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PHRM 828 > Knipp 2 > Flashcards

Knipp 2 Flashcards

1
Q

coatings

A

control diffusion rates by modulating release properties

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2
Q

solid coatings

A

protect agent from air/humidy
mask taste
provide special drug release
aesthetics
prevent inadvertant contact w/ drug

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3
Q

aqueous coatings

A

film-forming polymers
plasticizers for flexibility and eslastic
colorant and opafier
vehicle

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4
Q

disinigrants

A

control regions of release based on physiological properties

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5
Q

lubricants

A

can slow dissolution based on properties

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6
Q

internal excipients

A

used to modify the release rate as well: swellable matrices, non-swelling matrices, inert plastics

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7
Q

enteric coating

A

add to dosage form to prevent early release of API.
1. prevent acid sensitive API from gastric fluids
2. prevent gastric distress from the API
3. target API delivery to site in intestine
4. to provide delayed/sustained release
5. deliver API in higher local conc in intestine for better absorption

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8
Q

sustained release

A

pharm dosage form to slow release therapeutic agent such that appearance in systemic circulation is delayed/prolonged. AKA onset pharmalogic action is delayed but therapeutic effect has sustained duration

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9
Q

controlled release

A

goes beyond sustained release and reproducibility/predictability

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10
Q

examples of traditional controlled release formulations

A

coated beads, granules, microspheres: coating on the beads controls release by programmed erosion
multitablet system: small tabs placed in gelatin
microencapsulated: solids, liquids, gases encapped in walled material allowing microparticles across surface
drug embed in slow eroding or hydrophilic matrix: drug is homogenously dispersed in eroding matrix and release is controlled by eosion rate

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11
Q

steady state

A

rate going into the body must be equal to diposition (rate distributed/metabolized/excreted throughout the body)

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12
Q

characteristics of drugs best for oral controlled release

A

either slow/fast rate of absorption/secretion
uniformly absorbed from GI tract
administered in relative small doses
have good safety/therapeutic window
chronic therapies better suited than acute

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13
Q

physiological factors affecting absorption

A

absorbing surface area
residence time at absorption site
pH changes in lumen (unionized will get absorbed)
permeability
dietary fluctuations/effects
complexation/protein binding
biliary uptake and clearance

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14
Q

epithelia

A

predominantly used for external surfaces although endothelial cells are epitheliod
simple squamous
simple columnar
translational
stratified squamous

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15
Q

composition of bio membranes

A

most of surface area
all living cells are enclosed with 1+ membranes
membrane isolates cellular components from environment
cell membrane is semi-permeable membrane, permits rapid passage of chemicals while slowing others
cellular lipid composition is polarized, so outter is different from inner

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16
Q

cholesterol effects on membrane?

A

no. it provides fluidity at lower levels. when exceeds a certain level in membrane, it causes a phase of transition and forms liquid crystalline state. called hardening atherosclerosis when occurs in vasculature

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17
Q

intestinal transport mechanisms

A

passive(non saturable): paracellular (between cells), transcellular (through cells)
carrier-mediated(saturable): active (energy), facilitated diffusion (no energy)

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18
Q

general interpretation of caco-2 vs pampa

A

passive difussion
has linear relationship between active transport and efflux

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19
Q

drug transporters

A

membrane-bound proteins involved in clearance
role is to move important molecules across membranes
crucial determinant of tissue and cellular distribution of drugs
variation can be determinant of drug response
primarily been identified in adults

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20
Q

SLC (solute carrier)

A

43 subfamilies
300 members identified
generally influx or secretory efflux transporters

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21
Q

ABCs

A

7 subfamilies
50 members
generally efflux-multidrug resistant transporters
PgP, MRPs

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22
Q

Absorption

A

many routes of permeation:
influx transport mediated
passive transcellular influx + efflux
passive paracellular
metabolism
efflux of the metabolite

23
Q

conventional terminology

A

influx: transporters transfer into cells
efflux: transporters pump substrate out of cell back into compartment
absorptive: transporters transfers substrate into systemic blood
secretory: transporters transfer their substrates from blood into bile, urine, GI lumen

24
Q

passive paracellular permeation

A

hydrophilicity
molecular size + shape
pKa of ionizable groups
linear increase in permeability w/ increasing conc
adjuvants can open tight junctions

