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Pharmacology exam 1 > Exam 1 > Flashcards

Exam 1 Flashcards

0
Q

What is a drug?

A

Any chemical agent that affects living protoplasm

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1
Q

What is pharmacology?

A

The study of drugs and their interactions with the human body

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2
Q

What is an adverse drug reaction?

A
  • Any response to a drug which is harmful and unintended at a normal therapeutic dose
  • Occurs at doses used in man for prophylaxis, diagnosis, or treatment
  • Side effects, drug allergies, and drug interactions
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3
Q

What is pharmacokinetics?

A
  • The absorption, distribution, metabolism, + elimination of drugs
  • The action of the body on a drug
  • The study of the fate of drugs in the body
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4
Q

What can understanding and applying pharmacokinetic principles do?

A

Increase the probability of therapeutic success and reduce the occurrence of adverse drug effects in the body

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5
Q

Tools used to design optimally beneficial drug therapy regimens

A
  • Proper drug
  • Route of administration
  • Dosing schedules
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6
Q

What is absorption?

A

Movement of a drug from its site of administration into the central compartment and the extent to which this occurs

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7
Q

For solid dosage forms, absorption first requires

A

Dissolution of the tablet or capsule, thus liberating the drug

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8
Q

The clinician is primarily concerned w/ bioavailability or absorption?

A

bioavailability

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9
Q

A drug should be _____ for absorption and site access

A

lipid soluble

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10
Q

Absorption occurs by

A

passive or active transport

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11
Q

Passive transport in absorption

A

Diffusion from higher to lower concentration

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12
Q

Active transport of absorption

A

Against a concentration gradient requiring energy

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13
Q

Absorption can occur as

A

ionized/non-ionized

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14
Q

Their is a high probability for drug interactions to occur during movement through

A

the GI tract

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15
Q

An example of a drug interaction in the GI tract

A

Theo-24 + food = ir and toxic levels

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16
Q

What is distribution?

A

After absorption, drug transported to site where it reacts w/ various bodily tissue, and/or receptors

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17
Q

Following absorption/systemic administration into the bloodstream, a dug distributes into

A

interstitial + intracellular fluids

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18
Q

What are things that effect distribution?

A

Cardiac output, regional blood flow, capillary permeability, + tissue volume determine the rate of delivery and potential amount of drug distributed into tissues

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19
Q

Initially during distribution, which organs receive the most amount of the drug

A

Liver, kidney, brain, + other well-perfused organs

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20
Q

Is the second distribution phase faster/slower?

A

slower

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21
Q

In the second distribution phase, delivery is made to

A

muscle, most viscera, skin, + fat

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22
Q

The second distribution phase involves a far larger fraction of

A

body mass

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23
Q

What accounts for most of the extravascularly distributed drug

A

second distribution phase

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24
Q

What are two important determinants for distribution

A

lipid solubility + transmembrane pH gradiets

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25
Q

What limits the concentration of free drug during distribution?

A

Binding of drug to plasma proteins + tissue macromolecules

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26
Q

In distribution, lipid soluble drugs have

A

A high affinity for adipose tissue where stored and since their is low blood flow here, lipid soluble drug reservoir causes prolonged drug effects

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27
Q

What are some highly lipid soluble drugs

A

Phenothiazines, benzodiazepines, barbiturates

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28
Q

What is metabolism in pharmacokinetics?

A

Convert active lipid soluble compounds to inactive water-soluble substances primarily excreted by the kidney

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29
Q

Most drugs are metabolized in the

A

liver, but also kidneys, lungs, + intestinal tract

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30
Q

The two metabolic processes are

A

Phase 1 and phase 2

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31
Q

Phase 1 of metabolism hepatic microsomal enzymes first

A

oxidize, demethylate, + hydrolize drugs

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32
Q

More clinically significant drug interaction are cause by which phase of metabolism?

A

Phase 1

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33
Q

Drugs w/ short half-lives and inactive metabolites almost entirely metabolize during

A

first pass, therefore less effected by drug interactions

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34
Q

What is phase 2 of metabolism

A

Large water soluble substances are attached to the drug (glucuronic acid, sulfate)

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35
Q

Compounds may circulate through one/both phases multiple times until

A

the water-soluble characteristic is present

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36
Q

Hepatic microsomal enzymes of phase one are

A

mixed function oxidases characterized by the cytochome p450 isoenzymes

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37
Q

Hepatic microsomal enzymes of phase 1 metabolism is more commonly _______ by other drugs

A

induced/inhibited

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38
Q

There are numerous forms of the hepatic microsomal enzymes of phase 1 metabolism about _________ different genes

A

20-200

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39
Q

The CP450 system which is how hepatic microsomal enzymes of phase 1 metabolism are characterized are responsible for

