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RU PA Pharm > ANS and FDA drugs > Flashcards

ANS and FDA drugs Flashcards

1
Q

vesamicol

A

Physiologic ACh antagonist

Presynaptically inhibits ACh uptake into synaptic vesicles by inhibiting vesicular ACh transporter (VAT)

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2
Q

Hemicholinium

A

Indirect ACh antagonist

Impairs synthesis of ACh presynaptically by preventing choline reuptake by Choline transporter (CHT)

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3
Q

Botulinum toxin

A

Cholinergic antagonist
Inhibit Soluble attachment protein receptors (SNARES)
SNARES mediat vesicle fusion with presynaptic membrane, mediate Ca++ dependent release of ACh from vesicles and into the synapse for long periods of time
-used as NMJ blocker to prevent mm contraction

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4
Q

Reserpine

A

Non specific VMAT inhibitor leading to peripheral and central depletion of NE, DA, 5HT
Lipid Soluble (Crosses BBB)
I: HTN, hyperkinesis from antipsychotics
AE: Decrease DA in CNS can lead to parkinsonism features, Decrease NE and 5HT in CNS can lead to depression
PK: Long duration (Days)

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5
Q

Tyramine

A

inhibits uptake of released NE by NET ( NE transporter, a NA+ counter transporter)
Sympathomimetic
Pressor amine family
Degraded by MAO
NE substrate
Sources: Pickled herring, Chianti wine, cheeses
-can cause hypertension if taken with MAO inhibitors

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6
Q

Cocaine, tricyclic antideprssants

A

allosteric inhibitor of NET (NE reuptake)

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7
Q

Bethanechol/Carbacol

A

non-specific cholinomimetic
Quaternary amine (Can’t cross BBB)
Longer half/life than ACh due to less affinity for AChE

Carbacol: -M and N agonist

Bethanechol:

  • full agonist of M1-M3, little effect on N
  • SLUDGEM effect
  • used post op for neurogenic ileus and urinary retention to stimulate bowl movement and urination
  • single dose is used for urinary retention if there is no OBSTRUCTION
  • can cause bronchospasm in asthmatics
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8
Q

Muscarine

A

-BOTH specific, direct acting muscarinic cholinomimetic

  • Muscarine: full agonist of M receptors
  • quartenary amine and doesn’t cross BBB, but can cause severe toxicity if large amounts of certain mushrooms are consumed
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9
Q

Nicotine/Lobeline

A

-mixed direct acting nicotinic agonist
-MAO: Direct acting Full Nn and NM(neurons and muscle) agonist. Activates SANS and PANS (Nn at ganglia, NM at striated muscle plates)
- tertiary amines, readily cross membranes, so nicotine can be absorbed subcut and used in smoking cessation
Toxicity: increased GI activity with nausea, vomiting and diahrrhea; increased BP and potential for seizure due to entry into CNS

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10
Q

Varenicline

A

Chantix (trade name)
MOA: alpha4Beta2 NN (DA release in CNS) receptor partial agonist
Agonist/antagonist (partially decreasing reinforcing effects of nicotine , as well as produces moderate DA release and reduces cravings and withdrawal symptoms)
I: Smoking cessation

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11
Q

Edrophonium

A 
AChEI, indirect acting cholinomimetic
-competitive and reversible
Quaternary amine
Alcohol (1st type of ACHEI)
MOA: Reversibly Binds to AChE at Active site (electrostatically and by H bonding) and competes with ACh at enzyme active site preventing ACh hydrolysis and breakdown thus increasing ACh levels at junction synapse.

-used in TENSILON TESTfor MG( more weakness-overmedicated, less weakness-undermedicated)

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12
Q

Neostigmine/Physostigmine

A

-carbamates; AChEI, indirect acting cholinomimetics
Nei Quaternary and physi tertiary amine
Carbamate (2nd type of AChEI)
MOA: Binds to AChE Active site and competes with ACh at enzyme active site preventing ACh hydrolysis and breakdown.
Blocks for hours due to slowing 2nd carbamoylation step of AChE
I: Postoperatively to reverse muscle relaxers used by anesthesia. Tx of Myasthenia Gravis

