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IPAP 21-2 Soph Semester > Drugs Only, Block 1 Pharm > Flashcards

Drugs Only, Block 1 Pharm Flashcards

1
Q

Pilocarpine

A

Cholinergic Agonist
IND:
EYE: Reduce IOP in ocular HTN, Prevent Post Op IOP
Oral: Xerostomia

ADE: DUMBELLS Decreased Far Visón

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2
Q

Bethanechol

A

Cholinergic Agonist
MOA: increases bladder contraction relaxes sphincter
IND: acute PostOP nonobstructive UOP retention, neurogenic stony of urinary bladder

ADE: DUMBBELLS
Contra: Obstruction, Asthma, PUD, Bradycardia

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3
Q

Edrophonium

A

Competive Indirect Cholinergic Agonist
MOA: Short acting that potentiates acetylcholine activity by inhibiting its destruction
IND: DDx of Myasthenia Gravis, Myasthenia Crisis, reverse the effects of non-depolarizing neuromuscular blocking agents (not succs)

ADE: DUMBBELLS
Contra: Obstruction of GU/GI, when the bladder wall strength is questionable

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4
Q

Physostigmine Salicylate

A

Indirect Cholinergic Agonist
MOA: competitive (reversible) acetylcholinesterase inhibitor that potentiates acetylcholine activity by inhibiting its destruction

IND: Reversal for OD on anticholinergics, reserved for severe life threatening cases (Extensive delirium or agitation, hallucination, hyperthermia, supraventricular tachycardia)

MAKE SURE TO MONITOR THE PT! ECG, VITALS.
ADE: SEVERE DUMBBELLS
Contra: Obstruction GI/GU, RR distress or SZR

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5
Q

Neostigmine

A

Indirect Cholinergic Agonist
MOA: Synthetic Competitive acetylcholinesterase inhibitor
Medium Acting
IND: Tx of Myasthenia Gravis, Reversal of no depolarizing blocking agents

(More polar than pheostigmine) (Less SZR)

Route: PO, IV
ADE: DUMBBELLS

Contra: Obstruction of GU/GI

CAUTION: Asthma, PUD, or Bradycardia

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6
Q

Pyridostigmine

A

Indirect cholinergic agonist

competitive (reversible) acetylcholinesterase inhibitor
Medium Acting
IND: Tx of myasthenia Gravis, reverse non depolarizing blocking agents, nerve agent pretreatment

ADE: DUMBBELLS
Contra: GI/GU obstruction, weak bladder wall

CAUTION: ASTHMA, PUD, Bradycardia

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7
Q

Echothiophate

A

Only noncompetitive acetylcholinesterase inhibitor used on a regular basis

MOA: indirect cholinergic agonist that contracts the ciliary muscle leading to increase aqueous humor outflow

IND: Gluacoma
ADE: Miosis, decreased accommodation (far vision)

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8
Q

Pralidoxime

A

MOA: Reactivate cholinesterase, detoxifies certain organophosphates, reverses the paralysis of respiratory muscles
IND: Anitdote for organophosphate OD and anti cholinesterase drugs

ADE: blurred vision, diplopia, impaired accommodation, dizziness, headache, drowsiness, nausea, tachycardia, increased systolic and diastolic blood pressure, hyperventilation, and muscular weakness when given parentally to normal people who have not been exposed to anticholinesterase poisons.

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9
Q

ATNAA

A

Antidote Treatment Nerve Agent Auto injector)

  • Atropine (anticholinergic agent)
  • Pralidoxime (reactivate cholinesterase)
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10
Q

CANA

A

(Convulsant Antidote for Nerve Agent)

Diazepam (benzodiazepine) to control nerve agent induced seizures

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11
Q

ALZHEIMERS DRUG LIST

A

Tacrine
Donepezil
Galantamine
Rivastigmine

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12
Q

Atropine

A

Anticholinergic (competitive)
MOA: Inhibits the muscarinic actions of acetylcholine (Central and Peripheral)
IND: EYE for Mydriasis/ Cycloplegic, Bradycardia, GI/GU antispasmodic (hypotonic radiography), Cholinergic OD

Route: PO, IV, IM, Eye ggts

MAKE SURE TO MONITOR PT ( HR, BP, AMS)
ADE: Blind, Mad, Red, Hot, Dry, Bowel Loose, Inc HR

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13
Q

Anti Cholinergics used in the eye

A

Atropine (we know this one)
Cyclopentolate
Tropicamide (we know this one)
MAO: produce mydriasis and cycloplegia, loss of accommodation

IND: Dx procedures, produces mydriasis and cycloplegia, eye exams

ADE: Photo sensitivity, inability to focus, anticholinergic affects ( Blind, Mad, Red, Hot, Bowel tone decreases, Tachycardia)

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14
Q

Anticholinergic for GU use

A 
Oxybutyin 
Derifenacin 
Solifenacin 
Tolterodine 
Fesoterodine 
Trospium

MOA: Decreases bladder tone resulting in detrusor muscle relaxation and sphincter constriction

IND: overactive bladder

ADE: Dry mouth, constipation, anticholinergic effects
(Less ADE with a transdermal patch)

