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Pharmacology by me > Pharm Basics-Exam 1 > Flashcards

Pharm Basics-Exam 1 Flashcards

1
Q

Bioavailability = F =

A

% of the drug that makes it into circulation.

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2
Q

Calculate amount of drug in circulation for a given bioavailability

A

Drug in circulation = F x dose

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3
Q

Calculate a new dose for a new administration mode

A

new dose = (old dose x old F) / new F

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4
Q

MEC

A

Minimum effective concentration

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5
Q

ADME

A

Administration
Distribution
Metabolism
Excretion

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6
Q

henderson hasselbach

A

pH = pKa + log (non-protonated / protonated)

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7
Q

partition coefficient

A

lipid solubility of the non ionized form

[organic drug] / [aqueous drug]

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8
Q

First order kinetics

A

most drugs follow this clearance
constant fraction of the drug is cleared
rate of elimination directly proportionate to [ ]

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9
Q

zero order kinetics

A

Phenytoin, ETOH, Aspirin
Saturates- constant amount cleared
independent of [ ]

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10
Q

clearance

A

volume of blood cleared of drug/unit time

CL = rate of elimination / C

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11
Q

Volume of distribution (Vd)

A

Vd= dose / C

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12
Q

half life (t1/2)

A

t1/2 = (0.7 x Vd) / CL

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13
Q

steady state

A

plateau

takes about 4-5 t1/2’s to get to the plateau

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14
Q

loading dose

A

loading dose = (Vd x TC) / F

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15
Q

maintenance dose

A

maintenance dose = (dose rate x dose interval) / F
or
md = (CL x TC) x dose interval / F
or
md =((rate of elim / C) x TC) x dose interval / F

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16
Q

dosing rate

A

dosing rate = CL x TC

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17
Q

What are some great examples of very rapidly dividing cells that would be damaged with chemotherapy?

A

Lymphocytes, epithelium, hair follicles, RBCs

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18
Q

Primary resistance

A

Resistance to drugs after the first treatment due to inherent resistance

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19
Q

Aquired resistance

A

Resistance developed from multiple treatments

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20
Q

Selective toxicity

A

Ability of a drug to harm a target while sparing the good guys

  1. Unique target in pathogen (cell wall)
    or
  2. Target must be structurally different in pathogen (ribosomes)
    or
  3. Target must be more important to pathogen than to host
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21
Q

5 important aspects to consider when selecting antibiotics

A
  1. organisms identity and sensitivity to agent
  2. site of infection
  3. safety of the agent
  4. patient factors (ie pregnancy, gender, age, etc…)
  5. cost of therapy
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22
Q

Combination broad spectrum antibiotics

A

Clindamycin and gentamicin

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23
Q

Single broad spectrum antibiotics

A

Imipenem and cilastatin

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24
Q

3 targets of selective toxicity

A

Disrupt cell wall
disrupt protein synthesis (ribosomes)
inhibit enzyme unique to bacteria (dihydrofolate reductase)

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25
Q

Sulfonamides

Trimethoprim

A

suppress bacterial growth by inhibiting folic acid synthesis from PABA.

Works great with trimethoprim, which binds to dihydrofolate reductase and inhibits the reduction of dihydrofolic acid (DHF)

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26
Q

Xenobiotics

A

Any foreign substance really

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27
Q

Bio transformation

A

The processing of xenobiotics for elimination

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28
Q

Two functions of biotransformation

A

Metabolism - phase 1, and elimination - phase 2

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29
Q

Sites of metabolism

A

LIVER, kidney, intestines, skin, lungs

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30
Q

Phase 1 reaction does what?

Who does the majority of the reactions?

A

Enzymes add a polar group to the molecule to make it somewhat more hydrophilic, allowing the drug to be conjugated. Drug is likely still active after phase 1.

Cytochrome p450 does the majority of the reactions (CYP)

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31
Q

Phase 2 reaction does what?

What is a possible negative effect of this reaction?

A

Phase 2 conjugates with endogenous stuff (OH, NH2, COOH, glucuronidation, acetylation, sulfation) making it quite polar and easily excreted. Drug probably inactive after phase 2.
ROS could result from conjugation!

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32
Q

Acetaminophen conjugation?

What about with overdose?

A

Normally, 95% of the drug is conjugated and excreted with no problems. 5% is converted via CYP450 to NAPQI which accumulates and forms protein adducts in the liver and kill you. GSH takes care of this problem under normal conditions, but with overdose, GSH gets saturated. He dead.

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33
Q

How does one treat an acetaminophen overdose?

A

N-acetylcysteine (NAC) binds the toxic proteins and creates conjugates that can be excreted.