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13
Q

Parathion/ Malathion

A

Indirect-acting cholinergic agonists (AchEIs)
Cross BBB
Organophosphate (3rd type of AChEI)
MOA: Irreversibly (covalently) binds to esteric site (allosteric site) of AChE preventing AChE from degrading ACh.
Antidote: Pralidoxime, if given before esteric site “ages” can rescue receptor and enzyme.
Actually considered pseudo-irreversible for this reason
AE: SLUDGEM, death

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14
Q

Sarin

A

Nerve gas
Cross BBB
Organophosphate (3rd type of AChEI)
MOA: Irreversibly (covalently) binds to esteric site (allosteric site) of AChE preventing AChE from degrading ACh.
Antidote: Pralidoxime, if given before esteric site “ages” can rescue receptor and enzyme.
Actually considered pseudo-irreversible for this reason
AE: SLUDGEM, death

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15
Q

Pralidoxime

A

Receptor generator
Antidote for organophosphate/ Nerve gas poisoning.
Binds to esteric site of AChE and regenerates it if given in time
Time varies on poison

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16
Q

Donepezil

A

Nootropic
Trade name: Aricept
Crosses BBB
MOA: Reversible noncompetitive G1 and G4 AChEI. Greater CNS/PNS selectivity
G1 and G4 ACh receptors found mostly in CNS
I: Improve Mental function in AD
PK: Half Life of 60 hrs, High PO bioavailability, renal excretion (less likely drug interactions)

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17
Q

Rivastigmine

A

Pseudo-irreversible competitive AChEITrade Name: Excelon
Crosses BBB
MOA: Pseudo-irreversible competitive AChEI (G1 and G4)
AD
PK: Long duration

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18
Q

Galantamine

A

Trade Name: Reminyl
Crosses BBB
MOA: Reversible, low potency, competitive AChEI (G1 and G4)
Also Noncompetitive NN agonist (Also aids with AD)
AD
PK: Half life of 5-6 hrs

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19
Q

Memantine

A

Indirect active Glutamate antagonist
MOA: NMDA indirect acting Glu antagonist.
Inhibits prolonged influx of Ca++ ions
I: Stage II and 3 AD
AE: Confusion, dizziness, drowsiness, HA, Insomnia, Agitation, hallucinations.

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20
Q

Tropicamide

A

Short acting antimuscarinic
Preferred for pupillary dilation
Better than scopolamine or atropine due to shorter action

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21
Q

Atropine

A

Enters CNS
Surmountable antagonist of M1-M5 (No N) receptors. (Reversed with AChEI)
Reduces PANS and also reduces sweat and salivary secretion
Temporary ENS modulator
Blocks receptor in inactive state
I: Asthma, COPD, diarrhea, motion sickness, dilate eyes, reduce airway secretions (M3)
CI: Glaucoma, GI obstruction, urinary obstruction, Intestinal atony.
AE: Hyperthermia, Blindness, Altered mental status, lack of secretions, tachycardia, arrhythmias. See anticholinergic toxicity
-reverces bradycardia

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22
Q

ipratropium

A

Quaternary Amine
MOA: M1-M5 antaginist, some NN
Aerosolized, does not easily cross lung endothelial membrane
I: Asthma, COPD, Reduce mucous production (Blocks M3)
PK: Doesn’t cross membranes easily and so stays in bronchial tree and has few systemic effects.

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23
Q

oxybutynin

A 
MOA: M3 preferring antagonist 
I: Hyperactive bladder
AE: Reduced GI motility, Dry mouth.
PK: Short half life and needs frequent dosage
Generic form is cheap though
24
Q

scopolamine

A

Lipid soluble (Crosses BBB)
Antagonist of M1-M5 and some NN receptors.
Reduces PANS and also reduces sweat and salivary secretion
Temporary ENS modulator
Blocks receptor in inactive state
Also NN Unlike atropine
I: Especially Motion Sickness. Also Asthma, COPD, diarrhea, dilate eyes, reduce airway secretions (M3)
CI: Glaucoma, GI obstruction, urinary obstruction, Intestinal atony.
AE: Hyperthermia, Blindness, Altered mental status, lack of secretions, tachycardia, arrhythmias. See anticholinergic toxicity
PK: Lipid soluble can be absorbed through skin via patch

