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Patho 2023 > ADMET (EXAM 3) > Flashcards

ADMET (EXAM 3) Flashcards

1
Q

Identify the portions of a concentration vs. time curve that produce a pharmacologic effect

A
  1. onset (how quickly exhibits effect)
    - reaches MEC
  2. duration (how long it exhibits effect)
    - remains above MEC
  3. intensity (magnitude of pharmacologic)
    - max conc. or when highest
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2
Q

Provide a route of administration, identify barriers that may reduce the amount of drug that reaches the site of action.

A
  1. tissue barriers (blood brain barriers)
  2. can go through the barrier it is going through first
  3. most require 1 or more passage for the drug to cross the systemic circulation
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3
Q

define disposition

A

the fate of a drug after it has entered the systemic circulation

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4
Q

define pharmacokinetics

A

study of absorption, distribution, biotransformation, and elimination of xenobiotics

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5
Q

define pharmacodynamics

A

the study of the molecular, biochemical, and physiological effects of xenobiotics and their mechanisms of actions

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6
Q

what percent of drugs currently fail in clinical trials due to problems with ADME?

A

<10%

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7
Q

what are the primary routes of administration?

A
  1. renal via kidney (most drugs)
  2. bile (feces)
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8
Q

Describe the four potential consequences of drug metabolism (biotransformation) as it relates to pharmacologic activity

A
  1. Active drug to inactive metabolite
  2. Active drug to active metabolite
  3. Inactive drug to active metabolite
  4. Active drug to reactive metabolite
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9
Q

what is the fastest route of admin?

A

IV

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10
Q

what is the slowest route of admin?

A

oral

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11
Q

a reduction in the extent of absorption will impact what effect?

A

intensity

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12
Q

a reduction in the speed of entry will impact what effect?

A

onset

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13
Q

mechanism of a drug to its effects

A
  1. drug given
  2. released
  3. particles in fluid
  4. dissolution
  5. drug in solution
  6. degradation –> tissues –> effect
  7. absorption
  8. liver
  9. excretion
  10. central compartment
  11. distribution
  12. tissues
  13. effect
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14
Q

Name the factors that determine drug absorption across the membrane.

A
  1. Characteristics of the membrane
  2. Mechanisms of passage across membranes
  3. Dwell time of drug-membrane interface
  4. Physicochemical characteristics of the drug
  5. pH of the microenvironment
  6. Surface area of absorptive surface
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15
Q

Identify the site in the GI tract where most drug absorption occurs.

A

small intestine
- SA is increased with folds

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16
Q

Identify the mechanism by which nanoparticles cross biological membranes.

A

endocytosis

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17
Q

what is FICK’s law of diffusion?

A

when it undergoes passive diffusion, the transport rate should increase as the concentration increases

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18
Q

in contrast to simple diffusion, carrier-mediated transport is ___

A

both saturable and subject to competitive inhibition

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19
Q

Differentiate the two forms of carrier-mediated absorption: facilitated diffusion and active transport.

A

a. facilitated diffusion
– With concentration gradient only
– Conformational change
– No energy and involves transport proteins
b. Active transport
– May go against gradient
– Needs energy

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20
Q

Describe the impact of efflux transporters on drug absorption from the small intestine.

A
  1. Efficiently remove drugs from cells that have entered via passive diffusion
  2. Can reduce the amount of drug that accumulates in certain tissues, such as brain
  3. Increases the amount of drug absorbed with pgp
  4. Can either move solutes in or facilitate their movement out of the cell
  5. in to out
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21
Q

what are the mechanisms by which drugs cross the biological membranes

A

transcellular, paracellular, carrier-mediated transport (facilitated diffusion and active transport)

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22
Q

what is transcellular diffusion

A

→ driven by conc. gradient
- 95% drugs absorbed here
- Can be increased by
1. Removing ionized groups
2. Increasing lipophilicity
3. Reducing size
- Compromise between solubility and permeability necessary

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23
Q

what is paracellular diffusion

A

→ driven by conc. gradient
- Tight junctions between cells
–> Small channels
–> MW <180 Da (polar mol.)
–> Very few drugs
–> Toxins can open junctions
–> Selective openings can active oral absorption of insulin and other proteins

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24
Q

describe the effects of drug distribution on the conc. vs. time curve

A
  • Can be different for different people
  • When in plasma it can be readily distributed and restricted to that area and be a declining linear line
  • When in other areas it will move to other tissues as the plasma or other area is declining and make a small to big then decreasing curve
  • A drug only distributed in the vascular space will exhibit mono exponential blood conc. Vs. time curve after IV admin
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25
Q

what is perfusion rate limited

A

Readily penetrates endothelial membrane so that the delivery rate of the drug to the tissue by perfusing blood is what determines how quickly a drug will appear in tissue

