Pharm Quiz 1 Flashcards
(72 cards)
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
2
Q
Pharmacology and PT Patient Management
A
Exam -> Eval -> Diagnosis -> Prognosis -> Interventions -> Outcomes (Discharge)
3
Q
What is pharmocology?
A
Study of drugs
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
5
Q
Subdivisions of Pharmacology
A
Pharmacotherapeutics and toxicology
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
7
Q
Toxicology
A
harmful effects of chemicals, side effects of AEs
8
Q
Pharmacokinetics
A
- what the body does to a drug
- movement of a drug into, through, and out of the body,
- involves ADME
9
Q
Pharmacodynamics
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- how a drug affects a body
- involves systemic (organ) and cellular effects of drugs
- includes MOA, potency, efficacy
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
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
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
13
Q
Off-label use
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- used for an unapproved indication or in an unapproved age group, dosage, or route of administration
- generally legal
- illegal to market off-label use
14
Q
Orphan drug act
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provide grants for drugs less likely to be studied
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
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
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
18
Q
Brand name drugs
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drug marketed under a proprietary, trademark-protected name
19
Q
Generic name drugs
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- 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
20
Q
OTC drugs
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- safe and effective for use by the general public w/o doctor’s Rx
- important to evaluate use due to AE, interactions, etc.
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
22
Q
Absorption
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process by which the drug is transferred from its site of administration to the systemic circulation
23
Q
Enteral route
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via GI tract
- oral tablet, capsule, syrup, buccal, etc.
- rectal
24
Q
Parenteral route
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not GI tract
- injection
- inhalation
- topical
- transdermal patch
- implant
25
Oral: Advantages and Disadvantages
- easy, safe, convenient
| - limited/erratic absorption; first-pass inactivation in liver
26
Sublingual: Advantages and Disadvantages
- rapid onset, no first-pass inactivation
| - must be easily absorbed from oral mucosa
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Rectal: Advantages and Disadvantages
- alternative to oral; local effect on rectal tissue
| - poor/incomplete absorption; rectal irritation; inconvenience
28
Inhalation: Advantages and Disadvantages
- Rapid onset; direct application for respiratory disorders; large surface area for systemic absorption
- chance of tissue irritation; compliance concerns
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Injection: Advantages and Disadvantages
- more direct administration to target tissue; rapid onset; no first-pass effect
- chance of infection, invasive
30
Topical: Advantages and Disadvantages
- local effects on skin surface
| - only effective treating outer layers of skin
31
Transdermal: Advantages and Disadvantages
- doesn't require breaking the skin; steady, prolonged delivery via medicated patch
- drug must be able to pass through dermal layers intact
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Implant: Advantages and Disadvantages
- continuous delivery
| - invasive
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3 main drug pathways:
- passive diffusion through lipid membrane
- passive diffusion through aqueous channel
- carrier-mediated (binds to protein)
34
What impacts drug movement?
- lipophilicity
- size of drug molecule
- membrane thickness
- acidic vs basic molecules
- concentration gradient
35
Blood brain barrier
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
Barriers to delivery
- user error
- lipid solubility
- fast/slow gastric interactions
- food or drug interactions
- first-pass metabolism/effect/elimination
- bioavailability
37
Bioavailabiliy
% 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
First-pass effect/metabolism/elimination
- 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
Distribution
- drug distributes to interstitial and intracellular fluids, and extravascular tissues
- measured as volume of distribution (Vd)
40
Distribution rate depends on:
- 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
Vd
total concentration of drug in body/plasma concentration
| -impacted by how much the drug crosses the membranes and plasma protein binding
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Higher Vd=
more drug in tissue than blood
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highly protein bound drug=
decreased active drug in tissue
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Protein binding is changed by..
disease states, nutrition, drug interactions
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Metabolism
how a drug is inactivated and prepared for elimination
46
Metabolism phases:
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
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What is a pro drug?
drugs that we take that have to be metabolized to an active derivative
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What are CP (CYP450) enzymes?
-catalyze reactions to break down drugs
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Why does CYP450 matter?
- 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
Elimination or Excretion
most common in urine via kidneys or fecal via liver
| -breath (exhalation), tears, breast milk, saliva, sweat
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First Order elimination
most common, elimination is proportional to concentration, constant half life (t1/2)
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Zero order elimination
elimination rate is constant and independent of conc., saturating elimination mechanisms slows down the rate, inconsistent t1/2
53
What is half life?
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
Why is knowledge half life important for PTs?
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
Steady state
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
5 t1/2 to clear --> _____ t1/2s to reach "steady state"
4-5
57
Length of t1/2s
shorter t1/2= more frequent dosing
| longer t1/2= less frequent dosing but longer to reach steady state
58
Changes with age: increased risk for ADRs/AEs with Polypharmacy (Pharmacokinetics)
taking multiple medications that cause drug-drug interactions and often side effects are mistaken for disease states
59
Changes with age: increased risk for ADRs/AEs with CYP450 (Pharmacokinetics)
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
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Changes with age: increased risk for ADRs/AEs with Decreased serum albumin (Pharmacokinetics)
poor nutrition status might result in more active drug in the blood bc drug does not have proteins to bind to
61
Changes with age: increased risk for ADRs/AEs with reduced renal and liver function (Pharmacokinetics)
- liver dysfunction results in altered drug metabolism
- kidney dysfunction can result in altered drug excretion
- both can potentially prolong half lives
62
Changes with age: increased risk for ADRs/AEs (Pharmacodynamics)
- changes in drug-receptor interactions
- increased sensitivity to sedative-hypnotics, analgesics due to changes in BBB
- reduced baroreceptor sensitivity: leads to OH
63
Body composition and lean muscle mass changes in age resulting in..
the way drugs are distributed
| -where there is increased body fat-> longer half lives of drugs
64
Pharmacogenetics
how variation in one single gene, influences the response of a single drug
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Pharmacogenomics
a broader term which studies how all of the genes in the genome can influence response to drugs
66
Genetic polymorphisms (CYP2D6)
highly morphic in the human pop. and metabolizes 1/4 of clinically useful meds resulting in inability to metabolize drugs
67
Genetic polymorphisms (Alpha2-adrenoreceptor)
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
Genetic polymorphisms (Cholinesterase deficiency)
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
Cholinesterase
an enzyme that metabolizes succinylcholine
70
Changes with disease
- 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
What issues can arise from having reduced CYP450?
whether the drug is an inhibitor or inducer, you may get too much of the drug in the system or not enough
72
How does exercise effect BF?
Intense exercise will shunt BF away from organs that metabolize, distribute, and eliminate drugs