A

Oxidation of many drugs

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40
Q

CYP450 system of phase 1 metabolism oxidizes these drugs:

A
  • warfarin
  • phenytoin
  • tolbutamide
  • quinidine
  • cyclosporin
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41
Q

The CYP in the CYP450 stands for

A

the superfamily

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42
Q

The number 4 in the CYP450 system stands for

A

the family

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43
Q

The 5 in the CYP450 system stands for the

A

subfamily-letter/arabic number

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44
Q

The 0 in the CYP450 system is the

A

individual gene

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45
Q

What are the families that are primarily involved with drug metabolism in the CYP450 system

A

CYP1, CYP2, CYP3, + CYP4

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46
Q

Drugs have been identified as ______, ______, + _____ of CYP metabolism

A

substrates, inhibitors, + inducers

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47
Q

Enzyme inhibitors decrease the rate of

A

metabolism of object drug by obstructing metabolizing enzymes

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48
Q

Enzyme inhibition leads to a _____ in enzyme concentration, and an ______ half life, accumulation, and side effects/toxicities

A

increase, increase

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49
Q

Examples of enzyme inhibitors

A

allopurinol, erythromycin, amidarone, fluoxetine, azoles, isoniazid, cimetidine, MAO inhibitors, ciprofloxain, metronidazole, bactrim, omeprazole, diltiazem, quinidine, ethanol, sulfonamindes, verapamil

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50
Q

Enzyme induction

A

stimulates the increase of CYP450 enzyme activity

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51
Q

Enzyme induction _____ the clearance of each drug and ____ the concentration available to site of action

A

increase, decrease

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52
Q

What is the prototype inducer

A

Phenobarbital

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53
Q

Enzyme inducers and substrates

A

Inducers: barbiturates, carbamazepine, ethanol (chronic), phenytoin, primidone, rifampin, rifabutin, + cigarette smoking
Substrates: warfarin, quinidine, verapamil, keto/itraconazole, cyclosporine, steroids, OCP’s, methadone, metronidazole

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54
Q

Excretion/elimination is

A

the process that removes the drug and its metabolites from the body primarily through urine mostly done in the kidneys

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55
Q

Excretion can also occur through

A

feces, lungs, + skin

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56
Q

Drugs are eliminated from the body either _____ by the process of excretion or _______

A

unchanged, converted to metabolites

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57
Q

Excretory organs, excluding the lungs, eliminate

A

polar compounds more efficiently than substances w/ high lipid solubility
*Lipid soluble drugs are NOT readily eliminated until they are metabolized to MORE POLAR compounds

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58
Q

Substances excreted in the feces are principally _______ orally ingested drugs/drug metabolites excreted either in the _____ or secreted directly into the ______ and not reabsorbed

A

unabsorbed, bile, intestinal

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59
Q

Excretion of drugs in breast milk is important not because of the _________, but because the excreted drugs are potential sources of ______ in he nursing infant

A

amounts eliminated, unwanted pharmacological effects

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60
Q

Excretion from the lung is important mainly for

A

The elimination of anesthetic gases

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61
Q

All four pharmacokinetic principles can __________, making it difficult to predict reactions to the medications

A

vary from patient to patient

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62
Q

Factors that affect the pharmacokinetic principle

A

age, sex, weight, disease states, genetic factors

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63
Q

Pharmacodynamics is

A
  • the action of the drug on the body

- The study of the biochemical + physiological effects of drugs + their mechanisms of action

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64
Q

The most common mechanism for drug interactions by pharmacodynamics include:

A

Synergism (additive effect), antagonism, altered cellular transport, + effects on receptor sites

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65
Q

Understanding pharmacodynamics can provide the basis for the ________ and ____________

A

rational therapeutic use of a drug, desin of new and superior therapeutic agents

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66
Q

The four most important parameters governing drug disposition in pharmacodynamics:

A
  • Bioavailability
  • Volume of distribution
  • Clearance
  • Elimination
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67
Q

Bioavailability(F) in pharmacodynamics is the

A

fractional extent to which a dose of drug reaches its site of action

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68
Q

Factors that decrease bioavailability (F)

A
  • GI absorption
  • First pass effect
  • Metabolism (enzymes, active transport)
  • Route of administration must be based on understanding of these conditions
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69
Q

Volume of distribution (V)

A
  • second fundamental parameter useful in considering processes of drug disposition
  • relates the amount of drug in the body to the concentration of the drug (C) in the blood or plasma depending on the fluid measured
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70
Q

Volume of distribution (V) does not necessarily refer to an identifiable physiological volume but rather

A

the fluid volume that would be required to contain all of the drug in the body at the same concentration measured in the blood or plasma

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71
Q

Half-life (t) is

A

the time it takes for the plasma concentration to be reduced by 50%

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72
Q

Half-life (t) reflects the

A

decline of systemic drug concentrations during a dosing interval at steady-state

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73
Q

State state is when ______=_______

A

rate in, rate out

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74
Q

Steady state is

A

the amount of drug administered in a given period (maintenance dose) is equal to the amount eliminated in that same period

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75
Q

Approximately how many half-lives does it take to reach steady state

A

5-7

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76
Q

If the half life of prozac is 7 days how long does it take to reach steady state?

