12: Toxidrome and Dietary Supplements Flashcards
toxidromes are based on
clinical sx associated with classes of toxins
5 main toxidromes
Sympathomimetics
anticholinergics
cholinergics
opioids
sedatives
which 2 classes are fast and furious
sympathomimetics and anticholinergics
which 2 classes are downers
cholinergics and opioids
the skin is _____ with anticholinergics
dry
the skin is _____ with sympathomimetics
wet
the skin is _____ with cholinergics
wet
what does PACED for bradycardia stand for
Propranolol/ poppies, anticholinesterase drugs, clonidine/ CCBs, ethanol, digoxin
what does FAST for tachycardia stand for
free base (cocaine), anticholinergics/ antihistamines/ amphetamines, sympathomimetics/ solvent abuse, theopylline
sympathomimetic key sx
Fast HR, high BP, sinus tachycardia, normal respiration, mydriatic eyes
CNS excitation, seizures, HPTN, sweating, hyperthermia, dehydration, rhabdomyolysis
list 3 common agents of sympathomimetic toxidrome
Amphetamines, cocaine, PCP, MOi, pseudoephedrine, phenylephrine, withdrawal form sedatives, SNRIs
what is the tx for sympathomimetic toxidrome
BZDs for agitation + prevent seizures
fluids
cooling
antihypertensives
how do anticholinergics cause their toxidrome?
Block PNS = unopposed sympathetic tone (anything that activates arousal will have large/ fast response)
Drugs have affinity for ACh receptor + antagonize muscarinic/ nicotinic receptors
what are the key sx to anticholinergic toxidrome
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)
list 3 common agents of anticholinergic toxidrome
atropine, antiemetics, scopolamine, antihistamines, herbal supplements, antipsychotics, TCAs
how to tx anticholinergic SEs
physostigmine
cholinergic toxidrome MOA
Inhibits cholinesterases = ↑ACh
or acts on both central and peripheral nicotinic and muscarinic receptors (rest and digest response)
cholinergic toxidrome sx
Low RR, slow HR, normal to low BP/temp, slow cardiac rhythm, miotic eyes
Sweating a lot + lots of secretions
hat does SLUDGE stand for
salivation, lacrimation, urination, diarrhea, GI upset, emesis
what does the killer Bs stand for
bradycardia, bronchospasm, bronchorrhea (atropine- a lot)
what does dumbels stand for
diarrhea, urination, miosis, bronchospasm, emesis, lacrimation, salivation
common agents to a cholinergic toxidrome
Organophosphates, insecticides, some mushrooms, chemical warfare agents (sarin nerve gas), nicotine, physostigmine, pilocarpine
how to treat cholinergic toxidrome
atropine
pralidoxime
what receptors does atropine act on
muscarinic
what receptors does pralidoxime act on
nicotinic
sedatives MOA
CNS depression leading to decreased consciousness, modulation of GABA activity
sedative toxidrome sx
Loss of airway protective reflexes, respiratory depression, autonomic effects minimal
Drop in temp, no change in pupils
Sedation, somnolence, some ataxia
which medications have sedative toxidromes
BZDs
barbiturates
ethanol
chloral hydrate
how to treat sx of sedative toxidrome
flumazenil
caution with flumazenil
can trigger withdrawal to sedatives = seizure and arrhythmia risk
which organs are primarily affected by opioids
CNS, ocular, GI, respiratory
sx of opioid toxidrome
Respiratory depression, hypotension, CNS depression, coma
↓ mentation, pupils (not always seen early), pulse, temp, GI motility
tx of opioid OD
naloxone
serotonergic toxicity results from excess serotonin in the _______ and mainly involve the ____________ receptors
CNS
5HT1A, 5HT2A
serotonin toxicity has effects on __________________
thermoreg
behavioral and regulation of neuronal networks in brain and spinal cord
sx of serotonin toxicity
Altered mental status, hyperthermia, muscle rigidity, hyperreflexia, tremors, sympathetic effects, myoclonus (key)
what is the key sx of serotonin toxicity
myoclonus
how to tx serotonin toxicity
d/c offending agents
supportive care
intubation/ ventilation
BZDs
alcohol withdrawal develops ______ after last drink
6-24h
sx of alcohol withdrawal
autonomic excitation, neuroexcitation, delirium tremens
what are delirium tremens
severe form of withdrawal that is lethal- altered mental state + sympathetic overdrive
