Drugs Only, Block 1 Pharm Flashcards
(197 cards)
1
Q
Pilocarpine
A
Cholinergic Agonist
IND:
EYE: Reduce IOP in ocular HTN, Prevent Post Op IOP
Oral: Xerostomia
ADE: DUMBELLS Decreased Far Visón
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
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
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
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
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
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)
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.
9
Q
ATNAA
A
Antidote Treatment Nerve Agent Auto injector)
- Atropine (anticholinergic agent)
- Pralidoxime (reactivate cholinesterase)
10
Q
CANA
A
(Convulsant Antidote for Nerve Agent)
Diazepam (benzodiazepine) to control nerve agent induced seizures
11
Q
ALZHEIMERS DRUG LIST
A
Tacrine
Donepezil
Galantamine
Rivastigmine
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
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)
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)
15
Q
Anticholinergics used in GI
A
Dicyclomine
Belladonna Alkoloids
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)
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
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)
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
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
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
22
Q
MOA of NMBA
A
Block acetycholine at the Nm (nicotinic muscle) at the neuromuscular junction at the skeletal muscle
23
Q
Order of paralysis with NMBA
A
Order of paralysis (peripheral to central): face/eyes; fingers; limbs; neck; trunk muscles; intercostal muscles; diaphragm
24
Q
Can cholinesterase inhibitors reverse depolroizing NMBA
A
Not in phase I, in phase II they potential can in late phase
25
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
26
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
27
Reversal agent for Malignant Hyperthermia
Dentrolene
28
What does atracurium metabolize to
Laudanosine ( can cross the BBB and cause SZR)
29
What is the NMBA DOC in renal and hepatic dz
Cisatracurium
30
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
31
What is the antidote for OnabotulinumtoxinA
Equine botulinum antitoxin
32
Brimonidine tartrate
Sympathetic agonist
MOA: decrease IOP, contracts radial muscle (mydriasis)
IND: OPEN ANGLE glaucoma or ocular HTN
33
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
```
34
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
35
What is the effect of EPI at low doses
| < 0.5 mcg/kg/min
Vasodilation predominates (B2)
36
What is the effect of Epi at high doses
| >0.5mcg/kg/min
Vasoconstriction predominates (a1)
37
What are the drug interactions of Epi
a- blockers, b-blockers, and increased the efficacy of MAOI and COMT inhibitors
38
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
39
NE
Direct acting catecholamine
MOA: direct-acting catecholamine that is an agonist at both α and β receptors (α effects >> β1 >>> 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
40
What the mortality difference when using dopamine or NE in Tx of shock
Dopamine>>NE
| No mortality difference
41
What are the drug interactions of NE
Same as EPI
| a-blockers, b-blockers, increase efficacy of MOAI and COMT inhibitors
42
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
43
What are the drug interactions of Isoproterenol
COMT inhibitors may prolong action, b-blockers result in physiologic anatogonism
44
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
45
What are the drug interactions with dobutamine
COMT inhibitors may prolong action
| b-blockers result in physiologic antagonism
46
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
47
Should low dose dopamine be used for renal protection
NO!
48
What are the drug interactions for Dopamine
A-blockers and b-blockers
| Increase efficacy of MAOI and COMTI
49
What receprtors does Epi hit
A1 and 2 (more) ,
| B1 and 2 (less)
50
What receptors does NE hit
A1 and 2 (more)
| B1 and 2 (less)
51
What receptors does isoproterenol hit
Only B1 and B2
52
What receptors does dobutamine hit
A1 and 2 (less)
B1 (most)
B2 (less)
53
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
54
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
55
What are the drug interactions of phenylephrine
A-blockers and MAO-I
56
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
57
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
58
What prodrug gets converted to desglymidodrine
Midodrine
59
What are the drug interactions for midodrine
MAO-I
60
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
61
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)
62
Brimonidine
Direct acting non catecholamine
MOA: ocular α2-agonist, decreases aqueous humor production
IND: Glaucoma
ADE: burning/ stinging
63
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
64
What are the drug interactions of B2 agonists
B- blockers (primarily non selective)
65
What is the B agonist of choice for acute respiratory relief in COPD and asthma
Albuterol
66
What drug is a R-isomer of Albuterol
Levalbuterol
67
What B 2 agonist does not end in -ol and is used to suppress premature birth
Terbutaline
68
What is arformeterol only approved for
COPD
69
Is formoterol approved for acute relief of asthma
No, despite its rapid onset of action (less than 5 min)
70
What is Indacterol only approved for
COPD
71
Mirabegron
Direct acting non catecholamine
Mechanism of Action: β3 agonist that relaxes the detrusor muscle, increases bladder capacity
IND: Overactive bladder
ADE; increases BP
72
What are the drug interaction of Mirabegron
Anticholinergics for the bladder, (increases urinary retention)
73
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
74
What are the clinical uses of indirect acting adrenergic agonist
ADHD
Narcolepsy
Obesity
Depression
(METH, COCAINE)
75
What are the ADE of dextroamphetamine and methamphetamine
Insomnia, irritability, tremor, panic, SI, psychosis, dependency, HTN, palpitations, N/V/D, anorexia, stunted growth
76
Dextro- and methamphetamine are contraindicated in what pts..