A

35 days/5 weeks b/c 7*5=35

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77
Q

Drug interactions are

A
  • pharmacological results either desired/undesired

- the effect of one drug (object drug/substrate) is changed by another drug (precipitant drug)

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78
Q

What are the two classifications of drug interactions

A

Pharmacokinetic/pharmacodynamic

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79
Q

What are the types of drug interactions?

A
  • Drug-drug
  • Drug-food
  • Drug-disease
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80
Q

Pharmacokinetic drug interactions occur when

A

Absorption, distribution, metabolism, + excretion (ADME) of one drug is affected by another drug/agent

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81
Q

How can absorption cause a drug interaction

A
  • GI
  • pH
  • Binding
  • Increase/decrease in motility (chrones/diabetes)
  • Changes in GI flora (OCP’s absorbed by bacteria in Gi tract so if given w/ ABX that wipe out that bacteria, OCP’s are ineffective)
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82
Q

How can distribution cause a drug interaction?

A
  • Plasma protein

- Bound vs. unbound (free drug)

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83
Q

How can metabolism cause a drug interaction?

A
  • Hepatic (liver) enzymes: CYP450, CYP3A4
  • Inducers: in addition to meds like cigarettes/phenytoin
  • Inhibitors: grapefruit juice (inhibits CYP4A4), + Tagamet
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84
Q

How can elimination cause a drug interaction?

A
  • Urinary pH

- Competition: Probenecid + PCN= increased PCN in the body (blocks PCN elimination in the case of syphilis), Lithium

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85
Q

Pharmacodynamic causes of drug interactions

A
  • Action of drug on the body
  • Additive effects (synergism): Beer+valium
  • Opposing effects: Tenormin+Sudafed (but heads may not get any effects)
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86
Q

Potentiation/synergism things that can cause drug interactions from pharmacodynamics are

A

interactions between two + drugs/agents resulting in a pharmacologic response greater than the sum of individual responses to each drug

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87
Q

Antagonism, a pharmacodynamic effect that can cause a drug interaction is

A

opposition in action/smaller combined effect than individual agents: 2+2=1 (opposite of synergism/potentiation)

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88
Q

Principles of pharmacodynamics apply to all biologic systems

A
  • In vivo, patients w/ specific disease

- In vitro, isolated receptors

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89
Q

A receptor is

A

A molecule to which a drug binds to bring a change in function of he biologic system

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90
Q

A receptor site is

A

the specific region of he receptor molecule which the drug binds

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91
Q

Inert binding molecule/site

A

Molecule to which a drug may bind w/out changing any function

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92
Q

Spare receptor

A
  • receptor that doesn’t bind drug when the drug concentration is sufficient to produce maximal effect
  • Present when K(d)>EC50
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93
Q

Effector

A

Component that accomplishes the biologic effect after the receptor is activated by an agonist (i.e. channel/enzyme molecule)

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94
Q

Efficiency, maximal efficiency (Emax)

A

The maximum effect that can be achieved w/ a particular drug regardless of dose

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95
Q

Potency

A

Amount of drug needed to produce a given effect, determined mainly by the affinity of the receptor for the drug, and # of receptors available

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96
Q

Graded dose-response curve

A

A graph of increasing response to increasing drug concentration/dose

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97
Q

Quantal dose-response curve

A

A graph of the fraction of a population that shows a specified response at progressively increasing doses

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98
Q

EC50

A

The CONCENTRATION hat causes 50% of the maximum effect/toxicity

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99
Q

ED50

A

The DOSE that causes 50%of the maximum effect/toxicity

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100
Q

TD50 (TC50)

A

The median toxic dose/concentration at which toxicity occurs in 50% of cases

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101
Q

LD50 (LC50)

A

The median lethal dose/concentration required to kill half the members of a tested population after a specified test duration

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102
Q

Kd

A

The concentration of drug that binds 50% of the receptors in the system

103
Q

Bmax

A

Max # of receptors bound

104
Q

Agonist

A

Drug that activates its receptor upon binding

105
Q

Partial agonist

A

Drug that binds to its receptor but produces a smaller effect at full dosage than a full agonist

106
Q

Allosteric agonist

A

A drug that binds to a receptor molecule w/out interfering w/ normal agonist binding but alters the response to the normal agonist

107
Q

Antagonist

A

Pharmacologic antagonist that binds w/out activating its receptor + thereby prevents activation by an agonist

