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Psychopharm > unit 1 > Flashcards

unit 1 Flashcards

1
Q

pharmacology

A

study of the action of drugs in organisms

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2
Q

neuropharmacology

A

drug induced changes in functioning of nerve cells

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3
Q

psychopharmacology

A

drug induced changes in behavioral responding

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4
Q

neuropsychopharmacology

A

drug induced changes in the function of select neurons that influence specific behaviors

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5
Q

drug action

A

molecular changes within cells produced by the drug binding to a particular target site/ receptor (VERY specific)

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6
Q

drug effect

A

molecular changes within and between cells that lead to alterations in physiological/ psych function (broader)

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7
Q

therapeutic effects

A

drug/ receptor interactions that produce the desired physiologic and or behavioral effect(s)

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8
Q

side effects

A

all other drug effects varying from annoying to deadly

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9
Q

specific drug effects

A

due to physical or biochemical interaction of a drug with a target

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10
Q

nonspecific drug effects

A

not based on drug/ target interaction due to individual characteristics (influences by experience or attitude or varied neurochemical state at time of exposure
-ex= placebo effect

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11
Q

pharmacokinetics

A 
how drugs move through the body (speed/ duration)
-multiple factors influence drug action in CNS
main factors:
-route of admission
-absorption and distribution
-binding characteristics
-inactivation
-elimination from system
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12
Q

proximal small intestine

A

most drugs are absorbed here (first 12 inches) and can take longer to absorb if food (especially fatty) is in way

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13
Q

enteric-coated formulations

A

used for drugs inactivated at low pH (coating protects drugs from stomach acid)`

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14
Q

buffered formulations

A

used for drugs that increase stomach acidity

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15
Q

absorption

A

drug movement from the site of administration to blood circulation

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16
Q

oral administration (PO)

A

most popular, safe, cheap, easy

  • capsules, pills, tablets, liquids
  • must dissolve in stomach and pass to small intestine and MUST be resistant to strong acids and enzymes in stomach
  • most PO drugs aren’t absorbed until reach SI
  • amount of food influences speed of absorption
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17
Q

first pass effect

A

PO drugs absorbed into blood stream go directly to liver and metabolism here reduces the amount of drug available to circulation and so concentration in blood is irregular and difficult to predict

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18
Q

intravenous administration (IV)

A

most rapid and accurate method (avoids first pass effect)

  • best for Med; worst for illicit
  • quick onset leaves little room for corrective measures
  • easy monitoring
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19
Q

intramuscular administration (IM)

A

slow and even delivery of drug (absorption usually 10-30 min post-injection); non-aqueous additives (lipophilic) provide slow release; often painful
-common IM sites= deltoid, ventrogluteal, rectus femurs, vastus lateralis

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20
Q

subcutaneous admin (SC)

A

absorption dependent upon blood supply to the site (point of injection); often slow and steady oil delivery (insulin at waist)

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21
Q

gaseous (inhalation) admin

A

rapid absorption due to large surface area of pulmonary capillary system (most dangerous for illicit bc hard to fix); quick drug onset

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22
Q

topical admin

A

direct application to mucosal membranes (nasal, vaginal, ocular, colon)= rapid absorption and rapid effects

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23
Q

transdermal application

A

slow absorption bc skin is a barrier for aqueous and need lipophilic… transdermal patches= lipids; controlled and sustained method

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24
Q

excipients

A

chemicals added to drugs to allow drugs to exist in diff forms
-formulation controls rate of delivery ONLY when liberation rate is less than absorption rate

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25
Q

bioequivalence

A

if two drug formations have equal bioavailability and rate of absorption then the resulting plasma level will be similar

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26
Q

tolerence

A

dose-dependent phenomenon (less tolerant to PO drugs)

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27
Q

rate of drug passage

A

=across various cell layers between sit of admin and blood is the single most important factor in determining plasma drug levels

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28
Q

lipid-soluble drugs

A

move across membranes via passive diffusion
-movement down concentration gradient
-depends on concentration gradient and lipid solubility
(extremely hydrophobic and hydrophilic don’t diffuse as easily because they get stuck in the plasma membrane)
-diffusion occurs in steps (two barriers= hydrophilic heads on both sides of the membrane)