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26
Q

what is permeability rate limited

A
  • Slowly passes across the endothelial membrane
  • Drug is delivered to tissues more quickly than moving to the blood then tissues
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27
Q

what is convection

A
  • Pressure is the driving force
  • Use of large molecules such as MABs
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28
Q

what is diffusion

A
  • Most drugs undergo here
  • Uses concentration gradient as driving force of movement
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29
Q

how can differences in pH result in drug trapping of drugs

A
  • When concentration of a drug within a tissues has pH differences that lead to ionization states of the drug to in the tissue environment
  • The inability for ionized drug to cross membranes can be used to enhance urinary excretion of drugs by changing urine pH
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30
Q

how can plasma protein binding effects distribution and effect of drugs

A
  • We want free drug as it can move back and forth
  • Drugs that are bound to RBCs, proteins, etc. can’t pass the membrane
    –>Blood brain barrier
    –Tight junctions have no permeation
    –Negative head groups limits diffusion for acids
    – High conc. of Pgp leads to high efflux activity
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31
Q

what are the 4 mechanisms drugs can reach the CNS

A
  • Appropriate physicochemical properties
  • Utilize an existing transporter
  • Disruption of BBB
  • Direct administration into the CNS
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32
Q

what molecule or drug is best for pregnancy women

A

large polar molecules

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33
Q

what are the 3 barriers of drug entry in the brain

A
  1. Blood-Brain Barrier
  2. Blood-Arachnoid Barrier
  3. Blood-CSF Barrier
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34
Q

Name the primary routes by which drugs are excreted from the body.

A

kidney(renal), biliary (feces)

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35
Q

Identify the processes involved in renal excretion

A

filtraction, reabsorption, secretion

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36
Q

what are the anatomical location s of the processes involved in renal excretion

A

filtration
- glomerulus
secretion
- proximal convoluted tubule
reabsorption
- distal convoluted tubule
biotransformation
- kidney and liver (vitamin D)

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37
Q

what are the mechanisms of hepatic elimination

A

metabolism and biliary excretion

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38
Q

Plot the relationship between MW and renal clearance.

A

Decrease in CLr with inc in MW

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39
Q

Plot the relationship between dose and urinary excretion rate for a drug that undergoes filtration only and one eliminated primarily through renal excretion.

A
  • With filtration only the excretion rate is an increase
    –> Increase in CLR with inc. in creatinine clearance
  • With active tubular secretion it increases but then reaches a saturation point due to being a carrier-mediated process
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40
Q

Plot the relationship between MW and percent excreted in the bile.

A

As MW inc. Bile inc.

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41
Q

Describe the impact of enterohepatic recirculation on drug half-life in the body.

A
  • EHR will increase the half-life because of it getting reabsorbed and continuing the process of reabsorption from the intestine
  • If used with some bile binding agent the half-life will decrease because it is not reabsorbed
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42
Q

what is the first-pass effect of pre systemic circulation

A

all blood from stomach and small intestine flow to the portal veinal absorbed drug passes through the liver before entering the rest of the body. if drug is metabolized or excreted in bile unchanged, a significant fraction of the dose may be eliminated before entering the systemic circulation

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43
Q

what is the passage of drug from the blood to the liver

A
  • from hepatic vein or artery from sinusoid
  • out to in
  • active transport
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44
Q

why are transporter proteins important

A

uptake and efflux from the blood and transport to bile

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45
Q

how does bile move

A

in to out

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46
Q

where does bile get collected

A

hepatic duct (canaliculi)

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47
Q

what is the passage from the liver to the intestine

A
  1. bile moves via hepatic duct to gall blader
  2. bile stored and concentrated in gall bladder
  3. bile released in intervals from gall bladder into intestine
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48
Q

what are the classes of agents

A

a,b,c

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49
Q

what is the enterohepatic cycles

A

small intestine –> portal vein –> liver –> bile duct
–> repeat

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50
Q

what is pulmonary excretion

A

any volatile compound that has potential for pulmonary excretion
- simple passive diffusion

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51
Q

what are other routes of excretion

A

hair, sweat and saliva, milk, tears

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52
Q

Describe how the physicochemical properties of a drug influence its filtration by the kidney

A
  • Located in the glomerulus
  • Determinants
    – Number of functional nephrons
    – Molecular size
    – >MW < or equal to 5000
    – Protein binding
    – Renal blood flow
53
Q

Describe how the physicochemical properties of a drug influence its, secretion by the kidney

A
  • Involves transporters
  • Is a carrier-mediated process
    » Saturable and involves competitive interactions
  • Also undergo stereoselective renal excretion
54
Q

Describe how the physicochemical properties of a drug influence its reabsorption by the kidney.

