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Ped cardiology board exam > Pharmacology > Flashcards

Pharmacology Flashcards

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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
diltiazem falls under what class of medication
CCB--more commonly used for atrial arrythmias than HTN
26
carvedilol is a **** B antagonist
non-selective B antagonist | -no intrinsic sympathomimetic activity
27
In adults carvedilol has been shown to *** risk of death, hospitalization, and *** NYHA class association. In pediatrics
decrease risk of death, hospitalization and improve NYHA classification -in pediatrics the data is inconclusive
28
we use carvedilol in pediatric chronic HF patients for these intended effects...
1) decrease afterload 2) decrease LV EDP 3) increase LV EF 4) beneficial effects on remodeling
29
how often can carvedilol be uptitrated in the outpatient setting?
q2h weeks as outpatient | target dose: 0.5mg/kg/dose bid
30
Is propanolol via the kidneys or liver cleared?
liver
31
propanolol is contraindicated in what patient population
heart block, decompensated HF | -use caution when using in asthmatics given risk of bronchospasm with B-blockers
32
of the following Bblockers which is selective? 1) esmolol 2) propanolol 3) carvedilol
esmolol--selective B1 antagonist
33
what can happen if both morphine and esmolol are administered together
morphine increases the effect of esmolol, leading to rebound HTN
34
tx of choice for rebound htn post CoA repair?
propanolol | -not renally based htn, 2/2 to sympathetic/adrengeric mediation and carotid baroreceptors
35
what are the clinical effects of digoxin
- inotrophy - vasodilation - decreased automaticity - speed of AV conduction - increased vagal tone
36
digoxin interacts with what medications
-amiodarone and CCB, reducing their clearance
37
digoxin is relatively contraindicated in what patient populations
- WPW - sinus bradycardia - AV block - renal insufficency
38
use of digoxin after stage I pallation showed what effect
decrease in interstage mortality with digoxin use...but there is more to come
39
how does digoxin toxicity present?
- N/V, CNS/vision changes | - PVCs, ST changes, PR prolongation, AV block
40
how do you tx digoxin toxicity
``` stop digoxin tx hypoK atropine for bradycardia -esmolol or lidocaine for refractory ventricular arrythmias -digibind (monoclonal Ab fragments) ```
41
what are some SE associated with prostaglandin?
- plt inhibition and increased risk of bleeding - gastric outlet obstruction wiht prolonged use - bone changes, cortical hyperotosis
42
what drugs can be given to close a PDA?
- indomethacin - ibuprofen - tylenol * high dose ibuprofen associated with higher rates of closure than the rest according to one paper
43
catecholamines work on what overall receptor class?
adrenergic
44
what adrenergic receptors are found on the myocardium?
B1 (sinus node/AV node/myocardium)--increase iontrophy (HR) and chronotrophy (contractility) alpha 1-coronary circulation-->vasoconstriction DA1-coronary circulation-->vasodilation
45
what happens on a cellular level after B1 activation?
- 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
what adrenergic receptors are found in peripheral vasculature?
- alpha1 (skin, pulmonary, renal)-->vasoconstriction - DA1 (renal)-->vasodilation - B2, DA2 (mesenteric and splanchnic)-->vasodilation - B2 (skeletal muscle) vasodilation)
47
what is the role of alpha 2 receptors?
- negative feedback loop for sympathetic nervous systme | - inhibits NE secretion
48
what happens after alpha receptor activation?
-G protein mediated, activation of phospholipase C--> DAG activates protein kinase C--> increased intracellular Ca + PK
49
what is the effect of low/moderate/high dose dopamine?
- 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
what is the MOA of vasopressin
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
when using vasopressin in the infant population what do you need to be cautious for (side effects)
- tissue necrosis with infiltrate | - NEC
52
what is levosimendan used for? what is its moa?
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
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
- 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
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
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
ketamine is used for? a) analgesia b) sedation c) anxiolysis d) amnesia What is MOA? SE?
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
what do you use to sedate in patients with impaired myocardial function
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
dexmedetomidine acts on what receptor and what is it used for?
- acts selective alpha2 receptor agonist - use for sedation, analgesia, sympatholysis - caution: can cause bradycardia and risk for AV block
58
propofol is not used too often in CICU because of what SE?
- 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
SE of inhaled anesthesetics
- 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
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
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
How do you manage a non-dihydropyridine overdose?
``` 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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