Poisons/Toxicities Flashcards by Stephanie Escobar

a life-threatening disorder characterized by hyperthermia (typically >104 F) associated with CNS dysfunction
(encephalopathy, syncope).

Nonexertional heat stroke (NHS)

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Medications promote Nonexertional heat stroke (NHS) by impairing diaphoresis:

Anticholinergic (amitriptyline, scopolamine) inhibit sweat

sympathomimetics (amphetamines, cocaine) inhibit vasodilation

dopamine antagonists (chlorpromazine, haloperidol) disrupt hypothalamic thermoregulation

diuretics
beta blockers

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Anemia in lead poisoning results from inhibition of ____ and δ-aminolevulinic acid (ALA) dehydratase in the heme biosynthesis pathway.

ferrochelatase

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elevated zinc protoporphyrin levels suggest

lead poisoning

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Physiologic adaptations in response to hypothermia include increased sympathetic activity and __ hormone release, shivering, and peripheral vasoconstriction.

thyroid

*These actions normalize body temperature by reducing heat loss and increasing metabolic rate (promoting thermogenesis).

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Symptoms of ____ are neurologic (cognitive impairment, irritability), gastrointestinal (constipation, abdominal pain), renal (interstitial nephritis), and hematologic (anemia).

lead poisoning

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Hypokalemia and hypercalcemia can present with

constipation

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Patients with ____ exhibit muscle weakness or arrhythmias, and/or constipation

hypokalemia

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Patients with ____ exhibit muscle weakness, confusion, renal insufficiency and/or constipation.

hypercalcemia

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Exercise-associated collapse typically occurs after intense exercise in well-conditioned athletes. It is characterized by loss of postural tone or syncope immediately following the cessation of exercise and occurs due to impaired

venous return to the heart

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can cause syncope and sudden cardiac death.

Left ventricular outflow obstruction (eg, hypertrophic cardiomyopathy)

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Elderly patients are at increased risk of developing heat-related illness due to several features of normal aging that impair normal thermoregulatory mechanisms, including tonic contraction of the peripheral____, reduced sweat gland density, and reduced effective ___ area available for heat transfer.

vasculature

epidermal

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Induces DNA damage (eg, double-strand breakage, free radical generation) that predominantly affects highly proliferative cells (eg, skin stem cells, hematogenous progenitors, intestinal crypt cells)

Ionizing radiation

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A patient who has ingested a quantity of rat poison (aka super Warfarin) sufficient to cause coagulopathy and abnormal bleeding (bloody vomit/stool, ecchymosis) requires immediate treatment with ___ in addition to ___.

fresh frozen plasma

vitamin K

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Serotonin syndrome:
altered mental status, mydriasis, sympathetic hyperactivity, hyperreflexia/clonus

what is the antidote?

Cyproheptadine

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Anticholinergic toxicity:
Agitated delirium with sympathetic hyperactivity
Mydriasis, dry skin/mucous membranes, flushed skin, urinary retention

what is the antidote?

Physostigmine

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Benzodiazepines toxicity:
Sedation with normal vital signs
Slurred speech, ataxia

what is the antidote?

Flumazenil

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Opioids toxicity:
Sedation with respiratory suppression
Miosis, decreased bowel sounds

what is the antidote?

Naloxone

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In the United States, the majority of overdose deaths are caused by

opioids

*including prescription analgesics and heroin

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a competitive inhibitor of alcohol dehydrogenase, is the preferred agent for treatment of ethylene glycol and methanol toxicity.

Fomepizole

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are toxic alcohols that cause anion gap metabolic acidosis and an elevated osmolar gap.

