Pharm (Q/A) Flashcards
Km
Measures the affinity of an enzyme for its substrate ( dec Km = inc affinity)
Vmax
Maximal velocity of an enzymatic reaction (proportional to enzyme concentration)
Competitive inhibition
Does not change Vmax (Lineweaver-Burke lines cross each other “competitively”)
Noncompetitive inhibition
Decreases Vmax (Lineweaver-Burke lines do not cross each other)
Volume of Distribution (Vd)
Drug in body / plasma drug concentration (low Vd (4-8L: in blood), medium Vd (in extracellular space), High Vd (> body weight: in tissues))
Clearance (CL)
Rate of elimination of drug / plasma drug concentration (OR Vd x Kc, where Kc is the elimination constant)
Half life (t1/2)
T1/2 = (0.7 x Vd) / CL
Concentration of a substance after X half lives (1,2,3,4)
1:50%, 2:75%, 3:87.5%, 4:93.75%
Loading dose
= Cp x (Vd / F); (Cp: target plasma conc., F: bioavailability, 1 if by IV)
Maintenance dose
= Cp x (CL / F); (Cp: target plasma conc., F: bioavailability, 1 if by IV; a renal patient would have decreased clearance, so they would need a decreased maintenance dose)
Common drugs that follow zero-order elimination
PEA (phenytoin, ethanol, aspirin)
Treating a weak acid overdose
Will get trapped in a basic environment, treat with bicarbonate
Treating a weak base overdose
Will get trapped in an acidic environment, treat with ammonium chloride
Reactions involved in phase I drug metabolism
(Cytochrome P450) 1. reduction, 2. oxidation, 3. hydrolysis (drugs became slightly polarized, may still be active)
Reactions involved in phase II drug metabolism
(Conjugation) 1. acetylation, 2. glucuronidation, 3. sulfonation (drugs become very polarized, are inactivated)
Effect of competitive antagonists on efficacy curves versus noncompetitive antagonists
Competitive antagonist shifts curve right, requires bigger dose of drug for effect (inc EC50); noncompetitive antagonist shortens curve, cannot reach same level of effect (dec efficacy)
Effect of partial agonists versus full agnoists on efficacy curves
Partial agonists will have a lower maximal efficacy than full agonists (however potency is independent, they may still be more potent or less potent than a full agonist)
Therapeutic index (TI)
TILE: TI = LD50 / ED50 (median toxic dose / median effective dose; Safer drugs have HIGHER TI values)
Nm receptors
Receptor location: NMJ; Function: skeletal muscle contraction; Mechanism: ion channel (Na influx)
Nn receptors
Receptor location: Ganglia; Function: stimulates sympathetics and parasympathetics; Mechanism: ion channel (Na influx);
M1 receptors
Receptor location: Nerve endings; Function: Gastric acid secretion; Mechanism: Gq protein;
M2 receptors
Receptor location: Heart; Function: Inhibitory, reduces heart rate; Mechanism: Gi protein;
M3 receptors
Receptor location: Smooth muscle, endothelium, glands; Function: bronchoconstriction, pupil constriction, accommodation, increases secretions; Mechanism: Gq proteins;
alpha1
Receptor location: Arterioles, glands; Function: vasoconstriction (smooth muscle), pupillary dilation, /\ intestine and bladder sphincter contraction; Mechanism: Gq protein;
alpha2
Receptor location: presynaptic nerve endings; Function: inhibitory, feedback inhibition of NT release, \/ insulin; Mechanism: Gi protein;
Beta1
Receptor location: heart, kidney; Function: heart stimulation, renin release; Mechanism: Gs protein;
Beta2
Receptor location: lungs, skeletal muscle; Function: Vasodilation, bronchiole dilation, ciliary process (makes aqueous humour), \/ uterine tone, /\ insulin, /\ lipolysis; Mechanism: Gs protein;
D1
Function: renal vasodilation; Mechanism: Gs protein;
D2
Function: Causes NT release in brain; Mechanism: Gi protein;
H1
Function: /\ mucus production, bronchiole constriction, pain, itching; Mechanism: Gq protein;
H2
Function: gastric acid secretion; Mechanism: Gs protein;
V1
Function: vasoconstriction (smooth muscle); Mechanism: Gq protein;
V2
