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Autonomic Drugs

Pharmacology: Autonomic

QuestionAnswer
What action does stimulation of β2 receptors mediate on the following tissues? 1. vasculature 2. bronchioles 3. pancreas 4. liver 5. uterus 1. vasculature → vasodilation 2. bronchioles → bronchodilation 3. pancreas → ↑ insulin release 4. liver → ↑ glycogenolysis 5. uterus → relaxation
Which adrenergic receptor: 1. ↑ vascular smooth muscle contraction 2. ↓ insulin release 3. ↑ insulin release 4. ↑ renin release 5. ↑ bladder sphincter contraction 1. α1 2. α2 3. β2 4. β1 5. α1
Functions of the following receptors: 1. D1 2. H1 3. H2 1. relaxes renal vascular smooth muscle 2. ↑ nasal and bronchial mucus production, contraction of bronchioles 2. ↑ gastric acid secretion in parietal cell
What effect do β blockers have on the RAAS system? inhibition of β1 receptors in the juxtaglomerular cells → ↓ renin release
Which pupillary muscle is acted upon by? 1. Sympathetic α1 stimulation 2. Parasympathetic M3 stimulation 1. radial muscle 2. sphincter muscle
What effect does muscarinic stimulation have on: 1. pupil size 2. near vision 1. Miosis 2. Accommodation
What effect does α1 stimulation have on: 1. pupil size 2. near vision 1. mydriasis 2. no effect
What effect does muscarinic (M3) antagonism have on: 1. pupil size 2. near vision 1. mydriasis 2. cycloplegia (loss of accommodation)
What drug: 1. inhibits choline uptake in presynaptic cell 2. inhibits ACh release 3. inhibits breakdown of ACh 1. Hemicholinium 2. Botulinum toxin (binds synaptobrevin) 3. Acetylcholinesterase Inhibitor
Used to treat postoperative and neurogenic ileus and urinary retention: 1. direct cholinergic agonist 2. anticholinesterase 2. What is its mechanism of action? 1. Bethanechol 2. Neostigmine
What are the following muscarinic agonists used for: 1. Methacholine 2. Pilocarpine 1. bronchial hyperreactivity (asthma diagnosis) 2. (M3 agonist) glaucoma and xerostomia (dry mouth as in Sjogrens)
1. What is the difference in structure of Physostigmine and Neostigmine? 2. How does this contribute to its location of action? 1. Physostigmine is a tertiary amine and is non-ionized while neostigmine is a quaternary amine and is ionized 2. the nonionized drugs can cross the blood brain barrier
What form of antagonism to acetylcholinesterase do the following drugs possess: 1. physostigmine 2. donepezil 3. organophosphates all ACh inhibitors exhibit reversible, competitive inhibition except for organophosphates which are irreversible, noncompetitive
Drug used to treat 1. atropine toxicity 2. organophosphate toxicity 1. Physostigmine (crosses BBB) 2. (organophosphates are cholinesterase inhibitors) Rx: atropine + pralidoxime (2-PAM)
Mechanism of action: 1. α-bungarotoxin 2. hexamethonium 3. Atropine 4. mecamylamine 5. succinylcholine 1. blocks muscle nicotinic receptors (Nm receptors) 2. blocks autonomic ganglia nicotinic receptors (Nn receptors) 3. blocks muscarinic receptors (M) 4. blocks Nn receptors in ganglia 5. blocks Nm receptors in muscle
rate limiting step in the synthesis of NE tyrosine hydroxylase
What are the effects of dopamine at: 1. low doses 2. medium doses 3. highest doses stimulates: 1. D1 receptors: ↑ renal blood flow, ↑ mesenteric blood flow 2. β1 receptors: ↑ cardiac contractility 3. α1 receptors: vasoconstriction
1. Which neurotransmitter activates β2 receptors? 2. Which receptor is more sensitive to activators and predominates at lower concentrations: α or β receptors? 1. epinephrine; β2 receptors are not innervated so norepi cannot reach them 2. β receptors
Which G-protein class goes with the receptor: 1. α1 2. α2 3. β1 4. β2 5. M1 6. M2 7. M3 1. q 2. i 3. s 4. s 5. q 6. i 7. q
