -> Increased intracellular calcium -> activation calcium-calmodulin complex -> calmodulin complex directly activates MLCK -> phosphorylation of myosin light chain -> smooth muscle contraction

43
Q

How do Beta2 receptors cause smooth muscle relaxation?

A

Gs -> increasing cAMP -> phosphorylation of myosin light chain kinase -> phosphorylation decreases activity of the kinase -> myosin light chain becomes dephosphorylated -> relaxation.

44
Q

How do non-DHP/DHP’s cause negative cardiac inotropy and smooth muscle relaxation, respectively, but no effect on the skeletal muscle?

A

L-type calcium channel is the primary channel on smooth muscle which controls Ca+2 influx to activate the calcium-calmodulin complex

Skeletal muscle does not rely on Ca+2 current as its primary source of contraction -> blockade of L-type calcium channel does not interrupt Ca+2 channel and RyR connectivity

45
Q

Do nitrates cause coronary artery vasodilation?

A

Only very minimally, at high levels of nitric oxide release.

Main effect is on venous vasodilation -> decrease preload

46
Q

What nitrates are used for maintenance therapy and why?

A

Oral isosorbide mononitrate / dinitrate, because there is extensive first pass metabolism and you need lots of it to combat this.

Sublingual nitroglycerin is insufficient for maintenance therapy.

47
Q

Why are nitrates good for pulmonary edema?

A

Decreasing preload to the heart prevents high LVEDV’s which back up into the lung when the heart isn’t working properly (i.e. heart failure, hypertensive emergency).

Furthermore, the mild afterload decrease is also beneficial to failing hearts -> some arterial vasodilation

48
Q

Why might nitrates need to be given with a beta blocker?

A

Causes blood to pool in venous circulation -> can cause orthostatic hypotension and reflex tachycardia, bad if you are trying to reduce ischemia.

49
Q

What are nitrites used in the treatment of?

A

Cyanide poisoning -> induce methemoglobinemia which allows binding to RBCs instead of complex IV of cells

50
Q

What is the most common untoward effect of nitrates?

A

Throbbing / pulsating headache - due to meningeal artery pulsations

51
Q

What are three key contraindications of nitrates?

A
  1. Hypertrophic cardiomyopathy - good preload is required to minimize LVOT obstruction
  2. PDE5 inhibitors within 24 hours - i.e. sildenafil -> too much cGMP-vasodilation
  3. Right ventricular infarction - RV preload is required to maintain systemic cardiac output in MI
52
Q

What are the two ways which HDL reduces peripheral cholesterol?

A
  1. Gives cholesterol to VLDL / LDL via the CETP - cholesterol ester transfer protein. These will eventually be uptake by the LDL receptor in the liver
  2. Directly dumps cholesterol from peripheral tissues to the liver via the scavenger B1 receptor (SR-B1)
    - > It’s all in the statins sketchy
53
Q

When should statin therapy be started? Are statins teratogenic?

A

Should be started post-ACS (banjo)
Post-ischemic stroke (atherosclerosis, black paint across head)
Peripheral artery disease (clogged pipe
High risk diabetic patients (think of the guy eating candy)

Yes they are teratogenic - think of the teratogenic tarantula being drawn on the HDL warship by the pirates

54
Q

What is the mechanism of action of the cholestyramine?

A

Cho-lobster-amine -> they inhibit enterohepatic circulation of bile salts

They are bile salt binding resins

55
Q

What do bile acid resins like cholestyramine do to triglycerides and why?

A

Increase triglycerides, because concomitant with the increased production of bile acids from cholesterol, they also increased VLDL synthesis. Think of that fucking lobster scaring away the VLDL warship.

56
Q

What do you worry about with giving cholestyramine to someone on warfarin?

A

Increased INR and bleeding events, since bile salt binding resins can cause fat malabsorption -> decreased absorption of fADEK

57
Q

Cholestyramine and statins are usually given in combination therapy. What do you have to remember about the way they are administered?

A

Give them 4 hours apart (think of the statin pirate and the cholestyramine lobster at odds with eachother)
-> This is because cholestyramine inhibits statin absorption to some extent as well.

58
Q

What is the mechanism of action of ezetimibe? What is the overall goal?

A

Think of the ezetimibe eel preventing the gold bars being from put in the chylomicron hot air balloon.
-> Prevent dietary cholesterol absorption at the brush border

Similar to bile acid resins -> lower LDL levels by causing increased LDL uptake by the liver. Generally given in combination with a statin as well so the liver can’t compensate by increasing production.

59
Q

What are the side effects of concern for ezetimibe?

A

Think of the eel in the water below, threatening the little worker dude raising an LFT flag -> remember the rare increase in LFTs.

60
Q

What is the mechanism of action of fibrates?

A

Think of the Jelly fish grabbing onto the VLDL warship, making all the triglyceride passengers fall off.

Also think of the PPARalpha newspaper on the lipoport light house

They upregulate LPL activity -> decrease triglycerides
They also downregulate hepatic VLDL production -> also leads to a modest reduction in LDL as a result (less VLDL -> less LDL is made)

61
Q

What effect do fibrates have on HDL levels?

A

Think of the jellyfish modestly lifting the HDL submarine
-> modest increase due to upregulation of ApoA production in liver. Niacin is really much more important for this function

62
Q

What are the side effects of fibrates?

A

Think of the pirate riding the jellyfish eating chicken -> increased risk of myopathy with statins (Especially gemfibrozil)

Also cholesterol gallstones - PPARa also downregulates 7-alpha hydroxylase which is the rate-limiting step of bile acid synthesis.

63
Q

What are the two primary lipid effects of niacin which you care about?

A

Loch Niacin monster

  1. Increase HDL levels** -> Think of the HDL submarine lifted WAY ontop of the monster’s head
  2. Moderately decreased TG levels -> due to inhibition of hepatic VLDL synthesis -> think of the monster eating the VLDL warship in the back.
64
Q

Does niacin affect LDL levels?

A

Yes, there is a modest effect because decreased hepatic VLDL production will also slightly drop LDL production (similar mechanism as fibrates in this regard).

65
Q

Other than prostaglandin-induced flushing, what are the other side effects of niacin therapy?

A
  1. Hyperglycemia - think of guy eating candy
  2. Hyperuricemia -> gout
  3. Severe hepatotoxicity -> think of burning liver in the background. NEED to monitor LFTs
66
Q

What is the mechanism of action of fish oil in improving cardiovascular outcomes?

A

It’s included in the niacin / fibrate sketch, so you know it has to lower VLDL

The omega-3-fatty acids suppress hepatic VLDL reduction and may reduce cardiovascular risk.

67
Q

What is calmodulin analogous to?

A

Troponin -> binds to calcium to activate contraction

Will activate MLCK

Step 1 Miscellanous (40 decks)

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