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pharm > exam 2: lecture 4 > Flashcards

exam 2: lecture 4 Flashcards

1
Q

Explain the cardiac AP .

A

phase 0 - NA channel open up, goes into and starts depolarizing the cell

phase 1 = K channels open up and goes out of the cell starts repolarizaing

phase 2: pleatue phase. L TYPE. Ca channels open and goes inside the cell

phase 3: Ca channels close and K remain open

phase 4 = goes back to resting potential and restarts at -65mV

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2
Q

what is the diff between enhanced automaticity and triggers automatciity?

A

enhanced auto = is when there is increased rate of spontaouse discharge starting at the SA node

triggered auto = electrocyte distubrances, early depolarization or delayed depolarization

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3
Q

what are the four classes Myles Von William made?

A

Class 1 - Na blocker
2- BB
3 - K blockers
4 - CCB

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4
Q

what are the drugs part to Na channel blockers?

A

Class 1A: (PQN) procainamide, quininide, disopyramide
Class 1B: lidocaine, mexliletide
Class 1C; flecanide

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5
Q

how did sodium channel blokcers come about?

A

it all started with cocaine. Cocaine blocks sodium channels in the neurons. cocaine were used as anestheics but was too strong.

it was changed to procaine then to lidociane which had better success

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6
Q

what is the MOA, indication and S/E for procainamide?

A

given PO IV IM
MOA: blocks NA channel in the cardiac myocyte = depressing effect of SA/AV node

  1. prolongs AP and RP
  2. blocks some K channels
  3. prolongs QRS and QT intervals

indication: 2-3rd agent for MI induced arrthymias

S/E: excesive slowing of Heart, prolong QT so torsade, fainting and lupus like syndrome if given PO

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7
Q

what are quinidine and disopyramide?

A

they are part of CLASS 1A drugs,

quinidine = similiar to procainamide but is anti malaria. it has anti muscarinic effect (dry mouth, consitpation, urinary retention)

dispyramide = similiar to procainamide but even way worse

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8
Q

what are the class 1B drugs ?

A

lidocaine
mexiletine

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9
Q

what is the MOA, indication, S/E for lidocaine?

A

MOA:
1. blocks NA channels in both active and inacttive channels
2. bascially just takes neruon out of commison
3. shorterns AP and shortens RP
4. WORKS BEST W ISCHEMIC HEART AND FAST HR

indication: MI with induced arrthymias, Vtach/Vfib, CV

S/E - THE LEAST CARDIOTOXICITY
- AMS, parethesia, psychosis, euphoria , stupor

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10
Q

what is mexiletine?

A

part of the class 1B Na blocker drugs

it is similiar to lidocaine but given PO
good for long term tx and for chronic pain syndrome

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11
Q

what is flecainide? MOA/indication?

A

part of class 1C of NA blocker

it works w NORMAL tissue w NORMAL HR

MOA: blocks NA channels and some K channels, decreases slope of phase 0, NO CHANGES TO AP OR RP, prolong QRS

indication: supraventricualr arrhythmias, PVC

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12
Q

what is BB MOA?

A

B1 normally casues influx of CA and NA which leads to + chronotropic and inotropic effect

but BB will block this and decrease CA influx so decrease contract

BEST for ishemica heart bc it lowers demand for O2 and work

IT SLOWS AV CONDUCTION

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13
Q

what are the BB drugs in CLASS 2?

A

propranolol - 1st gen drug, if given in high dose can mimik class 1 drugs - block NA

sotalol - verstailie drug, to go BB

metoprolol - 2nd gen drug

esmolol - short half life 8 mins

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14
Q

what is the indication of BB?

A

sinus tachy
Afib/aflutter
ventricular tachy
long QT syndrome
re entry circut

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15
Q

what are the class 3 drugs?

A

K blocker drugs
- K-ADDI-
amiodarone
dronedarone
dofetilide
ibutilde

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16
Q

what is the MOA of amiodarone?

A

Amiodarone is liek a thyroid hormkone so it interacts w thyroid hormone receptor in the cardiac myocyte

it blocks EVERYTHING!!
it blocks K channel WHICH prolongs AP and RP

  • andrenergic channels,
  • NA channels
  • Ca channels
17
Q

what is the indication and pharmacokinetics for amiodarone?

A

indication: 1st in line for Vtachy/Vfib
- it also does rate control for Afib (slowing conduction through AV node)

  • given IV or PO (long term)
  • metabolzied by CYP3A4
  • 3-6 months half life HAS A WIDE VOLUME OF DISTRUBUTION
18
Q

what are the S/E for class 3 drugs?

A
  1. bradycardia
  2. skin and corneal discoloration but no visual impartment
  3. GI: N/V
  4. Hyper/hypothyroidism = since amiodarone is like a thyroid hormone, it will bind to the thyroid hormone receptor OR it can inhibit thyroid uptake of iodine
  5. pulmonary fibrosis = the drug can accumulate O2 radically coupled
    • “ground glass” w pul infiltrates = pneuomonittis
19
Q

what are dronedarone, dofetilide, ibutitlide ?

