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Flashcards by ACAPUN INSTITUTE, updated more than 1 year ago
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Created by ACAPUN INSTITUTE
over 3 years ago
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| Question | Answer |
| Hydrocodone + APAP (Acetaminophen) | Vicodin |
| Oxycodone + APAP | Percocet |
| Composition 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 |
| Therapeutic and SEs of morphine | M 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 |
| Nitrous oxide tank color | blue |
| Oxygen tank color | green |
| Nitrous oxide | Sensation before onset = tingling of limbs/fingers SE = nausea Long term exposure --> peripheral neuropathy |
| Why give 3-5min oxygen after shutting off nitrous oxide? | to prevent diffusion hypoxia |
| Pharmacokinetics vs. Pharmacodynamics | Pharmacokinetics: What the BODY does on the drug Administration, absorption, distribution, metabolism, clearance Pharmacodynamics: What the DRUG does on the body |
| Systemic 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 |
| Bioavailability of drugs is only 100% if administered via _________. | IV |
| pH considerations | Weak acids: pH of environment < drug pKa Weak bases: pH of environment > pKa |
| First pass effect | The initial metabolism in the liver of a drug absorbed from the GI to the hepatic portal system Reason why bioavailability is reduced |
| Volume 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% |
| T/F: Binding to serum proteins lowers Vd and "traps" drugs in the blood as hydrophilic molecules. | True |
| Which tissue have lowest and highest water content? | Fat - lowest Brain/muscle - highest |
| Drug metabolism phase | Phase 1 - functionalization (redox + hydrolysis) by Cytochrome P450 Phase 2 - conjugation (glucouronide, glutathione, glycine) by UDP-glucouronosyltransferase |
| Drug clearance | Phase 1 --> urine Phase 2 --> GI |
| First-order vs. Zero-order elimination kinetics | First-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 |
| Induction vs. inhibition DDIs | Induction - 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 |
| Almost all drug targets are ________. | proteins |
| Agonist vs. Antagonist | Agonist: 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 |
| Competitive antagonist vs. non-competitive antagonist | Competitive - 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 |
| Inverse agonist | inhibits 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 |
| Type I vs. Type II dose response curve | Type I: dose vs. drug efficacy Usually in sigmoid/log form Type II: dose vs. patient response Usually 3 curves |
| Intrinsic 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 |
| Efficacy vs. Affinity vs. potency | Efficacy - 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 |
| Competitive antagonist vs. non-competitive antagonist effects on Type I dose response curve | Competitive --> shifts curve right Noncompetitive --> shifts curve down |
| Type II dose curve | ED50 - effective dose 50% of population TD50 - toxic dose 50% of population LD50 - toxic dose 50% of population |
| How is the therapeutic index calculated? | Human studies = TD50/ED50 The larger the TI, the safer it is. |
| Additive vs Synergistic effects | Additive: when the effect of 2 drugs together = each one individually Synergistic: when the effect of 2 drugs together is MORE than each one individually |
| Parasympathetic (PSNS) and sympathetic (SNS) nerves extend from which part of the spinal cord? | Cranial + sacral = PSNS Thoracic + lumbar = SNS |
| PSNS bodily effects | -pupil constriction -stimulated saliva -decreased heart rate -airway constriction -stimulated digestion -bladder constriction |
| SNS bodily effects | -pupil dilation -dry mouth -increased heart rate -airway relaxation -slowed digestion -bladder relaxation |
| Ionotropic vs Metabotropic receptors in the ANS | Ionotropic - ion channel; faster Metabotropic - G-protein coupled receptor; slower |
| 2 kinds of cholinergic receptors | Muscarinic (metabotropic) - ACh + muscarine =postganglionic PSNS Nicotinic (ionotropic) - ACh + nicotine =ganglion receptors |
| Adrenergic receptors | binds to epi/NE metabotropic postganglionic sympathetic |
| SNS and PSNS nerve length | SNS - short pre-ganglion, long post OR short-pre to adrenal medulla, then direct secretion into blood stream PSNS - long pre-ganglion, short post |
| T/F: All ganglion and adrenal medulla receptors are nicotinic (ionotropic) receptors, for both SNS and PSNS. | True |
| ACh synthesis | acetyl CoA + choline, catalyzed by choline acetyltransferase **reversed by acetylcholinesterase |
| Muscarinic receptors subtypes | M1, M4, M5 - CNS M2 --> bradycardia M3 --> smooth muscle relaxation |
| What 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 |
| Synthesis of epi/NE | Tyrosine --> L-DOPA --> dopamine --> NE --> epi |
| Catecholamines vs monamines | Catecholamine = dopamine, NE, epi Monamines = dopamine, NE, epi, serotonin, histamine |
| Adrenergic receptor subtypes | alpha 1, alpha 2 - vasoconstriction, urinary retention, pupil dilation (mydriasis) beta 1 - TACHYCARDIA, renin release from kidneys beta 2 - bronchodilation, vasodilation, stop peristalsis |
| sympathomimetic | agent 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) |
| T/F: When alpha 2 receptors are agonized, it will block SNS signal. | True, because these receptors are in CNS. |
| Epinephrine reversal | when 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 |