Which G-protein class goes with the receptor: 1. D1 2. D2 3. H1 4. H2 5. V1 6. V2 1. s 2. i 3. q 4. s 5. q 6. s
What is the function of the following receptors: 1. D1 2. D2 3. V1 4. V2 1. ↑ renal blood flow 2. modulates transmitter release in brain 3. ↑ vascular smooth muscle contraction 4. ↑ H2O reabsorption in collecting duct
Which receptors are stimulated by: 1. Isoproterenol 2. Dobutamine 3. Norepinephrine 4. Epinephrine 1. β1 = β2 2. β1 > β2 3. α1, α2, β1 4. α1, α2, β1, β2
How do the following change after isoproterenol administration: 1. pulse pressure 2. overall blood pressure 3. heart rate 1. ↑ pulse pressure: ↑ systolic (β1), ↓ diastolic (β2) 2. decrease 3. increase (β1)
Use of an α1 blocker can reverse hypertension in a patient receiving too much epinephrine but not norepi. Why? By blocking α1 receptors, the β2 receptors that are stimulated by epinephrine and not by norepinephrine are free to act and ↓ TPR
Which receptors are stimulated by epinephrine at the following doses and which other drug does its action mimic at each dose: 1. low-dose 2. medium-dose 3. high-dose 1. β1, β2 - isoproterenol 2. β1, β2, α1 - dobutamin (bc β2, α1 cancel out their effects) 3. β1, β2, α1 - norepinephrine (bc α1 predominates)
Where are the following enzymes found and which neurotransmitters do they metabolize: 1. MAO type A 2. MAO type B 1. liver; NE, 5HT, and tyramine 2. brain; dopamine
How does tyramine initiate a hypertensive crisis in a patient taking an MAO-A inhibitor? tyramine is metabolized by MAO-A. MAO inhibition can result in a built up of tyramine which acts as a catecholamine neurotransmitter releaser
How do Phentolamine and Phenoxybenzamine differ in their competitive properties to the α receptor 1. Phentolamine - competitive inhibitor 2. Phenoxybenzamine - noncompetitive (irreversible)
3 Clinical Symptoms of a muscarinic antagonist overdose 3 C's 1. cardiotoxicity 2. convulsion 3. coma
Symptoms of cholinergic crisis DUMBBELSS 1. Diarrhea 2. Urination 3. Miosis 4. Bronchospasm 5. Bradycardia 6. Excitation of skeletal muscle and CNS 7. Lacrimation 8. Sweating 9. Salivation
Atropine mechanism of action Antagonizes muscarinic receptors
Where are the following receptors located: 1. M1 2. M2 3. M3 1. CNS, enteric nervous system 2. heart 3. most other sites (exocrine gland, bladder, lung)
Use of these muscarinic antagonists: 1. Benztropine 2. Scopolamine 3. Ipratropium 4. Oxybutynin 5. Methscopolamine 1. Parkinson's 2. Motion sickness 3. Asthma, COPD 4. ↓ bladder spasms in mild cystitis 5. peptic ulcer
Mechanism of action and use: 1. Ritodrine 2. Clonidine 3. Phenylephrine 4. Prazosin 5. Mirtazepine 1. β2 agonist, ↓ premature contractions 2. α2 agonist, hypertension 3. α1 > α2 agonist, nasal decongestion 4. α1 blocker, HTN and BPH 5. α2 blocker, depression
Mechanism of action: 1. Reserpine 2. Guanethidine 1. inhibits monoamine vesicular uptake in presynaptic terminal 2. inhibits NE release from synaptic nerve ending
1. Which drug/test is used to differentiate Myasthenia gravis from cholinergic crisis? 2. How does this test work? 1. Edrophonium/Tensilon Test 2. Edrophonium is an ACh esterase inhibitor that will improve muscle weakness in myasthenia patients but worsen that of cholinergic crisis
What is the cause of a cholinergic crisis? excess acetylcholine leads to overstimulation at the neuromuscular junction and desensitization of ACh receptor
Name the sympathetic and parasympathetic action and receptors for the following organs? 1. Bladder walls 2. Bladder sphincters 1. sympathetic: β₂ relaxes 1. parasympathetic: M₃ contracts 2. sympathetic: α₁ contracts 2. parasympathetic: M₃ relaxes
Which ganglia are found in the sympathetic chain? paravertebral ganglia
Mechanism of action: methyldopa α2 agonist used in hypertension
Created by: amichael87