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Ped cardiology board exam > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is the mechanism of action of loop diuretics?

A

Blocks Na/K/Cl transporter within the loop of henle

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2
Q

What are some side effects of loop diuretics?

A

hypoK

ototoxicity

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3
Q

What do NSAIDs do to the efficacy of loop diuretics?

A

decrease it!

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4
Q

What medication do you have to be mindful of when using loop diuretics?

A

digoxin, especially with low K

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5
Q

What is the mechanism of action of digoxin?

A

Blocks Na/K ATPase pump within plasma membrane of cardiac myocytes, leading to increased intracellular Ca+

slows and strengths the heart

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6
Q

Why are we cautious about use of loop diuretics in neonates?

A

risk of nephrocalcinosis

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7
Q

what is the IV–>oral dose adjustment required?

1) loop diuretics
2) thiazide diuretics

A

1) increase dose by 50%

2) increase dose by 20%

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8
Q

MOA of thiazide diuretics

A

inhibits Na/Cl cotransporter in the distal tubule

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9
Q

which diuretic can cause photo sensitivity?

A

thiazide

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10
Q

what is the MOA of spironolactone?

A

competitive aldosterone receptor for Na/K exchange sites in distal tubule
-used for K sparing affect

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11
Q

gyneocmastia is a side effect of what medication

A

spironolactone

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12
Q

what is the MOA of acetazolamide

A

CA inhibitor in the proximal convulted tuble

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13
Q

why do we use acetazolamide

A

weak diuretic, tx metabolic alkolosis 2/2 to diuretic use

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14
Q

SE of acetazolamide?

A

can cause severe reactions in patients with sulfonamide sensitivity–>SJS, TENS, bone marrow suppresion, hepatic necrosis

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15
Q

what is the clinical effect of nitroprusside

A

direct vasodilation with decrease in SVR, PVR, and preload

-NO donor–> increase cGMP and secondarily increase in CO

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16
Q

what drug do you have to worry about cyanide toxicity with? How does it present? what subset of patients is more at risk for developing cyanide toxicity?

A

nitroprusside

  • potential for developing methmoglobinemia
  • cyanide binds to cytochrome oxidase (enzyme critical in production of ATP), causing transition to anaerobic metabolism leading to tissue hypoxia and therefore presents with a metabolic acidosis with an increased SvO2
  • there is decreased O2 utilization, leading to high SvO2, bright red blood, and patients appear flushed or cherry red
  • higher risk in prolonged use, higher droses, or those with hepatic dysfxn
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17
Q

does nitroglycerin have a greater vasodilatory effect on the venous or arterial system?

A

venous!

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18
Q

what is the MOA of cough seen in ACEi

A

increased bradykinin

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19
Q

which ACEi can be used with once daily dosing?

A

enalapril (tho more classically use BID dosing)

lisinopril

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20
Q

ARBs are typically used as second line oral afterload reduction agents for patients that don’t tolerate ACEi. Except in the following patient population:

A

Aortic root dilation in setting of connective tissue d/o (Marfan, Loeys-Dietz)

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21
Q

when do we use CCB?

A

afterload reduction when unable to use ACEi (renal failure) or atrial arrythmias (dilitiazem)

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22
Q

CCB should be used in caution with what two patient populations

A

1) neonates–risk for CV collapse and AV block

2) ventricular dysfxn

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23
Q

nicardipine falls into what class of medications?

A

calcium channel blocker

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24
Q

amlodopine falls under what class of medication

A

CCB

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25
Q

diltiazem falls under what class of medication

A

CCB–more commonly used for atrial arrythmias than HTN

26
Q

carvedilol is a ** B antagonist

A

non-selective B antagonist

-no intrinsic sympathomimetic activity

27
Q

In adults carvedilol has been shown to ** risk of death, hospitalization, and ** NYHA class association. In pediatrics

A

decrease risk of death, hospitalization and improve NYHA classification

-in pediatrics the data is inconclusive

28
Q

we use carvedilol in pediatric chronic HF patients for these intended effects…

A

1) decrease afterload
2) decrease LV EDP
3) increase LV EF
4) beneficial effects on remodeling

29
Q

how often can carvedilol be uptitrated in the outpatient setting?

A

q2h weeks as outpatient

target dose: 0.5mg/kg/dose bid

30
Q

Is propanolol via the kidneys or liver cleared?

A

liver

31
Q

propanolol is contraindicated in what patient population

A

heart block, decompensated HF

-use caution when using in asthmatics given risk of bronchospasm with B-blockers

32
Q

of the following Bblockers which is selective?

1) esmolol
2) propanolol
3) carvedilol

A

esmolol–selective B1 antagonist

33
Q

what can happen if both morphine and esmolol are administered together

A

morphine increases the effect of esmolol, leading to rebound HTN

34
Q

tx of choice for rebound htn post CoA repair?

A

propanolol

-not renally based htn, 2/2 to sympathetic/adrengeric mediation and carotid baroreceptors

35
Q

what are the clinical effects of digoxin

A
  • inotrophy
  • vasodilation
  • decreased automaticity
  • speed of AV conduction
  • increased vagal tone
36
Q

digoxin interacts with what medications

A

-amiodarone and CCB, reducing their clearance

37
Q

digoxin is relatively contraindicated in what patient populations

A
  • WPW
  • sinus bradycardia
  • AV block
  • renal insufficency
38
Q

use of digoxin after stage I pallation showed what effect

A

decrease in interstage mortality with digoxin use…but there is more to come

39
Q

how does digoxin toxicity present?

A
  • N/V, CNS/vision changes

- PVCs, ST changes, PR prolongation, AV block

40
Q

how do you tx digoxin toxicity

A 
stop digoxin
tx hypoK
atropine for bradycardia
-esmolol or lidocaine for refractory ventricular arrythmias
-digibind (monoclonal Ab fragments)
41
Q

what are some SE associated with prostaglandin?

