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AAA PA: Pharm I > Exam 1 > Flashcards

Exam 1 Flashcards

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1
Q

What are the phases of FDA approval and clinical trials? ***

A

(Safeguard #1)
- Preclinical: lab & animal studies
- Phase I: for safety, small group healthy volunteers, ADME,
- Phase II: for safety, medium group with disease, ID SE
- Phase III: for effectiveness, large group, serious AE, dose, double blind, ++yrs
- Phase IV: on market, long-term SE & effectiveness

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2
Q

What is the FDA fast track?

A
  • more frequent communication & review
  • Breakthrough therapy: serious condition & show substantial improvement over current
  • Accelerated approval: effectiveness morbidity/mortality
  • Priority review: 6 instead 10 mo.
  • Emergency Use Authorization: Public health emergency (COVID vac & remdesivir)
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3
Q

How does the U.S. Drug Enforcement Agency prevent the misuse of drugs?

A
  • Providers must register with the DEA
  • DEA number required for prescribing controlled substances
  • Drug schedules (five classes)
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4
Q

What is the difference between generic and brand name drugs?

A
  • The name. There is the same drug formula
  • Cheaper
    (Required to show therapeutic equivalence–quality, purity, strength, potency)
  • Bioequivalence ratings: A - therapeutically equivalent (TE) B- not TE AB- somewhere in between
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5
Q

What are the five drug schedules?

A

I: no currently accepted medical use & high potential for abuse (heroin, LSD, marijuana, MDMA)
II: high potential for abuse and dangerous (cocaine, methamphetamine, methadone)
III: Moderate or low potential for dependence (ketamine, anabolic steroids, test)
IV: low potential for abuse and low risk dependence (Xanax, Valium, Ambien)
V; lower potential for abuse (Lomotil, Motofen, Lyrica)

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6
Q

What is the difference between prescription and non prescription drugs?

A
  • If they need a prescription
  • The FDA approves both
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7
Q

What factors may lead to adverse drug events?

A
  • Diet (herbals - natural X= harmless)
  • Different genes
  • Lack of drug knowledge
  • Lack of patient information: therapeutic effect, SE & management, Black Box Warnings - serious/permanent/fatal SE, simple language, one pharmacy
  • Poor Communication
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8
Q

What are all the pieces of information for a legal prescription?

A
  • Prescriber name, address, phone #
  • Pt name (DOB & address X req)
  • Date
  • Med name (generic safest) & strength: leading zeros (0.4), no trailing (0.40), correct metric
  • Quantity, dosage, instructions/sig:, refills, frequency
    (PRN must have a reason)
  • Signature
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9
Q

What are common Sigs on prescriptions?

A

(Instructions)
po - by mouth
qd - as needed
bid - twice a day
tid - three times a day
quid - for times a day
q4h - every 4 hours
q12h - every 12 hrous
qhs - at bedtime

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10
Q

What is absorption? And what affects it?

A
  • Medications reach bloodstream
    (plasma concentration gives idea of concentration at receptor)
  • Deals with bioavailability - how much of drug reaches bloodstream (IV - 100%)
  • Affected by:
    – cell membranes (allows lipid-soluble & small),
    – proteins (pores, AT),
    – passive diffusion (down concentration),
    – Fick’s Law (> distance & size = slower diffusion)
    – Solubility: > diffusion in
    – most in small intestine
    – most by endocytosis
    neutral, non-ionized form
    – pharmaceutical preparation (local/systemic admin, immediate/extended/sustained release)
    – blood flow
    – GI motility: Decreased gastric emptying (high fat meals/solid foods) delays absorption
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11
Q

What is the difference between pharmacokinetics and pharmacodynamics?

A
  • Pharmacokinetics: what the body does to the drug (ADME)
  • Pharmacodynamics: what the drug does to the body (binding sites, dose-response curve)
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12
Q

What are the types of routes of administration?

A
  • Enteral administration: oral (po), sublingual (SL), rectal (PR)
  • Parental administration: IV, IM, SC, topically (bypasses GI), inhalation, transdermal
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13
Q

What is first-pass effect? Bioavailability formula?

A

The liver may degrade dugs that are absorbed from the GI
- bioavailability = fraction/% drug reach circulation after first pass effect
- bioavailability = AUCroute/AUCiv

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14
Q

What is therapeutic index?

A
  • difference between the median toxic dose (TD50) and the median effective dose (ED50)
  • Farther from 1 the better (higher index safer)
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15
Q

What medications have a narrow margin of safety?