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29
Q

salt forms of drugs

A

substitute hydrobromide/ sulfate for hydrogen

  • useful for long-lasting drugs (popular, many applications, save money and time)
  • dosage delivery can be an issue (drug weight includes the salt- less drug)
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30
Q

drug acidity

A

closer to neutral the drug is, the easier it is to be absorbed

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31
Q

drug ionization characteristics (pKa)

A

weak acids ionize more in basic environment- weaker acids ionize less in acidic environment

  • highly ionized drugs are poorly absorbed in body and cannot be admin orally
  • drugs closer to non-ionized the better (increases movement and goes into cells)
32
Q

distribution of drug influences

A

blood flow and diffusion of drug out of circulation to target sites
and selective barriers to diffusion

33
Q

apparent volume (Vd)

A

describes distribution ability of drug to the body- heavily influenced by lipid solubility (greater Vd= increased lipid solubility)
Vd= amount of drug that leaves circulation and enters the body (defined in L)
-total body volume= 42L, so drug with Vd=42L will distribute to the whole body

34
Q

first phase

A

due to preferential blood flow to brain, it receives blood first and drug conc in blood decreases as drug conc in brain increases

35
Q

second phase

A

due to drug solubility in other body tissues

  • drug entering other body tissues reduces overall drug concentration in the blood
  • drug leaves brain for blood
36
Q

third phase

A

drug leaves blood to enter fat stored in reservoir

37
Q

redistribution

A

process of drug leaving one site for another based on blood flow and lipid solubility

38
Q

blood brain barrier

A

vascular endothelial cells- connect by tight junctions and secrete basement membranes (tight junction and basement membrane force mcls to diffuse through matrix, which forces bigger toxins to not enter)

39
Q

astrocytes

A

project astrocytic feet around basement membrane- together they form the barrier to diffusion of polar molecules (force drugs to diffuse across basement membranes)

40
Q

fenestration

A

molecules can leave blood through these gaps in capillary covering

41
Q

chemoreceptor trigger zone

A

area postrema- has no BBB, so it can sense toxins and cause emesis (vomiting)- has 5HT and DA receptors

42
Q

plasma binding

A

in blood- affects distribution and alters extent and duration of drug action

  • drug binding in blood occurs at inactive sites and these are called drug depots= plasma proteins in blood that bind drugs
  • only unbound drugs can diffuse across membrane
  • binding to drug depots is non-selective (competition between drugs with diff affinities)
43
Q

drug metabolism

A

breakdown of drugs by the microsomal system (p450 system) in liver- several isoforms of enzymes exist and large gene family leads to variability

44
Q

pharmacogenetics

A

study of inherited genetic differences in drug metabolic pathways- which can affect individuals

45
Q

two phases of biotransformation

A

phase 1- oxidation, hydrolysis, reduction of parent structure; slight charge; usually not enough to metabolize drug from system
phase 2- conjugation w glucuronide, sulfate, acetate, or amino acid; produces highly ionized, biologically inactive molecules

46
Q

drug half life

A

time it takes for removal of 50% of the drug in blood

47
Q

first order transformation (kinetics)

A

drug clearance rate proceeds exponentially
=enzymes are in excess and the concentration of the drug determines rate of biotranformation
-rapid clearance from system

48
Q

zero order transformation

A

drug clearance rate is FIXED- around of drug to transform exceeds the concentration of converting enzymes (rate depends on amount of enzymes)
-slow clearance

49
Q

factors influencing drug metabolism

A
  • enzyme induction
  • enzyme inhibition
  • drug competition
  • individual characteristics
50
Q

enzyme induction

A

increase in concentration of enzymes available for biotransformation

  • increase in biotransformation rate of all drugs in system
  • ex= excessive alcohol use leads to increased enzyme activity
51
Q

enzyme inhibition

A

some drugs directly inhibit metabolizing action of enzymes- decrease in biotransformation rate of all drugs in system; decrease in the biotransf rate of other naturally occurring biomolecules

