567 Pharm Quiz 2

Front 1

sources
constituents
dosage forms
routes of administration
stability
storage (follow directions of how to handle)

Back 1

What is pharmaceutic phase?

Front 2

plants, minerals, animals, (marine life)

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I. Sources of Drugs (pharmaceutic phase)

Front 3

fillers; don’t include the active ingredient; nontherapeutic chemical

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II. EXCIPIENTS USED IN DRUGS

Front 4

disintegrate
dissolution
rate of absorption
stability of storage
(nurses should follow instructions – honor the rules of pharmaceutics)

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What are the purposes of using excipients?

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diluents
fillers
binders
disintegrators
dissolution enhancers
retardants
lubricants
wetting agents
anti=adherants
antioxidants
preservatives
pH stabilizers
coatings
flavorings
colorings

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What are the substances that are used as excipients?

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1. oral
2. enteral
3. parenteral
4. topical
5. intradermal implants

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II. What are drug routes?

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1. intradermal
2. subq
3. intramuscular
4. intravenous
5. intraarterial
6. intrathecal (subarachnoid, subdural, cerebrospinal fluid)
7. intraspinal
8. intraarticular

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What are parenteral drug routes?

Front 8

anything absorbed across a membrane;
inhalants
skin
nasal
suppositories
eyes

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What are topical drug routes?

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These are written as part of the prescriptive process.

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IV. What are dosage forms and preparations?

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TABLETS - most complex dosage forms
Buccal tablet - held between cheek & gum
Sublingual t. - under tongue
coated t. - outside layer for taste
enteric-coated t. - coating to prevent disintegration in gastric juices or protect stomach
effervescent t. - have Nabicarb and acidulant to generate CO2 when added to
H20
sustained-release t. - time-release dose of coated particles
capsules - gelatin cases enclosing solid drugs, melt
caplets - tablets that resemble capsules in shape

powders
patches
pellets or needles - surgically implanted
troches - oral or vaginally
lozenges - oral

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What are NAMES of VARIOUS SOLID FORMULATIONS?

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what the body does to the drug

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pharmacokinetics

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what the drug does to the body

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pharmacodynamics

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ABSORPTION
DISTRIBUTION
BIOTRANSFORMATION
EXCRETION

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What are the 4 basic process of pharmacokinetics?

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- determine # of drug molecules to reach site
- regulate plasma concentration of drug
intensity of drug action
- regulate the duration of drug action

*translates into the planning of the dose

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The collective effect that is determined by the processes of pharmacokinetics.

Front 15

genetics
physiological status
psychological state
environmental factors – *ex. outside temp and sun

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What are the patient variables that modify the general principles of pharmacokinetics ?

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The most common way drugs move across membranes.

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diffusion is the most common method of drug movement across membranes

also, drugs that are more neutral are more fat soluble

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Process of a drug passing from site of administration to venous or lymphatic circulation.

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Absorption

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Proportion of administered drug available to produce effects.

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Bioavailability

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Drug solubility
surface area
blood flow
lipid solubility
pH partitioning

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Components of Absorption

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1. the physical and chemical properties of the drug
2. the anatomical and physiological factors of the absorptive surface.

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What affects the rate of drug absorption?

Front 21

This drug type crosses membranes more easily.

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1. lipid (vs. non lipid soluble)
2. polar (vs. nonpolar)

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barriers to absorption: none
absorption pattern: instantaneous and complete
advantages: rapid onset, control, use of large fluid volumes, use of irritant drugs (rapidly diluted in blood)
disadvantages: high cost, inconvenient, difficult, irreversible, dangerous, fluid overload, infection, embolism

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IV absorption characteristics

Front 23

barriers to absorption: no significant barriers, just the capillary wall
absorption pattern: rapid or slow, determined by water solubility of the drug and blood flow to the site of administration
advantages: for parenteral administration of poorly soluble drug, administer depot preparations – effects can persist for days to months reducing # of injections
Ex. benzathine penicillin G – a month or more following injection
disadvantages: discomfort and inconvenience