Ethylene glycol and methanol

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Mathanol is converted to formaldehyde via

alcohol dehydrogenase

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Formaldehyde is then turned into formic acid causing (2)

AKI

Blindness

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Ethylene glycol (anti-freeze) is turned to glycolic acid via

alcohol dehydrogenase

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Toxicity Clinical features: Visual deficits Altered mentation Labs: ↑ Osmolar gap ↑ Anion gap metabolic acidosis

Methanol

Toxicity Clinical features: Renal failure/flank pain Altered mentation Labs: ↑ Osmolar gap ↑ Anion gap metabolic acidosis Calcium oxalate crystals in urine

Ethylene glycol

Toxicity Clinical features: Altered mentation Labs: ↑ Osmolar gap No increased anion gap or metabolic acidosis

Isopropyl Alcohol

Toxicity Clinical features: Altered mentation Labs: ↑ Osmolar gap ↑ Anion gap metabolic acidosis (ketosis)

Ethanol | Ketoacidosis

The patient is disoriented, tremulous, and diaphoretic Tachycardia, HTN, Diaphoresis Neurologic examination reveals pupillary dilation, bilateral hyperreflexia in the lower extremities, and bilateral, inducible ankle clonus. Toxicity?

Seretonin Syndrome | Tryptophan converted to Seretonin

Mental status changes (eg, anxiety, agitation, delirium) Autonomic dysregulation (eg, diaphoresis, hypertension, tachycardia, hyperthermia, vomiting, diarrhea) Neuromuscular hyperactivity (eg, tremor, myoclonus, hyperreflexia)

Seretonin Syndrome

excess muscarinic stimulation (eg, increased salivation, miosis, bronchospasm, bradycardia) caused by

Organophosphates | Cholinesterase Inhibitors

Organophosphates are cholinesterase inhibitors that are commonly used as pesticides. Atropine can be used to counteract the effects of excess muscarinic stimulation However, patients remain at risk of PARALYSIS due to nicotinic overactivation, and so also require treatment with

pralidoxime

a cholinesterase reactivating agent

pralidoxime

____ toxicity, likely from encountering jimsonweed (Datura stramonium) while working in their yard

anticholinergic

___ toxicity presents with altered mental status (lethargic/confused) seizures cardiovascular collapse (lung crackles/ HTN) lactic acidosis bright red venous blood (seen on venous blood gas and funduscopy).

Cyanide

Antidotal treatment of cyanide toxicity can be achieved by 3 different strategies: direct binding of cyanide ions (_____), induction of methemoglobinemia (_____), and use of detoxifying sulfur donors (_____).

hydroxocobalamin sodium nitrite sodium thiosulfate

Symptoms of _______ overdose include : seizures anticholinergic toxicity (Tachycardia, Flushing, Mydriasis) hypotension cardiac toxicity (QRS widening, ventricular arrhythmias).

tricyclic antidepressant

Acute ____ poisoning impairs cellular respiration and presents with abdominal pain, vomiting, diarrhea, hypotension, tachycardia, and a garlic odor on the breath

arsenic *treat with Dimercaprol (chelating agent)

Impairs celliular respiration | causes garlic odor breath

arsenic poisoning

presents with gray- or blue-colored skin, shortness of breath, and "chocolate-colored" blood.

Methylene blue

``` act as competitive antagonists for endogenous catecholamines; therefore, toxicity presents with: delayed capillary refill hypotension bradycardia bronchospasm (+/- wheezing) hypoglycemia. ```

Beta blockers

Its major adverse effect is hypotension (especially postural hypotension).

Prazosin | alpha-1 adrenergic blocker

Naloxone frequently requires ___ to prevent recurrent overdose symptoms due to its short half-life (<1 hr).

redosing

Benzodiazepine overdose does NOT cause

miosis

pralidoxime should be given only after atropine because it can cause transient ____ inhibition, which can momentarily worsen symptoms

acetylcholinesterase

____ reverses nicotinic and muscarinic symptoms (reactivates cholinesterase) in organophosphate poisoning

Pralidoxime Give AFTER Atropine though

Manifestations of Organophosphate poisoning | Cholinergic excess

``` Muscarinic: Diarrhea/diaphoresis Urination Miosis Bronchospasms, bronchorrhea, bradycardia Emesis Lacrimation Salivation ``` Nicotinic: muscle weakness, paralysis, fasciculations

First-line therapy is _____, a competitive inhibitor of acetylcholine at the muscarinic receptor

atropine

atropine a competitive inhibitor of ____ at the muscarinic receptor

acetylcholine

Insecticides and contaminated water are common sources of

arsenic

Dapsone Local/topical anesthetics (benzocaine, teething medications) Nitrates/nitrites (drinking ground water) can cause

Methemoglobinemia

patient with cyanosis that does not improve with supplemental oxygen has acquired ____ due to topical anesthetics

methemoglobinemia *functional anemia

result in the conversion of Fe2+ to Fe3+, which results in functional anemia and a left shift of the oxygen dissociation curve.

methemoglobinemia

Seizures & Tachyarrhythmias are the major cause of morbidity and mortality from ____ intoxication.

theophylline

__ poisoning can cause hematemesis and melena as it is directly toxic to gastric mucosal cells.

Iron

Toxicity presents with: Tinnitus Hyperventilation/Tachypnea (primary respiratory alkalosis) Vomiting Hyperthermia Altered mental status (lethargic/confused) Elevated anion gap & lactate*

Acute salicylate poisoning

Acute _____ poisoning causes: Direct medullary stimulation (respiratory center, chemoreceptor trigger zone) Impaired oxidative phosphorylation Decreased prostaglandin synthesis

salicylate poisoning

The toxicity of salicylate is caused mostly by its protonated/uncharged, salicylic acid form, which is ____ and readily passes into the tissues

lipophilic

The toxicity of salicylate is caused mostly by its ___, salicylic acid form

protonated/uncharged

___ toxicity typically presents with mixed primary respiratory alkalosis and anion gap metabolic acidosis.

Salicylate

Sodium bicarbonate facilitates the conversion of salicylate to its ____, ionized/charged form which traps much it in the bloodstream and increases its urinary excretion.

lipophobic *recall ionized/charged molecules do not penetrate tissue very well

Sodium bicarbonate facilitates conversion to the lipophobic, ionized form of salicylate, which ___ & ___.

traps salicylate in the blood | and increases its urinary excretion

____ facilitates the conversion of salicylate to its lipophobic, ionized form, which traps much of the compound in the bloodstream and increases its urinary excretion.

Sodium bicarbonate (given intravenously) *bicarbonate acts as a base to bind free hydrogen ions in the blood. It also alkalinizes the urine to make it lipophobic

Activated ____ is commonly given orally to patients with acute salicylate toxicity because it binds to salicylate in the gastric lumen and prevents absorption of the drug. *only works within the first 4 hours

charcoal

Salicylate is metabolized mostly via hepatic ____

glucuronidation

Normal pH Very Low PaCO2 (alkalosis) Very Low Bicarb (acidosis) + Hyperthermia, Tachypnea, Tinnitis Diagnosis?

Acute salicylate poisoning

Primary respiratory ____ occurs because salicylates directly stimulate the medullary respiratory center, resulting in increased ventilation and loss of CO2 in the expired air.

alkalosis *basic bitches hyperventilate

Primary anion gap metabolic ____ develops because toxic salicylate levels: increase lipolysis, uncouple oxidative phosphorylation, inhibit TCA This results in the accumulation of unmeasured organic acids in the blood (ketoacids, lactate), increasing the anion gap.

acidosis

Activation of __ receptors promotes synthesis of nitric oxide (NO), an endothelium-derived relaxing factor.

NO diffuses into vascular smooth muscle cells, activating guanylate cyclase and increasing intracellular

cyclic-GMP

Increased levels of cyclic-GMP activate myosin light chain phosphatase, which resulting in smooth muscle

relaxation and vasodilation

M3 activation causes smooth muscle relaxation in ____ (1) contraction in ____ (4)

peripheral vasculature Lungs, bladder, eyes (miosis), GI tract

Amatoxins are found in a variety of poisonous mushrooms and are potent inhibitors of ____

RNA polymerase II | halting mRNA synthesis = apoptosis

RNA Polymerase I makes

ribosomal RNA

RNA Polymerase II makes

messenger RNA

RNA Polymerase III makes

transfer RNA

Symptoms typically start 6-24 hours after ingestion and include abdominal pain, vomiting, and severe, cholera-like diarrhea that may contain blood and mucus. Severe poisoning can lead to acute hepatic and renal failure. Urine testing for α-amanitin can confirm suspected _____ poisoning.

amatoxin (mushroom)

Poisons/Toxicities Flashcards

(77 cards)