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236 Cards in this Set
- Front
- Back
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____ stimulates fusion of synaptic vesicles with nerve terminal plasma membraine causing ACh release |
Ca |
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Which muscarinic R are excitatory? |
1,3,5 - "odd people are exciting" |
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Which muscarinic R are inhibitory |
2,4 |
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Where does Hemicholinium work? |
Choline (starting material for ACh) and Na symporter |
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Where does vesamicol work? |
Prevents ACh from entering potential release vessicle |
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Where does botulinum work? |
Prevents exocytosis of vessicle |
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What enzyme is used for AcCoA + Choline --> ACh |
Choline Acetyltransferase |
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What 3 drugs cause Na channel block? |
Tetrodotoxin Scorpion Toxin Local Anesthetics |
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What drugs disrupt ACh synthesis, storage, release, etc (3) |
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What drugs Act on ACh R (3) |
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What 2 drugs prolong the action of ACh by working on esterase |
Nerve gases Esterase inhibitors |
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What 2 drugs result on changes on physiologic target tissue |
Ca Tetrodotoxin |
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T/F M1, M3, M5 Ach signaling uses IP3 to act on Ca stores in cell? |
T |
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T/F Nicotinic Receptor Signaling results in membrane depolarization |
T |
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What signaling method is used by M2 and M4? |
cAMP and activating K channels |
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How are K+ channels activated? |
by hyperpolarization of the plasma membrane |
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What type of M Receptors are found in the CNS |
M1; IP3 and DAG |
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What type of M Receptors are found in the Heart |
M2 |
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What type of M Receptors are found in the exocrine glands |
M3 |
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What type of M Receptors are found in the CNS; possibly vagal nerve endings |
M4 |
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What type of M Receptors are found in the Vascular endothelium |
M5 |
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How does M1 signaling work |
IP3 and DAG, Increased intracellular Ca2+ |
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How does M2 signaling work |
Opens K+ channels, inhibits adenylyl cyclase |
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How does M3 signaling work |
Like M1 |
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How does M4 signaling work |
Like M2 |
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How does M5 signaling work |
Like M1 |
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Where are Nicotinic Nn found |
Postganglionic Neurons |
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Where are Nm R found |
Skeletal muscle |
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How do nicotinic R signal |
Opening of Na and K channels --> Depolarization |
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What are the 2 classes of direct Muscarinic R agonists |
Choline Esters Cholinomimetic Alkaloids |
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T/F Choline esters are charged at physiological pH and therefore cross the BBB |
F; they cant cross because of their charged state |
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What are the 2 Cholinomimetic Alkaloids |
Muscarine: From Toxic mushroom Pilocarpine: Especially active on sweat glands |
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What happens if you eat the toxic amanita mushroom? |
overstimulation of autonomic organs |
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What is pilocarpine used for (2) |
Miotic in Glaucoma Stimulate salivation |
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Effects of Muscarinic Cholinergic agents on Eyes (2) |
Miosis Accomodation (Contracts iris sphincter and ciliary muscle) |
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Effects of Muscarinic Cholinergic agents on Lungs (2) |
Contraction of SM Increase secretions |
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T/F Muscarinic Cholinergic agents on bladder cause urinary retention |
F; voiding |
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Effects of Muscarinic Cholinergic agents on GI |
Increase Secretions + Motor activity |
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T/F Ca+ stimulates Gi and cAMP relaxes |
T |
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Effects of Muscarinic Cholinergic agents on secretions (NON GI) (3) |
Increases lacrimal Increases Nasopharyngeal Increases Sweating |
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What causes GI stimulation? GI Inhibition? (contraction) |
Ach --> Stimulate NE --> Inhibits |
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What are the 4 Primary effects of ACh on CV system |
Vasodilation Negative Chronotropy (beating rate) Negative Dromotropy (conduction Velocity) Negative Inotropy (force of contraction) |
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Low does ACh leads to |
Transient fall in BP --> reflex tachycardia |
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Larger doses of ACh leads to |
bradycardia |
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The ability of atropine to block ACh effects on BP tells us what? |
ACh is working on muscarinic R |