A
  • plt inhibition and increased risk of bleeding
  • gastric outlet obstruction wiht prolonged use
  • bone changes, cortical hyperotosis
42
Q

what drugs can be given to close a PDA?

A
  • indomethacin
  • ibuprofen
  • tylenol
  • high dose ibuprofen associated with higher rates of closure than the rest according to one paper
43
Q

catecholamines work on what overall receptor class?

A

adrenergic

44
Q

what adrenergic receptors are found on the myocardium?

A

B1 (sinus node/AV node/myocardium)–increase iontrophy (HR) and chronotrophy (contractility)
alpha 1-coronary circulation–>vasoconstriction
DA1-coronary circulation–>vasodilation

45
Q

what happens on a cellular level after B1 activation?

A
  • activation of Gprotein leading to activation of adenyl cyclase
  • conversion of ATP to cAMP
  • cAMP activates protein kinase–>increases intracellular Ca+ and binds troponin
46
Q

what adrenergic receptors are found in peripheral vasculature?

A
  • alpha1 (skin, pulmonary, renal)–>vasoconstriction
  • DA1 (renal)–>vasodilation
  • B2, DA2 (mesenteric and splanchnic)–>vasodilation
  • B2 (skeletal muscle) vasodilation)
47
Q

what is the role of alpha 2 receptors?

A
  • negative feedback loop for sympathetic nervous systme

- inhibits NE secretion

48
Q

what happens after alpha receptor activation?

A

-G protein mediated, activation of phospholipase C–> DAG activates protein kinase C–> increased intracellular Ca + PK

49
Q

what is the effect of low/moderate/high dose dopamine?

A
  • low dose (< 5mcg/kg/min): works on DA1+DA2 receptors primarily renal + mesentaric effects–> vasodilation inhibition of NE
  • moderate (5-15): B1 (iontropy, chronotrophy) and then Alpha1 (vasoconstriction
  • high dose ( > 15): alpha1 dominates

dopamine is a precursor to NE + Epi

50
Q

what is the MOA of vasopressin

A

related from posterior pituitary 2/2 to hypotension

  • acts at V1–potent vasoconstriction
  • V2 (Renal DCT, collecting ducts) increases water permatability and water retention
  • use for vasodilatory shock
51
Q

when using vasopressin in the infant population what do you need to be cautious for (side effects)

A
  • tissue necrosis with infiltrate

- NEC

52
Q

what is levosimendan used for? what is its moa?

A

calcium sensitizing agent

  • enhances myocardial response to Ca adn sensitivity of the myocardial apparatus to calcium
  • used experimentally or for compassionate use in decompensated HF
53
Q

fentanyl vs morphine

  • what class of drugs are they
  • which is more potent
  • which causes more histamine release
  • which is more lipophilic
  • which is more hemodynamically neutral
  • which can cause rigid chest
A
  • opoids
  • fentanyl more potent
  • morphine causes more histamine release
  • fentanyl is lipophilic so patients with fat stores can have drug build up and more lasting effect
  • fentnayl is also more hemodynamically neutral
  • rapid administration of fentanyl–>rigid chest
54
Q

which of the following is midazolam used for

a) analgesia
b) sedation
c) anxiolysis
d) amnesia

What is the class of drugs? MOA? SE? reversal agent

A

b-d
–it has no effect on modifying pain

MOA: binds to benzo site on GABA receptor and upregulates GABA
SE: respiratory depression, hypotension
reversal w/ flumazenil

55
Q

ketamine is used for?

a) analgesia
b) sedation
c) anxiolysis
d) amnesia

What is MOA? SE?

A

all of the above
MOA: dissociative, acts via inhibition of NMDA receptor
analgesia and amnesia
-preserved respiratory drive at moderate doses
-can lead to hypertension 2/2 to intrinsic catecholamine release
-monitor for emergence reactions and nightmare, increased secretions

56
Q

what do you use to sedate in patients with impaired myocardial function

A

etomidate

  • hemodynamically neutral
  • quick onset with duration of action < 10 minutes
  • think of this with impaired dysfxn or PH
  • caution: can cause adrenal suppression, may require supplemention with stress dose steriods
57
Q

dexmedetomidine acts on what receptor and what is it used for?

A
  • acts selective alpha2 receptor agonist
  • use for sedation, analgesia, sympatholysis
  • caution: can cause bradycardia and risk for AV block
58
Q

propofol is not used too often in CICU because of what SE?

A
  • can lead to hypotension and depressed myocardial contractility
  • long term use limited by propofol infusion syndrome: potentially fatal combo of metabolic deranagements and organ failure
59
Q

SE of inhaled anesthesetics

A
  • dose related vasodilation (drop in BP, SVR, contractility)
  • life threatening malignant hyperthermia: AD inheritance, block the regulatory effect of Mg on skeletal muscle SR, leading to disregulated Ca release
  • tachycardia, tachypnea, muscle spasm, unexplained hypercarbia
60
Q

When considering which type of CCB had a worse SE in the setting of overdose is it the dihydropyridine or non-dihydropyridine? Name the meds

A

non-dihydropyridines—> impact both vascular smooth muscle ++myocardial contractilty, diltazem and verapamil

dihydropyridine-nicardipne and nifedipine ARE selective and impact the vascular smooth muscle but NOT the heart
Ie why we feel so comfortable using them in the CICU!

61
Q

How do you manage a non-dihydropyridine overdose?

A 
Atropine or pacing for HR
Iontropes for contractilty
Lipid infusion to bind free drug
Insulin/dextrose for hyperglycemia 
May need ECMO temporarily

Ped cardiology board exam (3 decks)

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