UWorld - CK - poisoning/environmental

Physostigmine

-Anticholinesterse --> increases ACh!! -Used in anticholinergic toxicity -Crosses the blood-brain barrier (CNS)

when is activated charcoal given to a patient with salicylate poisoning?

Activated charcoal is indicated in alert patients within 2 hours of acute ingestion to bind salicylate in the gastrointestinal tract, thereby decreasing its absorption. It would not be appropriate in this patient with altered mental status (aspiration risk) and chronic (rather than acute) toxicity

which medication needs to be given immediately for organophosphate poisoning?

Atropine --> resolution if muscarinic symptoms

how does TCA overdose cause cardiac toxicity?

Cardiac toxicity is caused by TCA inhibition of fast sodium channels in the His-Purkinje system and myocardium. This decreases conduction velocity, increases the duration of repolarization, and prolongs absolute refractory periods. QRS prolongation and ventricular arrhythmias (eg, ventricular tachycardia, ventricular fibrillation) may result

how to confirm lead poisoning?

Confirmatory venous lead measurement is required to confirm the diagnosis of elevated lead level if a screening capillary lead level is ≥5 µg/dL.

a house fire can lead to which type of toxicity?

Cyanide (HCN) Treatment: 1. Cyanide toxicity can be treated with an antidote such as hydroxocobalamin or sodium thiosulfate, which directly binds cyanide molecules. 2. An alternate treatment is induction of methemoglobinemia with nitrites to increase ferric iron (Fe3+) in circulating hemoglobin. Cyanide binds avidly to Fe3+, and so methemoglobinemia provides an alternate binding site.

how to differentiate between methanol poisoning and eythelne glycol poisoning?

Ethylene glycol and methanol poisoning share similarities (eg, substitutes for ethanol, anion gap metabolic acidosis, increased osmolar gap). However, whereas methanol damages the eyes due to the effects of its formate metabolite, ethylene glycol damages the kidneys (eg, elevated creatinine) due to glycolate-induced tubule damage.

patient with frostbite undergoes rewarming however hand doesn't look any better. management?

Failure to improve with rewarming measures (eg, persistent sensory loss, gray color) may indicate continued ischemiadue to vascular thrombosis. In such cases, angiography (most commonly fluoroscopic digital subtraction angiography) or technetium-99m scintigraphy can help assess perfusion within the affected tissues and identify patients who are candidates for thrombolysis

snake bite management

Given the risk of anaphylaxis, patients with mild envenomation (eg, mild, localized swelling; normal laboratory studies) should not receive antivenom but should be observed for 12-24 hours because delayed toxicity can occur. Patients with progressing or pronounced symptoms (eg, pronounced swelling and ecchymosis), abnormal coagulation (eg, oozing), or cardiovascular compromise (eg, hypotension) should receive antivenom and be admitted to the intensive care unit.

when is hemodialysis given to patients with salicylate poisoning?

Hemodialysis: Indicated in patients unlikely to tolerate the large volumes of bicarbonate required, such as those with end-stage renal disease, renal failure, and salicylate-induced pulmonary edema (as with this patient). Hemodialysis is also indicated with severe ingestions (eg, shock, seizures), refractory acidosis, or clinical worsening despite sodium bicarbonate therapy.

exertional hyponatremia, and hypochloremic dehydration are seen in patients with which disease?

Individuals with cystic fibrosis excrete excessive sodium and chloride in their sweat.

when is sodium bicarbonate given to patient with salicylate poisoning?

Intravenous sodium bicarbonate therapy: Indicated in symptomatic patients with elevated salicylate levels to alkalinize the urine and serum, thereby increasing salicylate (anion) excretion. However, large volumes are required

organophosphates pathophysiology

Irreversible inhibition of acetylcholinesterase → ↑ acetylcholine levels → activation of muscarinic and nicotinic acetylcholine receptors INCREASED ACH LEVELS!!!!

why does metabolic acidosis occur in cyanide toxicity?

It binds to ferric iron (Fe3+), inhibiting its reduction to ferrous iron (Fe2+) and blocking production of ATP from oxidative phosphorylation. Cells then switch to anaerobic metabolism, leading to lactic acid formation and causing metabolic acidosis. Serum bicarbonate levels fall in an attempt to buffer excess acid

opioid withdrawal symptoms?

Manifestations frequently include nausea, vomiting, cramps, diarrhea, restlessness, rhinorrhea, lacrimation, myalgias, and arthralgias. Examination can show hypertension, tachycardia, mydriasis, piloerection, and hyperactive bowel sounds Patients with opioid dependence typically develop withdrawal symptoms within 6-12 hours of the last dose of a short-acting opioid, with a peak 24-48 hours after symptom onset.

is atropine enough for organophosphate poisoning?

