Karteikarten
Pharmacology IX(100 Flash Cards)
Karten in diesem Stapel (100)
- 1Hydrocodone + APAP (Acetaminophen)Vicodin
- 2Oxycodone + APAPPercocet
- 3Composition of Tylenol 1-4?300mg APAP +
8mg codeine (Tylenol 1)
15mg codeine (Tylenol 2)
30mg codeine (Tylenol 3)
60 mg codeine (Tylenol 4)
codeine dosage increases by 2 between each level - 4Therapeutic and SEs of morphineM iosis (constricted pupil) and Medulla affected
O ut of it
R espiratory depression
P neumonia
H ypotension
I nfrequency (holding in urine)
N ausea and vomiting
E uphoria and dysphoria - 5Nitrous oxide tank colorblue
- 6Oxygen tank colorgreen
- 7Nitrous oxideSensation before onset = tingling of limbs/fingers
SE = nausea
Long term exposure --> peripheral neuropathy - 8Why give 3-5min oxygen after shutting off nitrous oxide?to prevent diffusion hypoxia
- 9Pharmacokinetics vs. PharmacodynamicsPharmacokinetics: What the BODY does on the drug
Administration, absorption, distribution, metabolism, clearance
Pharmacodynamics: What the DRUG does on the body - 10Systemic drugs cross through what layers to get through to the bloodstream?Lumen - apical membrane - basal lateral membrane - interstitial fluid - endothelium of blood vessel
via passive diffusion (must be non-ionized), facilitated diffusion, active transport - 11Bioavailability of drugs is only 100% if administered via _________.IV
- 12pH considerationsWeak acids: pH of environment < drug pKa
Weak bases: pH of environment > pKa - 13First pass effectThe initial metabolism in the liver of a drug absorbed from the GI to the hepatic portal system
Reason why bioavailability is reduced - 14Volume of distribution (Vd)Vd = (amount of drug in the body) / (plasma drug concentration)
Distribution of drug across the 3 body water departments (60% body weight):
Plasma 4%
Interstitial 16%
Intracellular 40% - 15T/F: Binding to serum proteins lowers Vd and "traps" drugs in the blood as hydrophilic molecules.True
- 16Which tissue have lowest and highest water content?Fat - lowest
Brain/muscle - highest - 17Drug metabolism phasePhase 1 - functionalization (redox + hydrolysis) by Cytochrome P450
Phase 2 - conjugation (glucouronide, glutathione, glycine) by UDP-glucouronosyltransferase - 18Drug clearancePhase 1 --> urine
Phase 2 --> GI - 19First-order vs. Zero-order elimination kineticsFirst-order (more common) - constant FRACTION of drug is eliminated per time (%/hour)
Zero-order - constant AMOUNT of drug is eliminated per unit time (mg/hour); higher risk of drug accumulation - 20Induction vs. inhibition DDIsInduction - Drug #1 induces liver cytochrome enzymes --> INCREASED metabolism + REDUCED effect of Drug #2
Inhibition - Drug #1 competes or directly inhibits liver cytochrome enzymes --> DECREASED metabolism + INCREASED toxicity of Drug #2 - 21Almost all drug targets are ________.proteins
- 22Agonist vs. AntagonistAgonist: medication binds to the same site as an endogenous substance (e.g., neurotransmitter) to produce similar response
Antagonist: Medication binds to a receptor and thus, prevents the binding and action of an agonist - 23Competitive antagonist vs. non-competitive antagonistCompetitive - binds to the same active site as agonist
Non-competitive - binds to a different active site (allosteric site) on the enzyme receptor, but prevents agonist from binding - 24Inverse agonistinhibits the basal activity of a receptor in the absence of the normal agonist
binds to a special kind of receptor that is active at rest in order to inhibit its basal activity - 25Type I vs. Type II dose response curveType I:
dose vs. drug efficacy
Usually in sigmoid/log form
Type II:
dose vs. patient response
Usually 3 curves - 26Intrinsic activity (efficacy)Ability of a drug to activate a receptor and produce an effect
Full agonist has intrinsic activity = 1
Partial agonist = 0-1
Antagonist = 0 - 27Efficacy vs. Affinity vs. potencyEfficacy - effect of a drug as a function of binding
Affinity - attractiveness of a drug to its receptor
Lower dissociation constant (Kd) = higher affinity
Potency - power of a drug at a specific concentration, measured with EC50 - 28Competitive antagonist vs. non-competitive antagonist effects on Type I dose response curveCompetitive --> shifts curve right
Noncompetitive --> shifts curve down - 29Type II dose curveED50 - effective dose 50% of population
TD50 - toxic dose 50% of population
LD50 - toxic dose 50% of population - 30How is the therapeutic index calculated?Human studies = TD50/ED50
The larger the TI, the safer it is. - 31Additive vs Synergistic effectsAdditive: when the effect of 2 drugs together = each one individually
Synergistic: when the effect of 2 drugs together is MORE than each one individually - 32Parasympathetic (PSNS) and sympathetic (SNS) nerves extend from which part of the spinal cord?Cranial + sacral = PSNS
