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Pharmacology > Pharm Quiz 1 > Flashcards

Pharm Quiz 1 Flashcards

1
Q

Learning Objectives of Pharm as a PT

A
  • Infer past medical history based on meds
  • drugs may alter a patients clinical presentation and/or course of therapy
  • knowledge of drug classes and MOAs
  • be able to identify and avoid/limit common AE’s relevant to rehab
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2
Q

Pharmacology and PT Patient Management

A

Exam -> Eval -> Diagnosis -> Prognosis -> Interventions -> Outcomes (Discharge)

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3
Q

What is pharmocology?

A

Study of drugs

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4
Q

What is a drug?

A
  • any substance that, when taken, may modify one or more of your functions
  • alters physiology
  • benefit or harm
  • synthesized or naturally occurring compound
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5
Q

Subdivisions of Pharmacology

A

Pharmacotherapeutics and toxicology

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6
Q

Pharmacotherapeutics

A

study of the therapeutic use and effects of drugs in the treatment or prevention of disease
-further broken down into pharmacokinetics and pharmacodynamics

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7
Q

Toxicology

A

harmful effects of chemicals, side effects of AEs

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8
Q

Pharmacokinetics

A
  • what the body does to a drug
  • movement of a drug into, through, and out of the body,
  • involves ADME
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9
Q

Pharmacodynamics

A
  • how a drug affects a body
  • involves systemic (organ) and cellular effects of drugs
  • includes MOA, potency, efficacy
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10
Q

What is the FDA?

A

branch of government to design drug development policy and approve new drugs/indications
-they go through an approval process for new drugs

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11
Q

Clinical Trials for drugs

A

Phase 1: safety, small # of people, healthy subjects unless possibly very toxic
Phase 2: efficacy, small # of subjects, in patients with disease, compare to placebo/current drug
Phase 3: Larger and longer, larger group of p’s (>10k), randomized, double-blind
Phase 4: After FDA approval, post-marketing, general pop. are a part of this trial

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12
Q

Going “off-patent”

A
  • takes about 20 years

- meaning it is no longer owned by that original manufacturer and others can sell it for less at a different name

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13
Q

Off-label use

A
  • used for an unapproved indication or in an unapproved age group, dosage, or route of administration
  • generally legal
  • illegal to market off-label use
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14
Q

Orphan drug act

A

provide grants for drugs less likely to be studied

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15
Q

Drug recalls

A

remove defective or potentially harmful from market

  • by a company’s own initiative or FDA request
  • public is notified only of widely distributed or serious harm
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16
Q

Class levels of drug recalls

A

Class 1: a dangerous or defective that could cause serious health problems or death
Class 2: might cause temporary health problem, or pose slight threat
Class 3: unlikely to cause adverse health reaction but violates FDA labeling or manufacturing laws

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17
Q

Drug nomenclature

A

Chemical name: specific structure
Generic name: official name, used by anyone, based on chemical, first letter lowercase, used in clinicals trials, varies by country
Brand name: proprietary name assigned/owned by manufacturer but FDA approved, first letter capitalized, catchy

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18
Q

Brand name drugs

A

drug marketed under a proprietary, trademark-protected name

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19
Q

Generic name drugs

A
  • same as brand name drug in dosage, strength, administration, performance and quality
  • must provide “therapeutic equivalence” per FDA
  • identical amount of active ingredients but inactive ingredients may vary
  • cheaper
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20
Q

OTC drugs

A
  • safe and effective for use by the general public w/o doctor’s Rx
  • important to evaluate use due to AE, interactions, etc.
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21
Q

Pharmokinetics is the..