Contraindicated in patients with hypertension, CV diseases, hyperthyroidism, and glaucoma
77
What are the drug interactions with Dextro- and methamphetamine
MAO-I
78
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
79
Patients taking a mono amine oxidase inhibitors (MAOI) who eat tyramine containing foods can develop?>
HTN crisis
80
What it tyramine
Tyramine is an indirect sympathomimetic that will release stored epinephrine and norepinephrine causing: hypertension, tachycardia, nausea, arrhythmias and stroke
81
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
82
At what dose is cocaine fatal
1.2 grams, with severe toxic effects reported as low as 20 mg
83
What are the Mixed- action Adrenergic Agents
Ephedrine and Ephedra
84
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
85
What are the drug interactions for ephindrine and ephedra
A-blockers
86
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
87
What are the drug interactions for pseudoephedrine
A-blockers
88
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
89
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
90
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
91
What is the IND for a1 blockers
Hypertension
BPH
Raynaud’s Disease (reduced blood flow)
Pheochromocytoma
92
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
93
Alfuzosin is contraindicated in pts with
Potent CYP3A4 inhibitors (-azole and antifungals)
94
Should a1 and a1a blockers be used together
No
95
Should a1 and PDE5 inhibitors (sildenafil) be used together
No
96
What is prazosin used for
A1 blocker
PTSD and nightmares
NOT APPROVED FOR BPH
97
What is doxazosin approved for
A1 blocker
| HTN and BPH
98
What is the only XR a1 blocker approved for BPH
Doxazosin
99
What is terazosin approved for
A1 blocker approved for BPH and HTN
100
What is alfuzosin approved for
A1 blocker approved ONLY for BPH
Not selective for a1a receptor
101
Drugs that in in -Osin are
A(1a) blockers
102
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)
103
What are the drug interactions of Tamsulosin and Silodosin
caution in patients using phosphodiesterase 5 (PDE5) inhibitors (i.e. sildenafil, tadalafil
104
Tamsulosin may cause what undesirable penis complication
Priapism
105
What pts is Silodosin contraindicated in
Pts with severe hepatic and renal impairment
106
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
107
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
```
108
What are the drug interactions of B blockers
B agonists
Non-dihydropyridine
Calcium Channel blockers
109
What is the b blocker DOC in thyroid storm
Propranolol
110
Since propranolol crosses the BBB ( lipophilic) it is useful in the Tx of
Migraine prophylacxsis
111
Which b blocker is most likely to cause b blocker blues
Propranolol
112
What is nadolol approved for
Migraine prophylaxis , has a long t 1/2
113
What is the route admin for Timolol
PO and its rarely used (opthamolic)
114
Does atenolol cross the BBB
No
115
What should be used instead of timolol
Betaxolol
| It’s more beta than tim
116
Does bisoprolol cross the BBB
Yes
117
What is esmolol approved for
Thyroid storm, for Tachy cardia and HTN ( perioperative in the OR)
118
Which b blocker produces a N.O. Potentiating vasodilation effect
Nebivolol
119
Which b blocker is a B1 specific blockade
acebutolol
Ace is number 1
120
What b blocker is a non specific b blockade
Pinolol and penbutolol
Can’t pin it down to one
121
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
122
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
123
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)
124
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
125
What pt population is labetalol most useful in
Elderly or black HTN pts who cannot tolerate increase PVR
126
At what HR should you decrease the dose of Carvedilol
<55 BPM
127
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
128
What are the general contraindication for B blocker
Bradycardia (<55BPM)
PR-interval >0.24, or 2nd/3rd degree heart block
Decompensated Heart Failure
Asthma
129
What are the three non selective B blockers
Propranolol (Inderal)
Nadolol (Corgard)
Timolol (Timoptic) – eye drop
130
What are the 4 B1 selective blockers
Atenolol (Tenormin)
Bisoprolol (Zebeta)
Esmolol (Brevibloc) – Extremely short half life
Metoprolol (Toprol XL or Lopressor)
131
What are the 2 Mixed a1 and nonspecific b blockers
Labetalol and Carvedilol
132
What are the 3 ISA beta blockers
Acebutolol (Sectral)
Pindolol (Visken)
Penbutolol (Levatol)
133
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)
134
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
135
What does metoclopramide do
Aspiration pneumonitis prophylaxis, prevents post surgical N/V
Antiemetic/ Gastric motility stimulant
136
h2 receptor antagonist do what
Reduce gastric acidity and volume, reducing risk of aspiration
137
What does ranitidine (Zantac) and famotidine (Pepcid) do
Prevents gastric acid excretion
| -h2 receptor antagonists
138
How are anitcholinergics like atropine, glycopyrrolate, and scopalamine used in pre anesthesia
Prevent N/V, Tx Brady hr, and decrease salivation for intubation
139
How is diphenhydramine used in pre anesthesia
Used to prevent allergic RXN
140
What is General anesthesia
analgesia, amnesia, unconsciousness, sensory and autonomic reflex suppression, and in many cases muscle relaxation
141
What is induction
time from the onset of administration of the potent anesthetic to the development of effective surgical anesthesia
142
What determines induction speed
How fast effective concentrations of the anesthetic drug reach the brain determines induction
143
What is maintenance anesthesia
sustained surgical anesthesia
144
What is recovery/ emergency from anesthesia
time from discontinuation of anesthesia until consciousness and protective physiologic reflexes are regain