Thoracic + lumbar = SNS - 33PSNS bodily effects-pupil constriction
-stimulated saliva
-decreased heart rate
-airway constriction
-stimulated digestion
-bladder constriction - 34SNS bodily effects-pupil dilation
-dry mouth
-increased heart rate
-airway relaxation
-slowed digestion
-bladder relaxation - 35Ionotropic vs Metabotropic receptors in the ANSIonotropic - ion channel; faster
Metabotropic - G-protein coupled receptor; slower - 362 kinds of cholinergic receptorsMuscarinic (metabotropic) - ACh + muscarine
=postganglionic PSNS
Nicotinic (ionotropic) - ACh + nicotine
=ganglion receptors - 37Adrenergic receptorsbinds to epi/NE
metabotropic
postganglionic sympathetic - 38SNS and PSNS nerve lengthSNS - short pre-ganglion, long post
OR short-pre to adrenal medulla, then direct secretion into blood stream
PSNS - long pre-ganglion, short post - 39T/F: All ganglion and adrenal medulla receptors are nicotinic (ionotropic) receptors, for both SNS and PSNS.True
- 40ACh synthesisacetyl CoA + choline, catalyzed by choline acetyltransferase
**reversed by acetylcholinesterase - 41Muscarinic receptors subtypesM1, M4, M5 - CNS
M2 --> bradycardia
M3 --> smooth muscle relaxation - 42What patients should not be given M agonists?Those with:
-peptic ulcers
-asthma/COPD
-CHF
You don't want to increase gastric acid production and bronchoconstriction or decrease cardiac output - 43Synthesis of epi/NETyrosine --> L-DOPA --> dopamine --> NE --> epi
- 44Catecholamines vs monaminesCatecholamine = dopamine, NE, epi
Monamines = dopamine, NE, epi, serotonin, histamine - 45Adrenergic receptor subtypesalpha 1, alpha 2 - vasoconstriction, urinary retention, pupil dilation (mydriasis)
beta 1 - TACHYCARDIA, renin release from kidneys
beta 2 - bronchodilation, vasodilation, stop peristalsis - 46sympathomimeticagent that mimics the effects of the sympathetic nervous system, but either releasing NE stores or causing re-uptake
examples: cocaine, TCAs, MAOIs, tyramine (wine, cheese, chocolate) - 47T/F: When alpha 2 receptors are agonized, it will block SNS signal.True, because these receptors are in CNS.
- 48Epinephrine reversalwhen epinephrine is administered in the presence of an alpha blocker (Prazosin or Chlorpromaxine), will cause decrease in BP rather than increase because beta-mediated vasodilation predominates
- 49Vasovagal reflexNE can activate baroreceptors --> stimulate vagal reflex --> reduce HR, which is an opposite response to what NE usually does
- 50_________ blocks the vasovagal reflex.Atropine
- 51What contributes to BP?BP = CO x PR
OR
BP = SV x HR x PR
because CO = SV x HR - 52Preload vs. afterloadPreload - pressure in ventricles before heart contracts
Afterload - pressure in arteries against which the ventricles must pump - 53Diuretic antihypertensive MOAdecreases renal reabsorption of Na+ --> net fluid loss --> BP reduction
- 54Furosemide, HCTZ, SpironolactoneAntihypertensive diuretics
Furosemide - loop
HCTZ - Thiazide (distal tubule); HYPOKalemia risk
Spironolactone - K+ sparing (collecting duct; HYPERKalemia risk - 55Antihypertensive vasodilators and CCB MOAVasodilator - opens K+ channels --> hyperpolarizes inside --> vasodilation
- ex: Hydralazine
CCBs - blocks Ca2+ influx --> hyperpolarizes inside --> vasodilation
- ex: Verapamil, Dilitiazem, Amlodipine, Nifedipine - 56SE of CCBsgingival hyperplasia
- 57Angiotensin IIincreases blood pressure by stimulating kidneys to reabsorb more water and by releasing aldosterone
- 58Renin-Angiotensin-Aldosterone system-decreased blood pressure causes the juxtaglomerular cells of kidneys to secrete renin which converts angiotensinogen (inactive) to angiotensin I (active) which is then converted into angiotensin II by angiotensin-converting enzyme (ACE)
-Angiotensin II stimulates the adrenal cortex to secrete aldosterone
- leads to absorption of Na and increased blood pressure
-once blood pressure is restored, there is a decreased drive to stimulate renin release - 59Antihypertensive ACE inhibitors (-prils)blocks ACE, which converts angiotensin I into angiotensin II (vasoconstrictor)
- 60Nitroglycerin, propranolol, CCBs belong to what family of meds?Antianginals (insufficient O2 to cardiac muscle)
-NTG - vasodilates smooth muscle in coronary arteries
-Propranolol - reduces O2 demand by relaxing heart
- CCBs - reduces O2 demand by reducing peripheral resistance via vasodilation - 61Heart attack emergency responseMONA
Morphine, O2, NTG, Aspirin - 62Anti-CHF drugs should be given when......heart fails to pump enough blood
Cardiac glycosides + ACE inhibitors - 63Cardiac Glycosides (Digoxin) MOADirect inhibition of Na+/K+ ATPase --> increase Ca2+ influx --> positive inotropy in cardiac muscle cells.