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At HUGE doses of Ach with atropine what happens? |
Increase in BP and Vasoconstriction Due to ACh stimulating adrenals |
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What are Chol. agents used for |
Closed Angle Glaucoma Urinary/GI Retention Sjogrens to increase tears and saliva |
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What are the 2 major Anti-Cholinergics |
Atropine Scopolamine |
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T/F anti cholinergics can be used on Nicotinic and Muscarinic Rs |
T |
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T/F Tertiary amine drugs are highly specific for Muscarinic while quaternary are less specific |
T |
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Effect of Atropine on eyes |
Mydriasis and loss of accomodation |
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What drug is used on eyes becuase of it's short acting duration |
Tropicamide |
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Atropine effets on GI (2) |
Inhibits saliva (M1 and M3) Gastric Secretion is reduced |
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Atropine effects on CV |
Tachycardia by inhibiting vagal N (M2) |
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T/F Atropine can abolish reflex vagal-mediated bradycardia |
T |
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T/F Atropine can block vasodilation by acting on M2 on endothelial vasculature |
F; M3 R |
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Effect of Atropine on infants and children |
Atropine Fever |
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T/F Atropine can cross BBB and can cause depression and drowsiness |
T |
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Atropine is a bronchoconstrictor |
F; Bronchodilator and inhibits mucus secretions and movement |
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What drug is best as a bronchodilator as it doesnt inhibit mucus |
Ipratropium |
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What drugs are used for OAB |
Oxybutynin Darifenacin Tolterodine (pro-drug) |
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Atropine Toxicity |
Blind as Bat Dry as Bone Red as Beet Hot as Hare Mad as Hatter |
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Atropine Tox treatment: |
Anti-AChE Physostigmine/Neostigmine |
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3 Types of Cholinesterase Inhibitors |
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What cholinesterase inhibitor is used to test for MG |
Edrophonium* |
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3 Reversible Chol. inhibitors |
Edrophonium Tacrine Donezepil T and D used for alzheimers and have muscarinic side effects |
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Carbamate Esters form carbamylated esters which are quickly hydrolyzed leading to longer 1/2 life |
F; are slowly hydrolyzed |
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Name 3 Carbamate Esters |
Physostigmine Neostigmine Pyridostigmine |
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T/F Organophosphates are irreversible |
T |
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Name 5 Organophosphates |
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What can you give to reactivate enzyme that has been phosphorylated by Organophosphate, PRIOR to "aging" |
Pralidoxime |
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6 uses of Anti-Chols |
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MG is an autoimmune disease in which Anti_____ Abs are made |
Ach R |
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MG leads to destruction of _____ in the ______ |
Neuromuscular junction; head and neck |
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What treatments are given for MG |
Neostigmine Physiostigmine |
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Why doe Neostig and Physostig help in MG |
Increase amount of ACh available |
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Why is edrophoinium used for diagnosis |
Rapid onset and short duration of action |
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T/F Physostigmine can be used for belladona poisoning |
T |
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Cholinergic Syndrome: Respiratory |
Bronchial Constriction |
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Cholinergic Syndrome: GI |
Vomiting, diarrhea, salivation |
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Cholinergic Syndrome: CV |
Bradycardia, Hypotension, collapse |
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Cholinergic Syndrome: Skeletal muscle/skin |
Sweating Fasciculations then paralysis |
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How does death occur from Anti-AchE |
Respiratory failure from muscle paralysis Bronchial constriction and airway blockage CV collapse |
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Similarities between Cholinergic Crisis and MG |
Muscle weakness Excessive Muscarinic stimulation |
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5 Methods to treat Cholinergic Crisis |
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T/F Succinylcholine is depolarizing skeletal muscle blocker |
T |
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4 Times to use NM block |
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What are the 2 types of NMJ blockers |
Competitive - Non-depolarizing Depolarizing |
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Name one competitive NMJ blocker |
D-tubocurarine |
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MOA of D-tubocurarine |
Competes with Ach |
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Pharmacological effects of D-tubocurarine |
Muscle Relaxation Hypotension |
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Does d-tubocurarine have CNS effects |
no |
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Does d-tubocurarine have sensory or pain R effects |
No |
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Adverse effects of NMJ blockers |
