chapters 1-3

Question 1

the goal of clinical guidlines

Answer 1

set standard guidelines using best evidence

Question 2

the best guidelines integrate

Answer 2

clinical experience and research evidence

Question 3

purpose of clinical guidelines is to

Answer 3

standardize care, improve pt outcomes, and ensure safety

Question 4

things to keep in mind

Answer 4

may not represent underrepresented groups
may change
personalized recommendations to pts

Question 5

benefits of clinical guidelines

Answer 5

shared decision making
id underrepresented populations- cheapest, least invasive options

Question 6

limitations of clinical guidelines

Answer 6

lacking evidence
rigid guidelines

Question 7

recommendations should be based on

Answer 7

Effective size of the main outcomes
Quality of the evidence
Application of the evidence into specific practice settings
Baseline risk to the population
Cost of the intervention relative to the added benefit to the patient

Question 8

must consider when making recommendations

Answer 8

pt values and preferences

Question 9

strength of a recommendation is influenced by

Answer 9

the balance of the risks
the burdens and benefits of an intervention to a specific population
the quality of the evidence supporting the treatment outcomes

Question 10

good guideline is based on

Answer 10

1) based on the consistent and systematic judgement of the evidence
2) clear in its recommendations
3) translatable into practice.

Question 11

tells how drug moves through body

Answer 11

pharmacokinetics

Question 12

-applies the fundamentals of PK to dose calculations, infusion rates, predictions of drug concentrations, dosing intervals, and time to eliminate the drug from the body.
-can be affected by numerous covariates, such as age, genetics, gender, race, comorbid disease states, and concomitant medications, resulting in drug interactions. These factors should be considered in the dosing regimen for each patient.

Answer 12

pharmacokinetics

Question 13

The primary objective of clinical PK is to maximize efficacy while minimizing toxicities through a process called

Answer 13

therapeutic drug monitoring (TDM)

Question 14

can provide insight into patients’ metabolism, distribution, and excretion, or perhaps pharmacological response or toxicities, further maximizing patient outcomes.

Answer 14

genetic information

Question 15

clinical practice of measuring specific drug levels in a patient’s blood at designated intervals to ensure that the drug concentration stays within atherapeutic range—high enough to be effective, but low enough to avoid toxicity

Question 16

things that effect how the body acts on a drug

Answer 16

introduction to body- iv, oral, buccal
delivery to target tissues- rate, passive diffusion, carrier-mediated membrane transport
clinical expression- determined by the bioavailibility conc. in plasma

Question 17

acronym for PK

Answer 17

ADME
absorbed
distributed
metabolized
excreted

Question 18

most common absorbed method

Answer 18

passive distribution

Question 19

• Lipophiliic (fat soluble) vs Hydrophilic (Water Soluble)
  -Dependent on tissue permeability, organ/tissue size, and
  -Binding of drugs

Answer 19

distributed

Question 20

The process by which the body modifies drugs into compounds that can be eliminated

Answer 20

metabolized

Question 21

drug concentration is greatly reduced before it reaches systemic circulation (po meds)
-most oral medications. taken orally and passes through liver by portal vein

Answer 21

first-pass metabolism

Question 22

The removal of drugs from the body, either as a metabolite or an unchanged drug
important to understand where- urine, skin, gi tract, tears, breast

Answer 22

excreted

Question 23

active protein/medication that causes effects are

Answer 23

free/unbound

Question 24

acidic drugs binds to

Answer 24

albumin

Question 25

low nutrition shows low

Answer 25

albumin

Question 26

low nutrition given drug that binds to albumin but have low albumin leads to

Answer 26

high effects

Question 27

Basic drugs bind to α1-acid glycoprotein (AAG) AAG can increase in response to stress, trauma, inflammation) so dosing needs to be

Answer 27

higher

Question 28

many drug interactions involve

Answer 28

cytochrome P450 enzyme system.

