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100 Cards in this Set
- Front
- Back
nicotinic type I receptors
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autonomic ganglia
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N1 agonists
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ACh and nicotine (enhance Na conductance)
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N1 antagonists (ganglionic blocking drugs)
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trimethaphan, hexamethonium
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nicotinic type II receptors
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skeletal muscle motor endplate
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N2 agonists
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ACh, nicotine, succinylcholine = enhance Na conductance
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N2 antagonists
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d-tubocurarine (d-tc), pancuronium, Mg++ = the -curiums and -roniums
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sodium channels of cardiac fast fibers
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atria, ventricles
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cardiac class IA drugs
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procainamide, disopyramide, quinidine
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cardiac class IB drugs
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lidocaine - only affects ventricles
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sodium channels in CNS
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the antiepileptic drugs phenytoin, carbamazepine, & valproate inhibit the spread of electrical signals by prolonging the state of inactivation of the sodium channel
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Na+ channels in sensory nerve fibers
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the cationic form of local anesthetic drugs (cocaine, procaine, lidocaine) blocks Na+ conductance by binding to a
site in the channel on the axoplasmic side (inside cell) |
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Sodium channels coupled to 5-HT3 receptors in CTZ
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= induce nausea/emesis, blocked by ondansetron
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Ca++ channel blockers
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nifedipine, diltiazem & verapamil = block L-type channels in heart and vascular smooth muscle (VSM)
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Ca++ channels in SM of GI tract blocked by
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Al, Fe, diltiazem and verapamil
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Ca++ channels in SM of uterus blocked by
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Mg++
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T-type Ca++ channels in CNS blocked by
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ethosuximide
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Felbamate prevents seizures by
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blocking NMDA receptors
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Glutamate stimulation of NMDA receptors coupled to
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Ca++ channels
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Ketamine and phencyclidine (“angel dust”) block
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NMDA receptors and prevent the excitatory effects of glutamate to cause “dissociative” anesthesia and hallucinations.
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DOC for tx of neuroleptic malignant syndrome and anesthesia-induced malignant hyperthermia (hyperpyrexia)
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dantrolene, Internal Ca++ channels of SR blocked which prevents the release of “trigger” Ca++
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Drugs acting through potassium channels
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hyperpolarize and inhibit
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Muscarinic receptors at the SA node
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coupled to a K-channel via a G-protein
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M agonists at SA node
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ACh, pilocarpine
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M antagonists at SA node
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atropine et al., pancuronium, quinidine, TCA’s, older antihistamines like diphenhydramine
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buspirone is a partial agonist at
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5-HT1A-receptors in the CNS, for tx of anxiety
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hydralazine, minoxidil, diazoxide
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arterial vasodilators
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arterial vasodilators activate
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ATP-modulated K-channels = hyperpolarization = relaxation = vasodilation
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Fast cardiac fibers
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antiarrhythmic drugs
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procainamide, disopyramide & quinidine as antidysrhythmics
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prolong repolarization (APD & ERP increased); only quinidine actually widens the QRS and increases the Q-T interval
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lidocaine as antidysrhythmic
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accelerates repolarization (APD decreased)
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Amiodarone and sotalol as antidysrhythmics
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delay ventricular repolarization via block of K+ channels; APD, ERP and Q-T interval increase
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Terfenadine blocks
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K+-channels and delays repolarization in the ventricles, but is completely metabolized by CYP450 to its active metabolite fexofenadine. The macrolide erythromycin inhibits this CYP450, so terfenadine inhibits repolarization and can increase the Q-T interval enough to cause torsades de pointes = polymorphic ventricular tachycardia
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Cisapride cardiac s/e
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torsades by partially inhibiting the K-repolarization current.
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tolbutamide, chlorpropamide, glypizide MOA at K channel
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in pancreatic Beta-islet cells, close K+-channels causing the cell to depolarize; depolarization opens voltage-sensitive channels; Ca++ flows in to activate PLC which increases IP3 which release more Ca++ from the SR; increased free intracellular Ca++ causes insulin secretion
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Diazoxide opens
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ATP-regulated K+-channels to prevent depolarization and thus inhibit insulin secretion
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Baclofen enhances GABA-mediated K+ conductance at
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presynaptic terminals and thus reduce the release of an excitatory NT glutamate in the spinal cord. Baclofen used to tx spasticity ass w cerebral palsy, multiple sclerosis and stroke. Baclofen is as effective as BZ’s, but causes less sedation. Baclofen also causes less of a decrease in muscle strength than does dantrolene
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Opiates (morphine) hyperpolarize neurons via
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mu receptors
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dopamine, bromocriptine and pergolide hyperpolarize cells to prevent prolactin release at the __ receptors in the _____ _______.