A
  • Passive reabsorption (most drugs)
    »Driven by conc. gradient
    »Determined by lipophilicity, pKa of drug
    »Influenced by urine flow and urine pH
  • Carrier-mediated reabsorption
    »Saturable (capacity-limited)
    »Ascorbic acid, glucose are examples
  • The high fraction of filtrate reabsorbed results in a marked conc. Of solutes that remain in the tubules
  • As solutes transverse to tubules, conc. Due to reabsorption of water
    »Fluid below one favors plasma
    »Fluid above one favors tubular fluid
  • Contributes to poor relationship between ascorbic acid and plasma conc.
55
Q

what is the optimal MW for biliary excretion

A

> 300-400
- optimal 500-600

56
Q

name the primary organ in drug metabolism

A

the liver

57
Q

what are the 2 phases of drug metabolism

A

phase 1 and phase 2

58
Q

what is phase 1 drug metabolism

A

Biotransformation of xenobiotics that includes oxidation, hydroxylation, and related changes that either introduce or expose a functional group

59
Q

what is phase 2 drug metabolism

A

Biotransformation of xenobiotics that involves conjugation with a polar group yielding a polar metabolite that can be more readily excreted in the bile or urine
–>Sometimes referred to as conjugation reactions and can be influenced b the availability of the co-substrate

60
Q

primary substrates for CYP3A4

A

midazolam, indinavir

61
Q

primary inducers for CYP3A4

A

rifampin, st. johns wort

62
Q

primary inhibitors for CYP3A4

A

ritonavir, ketoconazole

63
Q

substrates for CYP2D6

A

codeine, fluoxetine

64
Q

inhibitors for CYP2D6

A

fluoxetine, quinidine

65
Q

inducers for CYP2D6

A

no clinical relevance

66
Q

substrates for CYP2C9

A

ibuprofen, s-warfarin

67
Q

inducers for CYP2C9

A

rifampin, secobarbital

68
Q

inhibitors for CYP2C9

A

fluconazole, amiodarone

69
Q

Given a specific CYP450, identify the subfamily, family, individual gene, and allelic variant.

A
  1. superfamily –> CYP
  2. sub family –> first number
  3. family –> letter after number
  4. gene –> second number
  5. allele –> the number&letter after *
70
Q

describe reversible inhibition

A
  • Sometimes metabolite
  • Compete with substrates for binding at or near the active site of the enzyme.
    –> Similar to receptor antagonist
  • Nitrogenous compounds that can serve as the sith axial ligand for iron in the heme are especially potent inhibitors of CYP450
    –> Stronger affinity
  • Additional hydrophobic contacts stabilize ligand-protein binding
71
Q

describe irreversible inhibition

A
  • Mechanism-based inhibition
  • Metabolism of substrate generates reactive metabolite that irreversibly interacts with the heme or residues in the binding site
  • further metabolism of same or other drug is delayed as CYP needs to be resynthesized so it has the longest lasting inhibition
72
Q

Explain why an enzyme inducer may increase the metabolism of the drugs metabolized by different CYP450s.

A
  • It can exhibit cross-talk
    –> Induce expression of several different families and subfamilies of CYP450 enzymes
    –> Can turn on multiple genes from substrates binding to receptor and turning on many CYPs
73
Q

Provided a reaction, name the phase 2 metabolic process.

A
  • UGT
    –> Chair conformation form
  • SULT
    –> Adds a sulfate
  • NAT
    –> Adds the double bonded o and methyl
74
Q

Explain why genetic variation in metabolism is often the most important factor in determining variation in drug concentrations

A

-It can be an important determinant of the variability of drug metabolism, other sources of variability are often more important than genetic variation
-So many things contribute and modulate the metabolism of drugs

75
Q

what are the factors determining binding strength in reversible inhibition of CYP450

A
  1. Coordination
    –> Strength with heme iron
  2. Hydrophobic
    –> Contacts with site of CYP
  3. Specific contacts
    –> Binding site residues
76
Q

deine toxicology.