52
Q

drug competition

A

some drugs share metabolizing enzymes

  • decrease in biotransformation rate of both drugs in a system
  • produce potentially dangerous drug interactions (both need enzymes and set number of enzymes, decrease rate of clearance)
53
Q

individual characteristics

A

individual genetics characteristics/ environment differences that can decrease or increase the biotransf rate of drugs in a system

54
Q

pharmacodynamics

A

study of physiological and biochemical interactions of a drug with target tissue that is responsible for the drugs effects

  • drugs change the system over time
  • membrane bound receptors have local effect, cellular receptors often change genetic info and cause widespread effects
55
Q

first (traditional) view of ligand

A

receptor interaction= IONOTROPIC

  • lock and key model
  • ligand binds to R, conformational change, ions can enter
56
Q

second view of ligand

A

receptor interaction= METABOTROPIC
-most common.. Rs have acceptor site for ligand and binding causes cascade of action; results in synthesis of secondary messengers (cAMP, DAG, Ca2+)

57
Q

agonist

A

binding produces specific cellular response= mimic= potent

58
Q

antagonist

A

doesn’t produce cellular response= blocks

59
Q

dose response curve

A

describes the amount of biologic/ behavioral effect for a given drug concentration
(increased dose= more receptors occupied and more response seen)

60
Q

ED50

A

produces half the maximal effect (50% effective dose)

  • drugs with different potencies have differing ED50s
  • drugs with different response curve slopes have different mechanisms of action
61
Q

TD50

A

does at which 50% patients experience toxic effect- can have multiple TD50s for differing effects

62
Q

therapeutic range (TR)

A

gives working range of plasma levels- minimum plasma concentration which benefits vs minimum plasma concentration which is toxic

63
Q

therapeutic index

A

calculates the margin of drug safety

=TD50/ED50

64
Q

direct acting agonist

A

affinity and efficacy (potency) at NT-R site

  • binds R and mimics NT action
  • R subtype selective (DAD2 agonist
  • R subtype non selective (D1 and D2 agonist)
65
Q

indirect acting agonist

A

enhances NT action at R but indirectly

  • do not bind receptors but do activate them
  • ex= drugs that increase levels of endogenous Its/ extend availability over time)
66
Q

direct acting antagonist

A

affinity but no efficacy- bind Rs but do not produce biologic action

67
Q

competitive antagonist

A

ligand binding at receptor site- competes with natural NT for binding site (can be reversible or irreversible (deadly toxin))

68
Q

non-competitive antagonist

A

binding to regulatory site on R to inhibit access of NT to R

-antagonists increase overall NT amount (left in synapse bc can’t bind)

69
Q

indirect acting antagonist

A

decreased action of NT at receptor

-decreases naturally occurring NTs

70
Q

tolerance

A

chronic drug use can change drug potency in body= usually the more you take the less response you are to it

71
Q

pharmacodynamic tolerance

A

due to chronic drug exposure
-decreased potency due to decrease in efficacy through which drug carries out which action
A) decreased number receptors
B) desensitization- increased phosphorylation of NT-Rs reduces ability of Rs to produce secondary messengers

72
Q

pharmacokinetic tolerance (biodispositional)

A

biologic system responds to drug by decreasing drug concentration delivered to target site due to altered pharmacokinetic parameters
-drugs make metabolizing system faster- causes drug dependency

73
Q

physiological tolerance

A

due to secondary consequences of drug action- upstream chain effect of drug causes large downstream effects
-review haloperidol example in ppt

74
Q

behavioral tolerence

A

decreased potency of drug secondary to intentional change in behavior of consumer based on anticipation of adverse effects

75
Q

acute tolerance

A

rapid induction of tolerance (2-24hrs) due to rapid effect on neurons (LSD)

76
Q

cross tolerance

A

tolerant to one drug= tolerant to others in same class

-decreased potency of one drug bc of exposure to another drug in the same class

77
Q

reverse tolerance= sensitization

A

increased potency of drug following continued exposure to drug- stimulants

Psychopharm (2 decks)

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