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100 Cards in this Set

  • Front
  • Back
nicotinic type I receptors
autonomic ganglia
N1 agonists
ACh and nicotine (enhance Na conductance)
N1 antagonists (ganglionic blocking drugs)
trimethaphan, hexamethonium
nicotinic type II receptors
skeletal muscle motor endplate
N2 agonists
ACh, nicotine, succinylcholine = enhance Na conductance
N2 antagonists
d-tubocurarine (d-tc), pancuronium, Mg++ = the -curiums and -roniums
sodium channels of cardiac fast fibers
atria, ventricles
cardiac class IA drugs
procainamide, disopyramide, quinidine
cardiac class IB drugs
lidocaine - only affects ventricles
sodium channels in CNS
the antiepileptic drugs phenytoin, carbamazepine, & valproate inhibit the spread of electrical signals by prolonging the state of inactivation of the sodium channel
Na+ channels in sensory nerve fibers
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)
Sodium channels coupled to 5-HT3 receptors in CTZ
= induce nausea/emesis, blocked by ondansetron
Ca++ channel blockers
nifedipine, diltiazem & verapamil = block L-type channels in heart and vascular smooth muscle (VSM)
Ca++ channels in SM of GI tract blocked by
Al, Fe, diltiazem and verapamil
Ca++ channels in SM of uterus blocked by
T-type Ca++ channels in CNS blocked by
Felbamate prevents seizures by
blocking NMDA receptors
Glutamate stimulation of NMDA receptors coupled to
Ca++ channels
Ketamine and phencyclidine (“angel dust”) block
NMDA receptors and prevent the excitatory effects of glutamate to cause “dissociative” anesthesia and hallucinations.
DOC for tx of neuroleptic malignant syndrome and anesthesia-induced malignant hyperthermia (hyperpyrexia)
dantrolene, Internal Ca++ channels of SR blocked which prevents the release of “trigger” Ca++
Drugs acting through potassium channels
hyperpolarize and inhibit
Muscarinic receptors at the SA node
coupled to a K-channel via a G-protein
M agonists at SA node
ACh, pilocarpine
M antagonists at SA node
atropine et al., pancuronium, quinidine, TCA’s, older antihistamines like diphenhydramine
buspirone is a partial agonist at
5-HT1A-receptors in the CNS, for tx of anxiety
hydralazine, minoxidil, diazoxide
arterial vasodilators
arterial vasodilators activate
ATP-modulated K-channels = hyperpolarization = relaxation = vasodilation
Fast cardiac fibers
antiarrhythmic drugs
procainamide, disopyramide & quinidine as antidysrhythmics
prolong repolarization (APD & ERP increased); only quinidine actually widens the QRS and increases the Q-T interval
lidocaine as antidysrhythmic
accelerates repolarization (APD decreased)
Amiodarone and sotalol as antidysrhythmics
delay ventricular repolarization via block of K+ channels; APD, ERP and Q-T interval increase
Terfenadine blocks
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
Cisapride cardiac s/e
torsades by partially inhibiting the K-repolarization current.
tolbutamide, chlorpropamide, glypizide MOA at K channel
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
Diazoxide opens
ATP-regulated K+-channels to prevent depolarization and thus inhibit insulin secretion
Baclofen enhances GABA-mediated K+ conductance at
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
Opiates (morphine) hyperpolarize neurons via
mu receptors
dopamine, bromocriptine and pergolide hyperpolarize cells to prevent prolactin release at the __ receptors in the _____ _______.
D2-receptors in the anterior pituitary
clonidine hyperpolarizes to inhibit peripheral sympathetic outflow at the
__ receptors in the _____ _______.
alpha 2-adrenoceptors in the medulla
Effect of GABA enhanced by:
ethanol, propofol, volatile anesthetic agents, BZ’s (increased frequency of channel opening) and barbiturates (increased duration of channel opening)
GABAA-receptors =
hyperpolarization = inhibition
Valproate increases [GABA] by
increasing glutamic acid dehydrogenase and inhibiting GABA transaminase
Gabapentin releases
GABA from its neurons
Glycine released from Renshaw cells to
inhibit alpha-motor neurons
strychnine blocks
glycine receptors in the spinal cord = no alpha-motor neuron inhibition = convulsions
Beta1-adrenoceptor effects
heart = increase heart rate, contractility & impulse conduction; decrease APD and ERP
adipocyte = lipolysis = increased plasma free fatty acids
renal JG cells = increased renin release
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
D1-dopamine receptors effects
vasodilation in the kidney, blocked by D1- D2-receptor blockers like haloperidol
H2-histamine receptors actions
relaxation of VSM (direct and through NO) causes vasodilation
increased gastric acid secretion from oxynitic cells
PGI2 (prostacyclin) and PGE receptors effects
relaxation of vascular smooth muscle = vasodilation
decreased platelet aggregation
V2-AVP receptors (renal collecting duct) =
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.