A

The study of the adverse effects of chemical or physical agents on living systems

77
Q

define toxin and examples

A

Toxin: a poisonous substance produced by living cells
Examples: venoms, mycotoxins, microbial toxins, alkaloid, marinobufagenin

78
Q

define toxicant and examples

A

Toxicant: a man-made chemical introduced into environment that produces toxic effects on living cells
Examples: bisphenol, dioxin, ethylene glycol, sarin, phosgene, carbon tetrachloride

79
Q

what is descriptive toxicology

A

Descriptive: identify phenotypic changes resulting from exposure to toxic substances
Is it toxic?

80
Q

what is mechanistic toxicology

A

Mechanistic: identify how toxic substances alter normal cellular function
Why is it toxic?

81
Q

what is regulatory toxicology

A

Regulatory: assess the safety of exposure levels of toxic substances
What should we do about it?

82
Q

local vs. systemic

A

Local: effect observed at site of contact or portal of entry (confined area)
Systemic: effect observed at site distant from contact or portal of entry

83
Q

immediate vs. delayed

A

Immediate: seconds to hours
Delayed: days to years

84
Q

reversible vs. irreversible

A

Reversible: effects abates after stopping exposure
Irreversible: effects persists after stopping exposure

85
Q

wha tare the 3 phases of toxic responses that are ongoing

A

Exposure
–> Source (how were they exposed?)
Disposition
–> More complex with it varying in tissues and reservoirs with differ toxicology
Toxicodynamics
–> The cellular response

86
Q

what are the 3 means by which toxic responses may be mitigated

A
  1. prevent/ reduce exposure
  2. Enhance elimination in body
  3. block/ repair cellular effects
87
Q

what are the 3 levels of risk-benefit analysis that can occur related to drug therapy?

A

accessibility, acceptability, applicability

88
Q

what is accessibility?

A

FDA evaluates benefits/risks for the population

89
Q

what is applicability?

A

Provider evaluates benefits/risks for a patient

90
Q

what is acceptability?

A

Patient evaluates benefits/risks in terms of personal values

91
Q

State 3 elements of info needed for application of an investigational new drug with FDA.

A
  1. animal pharmacology and toxicology
  2. manufacturing information
  3. clinical protocol and investigator information
92
Q

What are the steps to predict the first dose in man for a new drug?

A
  1. Determine NOAEL in appropriate animal species
  2. Calculated human equivalent dose (HED) from appropriate species
  3. Determine a safety factor ( usually 10 )
  4. Divide HED by safety factor to determine max recommended starting dose
93
Q

what is NOAEL

A
  • no observable adverse effect level
  • highest dose where it has no effect
94
Q

what is MABEL?

A
  • Minimal anticipated biological effect level
  • Needed to result in biological effect in participants of a clinical trial
95
Q

Identifying primary reasons adverse drug events are often not detected until after the drug is approved and marketed for a period of time.

A
  1. rare events vs. patient numbers in clinical trails
    –> Only 10,000 or less people studied and sometimes we don’t get information until 100,000s of people
  2. common events vs. patient numbers and duration in clinic trials
96
Q

Provided key info about potential pharmaceutical excipients determine whether or not preclinical studies are needed in dosage form.

A
  1. GRAS
    - generally recognized as safe
    - a group of compound whose safety in humans has been established through careful studies or widespread use
    - if included in a drug formulation as excipients, specific toxicology data is not needed for those compounds
97
Q

Name 5 categories of preclinical studies completed for new drug development.

A
  1. acute studies
  2. repeated dose studies
  3. genetic toxicity
  4. reproductive toxicity
  5. carcinogenicity
98
Q

what are acute studies?

A
  • effect of single dose
  • at least 2 species
99
Q

what are repeated dose studies?

A
  • length depends on anticipated therapy
  • at least 2 species
100
Q

what is genetic toxicity?

A
  • determine likelihood compound is mutagenic or carcinogenic
101
Q

what is reproductive toxicity?

A
  • needs depends on target population
  • multiple species
102
Q

what is carcinogenicity?

A
  • only for compounds used in chronic or recurring conditions
103
Q

what are the three ways to identify the nature of adverse reactions?

A
  1. side effects
  2. augmented response
  3. toxic reactions
104
Q

describe side effects.

A
  • off target response
  • marginal impact on health
  • impact patient compliance
  • Ex: dry mouth with antidepressants
105
Q

describe augmented responses.

A
  • extension of pharmacologic effect
  • usually dose-dependent
  • May impair health seriously
  • Ex: bradycardia with propranolol
106
Q

describe toxic reactions

A
  • Not predicted pharmacology of drug
  • sometimes not dose-dependent
  • seriously impact health
  • Ex: carbamazepine-induced liver injury
107
Q

Given a cell type that experiences genomic damage, identify clinical outcome.