25
Q

Atracurium/Rocuronium

A
  • non-depolarizing NMJ blocker
    MOA: Direct acting, competitive NM (Some NN) antagonist
    Reversed with AChEI
    Causes NMJ blockade, weakness, flaccid paralysis
    I: Induction for intubation
    AE: Respiratory compromise (If you consider paralysing the diaphragm and killing them compromise then sure, I’ll buy that), Histamine release, hypotension, muscle weakness.
    peripheral effects, not lipid soluble
    Poorly lipid soluble-Peripheral effects
26
Q

Pancuronium

A

-non-depolarizing NMJ blocker, Nm antagonist at the NMJ
-longest acting
-used in surgery for mm relaxation, causes NMJ blockade and paralysis; can lead to respiratory paralysis in high doses
peripheral effects, not lipid soluble

27
Q

Succinylcholine

A

-Depolarizing NMJ blocker (Different than others)
Combination of 2 ACh molecules
MOA: Irreversible agonist of full specific NM.
Blocks by inducing a depolarization blockade in 2 phases
Phase 1) Occupies receptor preventing end plate depolarization.
Repolarization needed to reset excitation contraction coupling
Phase 2) Desensitization phase: Slow recovery
Not fully understood
Leads to muscle fasciculations than flaccid paralysis
I: Induction for intubation
AE: Histamine release, respiratory paralysis, hypotension, increased intraocular pressure, hyperkalemia (especially in burns), genetic variation can lead to extended desensitization blockade.

28
Q

a- Bungarotoxin

A
  • in venom of elapid snake (cobra and coral snakes)
  • inhibits NMJ
  • risk: breathing mm can be paralyzed
29
Q

a-latrotoxin

A

Black Widow spider
Produces presynaptic release of Neurotransmitters (Including ACh) from sensory motor neurons)
Creates a depolarization blockade similar to succinylcholine
Binds to vesicles and facilitates their binding to the presynaptic membrane via synaptotagmin.

30
Q

Trimethaphan

A

-ganglionic blocker, competitive antagonist at Nn receptor
Uses difference in esteric and anionic sites on ACh receptor. NN= more narrow and thus specific. Has NN effects and little NM. Block all ANS outflow.

E: Reduce ANS outflow overall. Peripheral NN block, loss of tone, Increased HR, Vasodilation, Decreased GI activity, Urinary hesitancy, Decreased sexual function (Sad panda disorder,) reduced sweat production.
I: HTN emergency, CNS bleeding, Not well tolerated (limited use)
PK: Very short acting

31
Q

Phenylephrine

A

MOA: Direct acting competitive A1 agonist (Specific)
E: Smooth muscle contraction and other A1
I: Decongestant. Reverse anesthetic hypotension due to mild inotropic and chronotropic effects. Decreased HR due to baroreceptor reflex. Priapism (Direct injection)
AE: HTN (Risk for Dissecting aneurysm if predisposed), Seizures (CNS effects) at high dose.
PK: Substrate for MAO-A. Significant 1st pass effect. Often used locally as nasal spray

32
Q

Clonadine

A

Used for sympatholytic effects
MAOL Direct acting A2 Competitive agonist
E: Activates A2 receptors and reduces NE release.
PO: leads to mild SANS reduction outflow from CNS and mild A2 effects reduce NE release, leading to reduced sympathetic tone and lower BP.
IV rout: Vasoconstriction due to direct effects on A2 postsynaptically: Postsynaptic A2 in CNS and periphery.
I: ADHD (3rd line, CNS effects), Opiate withdrawal (rebound NE release in amygdala), Antihypertensive by reducing NE and SANS outflow, Mild sedation (Reduction in ventral alertness system)
AE: Orthostatic hypotension, tachycardia, dizziness, HA, depression.

33
Q

Isoproterenol

A

MOA: Direct acting competitive B1, 2, 3 agonist
E: Activates all B directly with very little Alpha
I: Asthma (not any longer due to cardiac issues), EP studies
AE: High dose leads to increased HR, initial increase in BP, arrhythmias.

34
Q

Dobutamine

A

-MOA: Direct acting B1 selective agonist. But racemic mixture has A1 and A2 interactions.
A1 agonist and A2 antagonist.
I: Acute (reversible) heart failure during; surgery, sepsis, cardiogenic shock. Also cardiac stress testing.
AE: Angina, HTN, Tachycardia, arrhythmias.