| Vasovagal reflex | NE can activate baroreceptors --> stimulate vagal reflex --> reduce HR, which is an opposite response to what NE usually does |
| _________ blocks the vasovagal reflex. | Atropine |
| What contributes to BP? | BP = CO x PR OR BP = SV x HR x PR because CO = SV x HR |
| Preload vs. afterload | Preload - pressure in ventricles before heart contracts Afterload - pressure in arteries against which the ventricles must pump |
| Diuretic antihypertensive MOA | decreases renal reabsorption of Na+ --> net fluid loss --> BP reduction |
| Furosemide, HCTZ, Spironolactone | Antihypertensive diuretics Furosemide - loop HCTZ - Thiazide (distal tubule); HYPOKalemia risk Spironolactone - K+ sparing (collecting duct; HYPERKalemia risk |
| Antihypertensive vasodilators and CCB MOA | Vasodilator - opens K+ channels --> hyperpolarizes inside --> vasodilation - ex: Hydralazine CCBs - blocks Ca2+ influx --> hyperpolarizes inside --> vasodilation - ex: Verapamil, Dilitiazem, Amlodipine, Nifedipine |
| SE of CCBs | gingival hyperplasia |
| Angiotensin II | increases blood pressure by stimulating kidneys to reabsorb more water and by releasing aldosterone |
| Renin-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 |
| Antihypertensive ACE inhibitors (-prils) | blocks ACE, which converts angiotensin I into angiotensin II (vasoconstrictor) |
| Nitroglycerin, 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 |
| Heart attack emergency response | MONA Morphine, O2, NTG, Aspirin |
| Anti-CHF drugs should be given when...... | heart fails to pump enough blood Cardiac glycosides + ACE inhibitors |
| Cardiac Glycosides (Digoxin) MOA | Direct inhibition of Na+/K+ ATPase --> increase Ca2+ influx --> positive inotropy in cardiac muscle cells. Stimulates vagus nerve--> decrease HR. |
| 4 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 |
| Dopamine, serotonin, GABA receptor effects | Dopamine & serotonin - excite GABA - depress |
| Antipsychotics | 1st gen (Haloperidol, Phenothiazines) - D2 blocker SE: tardive dyskinesia 2nd gen (Clozapine) - D and 5HT blocker Not many SEs |
| Antidepressant drugs | SSRIs - Fluoxetine, Citalopram, Trazodone SNRIs/TCAs MAOIs SEs: anticholinergic |
| Choice drug for bipolar disorder? | Lithium |
| Ideal drug for oral sedation in dental setting? | Benzos |
| Benzos & barbiturates (sedatives) MOA | increases GABA binding and Cl- ion influx to slow down CNS |
| Propylene glycol can induce ___________ in large veins. | thrombophlebitis |
| Barbiturate contraindications | intermittent porphyria, will aggravate the disease |
| Barb overdose -- | >respiratory depression |
| T/F: Sedatives provide no pain relief. | True |
| Stages of General Anesthesia | I - analgesia II - delirium III - surgical anesthesia IV - medullary paralysis |
| The more soluble the general anesthetic agent in blood, the (more/less) you need to reach critical tension in the brain. | More |
| Halothane's (GA) SE | hepatotoxicity |
| Cause of Parkinson's? | dopamine deficiency in brain |
| T/F: Dopamine cannot cross the BBB. | True, but its precursor (L-DOPA) can |
| Carbidopa is administered w/ L-DOPA because | it blocks DOPA decarboxylase to maintain L-DOPA's structure, so that it can cross the BBB before converting to dopamine |
| Neostigmine | inhibits ACH-ase activity |
| Pharmacodynamics | what the drug does to the body -affinity to R -selectivity |
| Affinity | tightness of binding attractiveness of a drug for its R measured w/ Kd |
| Kd | disassociation constant (↓Kd = ↑affinity) measures drug affinity to R |
| Selectivity | ability to elicit an effect at a R |
| Pharmacokinetics | what the body does to the drug (absorption, distribution, metabolism, excretion) |
| Pharmacovigilance | the safety of the drug - aka toxicity |
| Pharmacogenomics | variations in response due to genetic differences |
| List the 5 main R types | Ion channels = fastest Transmembrane GPCR Transmembrane enzymatic cytosolic domain R: drug binds --> dimerization -ex = tyrosine kinase Intracellular R = slowest, regulates transcription -ex = steroids Adhesion R |
| Type 1 graded dose-response curve | effect of various [drug] on an individual determined w/ efficacy (EC50) determines agonist + antagonist activity |
| Potency | response of a drug over a range of concentrations most potent drug = effect seen at lowest dose |
| Type 2 quantal dose response curve | #subjects responding to a drug Effective dose (ED50) Toxic dose (TD50) lethal dose (LD50) Therapeutic window |
| Therapeutic Window | [drug] electing an effect + no adverse effect seen Measured w/ Therapeutic Index B/w Minimum Toxic Concentration + MEC |
| Therapeutic index | margin of safety of drug TI = TD50 / ED50 ↑Therapeutic index = ↑safety |
| pH pKA Henderson-Hasselbach equation | pH: negative log of [H+] pKa : pH where protonated + unprotonated species are in [equal] Henderson-Hasselbach equation: pH = PkA + Log [conjugate base/acid] |
| Volume 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 |
| Metabolism -phase 1 rxns -phase 2 rxns | phase 1 = oxidation, reduction, hydrolysis phase 2 = synthesis -conjugation (more water soluble) = glucuronidation + sulfonation -acetylation/methylation (less water soluble) |
| Catecholamine Synthesis | Tyrosine --> (tyrosine hydroxylase) --> DOPA --> (Aromatic L-Amino Acid Decarboxylase) --> Dopamine --> NE --> E |
| Drug Clearance | plasma V from which all solute is removed per unit time |
| Flow Dependent Elimination | cleared readily by the organ of elimination |
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