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15
Q

Anticholinergics used in GI

A

Dicyclomine

Belladonna Alkoloids

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16
Q

Dicyclomine

A

Anticholinergics for Gastrointestinal Use
MOA: Blocks Ach
IND: IBS
ADE: Anticholinergic effects, CNS defects, drowsiness, blurred vis. AMS, Psychosis/ delirium, Diarrhea

CAUTION: D/C Tx if diarrea occurs (sign of Incomplete obstruction)

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17
Q

Belladonna Alkaloids

A

Combination of Hyoscyamine, Atropine, Scopolamine, and Phenobarbital
Anticholinergics for Gastrointestinal Use

MOA: Inhibits Muscarinic reseptors
IND: IBS, acute enterocolitis, duodenal ulcer

ADE: Anticholinergic effects, CNS depression, Drowsiness, Psychosis/ delirium, Diarrhea

CAUTION: D/C Tx w/ Diarrhea, sign of incomplete obstruction

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18
Q

Anticholinergics used in the Lungs

A

Ipatropium (short acting)
Tiotropium ( long acting)

MOA: cholinergic antagonist that causes bronchodilation, decreases resp secretions
IND: COPD
ADE: Anticholinergic effects, (inhalation minimizes ADE)
(Less Efficacy in ASTHMA when compared to B2 agonists)

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19
Q

Should anticholinergics be used to treat acute asthma

A

No

Compared to β2 agonists, anticholinergics have similar or greater efficacy for COPD, but less efficacy for asthma
Anticholinergics are NOT appropriate for relief of acute asthma symptoms

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20
Q

Scopalamine

A

Belladonna Alkaloid
MOA: cholinergic antagonist with greater central than peripheral effects
IND: motion sickness, decreases saliva, blocks short term memory (surgical adjunct)
BE SURE TO MONITOR PT: HR, TEMP, UOP
ADE: Drymouth, drowsiness, Anticholinergic effects

CAUTION: Wash hands after handling the patch

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21
Q

Anticholinergics used for Parkinson’s

A

Benztropine (controls extrapyramidal d/o except dyskinesia)
Trihexyphenidyl

MOA: centrally-acting cholinergic antagonist in an attempt to restore its balance with dopamine levels

IND: Parkinson’s, adjunct with L-dopa and phenothiazines

ADE: anticholinergic effects

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22
Q

MOA of NMBA

A

Block acetycholine at the Nm (nicotinic muscle) at the neuromuscular junction at the skeletal muscle

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23
Q

Order of paralysis with NMBA

A

Order of paralysis (peripheral to central): face/eyes; fingers; limbs; neck; trunk muscles; intercostal muscles; diaphragm

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24
Q

Can cholinesterase inhibitors reverse depolroizing NMBA

A

Not in phase I, in phase II they potential can in late phase

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25
Q

Can AchE inhibitors reverse nondepolarizing NMBA

A

Yes, increasing Ach can compete with Nondepolaring NMBA as well as AchE inhibitors (Indirect Ach Agonists) such as neostigmine, pyridostigmine, and edrophonium

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26
Q

Succinylcholine

A 
NMBA 
MOA: NMBA Depolarizing Agent
IND: DOC from rapid sequence intubation, procedures lasting < 3min, Endoscopic exams, Convulsion therapy, 
Duration: 4-6 min 
DO NOT GIVE AS INFUSION 
MONITOR: Sedation, Temp, RR, K*

ADE: malignant hyperthermia, Apnea, HyperK*
Contra: Pmhx of Malignant Hyperthermia, muscle myopathies

Drug interactions: digoxin

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27
Q

Reversal agent for Malignant Hyperthermia

A

Dentrolene

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28
Q

What does atracurium metabolize to

A

Laudanosine ( can cross the BBB and cause SZR)

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29
Q

What is the NMBA DOC in renal and hepatic dz

A

Cisatracurium

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30
Q

OnabotulinumtoxinA

A

MOA: NMBA

Inhibits the release of acetylcholine from cholinergic nerve fibers at neuromuscular junctions
Produced by the bacteria clostridium botulinum

IND: Chronic Migraines ( 2nd line agent), Cervical Dystonia, Blepharospasm, Cosmetic Procedures : Glabellar lines, Rhytides, crows feet’s.

ADE: Double vision, blurred vision, eyelids droop, slurred speech, the head sags, the legs lose their ability to support one’s body, breathing stops, Pain at injection site
CAN BE A BIO WEAPON

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31
Q

What is the antidote for OnabotulinumtoxinA

A

Equine botulinum antitoxin

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32
Q

Brimonidine tartrate

A

Sympathetic agonist
MOA: decrease IOP, contracts radial muscle (mydriasis)
IND: OPEN ANGLE glaucoma or ocular HTN

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33
Q

Timolol

A 
non-selective β-blocker
B Antagonist 
MOA: decrease aqueos humor production 
With no effect on pupil 
IND: reduction of elevated IOP in OPEN ANGEL glaucoma or ocular HTN
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34
Q

Epi

A

Direct acting catecholamine
MOA: direct-acting catecholamine released by the adrenal medulla that is an agonist at both α and β receptors
(α1=α2; β1~β2)
Increase HR, CO, Inc SysBP, Bronchodialation, prolongs anesthetics.

