Drugs Only, Block 1 Pharm Flashcards
Pilocarpine
Cholinergic Agonist
IND:
EYE: Reduce IOP in ocular HTN, Prevent Post Op IOP
Oral: Xerostomia
ADE: DUMBELLS Decreased Far Visón
Bethanechol
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
Edrophonium
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
Physostigmine Salicylate
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
Neostigmine
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
Pyridostigmine
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
Echothiophate
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)
Pralidoxime
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.
ATNAA
Antidote Treatment Nerve Agent Auto injector)
- Atropine (anticholinergic agent)
- Pralidoxime (reactivate cholinesterase)
CANA
(Convulsant Antidote for Nerve Agent)
Diazepam (benzodiazepine) to control nerve agent induced seizures
ALZHEIMERS DRUG LIST
Tacrine
Donepezil
Galantamine
Rivastigmine
Atropine
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
Anti Cholinergics used in the eye
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)
Anticholinergic for GU use
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)
Anticholinergics used in GI
Dicyclomine
Belladonna Alkoloids
Dicyclomine
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)
Belladonna Alkaloids
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
Anticholinergics used in the Lungs
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)
Should anticholinergics be used to treat acute asthma
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
Scopalamine
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
Anticholinergics used for Parkinson’s
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
MOA of NMBA
Block acetycholine at the Nm (nicotinic muscle) at the neuromuscular junction at the skeletal muscle
Order of paralysis with NMBA
Order of paralysis (peripheral to central): face/eyes; fingers; limbs; neck; trunk muscles; intercostal muscles; diaphragm
Can cholinesterase inhibitors reverse depolroizing NMBA
Not in phase I, in phase II they potential can in late phase
Can AchE inhibitors reverse nondepolarizing NMBA
Yes, increasing Ach can compete with Nondepolaring NMBA as well as AchE inhibitors (Indirect Ach Agonists) such as neostigmine, pyridostigmine, and edrophonium
Succinylcholine
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
Reversal agent for Malignant Hyperthermia
Dentrolene
What does atracurium metabolize to
Laudanosine ( can cross the BBB and cause SZR)
What is the NMBA DOC in renal and hepatic dz
Cisatracurium
OnabotulinumtoxinA
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
What is the antidote for OnabotulinumtoxinA
Equine botulinum antitoxin
Brimonidine tartrate
Sympathetic agonist
MOA: decrease IOP, contracts radial muscle (mydriasis)
IND: OPEN ANGLE glaucoma or ocular HTN
Timolol
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
Epi
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
What is the effect of EPI at low doses
< 0.5 mcg/kg/min
Vasodilation predominates (B2)
What is the effect of Epi at high doses
>0.5mcg/kg/min
Vasoconstriction predominates (a1)
What are the drug interactions of Epi
a- blockers, b-blockers, and increased the efficacy of MAOI and COMT inhibitors
Dipiverfin
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
NE
Direct acting catecholamine
MOA: direct-acting catecholamine that is an agonist at both α and β receptors (α effects»_space; β1»_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
What the mortality difference when using dopamine or NE in Tx of shock
Dopamine»NE
No mortality difference
What are the drug interactions of NE
Same as EPI
a-blockers, b-blockers, increase efficacy of MOAI and COMT inhibitors
Isoproterenol
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
What are the drug interactions of Isoproterenol
COMT inhibitors may prolong action, b-blockers result in physiologic anatogonism
Dobutamine
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
What are the drug interactions with dobutamine
COMT inhibitors may prolong action
b-blockers result in physiologic antagonism
Dopamine
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
Should low dose dopamine be used for renal protection
NO!
