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401 - Toxicology, Drug Abuse, Pharmacology > 8: Organ Toxicity > Flashcards

8: Organ Toxicity Flashcards

1
Q

5 types of hepatotoxiicty

A

hepatocellular necrosis
steatosis
chronic hepatitis
cholestasis
fibrosis/ cirrhosis

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2
Q

what is hepatocellular necrosis

A

ncrotic cell loss

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3
Q

what is steatosis

A

abnormal accumulation of fat in hepatocytes

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4
Q

what is chronic hepatitis

A

hepatic inflammation

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5
Q

what is cholestasis

A

obstruction of the flow of bile salts

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6
Q

what is fibrosis/ cirrhosis

A

pathological wound healing, scarring, increased connective tissue

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7
Q

DILI is ____ but _____ and often ______ to manage/ diagnose
fill in the blanks: common/ uncommon, clinically important/ unimportant, difficult/ easy to manage

A

uncommon
clinically important
difficult to diagnose /manage

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8
Q

which of the following is dose related and predictable
1. direct hepatotox
2. idiosyncratic hepatotox
3. indirect hepatotox

A

1

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9
Q

causes of direct hepatotoxicity

A

intrinsic hepatotoxicity when agent given in high doses

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10
Q

causes of idioxyncratic hepatotoxicity

A

indiosyncratic metabolic or immunologic reaction

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11
Q

causes of indirect hepatotoxicity

A

indirect action of agent on liver/ immune system

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12
Q

T or F: toxins can affect any part of the kidney but not all result in decreased GFR

A

T

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13
Q

nephrotoxicity results ini

A

AKI, CKD, and functional kidney disorders

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14
Q

damage to the kidneys, reusltilng in AKI, CKD, and others see changes such as (3)

A

decreased ability to excrete wastes
disruption to fluid and electrolyte homeostasis
renal hormones impacted (ex- erythropoietin)

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15
Q

which of the following is false about the CNS
1. the CNS has high cellular interdependence
2. the CNS has high metabolic demant
3. there is a limited understasnding of its normal chemical and molecular function
4. it is a complex system requiring a 3 basic cell types

A

4

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16
Q

neuropathies =

A

degeneration of neurons

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17
Q

peripheral neuropathy is

A

damage to sensory, motor, or autonomic PNS

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18
Q

what is excitotoxicity

A

energy needs exceeds production = no ATP to restore or maintain ion gradients

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19
Q

demyelination impacts

A

the production and maintenance of myelin

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20
Q

MAOi inhibits

A

presynaptic metabolism

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21
Q

amphetamimnes stimulate

A

neuronal release of NT

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22
Q

ACh esterase inhibitors inhibit

A

synaptic degradation of ACh

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23
Q

botulinum toxins inhibit

A

release of neurotransmitters

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24
Q

respiratory toxicity can manifest as

A

pulmonary irritation, asthma/ bronchitis, reactive airway disease, emphysema, allergic alveolitis, fibrotic lung disease, pneumoconiosis, lung cancer

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25
Q

what is the central compartment of PK

A

blood

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26
Q

what has direct contact with every systemic xenobiotic

A

blood

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27
Q

because blood comes into contact with almost all toxins, toxins in the blood can disrupt

A

homeostasis

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28
Q

3 functions of skin

A

shields internal organs
maintains homeostasis
prevents infections

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29
Q

3 main components of skin

A

epidermis, dermis, hypodermis

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30
Q

what is one of the most common body systems for ADRs

A

skin

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31
Q

transdermal xenobiotic absorption depends on

A

passive diffusion
lipid solubility
concentration gradient
MW
skin permeability

32
Q

burns are mostly ________ rather than ________

A

chemical reactivity rather than thermal damage

33
Q

chemical reactivity burns may be caused by

A

oxidizing or reducing agents, corrosives, protoplasmic poisons, desiccants, or vessicants

34
Q

chemical burns often appear _________ but can _________

A

mild/ superficial
can progress in 24-36hrs to necrosis

35
Q

list 3 systemic injuries/ diseases that manifest dermatologically

A

cyanosis
xanthoderma
pruritus
flushing
sweating
dyspigmentation

36
Q

urticaria is a type ___ reaction

A

1- IgE

37
Q

bullous reactions are often _____ or _____ related

A

xenobiotic or autoimmune

38
Q

drug induced hypersensitivity sx is characterized by

A

fever, skin eruptions, internal organ involvement

39
Q

drug induced hypersensitivity sx is more common in patients with underlying diseases like

A

hepatitis, interstitial nephritis, vasculitis, pneumonitis, autoimmune hypothyroidism

40
Q

anticoagulant induced skin necrosis is usually due to ______ and starts ______

A

warfarin
3-5 days after initiation

41
Q

anticoagulant induced skin necrosis corresponds to ________________________ from warfarin tx. it results from _________________