IND: Bronchospasms, Anaphylaxis, Cardiac Arrest, Anesthetic adjunct.

ADE: Anxiety, tremor, HTN, Tachy HR, Cerebral Hemorrhage, Mydriasis, Hyperglycemia, Extravasation

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35
Q

What is the effect of EPI at low doses

< 0.5 mcg/kg/min

A

Vasodilation predominates (B2)

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36
Q

What is the effect of Epi at high doses

>0.5mcg/kg/min

A

Vasoconstriction predominates (a1)

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37
Q

What are the drug interactions of Epi

A

a- blockers, b-blockers, and increased the efficacy of MAOI and COMT inhibitors

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38
Q

Dipiverfin

A

MOA: prodrug metabolized to epinephrine in the eye that decreases IOP by contracting the radial muscle that opens the trabecular network to increase aqueous humor outflow

IND: OPEN ANGEL glaucoma
ADE: mydriasis, burning/ stinging

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39
Q

NE

A

Direct acting catecholamine
MOA: direct-acting catecholamine that is an agonist at both α and β receptors (α effects&raquo_space; β1&raquo_space;> β2)

Increases Vasoconstriction and inotropic effect.
SBP AND DBP

IND: short term treatment of shock, Arrhythmia

ADE: Anxiety, fear, tremor, HTN, Cerebral hemorrhagic 2/2 increased BP, extravasation

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40
Q

What the mortality difference when using dopamine or NE in Tx of shock

A

Dopamine»NE

No mortality difference

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41
Q

What are the drug interactions of NE

A

Same as EPI

a-blockers, b-blockers, increase efficacy of MOAI and COMT inhibitors

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42
Q

Isoproterenol

A

Direct acting catecholamine
MOA: Direct-acting catecholamine that is a non-selective agonist at β1 and β2 receptors (β1 = β2)

IND: bradyarrythmias, 3rd degree HB (temporary use)
MONITOR: EKG
ADE: Anxiety, fear, tremor, tachycardia, hyperglycemia

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43
Q

What are the drug interactions of Isoproterenol

A

COMT inhibitors may prolong action, b-blockers result in physiologic anatogonism

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44
Q

Dobutamine

A

Synthetic Direct Acting Catecholamine
MOA: synthetic, direct-acting catecholamine that is a selective β1 agonist
IND: increase CO in Acute decompensated HF
MONITOR: EKG
ADE: Headache, A fib

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45
Q

What are the drug interactions with dobutamine

A

COMT inhibitors may prolong action

b-blockers result in physiologic antagonism

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46
Q

Dopamine

A

Direct acting catecholamine
MAO: Direct-acting catecholamine that stimulates α, β, and dopamine (D) receptors, depending on dose
IND: Low dose: cardiac and septic shock, alternative to NE
MONITOR: EKG, VITAL SIGNS, UOP

ADE: Anxiety, tremor, tachy HR, HTN, Extravasation

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47
Q

Should low dose dopamine be used for renal protection

A

NO!

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48
Q

What are the drug interactions for Dopamine

A

A-blockers and b-blockers

Increase efficacy of MAOI and COMTI

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49
Q

What receprtors does Epi hit

A

A1 and 2 (more) ,

B1 and 2 (less)

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50
Q

What receptors does NE hit

A

A1 and 2 (more)

B1 and 2 (less)

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51
Q

What receptors does isoproterenol hit

A

Only B1 and B2

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52
Q

What receptors does dobutamine hit

A

A1 and 2 (less)
B1 (most)
B2 (less)

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53
Q

What receptors does dopamine hit

A

Dose dependent
Low dose B1 and D1
Medium dose B1, B2, D1 and minimal A1
High Dose A1, B1, B2, and no D1

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54
Q

Phenylephrine

A

Direct acting non-catecholamine
MOA: synthetic α1-agonist

Increases BP (SBP & DBP), dilates the pupil, constricts engorged ocular, nasal, and rectal vasculature to decrease redness and congestion, and shrinks hemorrhoids

IND: Tx of HOTN 2/2 Shock, Mydriasis for Eye exams, Relief of eye redness, hemorrhoids, and nasal decongestant.
MONITOR: BP (drug increases it)
ADE: Extravasation, HTN HA, Rebound Congestion

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55
Q

What are the drug interactions of phenylephrine

A

A-blockers and MAO-I

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56
Q

Oxymetazoline (AFRIN, Visine)

A

Direct acting non-catecholamine
MOA: Direct-acting α1 and α2 agonist

Eye drops or nasal spray produces vasoconstriction that decreases blood flow resulting in decreases ocular redness and nasal congestion

IND: Relief of red eye and congestion
ADE: rebound hyperemia and congestion, stinging/ burning sensation

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57
Q

Midodrine

A

Direct acting non catecholamine
MOA: Prodrug that forms an active metabolite, desglymidodrine, an α1 agonist

Causes vasoconstriction, increases SBP & DBP

IND: Orthostatic HOTN
ADE: HTN, Brady HR, Piloerection (GOOSEBUMPS), Paresthesia

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58
Q

What prodrug gets converted to desglymidodrine

A

Midodrine

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59
Q

What are the drug interactions for midodrine

A

MAO-I

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60
Q

Clonidine

A

Direct acting non catecholamine
MOA: Stimulates α2 presynaptic receptors in the brain stem (central)