108
Q

Competitive antagonist

A

A pharmacologic antagonist that can be overcome by increasing the concentration of the agonist

109
Q

Irreversible antagonist

A

A pharmacologic antagonist that cannot be overcome by increasing agonist concentration

110
Q

Physiologic antagonist

A

Drug that counters effects of another by binding to a different receptor + causing opposing effects

111
Q

Chemical antagonist

A

A drug that counters the effects of another by binding the agonist drug NOT THE RECEPTOR

112
Q

Allosteric anagonist

A

A drug that binds to a receptor molecule without interfering w/ normal antagonist binding but alters the response to the normal antagonist

113
Q

Therapeutic index (TI)

A

Td50/LD50:ED50

114
Q

Signaling

A

Once an agonist drug has bound to its receptor, some effector mechanism is activated

115
Q

What are the receptor-effector systems of signaling

A

Enzyme in intracellular space:
-cyclooxygenase, target for NSAIDS

Neurotransmitter reuptake transporters:
-NE + DA transporters for cocaine

Voltage-activated ion channels:
-Antiarrythmic drugs target Na+, K+, + Ca2+ calcium channels

116
Q

Classic drug-receptor interactions of signaling

A
  • drug is present in the extracellular space, effector mechanism resides inside the cell + modifies some intracellular process
  • Involves signaling across the membrane
117
Q

5 major types of transmembrane-signaling mechanisms

A
  1. transmembrane diffusion of drug to bind to an intracellular receptor
  2. transmembrane enzyme receptors, whose outer domain provides the receptor function + inner domain provides the effector mechanism converting A to B
  3. Transmembrane receptor that after activation by an appropriate ligand, activate separate cytoplasmic tyrosine kinase molecules (JAKs) which phosphorylate STAT molecules that regulate transcription (Y, tyrosine, P, phosphate)
  4. transmembrane channels that are gated open/closed by the binding of a drug to receptor site
  5. G protein-coupled receptors, which use coupling protein to activate a separate effector molecule
118
Q

Receptors that are intracellular

A
  • More lipid-soluble/diffusible agents (steroid hormones, nitric oxide)
  • May cross membrane + combine w/ an intracellular receptor that affects an intracellular effector molecule
  • Receptor + effector may/may not be the same molecule, but no specialized transmembrane signaling device is required
119
Q

Receptors located on membrane-spanning enzymes

A

-Drugs that affect membrane-spanning enzymes combine w/ a receptor site on the extracellular portion of the molecule + modify its intracellular activity (insulin + tyrosine kinase)

120
Q

Receptors located on membrane-spanning molecules binding seperate intracellular TK molecules

A
  • Appropriate drug (cytokine) activates extracellular receptor site
  • Associate but separate tyrosine kinase molecules (JAKS) activated
  • Results in phosphorylation of STAT molecules (signal transducers + activators of transcription)
  • STAT dimers (effectors) then travel to the nucleus + regulate transcription
121
Q

Receptors located on membrane ion channels

A
  • Directly cause opening of channel (ACh at nicotinic receptor)
  • Modify channel’s response to other agents (BZD’s at GABA-activated Cl- channel)
  • The channel molecule acts as both receptor + effector (resulting in a change in transmembrane electrical potential)
122
Q

Receptors linked to effectors via G Proteins

A
  • Drug bind to receptors that are linked by coupling proteins to intracellular/membrane-bound effectors (sympathomimetics-activate/inhibit adenylyl cyclase (effector) by multistep process)
  • When G-coupled receptors bind agonist, G-protein activated
123
Q

3 most important G-proteins

A
  • receptor: M2, M3, a1 G protein: GQ Effector: phospholipase C Effector substate:membrane lipids second messenger response: increased IP3, DAG Result: Increased CA2+ and protein kinase activity
  • receptor: B, D1 G protein: GS effector: adenylyl cyclase Effector substrate: ATP second messenger response: ^cAMP result: ^Ca2+ influx + enzyme activity
  • receptor: a2, M2 G protein: GI effector:adenylyl cyclase effector substrate:ATP second messenger response: dec. cAMP result: decreased CA2+ influx + enzyme activity, ^ K+ efflux
124
Q

Receptor regulation in

A

number, location, + sensitivity

125
Q

Receptor regulation can have changes that occur

A

over a short time (minutes) or longer periods (days)

126
Q

Tachyphylaxis of receptor regulation

A
  • An acute (sudden) decrease in the response to a drug after its administration
  • Frequent/continuous exposure to agonists, resulting in short-term reduction of receptor response
  • Can occur via several mechanisms
127
Q

Mechanisms of tachyphylaxis the sudden decrease in the response to a drug after its administration

A
  • Blockage of G proteins responsible for receptor activation + sensitization
  • Agonist-receptor complexes may be internalized, removing them from further exposure/activation by agonists
  • Continuous activation of the receptor-effector system that may lead to depletion of essential substrates needed for effect expression
128
Q

Down regulation

A

Long-term reduction in receptor number which occur in response to continuous exposure to agonists

129
Q

Up-regulation

A

Increases in receptor number which occur when receptor activation is blocked for prolonged periods (several days) by pharmacologic antagonists/denervation

130
Q

Do you want a high or low TD50?