5-HT1-receptors effects
relaxation of vascular smooth muscle causes sustained vasodilation
hormones = ACTH, FSH, LH, glucagon, PTH activate (which intracellular messenger)
adenyl cyclases
phosphodiesterase inhibitors
theophylline, aminophylline
amrinone and milrinone
DOC for tx of neonatal apnea
theophylline, aminophylline = bronchodilation
DOC for penile erection
phosphodiesterase inhibitors like papaverine = relaxation of s.m. in the corpus cavernosa
decreased platelet aggregation when used with aspirin
amrinone and milrinone =
increased cardiac dp/dt (tx of terminal CHF)
Signal transduction via cyclic GMP (CGMP)
THINK antianginal drugs!
nitrate vasodilators (nitroglycerin) and Na nitroprusside are converted to NO which
activates guanyl cyclase: CGMP relaxes arterial/venous VSM (a kinase dephosphorylates the MLC’s) and inhibits platelet aggregation
Atrial natriuretic factor (ANF) also decreases BP by
activation of guanyl cyclase and increases [CGMP]
sildenafil causes erection by inhibiting
the type V PDEase which degrades CGMP
MOA of IP3 and DAG
IP3 releases Ca++ from the SR; Ca++ binds to calmodulin which then activates enzymes (E’s) = smooth muscle contraction or secretion
muscarinic receptors are found at
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
alpha1-adrenoceptors are found at
radial muscle of eye, vascular SM, trigone and internal sphincter of GU tract, SM of urethra/prostate, pilomotor muscles, salivary glands
Ang II receptors are found in
TXA2 receptors are found in
V1-AVP receptors are found in
Vascular smooth muscle
H1-histamine receptors are found in
vascular endothelial cells, SM of bronchioles and GI tract
5-HT2-receptors are found in
PGE receptors are found in
SM of uterus and GI tract
Li+ inhibits (which intracellular messenger)
the recycling of PIP2 and thus interrupts the IP3 signaling pathway
Cardiac glycosides
digoxin & digitoxin
digoxin & digitoxin effect on ion transport
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
Gastric H+-K+ ATPase (proton pump) inhibited by:
Na+: K+:2Cl- symporter in ascending limb of Henle’s loop is blocked by
furosemide and ethacrynic acid
Na+: Cl- symporter in renal DT inhibited by
thiazide diuretic drugs
Na+ channels in principal cells of LDT/CD blocked by
amiloride and triamterene
H+ ion secretion in renal PT and DT decreased by
acetazolamide because it inhibits CA
H+ ion secretion from LDT/CD blocked by
amiloride and triamterene
thyroxine's effect on gene transcription
increase beta-receptors & mitochondrial E’s for oxidative phosphorylation (ATP)
aldosterone 's effect on gene transcription
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
glucocorticoids's effect on gene transcription
- 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)
cyclosporine's effect on gene transcription
decreased transcription of gene for IL-2 in helper T-cells
androgens' effect on gene transcription
increased erythropoesis and hepatic synthesis of C1-esterase inhibitor of complement
estrogens' effect on gene transcription
increased hepatic protein synthesis = transcortin (CBG), thyroxine-binding globulin (TBG), angiotensinogen (renin substrate), transferrin, fibrinogen and clotting factors 2, 7, 9 and 10.
NSAID’s effect on gene transcription
prevent the activation of nuclear factor kappa-B: this action prevents the increased expression of the genes which code for many inflammatory mediators.
examples of glucocorticoids
cortisone, hydrocortisone, prednisone, prednisolone,
beclomethasone, triamcinolone
effect of Plasma pseudocholinesterase deficiency
the NMB caused by succinylcholine last hours instead of minutes.
Barbiturates idiosyncratic drug reaction
produce excitation and anxiety instead of sedation in older patients
idiosyncratic drug reaction of The older antihistamines (e.g. diphenhydramine)
cause excitation instead of sedation in very young children and older patients.
idiosyncratic drug reaction of Aspirin and other NSAID's
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.
idiosyncratic drug reaction of primaquine, isoniazid, sulfonamides, nitrofurantoin or eating fava beans
hemolytic anemia because of Glucose-6-phosphate dehydrogenase deficiency
slow acetylators
SHIP - sulfasalazine, hydralazine, isoniazid, and procainimide
Malignant hyperthermia (hyperpyrexia)
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
Neuroleptic malignant syndrome
- 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)
procainamide in slow acetylators
SLE-like syndrome
isoniazid in slow acetylators
hepatic damage, peripheral neuropathy - tx neuropathy w pyridoxal phosphate (vitamin B6)
sulfapyrazine aka sulfasalazine in slow acetylators
hemolytic and aplastic
anemia, hepatic damage.
hydralazine in slow acetylators
SLE-like syndrome