Reduces sympathetic outflow from the CNS and decreases peripheral resistance, renal vascular resistances, heart rate, and blood pressure

IND: HTN, ADHD, (REMEMBER LUAREN SCHOOLED YOU), Tourette’s, Opiod WTDRWL, NICOTINE WTHDRWL

CAUTION: DO NOT D/C SUDDENLY

ADE: Drowsiness, Dizzy, Dry mouth, constipation, Itching, redness, Sodium and Water retention

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61
Q

What are the drug interactions of Clonidine

A

Enhances B-blockers (AV blocking effect)

Withdrawal b-blocker several days before clonidine withdrawal when possible (monitor BP closely)

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62
Q

Brimonidine

A

Direct acting non catecholamine
MOA: ocular α2-agonist, decreases aqueous humor production

IND: Glaucoma
ADE: burning/ stinging

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63
Q

b2 agonists

A

All end in -ol
MOA: β2 agonist that relaxes bronchial smooth muscle resulting in bronchodilation
IND: Asthma, COPD
MONITOR: Peak Expiratory Flow Rate (PEFR) and Pulmonary Function Tests (PFTs)

ADE: Increase BP, Tachy HR, Nervousness, restlessness, Hypo K*, hyperglycemia

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64
Q

What are the drug interactions of B2 agonists

A

B- blockers (primarily non selective)

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65
Q

What is the B agonist of choice for acute respiratory relief in COPD and asthma

A

Albuterol

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66
Q

What drug is a R-isomer of Albuterol

A

Levalbuterol

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67
Q

What B 2 agonist does not end in -ol and is used to suppress premature birth

A

Terbutaline

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68
Q

What is arformeterol only approved for

A

COPD

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69
Q

Is formoterol approved for acute relief of asthma

A

No, despite its rapid onset of action (less than 5 min)

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70
Q

What is Indacterol only approved for

A

COPD

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71
Q

Mirabegron

A

Direct acting non catecholamine

Mechanism of Action: β3 agonist that relaxes the detrusor muscle, increases bladder capacity

IND: Overactive bladder

ADE; increases BP

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72
Q

What are the drug interaction of Mirabegron

A

Anticholinergics for the bladder, (increases urinary retention)

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73
Q

Fenoldopam

A

Direct acting non catecholamine
MOA: D1 agonist that bind with moderate affinity to α2 receptors

Rapid acting vasodilator
Decreases peripheral vascular resistance and BP secondary to increased renal blood flow, and natriuresis/diuresis

IND: In hospital tax of severe HTN with renal compromise
-6x more potent as dopamine in producing renal vasodilation

ADE: HA, Flushing, Dizzyness, N/V, Reflex Tachy HR, Hypokalemia

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74
Q

What are the clinical uses of indirect acting adrenergic agonist

A

ADHD
Narcolepsy
Obesity
Depression

(METH, COCAINE)

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75
Q

What are the ADE of dextroamphetamine and methamphetamine

A

Insomnia, irritability, tremor, panic, SI, psychosis, dependency, HTN, palpitations, N/V/D, anorexia, stunted growth

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76
Q

Dextro- and methamphetamine are contraindicated in what pts..

A

Contraindicated in patients with hypertension, CV diseases, hyperthyroidism, and glaucoma

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77
Q

What are the drug interactions with Dextro- and methamphetamine

A

MAO-I

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78
Q

What are the drug interactions with tyramine

A

Like amphetamines, tyramine can enter nerve terminals and displace norepinephrine, which then acts on α-receptors.

Found in fermented foods.

Patients taking a mono amine oxidase inhibitors (MAOI) who eat tyramine containing foods can develop hypertensive crisis

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79
Q

Patients taking a mono amine oxidase inhibitors (MAOI) who eat tyramine containing foods can develop?>

A

HTN crisis

80
Q

What it tyramine

A

Tyramine is an indirect sympathomimetic that will release stored epinephrine and norepinephrine causing: hypertension, tachycardia, nausea, arrhythmias and stroke

81
Q

Cocaine (C-II)

A

Indirect acting agonist
MOA: Inhibits the reuptake of norepinephrine/epinephrine back into the synaptic vesicles
Blocks the initiation or conduction of the nerve impulse following local application

IND: topical anesthesia to accessible mucous membranes of the oral, laryngeal, and nasal cavities

ADE: CNS STIM/ Depression, Bradycardia at low dose, TACHY HR at high dose, vasoconstriction

82
Q

At what dose is cocaine fatal

A

1.2 grams, with severe toxic effects reported as low as 20 mg

83
Q

What are the Mixed- action Adrenergic Agents

A

Ephedrine and Ephedra

84
Q

Ephedrine and Ephedra

A

Mixed action adrenergic agonist
MOA: direct acting α and β agonist, while also displacing NE from storage sites

IND: Ephedrine: (1) bronchospasms; (2) nasal congestion; (3) hypotension ( can be used to temp relieve SOB, chest tightness, and wheezing due to bronchial asthma

Ephedra: Wt loss, Energy Booster, Inc Athletic performance (Currently Banned for life threatening CV RXN)