A

high b/c takes longer to produce signs of toxicity

131
Q

Do you want a high or low TI?

A

High because it gives you a high therapeutic window which means there is a large difference of a drug giving a desired effect + toxic effects

132
Q

Don’t ever compare potency w/out

A

efficiency

133
Q

What is the base value of TI?

A

100

134
Q

Is T1 always reliable?

A

No sometimes ED50 + LD50 overlap

135
Q

Pharmacokinetics helps decide

A

instructions of using a drug

136
Q

Only ______ drugs can diffuse through capillary walls + produce a pharmacological effect + be metabolized + excreted

A

unbound free

137
Q

What type of molecules can enter into the brain

A

Nonionized molecules not easily bound to plasma proteins b/c lipid-soluble

138
Q

A decreased bioavailability would mean that

A

poorly absorbed in GI tract or partially metabolized in the liver

139
Q

Pharmacodynamics is the relationship between _____ and ___+___

A

drug concentration and therapeutic and toxic effects

140
Q

Pharmacokinetics is the relationship between ____ + _____

A

dosage regimen + drug concentrations

141
Q

Kinetic interactions are changes in effect that are the result of changes in the relationship between _____ + ______

A

dose, concentration

142
Q

Dynamic interaction changes in effect are the result of changes in relationship between ___ + ___

A

concentration, effect

143
Q

The pharmacological effect of kinetic interactions has changes as a result in the change in the

A

drug concentrations

144
Q

The pharmacological effect of a dynamic interaction has changed despite the lack of change in the _______

A

concentration

145
Q 
Is this a pharmacodynamic/pharmacokinetic reaction and why?
Drug C (50mg) --> Cp peak 100mcg/ml--> efficiency w/out toxicity
Drug C (50mg) + Drug D--> Cp peak 100mcg/ml--> toxicity
A

Pharmacodynamic because the concentration stays the same but their must be an interaction at the receptor level that is producing toxicity

146
Q 
Is this a pharmacokinetic/pharmacodynamic relationship + why?
Drug A (10mg) --> drug A cp peak 8mcg/ml --> Efficiency w/out toxicity
Drug A (10mg) + Drug B --> Drug A cp peak 16 mcg/ml --> toxicity
A

Pharmacokinetic because the concentration changes with the same dose administered probably due to drug B inhibiting the metabolism of drug A

147
Q

The more _____ substances may move more freely across the membrane

A

lipid-soluble because they must pass through the phospholipid “barrier”

148
Q

Substances that are less lipid soluble may need to cross the membranes via

A

Other mechanisms (protein channels/carrier proteins) because they are polar substances, relatively insoluble, including ionized substances

149
Q

What is the only administration method which bypasses the absorption process?

A

IV b/c administered directly into systemic circulation

150
Q

An increase in bioavailability is equal to an _____ in systemic drug exposure

A

increase

151
Q

The area under the curve that is that is produced w/ a graph of serum concentration vs. time (AUC) is

A

bioavailability

152
Q

What is the pharmacokinetic parameter which quantifies drug exposure?

A

Bioavailability

153
Q

An increased AUC means an ______ in systemic drug exposure?

A

increase

154
Q

How is bioavailability expressed?

A

As a percentage/fraction of the drug administered which reaches th systemic circulation

155
Q

If 90% of the drug from an administered dose reaches the systemic circulation, the drug in that dose form has a ____ bioavailability?

A

90%

156
Q

With oral administration, the fraction reaching the systemic circulation (bioavailability) is dependent on

A
  • absorption characteristics of the drug dose form
  • amount of metabolism that occurs prior to the drug reaching the systemic circulation (intestinal wall/liver hepatic first pass metabolism)
  • Presence of interacting substances (drugs, food, type of food)
157
Q

With a first pass effect you would ____ a lot of the drug

A

lose

158
Q

CPmax ng/ml is

A

maximum concentration

159
Q

Tmax (hrs)

A

time to achieve maximum concentration after administration

160
Q

AUC

A

area under the curve produced by graphing the drug concentrations over time

161
Q

What is the approximate absolute bioavailability of a 30mg tablet if the AUC for the tablet is 27.3 and the AUC for IV is 4290?

A

0.64% because 27.3/4290=x/100

162
Q

What is the approximate bioavailability of a 30mg dose of oral aqueous solution if the AUC is 26.1 and the AUC for IV is 4290?

