Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MDTI > Pharmacology - Sheet1 > Flashcards

Pharmacology - Sheet1 Flashcards

1
Q

pharmacokinetcs

A

What the body does to the drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

pharmacodynamics

A

What the drug does to the body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Important disadvantage oral administration

A

First pass effect, variable response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

First Pass effect

A

Drug must first pass through portal vein to liver before reaching other organs. Metabolized and changed. Affects oral and to some extenct rectal. NOT sublingual

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

IM aqueous advantage

A

fast onset of action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

IM non aqueous advantage

A

slow sustained response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What determines absorption in transdermal

A

lipid solubility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

pH rule of thumb regarding absorption

A

weak acids stomach, weak bases intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

bioavailability formula

A

AUC oral/AUC injected x 100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

distribution

A

process of leaving blood and entering other areas. 3 main areas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

3 Compartments and relative size for distribution

A

Plasma - 4L, ECF - 14L, Total Body Water - 42L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Factors affecting distribution

A

blood flow, capillary permeability, degree of hydrophobicity, binding to plasma proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Important factor when drugs are displaced from plasma binding

A

Must assess their Volume of distribution. If small at higher risk of toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Volume of distribution equatino

A

bioavailability of dose/concentration of plasma at initial time.
hypothetical volume of fluid into which a drug is disseminated and prior to elimination.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Phase 1 Drug Metabolism

A

oxidation involving cytochrome p450

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Phase 2 Drug metabolism

A

coupling endogenous substrate to a drug or phase 1 metabolite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cytochrome p450

A

made of many families of heme containing isozymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

CYP families most involved in metabolizine enzymes

A

CYP 1,2,3 and CYP3A4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What can increase CYP3A4

A

Rifampin (TB), St John’s Wort. Effect is increased metabolism of the drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What can decrease CYP3A4

A

grapefruit juice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Which CYP polymorphisms are important

A

CYP2D6, CYP2C19

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

3 processes renal excretion

A

glomerular filtration, active tubular secretion, passive tubular transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

clearance equation

A

rate of elimination/concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Type of clearance kinetics for most drugs

A

first order so increasing amount leads to an equal increasing excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Relation of steady state to rate of elimination

A

Both require 4-5 half lives to reach steady state, indpeendent of dose or rate of dosing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Graded dose response

A

increase dose - increase response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

quantal

A

all or none resopnse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Intrinsic activity vs potency

A

Potency has to do with how much you must give to get 100% response. intrinsic activity has to do with highest % response you can achieve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Agonist K3 value

A

1, antagonist is 0

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Muscarininc chlinergic agonist

A

ACH, muscarine, pilocarpine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Muscarininc cholinergic antagonist

A

Atrpoine, Scopolamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Nicotinic chlinergic agonist

A

ACH, nicotine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Nictinic cholinergic antagonist

A

Curare, succinylcholine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Alpha- adrenergic agonists

A

norepinephrine, epinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Alpha 1 adrenergic antagonists

A

Prazosin, phentolamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Beta 1 adrenergic agonists

A

Epinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Beta 1 adrenergic antagonists

A

propranolol, metoprolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

4 Types of antagonism

A

competitive, noncompetitive, chemical, physiologic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Physiologic antagonism

A

One drug does exact opposite of another and works on entirely separate mechanism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Therapeutic index

A

Take the 50 cumulative percent of negative outcom/positive outcome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Safety Index Formula

A

Lethal Dose 01%/Effective Dose 99%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Mineralcorticoids, location and function

A

Zona glomerulosa adrenal cortex - salt and water regulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Glucocorticoids location

A

Zona fasiculata

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Androgen/estrogen location

A

Zona reticularis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Which two chaperone proteins does GR interact with LBD

A

Hsp90 and Hsp56

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Which end is AF2

A

C terminal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

AF2 function

A

ligand dependent transactivation domain. Only recruit co-regulators after steroid binds GR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Which end is AF1

A

N terminal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

AF1 Function

A

ligand independent transactivation domain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

role of Heat shock proteins in Glucocorticoid receptor

A

Keeps the receptor ligand friends. 2Hsp90 and 1 HSP 56 subunit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

2 Examples of how glucocorticoids affect gene expression

A

Increase expression of lipocortin, downregulating PLA2 decreasing synthesis of PGs and lueoktrienes
inhibits production of IL-6 and IL-8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