ADE: anxiety, insomnia, HTN, TACHY HR, false positive for meth

85
Q

What are the drug interactions for ephindrine and ephedra

A

A-blockers

86
Q

Psuedoephedrine (Sudafed)

A

Mixed action adrenergic agonist
MOA: direct acting a and b agonist, while also displacing NE from storage sites

IND: Relief of nasal congestion
ADE: HTN, Tachy HR, Used to make meth, false postive for meth

87
Q

What are the drug interactions for pseudoephedrine

A

A-blockers

88
Q

Phenoxybenzamine

A

A blocker
MOA: Nonselective, noncompetitive (irreversible) α1 and α2 antagonist

Prevents α-vasoconstriction, decreases BP

IND: Pheochromocytoma

ADE: orthostatic HOTN, reflex TACHY HR, Nasal Decongestion, N/V

89
Q

Phentolamine

A

A blocker
MOA: Antagonizes a-constriction, prevents secondary necrosis to HTN , increases HR and contraction (presynaptic a2 blocker)

IND: Dx of pheochromcytoma, Tx for Extravasation, Impotence (rarely used)

ADE: Orthostatic HOTN, Reflex Tachy HR, Nasal congestion

90
Q

What is the MOA of a1 blockers

A

Competitive α1 receptor blocker

Blocks α-receptors to prevent vasoconstriction

Decrease BP secondary to arterial and venous dilation

Benign Prostatic Hyperplasia (BPH) symptoms improve
secondary to relaxation of the smooth muscle in the bladder and prostate

Improves blood flow to extremities, possibly reducing sensitivity to cold

91
Q

What is the IND for a1 blockers

A

Hypertension
BPH
Raynaud’s Disease (reduced blood flow)
Pheochromocytoma

92
Q

What are the ADE and Contra for a1 blockers

A

ADE: Orthostatic HOTN, Syncope after 1 dose, Reflex Tachy HR, Angina, HA, drowsiness, asthenia (weakness)
nasal congestion, inhibition of ejaculation

Contra: alfuzoin in patients with moderate to severs hepatic dz

93
Q

Alfuzosin is contraindicated in pts with

A

Potent CYP3A4 inhibitors (-azole and antifungals)

94
Q

Should a1 and a1a blockers be used together

A

No

95
Q

Should a1 and PDE5 inhibitors (sildenafil) be used together

A

No

96
Q

What is prazosin used for

A

A1 blocker
PTSD and nightmares

NOT APPROVED FOR BPH

97
Q

What is doxazosin approved for

A

A1 blocker

HTN and BPH

98
Q

What is the only XR a1 blocker approved for BPH

A

Doxazosin

99
Q

What is terazosin approved for

A

A1 blocker approved for BPH and HTN

100
Q

What is alfuzosin approved for

A

A1 blocker approved ONLY for BPH

Not selective for a1a receptor

101
Q

Drugs that in in -Osin are

A

A(1a) blockers

102
Q

Tamsulosin and Silodosin

A

A (1a) blockers
MOA: Uroselective; competitive α1A-blockers, relieving bladder outlet obstruction and reducing symptoms associated with BPH

IND: BPH ( NOT HTN)

Monitor: IPSS (BPH SCORE) and Qmax/ UOP retention

ADE: Orthostatic HOTN, syncope, Floppy iris, abnormal ejaculation, nasal congestion, weakness, dizzynyess (more with tamsulosin)

103
Q

What are the drug interactions of Tamsulosin and Silodosin

A

caution in patients using phosphodiesterase 5 (PDE5) inhibitors (i.e. sildenafil, tadalafil

104
Q

Tamsulosin may cause what undesirable penis complication

A

Priapism

105
Q

What pts is Silodosin contraindicated in

A

Pts with severe hepatic and renal impairment

106
Q

To minimize the risk of intraoperative floppy iris syndrome (IFIS)…patients using α1 blockers should have a medication washout period for how long

A

2 weeks prior to cataract surgery

107
Q

B blockers MOA, IND, ADE

A

MOA:
B1 antagonist: decrease HR (SA and AV nodes), decreases strength of contraction, decrease renin release, decrease BP, PVR, Myocardial O2 demand.

B2 antagonist: inhibits skeletal muscle vasodilation (makes PVR worst), Smooth muscle relaxation (bronchoconstriction) Blunts and masks hypoglycemic response

-decreases IOP without affecting pupil size

IND: Hypertension
Angina
Congestive Heart Failure (CHF)
Tachyarrhythmias
Myocardial Infarction (MI)
Glaucoma
Hyperthyroidism 
Pheochromocytoma
ADE: Hypotension
Bronchoconstriction
Bradycardia
Depression (β-blocker blues)
Metabolic disturbances (i.e., lipolysis , etc.)
Burning/stinging (ocular)
Erectile Dysfunction
108
Q

What are the drug interactions of B blockers

A

B agonists
Non-dihydropyridine
Calcium Channel blockers

109
Q

What is the b blocker DOC in thyroid storm

A

Propranolol

110
Q

Since propranolol crosses the BBB ( lipophilic) it is useful in the Tx of

A

Migraine prophylacxsis

111
Q

Which b blocker is most likely to cause b blocker blues

A

Propranolol

112
Q

What is nadolol approved for

A

Migraine prophylaxis , has a long t 1/2

113
Q

What is the route admin for Timolol

A

PO and its rarely used (opthamolic)