A

rate at which drug concentrations accumulate in and are eliminated from various organs of the body

  • what the body does to a drug
  • involves ADME
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22
Q

Absorption

A

process by which the drug is transferred from its site of administration to the systemic circulation

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23
Q

Enteral route

A

via GI tract

  • oral tablet, capsule, syrup, buccal, etc.
  • rectal
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24
Q

Parenteral route

A

not GI tract

  • injection
  • inhalation
  • topical
  • transdermal patch
  • implant
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25
Q

Oral: Advantages and Disadvantages

A
  • easy, safe, convenient

- limited/erratic absorption; first-pass inactivation in liver

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26
Q

Sublingual: Advantages and Disadvantages

A
  • rapid onset, no first-pass inactivation

- must be easily absorbed from oral mucosa

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27
Q

Rectal: Advantages and Disadvantages

A
  • alternative to oral; local effect on rectal tissue

- poor/incomplete absorption; rectal irritation; inconvenience

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28
Q

Inhalation: Advantages and Disadvantages

A
  • Rapid onset; direct application for respiratory disorders; large surface area for systemic absorption
  • chance of tissue irritation; compliance concerns
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29
Q

Injection: Advantages and Disadvantages

A
  • more direct administration to target tissue; rapid onset; no first-pass effect
  • chance of infection, invasive
30
Q

Topical: Advantages and Disadvantages

A
  • local effects on skin surface

- only effective treating outer layers of skin

31
Q

Transdermal: Advantages and Disadvantages

A
  • doesn’t require breaking the skin; steady, prolonged delivery via medicated patch
  • drug must be able to pass through dermal layers intact
32
Q

Implant: Advantages and Disadvantages

A
  • continuous delivery

- invasive

33
Q

3 main drug pathways:

A
  • passive diffusion through lipid membrane
  • passive diffusion through aqueous channel
  • carrier-mediated (binds to protein)
34
Q

What impacts drug movement?

A
  • lipophilicity
  • size of drug molecule
  • membrane thickness
  • acidic vs basic molecules
  • concentration gradient
35
Q

Blood brain barrier

A

cells serving as boundary between blood and CNS fluid; semipermeable

  • BBB more permeable in some disease (MS)
  • some meds cross BBB easier
  • when meds cross, may have more CNS related ADR’s (dizziness and falling)
36
Q

Barriers to delivery

A
  • user error
  • lipid solubility
  • fast/slow gastric interactions
  • food or drug interactions
  • first-pass metabolism/effect/elimination
  • bioavailability
37
Q

Bioavailabiliy

A

% of drug that makes it into systemic circulation

  • highly variable- depends on local pH, food, gut mobility
  • ex: metoprolol has 100% bioavailability when given by IV but 50% bioavailability when given orally
38
Q

First-pass effect/metabolism/elimination

A
  • when the concentration of the drug is reduced before it reaches the systemic circulation during the absorption process
  • mainly occurs in the liver
  • only a problem for oral meds
39
Q

Distribution

A
  • drug distributes to interstitial and intracellular fluids, and extravascular tissues
  • measured as volume of distribution (Vd)
40
Q

Distribution rate depends on:

A
  • lipid solubility and degree of drug ionization in the different compartments
  • organ BF
  • molecular weight
  • local metabolism if any tissue other than the target organ
  • binding to plasma proteins
41
Q

Vd

A

total concentration of drug in body/plasma concentration

-impacted by how much the drug crosses the membranes and plasma protein binding

42
Q

Higher Vd=

A

more drug in tissue than blood

43
Q

highly protein bound drug=

A

decreased active drug in tissue

44
Q

Protein binding is changed by..

A

disease states, nutrition, drug interactions

45
Q

Metabolism

A

how a drug is inactivated and prepared for elimination

46
Q

Metabolism phases:

A

Phase 1: catabolic process, catalyzed by CYP450 enzyme, large->small molecule
Phase 2: usually inactive, sometimes active (pro drugs: codeine and diazepam)
Phase 3: conjugation reaction, add hydrophillic group=less lipid soluble= more likely to excrete via kidneys

47
Q

What is a pro drug?

A

drugs that we take that have to be metabolized to an active derivative

48
Q

What are CP (CYP450) enzymes?

A

-catalyze reactions to break down drugs

49
Q

Why does CYP450 matter?