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D2-receptors in the anterior pituitary
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clonidine hyperpolarizes to inhibit peripheral sympathetic outflow at the
__ receptors in the _____ _______. |
alpha 2-adrenoceptors in the medulla
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Effect of GABA enhanced by:
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ethanol, propofol, volatile anesthetic agents, BZ’s (increased frequency of channel opening) and barbiturates (increased duration of channel opening)
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GABAA-receptors =
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hyperpolarization = inhibition
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Valproate increases [GABA] by
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increasing glutamic acid dehydrogenase and inhibiting GABA transaminase
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Gabapentin releases
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GABA from its neurons
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Glycine released from Renshaw cells to
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inhibit alpha-motor neurons
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strychnine blocks
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glycine receptors in the spinal cord = no alpha-motor neuron inhibition = convulsions
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Beta1-adrenoceptor effects
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heart = increase heart rate, contractility & impulse conduction; decrease APD and ERP
adipocyte = lipolysis = increased plasma free fatty acids renal JG cells = increased renin release |
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Beta2-adrenoceptors
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lungs = (bronchial SM) = relaxation = bronchodilation = increased FEV1
vascular smooth muscle = relaxation = vasodilation of arteries and veins uterus = relaxation (inhibition of parturition) liver = glycogenolysis via protein kinase activation of phosphorylase a mast cell = decreased free intracellular calcium inhibits degranulation |
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D1-dopamine receptors effects
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vasodilation in the kidney, blocked by D1- D2-receptor blockers like haloperidol
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H2-histamine receptors actions
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relaxation of VSM (direct and through NO) causes vasodilation
increased gastric acid secretion from oxynitic cells |
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PGI2 (prostacyclin) and PGE receptors effects
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relaxation of vascular smooth muscle = vasodilation
decreased platelet aggregation |
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V2-AVP receptors (renal collecting duct) =
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AVP (ADH) increases water reabsorption
This cyclase inhibited by PGE’s, atrial natriuretic factor, lithium and demeclocycline Antidiuretic effect of AVP potentiated by chlopropramide and carbamazepine. |
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5-HT1-receptors effects
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relaxation of vascular smooth muscle causes sustained vasodilation
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hormones = ACTH, FSH, LH, glucagon, PTH activate (which intracellular messenger)
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adenyl cyclases
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phosphodiesterase inhibitors
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theophylline, aminophylline
papaverine dipyridamole amrinone and milrinone |
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DOC for tx of neonatal apnea
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theophylline, aminophylline = bronchodilation
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DOC for penile erection
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phosphodiesterase inhibitors like papaverine = relaxation of s.m. in the corpus cavernosa
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dipyridamole
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decreased platelet aggregation when used with aspirin
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amrinone and milrinone =
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increased cardiac dp/dt (tx of terminal CHF)
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Signal transduction via cyclic GMP (CGMP)
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THINK antianginal drugs!
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nitrate vasodilators (nitroglycerin) and Na nitroprusside are converted to NO which
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activates guanyl cyclase: CGMP relaxes arterial/venous VSM (a kinase dephosphorylates the MLC’s) and inhibits platelet aggregation
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Atrial natriuretic factor (ANF) also decreases BP by
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activation of guanyl cyclase and increases [CGMP]
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sildenafil causes erection by inhibiting
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the type V PDEase which degrades CGMP
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MOA of IP3 and DAG
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IP3 releases Ca++ from the SR; Ca++ binds to calmodulin which then activates enzymes (E’s) = smooth muscle contraction or secretion
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muscarinic receptors are found at
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sphincter muscle of iris, SM of bronchioles, bronchial glands, SM of GI tract and gall bladder, detrusor muscle of urinary bladder, pancreatic acini and alpha-islet cells (glucagon); salivary glands, lacrimal glands, nasopharyngeal glands
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alpha1-adrenoceptors are found at
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radial muscle of eye, vascular SM, trigone and internal sphincter of GU tract, SM of urethra/prostate, pilomotor muscles, salivary glands
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Ang II receptors are found in
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VSM
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TXA2 receptors are found in
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VSM
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V1-AVP receptors are found in
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Vascular smooth muscle
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H1-histamine receptors are found in
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vascular endothelial cells, SM of bronchioles and GI tract
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5-HT2-receptors are found in
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VSM
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PGE receptors are found in
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SM of uterus and GI tract
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Li+ inhibits (which intracellular messenger)
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the recycling of PIP2 and thus interrupts the IP3 signaling pathway
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Cardiac glycosides