114
Q

Does atenolol cross the BBB

A

No

115
Q

What should be used instead of timolol

A

Betaxolol

It’s more beta than tim

116
Q

Does bisoprolol cross the BBB

A

Yes

117
Q

What is esmolol approved for

A

Thyroid storm, for Tachy cardia and HTN ( perioperative in the OR)

118
Q

Which b blocker produces a N.O. Potentiating vasodilation effect

A

Nebivolol

119
Q

Which b blocker is a B1 specific blockade

A

acebutolol

Ace is number 1

120
Q

What b blocker is a non specific b blockade

A

Pinolol and penbutolol

Can’t pin it down to one

121
Q

Which B blocker was designed to weakly stimulate B1 and b2 receptors

A

Penbutolol

They are pen palls with B1 and b2 receptors event tho they are blockers

122
Q

Carvedilol

A

Mixed α1 and nonspecific β-blockers

MOA: In hypertension, decrease’s rate and strength of contraction of heart without reflex vasoconstriction (α1 antagonism)
In CHF, decreases afterload by inhibiting vasoconstriction (α1 antagonism) while decreasing SNS tone via β-blockade

IND: HTN and CHF

ADE: Orthostatic HOTN, Brady HR

CONTRA: asthma, 2nd and 3rd * HB, severe Brady HR, or liver failure

123
Q

What are the drug interactions of Carvedilol

A

Physiological Antagonism: α and β agonist

Additive Effect: α and β antagonist

Cumulative Negative Inotropic Effect: non-Dihydropyridine Calcium Channel Blockers (DHP CCBs)

124
Q

Labetalol

A

Mixed α1 and nonspecific β-blockers

MOA:
In hypertension, decrease’s rate and strength of contraction of heart without reflex vasoconstriction (α1 antagonism)

In CHF, decreases afterload by inhibiting vasoconstriction (α1 antagonism) while decreasing SNS tone via β-blockade

IND: HTN PO Offlabel use in pregnancy, SEVERE HTN (IV)

ADE: Diabetics and Asthma
Orthostatic HOTN

125
Q

What pt population is labetalol most useful in

A

Elderly or black HTN pts who cannot tolerate increase PVR

126
Q

At what HR should you decrease the dose of Carvedilol

A

<55 BPM

127
Q

What are teh 4 types of b blockers

A

Non-selective Beta-1 & Beta 2 blockers

Selective Beta-1 blockers

Intrinsic Sympathomimetic Activity (ISA) Beta blockers

Mixed alpha & non-selective Beta-bloc

128
Q

What are the general contraindication for B blocker

A

Bradycardia (<55BPM)

PR-interval >0.24, or 2nd/3rd degree heart block

Decompensated Heart Failure

Asthma

129
Q

What are the three non selective B blockers

A

Propranolol (Inderal)
Nadolol (Corgard)
Timolol (Timoptic) – eye drop

130
Q

What are the 4 B1 selective blockers

A

Atenolol (Tenormin)

Bisoprolol (Zebeta)

Esmolol (Brevibloc) – Extremely short half life

Metoprolol (Toprol XL or Lopressor)

131
Q

What are the 2 Mixed a1 and nonspecific b blockers

A

Labetalol and Carvedilol

132
Q

What are the 3 ISA beta blockers

A

Acebutolol (Sectral)
Pindolol (Visken)
Penbutolol (Levatol)

133
Q

What is the role of BZD in pre anesthesia

A

Used to relieve anxiety, facilitate amnesia and produce sedation

Examples: Diazepam (Valium), Lorazepam (Ativan), and Midazolam (Versed)

134
Q

What is the role of Opiods in pre-anesthesia

A

Administered pre-operatively as adjuncts to inhalation and IV anesthetics to reduce pain – may cause respiratory depression and oxygen desaturation, pt needs to be monitored

Examples: Morphine, Meperidine (Demerol) and Fentanyl (Sublimaze), Sufentanyl, and Remifentanyl

135
Q

What does metoclopramide do

A

Aspiration pneumonitis prophylaxis, prevents post surgical N/V

Antiemetic/ Gastric motility stimulant

136
Q

h2 receptor antagonist do what

A

Reduce gastric acidity and volume, reducing risk of aspiration

137
Q

What does ranitidine (Zantac) and famotidine (Pepcid) do

A

Prevents gastric acid excretion

-h2 receptor antagonists

138
Q

How are anitcholinergics like atropine, glycopyrrolate, and scopalamine used in pre anesthesia

A

Prevent N/V, Tx Brady hr, and decrease salivation for intubation

139
Q

How is diphenhydramine used in pre anesthesia

A

Used to prevent allergic RXN

140
Q

What is General anesthesia

A

analgesia, amnesia, unconsciousness, sensory and autonomic reflex suppression, and in many cases muscle relaxation

141
Q

What is induction

A

time from the onset of administration of the potent anesthetic to the development of effective surgical anesthesia

142
Q

What determines induction speed

A

How fast effective concentrations of the anesthetic drug reach the brain determines induction