2 glucocorticoid drugs that are very specific for glucocorticoid effects

A

Dexamethasone and Betamethasone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Effect of prolonged steroids on hypothalmic pituitary axis

A

suppress the axis and supress endogenous cortisol production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Addisonian Crisis

A

acute adrenal insufficiency bc sudden withdrawal of therapeutic glucocorticoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Which effector T cells can mediate steroid resistant rejection

A

Th17 producing IL 17,21,22

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Th1 produces

A

IFN gamma, IL-2, TNFalpha - T cell Drive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Th2 produces

A

IL4,5,13 - B cell drive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

T regulatory

A

IL10 - TGF beta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What downregulates Th2

A

INF-gamma

60
Q

What downregulates Th1

A

IL-10

61
Q

Basiliximab limitation

A

can be used to prevent induction but not to treat rejection because it is useless once the T cell has already received signal 3

62
Q

Equine anti-thymphocyte globulin use

A

anplastic anemia

63
Q

rabbit anti-thymocyte globulin

A

transplant

64
Q

Important liitation of polyclonal antibodies

A

risk of antibody response, toxicity, immunosuppresion

65
Q

Belatacet mechansim

A

Binds to CD80/86 better than CD28 and stops costimulation

66
Q

Belatacept major risk

A

increased risk of post-transplant lyphoproliferative disorder.
only use when have some other viral infection?

67
Q

High dose steroid effect

A

apoptosis of activated T and B cells

68
Q

Calcineurin examples

A

tacrolimus and Cyclosporine binding to FK binding protein-12 and cyclophilin

69
Q

Calcineurin mechanis

A

prevents calccineurin phosphatase. Inhibits IL-2 mediated response and transcription of IL-2, GM-CSF, TNFalpha and INF gamma

70
Q

Calcineurin metabolized by

A

CYP3A4 means you have to monitor levels differently. If on it need to give higher levels.

71
Q

Increased risk hyperglycemia/neurotoxicity (calcineurin)

A

tacrolimus

72
Q

increased risk hypertension, hyperlipidemia, hyperuricemia

A

cyclosporine

73
Q

Hirsutis/gingival hyperplasia

A

cyclosporine

74
Q

mTOR inhibitors

A

Sirolimus and everolimus

75
Q

mTOR inhibotor mechanism

A

inhibits protien kinase

76
Q

mTOR effect

A

decrease cytokine dependent cellular proliferation, at G1 to S, induce T cell cycle arrest. Inhibit activation and proliferation

77
Q

mTOR metabolized by

A

CYP3A, longer half-life than calcineurin so don’t need to monitor as much

78
Q

mTOR major toxicity

A

wound healing impairment

79
Q

Azathioprine mechanism

A

blocks denotovo and salvage of purines. prevents DNA relplication

80
Q

Mycophenolic acid products

A

block de novo purine synthesis, prevent DNA replication

81
Q

Methotrexate

A

Folic acid antagonist. Arrest cells at S phase

82
Q

Common drug interaction with azathioprine

A

Allopurinol inhibits xanthine oxidase which normally metabolizes azathioprine. So when both need to keep azathioprine levels lower

83
Q

Monoclonal antibodies, IL2 receptor agonist

A

binds to alpha subunit of IL-2 receptor.

84
Q

Basiliximab common use

A

used as an induction agent in organ transplant

85
Q

basiliximab mechanism

A

anti CD-25 antbody that acts on activated T cells.

86
Q

basilixmab cannot be used for

A

treating rejection

87
Q

Induction therapies

A

basiliximab or rabbit antiglobulin

88
Q

Maintinence therapies

A

calcineurin or mTOR w azathioprine or MPA w prednisone

89
Q

3 types of Eicosanoids

A

Prostanoids, Leukotrienes, HETES and EETS

90
Q

Eicosanoids derived from

A

arachidonic acid in cell membrane

91
Q

Isoeicosanoids

A

products that do not depend on enzymes and are driven by free radicals

92
Q

Phospholipase A2 function

A

catalyzes release of Arachidonic acid from embrane

93
Q

COX function

A

AA to intermediary PGG2/PGH2

94
Q

PGG2 platelet synthesize

A

TxA2

95
Q

GI Endothelial cells PGG2 synthesize

A

PGE2

96
Q

Vascular endothelial cels PGG2 synthesize

A

prostacyclin PGI2

97
Q

Phospholipase A2 forms

A

cytosolic and inducible

98
Q

Cox 1 function

A

constitutive activity

99
Q

Cox 2 function

A

inducible and not in all cells

100
Q

Platelet Cox form

A

Cox 1

101
Q

Enthothelial cell Cox form

A

Cox 2

102
Q

PGE2 ligand for

A

EP receptors (1-4)