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digoxin & digitoxin
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digoxin & digitoxin effect on ion transport
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Depolarization allows Ca++ to move into the cell via L-type (voltage-sensitive) Ca++ channels. Some of the Ca++ is pumped into the SR. Additional Ca++ is extruded by a Na+- Ca++ antiporter which uses the high outside/low inside Na+ gradient to move Ca++ out against its concentration gradient. This utside/inside Na+- gradient is maintained by the membrane Na+- K+ ATPase. Digoxin partially blocks the Na+- K+ ATPase; the outside/inside Na gradient is decreased; less Ca++ is extruded via Na+- Ca++ exchange; this excess Ca++ in the cell is stored in the SR; the next depolariaztion results in a greater release of Ca++ from the SR
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Gastric H+-K+ ATPase (proton pump) inhibited by:
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omeprazole
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Na+: K+:2Cl- symporter in ascending limb of Henle’s loop is blocked by
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furosemide and ethacrynic acid
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Na+: Cl- symporter in renal DT inhibited by
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thiazide diuretic drugs
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Na+ channels in principal cells of LDT/CD blocked by
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amiloride and triamterene
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H+ ion secretion in renal PT and DT decreased by
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acetazolamide because it inhibits CA
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H+ ion secretion from LDT/CD blocked by
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amiloride and triamterene
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thyroxine's effect on gene transcription
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increase beta-receptors & mitochondrial E’s for oxidative phosphorylation (ATP)
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aldosterone 's effect on gene transcription
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increase basolateral ATPase, Na+ channels and E’s for oxidative phosphorylation (ATP) in the LDT/CD; increased deposition of fibrillar collagen in the extracellular matrix of the heart
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glucocorticoids's effect on gene transcription
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- increased transcription of the genes for lipocortin (inhibits PLA2), the inhibitor of NFKappaB and enzymes (E's) for gluconeogenesis
- decrease transcription of genes for COX-2; IL-1 & IL-6 in monocytes & macrophages; gene for NFKappaB, and E’s for glycogen storage (except glycogen synthetase) |
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cyclosporine's effect on gene transcription
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decreased transcription of gene for IL-2 in helper T-cells
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androgens' effect on gene transcription
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increased erythropoesis and hepatic synthesis of C1-esterase inhibitor of complement
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estrogens' effect on gene transcription
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increased hepatic protein synthesis = transcortin (CBG), thyroxine-binding globulin (TBG), angiotensinogen (renin substrate), transferrin, fibrinogen and clotting factors 2, 7, 9 and 10.
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NSAID’s effect on gene transcription
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prevent the activation of nuclear factor kappa-B: this action prevents the increased expression of the genes which code for many inflammatory mediators.
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examples of glucocorticoids
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cortisone, hydrocortisone, prednisone, prednisolone,
beclomethasone, triamcinolone |
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effect of Plasma pseudocholinesterase deficiency
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the NMB caused by succinylcholine last hours instead of minutes.
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Barbiturates idiosyncratic drug reaction
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produce excitation and anxiety instead of sedation in older patients
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idiosyncratic drug reaction of The older antihistamines (e.g. diphenhydramine)
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cause excitation instead of sedation in very young children and older patients.
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idiosyncratic drug reaction of Aspirin and other NSAID's
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precipitate an anaphylactic-like reactions (a.k.a. aspirin
hypersensitivity) in patients with nasal polyps. Blockade of PG synthesis by the NSAID shunts all the arachidonic acid to leukotriene synthesis.... LT's cause rhinoconjunctivitis, angioedema and urticaria. |
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idiosyncratic drug reaction of primaquine, isoniazid, sulfonamides, nitrofurantoin or eating fava beans
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hemolytic anemia because of Glucose-6-phosphate dehydrogenase deficiency
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slow acetylators
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SHIP - sulfasalazine, hydralazine, isoniazid, and procainimide
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Malignant hyperthermia (hyperpyrexia)
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a gene defect prevents Ca++ from being sequestered correctly in the sarcoplasmic reticulum (SR) of skeletal muscle.
anesthesia with a volatile anesthetic agent (e.g., halothane) plus the administration of succinylcholine causes the massive release of Ca++ = masseter muscle spasm S/S = inc BP, HR, & muscle contraction w hyperthermia, lactic acidosis and cardiac dysrhythmias - tx w dantrolene sodium which prevents the release of Ca++ from the SR |
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Neuroleptic malignant syndrome
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- etiology NOT related to malignant hyperthermia
= produced by rapid blockade of central DA receptors with the typical antipsychotic drugs like haloperidol S/S = resembles severe Parkinson's dx w catatonia = EPS, stupor, hyperthermia, increase CPK, myoglobinuria, ARF -Tx w dantrolene sodium + bromocriptine (a D2-receptor agonist) |
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procainamide in slow acetylators
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SLE-like syndrome
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isoniazid in slow acetylators
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hepatic damage, peripheral neuropathy - tx neuropathy w pyridoxal phosphate (vitamin B6)
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sulfapyrazine aka sulfasalazine in slow acetylators
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hemolytic and aplastic
anemia, hepatic damage. |
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hydralazine in slow acetylators
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SLE-like syndrome
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