143
Q

What is maintenance anesthesia

A

sustained surgical anesthesia

144
Q

What is recovery/ emergency from anesthesia

A

time from discontinuation of anesthesia until consciousness and protective physiologic reflexes are regain

145
Q

What is stage I anesthesia

A

Going from an awake state to loss of consciousness

Analgesia

146
Q

What is stage II anesthesia

A

“Hyperexcitable state” or state of autonomic instability and dysfunction of reflexes

147
Q

What is the solution to Stage II hyperexitabily anesthesia

A

Fast acting drug like propofol

148
Q

What is stage III anesthesia

A

Ideal stage for surgery

149
Q

What is stage IV anesthesia

A

Medullary Paralysis results as an overdose of anesthetic drugs

DEATH if not on ventilation

150
Q

What is the MOA of inhaled anesthesia

A

Alter activity of neuronal ion channels, particularly the fast synaptic neurotransmitter receptors (nicotinic acetylcholine, GABA, and glutamate receptors)

151
Q

What is the benefit of inhaled anesthesia

A

Rapid elimination and faster pt recovery

152
Q

When are inhaled anesthetics usually used

A

Used primarily for the maintenance of anesthesia after administration of an intravenous agents

Usually supplemented with analgesics, a skeletal muscle relaxant, and an anti-muscarinic agent

153
Q

What are three Inhaled anesthetics

A

NO, Desflurane, sevoflurane

154
Q

What is the risk with using sevoflurane

A

Nephrotoxicity

155
Q

What is the risk with using NO

A

prolonged exposure to nitrous oxide decreases methionine synthase activity; risk of megaloblastic anemia

156
Q

What risk is common with succs and inhaled anesthetics

A

Malignant Hyperthermia

157
Q

Can NO produce surgical anesthesia

A

No, isn’t potent enough

158
Q

Desflurane (inhaled anesthetic) is often preferred for which pts

A

Outpatient surgical procedures

159
Q

What inhaled anesthetict is often used for pediatric pts

A

Sevoflurane

Potential nephrotoxic

160
Q

What are IV anesthetics used for

A

Ensure rapid induction, unconsciousness in 30-40 seconds

Avoids stage II delirium

161
Q

Diazepam, lorazepam, midazolam are all

A

BZD

162
Q

What is the advantage of midazolam over diazapam and lorazepam

A

Midazolam has more rapid onset and shorter elimination time frame than diazepam and lorazepam

163
Q

What is the indication of BZD

A

Preoperatively for sedation and to reduce anxiety

Intraoperatively with other drugs as part of balanced anesthesia

Useful as sole agents for surgical and diagnostic procedures that do not require analgesia (endoscopy, cardiac catheterization, changing burn dressings)

Midazolam can induce a clinically useful form of anterograde amnesia in which the patient retains memory of past events, but new information is not transferred into long-term memory

164
Q

What are morphine, meperidine, fentanyl, sufentanyl, and remifentanyl

A

Opiods

165
Q

What is the site of action for ketamine

A

NMDA receptor

166
Q

What is the site of action for propofol and etomidate

A

GABA receptor

167
Q

Describe the GABA receptor

A

When GABA binds to the GABA receptor it results in relaxation and sedation

Major inhibitor receptor

Cl- channel

168
Q

What is the MOA of the GABA receptor

A

Bind to specific high affinity sites on the cell membrane separate but adjacent to the GABA receptor (allosteric binding)

Enhancement of the inhibitory effect of GABA on neuronal excitability (increase chloride influx)

169
Q

Ketamine

A

MOA: Involves blockade of excitatory membrane effects of (NMDA) receptor
causes stimulation of the heart (increased BP, HR and CO)
Short-acting (non-barbiturate) produces a dissociated state -does not feel pain
Provides sedation, amnesia, immobility and analgesia

IND: induction and maintenance of anesthesia, supplement low potency agents ( NO),

170
Q

What is the role of ketamine in TCCC

A

Option 3 mediation
50 mg IM or IN q30min
2o mg IV or IO q20min

Endpoint; nystagmus

171
Q

What are the downfalls of ketamine

A

Increases BP, HR, and CO may be detrimental in some patients

Increased cerebral blood flow and O2 consumption

Increased intracranial pressure, potential to worsen severe TBI

Post-op disorientation

Sensory and induce post-op hallucinations and vivid dreams

Dose dependent nystagmus

172
Q

Propofol

A

MOA: Potentiates the actions of GABA

IND: Induction and maintenance of anesthesia
Produces prolonged sedation in critical care when given as a continuous infusion
(Produces no analgesic effects)

Contra: bacterial infx, allergies to eggs, soybean oil

173
Q

What is the advantage of propofol

A

High lipid emulsion Crosses bbb easily,

Rapid onset 30-45 Sec; Short duration 2-8 min;
no renal/hepatic adjustment

Antipruritic properties; less risk N/V
Antipruritic properties;
Opioids can cause pruritus

Bronchodilatory properties with decreased airway resistance

Anticonvulsant properties;
Reduces ICP and cerebral blood flow

174
Q

What is the down fall of propofol

A

Hypertriglyceridemia: order baseline triglycerides

Nutrition: must consider lipid contribution when evaluating peripheral/ enteral nutrition and diabetes