34
Q

factors that affect biotransformation

A

Genetic (race) age, sex, diet, environment, metabolic drug interactions, disease

35
Q

CYP2D6 polymorphism (phase 1)

A

ultra metabolizers need more drug to have the same therapeutic effects in the treatment of depression. Codine is also metabolized to morphine much more rapidly. Ethiopians and Saudi Arabians have this polymorphism often.

36
Q

CYP2C19 polymorphism (phase 1)

A

poor metabolizers (japanese) don’t metabolize the S form of the racemic mixture of mephenytoin, and get a more profound effect. Ataxia and sedation.

Mephenytoin is a hydantoin, used as an anticonvulsant.

37
Q

CYP2C9 polymorphism (phase 1)

A

Much more sensitive to warfarin. This can lead to bleeding and death. Much smaller dose is needed!

38
Q

Slow acetylater phenotype (phase 2)

A

isoniazid (treatment of TB) accumulates and can lead to induced peripheral neuritis, bladder cancer and autoimmune diseases

Note: INH is known to reduce cytochrome P450 and in theory promotes the efficacy of contraceptives. Therapy is often combined with rifampin. Rifampin increases the P450 enzyme and also can reduce the efficacy of contraceptives. Alternative means of birth control should be used when taking these medications.

39
Q

Chloramphenicol and newborns

A

newborn livers don’t conjugate the oxidative metabolite of chloramphenicol very well, and it accumulates toxically and leads to “gray baby syndrome”

40
Q

Diet and environment effects on biotransformation

  1. grapefruit juice
  2. st johns wart
  3. cigarette smoke
  4. lead
A
  1. inhibits 3A4 (could cause pregnancy)
  2. induces 3A4 (depression meds metabolized)
  3. induces 1A1, 1A2, 2E1
  4. induces heme-oxygenase that breaks down P450
41
Q

metabolic drug/drug interactions

A

Rifampin induces 3A4

Erythromycin metabolite complexes with 3A4 and inactivates it!

42
Q

Diseases affect metabolism

A

Cardiac-changes blood flow
liver- main metabolizer
thyroid- metabolism rate
kidney- drug excretion rate

43
Q

3 mechanisms of antibiotic resistance

A

Failure of drug to reach target (most common)
Drug is inactivated
Target is altered

44
Q

How might an antibiotic not reach its target?

Example drugs?

A

Drug could get metabolized before reaching target. Porins that once let the drug in may mutate.

Efflux pumps can confer multi drug resistance.
Tetracyclines, chloramphenicol, floroquinolones, macrolids, beta-lactam antibiotics

45
Q

How might an antibiotic be inactivated?

A

Beta-lactamase is an enzyme that alters the drug and renders it ineffective. A prodrug like anti-beta lactamase can help to fix this issue.

46
Q

Three principle factors for choosing antibiotics:

Hint: its pretty obvious

A

Identity of organism
Drug sensitivity of organism
Host factors such as infection site and host defense status
Drug with great efficacy, low toxicity, and narrow spectrum

47
Q

Why might the first drug of choice not be used?

A

Allergy, inability of drug to penetrate to site of infection (gentamicin), and unusual susceptibility of pt to toxicity of drug

48
Q

When should sulfonamides not be used?

A

Produces kernictorus in newborns, a severe neurologic disorder caused by displacement of bilirubin from plasma membranes

49
Q

Urine pH and drug elimination: weak acid (aspirin) overdose

A

alkalize the urine with bicarbonate

50
Q

Urine pH and drug elimination: weak base overdose

A

acidify the urine with ammonium chloride

51
Q

Therapeutic index

A

Measures drug safety. High values are safer.

TI = LD50 / ED50

52
Q

Therapeutic Index redefined as Margin of safety

A

LD1 / ED99 I guess it accounts for the slope better.

53
Q

Drug Efficacy

A

Maximal effect a drug can produce

54
Q

Therapeutic window

A

Measure of clinical drug safety. Range of min effective dose to min toxic dose.

55
Q

Spare receptor concept

A

Occupancy theory states that maximum effect is when all the receptors are occupied. Physiologically, a maximum effect is obtained when only a fraction of the receptors are occupied, so not all receptors are necessary. Receptors vs effectors may be the solution; there could be more receptors that effectors, thereby increasing sensitivity to ligand.

56
Q

Drug potency

A

amount of drug needed for given effect

57
Q

competitive antagonist

A

competes with the agonist for the binding site on the receptor. reversible, and if the [agonist] is high, 100% of response is still possible. Antagonist changes potency, not efficacy.

58
Q

receptor agonist

A

produces the proper response of the receptor. can reach 100% of the effect.

