ANS and FDA drugs Flashcards

Question

Atracurium/Rocuronium

Answer 1

- 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

Answer 2

-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

Answer 3

-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.

Answer 4

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

Answer 5

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.

Answer 6

-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

Answer 7

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

Answer 8

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.

Answer 9

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.

Answer 10

-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.

Answer 11

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

Answer 12

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

Answer 13

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.

Answer 14

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.

Answer 15

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.

Answer 16

-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

Answer 17

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.

Answer 18

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

Answer 19

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

Answer 20

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

Answer 21

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

Answer 22

-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

Answer 23

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

Answer 24

cardio selective, beta 1 specific blocker | -very short acting, used in ICU for management of arrythmias

Answer 25

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

Answer 26

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.

Answer 27

-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

Answer 28

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

Answer 29

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

Answer 30

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

Answer 31

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

Answer 32

-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

ANS and FDA drugs Flashcards

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