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Foundations II > Exam 4 vocab > Flashcards

Exam 4 vocab Flashcards

(86 cards)

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1
Q

How do you measure a drug’s potency?

A

ED50 or EC50

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2
Q

How do you measure a drug’s efficacy?

A

Emax

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3
Q

Occupancy theory

A

the response is directly proportional to the number of drug-receptor complexes formed

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4
Q

Agonist

A

binds to a receptor and elicits a response

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5
Q

Intrinsic activity

A

the capacity of a drug molecule to activate transduction as a function of binding to its receptor

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6
Q

Full agonist

A

a drug that causes the maximal response observed in a system. Efficacy is equal to 1 or 100%

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7
Q

Partial agonist

A

a drug that fails to cause the maximal response even when all receptors are bound. Intrinsic activity and efficacy are less than 1

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8
Q

Inverse agonist

A

a drug that causes an effect opposite of a ‘typical’ agonist; you lose basal activity and major upregulation results because all receptors are stabilized in the inactive form. Efficacy and intrinsic activity are less than 0. These are most obvious in a system with a high level of basal activity in absence of a drug.

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9
Q

Antagonist

A

a drug that upon binding to a receptor has no effect - doesn’t change the basal activity. Efficacy and intrinsic activity are 0.

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10
Q

Two state receptor theory

A

most receptors are limited to two states - off and on

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11
Q

Multi-state receptor theory

A

different agonists cause different activity

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12
Q

Summation of agonists

A

the effect of two agonists in combination is the predicted sum of the effect of each in isolation. The agonists may nor may not

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13
Q

Potentation

A

the effect of one agonist in combination with an ineffective drug is greater than the effect of the agonist by itself. The two drugs must be acting by different mechanisms - the compound causing the effect doesn’t even have to be a drug. An example is CYP induction/inhibition.

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14
Q

Allosteric agonist

A

bind to a different site on the receptor than a full agonist and elicit an effect

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15
Q

Chemical antagonist

A

chelation

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16
Q

Physiologic antagonist

A

a drug that acts at a different receptor site (agonist at this site) to cause an effect that is opposite of an agonist in the system. These two agonists act together to cancel each other out

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17
Q

Difference between an physiologic antagonist and an inverse agoninst

A

a physiologic antagonist is on a different receptor site and an inverse agonist acts on the same receptor site

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18
Q

Pharmacological antagonist

A

binds receptors and does not cause a response, but blocks agonist-receptor interactions

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19
Q

Mixed agonist/antagonist

A

a drug that has different effects at different receptor subtypes

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20
Q

Selective response modulator

A

a drug that has different effects at the same receptor subtypes in different tissue types

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21
Q

Spare receptors

A

some full agonists only bind to a fraction of the receptors yet elicit a full response. Spare receptors occur because the signal transduction proteins are limiting

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22
Q

Threshold of Toxicological Concern

A

a concept that is used when there is no chemical-specific data. We assume there is no appreciable risk to human health based on the chemical structure and level of exposure

