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77 Cards in this Set
- Front
- Back
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Parasympathetic Neurotransmitter
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Ach
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Parasympathetic Pre-ganglionic location and receptor
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location: near/on receptor organ
Receptor = Nicotinic |
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Parasympathetic Post-ganglionic location and receptor
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location: near/on receptor organ
Receptor = Muscarinic |
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Sympathetic Pre-ganglionic location and receptor
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Location: ganglion; far away from receptor organ
Receptor: nicotinic |
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What are the 5 dif. fates of NE?
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1. re-uptake = most active.
2. binds alpha 2 presynaptically = regulates NE release 3. binds alpha 1 or beta on post-snaptically = causes effect 4. diffusion 5. Metabolized by MAO (monoamine oxidase) or COMT |
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steps in the synthesis of NE?
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Tyrosine --> DOPA --> Dopamine --> NE
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Steps in synthesis of Epi?
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Tyrosine --> DOPA --> Dopamine --> vesicle-enclosed NE --> PNMT (phenylehtanolamine-N-methyltransferase) converts NE to EPI
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Fates of Epi?
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same as NE
1. re-uptake = most active. 2. binds alpha 2 presynaptically = regulates NE release 3. binds alpha 1 or beta on post-snaptically = causes effect 4. diffusion 5. Metabolized by MAO (monoamine oxidase) or COMT |
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Synthesis of Ach?
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Glucose --> Acetyl CoA and Choline --> CAT (cholinacetyltransferase) used to convert to vesicle enclosed Ach to
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Fate of Ach?
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1. Binds M receptor (G proteins signal transduction)
2. Binds Nicotinic receptor = inc. Na+ influx K= efflux = depol. 3. Broken down by acetylcholinesterase into acetate and choline then taken back up 4. Diffusion into blood vessels (Butyryl Che Breaks it down) |
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What does Gs Protein Activate?
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Adenylyl Cyclase
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What does Gq Protein Activate?
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Phospholipase CB
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What does Gi Protein Inhibit?
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Adenylyl Cyclase
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Chronic Agonist leads to what in terms of the Receptor?
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Receptor Down Regulation
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Chronic Antagonist leads to what in terms of the Receptor?
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Receptor Up-Regulationg
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What produces aqueous humor in the eye?
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ciliary body
Aqueous humor moves from post --> ant. eye through trabecular network through canal of schlem |
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What is the cause of open angle glaucoma?
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histological change in trabecular meshwork that slows outflow of aqueous humor
=inc. aqueous humor in eye and inc. IO pressure |
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what is the cause of narrow angle glaucoma?
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structural defect in eye that causes narrow angle between iris and cornea
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What is the preferred drug and its mechanism of action in treatment of HEMORRHAGE?
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Epi --> alpha 1's activated = vassoconstriction
CUTANEOUS Blood Vessels have many aplha 1's |
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What is the preferred drug and its mechanism of action in treatment of ANAPHYLAXIS?
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Anaphylaxis = Allergic Reaction
Angioedema = EPI (alpha 1's activated = constricts capillary beds) Bronchoconstriction = EPI activates B2's = bronchodilation Pruritis or Urticaria = Hives. EPI activates B receptors = suppress histamine release from mast cells Hypotension = EPI activates A1's and B1's = vasoconstriction and raises BP WITHOUT REFLEX BRADYCARDIA |
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Difference between Phenylephrine, Xylometazoline, Oxymetazoline, Ephedrine and Pseudoephedrine in treatment of NASAL CONGESTION
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-"zolines" plus phenylephrine and midrodrine = alpha 1 agonists
Phenylephrine, Xylometazoline, and Oxymetazoline act DIRECTLY on A1's Epehdrine and Pseudoephedrine act directly (on A1's) and indirectly via NE release which activates A1's Ephedrine = NO REBOUND EFFECT Phenylephrine = short DOA Ephedrine and Pseudoephedrine = ORAL, pseudoephedrine = less side effects than ephedrine |
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Compare B Agonists, Ephedrine, Atropine, Ipratropium Bromide in Treatment of Asthma and COPD
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-"erol" plus terbutaline = B2 Agonists = activate B2 on lungs = bronchodilation
Ephedrine = Inc. NE = B2 activated. Not used b/c of side effects like CV stimulation, and CNS affects like insomnia, nervousness, anxiety Atropine = M Blocker = doesn't allow lung to bronchiconstrict. Better used for COPD instead of asthma Ipratropium Bromide = M blocker. Short DOA. Less side effects than B Agonists. |
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Difference between Phenylephrine, Atropine, Scopolamine, and Tropicamide in dilating the eye
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Phenylephrine = A1 Agonist = iris radial sm. m. contracts = eye constricts W/O CYCLOPLEGIA (=ciliary m. paralysis)
Atropine/Scopolamine = M Blocker on iris sphincter sm. m. LONG DOA. W/ CLYCLOPLEGIA Tropicamide = M blocker. SHORT DOA. W/ CYCLOPLEGIA |
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Side Effects of ADRENOMIMETICS?