What are the drug interactions for Dopamine
A-blockers and b-blockers
Increase efficacy of MAOI and COMTI
What receprtors does Epi hit
A1 and 2 (more) ,
B1 and 2 (less)
What receptors does NE hit
A1 and 2 (more)
B1 and 2 (less)
What receptors does isoproterenol hit
Only B1 and B2
What receptors does dobutamine hit
A1 and 2 (less)
B1 (most)
B2 (less)
What receptors does dopamine hit
Dose dependent
Low dose B1 and D1
Medium dose B1, B2, D1 and minimal A1
High Dose A1, B1, B2, and no D1
Phenylephrine
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
What are the drug interactions of phenylephrine
A-blockers and MAO-I
Oxymetazoline (AFRIN, Visine)
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
Midodrine
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
What prodrug gets converted to desglymidodrine
Midodrine
What are the drug interactions for midodrine
MAO-I
Clonidine
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
What are the drug interactions of Clonidine
Enhances B-blockers (AV blocking effect)
Withdrawal b-blocker several days before clonidine withdrawal when possible (monitor BP closely)
Brimonidine
Direct acting non catecholamine
MOA: ocular α2-agonist, decreases aqueous humor production
IND: Glaucoma
ADE: burning/ stinging
b2 agonists
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
What are the drug interactions of B2 agonists
B- blockers (primarily non selective)
What is the B agonist of choice for acute respiratory relief in COPD and asthma
Albuterol
What drug is a R-isomer of Albuterol
Levalbuterol
What B 2 agonist does not end in -ol and is used to suppress premature birth
Terbutaline
What is arformeterol only approved for
COPD
Is formoterol approved for acute relief of asthma
No, despite its rapid onset of action (less than 5 min)
What is Indacterol only approved for
COPD
Mirabegron
Direct acting non catecholamine
Mechanism of Action: β3 agonist that relaxes the detrusor muscle, increases bladder capacity
IND: Overactive bladder
ADE; increases BP
What are the drug interaction of Mirabegron
Anticholinergics for the bladder, (increases urinary retention)
Fenoldopam
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
What are the clinical uses of indirect acting adrenergic agonist
ADHD
Narcolepsy
Obesity
Depression
(METH, COCAINE)
What are the ADE of dextroamphetamine and methamphetamine
Insomnia, irritability, tremor, panic, SI, psychosis, dependency, HTN, palpitations, N/V/D, anorexia, stunted growth
Dextro- and methamphetamine are contraindicated in what pts..
Contraindicated in patients with hypertension, CV diseases, hyperthyroidism, and glaucoma
What are the drug interactions with Dextro- and methamphetamine
MAO-I
What are the drug interactions with tyramine
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
Patients taking a mono amine oxidase inhibitors (MAOI) who eat tyramine containing foods can develop?>
HTN crisis
What it tyramine
Tyramine is an indirect sympathomimetic that will release stored epinephrine and norepinephrine causing: hypertension, tachycardia, nausea, arrhythmias and stroke
Cocaine (C-II)
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
At what dose is cocaine fatal
1.2 grams, with severe toxic effects reported as low as 20 mg
What are the Mixed- action Adrenergic Agents
Ephedrine and Ephedra
Ephedrine and Ephedra
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
What are the drug interactions for ephindrine and ephedra
A-blockers
Psuedoephedrine (Sudafed)
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
What are the drug interactions for pseudoephedrine
A-blockers
Phenoxybenzamine
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
Phentolamine
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
What is the MOA of a1 blockers
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
What is the IND for a1 blockers
Hypertension
BPH
Raynaud’s Disease (reduced blood flow)
Pheochromocytoma
What are the ADE and Contra for a1 blockers
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
Alfuzosin is contraindicated in pts with
Potent CYP3A4 inhibitors (-azole and antifungals)
Should a1 and a1a blockers be used together
No
Should a1 and PDE5 inhibitors (sildenafil) be used together
No
What is prazosin used for
A1 blocker
PTSD and nightmares
NOT APPROVED FOR BPH
What is doxazosin approved for
A1 blocker
HTN and BPH
What is the only XR a1 blocker approved for BPH
Doxazosin
What is terazosin approved for
A1 blocker approved for BPH and HTN
What is alfuzosin approved for
A1 blocker approved ONLY for BPH
Not selective for a1a receptor
Drugs that in in -Osin are
A(1a) blockers
Tamsulosin and Silodosin
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)
What are the drug interactions of Tamsulosin and Silodosin
caution in patients using phosphodiesterase 5 (PDE5) inhibitors (i.e. sildenafil, tadalafil
Tamsulosin may cause what undesirable penis complication
Priapism