Stimulates vagus nerve--> decrease HR. - 644 types of Anti-arrhythmic Drugs:Type 1 - Na+ channel blockers for cardiac muscle
1A - lengthens refractory period to slow HR
1B (Lido)- shortens refractory period to speed up HR
Type 2 - beta blockers
Type 3 - K+ channel blockers
Type 4 - CCBs - 65Dopamine, serotonin, GABA receptor effectsDopamine & serotonin - excite
GABA - depress - 66Antipsychotics1st gen (Haloperidol, Phenothiazines) - D2 blocker
SE: tardive dyskinesia
2nd gen (Clozapine) - D and 5HT blocker
Not many SEs - 67Antidepressant drugsSSRIs - Fluoxetine, Citalopram, Trazodone
SNRIs/TCAs
MAOIs
SEs: anticholinergic - 68Choice drug for bipolar disorder?Lithium
- 69Ideal drug for oral sedation in dental setting?Benzos
- 70Benzos & barbiturates (sedatives) MOAincreases GABA binding and Cl- ion influx to slow down CNS
- 71Propylene glycol can induce ___________ in large veins.thrombophlebitis
- 72Barbiturate contraindicationsintermittent porphyria, will aggravate the disease
- 73Barb overdose -->respiratory depression
- 74T/F: Sedatives provide no pain relief.True
- 75Stages of General AnesthesiaI - analgesia
II - delirium
III - surgical anesthesia
IV - medullary paralysis - 76The more soluble the general anesthetic agent in blood, the (more/less) you need to reach critical tension in the brain.More
- 77Halothane's (GA) SEhepatotoxicity
- 78Cause of Parkinson's?dopamine deficiency in brain
- 79T/F: Dopamine cannot cross the BBB.True, but its precursor (L-DOPA) can
- 80Carbidopa is administered w/ L-DOPA becauseit blocks DOPA decarboxylase to maintain L-DOPA's structure, so that it can cross the BBB before converting to dopamine
- 81Neostigmineinhibits ACH-ase activity
- 82Pharmacodynamicswhat the drug does to the body
-affinity to R
-selectivity - 83Affinitytightness of binding
attractiveness of a drug for its R
measured w/ Kd - 84Kddisassociation constant (↓Kd = ↑affinity)
measures drug affinity to R - 85Selectivityability to elicit an effect at a R
- 86Pharmacokineticswhat the body does to the drug (absorption, distribution, metabolism, excretion)
- 87Pharmacovigilancethe safety of the drug - aka toxicity
- 88Pharmacogenomicsvariations in response due to genetic differences
- 89List the 5 main R typesIon channels = fastest
Transmembrane GPCR
Transmembrane enzymatic cytosolic domain R: drug binds --> dimerization
-ex = tyrosine kinase
Intracellular R = slowest, regulates transcription
-ex = steroids
Adhesion R - 90Type 1 graded dose-response curveeffect of various [drug] on an individual
determined w/ efficacy (EC50)
determines agonist + antagonist activity - 91Potencyresponse of a drug over a range of concentrations
most potent drug = effect seen at lowest dose - 92Type 2 quantal dose response curve#subjects responding to a drug
Effective dose (ED50)
Toxic dose (TD50)
lethal dose (LD50)
Therapeutic window - 93Therapeutic Window[drug] electing an effect + no adverse effect seen
Measured w/ Therapeutic Index
B/w Minimum Toxic Concentration + MEC - 94Therapeutic indexmargin of safety of drug
TI = TD50 / ED50
↑Therapeutic index = ↑safety - 95pH pKA Henderson-Hasselbach equationpH: negative log of [H+]
pKa : pH where protonated + unprotonated species are in [equal]
Henderson-Hasselbach equation: pH = PkA + Log [conjugate base/acid] - 96Volume of Distribution (Vd)amount of drug in the body to the [plasma]
↑ Vd = ↓[drug] in plasma = mostly distributed to tissue
↓Vd = drug still in the blood - 97Metabolism -phase 1 rxns -phase 2 rxnsphase 1 = oxidation, reduction, hydrolysis
phase 2 = synthesis
-conjugation (more water soluble) = glucuronidation + sulfonation
-acetylation/methylation (less water soluble) - 98Catecholamine SynthesisTyrosine --> (tyrosine hydroxylase) --> DOPA --> (Aromatic L-Amino Acid Decarboxylase) --> Dopamine --> NE --> E
- 99Drug Clearanceplasma V from which all solute is removed per unit time
- 100Flow Dependent Eliminationcleared readily by the organ of elimination
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- Praxis Flashcards: Pharmacology Karteikarten am Pharmacology IX(100 Flash Cards) , erstellt von ACAPUN INSTITUTE am 15/07/2021.
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