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"THAMPAN" plus inc. vasoconstriction and dec. PVR
Tachycardia Hyperglycemia Angina Mydriasis Palpitations Arrhythmias Nasal Congestion Inc. Vasoconstriction Dec. PVR |
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What happens if a pt. is given a drug that inhibits MAO?
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Tyramine = from gut bacteria.
Promotes release of NE Metabolized by MAO (in Liver) (monoamine oxidase) If MAO inhibited, Tyramine will cause Ca2+ independent release of NE |
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Ability of Catecholamines, Ephedrine and Pseudoephedrine to cross BBB?
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Catecholamines = NE, Epi, Domapine ALL CROSS BBB
Ephedrine = taken orally. Releases NE from nerve terminals indirectly. CROSSES BBB. Asthma and COPD Pseudoephedrine = Releases NE from Nerve Terminal. Activates CNS to a lesser extent. Used as Nasal Decongestant |
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What is Raynaud's Disease?
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When Cold leads to Vasospasm in fingers and toes.
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What is the mechanism of treatment for Raynaud's Disease?
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A1 Blockers will prevent vasospasm in fingers and toes.
(NOTE- You would NOT use Tasulosin bc its specific for A1a receptors in prostate) |
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Difference between Pilcarpine, Cevimeline, in treatment of dry mouth, associated with Sjogren's Syndrome or radiation of head/neck?
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Pilocarpine - M Agonist, Oral,
Cevimeline - M Agonist, for Sjogren's because it works more selectively on Salivary glands, works longer, and has less side effects than pilocarpine |
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What is Sjogren's Syndrome?
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Autoimmune Disease that causes dry mouth and dry eyes.
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Difference between Muscarnic Antagonists, A1 Agonists, Neostigmine, and Bethanechol in treatment of Urinary Problems?
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Muscarinic Antagonists --> Treat Urinary Incontinence
A1 Agonist and Neostigmine --> Treat Urinary Retention Bethanechol --> Treats Non-Obstructive Urinary Retention |
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Advantage of using Tamsulosin in treatment of BPH?
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Tasulosin has a greater affinity for A1a receptor than other subtypes of A1 Antagonists.
A1a receptor is the subtype of receptor in the prostate Tamsulosin blocks A1a receptor at base of bladder = relaxes sm. m. at base of prostate and bladder |
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Whats the difference in Poisoning Symptoms caused by muscarine and scopolamine/atropine?
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Muscarine = M Agonist
Symptoms = salication, sweating, gastric acid secretion, intestinal cramps, bradycardia, pupil constriction = near vision Scopolamine/Atropine = M Blocker Symptoms = opposite of those above. |
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Side Effects of Muscarinic Agonists?
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salivation
sweating Intestinal cramps Increased Gastric Acid Secretion --> aggravates ulcers Blood Vessel Dilation = BP dec. = Inc. HR as reflex |
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What do you give a pt. who has OD'ed on Neostigmine, Pyridostigmine, or Edrophonium?
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Stigmine's plus Edrophonium = Reversible AchE Inhibitor
M Antagonist |
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What do you give a pt. who has OD'ed on Organophosphates?
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Organophosphates = Irreversible AchE Inhibotors
Give them M Blocker OR Pralidoxime = AchE reactivator |
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Ability of Physostigmine, Neostigmine, Pyridostigmine, and Organophosphates to cross BBB?
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Physostigmine - Cross BBB
Neostigmine - DOESN'T Crosss BBB Pyridostigmine Organophosphates - Crosses BBB |
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Which A1 Blockers Treat Hypertension?
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Prazosin, Terazosin, Doxazosin
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What is Pheochromocytoma?
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Tumor in Adrenal Medulla
Causes Inc. Epi and NE |
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What drugs treat Pheochromocytoma?