A

expected early decline in protein C function

results from antibodies that bind to complexes of heparin and platelet factor 4 and induce aggregation

42
Q

SJS/ TENs is due to drugs activating ________________ = triggering extensive apoptosis

A

cytotoxic T lymphocytes + Fas ligand/ perforin granzyme pathways

43
Q

SJS/ TENs is a ____ mediated, type ___ hypersensitivity

A

T cell mediated
type 4 hypersensitivity

44
Q

_______ dermatitis occurs when a xenobiotic comes into contact with skin

A

xenobiotic

45
Q

allergic contact dermatitis is a type ___ hypersensitivity reaction

A

4

46
Q

What is the difference between allergic and irritant contact dermatitis

A

irritant contact dermatitis does not require prior antigen sensitization

47
Q

what is the pathophys of nonreversible CV toxicity

A

cell loss through necrosis/ apoptosis

48
Q

what is usually seen on diagnosis of nonreversible CV toxicity

A

injury marker release, progressive contractile dysfunction, cardiac remodeling

49
Q

what are some manifestations of nonrev cardio tox

A

cardiomyopathy, HF, MI, thrombosis- progressive in nature

50
Q

what is the pathophys of reversible CV damage

A

cellular dysfunction

51
Q

upon diagnosis of reversible CV toxicity, what is usually seen

A

no injury marker release, reversible contractile dysfunction, reversible arterial hypertension

52
Q

reversible CV toxicity manifestations include

A

temporary contractile dysfunction, vasospastic angina, arterial hypertension - normalizes over time

53
Q

list 3 possible characteristics of cardiotoxicity

A

abnormalities in repolarization
reduced ventricular ejection
fibrosis
HF
altered hemodynamics
hemostasis and thrombosis

54
Q

when xenobiotics imapct cardiac contractility, there are changes in

A

ejection fraction, CO, BP

55
Q

inotrophy is dependent on

A

sympathetic/ parasympathetic NS, preload/ afterload, HR, catecholamines

56
Q

mechs of cardiotox are usually _______ and/or _______

A

multifactorial
unknown

57
Q

Xenobiotics can directly cause dysrhythmias/ cardiac conduction abnormalities by affecting _________ or indirectly via _________

A

the cell membrane
metabolic effects

58
Q

how does atropine affect the HR + MOA

A

rises HR- blocks inhibitor effect of vagal influence

59
Q

phenylephrine effect on HR

A

bradycardia

60
Q

arrhythmias result from alterations of

A

impulse formation or conduction

61
Q

what 2 drug classes cause hyperkalemia

A

Cardioactive steroids
Beta adrenergic blockers

62
Q

3 classes of drugs that cause hypokalemia

A

loop diuretics, insulin, thiazide diuretics

63
Q

list the ECG changes that occur with increasing K+ conc

A

peaked T waves - PR prolongation - loss of P wave - QRS widening - sine wave

64
Q

describe the ECG changes that occur with decreasing K+ conc

A

flattening of T wave- appearance of U waves - depression of ST segments

65
Q

which 5 drugs cause hypercalcemia

A

All trans retinoic acid
Androgens
Antacids
Lithium
Thiazide diuretics

66
Q

xenobiotics more commonly cause _______ than _________
- calcium changse

A

hypocalcemia > hypercalcemia

67
Q

T or F: ECG abnormalities from calcium changes are common, but life threatening dysrhythmias are rare

A

T

68
Q

the hERG gene encodes a _________

A

pore forming subunit of rapidly activating delayed rectifier cardiac K+ channel

69
Q

xenobiotics cause HPTN by

A

CNS synpathetic overactivity
increased myocardial contractility
increased peripheral resistance

70
Q

xenobiotics cause hypotension by

A

decreasing peripheral vascular resistance
decreasing myocardial contractility
dysrhythmias
depletion of intravascular volume

71
Q

the antitumor properties of anthracyclines come from

A

inhibition of topoisomerase and DNA synthesis

72
Q

LT AEs of anthracyclines

A

cardiomyopahty and congestive HF

73
Q

_________ is inflammation of the myocardium

A

myocarditis

74
Q

what is the most common cause of myocarditis

A

viral infection

75
Q

list 3 RFs for cardiotoxicity in cardiooncology

A

Prior anthracycline based tx or combined trastuzumab/ anthracycline
Elderly (>75yrs)
Prior mediastinal or chest radiotherapy
HPTN, diabetes
Smoker
Very young (<10yrs)
Elevated cardiac biomarkers
Baseline abnormal LV systolic function (LVEF <50%)

401 - Toxicology, Drug Abuse, Pharmacology (32 decks)

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