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IM absorption characteristics

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barriers to absorption: no significant barriers, just the capillary wall
absorption pattern: rapid or slow, determined by water solubility of the drug and blood flow to the site of administration
advantages: for parenteral administration of poorly soluble drug, administer depot preparations – effects can persist for days to months reducing # of injections
disadvantages: discomfort and inconvenience

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SC absorption characteristics

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Barriers to absorption: layer of epithelial cells (must pass through cells) and the capillary wall (pass between cells)
absorption pattern: highly variable, factors contributing:
1. solubility and stability of drug
2. gastric and intestinal pH
3. gastric emptying time
4. food in the gut
5. coadministration of other drugs
6. special coatings on the drug
advantages: easy, convenient, inexpensive; no risk for fluid overload, infection, embolism; potentially reversible
disadvantages: variability – difficult to control onset, intensity, duration; inactivation (“first-pass effect”); pt requirements – conscious, cooperative; local irritation
*generally preferred to parenteral

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Oral route characteristics

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fastest to slowest
liquids --> suspensions --> powders -->capsules --> tablets --> coated --> enteric coated

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oral preparations

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fastest to slowest
IV --> IM --> SC --> Intrathecal --> epidural

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parenteral preparations

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-emergencies
-tightly controlled plasma drug levels
-for drugs destroyed by GI
-drugs that cannot cross membranes
-drugs that cause irritation to GI or mouth
-desire depot effect
-pt will not swallow drugs

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When would parenteral administration be preferred?

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when drugs contain the same amount of the identical chemical compound

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chemical equivalence

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if the drug is absorbed at the same rate and to the same extent

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bioavailability

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Movement of drugs throughout the body, as determined by blood flow to tissues, ability of the drug to exit the vasculature, ability of drug to enter cells.

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distribution

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transportation of drug molecules to active site by body fluids (also non active site!)

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distribution

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1. Cardiac output and regional bloodflow
2. Plasma-binding protein
3. Drug concentration
4. Physiologic barriers
5. Drug reservoirs (storage sites)

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Factors than influence distribution

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plasma-bind inactivates drug (can’t cause therapy)
reversible (then it causes therapy)
low to high affinity of drug for protein
nonspecific binding: protein + drug competitive binding
*too much free drug in blood can cause toxicity, because it’s actively therapeutic

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How dose plasma-binding protein - Albumin affect distribution?

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BBB – blood brain barrier
placental barrier
milk barrier

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What are physiological barriers to distribution?

Front 36

storage sites:
fat, bone, teeth, kidneys;
release drug long after administration

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What are drug resevoirs?

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-enzyme mediated modification of chemical structure of a drug. (* use biotransformation) metabolism is ALL chemical rxns, biotransformation is unique to substances that enter the body
-enzymatic alteration of drug structure (usually in the liver) – Hepatic microsomal enzyme system (P450) CYP1, CYP2, CYP3 metabolize drugs

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Biotransformation

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chemicals resulting from drug modification

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metabolites

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1.increase drug polarity for accelerated renal excretion (ionized)- convert lipid-soluble to polar; most important
2.drug inactivation - convert pharmacologically active compounds to inactive forms (nonreversible)
3.increased effectiveness
4.activation of prodrugs - pharmacologically inactive as administered, prodrugs get converted into their active forms via metabolism
5.increased or decreased toxicity

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5 therapeutic consequences of biotransformation

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Liver, placenta, kidneys, lungs, blood plasma, intestinal mucosa

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sites of biotransformation

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-microsomal enzymes (cytochrome P450 system)located in smooth endoplasmic reticulum
-12 closely related enzyme families
CYP1, CYP2, CYP3 - metabolize drugs
CYP4-CYP12 - metabolized endogenous compounds
- many drugs are metabolized by non-specific enzymes

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hepatic metabolism

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1.Age
2.Induction of enzymes
3. first pass effect or phenomenon
4. Nutritional status
5. Competition between drugs
6. Genetic variability in enzymes (pharmacogenetics)

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factors affecting biotransformation