What pts is Silodosin contraindicated in
Pts with severe hepatic and renal impairment
To minimize the risk of intraoperative floppy iris syndrome (IFIS)…patients using α1 blockers should have a medication washout period for how long
2 weeks prior to cataract surgery
B blockers MOA, IND, ADE
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
What are the drug interactions of B blockers
B agonists
Non-dihydropyridine
Calcium Channel blockers
What is the b blocker DOC in thyroid storm
Propranolol
Since propranolol crosses the BBB ( lipophilic) it is useful in the Tx of
Migraine prophylacxsis
Which b blocker is most likely to cause b blocker blues
Propranolol
What is nadolol approved for
Migraine prophylaxis , has a long t 1/2
What is the route admin for Timolol
PO and its rarely used (opthamolic)
Does atenolol cross the BBB
No
What should be used instead of timolol
Betaxolol
It’s more beta than tim
Does bisoprolol cross the BBB
Yes
What is esmolol approved for
Thyroid storm, for Tachy cardia and HTN ( perioperative in the OR)
Which b blocker produces a N.O. Potentiating vasodilation effect
Nebivolol
Which b blocker is a B1 specific blockade
acebutolol
Ace is number 1
What b blocker is a non specific b blockade
Pinolol and penbutolol
Can’t pin it down to one
Which B blocker was designed to weakly stimulate B1 and b2 receptors
Penbutolol
They are pen palls with B1 and b2 receptors event tho they are blockers
Carvedilol
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
What are the drug interactions of Carvedilol
Physiological Antagonism: α and β agonist
Additive Effect: α and β antagonist
Cumulative Negative Inotropic Effect: non-Dihydropyridine Calcium Channel Blockers (DHP CCBs)
Labetalol
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
What pt population is labetalol most useful in
Elderly or black HTN pts who cannot tolerate increase PVR
At what HR should you decrease the dose of Carvedilol
<55 BPM
What are teh 4 types of b blockers
Non-selective Beta-1 & Beta 2 blockers
Selective Beta-1 blockers
Intrinsic Sympathomimetic Activity (ISA) Beta blockers
Mixed alpha & non-selective Beta-bloc
What are the general contraindication for B blocker
Bradycardia (<55BPM)
PR-interval >0.24, or 2nd/3rd degree heart block
Decompensated Heart Failure
Asthma
What are the three non selective B blockers
Propranolol (Inderal)
Nadolol (Corgard)
Timolol (Timoptic) – eye drop
What are the 4 B1 selective blockers
Atenolol (Tenormin)
Bisoprolol (Zebeta)
Esmolol (Brevibloc) – Extremely short half life
Metoprolol (Toprol XL or Lopressor)
What are the 2 Mixed a1 and nonspecific b blockers
Labetalol and Carvedilol
What are the 3 ISA beta blockers
Acebutolol (Sectral)
Pindolol (Visken)
Penbutolol (Levatol)
What is the role of BZD in pre anesthesia
Used to relieve anxiety, facilitate amnesia and produce sedation
Examples: Diazepam (Valium), Lorazepam (Ativan), and Midazolam (Versed)
What is the role of Opiods in pre-anesthesia
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
What does metoclopramide do
Aspiration pneumonitis prophylaxis, prevents post surgical N/V
Antiemetic/ Gastric motility stimulant
h2 receptor antagonist do what
Reduce gastric acidity and volume, reducing risk of aspiration
What does ranitidine (Zantac) and famotidine (Pepcid) do
Prevents gastric acid excretion
-h2 receptor antagonists
How are anitcholinergics like atropine, glycopyrrolate, and scopalamine used in pre anesthesia
Prevent N/V, Tx Brady hr, and decrease salivation for intubation
How is diphenhydramine used in pre anesthesia
Used to prevent allergic RXN
What is General anesthesia
analgesia, amnesia, unconsciousness, sensory and autonomic reflex suppression, and in many cases muscle relaxation
What is induction
time from the onset of administration of the potent anesthetic to the development of effective surgical anesthesia
What determines induction speed
How fast effective concentrations of the anesthetic drug reach the brain determines induction
What is maintenance anesthesia
sustained surgical anesthesia
What is recovery/ emergency from anesthesia
time from discontinuation of anesthesia until consciousness and protective physiologic reflexes are regain
What is stage I anesthesia
Going from an awake state to loss of consciousness
Analgesia
What is stage II anesthesia
“Hyperexcitable state” or state of autonomic instability and dysfunction of reflexes
What is the solution to Stage II hyperexitabily anesthesia
Fast acting drug like propofol
What is stage III anesthesia
Ideal stage for surgery
What is stage IV anesthesia
Medullary Paralysis results as an overdose of anesthetic drugs
DEATH if not on ventilation
What is the MOA of inhaled anesthesia
Alter activity of neuronal ion channels, particularly the fast synaptic neurotransmitter receptors (nicotinic acetylcholine, GABA, and glutamate receptors)
What is the benefit of inhaled anesthesia
Rapid elimination and faster pt recovery
