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
what receptors does pralidoxime act on
nicotinic
26
sedatives MOA
CNS depression leading to decreased consciousness, modulation of GABA activity
27
sedative toxidrome sx
Loss of airway protective reflexes, respiratory depression, autonomic effects minimal Drop in temp, no change in pupils Sedation, somnolence, some ataxia
28
which medications have sedative toxidromes
BZDs barbiturates ethanol chloral hydrate
29
how to treat sx of sedative toxidrome
flumazenil
30
caution with flumazenil
can trigger withdrawal to sedatives = seizure and arrhythmia risk
31
which organs are primarily affected by opioids
CNS, ocular, GI, respiratory
32
sx of opioid toxidrome
Respiratory depression, hypotension, CNS depression, coma ↓ mentation, pupils (not always seen early), pulse, temp, GI motility
33
tx of opioid OD
naloxone
34
serotonergic toxicity results from excess serotonin in the _______ and mainly involve the ____________ receptors
CNS 5HT1A, 5HT2A
35
serotonin toxicity has effects on __________________
thermoreg behavioral and regulation of neuronal networks in brain and spinal cord
36
sx of serotonin toxicity
Altered mental status, hyperthermia, muscle rigidity, hyperreflexia, tremors, sympathetic effects, myoclonus (key)
37
what is the key sx of serotonin toxicity
myoclonus
38
how to tx serotonin toxicity
d/c offending agents supportive care intubation/ ventilation BZDs
39
alcohol withdrawal develops ______ after last drink
6-24h
40
sx of alcohol withdrawal
autonomic excitation, neuroexcitation, delirium tremens
41
what are delirium tremens
severe form of withdrawal that is lethal- altered mental state + sympathetic overdrive
42
sedative hypnotic withdrawal develops _____ after abruptly stopping
2-10 days
43
sedative withdrawal sx
Agitation, insomnia, inattention, palpitations, hallucinations, spasticity, photophobia (mainly sympathetic response)
44
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
4
45
_____________: aromatic plants (ethereal or essential oils), evaporate at RT, odor, many are mucus membrane irritants, CNS activity (ex- catnip, chamomile, garlic)
volatile oil
46
_____________ are esters of long chain fatty acids + alcohols, used as emollients, demulcents, bases of other products
fixed oils
47
what kind of oils are the least dangerous
fixed oils
48
__________ are heterogeneous group of alkaline and nitrogenous compounds, found throughout plants, many active and toxic compounds (ex- acotnium, goldenseal, Jimson weed)
alkaloids
49
metal clay products are products used to
relieve joint pain, muscle, or other chronic diseases
50
clay acidic extracts suppress
nitric oxide production and reduce inflammation
51
st john's wort chronic use causes
increased P-gp levels = more excretion and less absorption
52
st john's wort induces
CYP 3A4, 2E1, 2C19
53
st/ john's wort inhibits
MAO reuptake = more 5HT, NE, DA COX 1 in platelets and TxA2
54
which water soluble supplements have associated toxicity
ascorbic acid (vit C), nicotinic acid (VitB2), and pyridoxine (vit B6)
55
which fat soluble vitamins have toxicity with OD/ chronic use
ADE
56
vit K AEs
severe or fatal anaphylactoid reaction
57
2 forms of vit A and their functions
retinol = storage form carotenoid = precursor
58
vit A is essential for
growth and differentiation of epithelial cells in mucus secreting or keratinizing tissues
59
vit A is primarily stored in the
liver
60
retinoid acid AEs
influences gene expression hepatotoxicity idiopathic intracranial hypertension
61
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
1- more with chronic ingestions
62
acute management of vit A OD
GI decontamination with activated charcoal
63
vit D deficiency results in
rickets
64
vit D must be metabolized by the ______ to active form
liver
65
which vitamin regulates calcium
vit D
66
T or F: toxic dose for vit D varies
T
67
what are the early manifestations of vit D OD
weakness, fatigue, somnolence, irritability, muscle and bone pain, N/V, abd pain
68
chronic vit D OD results in
polyuria and polydipsia, nephrolithiasis (kidney stones)
69
severe vit D OD sees
ataxia, confusion, psychosis, seizures, AKI, cardiac dysrhythmias
70
how to tx vit D OD
Discontinue + supportive care Oral or IV fluids Calcitonin to sequester some vit D
71
vit E has _____ properties, protects polyunsaturated FA from _____ and binds to ___________
antioxidant oxidation peroxyl radicals
72
high doses of vit E act as
prooxidant
73
vit D OD SEs
N/D, abd cramps
74
vit ___ antagonizes vit K by increasing _________ to inactive form
E eposidation
75
how to tx vit E OD
d/c and supportive care
76
vit C supposed "benefits" with little to no objective data include
reported antioxidant properties, scurvy, wound healing, cataracts, aging, mental attentiveness, decrease stress
77
how is vit D absorbed
active transport in intestines
78
vit ___ is a cofactor in several hydroxylation and amidation reactions
C
79
vit ___ has prooxidant properties and high concs
C
80
vit C AEs
oxalosis and kidney stones GI effect- localized esophagitis, diarrhea
81
vit B6 is absorbed in ___, metabolized, and excreted ______
intestinal tract renal excretion
82
what is the active form of vit B6 and what does it do
PLP = active form coenzyme for synthesis of GABA
83
vit ____ is used as tx of N/V in pregnancy
V6
84
deficiency and excess of vit B6 is characterized by
neurologic effects, peripheral sens effects
85
vit B6 toxicity sx
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
vit B3 is also known as
niacin
87
niacin is converted into _________ and incorporated int ________
nicotinamide cofactor NAD
88
vit B3 decreases
TG and VLDL synthesis LCL-C
89
vit B3 increases
HDL-C
90
deficiency of B3 =
pellegra
91
excess of B3 =
flushing
92
flushing from B3 is due to
production of PGD2 and PGE2
93
IR AEs of B3
flushing, dyspepsia
94
ER AEs of B3
Gi effects, hepatotoxicity
95
severe cases of B3 OD =
fulminant hepatic failure, hepatic encephalopathy
96
tx for B3 toxicity
NSAID (aspirin) prior to admin = inhibit COX Take with food (avoid EtOH, spicy) Gradual increment of dosing Tolerance to flushing develops in weeks