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Pharmacology 1 > Pharm 1 Final > Flashcards

Pharm 1 Final Flashcards

1
Q

no drugs are completely ________

A

safe

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2
Q

elicits response with no side effects

A

selectivity

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3
Q

study of drugs and their interactions with living systems

A

pharmacology

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4
Q

use of drugs in the treatment and prevention of disease or conditions

A

pharmacotherapeutics

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5
Q

any chemical agent that affects the process of living

A

drug

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6
Q

the study of absorption, distribution, metabolism, and excretion of drugs

A

pharmacokinetics

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7
Q

the study of the biochemical and physiologic effects of drugs on the body

A

pharmacodynamics

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8
Q

no medicinal value and greatest abused

A

1

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9
Q

high potential for abuse but medical use

A

2

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10
Q

cough syrup; sign for and some don’t have prescription

A

5

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11
Q

T1/2 time required for amount of drug in the body to decline by 50%.

A

half life

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12
Q

Warfarin 1/2 life = 24 hours

A

Give 1 q day

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13
Q

point at which the amount of drug eliminated between doses equals the amount of drug administered

A

steady state

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14
Q

steady state is reached in __ drug half lives.

A

4

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15
Q

what is the most reliable way to evaluate all new drugs

A

random controlled trials RCT

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16
Q

performed in animals 1-5 years.

A

preclinical testing

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17
Q

in healthy volunteers

A

phase 1

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18
Q

testing in patients

A

phase 2

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19
Q

tests safety and effectiveness

A

phase 3

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20
Q

post marketing surveillance–monitor side effects

A

phase 4

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21
Q

molecules which activate receptors

A

agonist

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22
Q

molecules which prevents receptor activation by endogenous regulatory molecules (a blockers)

A

antagonist

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23
Q

can act as both a antagonist and agonist (can block or stimulate and same time)

A

partial agonist

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24
Q

decrease responsiveness to a drug as a result of repeated drug administration

A

tolerance

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25
Q

uncommon drug response resulting from genetic predisposition (we don’t know they occur until they happen)

A

idiosyncratic effect

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26
Q

disease produced by physician (drug caused disease)

A

iatrogenic disease

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27
Q

drug induced birth defect

A

teratogenic

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28
Q

cancer causing

A

carcinogenic

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29
Q

space between toxic and MEC minimal effective concentration

A

therapeutic index/range

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30
Q

lowers level of object drug

A

induction

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31
Q

increases level of object drug

A

inhibition

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32
Q

any noxious unintended and undeserved effect that occurs at a normal range

A

adverse drug reaction

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33
Q

any preventable event that may cause or lead to inappropriate medicine use or patient harm, while in control of health care worker

A

med error

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34
Q

numerical parameter which indicates extent of drug distribution in body; the measure of appropriate space in the body available to contain the drug (larger the # the more it goes through your body)

A

volume of distribution

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35
Q

renal function declines with age and is a big deal with the elderly

A

creatine clearance

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36
Q

the #1 reason for ADRs in the elderly

A

declining renal function

37
Q

what are the teratogenic categories

A

X-no
A-ok
B-safe on animals and appears safe for pregnancy

38
Q

drugs pass through membranes easily by:

A

nonpolarized
nonionized
lipid solubility
minimal protein binding

39
Q

most potent vasoconstrictor

A

angiotensin II

40
Q

sodium retention and K wasting so increase volume overtime

A

aldosterone

41
Q

causes membranes to be permeable to H2O. Pulls free H2O into body and makes it more permeable to H2O-concentrates urine

A

anti-diuretic hormone

42
Q

causes hypokalemia (most dangerous), decrease Na, Cl, Mg, Ca, hypotension, hyperglycemia, hyperuricemia

A

side effects of diuretics

43
Q

MOA-work through reducing levels of angiotensin II so dilate blood vessels, preload and afterload reduce

A

ACE inhibitors

44
Q

good for HTN, heart failure, MI, diabetic nephropathy

A

ACE inhibitors

45
Q

hypotension, cough from bradykinins, increased K, renal failure, fetal injury, angioedema

