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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
uncommon drug response resulting from genetic predisposition (we don't know they occur until they happen)
idiosyncratic effect
26
disease produced by physician (drug caused disease)
iatrogenic disease
27
drug induced birth defect
teratogenic
28
cancer causing
carcinogenic
29
space between toxic and MEC minimal effective concentration
therapeutic index/range
30
lowers level of object drug
induction
31
increases level of object drug
inhibition
32
any noxious unintended and undeserved effect that occurs at a normal range
adverse drug reaction
33
any preventable event that may cause or lead to inappropriate medicine use or patient harm, while in control of health care worker
med error
34
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)
volume of distribution
35
renal function declines with age and is a big deal with the elderly
creatine clearance
36
the #1 reason for ADRs in the elderly
declining renal function
37
what are the teratogenic categories
X-no A-ok B-safe on animals and appears safe for pregnancy
38
drugs pass through membranes easily by:
nonpolarized nonionized lipid solubility minimal protein binding
39
most potent vasoconstrictor
angiotensin II
40
sodium retention and K wasting so increase volume overtime
aldosterone
41
causes membranes to be permeable to H2O. Pulls free H2O into body and makes it more permeable to H2O-concentrates urine
anti-diuretic hormone
42
causes hypokalemia (most dangerous), decrease Na, Cl, Mg, Ca, hypotension, hyperglycemia, hyperuricemia
side effects of diuretics
43
MOA-work through reducing levels of angiotensin II so dilate blood vessels, preload and afterload reduce
ACE inhibitors
44
good for HTN, heart failure, MI, diabetic nephropathy
ACE inhibitors
45
hypotension, cough from bradykinins, increased K, renal failure, fetal injury, angioedema
ACE inhibitor side effects
46
blocks receptors for aldosterone
aldosterone antagonist
47
examples of aldosterone antagonist
spironolactone and eplerenone
48
what is an aldosterone antagonist used for | SE
HTN and heart failure | K
49
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
diuretics
50
act on the ascending loop of henle, block absorption 20%
loop diuretics
51
block reabsorption of Na and Ca in the early distal tubule 10%
thiazides HCTC
52
pee out sugar with water
osmotic diuretics-mannitol
53
aldosterone antagonist and non a
potassium sparing
54
loss of H2O is greater than Na. Excessive sweating, burn victims, uncontrolled diabetes
hypertonic contraction
55
DOC for HTN because it dilates the arteries and lower BP other than fluid loss. must have GFR > 30.
thiazides HCTC
56
three factors for blood flow in vessels:
vessel diameter vessel length blood viscosity
57
Na and H2O lost in equal proportions. Give NS 0.9%
Isotonic contraction
58
Losing more Na as opposed to H2O. Caused by kidney problems, lack of aldosterone, excessive use of diuretics.
Hypotonic Contraction
59
Primary intracellular ion
K
60
Primary extracellular ion
Na
61
force against what the heart has to pump, what the heart must overcome
afterload
62
the biggest determinant of venous dilation, venous constriction
preload
63
cardiac output is
HRxSV
64
7.5 causes arrhythmia's and cardiac arrest. Infuse Ca salt if heart acts funny. Insulin drip. K-exalate exchange.
Treatment of hyperkalemia
65
hyperventilation causes
respiratory alkalosis
66
hypoventilation causes
respiratory acidosis
67
increase in bicarb or loss of acid such as gastric suctioning or vomiting
metabolic alkalosis
68
increase in acid or loss of bicarb such as chronic renal failure, excessive acid production, diarrhea
metabolic acidosis
69
in an acidotic state what increases
K
70
what catalyzes the conversion of angiotensinogen to AT 1
renin
71
where is renin produced
JG apparatus
72
what converts AT1 to AT2
ACE
73
what stimulates the activation of the RAAS system
poor renal profusion
74
drug used for sulfa allergic patient (diuretic)
ethacrynic acid
75
if you have a sulfa allergy you can't take
sulfaureas
76
when you take and ACE inhibitor you have a cough caused by
bradykinins
77
potentially fatal; swelling and edema in tongue, glottis, mouth when taking ACE inhibitor
angioedema
78
block AT II receptors so have similar effects to ACE but no accumulation of bradykinins so no cough or angioedema
ARBS ATII Receptor Blocking (sartan drugs)
79
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
ACE Inhibitors
80
Helps: HTN Heart failure
Aldosterone Antagonist
81
released to protect cardiac system with volume overload. reduce bv by increasing diuresis and dilate arteries and veins
natriuretic peptides
82
peripheral vascular resistance x cardiac output
arterial blood pressure
83
force of ventricular contraction is proportional to the stretch
frank sterling law
84
neostigmne, physostigmine, edophoniusm
Acetylcholinesterase Inhibitors
85
cause muscaranic man
acetylcholinesterase inhibitors
86
used for myasthenia gravis, reverse anticholinergic toxicity, reverse non depolarizing neuromuscular blockage and Alzheimer's
acetylcholinesterase inhibitors
87
recycled after disassociation and stored again; used again or gobbled up by MAOs
NE
88
only one that stimulates beta 2; once released by adrenal medulla, disassociates and floats away; metabolized later
Epinephrine

Pharmacology 1 (3 decks)

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