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401 - Toxicology, Drug Abuse, Pharmacology > 12: Toxidrome and Dietary Supplements > Flashcards

12: Toxidrome and Dietary Supplements Flashcards

1
Q

toxidromes are based on

A

clinical sx associated with classes of toxins

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2
Q

5 main toxidromes

A

Sympathomimetics
anticholinergics
cholinergics
opioids
sedatives

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3
Q

which 2 classes are fast and furious

A

sympathomimetics and anticholinergics

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4
Q

which 2 classes are downers

A

cholinergics and opioids

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5
Q

the skin is _____ with anticholinergics

A

dry

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6
Q

the skin is _____ with sympathomimetics

A

wet

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7
Q

the skin is _____ with cholinergics

A

wet

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8
Q

what does PACED for bradycardia stand for

A

Propranolol/ poppies, anticholinesterase drugs, clonidine/ CCBs, ethanol, digoxin

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9
Q

what does FAST for tachycardia stand for

A

free base (cocaine), anticholinergics/ antihistamines/ amphetamines, sympathomimetics/ solvent abuse, theopylline

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10
Q

sympathomimetic key sx

A

Fast HR, high BP, sinus tachycardia, normal respiration, mydriatic eyes
CNS excitation, seizures, HPTN, sweating, hyperthermia, dehydration, rhabdomyolysis

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11
Q

list 3 common agents of sympathomimetic toxidrome

A

Amphetamines, cocaine, PCP, MOi, pseudoephedrine, phenylephrine, withdrawal form sedatives, SNRIs

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12
Q

what is the tx for sympathomimetic toxidrome

A

BZDs for agitation + prevent seizures
fluids
cooling
antihypertensives

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13
Q

how do anticholinergics cause their toxidrome?

A

Block PNS = unopposed sympathetic tone (anything that activates arousal will have large/ fast response)
Drugs have affinity for ACh receptor + antagonize muscarinic/ nicotinic receptors

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14
Q

what are the key sx to anticholinergic toxidrome

A

Similar charac to sympathomimetic toxidrome
Layered mental state (delirium), distinct speech, picking behavior of things in the air
High temp
dry skin + no secretions (dry mouth, no tears)

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15
Q

list 3 common agents of anticholinergic toxidrome

A

atropine, antiemetics, scopolamine, antihistamines, herbal supplements, antipsychotics, TCAs

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16
Q

how to tx anticholinergic SEs

A

physostigmine

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17
Q

cholinergic toxidrome MOA

A

Inhibits cholinesterases = ↑ACh
or acts on both central and peripheral nicotinic and muscarinic receptors (rest and digest response)

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18
Q

cholinergic toxidrome sx

A

Low RR, slow HR, normal to low BP/temp, slow cardiac rhythm, miotic eyes
Sweating a lot + lots of secretions

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19
Q

hat does SLUDGE stand for

A

salivation, lacrimation, urination, diarrhea, GI upset, emesis

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20
Q

what does the killer Bs stand for

A

bradycardia, bronchospasm, bronchorrhea (atropine- a lot)

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21
Q

what does dumbels stand for

A

diarrhea, urination, miosis, bronchospasm, emesis, lacrimation, salivation

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22
Q

common agents to a cholinergic toxidrome

A

Organophosphates, insecticides, some mushrooms, chemical warfare agents (sarin nerve gas), nicotine, physostigmine, pilocarpine

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23
Q

how to treat cholinergic toxidrome

A

atropine
pralidoxime

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24
Q

what receptors does atropine act on

A

muscarinic

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25
Q

what receptors does pralidoxime act on

A

nicotinic

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26
Q

sedatives MOA

A

CNS depression leading to decreased consciousness, modulation of GABA activity

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27
Q

sedative toxidrome sx

A

Loss of airway protective reflexes, respiratory depression, autonomic effects minimal
Drop in temp, no change in pupils
Sedation, somnolence, some ataxia

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28
Q

which medications have sedative toxidromes

A

BZDs
barbiturates
ethanol
chloral hydrate

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29
Q

how to treat sx of sedative toxidrome

A

flumazenil

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30
Q

caution with flumazenil

A

can trigger withdrawal to sedatives = seizure and arrhythmia risk

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31
Q

which organs are primarily affected by opioids

A

CNS, ocular, GI, respiratory

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32
Q

sx of opioid toxidrome

A

Respiratory depression, hypotension, CNS depression, coma
↓ mentation, pupils (not always seen early), pulse, temp, GI motility

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33
Q

tx of opioid OD

A

naloxone

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34
Q

serotonergic toxicity results from excess serotonin in the _______ and mainly involve the ____________ receptors

A

CNS
5HT1A, 5HT2A

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35
Q

serotonin toxicity has effects on __________________

A

thermoreg
behavioral and regulation of neuronal networks in brain and spinal cord

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36
Q

sx of serotonin toxicity

A

Altered mental status, hyperthermia, muscle rigidity, hyperreflexia, tremors, sympathetic effects, myoclonus (key)

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37
Q

what is the key sx of serotonin toxicity

A

myoclonus

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38
Q

how to tx serotonin toxicity

A

d/c offending agents
supportive care
intubation/ ventilation
BZDs

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39
Q

alcohol withdrawal develops ______ after last drink

A

6-24h

40
Q

sx of alcohol withdrawal

A

autonomic excitation, neuroexcitation, delirium tremens

41
Q

what are delirium tremens

A

severe form of withdrawal that is lethal- altered mental state + sympathetic overdrive

42
Q

sedative hypnotic withdrawal develops _____ after abruptly stopping

A

2-10 days

43
Q

sedative withdrawal sx

A

Agitation, insomnia, inattention, palpitations, hallucinations, spasticity, photophobia (mainly sympathetic response)