Function: /\ H20 permeability, reabsorption in collecting tubules in kidney; Mechanism: Gs protein;
$V2 is found in the 2 kidneys$
Mnemonic for gprotein receptors used for D, H, and V receptors
Sick of sex (SIQ, SQS) D1,D2, H1, H2, V1, V2
Function of Gq protein receptors
Gq protein activates PLC, IP3 + DAG, inc Ca++ (IP3) and activate PKC (DAG)
Function of Gi protein receptors
Gi protein activates K+ channels, inhibition of adenylate cyclase, reduction of cAMP
Function of Gs protein receptors
Gs protein activates adenylate cyclase, increases cAMP
Symptoms of cholinesterase inhibitor poisoning (I.e. organophosphates like PARATHION) + Tx
DUMBBELSS (Diarrhea, urination, miosis, bronchospasm, bradycardia, excitation (of skeletal muscle), lacrimation, sweating, salivation); treatment: atropine (reverses symptoms) + pralidoxime (regenerates cholinesterase)
$Ooze from every oriface$
Symptoms of muscarinic antagonist overdose
Hot as a hare (inc temp), Dry as a bone (dec secretions), Red as a beet (flushed skin), Blind as a bat (cycloplegia), Mad as a hatter
Direct cholinergic agonist drugs
Bethanechol, carbachol, pilocarpine, methacholine
Direct cholinergic agonist; activates bowel and bladder post operation
Bethanechol
Direct cholinergic agonist; used in glaucoma (causes pupillary contraction and reduces ICP)
Carbachol
Direct cholinergic agonist; potent stimulator of sweat and tears
Pilocarpine (PILE on the sweat and tears)
Direct cholinergic agonist; challenge test for asthma diagnosis
Methacholine
Indirect cholinergic agonist drugs (anticholinesterases)
(-stigmine, Ed PHYSted the MAiLman and it ECHOed) Neostigmine, pyridostigmine, physostigmine, edrophonium, echothiophate, malathion
Indirect cholinergic agonist; used in post operative reversal of NMJ block; does NOT penetrate the CNS
Neostigmine (NEO CNS)
Indirect cholinergic agonist; used for myasthenia gravis (due to it’s long action); does NOT penetrate the CNS
Pyridostigmine
Indirect cholinergic agonist; Used for glaucoma and atropine overdose (does cross CNS)
Physostigmine (PHYS is for EYES)
Indirect cholinergic agonist; Used to diagnose myasthenia gravis (extremely short action)
Edrophonium
Indirect cholinergic agonist; used for glaucoma
Echothiophate
Muscarinic antagonist drugs
Atropine, homatropine, tropicamide, benztropine, scopolamine, ipratropium, methscopolamine, oxybutynin, glycopyrrolate, pirenzepine, propantheline
Muscarinic antagonist drug(s); produces mydriasis and cycloplegia (eye)
Atropine (or homatropine, tropicamide)
Muscarinic antagonist drug; treatment for parkinson’s (CNS)
Benztropine (PARK my BENZ)
Muscarinic antagonist drug; treatment of motion sickness (CNS)
Scopolamine
Muscarinic antagonist drug; treats asthma and COPD (respiratory)
Ipratropium
Muscarinic antagonist drug(s); Reduces bladder urgency in cystitis and bladder spasms (GI)
Methscopolamine (or oxybutynin, glycopyrrolate)
Muscarinic antagonist drug(s); treatment of peptic ulcers (GI)
Pirenzepine (or propantheline)
Muscarinic antagonist drug; Used to block DUMBBELSS; Toxicity: hot as a hare, dry as a bone, red as a beet, blind as a bat, mad as a hatter
Atropine
Nicotinic antagonist; ganglion blocker, used in experimental models to prevent vaga reflex responses to BP changes
Hexamethonium
Low doses of epinephrine are selective for what receptor?
B1
Drug used for anaphylaxis, open angle glaucoma, asthma and hypotension. Binds a1, a2, B1 and B2 receptors.
Epinephrine
Drug used for hypotension. Binds a1, a2 > B1
Norepinephrine
Drug that binds B1 = B2. Used rarely for AV block
Isoproterenol
Drug used for shock (by increased renal perfusion), and heart failure. Binds D1 = D2 > B > a.
Dopamine
Drug used for shock, heart failure, and cardiac stress test. Bind B1 > B2.
Dobutamine
What is the difference in inotropy and chronotropy between dopamine and dobutamine.
Dopamine is inotropic and chronotropic, Dobutamine is inotropic but not chronotropic.