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movement of drugs and/or their metabolites
from tissues ‡circulation ‡excretory organs
skin - sebaceous, lungs, liver, kidneys, colon

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excretion

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rate of removal of drug from body (amt/time)

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clearance

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passive diffusion from blood vessels in kidney in the t-tubule (place where blood meets urine)

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glomerular filtration rate

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renal excretion

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how most drugs are excreted

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drug is removed via bile into feces

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hepatic excretion

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drug metabolites are exhaled

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pulmonary excretion

Front 49

water soluble
ionized

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Forms of metabolites necessary for renal excretion - to get them out with the urine

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NOT lipid soluble; have uneven distribution of charge (water – electrons stay by the O rather than the H); but NO net charge

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polar molecules

Front 51

Not lipid soluble; have a net electrical charge (+ or -). Except for very small molecules ions are unable to cross membranes.

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ions

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1. passage through channels or pores (least common – too small)
2. passage with the aid of a transport system (most drugs lack a transport system that will help them cross)
3. direct penetration of the membrane itself (most common) – drug must be lipid soluble

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3 ways drugs cross membranes

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beyond therapeutic levels - side effects could be damaging.

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toxic concentration

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smallest amt to give effective therapeutic response.

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Minimum effective concentration (MEC)

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Between MEC and Toxic concentration

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Therapeutic Range

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This is a dynamic process that changes over time
Measure blood drug concentration (plasma drug level)
1. correlate with anticipated therapeutic response
2. assess absorption, distribution, metabolism, excretion

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how pharmacokinetics affect drug plasma levels

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1. Time course or time response
a. onset of action – time it takes to start to see therapy
b. peak serum level
c. time to peak action
d. duration of action

2. Plasma or biological half-life of drug
a. length of time required to reduce serum concentration by 50%
b. biotransformation and excretion

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time-course of single-dose administration

Front 58

how long and how many doses to reach plasma concentration plateau

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plateau principle of repeated drug administration

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usually double (take 2 pills right now, and every 12 hrs. take one; or give an injection and give the rest oral)

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loading dose principle of repeated drug administration

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once plateau is reached, how much to keep at plateau.

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maintenance dose principle of repeated drug administration

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Usual: 94% of drug will be eliminated in a time frame approximate to 4 half lives of the drug when drug administration is stopped.

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repeated drug administration: decline from plateau

Front 62

do not give a loading dose with these type of drugs

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low therapeutic impact

Front 63

-Noncharged
-lipid soluble and cross cell plasma membranes
-reabsorbed in kidney - not excreted
-need to be biotransformed to ionized form so that kidney can excrete

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nonionized

Front 64

-charged
-dissolution and absorption affected by pH
-water soluble
-do not readily cross plasma membranes
-positive charged: alkaloids, bases, and metallic radicals
-negative charged: acids and radicals
-ionized trapped by kidney and excreted

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ionized

Front 65

-drug inactive when bound
-drug can not cross plasma membranes when bound
-drug can not cross filter across kidney glomerulus when bound

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What happens when a drug is bound to a protein (albumin)?

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physiological response to a drug
mechanism of acton
the study of the biochemical and physiological effects of drugs and the molecular mechanisms by which those effects are produced.
-what drugs do to the body and how they do it.

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pharmacodynamics

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1. Drug action – drug-->target organ (or molecule) interaction
2. Drug effect – drug action-->body response
3. Drugs affect natural processes of body
4. Drugs DO NOT elicit new functions

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theories of drug action

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1. Chemical alteration intra or extra cell space
2. Physical alteration cell environment

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what nonspecific drugs do

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Drug receptor interactions
a. membrane protein, nucleic acids, lipids, enzymes, CHO residues
b. lock and key
c. affinity
d. agonist
e. antagonist

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what specific drugs do

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1. drugs can mimic the actions of endogenous hormones or neurotransmitters, and elicit a response; or
2. drugs can block the action of endogenous hormones or neurontransmitters and prevent a response.
*drugs can’t make a body do anything it isn’t already capable of doing (except gene Tx)

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What effects can happen when a drug binds to a receptor.