Question 29

lead to increased metabolism of drugs , resulting in a reduction in plasma concentration of the drug substrates, which may lead to decreased therapeutic effects ( increase metabolism = decrease amount in plasma)

Answer 29

inducers ETOH

Question 30

decrease drug metabolism increase plasma conc of drug increase pharm effects and toxicity

Answer 30

inhibitors

Question 31

ex of inducers

Answer 31

statins with grapefruit juice

Question 32

of cytochrome P450 enzymes , which decrease the metabolism of drugs that are substrates. The increase in substrate plasma concentration may result in enhanced pharmacological effects and enhanced toxicological effects, decrease metabolism = increase amount in plasma.

Answer 32

inhibibitors

Question 33

decrease concentration of drug decrease therapeutic effects

Answer 33

inducers

Question 34

the rate and extent of drug absorption, or the percentage/fraction that reaches systemic (plasma) circulation.

Answer 34

bioavailability

Question 35

bioavailibity is dependent on

Answer 35

Route of administration Rate of administration Presence of food Drug-drug interactions GI motility

Question 36

when taken orally compared to iv, the bioavailability is

Answer 36

lower

Question 37

dka want to give what route

Answer 37

IV

Question 38

is an independent PK parameter quantifying the rate at which the body eliminates a drug. It is defined as the volume of blood that is completely cleared of the drug per unit time.

Answer 38

clearance

Question 39

clearance is dependent on

Answer 39

on liver function, renal excretion, chemical decomposition, fecal excretion, loss through the skin (sweat, sloughing), and loss through breathing

Question 40

liver is responsible for

Answer 40

drug metabolism

Question 41

kidney is responsible for

Answer 41

parent drug and metabolite excretion (filtration and secretion)

Question 42

is an appropriate measure of renal function for determining dosage adjustments in renal impairment.

Answer 42

gfr

Question 43

is often used as a method of estimating GFR. 

Answer 43

Cockcroft-Gault equation 

Question 44

is the creatinine clearance in mL/min

Answer 44

ClCr

Question 45

the ideal body weight of the pt in kg

Answer 45

IBW

Question 46

serum creatinine

Answer 46

SCr

Question 47

utilizes serum creatinine, which is a by-product of muscle metabolism and is freely filtered by the glomerulus (pt with more muscle mass produces more creatinine & pt with low muscle mass creatinine may appear normal or low even if kidney function is impaired).

Answer 47

The Cockcroft-Gault equation

Question 48

determins by the properties of a drug, the extent of protein binding, and the influence of tissue binding.

Answer 48

volume distribution

Question 49

determines the loading dose

Answer 49

volume of distribution

Question 50

Drugs with a large distribution volume generally require

Answer 50

a higher loading dose to achieve therapeutic levels.

Question 51

Does the drug remain in plasma or redistribute? High Vd -> More distribution to other tissue HIGHER dose is needed Low Vd -> Less distribution to other tissues LOWER dose needed

Question 55

clinical significance of T1/2

Answer 55

Avoid drug toxicity or (subtherapeutic levels): Overdosed Received an incorrect amount of a particular drug Renal or hepatic failure

Question 56

Illustrates how repeated dosing (every 4 hours) leads to a gradual accumulation of the drug. After about 4–5 half-lives, the drug reaches a steady state, where the amount administered equals the amount eliminated

Answer 56

steady state

Question 57

what the drug does to the body or how the drug produces its therapeutic effect

Answer 57

pharmacodynamics

Question 58

Shows a constant increase in effect with increasing dose. The effect of the drug increases in proportion to the dose. Doses are predictable and easier to manage.

Answer 58

linear- the more you give, the more effect it has

Question 59

Starts slow (lag phase), increases rapidly (linear phase), then levels off (plateau phase) as receptors become saturated. Most drugs follow this pattern, especially those that act on specific receptors. Involves saturation of metabolic pathways, making dosing more complex and requiring careful monitoring.

Answer 59

sigmoidal -receptors are saturated

Question 60

The therapeutic goal is to understand how changes in dose alter the patient’s response. A hypothetical dose-response curve has features that vary in potency (location of the curve along the dose axis) Maximal efficacy or ceiling effect (greatest attainable response) Slope (change in response per unit dose)

Answer 60

the dose-response curve

Question 61

Reaches maximum effect at a low dose. Produces a strong response.