No. atropine does not have activity at the nicotinic receptors and cannot treat neuromuscular dysfunction. Therefore, pralidoxime, a cholinesterase-reactivating agent that has both nicotinic and muscarinic activity, should be given to treat neurotoxicity. note: --> Pralidoxime should be given only after atropine, because pralidoxime can cause transient acetylcholinesterase inhibition, which can momentarily worsen symptoms.

pule oximetry in carbon monoxide poisoning shows

Pulse oximetry shows normal O2 saturation because it cannot differentiate between oxyhemoglobin and carboxyhemoglobin.

Calcium channel blockers (eg, nifedipine, amlodipine) are useful in the management of ?

Raynaud phenomenon.

patient swallowed substance now looks to have oesophageal injury (mucosal). next step?

Serial chest and abdominal x-rays should be obtained to identify any signs of perforation, such as pneumomediastinum, pleural effusions, or subdiaphragmatic air in the absence of perforation or severe respiratory distress, endoscopic evaluation within the first 24 hours is recommended to assess the severity of esophageal damage.

how does sodium bicarbonate treat cardiac toxicity due to TCA overdose

Sodium bicarbonate likely improves cardiac toxicity through the following mechanisms: 1. Increasing serum pH makes the TCA less pharmacologically active, decreasing its avidity for sodium channels. 2. Increasing extracellular sodium concentration raises the electrochemical gradient across cardiac cell membranes, decreasing the impact of the TCA-induced sodium channel blockade. 3. Sodium bicarbonate infusion also improves TCA-induced hypotension, which is caused by alpha-1 adrenergic receptor antagonism in combination with cardiac toxicity, and is the leading cause of mortality in TCA overdose.

patient takes too many acetimophen tablets two hours ago. management?

The initial management should be focused on gastric decontamination with activated charcoal if the patient presents within 4 hours of ingestion. --> Acetaminophen levels should be obtained at the same time

Fomepizole

Tx of ethylene glycol overdose Inhibits alcohol dehydrogenase (unlike disulfiram)-->decreased breakdown of ethylene glycol into toxic metabolites

Pain out of proportion to clinical findings is often the first presenting symptom of ?

acute compartment syndrome

patient's confusion, hyperthermia, tachypnea, elevated lactate, and anion gap metabolic acidosis raise suspicion for?

acute salicylate toxicity. note: look for fever

patient with cystic fibrosis developed nausea and presyncope associated with hyperthermia, tachycardia, and tachypnea while playing soccer, suggesting ?

an exertional heat illness cystic fibrosis may predispose patients to heat-related illnesses due to higher rates of sodium and chloride lost in sweat.

Crotalidae polyvalent immune Fab (ovine)

antivenom for North American snake bites

Hypo- and hyperpigmentation of the skin occurs early in __________, and hyperkeratosis and scaling of the soles and palms is often seen later

arsenic toxicity

patient with bradycardia, hypotension, and hypoglycemia most likely has a?

beta blocker overdose

a small ulcer developing at the site of a recent bite, is highly suggestive of a ?

brown recluse spider bite note: in some cases, a deep skin ulcer develops at the bite site over the course of a few days, with an erythematous halo and a necrotic center that can progress to an eschar.

Carboxyhemoglobin level is elevated in ?

carbon monoxide poisoning note: they are NOT feverish

when should chelating therapy be used in lead poisoning?

chelation therapy is not routinely administered for lead levels <45 µg/dL due to lack of evidence for improved neurologic outcomes 1. Dimercaptosuccinic acid (succimer) is typically used when lead levels are 45-69 µg/dL. 2. Dimercaprol (British anti-Lewisite) plus calcium disodium edetate (EDTA) should be administered on an emergency basis for levels ≥70 µg/dL or acute encephalopathy.

organophosphate poisoning leads to ______ toxicity

cholinergic

patient who developed diaphoresis, nausea and vomiting, fecal incontinence, and diffuse weakness with muscle fasciculation after working in an agricultural field has signs of?

cholinergic toxicity, likely due to organophosphate pesticide exposure

Sodium thiosulfate is the antidote for ?

cyanide poisoning, generally seen in the setting of fires or occupational exposure (eg, mining, pesticides). Patients with cyanide poisoning have markedly elevated lactate levels (typically >10 mEq/L)

patient with worsening joint pain (shoulders and elbows) after scuba diving 12 hours ago most likely has?

decompression sickness, an environmental emergency that occurs when dissolved gases (mostly nitrogen) form bubbles within the body with rapid ascent, the more abrupt decrease in ambient pressure may cause much of the dissolved nitrogen to come out of solution and form gas bubbles throughout the tissues and bloodstream, leading to pain and obstruction of blood flow tx: -intravenous fluids and 100% oxygen -Hyperbaric oxygen therapy

patient who collapsed after running a marathon but did not lose consciousness most likely has?