When are inhaled anesthetics usually used
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
What are three Inhaled anesthetics
NO, Desflurane, sevoflurane
What is the risk with using sevoflurane
Nephrotoxicity
What is the risk with using NO
prolonged exposure to nitrous oxide decreases methionine synthase activity; risk of megaloblastic anemia
What risk is common with succs and inhaled anesthetics
Malignant Hyperthermia
Can NO produce surgical anesthesia
No, isn’t potent enough
Desflurane (inhaled anesthetic) is often preferred for which pts
Outpatient surgical procedures
What inhaled anesthetict is often used for pediatric pts
Sevoflurane
Potential nephrotoxic
What are IV anesthetics used for
Ensure rapid induction, unconsciousness in 30-40 seconds
Avoids stage II delirium
Diazepam, lorazepam, midazolam are all
BZD
What is the advantage of midazolam over diazapam and lorazepam
Midazolam has more rapid onset and shorter elimination time frame than diazepam and lorazepam
What is the indication of BZD
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
What are morphine, meperidine, fentanyl, sufentanyl, and remifentanyl
Opiods
What is the site of action for ketamine
NMDA receptor
What is the site of action for propofol and etomidate
GABA receptor
Describe the GABA receptor
When GABA binds to the GABA receptor it results in relaxation and sedation
Major inhibitor receptor
Cl- channel
What is the MOA of the GABA receptor
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)
Ketamine
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),
What is the role of ketamine in TCCC
Option 3 mediation
50 mg IM or IN q30min
2o mg IV or IO q20min
Endpoint; nystagmus
What are the downfalls of ketamine
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
Propofol
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
What is the advantage of propofol
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
What is the down fall of propofol
Hypertriglyceridemia: order baseline triglycerides
Nutrition: must consider lipid contribution when evaluating peripheral/ enteral nutrition and diabetes
Bacterial Infections
Propofol ADE
HOTN, RR depression, Increase risk of INFX,
PRIS( 33% mortality)
-refractory Brady HR, met acidosis, Cardio collapse, rhabdo, hyperlipidemia, renal failure, hepatomegaly
Dexmedtomidine
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
What are the advantages of using dexmedetomidine
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)
What are the ADE of nondepolarizing agents
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)
What are the drug interactions with NMBA (nondepolarizing)
- Actylcholinesterase inhibitors (reverses effects)
Aminoglycoside antibiotics (enhance blockade)
Calcium-channel blockers (enhance blockade)
How do local anesthesics work
prevent propagation of the action potential, so sensation cannot be transmitted from the source of the stimulation to brain
What channel do local anesthetics block
Sodium channels, stops action potentials
How does epinephrine adjunct local anesthetic
Reduces vascular blood flow
Increase the duration of action
Reduces systemic absorption
Minimizes systemic toxicity
What are the ADE of local anesthetics
SZR, Arrythmias, Methemolobinemia, Allergic RXN
As local anesthetics Benzocaine, lidocaine, and prolocaine are most common to cause what ADE
Methemoglobinemia
What kind of anesthetic is used in a epidural
A local anesthetic (nerve block)
What is the difference between esters and amides
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
What are the 5 local anesthesics
Benzocaine (topical) Tetracaine (local and spinal) Bupivacaine (nerve block, spinal) Dibucaine (topical) Ropivacaine (nerve block, spinal)
Lidocaine 5% patch
topical anesthetic for use on intact skin for relief of pain associated with post-herpetic neuralgia
Lidocaine/ PRilocaine cream
topical anesthetic for use on intact skin for local analgesia,
genital mucous membranes for superficial minor surgery, and pretreatment for infiltration anesthesia
TAC solution
(tetracaine 0.5%, adrenaline (epi) 1:2000, and cocaine 10-11.8%):
emergency treatment of uncomplicated lacerations
LET gel
(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
A1 receptor
Vascular constriction and peripheral resistance
Mydriasis
Decrease nasal secretions
Increase Salivary and Sweat activation
1a- closure of the internal sphincter (bladder)
A2 receptor
Presynaptic negative feedback to A1
Blocks NE release, inhibits vasoconstriction
Inhibition of lipolysis
Inhibition of insulin release
B1 receptor
Excitatory
Vascular smooth muscle
Increase contractility (inotropy) and conduction ( chronotropic) of the heart
Increase renin secretion in the kidney
B2 receptors
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)
Benzocaine and Tetracaine are esters or amides?
Esters
Buprivacaine, Bibuciane, Lidocaine, Ropivacaine are esters or amides ?
Amides
