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Foundations II > Exam 4 vocab > Flashcards

Exam 4 vocab Flashcards

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
Q

90 day chronic exposure

A

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

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26
Q

Long term toxicity/cardiogenicity

A

often evaluated at the same time; small exposures over prolonged time; lifetime exposure (2 yr)

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27
Q

Reproductive toxicity

A

decreased fertility

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28
Q

teratogenicity

A

test for congenital malformations/fetal effects

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29
Q

Therapeutic index calculation

A

TD50/ED50 or MTC/MEC

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30
Q

Hazard

A

an inherent property - the potential of something to cause harm

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31
Q

Risk

A

probability of a particular adverse outcome

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32
Q

pharmacokinetic considerations

A

drug concentrations differ at target receptor, body weight, age, sex-related differences, pregnancy and lactation, health and disease

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33
Q

pharmacodynamic considerations

A

sex-related differences, circadian rhythms, drug tolerance, drug resistance

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34
Q

idiosyncrasy

A

an unexpected response or unexpected sensitivity to a drug that is frequently genetically based

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35
Q

allergic response

A

an adverse response to a drug as a result of a previous exposure to the same drug

36
Q

cross sensitivity

A

an allergic reaction to a structurally similar drug without prior exposure

37
Q

tolerance

A

a change in the way the body adapts to the presence of drug over time

38
Q

classic tolerance

A

progressively decreased responsiveness resulting in the need for a larger dose to elicit the same response

39
Q

pharmacokinetic (indirect) tolerance

A

changes at the site separate from the agonist site of action resulting in a decreased drug response (includes increased metabolism)

40
Q

pharmacodynamic (direct) tolerance

A

a change due to a change at the receptor level or the ability of a cell to respond (includes downregulation)

41
Q

resistance

A

commonly used term with respect to anti-tumor and anti-microbial drugs - insensitivity or decreased sensitivity of cells to drugs

42
Q

intrinsic resistance

A

the organism is inherently insensitive and responds poorly

43
Q

acquired resistance

A

organism initially responds but subsequently does not

44
Q

passive poison prevention strategies

A

require no change by the patient/individual

examples: reduce manufacture/sale, decrease amount of poison in the consumer product, prevent access, change formulation

45
Q

classification of target organ toxicity

A

organs associated with the route of exposure, organs associated with metabolism and excretion, organs with selective vulnerability

46
Q

portal triad

A

bile duct, portal vein, hepatic artery

47
Q

what is the toxic metabolite of acetaminophen?

A

N-acetyl-p-benzo-quinone imine (NAPQI)

48
Q

stages of acute acetaminophen toxicity

A

GI distress –> hepatic toxicity and possible renal failure –> worsening hepatic necrosis and hepatic encephalopathy

49
Q

How would chronic acetaminophen toxicity present?

A

Elevated enzymes on liver function test

50
Q

Reversal of acute acetaminophen toxicity

A

within 1hr: ipecac syrup
within 4hr: activated charcoal
within 8hr: N-acetylcysteine

51
Q

ALT

A

alanine aminotransferase

most liver specific enzyme

52
Q

AST

A

aspartate aminotransferase

53
Q

ALP

A

alkaline phophatase

54
Q

GGT

A

gamma-glutamyl transpeptidase

55
Q

injury to the glomerulus

A

rare by drugs and more common by high blood pressure. Leads to altered permeability and proteinuria

56
Q

injury to the proximal tubule

A

most common site of nephrotoxicity, which results in degeneration, inflammation, and repair reactions

57
Q

injury to the loop of Henle/distal tubule/collecting duct

A

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
Q

analgesic nephropathy

A

chronic nephritis and renal papillary necrosis caused by chronic NSAID consumption and analgesic abuse

59
Q

interstitial nephritis

A

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
Q

tests for chronic renal disease

A

glomerular filtration rate, blood pressure, protein in urine, and creatinine levels in blood.

61
Q

aminoglycosides mechanism of nephrotoxicity

A

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
Q

amphotericin B mechanism of nephrotoxicity

A

it causes vasoconstriction and decreased renal blood flow

63
Q

calcineurin inhibitors mechanism of nephrotoxicity

A

renal blood flow and glomerular filtration rate are decreased due to vasoconstriction

64
Q

NSAID side effect

A

gastric irritation and stomach cramping due to disruption of the mucosa, which also leads to bleeding and ulceration

65
Q

Reye’s syndrome

A

syndrome associated with use of aspirin in children who had viral infections

66
Q

ototoxicity presentation

A

ringing in the ears (tinnitus), hearing loss, an inability to understand speech, loss of balance, dizziness, and spatial disorientation

67
Q

medications that can cause ototoxicity

A

aspirin and other NSAIDs, certain antibiotics, antimalarial drugs, benzodiazepines, certain anticonvulsants, cancer drugs, loop diuretics, and tricyclic antidepressants

68
Q

toxic interactions depend on…

A

concentration and duration of exposure

69
Q

types of damage toxins can cause to the heart

A

direct structural damage, functional alteration, or indirect action

70
Q

cardiovascular direct structural damage

A

inflammation, degeneration, and necrosis and can be difficult to distinguish from naturally occurring cardiovascular disease

71
Q

cardiovascular functional alterations

A

change in rhythm, rate, or contraction and lead to a lethal arrhythmia

72
Q

cardiovascular indirect action effects

A

secondary to a change in another organ system, including the autonomic nervous system, the central nervous system, and the endocrine system

73
Q

consequences of coronary blood vessel occlusions

A

angina pectoris and myocardial infarction

74
Q

angina pectoris

A

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
Q

types of angina

A

stable, unstable, and variant

76
Q

stable angina

A

most common. Predictable pain on exertion that’s helped by rest or medication (nitroglycerin)

77
Q

unstable angina

A

no pattern and is not helped by rest or medication. this is a dangerous, emergency situation that signals a heart attack.

78
Q

variable angina

A

rare and spasm rather than atherosclerosis. It is pain at rest and usually seen in younger individuals and caused by genetics

79
Q

how is the heart vulnerable to toxins

A

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
Q

effect of norepinephrine

A

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
Q

effect of acetylcholine

A

Acetylcholine (cholinomimetics) act at muscarinic receptors to decrease heart rate. They decrease the rate of depolarization, which decreases heart rate and ventricular contraction

82
Q

consequences of prolonged QT syndrome

A

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
Q

therapeutic target of digoxin

A

the Na+/K+ ATPase

84
Q

diagnostic tests for heart problems

A

electrocardiograms (ECG/EKG), chest X-ray, echocardiogram, angiogram, exercise stress test, and imaging such as computerized tomography (CT) or magnetic resonance imaging (MRI)

85
Q

biomarkers after myocardial infarction

A

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
Q

what lab is elevated with statin myalgia?

A

CK-MM

Foundations II (3 decks)

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