Answer 61

high potency, high efficacy

Question 62

Needs a higher dose to reach the same maximum effect. Still produces a strong response, just more slowly

Answer 62

low potency, high efficacy

Question 63

Reaches its maximum effect quickly, but the maximum is lower. Useful for comparing effectiveness, not just dose.

Answer 63

high potency, low efficacy

Question 64

a steeper curve means

Answer 64

more sensitive response

Question 65

left shifted curve means

Answer 65

higher potency

Question 66

the sweet spot in dosing. The range of drug doses that produces effective treatment without causing significant side effects or toxicity.

Answer 66

therapeutic window

Question 67

): the lowest concentration of a drug in the blood that still produces the desired therapeutic effect.

Answer 67

minimum effective concentration

Question 68

the lowest concentration at which the drug starts to produce toxic effects.

Answer 68

minimum toxic concentration

Question 69

A ratio that compares the amount of a drug that causes a therapeutic effect to the amount that causes toxicity. The ratio of the toxic dose to the effective dose.

Answer 69

therapeutic index

Question 70

the drug is safe, wide window

Answer 70

high therapeutic index

Question 71

means the drug requires careful monitoring (narrow window) because the effective and toxic doses are close together

Answer 71

low therapeutic index

Question 72

small doses=big effect changes

Answer 72

sigmoidal curve

Question 73

individual variability influencing pharmacodynamics

Answer 73

Genetic variations Age Sex Disease states

Question 74

factors influencing pharmacodynamics

Answer 74

individual variability drug interactions physiologic changes

Question 75

Drugs can bind to enzymes and receptors, altering their activity and producing therapeutic effects. The specificity of drug-receptor interactions, as well as enzyme-drug interactions, plays a crucial role in determining the efficacy and selectivity of drug action. 1. How does it affect a specific receptor? Many drugs bind to specific receptors on the surface of cells to cause an action. Morphine 2. Other medications inhibit specific enzymes for a desired effect. Monamine oxidase inhibitors (MAOIs)- monamine oxidase breaks down serotonin and dopamine, which blocks increase concentration of serotonin and dopamine in CNS increasing feelings of pleasure

Question 76

Drugs that occupy receptors and activate them

Answer 76

agonists

Question 77

Drugs that occupy receptors but DO NOT activate them Antagonists BLOCK receptor activation

Answer 77

antagonists

Question 78

Compete with an agonist for the same receptor binding site Their effects can be overcome by increasing the concentration of the agonist. In other words, you can often overcome the effect by increasing the dose of the agonist. Think of it like two people fighting for the same seat—if one pushes harder (higher dose), they can win. Example: Naloxone

Answer 78

COMPETITIVE ANTAGONISTS

Question 79

Bind to a different site on the receptor, either changing the receptor’s shape or function. Their effects cannot be overcome by increasing agonist concentration (higher doses will not change the effect). In other words, increasing the dose won’t help—so dosing strategies must be different. Like removing the seat altogether—no matter how many people want to sit, they can’t. Example Ketamine

Answer 79

NON-COMPETITIVE ANTAGONISTS

Question 80

enzymes and drug metabolism

Answer 80

1.Substrate enters the enzyme 2.Enzyme-substrate complex forms 3.Reaction happens 4.Products are released

Question 81

enzyme inhibitors can lead to stronger effect or toxicity. Grapefruit juice inhibits an enzyme (CYP3A4), which can

Answer 81

increase levels of certain medications

Question 82

what happens when enzyme is blocked

Answer 82

1. drug stays in the body longer 2. drug may not work at all 3. dangerous drug interactions

Question 83

Help control drug levels in the body. Can target specific disease processes. Allow fine-tuning of treatments with fewer side effects.

Answer 83

enzyme inhibitors

Question 84

4 medication ex. of enzyme inhibitors

Answer 84

1. HIV Treatment Protease inhibitors (block viral enzymes that HIV need to multiply) 2. Cancer Treatment Methotrexate (inhibits an enzyme needed for DNA synthesis) 3. GERD Treatment PPIs (block the enzyme that produces stomach acid 4.Antibiotics Penicillin (inhibits enzymes that bacteria use to build their cell walls)