A

0.61% b/c 26.1/4290=x/100

163
Q

What is absolute bioavailability?

A

One of the AUC’s is being compared to a dose form where there is 100% absorption (IV 100%)

164
Q

What is relative bioavailability?

A

How two dose forms compare in terms of the relative amount of the drug that reaches systemic circulation
*Used when we don’t have a gold standard like IV to compare to

165
Q

What is the relative bioavailability of the tablet relative to solution if the AUC of the tablet is 27.3 and the AUC of the solution is 26.1?

A

104.6% b/c 27.3/26.1*100

166
Q

What is the relative bioavailability of the solution relative to the tablet if the AUC of the solution is 26.1 and the AUC of the tablet is 27.3?

A

95.6% b/c 26.1/27.3*100

167
Q

What to do with relative/absolute bioavailability?

A

Determine whether to give a drug in a certain form based on the AUC and peak in case your method of form doesn’t provide relief of symptoms

168
Q

Volume of distribution (Vd) is used to account for

A

observed initial drug concentrations following administrations so researches calculate an “apparent” volume into which the drug is distributed

169
Q

When a researcher administers a drug, he measures the maximum concentration + calculates the volume of distribution with this equation

A

Cp max = dose/Vd

170
Q

CPmax= Dose/Vd allows the calculation of the ______ that should e produced when a certain dose is put into a certain volume

A

concentration

171
Q

If the researcher administers a drug and the concentration is very high, then the volume of distribution of that drug is

A

very small

172
Q

If the researcher administers a drug and the concentration is very low then the volume the drug appears to occupy is

A

very large

173
Q

Is the volume of distribution a true physiologic volume?

A

No it is “apparent”

174
Q

Physiologic volumes are used to help us understand

A

where the bulk of a drug resides in the body

175
Q

The volume of distribution provides an indication of

A

the extent of distribution

176
Q

The reason drugs have different Vd’s is a function of the drugs chemical characteristics which dictate its

A

lipid solubility, protein binding, + tissue binding

177
Q

For a given drug there is variability in Vd from pt to pt b/c of the pt characteristics + conditions like

A

pregnancy, fluid status, + disease states (CF, trauma)

178
Q

A high volume of distribution is due to

A

increased lipid solubility, decreased protein binding, and increased tissue binding

179
Q

Dose is calculated by

A

CP max*vd

180
Q

Average 70 kg person
A drug w/ <= 0.25 L/kg distributes into an apparent volume of 18L (70kg*0.25L/kg) means that the drug is primarily distributed in

A

extracellular fluid (interstitial fluid + plasma/blood)

181
Q

Average 70 kg person
Drug w/ 0.55-.70L/kg Vd distributes into an apparent volume of approximately 40-50L (70*.55-.7L/kg=40-50L) these drugs have a greater tendency to distribute

A

out of extracellular fluid compartment and into total body water

182
Q

70kg person

Drug Vd is >.7L/kg (>50L) is distributed

A

Extensively throughout the body and is NOT being allowed to reenter the central compartment due to tissue bind/affinity for specific cells/ion trapping

183
Q

Biotransformation (metabolism)

A

drug is chemically altered to form a metabolite that is more “excretable” then parent drug

184
Q

The byproduct of biotransformation (metabolism) is

A

a metabolite

185
Q

A prodrug

A

When the parent drug has no actiity and the metabolite does

186
Q

In phase 1 hepatic biotransformation either a ___ is added or a ___ is removed

A

oxygen, hydrogen

187
Q

Cytochrome P450 which primarily mediates oxidation in phase 1 hepatic biotransformation are most sensitive to substances that have the ability to ___ or ___ biotransformation

A

inhibit, induce (alcohol, drugs, smoking)

188
Q

An inducer ____ action and their is ____ metabolism and ____ concentrations

A

induce, more, less

189
Q

An inhibitor is ___ active, ____ metabolism, and ___ concentrations

A

less, less, more

190
Q

In phase 2 reactions of hepatic biotransformation the parent drug/metabolite is conjugated w/

A

glucuronic acid, a methyl group, an acetyl group, or a sulfate group

191
Q

Phase 2 reaction of hepatic biotransformation are primarily mediated by a group of enzymes known as

A

transferases

192
Q

Phase 2 reactions of hepatic biotransformation produce a metabolite which is more _____ and less ____. The more ____ molecules will be more likely to stay in the blood stream + be available for excretion via the kidneys

A

polar, lipophilic, polar

193
Q

Relatively polar substances made in phase 2 reactions of hepatic biotransformation are less likely to undergo

A

renal tubular reabsorption which means it will more likely stay in the renal tubule + be excreted

194
Q

How are drugs filtered through the kidney?