145
What is stage I anesthesia
Going from an awake state to loss of consciousness
Analgesia
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What is stage II anesthesia
“Hyperexcitable state” or state of autonomic instability and dysfunction of reflexes
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What is the solution to Stage II hyperexitabily anesthesia
Fast acting drug like propofol
148
What is stage III anesthesia
Ideal stage for surgery
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What is stage IV anesthesia
Medullary Paralysis results as an overdose of anesthetic drugs
DEATH if not on ventilation
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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)
151
What is the benefit of inhaled anesthesia
Rapid elimination and faster pt recovery
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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
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What are three Inhaled anesthetics
NO, Desflurane, sevoflurane
154
What is the risk with using sevoflurane
Nephrotoxicity
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What is the risk with using NO
prolonged exposure to nitrous oxide decreases methionine synthase activity; risk of megaloblastic anemia
156
What risk is common with succs and inhaled anesthetics
Malignant Hyperthermia
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Can NO produce surgical anesthesia
No, isn’t potent enough
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Desflurane (inhaled anesthetic) is often preferred for which pts
Outpatient surgical procedures
159
What inhaled anesthetict is often used for pediatric pts
Sevoflurane
| Potential nephrotoxic
160
What are IV anesthetics used for
Ensure rapid induction, unconsciousness in 30-40 seconds
| Avoids stage II delirium
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Diazepam, lorazepam, midazolam are all
BZD
162
What is the advantage of midazolam over diazapam and lorazepam
Midazolam has more rapid onset and shorter elimination time frame than diazepam and lorazepam
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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
164
What are morphine, meperidine, fentanyl, sufentanyl, and remifentanyl
Opiods
165
What is the site of action for ketamine
NMDA receptor
166
What is the site of action for propofol and etomidate
GABA receptor
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Describe the GABA receptor
When GABA binds to the GABA receptor it results in relaxation and sedation
Major inhibitor receptor
Cl- channel
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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)
169
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),
170
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
171
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
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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
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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
174
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
175
Propofol ADE
HOTN, RR depression, Increase risk of INFX,
PRIS( 33% mortality)
-refractory Brady HR, met acidosis, Cardio collapse, rhabdo, hyperlipidemia, renal failure, hepatomegaly
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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
177
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)
178
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)
179
What are the drug interactions with NMBA (nondepolarizing)
* Actylcholinesterase inhibitors (reverses effects)
Aminoglycoside antibiotics (enhance blockade)
Calcium-channel blockers (enhance blockade)
180
How do local anesthesics work
prevent propagation of the action potential, so sensation cannot be transmitted from the source of the stimulation to brain
181
What channel do local anesthetics block
Sodium channels, stops action potentials
182
How does epinephrine adjunct local anesthetic
Reduces vascular blood flow
Increase the duration of action
Reduces systemic absorption
Minimizes systemic toxicity
183
What are the ADE of local anesthetics
SZR, Arrythmias, Methemolobinemia, Allergic RXN
184
As local anesthetics Benzocaine, lidocaine, and prolocaine are most common to cause what ADE
Methemoglobinemia
185
What kind of anesthetic is used in a epidural
A local anesthetic (nerve block)
186
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
```
187
What are the 5 local anesthesics
```
Benzocaine (topical)
Tetracaine (local and spinal)
Bupivacaine (nerve block, spinal)
Dibucaine (topical)
Ropivacaine (nerve block, spinal)
```
188
Lidocaine 5% patch
topical anesthetic for use on intact skin for relief of pain associated with post-herpetic neuralgia
189
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
190
TAC solution
(tetracaine 0.5%, adrenaline (epi) 1:2000, and cocaine 10-11.8%):
emergency treatment of uncomplicated lacerations
191
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
192
A1 receptor
Vascular constriction and peripheral resistance
Mydriasis
Decrease nasal secretions
Increase Salivary and Sweat activation
1a- closure of the internal sphincter (bladder)
193
A2 receptor
Presynaptic negative feedback to A1
Blocks NE release, inhibits vasoconstriction
Inhibition of lipolysis
Inhibition of insulin release
194
B1 receptor
Excitatory
Vascular smooth muscle
Increase contractility (inotropy) and conduction ( chronotropic) of the heart
Increase renin secretion in the kidney
195
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)
196
Benzocaine and Tetracaine are esters or amides?
Esters
197
Buprivacaine, Bibuciane, Lidocaine, Ropivacaine are esters or amides ?
Amides