A
  • some drugs inhibit or induce CYP to change its activity or change gene expression so that more or less enzyme is produced
  • key in drug-drug interactions
50
Q

Elimination or Excretion

A

most common in urine via kidneys or fecal via liver

-breath (exhalation), tears, breast milk, saliva, sweat

51
Q

First Order elimination

A

most common, elimination is proportional to concentration, constant half life (t1/2)

52
Q

Zero order elimination

A

elimination rate is constant and independent of conc., saturating elimination mechanisms slows down the rate, inconsistent t1/2

53
Q

What is half life?

A

how long it takes to eliminate 50% of drug

  • at 5 half-lives is considered “cleared”
  • ex: t1/2=4 hours.. at time 0, drug conc.= 10 mg/L, thus 4 hours later= 5 mg/L
54
Q

Why is knowledge half life important for PTs?

A

we need to calculate half life sometimes to determine when the drug is cleared from the body and realize how long an adverse reaction due to a drug may last

55
Q

Steady state

A

when the amount of drug excreted in a specified period is equal to the amount of drug administered; often time to reach steady state is the time to reach therapeutic effect

56
Q

5 t1/2 to clear –> _____ t1/2s to reach “steady state”

A

4-5

57
Q

Length of t1/2s

A

shorter t1/2= more frequent dosing

longer t1/2= less frequent dosing but longer to reach steady state

58
Q

Changes with age: increased risk for ADRs/AEs with Polypharmacy (Pharmacokinetics)

A

taking multiple medications that cause drug-drug interactions and often side effects are mistaken for disease states

59
Q

Changes with age: increased risk for ADRs/AEs with CYP450 (Pharmacokinetics)

A

some cases in older adults there is an enzyme dysfunction -> increased drug-drug interaction and increase the amount of drug that is active in the system which increases AE’s

60
Q

Changes with age: increased risk for ADRs/AEs with Decreased serum albumin (Pharmacokinetics)

A

poor nutrition status might result in more active drug in the blood bc drug does not have proteins to bind to

61
Q

Changes with age: increased risk for ADRs/AEs with reduced renal and liver function (Pharmacokinetics)

A
  • liver dysfunction results in altered drug metabolism
  • kidney dysfunction can result in altered drug excretion
  • both can potentially prolong half lives
62
Q

Changes with age: increased risk for ADRs/AEs (Pharmacodynamics)

A
  • changes in drug-receptor interactions
  • increased sensitivity to sedative-hypnotics, analgesics due to changes in BBB
  • reduced baroreceptor sensitivity: leads to OH
63
Q

Body composition and lean muscle mass changes in age resulting in..

A

the way drugs are distributed

-where there is increased body fat-> longer half lives of drugs

64
Q

Pharmacogenetics

A

how variation in one single gene, influences the response of a single drug

65
Q

Pharmacogenomics

A

a broader term which studies how all of the genes in the genome can influence response to drugs

66
Q

Genetic polymorphisms (CYP2D6)

A

highly morphic in the human pop. and metabolizes 1/4 of clinically useful meds resulting in inability to metabolize drugs

67
Q

Genetic polymorphisms (Alpha2-adrenoreceptor)

A

mutation in this receptor means the person has increased bronchodilator desensitization so a drug taken to increase dilation of bronchioles will not bring expected results which can result in trouble breathing

68
Q

Genetic polymorphisms (Cholinesterase deficiency)

A

mutation in this receptor means the person has a decreased ability to terminate succinylcholine which is an anesthesia AKA trouble waking up from anesthesia

69
Q

Cholinesterase

A

an enzyme that metabolizes succinylcholine

70
Q

Changes with disease

A
  • Liver or kidney dysfunction -Increased serum levels of active drug remains in the body for increased time which can increase AEs
  • reduced activity of CYP450 enzymes due to viral infections
71
Q

What issues can arise from having reduced CYP450?

A

whether the drug is an inhibitor or inducer, you may get too much of the drug in the system or not enough

72
Q

How does exercise effect BF?

A

Intense exercise will shunt BF away from organs that metabolize, distribute, and eliminate drugs

Pharmacology (1 decks)

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