A
  • Warfarin
  • Theophylline
  • Lithium
  • Phenytoin
  • Gentamicin
  • Digoxin
    (Warning think last prescription {in} general don’t)
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16
Q

What is distribution? What affects it?

A
  • Med from circulation to body tissues
    Affected by
  • blood supply: (direct correlation amount & distribution)
  • proteins in the blood: cause binding: storage site, cannot exert effect (Warfarin highly protein bound)
  • Volume of distribution:
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17
Q

What is the volume of distribution?

A

hypothetical volume that accommodates all med in body
- lower: hydrophilic, larger, highly protein bound
- higher: hydrophobic, smaller, not protein bound (may cross BBB)
- vd = dose admin/plasma concentration
– Small: <3L primary in plasma
– >16: both
– >46L: possibly distributed throughout all compartments
- increased: Cirrhosis, Chronic Kidney disease (nephrotic syndrome- dec proteins), Fluid retention, impaired protein-binding (more free)
- higher Vd: required higher loading dose
- decreased: severe dehydrationt

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18
Q

What are the types of topical parental absorption?

A
  • ointments: occlusive, hydrating, prevent water absorption or evaporation (On to stay)
  • creams: water soluble & washable (Can be washed)
  • gels: most water soluble for large areas (Gone)
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19
Q

What is metabolism?

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A
  • Chemical change mostly by liver (kidneys, intestines, circulating enzymes) to water soluble readily excreted metabolite form
  • Activate–prodrug–or inactivate
  • By primarily Enzymes
    – E induction: inc enzymes –> dec drug concentration
    – E inhibition: dec production –> inc drug concentration
20
Q

What are the phases of metabolism?

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A

May not occur in sequence or together
- Phase I: by class of enzymes (Cytochromes–CYP450, lipid soluble) oxidation, hydrolysis or reduction
- Phase II: conjugation reactions (join with another compound)

21
Q

What is elimination?

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A
  • Loss of drug through chemical metabolism & physical excretion
  • Primarily kidney GI, lung, skin, glands
    – Proximal tubule: active secrete polar, water-soluble & passive: non-polar lipid-soluble,
22
Q

What does pH have to do with elimination?

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A

Strength of med and pH of urine
- Most meds weak acids/bases
- pKa = pH when concentrations of uncharged & charged forms of meds =
- Change urine pH affects reabsorption of acids/bases
- Alkaline urine (sodium bicarbonate) prevents reabsorption of weak acid (Aspirin OD)
- Acidic urine (ammonium chloride) prevents reabsorption of weak base (amphetamine OD)

23
Q

What affects elimination?

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A
  • Chronic kidney disease (filtration)
  • Hypotension (filtration)
  • Dehydration (filtration)
24
Q

How is the time required for the drug to be eliminated calculated?