Bacterial Infections

175
Q

Propofol ADE

A

HOTN, RR depression, Increase risk of INFX,
PRIS( 33% mortality)
-refractory Brady HR, met acidosis, Cardio collapse, rhabdo, hyperlipidemia, renal failure, hepatomegaly

176
Q

Dexmedtomidine

A

MOA: α2 adrenergic (pre-synaptic) agonist, similar to clonidine

IND: Adjunct to maintenance of anesthesia
Sedation of intubated and ventilated patients in an ICU setting
(Manufacturer recommends NTE 24 hours)
ADE: HOTN, variable elimination, Brady HR, Sinus arrest, Tranisent HTN

177
Q

What are the advantages of using dexmedetomidine

A

No effect on respiratory drive

Analgesic, sedative, anxiolytic, and sympatholytic properties

Decreases BP and systemic vascular resistance

Reduced post-op N/V

May reduce the duration of mechanical ventilation and intensive care unit (ICU)

178
Q

What are the ADE of nondepolarizing agents

A

Hypotension: secondary to histamine release

Tachycardia

Respiratory Depression: paralysis of respiratory muscle

Bronchospasm: patients with reactive airway disease more susceptible

Age: >70 y/o results in prolonged duration of action secondary to decreased hepatic and renal clearance

Atracurium: metabolized to laudanosine, which can cause seizures; hypotension/flushing/bronchoconstriction (secondary histamine release)

Pancuronium: tachycardia (vagolytic)

179
Q

What are the drug interactions with NMBA (nondepolarizing)

A
  • Actylcholinesterase inhibitors (reverses effects)

Aminoglycoside antibiotics (enhance blockade)

Calcium-channel blockers (enhance blockade)

180
Q

How do local anesthesics work

A

prevent propagation of the action potential, so sensation cannot be transmitted from the source of the stimulation to brain

181
Q

What channel do local anesthetics block

A

Sodium channels, stops action potentials

182
Q

How does epinephrine adjunct local anesthetic

A

Reduces vascular blood flow

Increase the duration of action

Reduces systemic absorption

Minimizes systemic toxicity

183
Q

What are the ADE of local anesthetics

A

SZR, Arrythmias, Methemolobinemia, Allergic RXN

184
Q

As local anesthetics Benzocaine, lidocaine, and prolocaine are most common to cause what ADE

A

Methemoglobinemia

185
Q

What kind of anesthetic is used in a epidural

A

A local anesthetic (nerve block)

186
Q

What is the difference between esters and amides

A 
Esters: Usually shorter duration of action
Metabolized by pseudocholinesterase
(More likely to cause a allergic RXN) 
Rapid metabolism 
Less likely to be toxic 
Breaks down in the sun 
Onset slow 
Pka: ph 8.5-8.9
Amides: Longer duration of action
Metabolized by P450 enzyme system – reduce dosage in hepatic failure
Slow metabolism
Toxicity more likely 
Allergic RXN rare 
Very stable compound 
Onset fast 
Ph: 7.6-8.1
187
Q

What are the 5 local anesthesics

A 
Benzocaine (topical) 
Tetracaine (local and spinal) 
Bupivacaine (nerve block, spinal) 
Dibucaine (topical) 
Ropivacaine (nerve block, spinal)
188
Q

Lidocaine 5% patch

A

topical anesthetic for use on intact skin for relief of pain associated with post-herpetic neuralgia

189
Q

Lidocaine/ PRilocaine cream

A

topical anesthetic for use on intact skin for local analgesia,

genital mucous membranes for superficial minor surgery, and pretreatment for infiltration anesthesia

190
Q

TAC solution

A

(tetracaine 0.5%, adrenaline (epi) 1:2000, and cocaine 10-11.8%):
emergency treatment of uncomplicated lacerations

191
Q

LET gel

A

(lidocaine 4%, epinephrine 1:2000, and tetracaine 0.5%): repair of wounds needing minor surgical procedures,

provides anesthesia for lacerations of the face and scalp in children and adults

192
Q

A1 receptor

A

Vascular constriction and peripheral resistance
Mydriasis
Decrease nasal secretions
Increase Salivary and Sweat activation

1a- closure of the internal sphincter (bladder)

193
Q

A2 receptor

A

Presynaptic negative feedback to A1

Blocks NE release, inhibits vasoconstriction

Inhibition of lipolysis
Inhibition of insulin release

194
Q

B1 receptor

A

Excitatory
Vascular smooth muscle

Increase contractility (inotropy) and conduction ( chronotropic) of the heart

Increase renin secretion in the kidney

195
Q

B2 receptors

A 
Vasodilation in vascular smooth muscle 
Decrease peripheral resistance 
BRONCHODILATION 
Increase glycogenolysis 
Increase release of glucagon

Decrease GI motility and secretions
Relax uterine smooth muscle (inhibits uterine contraction)
Promote bladder relaxation (decrease UOP)

196
Q

Benzocaine and Tetracaine are esters or amides?

A

Esters

197
Q

Buprivacaine, Bibuciane, Lidocaine, Ropivacaine are esters or amides ?

A

Amides

IPAP 21-2 Soph Semester (20 decks)

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