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23
Q

acute exposure

A

single event/dose - monitored for 14 days; 3 doses

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24
Q

sub-acute exposure

A

14 days - 14 doses repeating the same dose

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25
90 day chronic exposure
repeated dose for 90 days; study will usually be set up with 3 doses. Animals are monitored for signs of sickness, organs and tissues evaluated by a pathologist
26
Long term toxicity/cardiogenicity
often evaluated at the same time; small exposures over prolonged time; lifetime exposure (2 yr)
27
Reproductive toxicity
decreased fertility
28
teratogenicity
test for congenital malformations/fetal effects
29
Therapeutic index calculation
TD50/ED50 or MTC/MEC
30
Hazard
an inherent property - the potential of something to cause harm
31
Risk
probability of a particular adverse outcome
32
pharmacokinetic considerations
drug concentrations differ at target receptor, body weight, age, sex-related differences, pregnancy and lactation, health and disease
33
pharmacodynamic considerations
sex-related differences, circadian rhythms, drug tolerance, drug resistance
34
idiosyncrasy
an unexpected response or unexpected sensitivity to a drug that is frequently genetically based
35
allergic response
an adverse response to a drug as a result of a previous exposure to the same drug
36
cross sensitivity
an allergic reaction to a structurally similar drug without prior exposure
37
tolerance
a change in the way the body adapts to the presence of drug over time
38
classic tolerance
progressively decreased responsiveness resulting in the need for a larger dose to elicit the same response
39
pharmacokinetic (indirect) tolerance
changes at the site separate from the agonist site of action resulting in a decreased drug response (includes increased metabolism)
40
pharmacodynamic (direct) tolerance
a change due to a change at the receptor level or the ability of a cell to respond (includes downregulation)
41
resistance
commonly used term with respect to anti-tumor and anti-microbial drugs - insensitivity or decreased sensitivity of cells to drugs
42
intrinsic resistance
the organism is inherently insensitive and responds poorly
43
acquired resistance
organism initially responds but subsequently does not
44
passive poison prevention strategies
require no change by the patient/individual | examples: reduce manufacture/sale, decrease amount of poison in the consumer product, prevent access, change formulation
45
classification of target organ toxicity
organs associated with the route of exposure, organs associated with metabolism and excretion, organs with selective vulnerability
46
portal triad
bile duct, portal vein, hepatic artery
47
what is the toxic metabolite of acetaminophen?
N-acetyl-p-benzo-quinone imine (NAPQI)
48
stages of acute acetaminophen toxicity
GI distress --> hepatic toxicity and possible renal failure --> worsening hepatic necrosis and hepatic encephalopathy
49
How would chronic acetaminophen toxicity present?
Elevated enzymes on liver function test
50
Reversal of acute acetaminophen toxicity
within 1hr: ipecac syrup within 4hr: activated charcoal within 8hr: N-acetylcysteine
51
ALT
alanine aminotransferase | most liver specific enzyme
52
AST
aspartate aminotransferase
53
ALP
alkaline phophatase
54
GGT
gamma-glutamyl transpeptidase
55
injury to the glomerulus
rare by drugs and more common by high blood pressure. Leads to altered permeability and proteinuria
56
injury to the proximal tubule
most common site of nephrotoxicity, which results in degeneration, inflammation, and repair reactions
57
injury to the loop of Henle/distal tubule/collecting duct
relatively rare. Effects include changes in water regulation, electrolytes, and acid-base balance which leads to a concentrated, slightly acidic urine. Most frequent effects are crystalluria and renal papillary necrosis.
58
analgesic nephropathy
chronic nephritis and renal papillary necrosis caused by chronic NSAID consumption and analgesic abuse
59
interstitial nephritis
can be acute or chronic. associated with an allergic reaction to many drugs and analgesic abuse. results in the swelling of the tubules (inflammation and edema), decreased urinary output, fever, rash, and vomiting
60
tests for chronic renal disease
glomerular filtration rate, blood pressure, protein in urine, and creatinine levels in blood.
61
aminoglycosides mechanism of nephrotoxicity
It is excreted primarily by glomerular filtration; reabsorbed by earlier segments of the proximal tubule (PT). Enters PT by endocytosis and is stored in lysosomes; it accumulates here and causes changes in renal concentrating ability, proteinuria, enzymuria, and changes in acid-base balance.
62
amphotericin B mechanism of nephrotoxicity
it causes vasoconstriction and decreased renal blood flow
63
calcineurin inhibitors mechanism of nephrotoxicity
renal blood flow and glomerular filtration rate are decreased due to vasoconstriction
64
NSAID side effect
gastric irritation and stomach cramping due to disruption of the mucosa, which also leads to bleeding and ulceration
65
Reye's syndrome
syndrome associated with use of aspirin in children who had viral infections
66
ototoxicity presentation
ringing in the ears (tinnitus), hearing loss, an inability to understand speech, loss of balance, dizziness, and spatial disorientation
67
medications that can cause ototoxicity
aspirin and other NSAIDs, certain antibiotics, antimalarial drugs, benzodiazepines, certain anticonvulsants, cancer drugs, loop diuretics, and tricyclic antidepressants
68
toxic interactions depend on...
concentration and duration of exposure
69
types of damage toxins can cause to the heart
direct structural damage, functional alteration, or indirect action
70
cardiovascular direct structural damage
inflammation, degeneration, and necrosis and can be difficult to distinguish from naturally occurring cardiovascular disease
71
cardiovascular functional alterations
change in rhythm, rate, or contraction and lead to a lethal arrhythmia
72
cardiovascular indirect action effects
secondary to a change in another organ system, including the autonomic nervous system, the central nervous system, and the endocrine system
73
consequences of coronary blood vessel occlusions
angina pectoris and myocardial infarction
74
angina pectoris
ischemic chest pain and one of the first symptoms of occlusion. It occurs when the oxygen supply to the myocardium is insufficient for its needs.
75
types of angina
stable, unstable, and variant
76
stable angina
most common. Predictable pain on exertion that's helped by rest or medication (nitroglycerin)
77
unstable angina
no pattern and is not helped by rest or medication. this is a dangerous, emergency situation that signals a heart attack.
78
variable angina
rare and spasm rather than atherosclerosis. It is pain at rest and usually seen in younger individuals and caused by genetics
79
how is the heart vulnerable to toxins
it has an excitable membrane, is coupled to an intracellular contraction system (synchronized), requires a constant supply of oxygen and nutrients, and is regulated by the peripheral autonomic nervous system and epinephrine and norepinephrine that is synthesized in the adrenal medulla. Lots of drugs mimic endogenous substances that affect the heart
80
effect of norepinephrine
Norepinephrine (sympathomimetics) act at adrenergic receptors to speed up heart rate. They increase depolarization, which increases impulse transmission, which increases heart rate and force of contraction
81
effect of acetylcholine
Acetylcholine (cholinomimetics) act at muscarinic receptors to decrease heart rate. They decrease the rate of depolarization, which decreases heart rate and ventricular contraction
82
consequences of prolonged QT syndrome
increased risk of arrhythmia, ventricular tachycardia, torsade des points, hypotension, and fainting. These effects can be potentially fatal as it degenerates into ventricular fibrillation and can result in sudden death.
83
therapeutic target of digoxin
the Na+/K+ ATPase
84
diagnostic tests for heart problems
electrocardiograms (ECG/EKG), chest X-ray, echocardiogram, angiogram, exercise stress test, and imaging such as computerized tomography (CT) or magnetic resonance imaging (MRI)
85
biomarkers after myocardial infarction
creatine phosphokinase (CPK), heart CK-MB, skeletal muscle CK-MM, myoglobin, troponin, and lactate dehydrogenase (LDH), which is a nonspecific biomarker of cell membrane damage
86
what lab is elevated with statin myalgia?
CK-MM

Foundations II (3 decks)

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