44
Q

opioid withdrawal is
1. life threatening
2. onset time depends on specific drug
3. may cause an increase in HR and BP, lacrimation, and piloerection
4. 2+3

A

4

45
Q

_____________: aromatic plants (ethereal or essential oils), evaporate at RT, odor, many are mucus membrane irritants, CNS activity (ex- catnip, chamomile, garlic)

A

volatile oil

46
Q

_____________ are esters of long chain fatty acids + alcohols, used as emollients, demulcents, bases of other products

A

fixed oils

47
Q

what kind of oils are the least dangerous

A

fixed oils

48
Q

__________ are heterogeneous group of alkaline and nitrogenous compounds, found throughout plants, many active and toxic compounds (ex- acotnium, goldenseal, Jimson weed)

A

alkaloids

49
Q

metal clay products are products used to

A

relieve joint pain, muscle, or other chronic diseases

50
Q

clay acidic extracts suppress

A

nitric oxide production and reduce inflammation

51
Q

st john’s wort chronic use causes

A

increased P-gp levels = more excretion and less absorption

52
Q

st john’s wort induces

A

CYP 3A4, 2E1, 2C19

53
Q

st/ john’s wort inhibits

A

MAO reuptake = more 5HT, NE, DA
COX 1 in platelets and TxA2

54
Q

which water soluble supplements have associated toxicity

A

ascorbic acid (vit C), nicotinic acid (VitB2), and pyridoxine (vit B6)

55
Q

which fat soluble vitamins have toxicity with OD/ chronic use

A

ADE

56
Q

vit K AEs

A

severe or fatal anaphylactoid reaction

57
Q

2 forms of vit A and their functions

A

retinol = storage form
carotenoid = precursor

58
Q

vit A is essential for

A

growth and differentiation of epithelial cells in mucus secreting or keratinizing tissues

59
Q

vit A is primarily stored in the

A

liver

60
Q

retinoid acid AEs

A

influences gene expression
hepatotoxicity
idiopathic intracranial hypertension

61
Q

which of the following is false for vit A
1. toxic effects more frequent with acute large ODs
2. affects the skin, hair, bones, and liver
3. causes yellow- orange discolouring of skin and nails
4. causes hypertension, HA, visual disturbances

A

1- more with chronic ingestions

62
Q

acute management of vit A OD

A

GI decontamination with activated charcoal

63
Q

vit D deficiency results in

A

rickets

64
Q

vit D must be metabolized by the ______ to active form

A

liver

65
Q

which vitamin regulates calcium

A

vit D

66
Q

T or F: toxic dose for vit D varies

A

T

67
Q

what are the early manifestations of vit D OD

A

weakness, fatigue, somnolence, irritability, muscle and bone pain, N/V, abd pain

68
Q

chronic vit D OD results in

A

polyuria and polydipsia, nephrolithiasis (kidney stones)

69
Q

severe vit D OD sees

A

ataxia, confusion, psychosis, seizures, AKI, cardiac dysrhythmias

70
Q

how to tx vit D OD

A

Discontinue + supportive care
Oral or IV fluids
Calcitonin to sequester some vit D

71
Q

vit E has _____ properties, protects polyunsaturated FA from _____ and binds to ___________

A

antioxidant
oxidation
peroxyl radicals

72
Q

high doses of vit E act as

A

prooxidant

73
Q

vit D OD SEs

A

N/D, abd cramps

74
Q

vit ___ antagonizes vit K by increasing _________ to inactive form

A

E
eposidation

75
Q

how to tx vit E OD

A

d/c and supportive care

76
Q

vit C supposed “benefits” with little to no objective data include

A

reported antioxidant properties, scurvy, wound healing, cataracts, aging, mental attentiveness, decrease stress

77
Q

how is vit D absorbed

A

active transport in intestines

78
Q

vit ___ is a cofactor in several hydroxylation and amidation reactions

A

C

79
Q

vit ___ has prooxidant properties and high concs

A

C

80
Q

vit C AEs

A

oxalosis and kidney stones
GI effect- localized esophagitis, diarrhea

81
Q

vit B6 is absorbed in ___, metabolized, and excreted ______

A

intestinal tract
renal excretion

82
Q

what is the active form of vit B6 and what does it do

A

PLP = active form
coenzyme for synthesis of GABA

83
Q

vit ____ is used as tx of N/V in pregnancy

A

V6

84
Q

deficiency and excess of vit B6 is characterized by

A

neurologic effects, peripheral sens effects

85
Q

vit B6 toxicity sx

A

Chronic OD: progressive sensory ataxia and severe distal impairments of proprioception and vibratory sensation
Reflexes diminished or absent, but touch/ pain/ temp min affected

86
Q

vit B3 is also known as

A

niacin

87
Q

niacin is converted into _________ and incorporated int ________

A

nicotinamide
cofactor NAD

88
Q

vit B3 decreases

A

TG and VLDL synthesis
LCL-C

89
Q

vit B3 increases

A

HDL-C

90
Q

deficiency of B3 =

A

pellegra

91
Q

excess of B3 =

A

flushing

92
Q

flushing from B3 is due to

A

production of PGD2 and PGE2

93
Q

IR AEs of B3

A

flushing, dyspepsia

94
Q

ER AEs of B3

A

Gi effects, hepatotoxicity

95
Q

severe cases of B3 OD =

A

fulminant hepatic failure, hepatic encephalopathy

96
Q

tx for B3 toxicity

A

NSAID (aspirin) prior to admin = inhibit COX
Take with food (avoid EtOH, spicy)
Gradual increment of dosing
Tolerance to flushing develops in weeks

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

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