25
facilitative/active trans permeation
affinity, Vmax concentration dependent saturation expression level function(drug-drug & drug-nutrition interactions, competitive inhibition) exicpeints like surfactant can limit effects of efflux by PgP or BCRP
26
GI tract epithelia
oral cavity-buccal esophagus is comprised of strat squamous stomach is mainly columnar epithelial w/ mucus goblet cells small and large intestines have columnar epithelial cells rectum is best place for absorption w/ simple columnar and strat sqamous epithelia
27
stomach
digest food and control flow into intestine fast pH is <3 fed pH is 5-7 gastric emptying half-time is ~30 mins fasted emptying has 4 phases fed has no cycles
28
stomach anatomy
fundus - contains gas and produces contractions body - reservoir for ingested food and fluids antrum - lower part of stomach controls flow into small intestine
29
stomach phases
1) no activity 40-60 mins 2) mixing contractions 40-60 mins 3) stomach: powerful contractions intestine: peristalsis 4) stomach empty of digestible and indigestible food
30
intestine
mouth-anus: 24-32 hrs most absorption occurs in small intestine small intestine pH 5-6.5 colon drug absorption mainly occurs in ascending region nearest to SI
31
intestinal surface area
kercking folds villi microvilli all increase SA of SI
32
columnar epithelium
continuous layer of absorptive cells Crypt region: 3x more crypt than villi, comprised of undifferentiated cells that proliferate. globlet cells-mucus secreting Villus region: absorptive enterocytes, a few goblet cells do appear. cells from crypt migrate to villus tip and are extruded at tip lifetime of 2-3 days
33
colon characteristics
125 cm from caecum to anus responsible for water and electrolyte absorption to prevent dehydration and leads to formation of solid fecal matter
34
colon structure
serosa-squamous epithelium covered with adipose tissue submucosa and mucosa colonic mucusa: three layers-- muscularis mucosae, lamina propria, epithelium proximinal(ascending) colon is where enteric formulations target by oral admin distal colon: rectal + suppositories
35
anal muscles with age
as people age, anal muscles slow down their function
36
stomach vs. colon
stomach and colon have inverse relationship with drug concentration. as it decreases in the stomach, it increases in the colon
37
rectum
upper and lower region that transitions to strat squamous. stratified squamous, non-keratinized allows high drug absorption lots of high potency drugs that are delivered rectally gag reflex w/ pills so use suppositories
38
anal absorption
crystalline: form-low solubility amporphous: increased solubility free API: potential confounders are food, protein binding, pH, etc.
39
GI characteristics
GI volumes do not correspond with dissolution bath volumes
40
GI transit time variation
gastric residence differs a lot gastric emptying controls colonic absorption higher GI residence leads to higher absorption PT 2 has higher GI so capsule was voided much faster
41
GI transit fed state
capsule was admin 30 mins before breakfast and 4 hrs before lunch but gastric pH and residence changes still occurred
42
characteristics of GI fluids
jejunum: pH 7.08 ileum: pH 7.8 colon: pH 8.1
43
drug solubility changes in GI tract
factors influencing drug solubility: buffer capacity bile salts regional fluids other drugs potential issues from endogenous substrates
44
stomach emptying blood flow
stomach>jejunum 1> jejunum 2 > ileum 1> ileum 2> ileum 3> ileum 4> colon drug diffuses out, gets released, metabolized
45
challenges to assumptions of GI
transporters and enzymes vary in GI a lot of variability in GI fluid diet and chemical exposure vary pharmacogenetics and genomics are issues inter individual variation drug-nutrient + drug-drug interactions gut microbiome SO ONE SIZE FORMULATION DOES NOT FIT ALL
46
ADMET
Absorption Disposition: comprised of distribution and elimination Elimination: describes metabolism and excretion Toxicity: result of exposure
47
ADME
Absorption, Distribution, Metabolism, Excretion Drug is dissolved through intestinal tract Absorbed through portal vein to liver then blood then tissues Throughout these processes, theres metabolism of drug and excretion of it
48
Nature of pharmacokinetic processes
described by concentration time profiles: shape of profiles depend on conc compartments represent kinetically similar tissue/space processes can be reversible or irreversible processes can be linear or nonlinear fast and slow processes tend to disappear
49
blood level versus time curve
upward slope is absorption peak is Cmax + Tmax after peak is distribution, metabolism, excretion downward slope is disposition and elimination phase
50
biopharmaceutics terms
bioavailability - rate and extent of drug absorption absolute bioavailability - AUC of dosage compared to auc of same dose injected intravenously relative bioavailability - AUC of dosage form compared to arbitrary reference standard bioequivalent - does not mean therapeutic effects of two dosage forms are equivalent
51
concept and use of dose
amount of chemical in which organism is treated local concentration of the chemical at the biol response state relationship between dose and receptor concentration is a function of ADME
52
dosage form design
aborption begins declining as disposition begins to increase absorption rate Kabs is defined by drug properties of excipients/drug formulation and the physiological barriers between GI and systemic circulation
53
disease plasma levels
plasma levels peak in therapeutic window prolonged exposure to subtherapeutic doses or ineffective drugs can lead to development of disease becoming worse
54
dose relationship to toxic response
toxic repsonse - blood plasma is toxic level/ MTC safe and efficacious - blood plasma in therapeutic window/TW non efficacious - blood plasma not reached therapeutic level/ MEC

PHRM 828 (7 decks)

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