Front 71

any functional molecule to which a drug can bind to produce its effects.
USUALLY refers to the body’s own receptors for hormones, neurotransmitters and other regulatory molecules.

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receptor

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drugs that minic the body’s own regulatory molecules;
they activate receptors. Has high affinity and high intrinsic activity.

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agonist

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– drugs that block the actions of endogenous regulators; they prevent receptor activation by endogenous regulatory molecules and drugs. Has affinity but no intrinsic activity. Ex: drugs used to treat overdose (naloxone for opiods), antihistamines

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antagonist

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strength of attraction between drug and receptor. Drugs with high affinity can bind to receptors when present in low amounts and are effective at low doses – POTENT.

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affinity

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ability of the drug to activate the receptor once bound. Drugs with high intrinsic activity cause intense activity with low doses. It is reflected in its maximal efficacy.

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intrinsic activity

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A. Drug efficacy – ability to cause an effect
B. Drug RELATIVE potency – amount of drug for effect
C. Circadian rhythm - 24 hour body clock
D. Interethnic relationships - genetics

more potent drugs have a lower therapeutic index

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factors affection pharmacodynamics

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used to compare multiple drugs

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dose-response relationship curve

Front 78

Dose range that provides desired therapeutic effect with a minimum of adverse effects

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therapeutic index

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LD50 / ED50

lethal dose in 50% of subjects / effective dose in 50% of subjects

the larger the #, the safer

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therapeutic index

Front 80

A.Body size and weight
B.Gender
C.Age
D.Genetic factors
E.Ethnic differences
F.Pathophysiologic factors
G.Psychosocial factors
H.Nutritional factors
I.Environmental factors
J.Tolerance
K.Variability in absorption
L.Drug interactions
M.Compliance (failure to take medicine as instructed)

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factors that affect individual drug response

Front 81

any noxious, unintended, and undesired effect that occurs at normal drug doses. (maybe 4th leading cause of death?)
more common in elderly, very young, severely ill, and people taking multiple drugs (polypharmacy)

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Adverse Drug Reaction (ADR)
NOTE: terms used interchangeably - adverse drug reaction, iatrogenic, side-effect, toxic, idiosyncratic, drug-induced disease

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nausea, vomiting, dizziness, drowsiness, dry mouth, abdominal gas or distress, constipation, diarrhea

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most common adverse drug reactions

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Side effects
toxicity
allergic reaction
idiosyncratic effect
iatrogenic disease
tertogenic
mutagenic
carcinogenic
physical dependence

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Types of Adverse Drug Reactions

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nearly unavoidable secondary drug effect that occurs at therapeutic dose
predictable
effect is dose-dependent

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side effect

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caused by excessive drug dose or dosage
e.g. morphine coma

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toxicity

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immune mediated
prior sensitization
independent of drug dosage

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allergic reaction

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uncommon drug response due to genetic predisposition
e.g. CYP enzymes

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idiosyncratic effect

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disease produced by drugs
Dermatologic Hematoligic
Nephrotoxicity Hepatoxicity
Ocular toxicity Ototoxicity

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iatrogenic disease

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Modification of action of drug by another pharmacologically active CHEMICAL

response to drug combinations

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drug-drug interaction

Front 90

Complete summary of individual drug

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drug monograph

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Drug name- generic (Trade)
Drug Classification(s)
Pregnancy Category
Drug Schedule
Pharmacodynamics (Therapeutic actions, Actions, Mechanism of action)
Pharmacotherapeutics (Uses, Indications)
Contraindications (preexisting conditions that could lead to ADRs or affect therapeutic action; may chose not to use drug)
Precautions (life span, Pregnancy category, Proceed with caution observe carefully)
Pharmacokinetics
ADRs (side effects, undesired effects)
Interactions (drug, herb/supplement, environment, nutrition)
Patient Monitoring considerations (assessment, testing, evaluate)
Patient instruction issues (patient teaching points)

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drug monograph headings