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A
  • Half-life is time required for half the drug to be eliminates (3-5 = considered eliminated)
  • First order: more drug = faster eliminated, elimination fraction consistent (MOST DRUGS)
  • Zero order: constant rate regardless concentration
    – aspirin, phenytoin, ethanol, warfarin
25
What happens after a certain number of half-lives?
- 3-5 - considered eliminated - concentration curve reaches equilibrium for amount of drug entering and leaving body - longer half-life = longer time to achieve steady state
26
What is clearance?
The removal of drug from plasma or organ - Faster: greater Vd or smaller half life - Estimated: by creatine (from continual muscle breakdown & eliminated by glomerular filtration) - Creatine est GFR which est kidney function & clearance
27
What is the creatine clearance calculation we need to know?
Cockcroft-Gault formula C(Cr) = [((140-age) x weight)/(72 x S(Cr))] x 0.85 (if female) - Most helpful in pt over 65 and/or Scr >1.5mg/dL
28
Entero-hepatic Recirculation:
If travel through liver unchanged will potentially be reintroduced to intestine via bile and reabsorbed
29
What is a ligand? What does it bind to and what does that do?
- Ligand: any chemical (endo/exogenous) that interacts with a receptor - Binding capacity depends on size/shape dug & receptor - Receptor: classified by result, initiates chain that **alters/modifies** physiologic function (not new function)
30
What are the types of receptors?
- Gate ion channels: open/close channel for ion (nicotinic, acetylcholine, GABA) - Transmembrane receptors: bind on surface, enzyme in cytoplasm -- cytoplasmic enzyme/tyrosine kinase activated -- down regulate receptors, can generate second messenger - G protein-coupled receptors: extracellular receptor, intracellular G protein --> enzyme, ion channel, inc. 2nd messenger (alpha/beta-adrenergic, hormone) - Intracellular receptors: cross membrane direct changes in cell DNA transcription (glucocorticoids, sex hormones)
31
What are the drug-receptor interactions?
- Affinity: strongly bind (arnold P.) directly proportional to potency - Chirality: affinity different between diastereomers and enantiomers - Intrinsic Activity: ability to activate receptor, intensity of response to med, number bound receptors - Potency: amount needed for effect (smaller ED50) - Efficacy: Maximal effect (higher Emax, more efficacious) - Agonists: affinity w/ response - Antagonists: affinity w/o response (high enough, bump agonist)
32
What patient factors affect pharmacokinetics/dynamics?
- Body type - Weight - Pathophysiology: PK - renal failure, hepatic dysfunction, dec blood flow - Genetics: abnormal/absent enzymes (succinylcholine) - Age: very young/old metabolize less - Diet: tyramine-containing foods (wine, cheese) & MAOIs, grapefruit juice & CYP3A4 - Sex: PK - females >fat, PD - absence/presence hormones ie estrogen/progesterone - Ethnicity: genes & hepatic enzymes, cultural habits & traditions, diet & homeopathy
33
What causes drug-drug interactions?
- Pharmacokinetic (alter drug ADME) or pharmacodynamic factors (directly effect drug) - Object or target drug = drug w/ altered effect
34
What is synergism drug interactions?
When the effects of A & B are greater than the sum of their individual effects (Clopidogrel & Aspirin, acute MI)
35
What is additive drug interactions?
Effect of A & B is equal to the sum of their individual effects (Aspirin & acetominophen)
36
What is antagonism drug interactions?
Effect of A & B is less than sum of their individual effects
37
What are permissive drug interactions?
For A to have its full effect it needs B (Cortisol on catecholamine responsiveness)
38
What are tachyphylactic drug interactions?
Response from A decreases with repeated doses (Hydralazine, nitrates, niacin, phenylephrine)
39
What is potentiation drug interactions?
B has no therapeutic effect but enhances the action of A
40
How do drug-drug interactions affect absorption?
- Acidity: alter gastric pH -- ketoconazole/ferrous sulfate needs acidic pH, famotidine/esomeprazole increases pH - GI motility: alter rate -- metoclopramide (Reglan) increases -- anticholinergics decrease - Adsorption: agents bind (add) on surface forming complex -- most: cations - antacids (Mg2+, Ca2+, Al3+), -- Fe2+, Ca 2+, Vitamins + tetracyclines & fluoroquinolones dec antibiotic -- colestipol, cholestyramine - GI flora: metabolize drugs -- antibiotics (ABX) kill -- dec flora --> dec estradiol -- dec flora --> dec Digoxin metabolism --> **inc. availability**
41
How do drug-drug interactions affect distribution?
Two drugs high affinity for proteins - >90% protein bound) - narrow therapeutic index compete --> **more free** drug
42
How do drug-drug interactions affect metabolism generally?
- Liver, small intestine + (minor) kidneys, lungs, brain - 5 isoenzymes responsible for most metabolism-related drug interactions - poor metabolizers: drug build up or **prodrug** little effect - ultra-metabolizers: drug gone or **prodrug** a lot available - highest affinity drug binds more - inhibition: - induction:
43
How do drug-drug interactions affect metabolism for inhibition?
- dec. enzyme available - competitive: affinity for metabolism - non-competitive: affinity but metabolized elsewhere - half-life: proportional to duration of interaction (3-5 half-lives) - concentration: concentration must be reached to inhibit - toxic: (ketoconazole inhibits breakdown simvastatin {myopathy/rhabodmyolysis}, Bactrim inhibits warfarin {inc INR}) - efficacy: (omeprazole reduces active metabolite of clopidogrel --> less effective) - **warfarin**: P450 inhibited by fluconazole & grapefruit juice --> bleeding - **FAB5**: fluconazoles (azoles), fluoroquinolones, Flaguyl (metronidazole), Amiodarone, Bactrim (TMP/SMX) - P450 inhibitors
44
How do drug-drug interactions affect metabolism for induction?
- inc enzyme available - enhanced metabolism, inc hepatic blood flow & hepatic enzymes - shorter half-life = shorter induction - p450 induced by Rifampin degrading warfarin --> clotting -- LONG half-life so even when discontinued effect on warfarin remains b/c **half-life of the liver enzymes is longer than half-life of rifampin** - Rifampin, phenytoin, phenobarbital, carbamazepine, St. John's Wort
45

AAA PA: Pharm I (1 decks)

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