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Pathopharmacology > Exam #1 > Flashcards

Exam #1 Flashcards

1
Q

Pharmacology

A

“study of properties and effects of drugs on living systems”

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2
Q

Nomenclature (naming)

A

Chemical: acetyl salicylic acid

Generic: aspirin

Trade: Bayer

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3
Q

Drug

Agonist vs Antagonist

A

“chemical that interacts with specific molecule and exerts biological effect”

Agonist: stimulates response

Antagonist: inhibit response

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4
Q

Drug receptor

A

“functional macromoelcule to which drug binds and produces measureable effect”

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5
Q

Ligand-gated ion channel receptors

A

bind and open gate (ms)

Ex. ACH open Na channel (nicotinic receptors)

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6
Q

G-protein-coupled receptors

A

G protein load GTP and release alpha/beta second messengers (also gamma subunit)

Ex. AcH muscarinic receptors

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7
Q

Kinase linked receptors

A

Mebrane bind, conformational change activates a kinase which phosphorlyates 2nd messengers-

amino acids tyrosine, serine, threonine (cascade amplification)

Ex. Cytokine, insulin

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8
Q

**Nuclear receptors **

A

DNA coupled intracellular receptors–> stimulate gene transcriptio–> protein/enzyme synthesis

Ligand lipiphilic to cross membrane

Ex. Steroid hormones (estrogen, progesterone, cortisol, thyroid hormone)

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9
Q

Mechanism of Action

A

“specific cellular change mediated by a drug that cause clinically evident response”

Ex. Aspirin–>decrease CoX enzyme->decrease prostaglandin synthesis->decrease inflammation, edema, pain

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10
Q

Receptor occupancy

A

=number of receptors bound to drug

depends on concentration of drug and its affinity for a given receptor

(specificity and selectivity)

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11
Q

**Intrinsic activity **

A

how much effect does drug have on receptor action

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12
Q

**Sensitivity **

A

Up-regulation= more sensitive to drug due to increase # of receptors

Down-regulation= less sensitive due to less # of receptors or more tolerant to drug

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13
Q

Agonist

Antagonist

A

bind to receptor to trigger response

Can be competitive and bind depending on afinity and concentration

block receptor and access of drug to block flow of ions into and out of cell

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14
Q

Efficacy

Emax

A

“magnitude of drug response”

How well it does what its supposed to?

Emax= maximal drug response

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15
Q

**Potency **

ED50

A

“concentration of drug necessary for an effect”

ED50- effective dose to get 50% max response

desired response in 50% individuals

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16
Q

Competitive antagonist

Noncompetitive antagonist

A

=decrease ED50 but not Emax

=decrease Emax but not ED50

(agonist no longer induce same effect, not competing for same site so decrease overall magnitude of drug response)

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17
Q

Grade dose response curves

Quantal dose curves

A

% response over drug concentration

yes or no of individual responses

(# responding vs log10 dose)

Exampine descrete outcomes versus gradation of responses

18
Q

Toxicology

side-effect

adverse effect

toxic effect

A

“undesired effect of drugs and chemicals”

  • minor, uncomfortable
  • compromising or potentially harmful
  • major or life threatening at high dose
19
Q

TD50 or LD50

A

toxic or lethal dose

toxicity or death in 50% of animals tested

20
Q

**Therapeutic Index **

A

margin of safety

=TD50/ED50

Acetominophen=30 (30xs recommended dose get toxic)

Cancer drugs= 1

21
Q

Safety Margin

A

LD1/ED99

distance betweeb quantal dose-response curves for desired effect undesired effect

More concervative measure (how safe, risk vs benefit)

22
Q

_Biological variability _

Hyper-reactivity

Hypo-reactivity

Tolerance

Tachyphylaxis

Idiosyncrasy

Number-needed-to-treat (NNT)

A

=people respond differently to different medications

  • response at low dose
  • no response until high dose
  • hyporeactivity results from repeate administration
  • rapid onset of tolerance
  • unexpected deviation from normal

unexpected drug response

:# patients who must be expose to drug for 1 patient the deisred effect (takes into consideration individual variations among patients wieght, age, genetics)

23
Q

_Pharmodynamics _

Pharmokinetics

A

=biological, chemcial, physiological effects of drug

=dealing with absorption, distribution, metabolism, exretion of a drug

“rate at which drug concentration accumulates in and are broken down and eliminated from organs of body”

24
Q

**Bioavailability **

A

fraction of unchanged drug reaching systemic circulation

degrees to which drug reaches site of action

intravenously versus orally

25
Q

_Absorption _

A

=drug entry into systemic circulation from site of administration

rate influenced by route of administration

oral, sublingual, subcutaneous, topical, intravenously, intramuscular, inhalation