35
Q

Albuterol

A

MOA: Selective B2 (With little B1), direct acting agonist
R isomer is active ingredient. S is inactive and can produce inflammation.
E: Vasodilation of bronchial smooth muscle leading to bronchodilation. Also vasodilation of striated muscle vessels leading to pooling and thus reduced TPR and reflex increase in HR.
I: Asthma, COPD
AE: Tremor, anxiety (CNS entry), Tolerance and endogenous responsiveness is decreased possibly worsening asthma attacks. Genetic variant predisposes some to rapid tolerance. (Period of few weeks)
PK: Aerosolized, 10-15 min max onset, lasts 2-4 hours

36
Q

Salmeterol/formoterol

A

Second generation B2 agonist
Duration of action up to 12 hrs.
Prophylactic for COPD. Often combined with corticosteroid
MOA: Selective B2 (With little B1), direct acting agonist

37
Q

Amphetamin

A

Crosses BBB
Similar structure to catechol nucleus, but no hydroxyl prevents direct action at adrenergic receptors.
MOA:
1) Competitive reuptake inhibitor of NE by NET
2) Transports mobile pool to synaptic pool. Ca++ independent release. “ceiling effects”
3) Blocks MAO
E: Increases synaptic pool of NE: DA > 5HT, produces non-specific SANS effects at all NE and DA receptors; increased Heart rate and TPR, Alpha effects
CNS effects: Increased alertness, motor activity, increased temperature,
I: ADHD, narcolepsy, drug of abuse, Increased attention in fatigue, increased reaction time in fatigue, increased motor activity, increased anxiety, increased appetite, increased temperature, increased respirations.
AE: Stimulant vasculitis, prolonged vasoconstriction with ischemia and necrosis, hyperthermia, metabolic acidosis, death from hyperthermia and acidosis (Rare due to ceiling effect.

38
Q

methamphetamine

A

Similar to amphetamine
Greater CNS effects
More readily pyrolysed (smoked), insufflated (snorted), injected,
Meth biotransformed into amphetamine in liver.
Parent compound has more 5HT effects than amphetamine.

39
Q

Pseudoephedrine

A

Amphetamine like drug
Behind the counter
E: Vasoconstrictor effects which increase vascular tone.
CNS effects: alerting effect, mediated by NE working with in ventral arousal network, counteracts antihistamines (often given with pseudoephedrine)
I: Decongestant- constricts nasal vessels to reduce congestion
AE: Insomnia, anxiety, hallucinations (rare), can be used to make meth.

40
Q

Methylphenidate

A

-indirect acting adrenergic agonist, amphetamine like
Ritalin
Similar to amphetamine and pseudoephedrine
Slightly greater effects on DA and NE
I: ADHD- preferred drug due to slightly fewer ANS effec

41
Q

Atomoxetine

A

selective cocaine like, NE reuptake inhibitor
Selective NE reuptake inhibitor used for ADHD
Effects similar to amphetamine except that the drug potentiates actions of neurotransmitters that are released.
Unlike amphetamines, cannot induce release by itself.

42
Q

Phenoxybenzamine

A

non-selective alpha antagonist
MOA: Irreversible (Covalent) Alpha antagonist
Long acting
I: Control of pheochromocytoma, prior to surgery
HTN, tachycardia
AE: Orthostatic hypotension

43
Q

Phenoltalamine

A

non-selective alpha antagonist, reversible, competitive (so some efficacy of NE)
alpha 1=alpha 2
-used in management of pheochromocytoma during surgery and afterwards, short acting

44
Q

Prazosin/Tamsulosin

A

alpha 1 selective anatagonists
MOA: Specific Reversible Apha 1 competitive antagonist
Profound vascular tone blocking effects leading to orthostatic hypotension.
E: Reduction in TPR with little reflex tachycardia
I: Benign prostate hypertrophy (PBH)(Mostly), HTN

45
Q

Yohimbine

A

MOA: Competitive antagonist at A2 receptor on cholinergic terminals
E: Increased NE release, Increased A1 and B effects, Can increase ACh by inhibiting A2 receptor on cholinergic terminals.
I: Orthostatic hypotension and erectile dysfunction

