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N929 Pharmacology II > Test 2- Main points > Flashcards

Test 2- Main points Flashcards

1
Q

Class 1C agent main points

A

Slow dissociation; MFP- flecainide and propafenone

pro-arrhythmics, used for ventricular and atrial arrhythmias

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2
Q

Class 1A agent main points

A

intermediate dissociation, DQP- quinidine and procainamide, atrial and ventricular tachyarrhythmias
Concerns: lupus like syndrome & cardiotoxic leading to HF

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3
Q

Class 1B agent main points:

A

Fast dissociation, LMP- lidocaine, mexiletine
used in ventricular arrhythmias
-lidocaine has CYP450 metabolism so impaired by propranolol and cimetidine or induced by barbiturates, phenytoin, or rifampin
NOT A PRO-ARRhythmic due to fast dissociation
SE of lidocaine- can prolong NMBD

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4
Q

What drug is used in suppression of ventricular arrhythmias associated with digitalis toxicity?

A

Phenytoin (Class 1B)

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5
Q

Class II agents main points:

A

beta blockers; used to treat SVT, atrial and ventricular arrhythmias; decreases SA node firing and slows through AV node; blocks at phase 4

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6
Q

Class III agents main points:

A

Potassium channel blockers; work at phase 3, lengthening repolarization; used to treat SVT & ventricular arrhythmias, afib
**Super Pro-arrhythmic- torsades
AIDDS (amiodarone, ibutilide, dofetilide, dronedarone, sotalol)

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7
Q

Main points regarding amiodarone:

A

Class III anti-arrhythmic with 1, II, and 4 properties/activities
first line for VT/Vfib
29 day half-life
Adverse effects are huge: pulmonary fibrosis, thyroid abnormalities, pro-arrhythmic

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8
Q

Calcium channel blockers main points:

A

Work at phase 2 (shortens phase 2) of cardiomyocyte on L1a type receptors; decreases contractility of the heart; Verapamil and diltiazem on AV node and nifedipine on arterial bed
not used in ventricular arrhythmias (used in SVT, afib, and aflutter)
Side effects: prolongs neuromuscular blockers, hypotension and bradycardia
Can see reflex tachycardia with nifedipine

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9
Q

Calcium channel blockers and drug interactions:

A

-myocardial depression and vasodilation with inhalational agents
-can potentiate NMBDs
-Verapamil and beta blockers can cause heart block
-Verapamil increases risk of LA toxicity
-Verapamil & dantrolene can cause hyperkalemia
-Digoxin- can increase plasma concentration of digoxin
-H2 antagonists- can increase levels of CCB
toxicity of CCB can be reversed with calcium or dopamine

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10
Q

Calcium channel blockers require:

A

slow discontinuation or else may result in coronary vasospasm

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11
Q

Adenosine takeaways:

A

binds to A1 purine nucleotide receptors and increases K+ currents; slows AV nodal conduction
contraindicated in asthma and heart block

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12
Q

Digoxin takeaway:

A

cardiac glycoside
increases vagal activity, thus decreasing activity of the SA node and prolongs conduction through AV node
SEs: arrhythmias, heart block

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13
Q

Phenoxybenzamine

A

binds covalently A1>A2; pro-drug; decreases SVR and Vasodilation
used for pts with pheo & Raynaud’s
d/t less A2 we see less associated tachycardia

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14
Q

Phentolamine

A

non-selective alpha antagonist
-cause reflex mediated AND alpha 2 associated increases in HR & CO
Used for hypertensive emergences (pheo & autonomic hyperreflexia) & extravascular admin of sympathomimetic agents

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15
Q

Prazosin

A

selective alpha 1 antagonist (less likely to cause tachy)
dilates both arterioles and veins
uses: Pheo, HF, HTN, Raynaud’s

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16
Q

Yohimibine

A

alpha 2 selective blocker; increases the release of Norepi from post-synaptic neurone; used w/ orthostatic hypotension & impotence

17
Q

Terazosin & tamsulosin

A

selective alpha 1a for BPH

orthostatic hypotension is concern

18
Q

Relative contraindications to beta blockers:

A

reactive airway disease; DM (masking of hypoglycemia); heart blocks or AV node blocks; hypovolemia

19
Q

Propranolol:

A

non-selective
causes decreased HR & contractility and increased vascular resistance
chronic treatment: decreased clearance of local LAs and decreased pulm clearance of fentanyl

20
Q

Metoprolol

A

beta 1 selective (selectivity is dose related)

good for asthmatics

21
Q

Atenolol

A

MOST selective beta 1 antagonists with least CNS effects

used for HTN; good for asthmatics

22
Q

Esmolol

A

rapid onset and short DOA beta 1 selective blocker
metabolized by plasma esterases
does not cross BBB or placenta
treats HTN & tachy with laryngoscopy & thyroid storm, thyroidtoxicosis, and pheo