26
Q

Biological membranes

Simple diffusion

Facilitated diffusion

Active transport

A

=lipid soluble, water-filled channels, carrier proteins

  • small/nonpolar- with electrochemical gradient
  • big/charged- with electrochemical gradient
  • need ATP- against electrochemical gradient
27
Q

Absorption

Compatibility and blood flow

**Ionization **

A

depends on size, charge, ionization

Oral->GI lumen->GI epithemlium->mesenteric vessels-> blood flow

weak acids non-ionized (no charge) in acid solutions

weak based non-ionized basic solutions

= better diffusable/absorbed in like solutions

28
Q

Iontophoresis

A

-transcutaneous drug diffusion occurs via electrical repulsion push drug across membrane

(electicity may vasoconstrict holding drug in area- most drug passive diffusion)

29
Q

Absorption

**Disease effects **

A

GI disease decrease absorption

(digoxin blood levels decrease, malabsorption)

Inflammation decrease absorption

change ionization state of drug HA<->H+ + A-

Stomach pH 1-3

Small intestine pH 5-7

30
Q

Absorption

Drug/Food effects

A

Iron sulfate- form complex with many agents and decrease absorption (thyroxine, methyldopa, penicill)

Calcium can inhibit iron absorption

Neomycin and phenytoin cause malabsorption as side effect

Food/liquid can slow transit time (pop pH<3)

31
Q

Absorption

PT effects

Age effects

A

Exercise->decrease GI blood flow->decrease GI absorption

Intense exercise–>change GI pH->change drug solubility

Heat, massage, exercise–>increase local drug absorption administered transdermally

Secondary to cutaneous ateriodilation

-impaired GI (active) transport and decrease bioavailibility

32
Q

Distribution

A

“transfer drug from blood to extracellular fluids and tissues”

Interstitial=12 L

Intracellular= 24 L

Vascular= 5 L

33
Q

**Volume of distribution **

A

VD= dose/Co (plasma concentration at time 0)

Small= most drug stay in blood

Large= not concentrated in blood compartment (dilute)

34
Q

Factors of distribution

Tissue permeability

Blood flow

Drug bind plasma proteins

Bind subcellular components

A

Albumin: drug bind, not as bioavailable

Drug storage: Adipose- fat soluble drugs

Bone- heavy metals

Muscle- mefloquine-antimalarial drug

Organ- streptomycin in renal proximal tubule

35
Q

1st pass effect

A

drugs given orally are absorbed by small intestine through portal system to liver (limits bioavailibility)

36
Q

Distribution

Disease effects

Drug effects

A

Hypoalbuminemia- renal/hepatic disease

decrease bind drup typically bind to albumin–> increasing availability free drug (increase toxicity)

Chronic renal failure-

uremia decrease drug bound to protein–>

unbound phenytoin levels–>

increase toxic levels even when total blood levels normal

-protein bound drugs can be displaced at binding sites by other drugs

Ex. Warfarin displaced from binding protein by metronidazole= may result in hemorrhage

37
Q

Distribution

PT effects

Age-related

A

Redistribution by exercise, massage, heat, ultrasound

2ndary to increase blood flow

Exercise change blood pH and may change drug’s ability to cross tissue membrane

Increase body fat–>retention lipid soluble drugs

Decrease water content-> water soluble drugs more concetrated

Decrease serum albumin->increase biolavailbility albumin bound drugs

38
Q

Metabolism

Make drug hydrophilic

Make drug less active

Prodrugs

A

-Necessary for excretion in renal tubes

Enzyme increase regulatioin occur with repeated admin

-metabolite not as effective as parent drug

Exception: prodrugs

Metabolites more active- converted into more active

Ex. L-dopa->dopamine

Codeine-> morphine

39
Q

Metabolism

Inactivation, detoxification, or bioactivation

Phase 1

Phase 2

A
  1. Transform drug into more polar molecule- oxidations (cytochrome P-450s) , reduction, hydrolysis
  2. Nonpolar drug–>polar via conjugation with transferase

Ex. Glucaronide, glutathione

Morphine (prodrug)–> morphine glutathione

40
Q

Metabolism

Disease effects

Drug effects

A

Hepatic disease- impaired metabolism

Chronic heart failure alter hepatic perfusion (alter metabolism lidocaine, propanol)

Induction/Inhibition of metabolizing enzymes can increase or decrease 1/2 life of drug

Barbiturate/rifampin=increase metab oral anitcoagulants

Lovastatin/simvastatin+ketconozole/grapfruit=decr

Disulfirom (antabuse)= inhibit aldehyde dehydrogenase (alcoholism- alde dehydr help detox/digest ethanol)

41
Q

_Metabolism _

PT effects

Age-effects

A

Pathopharmacology (1 decks)

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