sedative hypnotic withdrawal develops _____ after abruptly stopping
2-10 days
sedative withdrawal sx
Agitation, insomnia, inattention, palpitations, hallucinations, spasticity, photophobia (mainly sympathetic response)
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
_____________: aromatic plants (ethereal or essential oils), evaporate at RT, odor, many are mucus membrane irritants, CNS activity (ex- catnip, chamomile, garlic)
volatile oil
_____________ are esters of long chain fatty acids + alcohols, used as emollients, demulcents, bases of other products
fixed oils
what kind of oils are the least dangerous
fixed oils
__________ are heterogeneous group of alkaline and nitrogenous compounds, found throughout plants, many active and toxic compounds (ex- acotnium, goldenseal, Jimson weed)
alkaloids
metal clay products are products used to
relieve joint pain, muscle, or other chronic diseases
clay acidic extracts suppress
nitric oxide production and reduce inflammation
st john’s wort chronic use causes
increased P-gp levels = more excretion and less absorption
st john’s wort induces
CYP 3A4, 2E1, 2C19
st/ john’s wort inhibits
MAO reuptake = more 5HT, NE, DA
COX 1 in platelets and TxA2
which water soluble supplements have associated toxicity
ascorbic acid (vit C), nicotinic acid (VitB2), and pyridoxine (vit B6)
which fat soluble vitamins have toxicity with OD/ chronic use
ADE
vit K AEs
severe or fatal anaphylactoid reaction
2 forms of vit A and their functions
retinol = storage form
carotenoid = precursor
vit A is essential for
growth and differentiation of epithelial cells in mucus secreting or keratinizing tissues
vit A is primarily stored in the
liver
retinoid acid AEs
influences gene expression
hepatotoxicity
idiopathic intracranial hypertension
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
acute management of vit A OD
GI decontamination with activated charcoal
vit D deficiency results in
rickets
vit D must be metabolized by the ______ to active form
liver
which vitamin regulates calcium
vit D
T or F: toxic dose for vit D varies
T
what are the early manifestations of vit D OD
weakness, fatigue, somnolence, irritability, muscle and bone pain, N/V, abd pain
chronic vit D OD results in
polyuria and polydipsia, nephrolithiasis (kidney stones)
severe vit D OD sees
ataxia, confusion, psychosis, seizures, AKI, cardiac dysrhythmias
how to tx vit D OD
Discontinue + supportive care
Oral or IV fluids
Calcitonin to sequester some vit D
vit E has _____ properties, protects polyunsaturated FA from _____ and binds to ___________
antioxidant
oxidation
peroxyl radicals
high doses of vit E act as
prooxidant
vit D OD SEs
N/D, abd cramps
vit ___ antagonizes vit K by increasing _________ to inactive form
E
eposidation
how to tx vit E OD
d/c and supportive care
vit C supposed “benefits” with little to no objective data include
reported antioxidant properties, scurvy, wound healing, cataracts, aging, mental attentiveness, decrease stress
how is vit D absorbed
active transport in intestines
vit ___ is a cofactor in several hydroxylation and amidation reactions
C
vit ___ has prooxidant properties and high concs
C
vit C AEs
oxalosis and kidney stones
GI effect- localized esophagitis, diarrhea
vit B6 is absorbed in ___, metabolized, and excreted ______
intestinal tract
renal excretion
what is the active form of vit B6 and what does it do
PLP = active form
coenzyme for synthesis of GABA
vit ____ is used as tx of N/V in pregnancy
V6
deficiency and excess of vit B6 is characterized by
neurologic effects, peripheral sens effects
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
vit B3 is also known as
niacin
niacin is converted into _________ and incorporated int ________
nicotinamide
cofactor NAD
vit B3 decreases
TG and VLDL synthesis
LCL-C
vit B3 increases
HDL-C
deficiency of B3 =
pellegra
excess of B3 =
flushing
flushing from B3 is due to
production of PGD2 and PGE2
IR AEs of B3
flushing, dyspepsia
ER AEs of B3
Gi effects, hepatotoxicity
severe cases of B3 OD =
fulminant hepatic failure, hepatic encephalopathy
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