59
Q

functional antagonist

A

binds to another receptor entirely, and although is has no change on the binding of the agonist, it antagonizes the EFFECTS of the agonist. this looks a lot like non-competitive antagonism.

60
Q

non-competitive antagonist

A

binds to receptor somewhere besides the active site, and changes the binding of the agonist. this changes the efficacy, and may alter the potency as well.

61
Q

inverse agonist

A

decrease the action of receptors that have intrinsic activity.

62
Q

partial agonist

A

these bind to the receptor site and elicit the some response as the agonist, but differ in intensity. partial agonists do not reach 100% efficacy.

clinical relevance is that they can be used to blunt a physiological response in a diseased population. partial agonists do not generate drug tolerance.

63
Q

Lipid soluble ligands and intracellular receptors

A

Receptors are located in the cytosol or nucleus.
Ligands must be lipophilic (steroids and gases).
Upon binding, cytosolic receptors translocate to nucleus.
Binds to specific DNA sequences.
Transcription, translation, and protein synthesis.

64
Q

3 intracellular receptor parts and how they are regulated

A
  1. ligand binding domain
  2. DNA-binding domain
  3. transcription activating domain

The receptors are kept inactive by chaperone proteins (hsp90), but upon ligand bonding, it dissociates and allows binding to DNA and transcription.

65
Q

G protein coupled receptors

A

First, the extracellular ligand selectively detected by a surface receptor. The receptor in turn triggers activation of the G protein located on the cytoplasmic face of the plasma membrane. The activated G protein then changes the activity of effector element, usually an enzyme or ion channel. This element then changes the concentration of the intracellular second messenger.

66
Q

Gs protein

A

Stimulatory
Beta-adrenergic, glucagon, histamine
Increase in adenylate cyclase and cAMP

67
Q

Gi protein

A

Inhibitory
Alpha-2 adrenergics, Muscarinics (M2,4)
Decrease adenylate cyclase and cAMP

68
Q

Gq protein

A

AchR (muscarinic M1,3,5)
Alpha-1 adrenergics
Histamine
Increase phospholipase C, PIP2, IP3 and DAG, and increase in cytoplasmic Ca2+

69
Q

Three drugs that do not fit into the receptor ligand model

A

Antimicrobials
Osmotic drugs
Antacids

70
Q

Proper approach to empiric therapy

A
  1. Make a clinical diagnosis of microbial infection
  2. Obtain specimens for lab
  3. Make microbiologic diagnosis
  4. Determine necessity for empiric therapy
  5. Institute treatment
71
Q

3 examples of antibiotic synergism

A
  1. Trimethoprim and sulfamethoxole
  2. Beta lactams and beta lactamase
  3. Penicillins and aminoglycosides(bind to the bacterial 30S ribosomal subunit)
72
Q

2 examples of antibiotic antagonism

A
  1. Tetracycline and penicillin
  2. Chloramphenicol and penicillin

Bacteriostatic and bactericidal don’t go well together.

73
Q

Chemotherapeutic index

A

CTI = toxicity to cancer / toxicity to normal cells

big # is better

74
Q

Cell cycle specific drugs

A

inhibit some aspect of cell division to kill cancer. some drugs affect S-phase and others M-phase.

75
Q

3 advantages to combination chemotherapy

A
  1. maximum cell kill
  2. broader range of coverage of resistant cell lines
  3. prevents or slows development of new drug resistance
76
Q

P-glycoprotein

A

increased expression in cancer causes multi drug resistance due to drug efflux (active transport)

77
Q

3 cell types and adverse effects of myelosuppression

A

myelosuppression = bone marrow suppression

  1. WBC- increased infection
  2. RBC- fatigue, headaches, etc…
  3. platelets- bruising, bleeding
78
Q

Serotonin receptor antagonists

A

First line and most effective antiemetic therapy, but rather costly. Tron drugs.

Dolasetron (ANZEMET)
Granisetron (KYTRIL)
Ondanisetron (ZOFRAN)

79
Q

antidopaminergics

A

second line antiemetic drugs selectively depress CTZ and to lesser extent, vomiting center

Prochlorperazine
Fluphenazine
Chorpromazine

80
Q

Bacterial conjugation

A

Common mechanism for gram negative rods as well as enterococci, and staphylococci

Multiple resistance genes can be transferred in a single event via plasmids. Extrachromosomal DNA is transferred. Donor guy must have code for mechanisms of transfer and the necessary sex equipment. Those two segments are called resistance factor.

81
Q

Pharmacodynamics

A

Action of the drug on the body

82
Q

Pharmacokinetics

A

The action of the body on the drug.

Pharmacology by me (5 decks)

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