A

somatic cells, germ cells, and developing embryos

108
Q

what do somatic cells do?

A

Cancers
Depends on route of exposure

109
Q

what do germ cells do?

A

Birth defects
Childhood cancers

110
Q

what do developing embryos do?

A

Miscarriages
Stillbirths
Birth defects
Occasional childhood cancers

111
Q

Provided specific gestational stages of women, identify whether a teratogen is likely to result in 1) embryo death, 2) major congenital anomalies, 3) functional defects and minor anomalies.

A

Embryo death
–> 1-2 weeks
Major congenital anomalies
–> 3-8 weeks
Function defects and minor anomalies
–> 9-38 weeks

112
Q

State the criteria for classification of an agent as a teratogen.

A
  1. Exposure results in characteristic set of malformations
  2. Effect occurs with exposure at a specific stage of development
  3. Effect is dose-dependent
113
Q

what are the mechanisms by drug producing toxic responses?

A

cellular dysfunction, cellular destruction, and genotoxicity

114
Q

what is cellular dysfunction

A
  1. Disruption of normal cellular function that does not result in embryo death
  2. Inc. in oxidative stress → inc in methemoglobin
  3. Dec. in G6PD → inc. methemoglobin
115
Q

what is cellular destruction

A
  1. Dysregulation of cellular process provoked by a toxicant resulting in the death of the cell
  2. Primary Targets:
    –> ATP depletion
    –> ROS/RNS generation
    –> Ca2+ accumulation
116
Q

what is genotoxicity

A
  • Damage to genetic material caused by an external agent
    –> Could have replication, transcription, cell division, synthesis, etc.
117
Q

what are some determinants of toxic responses

A
  1. Individual susceptibility
    –> Diet, genetics, environment, underlying disease
  2. Accessibility of drug to target
    –> ADME
    –> Blood stream
  3. Compensatory mechanisms
    –> Acidosis or alkalosis
  4. reactivity of drug with target
118
Q

what are the roles of reactive metabolites in drug response and their pathways and actions

A
  • There are 3 pathways
    –> Sulfate
    –> Liver injury
    –> Glucuronide
  • Is we deplete or induce one of the pathways it will either cause liver injury or it will not or if we inhibit CYP2E1 then it will reduce injury
    –> Depends
119
Q

define drug induced hypersensitivity

A

A low frequency serious adverse drug reaction with an immunological etiology to an otherwise safe and effective therapeutic agent

120
Q

what are the 4 characteristics of DIHR

A
  1. rare (implications)
  2. unpredicatable
  3. complex
  4. potentially fatal
121
Q

what are the 2 types of DIHR

A

immediate and delayed

122
Q

what is immediate hypersensitivity

A
  • occur within 1 hour
  • TYPE 1
  • IgE-mediated
123
Q

what is delayed hypersensitivity

A
  • occurs >1 hour
  • TYPE 3 and 4
  • T cell mediated
124
Q

State 2 primary reasons most people who claim to have an allergy to penicillin can tolerate it.

A
  • 50% of people with IgE-mediated PCN allergy lose sensitivity within 5yr; >80% by 10 yr
    –> loss of immunological memory
  • Some patients, rash caused by concurrent viral infection
125
Q

State 2 phases of DIHR.

A

sensitization
- may occur from prior exposure or earlier in the course of therapy for repeated dosing
effector
- hapten/antigen re exposure

126
Q

Identify the most common organ affected by DIHR.

A

the skin is the most common

127
Q

Describe how DRESS is differentiated from other DIHR.

A

CHARACTERISTICS: fever, skin rash, lymphadenopathy, hematological abnormalities, and internal organ involvement
ONSET: 2-8 weeks after start of therapy
MORTALITY: 10%
- Anticonvulsants, antibiotics, and allopurinol
STANDS FOR: drug reaction with eosinophilia and systemic symptoms

128
Q

State the time frame at which most drug eruptions occur.
EXANTHEMAS

A
  1. onset 4-14 days after therapy
  2. last 1 week
  3. self-limiting
  4. virus caused
    –> From penicillins, etc.
129
Q

State the time frame at which most drug eruptions occur.
TEN, SJS, ERYTHEMA MULTIFORME

A
  1. distinct reactions
  2. onset 1-3 weeks after start of therapy
  3. mortality is 10-30%
  4. causative agents: allopurinol, seizure meds

Patho 2023 (37 decks)

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