23
Q

Timolol

A

non-selective beta blocker used to treat glaucoma

eye drops can cause decreased BP, HR and increased airway resistance

24
Q

Betaxolol

A

cardioselective beta 1 blocker; better for pts with glaucoma and asthma

25
Q

Labetalol

A

alpha and beta 1 & 2 nonselective antagonist
used for HTN in OR but effects last longer than esmolol
no increase in HR b/c of beta 1 block
can cause bronchospasm, heart block, hypotension, CHF, bradycardia

26
Q

Centrally acting agents

A

reduce sympathetic outflow from vasomotor centers
clonidine is main one- used for HTN, sedation, decrease in anesthetic requirements, analgesia
can see rebound HTN with abrupt cessation
SEs: bradycardia, sedation, hypotension, dry mouth

27
Q

Vasopressin

A

endogenous- released in response to increased osmolality or hypovolemia
V1-vasoconstriction
v2- water reabsorption
v3- corticotropin
Uses: bleeding with Von Willebrand, refractory hypotension, cardiac shock following bypass, diuresis with diabetes insipidus
Concerns: GI ischemia, skin & digitalis ischemia, decreased CO

28
Q

Sodium nitroprusside

A

spontaneous breakdown to NO & cyanide
relaxation of arterial and venous smooth muscle
will see slight increase in HR, increased CBF and ICP
Uses CHF, controlled hypotension, HTN crisis, acute MI (limited d/t coronary steal)
Adverse effects: profound hypotension, cyanide toxicity (tissue anoxia, confusion, death), methemoglobinemia (tissue hypoxemia), thiocyanate accumulation (CNS related effects)
drug interactions: negative inotropes, general anesthetics, circulatory depression, phosphodiesterase 5 type inhibitors, guanylate cyclase stimulators

29
Q

Organic nitrates- nitroglycerin

A

require metabolism step to go through pathway
VENOUS capacitance vessels, dilates coronary arteries
will develop tolerance when you run out of metabolism factors
uses: angina, HTN, controlled hypotension during surgery, non STEMI, MI, HF
Adverse effects: HA, increased ICP, orthostatic hypotension, REFLEX TACHYCARDIA, methemoglobinemia
drug interactions: antihypertensive drugs, selective PDE-5 inhibitors, guanylate cyclase stimulating drugs

30
Q

Milrinone

A

inhibits breakdown of cAMP
inotropic, vasodilation
uses: HF, cardiogenic shock, heart transplant bridge or post op
adverse effects: arrhythmias, hypotension

31
Q

ACE-I

A

blocks the conversion of ANG I to ANG II–> prevents vasoconstriction, aldosterone secretion, decreasing NA & water retention
used for: CHF, HTN, Mitral regurg, post MI, diabetic neuropathy
useful for DM pts
NO REFLEX TACHY
“prils”
drug interaction: K+ sparing diuretic & K+ supplements
SEs: Hyperkalemia, hypotensive, contraindicated in bilateral renal artery stenosis, dry cough, angioedema, teratogenic

32
Q

ARBs

A

sartans- competitive antagonist at AT1 receptor
blocks effects of Ang II mediated by At1R
clinical effects, uses, drug interactions, and contraindications are same as ACE-I

33
Q

Aldosterone antagonist: spironolactone, eplerenone

A

competitive antagonist at mineralcorticoid receptor
effects: increased Na+, H20 excretion, mild diuresis, K+ reabsorption
uses: HTN, HF, K+ sparing diuresis, hyperaldosteronism, spironolactone has off label uses
AEs: hyperkalemia & broad with spironolactone

34
Q

Minoxidil

A

directly relaxes the arteriolar smooth muscle (no effect on venous capacitance) & increases efflux of K+ from VSMC resulting in hyperpolarization and vasodilation
used for HTN
AEs: tachycardia, increased myocardial workload, palpitations, angina, fluid retention
warnings: fluid retention, pericardial effusion/tamponade, rapid BP response sinus tachy, elderly

35
Q

Hydralazine

A

release of NO from endothelial cells, inhibition of Ca release
effects: vasodilates arterioles, minimal venous effect, decreased SVR, DBP reduced> SBP, increase HR, SV, CO
Clinical uses: HTN, HF
adverse effects: reflex tachy, tolerance, tachyphylaxis, sodium and water retention, angina, lupus, HA, sweating, palpitations
Contraindications: CAD, mitral valve, RH disease

N929 Pharmacology II (16 decks)

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