46
Q

Propranolol, Nadolol, Timolol, Sotolol,

A

-non-selective competitive beta blockers
-MOA: Competitive son-specific B antagonist with some local anesthetic action. Reduced corneal sensitivity while lowering intraocular pressure by reducing synthesis of aqueous humor.
E: Reduce B tone and B1 effects, decreased chronotropic, inotropic, dromotropic effects, Increase TPR from decreased B2 on striated muscle, decrease renin release, prevent bronchodilation and glycogenolysis in presence of hypoglycemia.
I: Arrhythmias, to decrease heart work, migraine HA, stage fright, sedation (CNS), physiological tremor, PTSD (controversial)
AE: Decrease heart rate, heart block. Bronchospasm, decrease glucagon response with hypoglycemia, increase in VLDL.
PK: Significant first pass (CYP3A4), significant interindividual variations in bioavailability, can have fast metabolizers.

Timolol doesn;t have local anesthetic effect, used in HTN and as eye drops to reduce IOP in glaucoma

47
Q

Metoprolol/Atenolol

A
  • cardio selective, beta 1 specific blockers
  • used in the management of HTN and arrhythmias
  • reduce the risk for asthmatics and diabetics
48
Q

Esmolol

A

cardio selective, beta 1 specific blocker

-very short acting, used in ICU for management of arrythmias

49
Q

Pindolol

A

Partial nonspecific Beta antagonist (B1)
Partial antagonist/agonist
Mildly reduces B tone, surmountable by high SNANS
Less hypotensive effects
Overcome by increased sympathomimetic activity (ISI) when need for increased SNAS
Competes with effects of EPI and NE at B receptor but doesn’t completely block receptor (ISI)
Also reduces renin release

50
Q

carvedilol

A

Similar to propranolol
MOA: Competitive son-specific B antagonist with some local anesthetic action. Reduced corneal sensitivity while lowering intraocular pressure by reducing synthesis of aqueous humor.
E: Reduce B tone and B1 effects, decreased chronotropic, inotropic, dromotropic effects, Increase TPR from decreased B2 on striated muscle, decrease renin release, prevent bronchodilation and glycogenolysis in presence of hypoglycemia.
I: Arrhythmias, to decrease heart work, migraine HA, stage fright, sedation (CNS), physiological tremor, PTSD (controversial)
AE: Decrease heart rate, heart block. Bronchospasm, decrease glucagon response with hypoglycemia, increase in VLDL.
PK: Significant first pass (CYP3A4), significant interindividual variations in bioavailability, can have fast metabolizers.

51
Q

Guanethidine

A

-NE depleting agent
MOA: Ligand for NET and Vesicular Monoamine Transporter (VMAT) where it enters vesicular pool of NE terminals and displaces NE.
Functional Sympathectomy
I: HTN

52
Q

tolterodine

A 
MOA: M3 preferring antagonist 
I: Hyperactive bladder
AE: Reduced GI motility, Dry mouth.
PK: Longer acting than oxybutynin
More expensive than oxybutynin
53
Q

epinephrine

A

Catecholamine
Limited CNS entry (more than NE)
A2>A1 B1=B2
Can affect the hypothalamus and CTZ

54
Q

dopamine

A

Catecholamine
E: Limited SANS function at low dose.
Vasodilates renal arterioles to preserve renal function via dopamine receptors in renal arterioles.
Natriuresis and diuresis via 2nd messenger systems dilates coronary vessels.
High dose: Increase inotropy via B1 also A1
I: Shock Tx while maintaining kidney perfusion.
Increased CO while maintaining kidney perfusion

55
Q

Terbutaline

A

Given Sub Q injection in emergency tx of asthma attack unresponsive to aerosols. Often used with epi pens.
MOA: Selective B2 (With little B1), direct acting agonist
E: Vasodilation of bronchial smooth muscle leading to bronchodilation. Also vasodilation of striated muscle vessels leading to pooling and thus reduced TPR and reflex increase in HR.
I: Asthma, COPD
AE: Tremor, anxiety (CNS entry), Tolerance

56
Q

Pilocarpine

A

-full M1-M3 agonist, very little effect on N
Pilocarpine:
-tertiary drug and crosses BBB
-SLUDGEM effect
-used primarily in glaucoma as an eye drop to constrict the pupil
-can precipitate bronchospasm in asthmatics

RU PA Pharm (5 decks)

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