A

At the nephron, filtered at the glomerulus + pass into the renal tubule + excreted in urine

195
Q

Some drugs may also be secreted into the tubules via

A

active transport proteins

196
Q

Drugs can also be excreted via other organs and of most relevance to kinetics is via

A

bile ducts

197
Q

What is enterohepatic recirculation?

A

When a metabolite may be excreted into the small intestine via bile and some may be reabsorbed and re-enter the systemic circulation

198
Q

These are less susceptible to change in the liver

A

Enzymes

199
Q

Drug elimination rate may be gleaned from two parameter

A

Clearance, elimination half-life

200
Q

Clearence

A

the volume of blood that is cleared of drug per time

201
Q

150ml/min clearance means

A

150ml of blood is cleared of drug every minute

202
Q

Elimination half-life

A

The time it takes for the concentration of drug to reduce by one-half and for most it is a constant value for a given drug

203
Q

A drug with a faster clearance or shorter elimination half-life will probably need to be dosed ______ frequently

A

more

204
Q

For a dug whose elimination processes are NOT easily maximized (Pk verbiage = NOT easily saturated) the elimination of that drug increases in _______ to the serum drug concentration (referred to as _______). For such a drug, the serum drug concentrations are _______ to the dose administered.

A

direct proportion, first pass elimination, directly proportional

205
Q

Half-life for first pass elimination is _____ and is _____ of drug serum concentrations

A

constant, independant

206
Q

First order reaction equation

A

elimination rate= serum concentration*constant

207
Q

Dose-serum concentrations hold true w/ IV administration but ____ with oral drug administration

A

May/may not be true b/c the AUC may not be directly proportional to dose b/c % absorption may decline w/ higher doses (maximized/saturated the absorption process)

208
Q

First order elimination is a linear relationship between

A

drug concentration + elimination, and dose + concentration

209
Q

For drugs whose elimination processes ARE easily maximized (PK verbiage=easily saturated) the elimination rate of that drug is ____ (referred to as ______). For such a drug, the serum drug concentration produced are _____ to the dose administered. Instead, small increases in dose will produce ______ increases in serum drug concentrations.

A

constant, zero-order elimination, disproportional, large

210
Q

Equation for zero-order elimination

A

Elimination rate = constant

211
Q

Half-life for zero-order elimination is

A

Dependent, the half-life changes based on serum concentrations

212
Q

The relationship of concentration and elimination in a zero-order elimination process is

A

non-line curves to the right where it plateaus, so even with high concentrations the elimination stays the same

213
Q

The relationship of serum concentration and dose in a zero-order elimination process is

A

non-linear, you may only increase the dose a little bit but the serum concentrations sky rocket so the curve goes far up to the right

214
Q

Neurotransmitters

A

transfer information from nerve terminals across the synaptic cleft and bind receptors to pass on the message

215
Q

Drugs have been found in nature + modified to

A

mimic or block the message getting to these receptors to cause a specific response

216
Q

Classification methods of the nervous system

A

Physical location: Peripheral vs. CNS (separates brain + spinal cord from everything else)
Function: Autonomic vs. somatic nervous system (actions that require conscious thought or not)

217
Q

Autonomic nervous system

A

Involves actions that are not under conscious control (visceral functions like cardiac output, blood flow to vital organs, + digestion)

218
Q

Somatic nervous system

A

conscious function: movement, respiration, posture

219
Q

Two major sections of the autonomic NS

A

sympathetic (thoracolumbar)

parasympathetic (craniosacral)

220
Q

Both sympathetic + parasympathetic originate in the

A

CNS

221
Q

Sympathetic NS fiber exit through

A

thoracic and lumbar spinal nerves

222
Q

Parasympathetic fibers of the autonomic NS exit through

A

cranial nerves + 3rd + 4th sacral spinal routes

223
Q

Efferent nerves

A
  • are preganglionic neurons that originate in the CNS + connect to ganglia in the peripheral NS
  • Ganglia act as relay stations to pass messages on to postganglionic nerves
  • Postganglionic neurons terminate on effector organs
224
Q

Afferent nerves of the autonomic nervous system

A
  • Regulate the autonomic nervous system by sensing actions + providing feedback to the CNS
  • Bring information from effector organ to CNS
  • CNS can then adjust its message to efferent nerves
225
Q

Two neurotransmitters of autonomic NS

A

Acetylcholine + norepinephrine

226
Q

Acetylcholine is released from

A
  • Cholinergic nerve fibers

- Include almost all efferent nerve fibers leaving CNS sympathetic and parasympathetic

227
Q

Norepinephrine is released from

A
  • adrenergic nerve fibers

- Include most postganglionic SYMPATHETIC nerve fibers

228
Q

The sympathetic portion of the nervous system have the ganglionic neurotransmitter ______ and a neuroeffector neurotransmitter ______ with a _____ receptor