103
Q

PGI2 ligand for

A

IP receptor

104
Q

TxA2 ligand for

A

TP receptor

105
Q

PGF2alpha ligand for

A

FP receptor

106
Q

TxA2 function

A

induce platelet aggregation, vasoconstriction, smooth muscle cell proliferation

107
Q

PGI2 (prostacyclin I2)

A

inhibits platelet aggregation and smooth muscle cell proliferation, vasodilator and pro-inflammatory

108
Q

Prostaglandin E1 and 2 function

A

cytoprotection in Gut w inhibition of gastric secretions

109
Q

Which Cox for inhibition of gastric secretions

A

Cox 1

110
Q

Prostaglandin E function on vessels

A

vasodilation (COX 1 and 2)

111
Q

Prostaglandin E function on homeostasis

A

Regulate sodium and water with renin release (COX 1 and 2)

112
Q

Prostaglandin E function, gastroutero muscles

A

contraction of smooth muscles COX1 and 2

113
Q

Prostaglandin E inflammatory effects

A

Controls body temperature. Pro-inflammatory through COX 2

114
Q

Prostaglandin F2 function

A

vascular smooth muscle and uterine contraction. Vasoconstrictor COX 1 and 2

115
Q

Prostaglandin D2 effect vessels

A

cutaenous vasodilation. Inhibitino of aggregation

116
Q

Prostaglandin D2 effect unusual

A

promotes sleep and changes hair follicle activity

117
Q

Prostaglandin D2 immune effect

A

produced by mast cells->chemotaxis Th2 lymphocytes

118
Q

Prostanoids in pain

A

PGE2, PGE1 PGI2

119
Q

Prostanoids in heat

A

PGE2 and PGE1

120
Q

Prostanoids in redness

A

PGE2, PGE1, PGI2

121
Q

Prostanoids in swelling

A

PGI2, PGE2, PGD2

122
Q

Reduces release of AA from membrane

A

steroids

123
Q

reduce AA to PGG2/PGH2

A

attack COX, NSAIDS

124
Q

Reduce production of prostanoids

A

target isomerases, Ridogrel

125
Q

Ridogrel

A

Inhibits throboxane synthase

126
Q

PGF2alpha medical function

A

causes luteal regression and induces smooth muscle contraction

127
Q

carbaprost

A

PGF2 analogue for abortifacient and post partum bleeding

128
Q

PGE2 PGE1 medical use

A

INduce uterine contraction

129
Q

Misoprostol

A

PGE2 analogue used as abortifacient and gastric cytoprotection

130
Q

Dinoprostone

A

PGE2 analogue for inducing labor

131
Q

NSAID basics

A

weak acids that have sleectivity for both COX

132
Q

Gold standard NSAID

A

Aspirin

133
Q

Aspirin mechanism

A

inhibition of COX by competing for active site

134
Q

Aspirin effect

A

acetylates SER-530 and causes irreversible inhibition

135
Q

NSAID side effect

A

limit cytoprotection = gastropathy

136
Q

Gastropathy mechanism

A

reduce PGE1,2 = reducegastric mucus and pH. Reduce TxA2 = inhibit clot = erosion, bleeding, ulcer

137
Q

Which COX causes gastropathy

A

COX 1 inhibition

138
Q

Coxib problem

A

inhibited only COX2 but had cardiovascular risks

139
Q

Coxib problem mechanism

A

get an imbalance of the TxA2 and PGI2. Endothelial cells need COX 2 for antiplatelet effects.

140
Q

NSAID renal adverse effects

A

renal disease need the vasodilation from prostaglandin. Inhibition leads to renal toxicities

141
Q

NSAID renal effect mechanis

A

PGE induced renin secretio causes elevated blood pressure bc sodium reabsorption

142
Q

Aspirin low dose

A

Inhibits platelet COX 1

143
Q

High dose Aspirin

A

analgesic

144
Q

Highest dose aspirin

A

anti-inflammatory

145
Q

Reyes syndrome (aspirin)

A

hepatic toxicity, limits pediatric use

146
Q

Salicylate toxicity (Aspriin

A

headache, tinnitus, dizziness. Ringing in ears most important

MDTI (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions