Poison and Toxicity Flashcards
Is used to treat serotonin syndrome
Cyproheptadine
- discontinue the offending meds
- benzodiazepines (to manage agitation & muscle rigidity)
- severe cases, serotonin antagonists like cyproheptadine
Medication used in management of neuroleptic malignant syndrome (NMS) and Malignant hyperthermia (MH)
Dantrolene
- NMS can develop in pts taking antipsychotic agents (quetiapine)
- Malignant hyperthermia (MH) in susceptible pts s/t inhalation anesthetics (halothane) or succinylcholine
——————
NMS (fever, ams, muscle rigidity, and autonomic dysfunction such as tachycardia and diaphoresis). often after the administration of antipsychotics.
Malignant hyperthermia (fever, muscle rigidity, tachycardia, and metabolic acidosis)
Functional anemia due to reduced oxygen delivery to tissues. Occurs after exposure to oxidizing agents (eg, dapsone, nitrates, topical/local anesthetics).
Methemoglobinemia
(iron oxidized to Ferric iron Fe3+)
Binds to ferric iron in CYTOchrome oxidase a3 in the mitochondrial ETC. This blocks oxidative phosphorylation and results in anaerobic metabolism, causing lactic acidosis.
Cyanide
Cyanide poisoning s/t fires, mines, nitroprusside, grilling, plastics
Cyanide poisoning causes what to build up in the body
lactic acid
(lactic acidosis)
Markedly elevated lactate level (eg, >10 mEq/L) areexpected.
Cyanide toxicity can be treated with an antidote such as [1st line] or [2nd line], which directly binds cyanide molecules.
hydroxocobalamin (Vit B12 derivative)
sodium thiosulfate (2nd line)
Alternate tx is induction of methemoglobinemia w/ nitrites for alt bind
Sodium nitrite + sodium thiosulfate is an alternate treatment but is contraindicated in CO poisoning
Ingested Cyanide Treated with Activated:
charcoal
Acute cyanide toxicity causes neurologic and cardiorespiratory stimulation which presents with:
* Lactic Acidosis
* Cherry Red Skin
* ____,
* vertigo,
* ____,
* hyperventilation,
* tachycardia,
* nausea, and
* vomiting.
headache
dizziness
Neurologic, respiratory, and cardiovascular DEPRESSION s/t untreated cyanide poisoning eventually results in
- coma,
- seizures,
- ____,
- hypotension, and
- ___
bradycardia
cardiorespiratory arrest
Early symptoms of carbon monoxide poisoning are neurological and include
agitation, ___, ____
confusion
& somnolence
Faulty indoor heating, Gas motors or inhalation of smoke from fire/grill, etc.
can cause ___ poisoning
carbon monoxide
CO binds to Hgb with greater affinity than O2 (displaces oxygen) creating ______.
* Reduces O2 carrying capacity (Left shift curve)
* Decreases O2 unloading (less O2 delivery)
* Impairs O2 utilization (disrupts mitochondrial oxidative phosphorylation)**
carboxyhemoglobin
carbon monoxide poisoning
Sodium nitrite + sodium thiosulfate is an alternate treatment but is contraindicated in carbon monoxide poisoning
Work up indicated for diagnosis of Carbon Monoxide poisoning (3)
ABG: ↑ carboxyhemoglobin level
ECG ± cardiac enzymes
Acute carbon monoxide (CO) poisoning can induce a ____
which is associated with increased mortality.
myocardial infarction (MI)
severe CO poisoning can cause:
*Cerebral hypoxia: Drowsiness, confusion, seizures, syncope, coma
*Lactic acidosis: impairs O2 use
*Myocardial injury: Arrhythmias, MI, or pulmonary edema
High-voltage Electrical injuries:
_ c/b
* Acute compartment syndrome (intracompartmental muscle swelling)
* Rhabdomyolysis (leakage of heme pigment into blood)
* Heme pigment–induced AKI (intratubular cast formation)
Seizures
* rarely, Brain Herniation
Interruption of normal cardiac impulse conduction
* arrhythmias (Ventricular Fibrillation)
* Cardiac Arrest
Skeletal muscle necrosis
- Acute compartment syndrome (intracompartmental muscle swelling)
- Rhabdomyolysis (leakage of heme pigment into blood)
- Heme pigment–induced AKI (intratubular cast formation)
Treatment is
Aggressive IVF resuscitation
High risk of hyperkalemia from rhabdo → avoid potassium-containing IVFs (LR, NS, Plasma LYTE)
___ ± ___ & ___
→ indicated for Methanol & Ethylene Glycol ingestion
Fomepizole
Hemodialysis in severe cases (end-organ damage)
IV NaHCO3 if pH <7.3
BOTH
Methanol/Ethylene Glycol toxicity presents with
Altered Mental Status
Early: CNS sedation & inebriation, osmolar gap
Late: anion gap metabolic acidosis + tachypnea (compensatory)
* Methanol ingestion causes _.
* Ethylene Glycol (anti-freeze) causes _ & _.
- vision changes (cloudy eyes)
- Flank pain + Hematuria
* Urine oxalate crystals, hypocalcemia, AKI
Organophosphate poisoning presents with DUMBELS.
List the mnemonic
Muscarinic:
* Diarrhea/diaphoresis
* Urination
* Miosis
* Bronchospasms, bronchorrhea, bradycardia
* Emesis
* Lacrimation
* Salivation
Nicotinic:
* muscle weakness
* paralysis
* fasciculations
____ poisoning presents with Muscarinic (DUMBELS) ± Nicotinic sxs
Organophosphate
Management of organophosphate toxicity includes:
* Stabilization of ABCs.
* Decontamination (remove soiled clothes, irrigation of skin) to stop further exposure.
* Administer antidote: ____ (reverses muscarinic sxs & cholinergic hyperstimulation)
* After antidote give: ____ (reverses nicotinic & muscarinic symptoms)
Atropine (competitive inhibitor of muscarinic acetylcholine receptor)
Pralidoxime (cholinesterase-reactivating agent ↑ Ach breakdown)
Atropine does not act on the nicotinic receptors.
Neuromusc sxs → pralid
Pralidoxime ONLY given after Atropine, because transient acetylcholinesterase inhibitionmomentarily worsen symptoms
What is the antidote for anticholinergic toxicity?
Anticholinergic toxicity toxidrome:
* Agitation (mad hatter)
* Tachycardia (fast fiddle)
* dilated pupils (blind bat)
* dry skin/mucous membranes (dry bone)
* urinary retention (full flask)
* hyperthermia (hot hare)
* decreased bowel sounds
* HTN
Physostigmine
(an indirect-acting CHOLINERGIC AGONIST)
Hydrofluoric acid burns (eg, glass etching, cleaning solutions) are corrosive & can cause local tissue destruction with life-threatening ___ ( s/t Hypomagnesemia & Hypocalcemia).
It’s a medical emergency that requires rapid treatment with (3)
cardiac arrhythmias
Treatment:
*copious irrigation
*topical calcium gluconate gel
*cardiac & electrolyte monitoring
Large Local Reaction
* Often s/t bites from bees, ants, wasps, etc
* ~10 cm+ localized swelling, erythema & warmth ____ w/ sting site
* Happens w/in 24 hr, peaks at 24-48 hr, resolve in 5-10 days
CONTIGUOUS
Pathophysiology: Exaggerated, IgE-mediated, local allergic response
Large Local Reaction treatment
* Cold compresses
* if moderate ____ or if severe ____
* oral antihistamines
* NSAIDS
Topical high-potency corticosteroids (clobetasol 0.05%)
or PO Prednisone, if severe
systemic sxs like vomiting, urticaria, swelling of the airway, bronchospasm, shock, hypotension)can also occur and should be treated similarly to anaphylaxis w/ IM or IV Epinephrine.
____: windshield wiper fluid, contaminated homemade liquor
____: automotive coolant/antifreeze, brake fluid
Industrial solvents & deicing solutions may contain either toxic alcohol
Methanol
Ethylene glycol
EG metabolized by alcohol dehydrogenase to glycolic acid & oxalic acid
What is the antidote for Methanol and Ethylene glycol poisoning?
Fomepizole
It inhibits alcohol dehydrogenase
What is the antidote for Methemoglobinemia?
Methylene blue
Methemoglobinemia develops after use of Dapsone or anesthetic agents.
What is the antidote for acetaminophen toxicity?
Can cause liver failure: Jaundice, elevated prothrombin time
N-acetylcysteine
activated charcol given for gastric decomtamination
Potentially toxic single dose of acetaminophen is >[ ] g
Ex: 20 tablets × 0.5 g/tablet = 10 g
> 7.5 g
Acetaminophen intoxication can be asymptomatic first 24hrs or non-specif
May develop severe liver injury after 24hrs
Initial management of Acetaminophen intoxication:
* Gastric decontamination with activated charcoal (if within 4 hours of ingestion)
* Obtain Acetaminophen levels (to calculate likelihood of hepatotoxicity)
When is N-acetylcysteine (NAC) administrered?
Acetaminophen concentration >10 µg/mL + unknown time of ingestion
or
Levels above treatment line in Acetaminophen concentration algorhythm
In hemodynamically stable patients who have ingested caustic liquids (solvents, cleaning solutions, etc.) with no evidence of perforation
What should be done within the** first 24 hours** to assess the severity of esophageal injury and guide further management.
endoscopy
Caustic alkali ingestion causes immediate esophageal injury with liquefactive necrosis.
Caustic acidic ingestion causes coagulative necrosis.
Within the first 24 hours
Toxicity can is marked by nausea/vomiting, anion gap metabolic acidosis, elevated lactate level,hyperthermia, tachypnea, & altered mental status
Tinnitus also commonly occurs.
Salicylate
Tx: supportive therapy & activated charcoal if aspirin was ingested.
2/2 overuse of Aspirin or other salicylate products (oil of wintergreen [methylsalicylate]).
Diagnosis is made with serum salicylate level
Serum level is elevated in carbon monoxide poisoning, which often presents with confusion, lactic acidosis, and anion gap metabolic acidosis.
Carboxyhemoglobin
Treatment of neuroleptic malignant syndrome (NMS), a hypermetabolic syndrome associated with some antipsychotic agents. NMS can cause
* hyperthermia
* muscle rigidity
* altered mental status
Dantrolene
____ overdose can present with CNS, cardiac, and anticholinergic findings.
Tricyclic antidepressant
What is used to treat cardiac toxicity, which is characterized by prolonged QRS duration (>100 msec) and ventricular arrhythmias (V-tach or V-Fib) associated with TCA overdose.
Sodium bicarbonate
Amitriptyline, Imipramine, Nortriptyline, Desipramine, Doxepin
Trimipramine
Calcium Channel Blockers are often used to prevent migraines.
CCB overdose causes hypotension and atrioventricular blocks.
What is the treatment for CCB overdose?
Calcium chloride
Toxicity presents with
* Abdominal pain/constipation
* Cognitive impairment/behavioral problems
* Encephalopathy
* Failure to thrive
or may be asymptomatic
Lead Poisoning
Lead poison management includes:
* Measuring Venous Lead levels (if screening performed by capillary sample)
* Identify & remove lead sources)
* Notify public health department
____ therapy if lead level ≥45 µg/dL
**Chelation Therapy **
* Dimercaptosuccinic acid (succimer) for levels 45-69 µg/dL.
* Dimercaprol (British anti-Lewisite) + calcium disodium edetate (EDTA) for levels ≥70 µg/dL or acute encephalopathy.
SSRI overdose patients are usually asymptomatic or have mild CNS depression.
If the pt presents with altered mental status or abnormal physical findings like respiratory depression, ____ should be investigated.
coningestion (eg, ethanol, benzodiazepine, Tylenol)
Beta blocker overdose presents within 6 hours of ingestion with bradycardia, hypotension, cardiogenic shock, bronchospasm, altered mental status, and seizures. Hypoglycemia is often seen.
Treatment consists of airway management, gastric decontamination, intravenous fluids, intravenous ____, and intravenous ____.
glucagon
atropine
Toxicity presents with nausea, vomiting, confusion, and changes in color vision. Patients specifically report xanthopsia, in which all objects and the environment appear yellow.
Digoxin
Bradycardia and hypotension are typical of overdose with calcium channel blockers (eg, diltiazem); however, unlike ____ overdose, altered mental status is not usually seen
beta blocker
Tricyclic antidepressant overdose can cause
what 3 forms of toxicity
- anticholinergic (fast as a fiddle)
- central nervous system toxicity (seizures)
- Cardiac toxicity (hypotension, QRS prolongation).
Patients with QRS prolongation should receive **sodium bicarbonate **
Acute iron poisoning presents with abdominal pain, diarrhea, and hematemesis.
Labs reveal an anion gap metabolic acidosis
X-ray may show _____
May develop hypovolemic shock w/i a few hrs s/t gastrointestinal losses
radiopaque tablets
Toxicity characterized as a triad of
* mental status changes (anxiousness, sleeplessness)
* autonomic dysregulation (HTN, Tachycardia)
* neuromuscular hyperactivity (increased muscle tone and reflexes)
Seretonin Syndrome
It may be an unintentional result of the combined use of serotonergic agents (eg, selective serotonin reuptake inhibitors and tramadol).
Certain opioids (eg, morphine) have active metabolites that can cause opioid toxicity in patients with _____
renal insufficiency
Opioids that have inactive metabolites (eg, fentanyl) or are not dependent on renal elimination (eg, methadone) are preferred.
Methemoglobinemia presents with low pulse oximetry saturation that does NOT improve with oxygen; The PaO2 level is High/Normal/Low?
Normal
The antidote for symptomatic methemoglobinemia or high levels of methemoglobin (as measured by co-oximetry) is _____ or _____.
methylene blue
or
high-dose ascorbic acid
if M. Blue is contraindicated (ex: G6PD deficiency)
A chelating agent, is most commonly used in the treatment of lead poisoning to increase the urinary and fecal excretion of lead.
Dimercaprol
Succimer
Antidote after the ingestion of a beta blocker or calcium channel blocker
by activating adenylate cyclase, which increases intracellular calcium and improves cardiac contractility
Glucagon
Acetaminophen poisoning antidote
N-acetylcysteine
Acetaminophen poisoning antidote
acts by restoring glutathione, which metabolizes acetaminophen’s toxic metabolite, N-acetyl-p-benzoquinone imine (NAPQI), to nontoxic metabolites.
Antidote for Cholinergic toxicity.
———
It is given after atropine and reactivates the cholinesterase enzyme.
Pralidoxime
—————
Cholinergic toxicity causes bradycardia, diarrhea, urination, etc.
Anticholinergic toxicity causes tachycardia, anuria, mydriasis, etc.
Presents with abdominal pain, hematemesis, shock, and anion gap metabolic acidosis.
Deferoxamine is the primary therapy.
Iron poisoning
Presents with pain, dysphagia, and oropharyngeal erythema and ulcerations. It does not cause alterations in consciousness.
caustic ingestion
Presents with pain, dysphagia, and oropharyngeal erythema and ulcerations. It does not cause alterations in consciousness.
caustic ingestion
These bites often lead to muscle pain (a prominent finding), abdominal rigidity (sometimes mimicking a surgical abdomen), and muscle cramps (seen in >60% of patients). Patients commonly develop nausea and vomiting within hours of the bite.
black widow spider bites
Brown Recluse leads to ulceraction and eschar of bite (not these symptoms)
What are some common causes of
Anticholinergic Toxicity (Mad as a Hatter, etc.)
- Antidepressants (e.g., TCAs like amitriptyline, certain SNRIs)
- Antipsychotics (especially older ones like haloperidol)
- Antihistamines (first-gen agents like diphenhydramine)
- Antiparkinsonian medications (benztropine)
- Antispasmodic medications (hyoscyamine)
- Certain plants and mushrooms containing anticholinergic compounds, if ingested accidentally or intentionally
Common cause of Cholinergic toxicity on exams
Organophosphates
Such as insecticides, herbicides, and nerve agents. They work by inhibiting the action of acetylcholinesterase, an enzyme responsible for breaking down the neurotransmitter acetylcholine. This inhibition leads to an accumulation of acetylcholine, resulting in overstimulation of cholinergic receptors throughout the body.
What is the antidote for:
- Anticholinergic toxicity (Fast as a Fiddle)
- Cholinergic toxicity (Dumbels)
- Physostigmine (try Benzo 1st)
- Pralidoxime (give Atropine 1st)