A

they are class 3 K blocker drugs

dronedarone is an analog of amiodarone BUT NO IDOINE OR NO THYROID EFFECT, DECREASE PUL TOXICITY

dofetilide / ibutilide = same class but not often used

20
Q

what is the MOA for class 4 CCB?

A

non dihydro (V and D) will block L type Ca channels on the SA and AV nodes

  • OVERALL: slows AP, increases RP, prolong repolarization of AV node also increase PR interval
21
Q

whats the indication and S/E for class 4 drugs?

A

indication: reentry rhythms, supraventricualr tachycarida, Afib, Aflutter

DONT GIVE IN VENTRICUALR ARRYHTMIAS due to poor CO

S/E = bradycarida SINCE were slowing heart

22
Q

what is the class, MOA, and indication for adenosine?

A

adenosine is part of the CLASS 1E

MOA: it works on adenosine receptor GPCR linked to Gi protein, it OPENS K, increases hyperpolarization which SLOWS AP DURATION and decrease HR
= it also decreases CA in the heart

NET EFFECT: prolong RP, prolong PT interval, slow AV conduction, reduce Ca

indication: supraventircualr and reentry since we are SLOWING conduction throuhg AV NODEw

23
Q

what is the MOA, class and pharmokinetics for ivabradine ?

A

ivabraidine is given PO
MOA = it blocks the Na funny channels in the SA node so it dramitcally decreases firing of SA NODE, which reduced HR

no change in ionotropic of the heart!!!

metabolized by CYP3A4

CLASS 0

24
Q

what is the indication and s/e for ivabradine?

A

class 0 drug

indication: Heart failure (you are not affecting the contraction but slowing the heart down/less O2 needed which is good for HF)

S/E: bradycardia!, visual disturbances, aFIB, HTN

25
Q

what are rx we learned that are anti muscarinic agents?

A

IT
ipratropium
tiotripium

USED FOR COPD

26
Q

what are rx we learned that are vasocontrictirs/decongestants?

A

PP
phenyleprhine
pseuodoephedrine

27
Q

what are rx we learned that are broncohdilators and corticoseriods?

A

albuterol, salmetrol = B2 agonist

beclomethasone, fluticasone, traimcinolone = decreases inflammtion, inhaled for asthma

28
Q

what are the anti-tussive drugs we learned?

A

CDH
codine
dextromethorphan = supresses couhg center in medulla
hydroconde = modifcation of semi syntehtic opioid

29
Q

what are the mucolytic/expectorant drugs we learned?

A

guaifesnsein = reduces viscoity, increwases water content, stimulates cillia

acetylcystenine = good for acetameophine overdose, splits disulfide bonds in muscus

30
Q

what are the leukotriene antagonist drugs ?

A

zileuton, zafirlukast, montelukast

31
Q

how do leukotreine antagonist drugs help those with asthma?

A

lipoxygense enzyme converts AA to leukotreines such as LD4 –> helps w vasoconstriction, vascular permability, and edema

leukotrienes antagonist inhibits this

Zileuton –> inhibits the enzyme that makes leukotrienes

Zafirlukast + montelukast –> bind to LD4 receptor and stops it

32
Q

whats the moa and S/E for leukotriene antagonist?

A

MOA: inhibits leukotreine production to stop inflammatory responses that casues astham

S/E: depression, psychosis, mental status changes

33
Q

what is the anti-eosinophilic drug MOA, pharmokinetics, indication, and S/E?

A

In asthma, IL5 induces maturation of eosinophils which drives the larger stages of inflammation

Benralizumab –> binds to IL5 receptor and prevents it from maturating eosinophils

Benralizumad –> also binds to NK cells and casues apoptosis of eosinophils

pharmokinetics: subQ every 4Q for first 3 months then q8 weeks/2 months after

indication: asthma duh

S/E: flu like sx, injection irrtation, Helminthic infection susceptibility (eosinophils fight of the parasitic illness, without them its bad *

34
Q

what is the MOA and pharmokinetics for Omalizumab?

A

Omalizumab is an anti IGE drug. FOR THOSE W SEVERE ASTHAM OR DRUGS THAT HAVE NO WORKED

it binds to IGE and prevents activation of mast cell and reduces histamine and infalmmation

given subQ q2-4 weeks or imn severe pt where other meds have no worked

35
Q

how does cromoyln and nedocromil sodium work? what are the indication?

A

these are drugs used for asthma.

they attack the CL channels on mast cells –> prevent mast cell from degranulation –> which stops it from secreting histamine

the drugs also effects the neurons –>goes through the inhalation route in the lungs and stops neruon from firing the cough reflex –>inhibits cough and inflammation!

indication: mild asthma, opthalmic formualtion which decreases eye inf, and rhinitis, GI

36
Q
A

pharm (13 decks)

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