Can interact with other drugs at NMJ CV: Bp and bradicardia, arrhythmias Histamine release respiratory paralysis |
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Which NMJB can cause overdose |
competitive |
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What can you give for d-tubocurarine OD |
neostigmine - increases availability of ACh |
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Long Acing Curare Short Acting curare |
Pipecuronium Pancuronium and Vecuronium Mivacuronium |
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Name a Depolarizing NMJ blocker |
Succinylcholine |
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What class of drug goes through Phase 1 and Phase 2 blocking |
Depolarizing NMJB |
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Phase I NMJB characterized by |
Constant and Diminished block |
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Phase II NMJB characterized by |
Fading block (similar to non-depolarizng) Desensitization |
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Side Effects of Succinylcholine: Duration Elimination Histamine Ganglion Block |
Ultrashort Plasma ChE Minimal Stimulation |
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Side Effects of Tubocurarine: Duration Elimination Histamine Ganglion Block |
Long Renal High High |
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Do the auto-alpha2 R on presynaptic R inhibit or stimulate NE |
Inhibit |
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Neuronal stimulation causes _____ dependent exycytosis of NE |
Ca |
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What R type does NE cause stimulation |
Beta |
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What 2 enzymes metabolize NE |
COMT MAO |
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Alpha 1 A,B,D R Agonist Preferences: |
Epi>= NE >> ISO Phenylephrine Oxymetazoline |
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Alpha 1 A,B,D R Antagonists |
Prazosin Tamsulosin (1A) Chloroethyl Clonidine (1B) |
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Alpha 1 Signaling |
Galpha-q; Increase in IP3 and DAG |
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Alpha 1 Tissue Responses |
Vascular SM contraction GU SM |
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Alpha 2 A,B,C Agonists |
Epi >= NE >> ISO
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Alpha 2 A,B,C Antags |
Yohimbine Prazosin (2B,C) |
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Alpha 2 A,B,C Signaling |
Ga-i decreases cAMP |
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Alpha 2 A,B,C Tissue Response (3) |
Decreases insulin secretion Platelet aggregation Decrease NE |
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Beta 1 Agonists |
Iso > NE >> NE Dobutamine |
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Beta 1 Antags |
Propranolol Metoprolol |
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Beta 1 Signaling |
Ga-s Increases cAMP |
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Beta 1 Key Tissue Response |
*Renin Release Cardiac Increases (Force, rate, conduction) |
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Beta 2 Agonists |
Iso > Epi >> NE Metroproterenol Albuterol |
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Beta 2 Antags |
Propanolol Butoxamine |
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Beta 2 Signaling |
Increases cAMP |
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Beta 2 Tissue Response |
SM relaxation in lung and BV Liver - gluconeo and glycogeno |
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Beta 3 Agonists |
Iso = NE > EPI Mirabegron |
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Beta 3 Antags |
Carvedilol |
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T/F Propanolol is a weak B3 Antag |
T |
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Beta 3 Signaling |
Increases cAMP |
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Beta 3 Tissue response |
Lipolysis (also B1 and B2) Bladder Retention |
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Dopamine 1 Agonists |
D1=D2 >> B1 >> A1 ibopamine |
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Dopamine 1 Antags |
NONE |
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Dopamine 1 signaling |
increases cAMP |
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Dopamine 1 tissue responses |
Selective Vasodilation* |
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Dopamine 2 Agonists |
Dopamine Bromocriptine |
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Dopamine 2 Signaling |
Decrease cAMP |
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Dopamine 2 Tissue response |
CNS Nerve Terminals TreatPD* |
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Imidazoline Agonist Agonist |
Clonidine |
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Imidazoline Antag |
NONE |
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Imidazoline tissue response |
Decrease Sympathetic output from brainstem |
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T/F Isoproteronol is a D2 Antag |
F; D2 have no antags |
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What 2 R result in decreasing cAMP |
Alpha2 (A,B,C) D2 |
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What R uses IP3 and DAG |
Alpha1 |
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T/F In general Subtypes 1 excite and 2 inhibit |
T |
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_____ mediate contraction of vascular smooth muscle |
A1 |
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_____ R located on nerve terminals mediate contraction of vascular smooth muscle |
A2 |
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______ mediate relaxation of bronchiole SM |
B2 |
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_______ R are excitatory, mediating cardiac stimulation |
B1 |
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What happens after prolonged exposure of sympathyolytics like propanolol |
R up-regulation |
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What 3 autonomous dysregulations are seen in chronic hypertension |
Decreased baroreceptor Increased chemoreflex CNS-RAAS changes |
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The 3 dysregulations in CH are the root cause of what |
Increased Sympatho Decreased Vagal |
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T/F Inflammation is heart healthy |
F |
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T/F autonomous dysregulation increases mortality |
T |
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T/F Immune system is powerful regulator of autonomic system |
F; autonomic system influences immune system |
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What R does pheocytoma work on to cause hypertension |
A1 R (catecholamine releasing tumor) |
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*What is the alpha response to Cutaneous and viceral blood vessels |
A1 constriction |
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What is the beta response to Cutaneous and viceral blood vessels |
NONE |
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What is the alpha response to skeletal muscle, liver |
NONE |
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What is the beta response to skeletal muscle, liver |
B2; Dilation |
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T/F Beta R increase arterial resistance |
F; Alpha |
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What R type plays predominant role in heart |
Beta; Increases CO all 3 ways (HR, Conduction Velocity, Contractility) |
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T/F Beta effects on the heart see increase in systolic and decrease in diastolic |
T |
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T/F Alpha R stimulation leads to mydriasis |
T |
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What R maintains intraocular P |
Alpha |
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What R produces Aq. humor |
Beta |
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What R are found in bronchioles (lead to dilation) |
B2 |
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What R are found in nasal passages that have decongestant action |
A1 |
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Sphincters in GI are ______ by A1 R |
Contracted |
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____ causes bladder contraction |
A1 |
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____ cause bladder relaxation* |
B3 |
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Apocrine (smelly) glands are stimulated by ___ r |
Alpha |
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Exocrine glands (theromo) are regulated by _____ |
Sympathetic Cholinergic N via AcH |
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What R does EPI have preference for? |
Beta 2 |
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T/F Isoproterenol is specific for Beta R |
T; vasodilator |
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Iso is great for what 3 things |
HR and CO increases Relaxes bronchioles Relaxes GI SM |
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What drug is specific for A1 R |
Phenylephrine; vasoconstriction and increase BP |
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What drug is used as Nasal decongestants (A1 agonists) |
Oxymetazoline |
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What is the effect of Clonidine on A2 R |
Decreases BP |
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What is the effect of Dobutamine* on B1 R? |
Increase CO. NO reflex bradycardia |
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What is the effect of B2 R agonists |
Dilates broncioles Great for asthma Albuterol |
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What R are involved with OAB |
B3 |
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What drug is B3 R selective |
Mirabegron |
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T/F Amphetamine results in the stimulation of both alpha and beta R |
T |
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Nicotine effects on CV |
Increases BP and HR (higher doses cause arrhythmias) |
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Nicotine effects on GI |
Increases Tone, Motility, secretion (high dose - nausea, vomiting, diarrhea) |
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Nicotine effects on Exocrine |
Increase salivation and bronchial secretion |
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Nicotine effects on CNS |
Tremors, Addiction |
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4 Methods to treat nicotine OD |
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2 Major Ganglia blockersq |
Hexamathonium Mecamylamine |
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Which Ganglia will a GB block? SNS or PnSN? |
Whatever branch has greatest influence; predominant tone |
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What 3 Sites have Sympathetic Predominant tones |
Arterioles Veins Sweat Glands |
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T/F Sweat glands are under control of adrenergic as they have sympathetic predominant tone |
F; sympathetic but CHOL |
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What 6 sites are under control of Parasympth |
Heart Iris Ciliary Muscle GI Bladder Salivary glands |
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Effect of block on Arterioles |
Vasodilation; increases peripheral blood flow |
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Effect of block on Veins |
Vasodilation; decreases CO |
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Effect of block on Heart |
Tachycardia |
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Effect of block on Iris |
Mydriasis (pupil dilation) |
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Effect of block on Ciliary muscle |
Cycloplegia - focused for far vision |
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Effect of block on Gi |
Decreases tone/motility/secretion |
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Effect of block on bladder |
urinary retention |
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Effect of block on salivary glands |
Dry mouth |
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Effect of block on sweat glands |
absence of sweating |
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Why would we use ganglia block |
Hypertensive Crisis Controled Hypotension To prevent massive symph discharge |
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Which of thefollowing is true in an individual with heart failure? A. There is alengthening of phase 2 of the fast response B. The parameter:stroke volume divided by end-diastolic volume is excessively low. C. There is increasedsystolic blood pressure relative to diastolic blood pressure. D. There is anincreased Frank-Starling effect (Starling’s law) relative to normal ventricularfunction. |
B. The parameter: stroke volume divided by end-diastolic volume is excessively low. |
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What is the best index of cardiac preload |
End-diastolic volume |
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Which is a mechanism for correcting bothlow blood pressure and hypovolemia (low blood volume)? |
Increase renin release from cells of the kidney |
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Epinephrine give to reduce bleeding works where |
Directly at target tissue; Post-ganglia (adrenergic synapse) |
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Cholinesterase inhibitors to produce excessive salivation works |
Target tissue; post-ganglia (nicotinic synapse) |
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Respiratory paralysis is due to succinylcholine and works where? |
Target tissue; NMJ of somatic neurons |
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Nicotine stimulates GI and Heart by acting on |
Preganglia of PSNS Preganglia of SNS |
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Prazosin works on prostate by acting at |
Target tissue; post-ganglia (adrenergic synapse) |
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T/F In treatment of BPH, Tamsulosin has few CV side effects that Prazosin because Tamsulosin lacks activity at Presynaptic A2 R |
F |
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Physostigmine can be used to reactivate phosphorylated acetylcholinesterase, provided that enzyme has not aged |
F |
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What Drug increases cAMP in cardiac muscle |
NE |
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What drug acts on Alpha 2 Adrenergic R |
Clondidne |
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What drug acts on B2 R |
Albuterol |
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What drug acts on A1 R |
Oxymetazoline |
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What drug acts on B3 R |
Mirabegron |
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What drug reverses CNS and peripheral actions of atropine |
Physostigmine |
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What drug effects Voltage gated Na channels |
Tetrodotoxin |
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What drug effects Muscle type nicotinic R |
Decamethonium |
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What drug effects Muscarinic AcH R |
Bethanechol |
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What drug effects Ganglionic type nicotinic Ach R |
Hexamethonium |
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The CV effects of ephedrine occurs because |
Stimulation of catecholamine release from Adrenergic Nerves |
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Atropine can be used to treat (4) |
Muscarine poisoning Vagal-induced bradycardia A-V node block Acetylcholinesterase inhibitor |
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What drug antagonizes both vascular and cardiac actions of NE |
Carvedilol |
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Which one of the following statements regardingd-tubocurarine (d-TC) is TRUE? A. The diaphragm and intercostal muscles are the mostsensitive to d-TC B. d-TC produces brief muscle twitches prior to muscleparalysis C. d-TC is very short acting lasting less than 5 minutes D. Acetylcholinesterase inhibitors can inhibit the effectsof d-TC E. d-TC blocks muscarinic receptors in the parasympatheticnervous system |
D. Acetylcholinesterase inhibitors can inhibit the effects of d-TC |
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Why is NE a potent vasoconstrictor |
Activates A1 R on blood vessesl |
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What will prevent reflex bradycardia after A1 R agonist |
Mecamylamine |
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What drug is used for OAB |
Oxybutynin |
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What drug is used for Asthma |
Ipratropium |
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What drug lowers intraocular pressure |
Timolol |
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At toxic doses,atropine can induce: 1. Mydriasis and cycloplegia 2. Inhibition of sweating 3. Inhibition of salivation 4. Hallucinations and delirium |
ALL 4 |
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Poisoning with DFP most likely would result in: |
Excessive Salivation Skeletal muscle paralysis |
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T/F Succinylcholine has a shorter duration of action than D-tubocurarine |
T |
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T/F Succinylcholine may cause prolonged apnea which can be treated by cholinesterease inhibitors |
T |
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T/F Succinylcholine may precepitate attacks of malignant hyperthermia |
T |
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T/F Succinylcholine is a competitive blockers at Nic. AcH R |
F |