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Phentolamine and Phenoxybenzamine
OR B Blocker but must he given with an A1 Blocker b/c slowed HR unopposed by blood vessels to Epi's affects = massive inc. in BP |
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Side Effects of A Blocker?
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"RHINOS"
Reflex Tachycarida Headache, Weakness, Dizzy Inhibition of Ejaculation Nasal Congestion Orthstatic Hypotension Salt and Water Retention |
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Side Effects of B Blockers?
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Dec. HR
Hypotension CNS: Nightmares, lassitude, depression, insomnia NVD (nausea, vomitting, diarrhea) Sexual Dysfunction Inc. Triglycerides/Dec. HDL-C |
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How do B Blockers treat Migraine or Essential Tremor?
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Migraine:
Block B2 = No Dilation OR Inhibit Renin Secretion Tremor: Block B2 on Muscle = Na+ doesn't come into cell = No Tremor |
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Whats the biggest fear of esophageal bleeding?
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Repetitive Vomitting of blood = lots of blood loss
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Whats the main cause of esophageal varices?
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Portal Hypertension (Cirrhosis of the liver can cause portal hypertension)
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What do you use to treat esophageal varices?
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non-selective B Blocker (B1's and B2s) b/c they will reduce amt. of blood going into esophageal veins.
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Whats the mechanism by which Reversible and Irreversible AchE inhibitors bind to and are hydrolyzed by the enzyme?
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Reversible AchE Inhibitors: Bind AchE and are slowly hydrolyzed = impairs AchE's breakdown of Ach. Clinical effects 2.5-4 hrs.
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Where do AchE inhibitors work?
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Anywhere there is AchE (all cholinergic synapses)
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What is Myasthenia Gravis?
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autoimmune disease where Ab's to nicotinic receptor in NM Junction cause down-regulation of receptor = Impairs Ach Action = Muscle Weakness
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Whats the mechanism of action of reversible AchE inhibitors in treatment of Myasthenia Gravis?
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Inhibit AchE in NM Junction = Ach effects prolonged
N receptors over a greater cross sectional area are exposed to Ach |
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Difference between Edrophonium, Neostigmine, Pyridostigmine in Masthenia Gravis?
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Edrophonium = SHORT DOA so used for diagnosis (3-4 min. duration, IV only) (Also can be used to test the adequacy of prescribed meds.)
Neostigmine = 2-4 hr. Duration Pyridostigmine = 3-6 hr. Duration (time release version lasts 12 hrs.) |
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Define causes of a Cholinergic Crisis in a pt. with myasthenia gravis
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Overexposure to meds.
Stimulation of M Receptors at effector organs and in CNS Stimulation then Paralysis of autonimic ganglia and skeletal muscle |
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Define causes of a Myasthenic Crisis in a pt. with myasthenia gravis
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Disease has flared up and they can't breathe very well
Weakness of Muscles |
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Difference between Cholinergic crisis and Myasthenic Crisis in pt. with myasthenia gravis?
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cholinergic crisis = overstimulation of M receptors
Myasthenic Crisis = M receptors blocked to a great degree I.e. these conditions are opposites of each other |
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Difference between Toxicity and Uses of Echothiophate, Malathion, Parathion and Sarin Gas?
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Least Toxic to Most Toxic:
Echothiophate (miotic pupils, glaucoma) Malathion (Insecticide) Parathion (Insecticide) Sarin Gas (Very Toxic, no clinical use) |
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Side Effects of AchE Inhibitors (both reversible and irreversible)
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LNM
Lens Opacities Neurotoxicity M Receptor Stimulation |
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Mechanism of action of Atropine and Palidoxime in treatment of Cholinergic crisis due to organophosphate poisoning?
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Atropine - M Blocker
Central and Peripheral Side Effects Used for Reversible AND Irreversible AchE Inhibitors Pralidoxime - Works at NM Junction and Autonomic Ganglia Has Peripheral Side Effects Used ONLY In ORGANOPHOSPHATE POISONING |
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Difference between Non-depolarizing and Depolarizing Neuromuscular Blockers?
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Non-depolarizing: Competitively inhibit Ach at Post Junction Nicotinic Receptor = NO DEPOLARIZATION
Succinylcholine = Depolarizing Nicotinic Receptor Agonist. Prevents stimulation of contraction by Ach. |
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Difference between Phase I and Phase II block for succinylcholine?