A

ACE inhibitor side effects

46
Q

blocks receptors for aldosterone

A

aldosterone antagonist

47
Q

examples of aldosterone antagonist

A

spironolactone and eplerenone

48
Q

what is an aldosterone antagonist used for

SE

A

HTN and heart failure

K

49
Q

MOA block Na and Cl reabsorption by doing this it limits passive reabsorption of water; degree of urine flow is directly proportional to the amount of Na and Cl reabsorption it blocks

A

diuretics

50
Q

act on the ascending loop of henle, block absorption 20%

A

loop diuretics

51
Q

block reabsorption of Na and Ca in the early distal tubule 10%

A

thiazides HCTC

52
Q

pee out sugar with water

A

osmotic diuretics-mannitol

53
Q

aldosterone antagonist and non a

A

potassium sparing

54
Q

loss of H2O is greater than Na. Excessive sweating, burn victims, uncontrolled diabetes

A

hypertonic contraction

55
Q

DOC for HTN because it dilates the arteries and lower BP other than fluid loss. must have GFR > 30.

A

thiazides HCTC

56
Q

three factors for blood flow in vessels:

A

vessel diameter
vessel length
blood viscosity

57
Q

Na and H2O lost in equal proportions. Give NS 0.9%

A

Isotonic contraction

58
Q

Losing more Na as opposed to H2O. Caused by kidney problems, lack of aldosterone, excessive use of diuretics.

A

Hypotonic Contraction

59
Q

Primary intracellular ion

A

K

60
Q

Primary extracellular ion

A

Na

61
Q

force against what the heart has to pump, what the heart must overcome

A

afterload

62
Q

the biggest determinant of venous dilation, venous constriction

A

preload

63
Q

cardiac output is

A

HRxSV

64
Q

7.5 causes arrhythmia’s and cardiac arrest. Infuse Ca salt if heart acts funny. Insulin drip. K-exalate exchange.

A

Treatment of hyperkalemia

65
Q

hyperventilation causes

A

respiratory alkalosis

66
Q

hypoventilation causes

A

respiratory acidosis

67
Q

increase in bicarb or loss of acid such as gastric suctioning or vomiting

A

metabolic alkalosis

68
Q

increase in acid or loss of bicarb such as chronic renal failure, excessive acid production, diarrhea

A

metabolic acidosis

69
Q

in an acidotic state what increases

A

K

70
Q

what catalyzes the conversion of angiotensinogen to AT 1

A

renin

71
Q

where is renin produced

A

JG apparatus

72
Q

what converts AT1 to AT2

A

ACE

73
Q

what stimulates the activation of the RAAS system

A

poor renal profusion

74
Q

drug used for sulfa allergic patient (diuretic)

A

ethacrynic acid

75
Q

if you have a sulfa allergy you can’t take

A

sulfaureas

76
Q

when you take and ACE inhibitor you have a cough caused by

A

bradykinins

77
Q

potentially fatal; swelling and edema in tongue, glottis, mouth when taking ACE inhibitor

A

angioedema

78
Q

block AT II receptors so have similar effects to ACE but no accumulation of bradykinins so no cough or angioedema

A

ARBS ATII Receptor Blocking (sartan drugs)

79
Q

Helps:
HTN: dilates veins and reduction of volume status
BP: decreases
heart failure: makes easier by dilating veins
MI: take within 30 min of MI
Diabetic Nephropathy
max. reduce MI, stroke, death

A

ACE Inhibitors

80
Q

Helps:
HTN
Heart failure

A

Aldosterone Antagonist

81
Q

released to protect cardiac system with volume overload. reduce bv by increasing diuresis and dilate arteries and veins

A

natriuretic peptides

82
Q

peripheral vascular resistance x cardiac output

A

arterial blood pressure

83
Q

force of ventricular contraction is proportional to the stretch

A

frank sterling law

84
Q

neostigmne, physostigmine, edophoniusm

A

Acetylcholinesterase Inhibitors

85
Q

cause muscaranic man

A

acetylcholinesterase inhibitors

86
Q

used for myasthenia gravis, reverse anticholinergic toxicity, reverse non depolarizing neuromuscular blockage and Alzheimer’s

A

acetylcholinesterase inhibitors

87
Q

recycled after disassociation and stored again; used again or gobbled up by MAOs

A

NE

88
Q

only one that stimulates beta 2; once released by adrenal medulla, disassociates and floats away; metabolized later

A

Epinephrine

Pharmacology 1 (3 decks)

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