A

ACh, Norepinephrine, Adrenergic receptor

229
Q

The parasympathetic portion of the autonomic nervous system includes ____ as the ganglionic neurotransmitter and he neuroeffector neurotransmitter ____ which has a _____ receptor

A

ACh, ACh, muscarinic

230
Q

Acetylcholine is made from

A

acetyl-CoA using the enzyme choline O-acetyltransferase

231
Q

Synthesis of ACh occurs in the nerve fiber

A

mitochondria

232
Q

Once formed ACh is transferred to neuronal terminal by a

A

choline transporter

233
Q

ACh is stored ass packages of

A

“quanta” in vesicles located on the surface of the nerve terminal facing the synapse

234
Q

Release of ACh

A
  • An action potential is generated in the nerve + reaches the terminal
  • Causes an influx of Ca++ into the nerve terminal
  • Calcium interacts w/ the vesicle membrane triggering fusion of the membrane to the terminal membrane
  • A pore opens into the synapse + subsequent release of hundreds of quanta into synaptic cleft
235
Q

Released ACh

A
  • ACh binds to and activates acetylcholine receptors (reversible)
  • Acetylcholinesterase present in the synaptic cleft breaks down unused ACh into choline + acetate in seconds
  • Terminates ACh action
  • Any ACh present in synapse will continue to interact with receptors until broken down
236
Q

NE is only on the

A

postganglionic side and through the sympathetic portion of the autonomic nervous system

237
Q

Adrenergic nerve fibers

A
  • Make up the postganglionic neurons of the sympathetic nervous system
  • Release norepinephrine
  • Make adjustments in response to stressful situations
238
Q

Adrenergic nerve fibers that release norepinephrine’s actions

A
  • Increase hr + BP
  • Mobilize energy stores
  • Increase blood flow to skeletal muscles
  • Divert blood flow from skin + internal organs
  • Dilate pupils + bronchioles
239
Q

Termination of adrenergic action occurs in three ways

A
  • NE metabolized by catalytic enzyme (monoamine oxidase MAO)
  • Diffusion away from receptor site (then metabolized)
  • Reuptake into terminal by norepinephrine transporter (NET) or other cells
240
Q

Receptors

A
  • Structures made of protein that are designed to bind endogenous molecules
  • Upon binding, the receptors pass on the message using signaling proteins
  • Highly specific + require special interaction w/ the molecules for proper binding
  • Many drugs are based on receptor-ligand interaction
241
Q

Cholinergenic receptors are named after

A

alkaloids that bind them (muscarinic + nicotinic)

242
Q

Norepinephrine receptors are based on

A

agonist + antagonist selectivity (a1 and B1 ad dopamine but not usually in the ANS)

243
Q

There is more to ANS then just norepinephrine + ACh

A

nitric oxide synthase, purines, substance P, calitonin gene-related peptide, cholecytokinin, dynorphin

244
Q

The parasympathetic system is sometimes referred to as

A

trophotopic which means leading to growth by resting + digesting conserving + storing energy and stimulating digestive activity

245
Q

The sympathetic system is sometimes referred to as

A

ergotrophic which means leading to energy expenditure activated in “fight or flight” stimulating heart, increasing blood sugar, + mediating vasoconstriction of blood vessels

246
Q

What is a major target of the autonomic NS

A

Cardiovascular system

247
Q

What are parasympathetic effects on the cardiovascular system

A

-bradycardia:decreased hr

248
Q

What are the sympathetic effects on the cardiovascular system

A
  • Alter peripheral vascular resistance to manage BP
  • Heart rate
  • Contraction force to manage cardiac output
  • Venous tone
  • Renin production to manage renal blood flow
249
Q

Control of autonomic function is done in order to

A
  • prevent overstimulation

- maintain effector organ functions w/in a narrow window of tolerance

250
Q

Control of autonomic function is done by

A
  • Presynaptic regulation

- Postsynaptic regulation

251
Q

Receptors on presynaptic nerves control

A

output of neurotransmitter

  • a1 receptors
  • B receptors
252
Q

A1 recetors

A
  • present on noradrenergic nerve terminals
  • Activated by binding of NE released from same nerves
  • Binding results in decreased release of NE
  • Example of autoreceptor b/c responds to NE released from same neuron
253
Q

B receptors

A
  • Present on some neurons

- Facilitate release of more NE

254
Q

2 mechanisms of postsynaptic regulation

A
  • Up or down regulate receptors

- Action of one receptor is affected by action of other receptors

255
Q

Up or down regulate receptors

A

Response to high or low activation from neurotransmitters or drugs that mimic neurotransmitters

256
Q

Effector organs

A
  • Multiple sites throughout the body sensitive to adrenergic/cholinergic action
  • Actions of NE + ACh are often opposite each other

Pharmacology exam 1 (3 decks)

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