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Phase I Block = Initial Action = Depolarize Membrane
Resistant to AchE Phase II Block = Occurs with higher Succinylcholine doses or continuous exposure. Depolarization then gradual Repolarization Like a competitive inhibitor AchE inhibitors may REVERSE Can directly stimulate muscle by electrical input |
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Compare ability of AchE inhibitors to reverse the effects of non-depolarizing and depolarizing NM Blocker
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AchE Inhibitors will enhance Phase I Block but can Reverse Phase II Block
i.e don't use Neostigmine during a Phase I Block, But you can Use it during a phase II Block |
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Compare the ability of AchE in NM Junction and Butyrylcholinesterase in plasma and liver to metabolize Succinylcholine
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AchE in NM Junction: Metabolizes Succ. MUCH MORE SLOWLY than Ach because of Succ's ability to resist hydrolysis
Butyrylcholinesterase in plasma and liver: Rapidly metabolizes Succ. and can lead to poison/death |
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Whats the difference between the DOA of Succ and Pancuronium?
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Succ = Depolarizing, Lasts 5 min. Elimination = Plasma
Pancuronium = Nondepolarizing, DOA 120-180 min. Elimination = Renal |
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Side Effects of Non-Depolarizing NM Blockers?
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PIMP-BHH
Post-Op Muscle Pain Intraocular Pressure Malignant Hyperthermia Paralysis Bradycardia Hyperkalemia Histamine Release |
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How can Succ. cause Hyperkalemia?
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Loss of Tissue K+ During Depolarization
nAchR Opens = K+ and Na+ cross membrane = Currents generated, and an excitatory post-synaptic potential generated Risk greater in pts. with burns, muscle trauma, spinal cord transections Can result in cardiac arrest or circulatory collapse |
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How can Succ. cause Malignant Hyperthermia in pts.?
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Can happen when Succ. used with general anesthetics. Pts. have genetic disorder of skeletal muscle
Excessive Ca2+ release from S.R. |
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What are the symptoms of Malignany Hyperthermia?
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Hyperthermia
Tachycardia Muscle Rigidity Accelerated muscle metabolism and contractures Potentially Fatal |
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Difference between the solubility of Atropine and Ipratropium Bromide?
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Atropine = Lipid Soluble = Cross BBB to have CNS Effects
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What are Atropine and Scopolamine used for?
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To Induce sedation, amnesia, and less oral secretions
Scopolamine more potent and more side effects |
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What is Atropine used for and what is it mechanism of action?
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Hyperactive carotid sinus syndrome and vagal-induced heart block
Blocks M2 receptors on Heart preventing over-stimulation |
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Whats the mechanism of action of scopolamine in motion sickness?
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Scopolamine blocks M receptors which are stimulated in vestibulocochlear ear during motion and it stops the reflex to vomit during motion
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What are the Anticholinergic Drugs used for urinary incontinence due to Detrusor Over-activity?
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M Blockers:
Tolterodine Oxybutynin Chloride Fesoterodine |
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Difference between the CNS effects of Scopolamine, Atropine, Ipratropium Bromide
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Scopolamine = most potent, then Atrpoine then Apratropium Bromide
CNS Effects: Sedation OR Excitement drowsiness, amnesia, fatigue, dreamless sleep Disorientation, memory loss, dizzy, restlessness, hallucinations, delirium, confusion |
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Difference between contraindications of adrenomimetics (NE and Epi Agonist) and cholinolytics (M Blocker) in Glaucoma
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In pts. with Glacoma, giving adrenomimetic or cholinolytic will cause eye dilation= Increased IO Pressure
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How is Open Angle Glaucoma treated?
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Either with B Blocker or A2 Agonist
--> Dec. Aqueous Humor Production by Ciliary Body = Dec. IO Pressure B Blockers used first, A2's given as alternative Epi given rarely |
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How to M Agonists (Cholinomimetics) work differently in Open angle and Closed angle glaucoma?
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Open Angle: Contracts Ciliary Muscle = opens trabecular meshwork
Closed Angle: Contracts Iris Sphincter m. = moves iris = aqueous humor can flow |
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What drugs are used to treat Glaucoma?
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Pilocarpine - used first (bc its most effective)
Pysostigmine - used second (less effective) Echothiophate - given as a last choice (its least effective and has most side effects) |
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What drugs are used to treat Open Angle Glaucoma?
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B Blockers used first
(All drugs used to treat open angle glaucoma are eye drops) Non-Selective: Timolol, Certeolol, Levobunolol B1-Selective: Betaxolol Levobetaxolol |