exercise-associated postural hypotension (EAPH) EAPH is thought to occur due to physiologic adaptations in endurance athletes, who have significantly higher cardiac output than unconditioned individuals due to hypertrophy and hyperplasia of the left ventricle (ie, athlete's heart). --> patients with EAPH remain alert with normal mental status --> Core temperature may be normal or mildly elevated

when is emergency management of opioid withdrawal with methadone permitted?

for up to 3 days if the treatment is inpatient and the primary disease is medical (eg, cellulitis).

heat exhaustion vs. heat stroke?

heat stroke = fever >40 and CNS dysfunction

altitude sickness + drowsiness?

high-altitude cerebral edema (HACE), a rare, life-threatening emergency. --> HACE is diagnosed clinically; -->treatment is aided by dexamethasone, which can decrease cerebral swelling and is administered at the first sign of symptoms. --> Definitive management requires immediate descent to lower altitude.

patient with severe burns now has persistent fever, tachycardia, and hypertension. In the absence of infection (eg, negative blood and wound cultures), the most likely cause is a ?

hypermetabolic response to severe burn injury It typically arises within the first 5 days postinjury, after an initial 24-48 hours of shock (eg, increased capillary permeability, myocardial depression). It is likely triggered by the profound release of inflammatory mediators from damaged tissue, leading to increased levels of catecholamines and glucocorticoids

deferoxamine is administered for

iron tablet poisoning a chelating agent that binds free iron, forming a complex that can be renally excreted. Because iron is rapidly taken up by various organs (eg, myocardial cells, hepatocytes), deferoxamine must be administered early to be effective.

child swallows unidentified pills. Imaging reveal small opacities in the stomach and intestines. pill?

iron tablets ( radiopaque )

how will physostigmine affect Ach levels

it is an anti cholinesterase inhibitor --> increases Ach!!

The exaggerated area (~10 cm) of swelling, induration, and redness on this patient's hand after a sting by a member of the Hymenoptera species (eg, bees, yellow jackets, wasps) is called a?

large local reaction (LLR) To be considered an LLR, the area of exaggerated swelling and erythema must be contiguous with the site of the sting

distilled alcohol can lead to _____ poisoning?

lead look for: -GI probs -neuro probs -anemia

methadone

long acting opioid agonist = heroin withdrawal

Cyclopentolate

muscarinic antagonist --> anticholinergic ts: physostigmine

Dantrolene treats?

neuroleptic malignant syndrome (NMS), a hypermetabolic syndrome associated with some antipsychotic agents. Although NMS can cause hyperthermia and altered mental status, severe muscle rigidity would be expected.

gas is colorless, tasteless, and often has a slight, fruity odor?

organophosphate exposure, possibly due to a chemical weapon (eg, sarin, soman)

the management of atropine and then pralidoxime is used in?

organophosphate poisoning

when a patient with an SSRI overdose has altered mental status (eg, not following commands and withdrawing to painful stimuli) or abnormal physical findings, next step mx?

other causes (eg, coingestions, infections) should be investigated.

how to identify infant botulism

patho: decreased Ach!!! Age <12 months Constipation, poor feeding, hypotonia Oculobulbar palsies (eg, absent gag reflex, ptosis) Symmetric, descending paralysis Autonomic dysfunction (eg, decreased salivation, fluctuating HR/BP) think MG symptoms...

Initial management of frostbite is based on?

rapid rewarming in a 37-39 C (98.6-102.2 F) water bath

Cyproheptadine is the antidote for ?

serotonin syndrome

treatment for prolonged QT interval

sodium bicarbonate note: mg is for tornado de pointes

A QRS interval >100 msec or ventricular arrhythmia in the setting of TCA overdose is an indication for?

sodium bicarbonate therapy

pathophysiology of high voltage electrical burns

tissue damage occurs from both the direct injury caused by electricity and from the secondary conversion of electrical energy to thermal energy. Because bone (with its high resistance to electrical current) generates the most heat as current passes through the body, thermal injury to internal tissues surrounding the bone (eg, skeletal muscle) often exceeds the visible injury to external tissues (eg, skin). Skeletal muscle necrosis in patients with high-voltage electrical injuries often leads to the following clinical features: 1. Acute compartment syndrome from intracompartmental muscle swelling 2. Rhabdomyolysis, with leakage of muscle contents, including heme pigment, into the circulation 3. Heme pigment-induced acute kidney injury

Sodium bicarbonate is used to treat cardiac dysrhythmias associated with ?

tricyclic antidepressant (TCA) overdose

patient with chronic pain has altered mental status, hypotension, signs of anticholinergic toxicity (eg, facial flushing, dry mouth), and a prolonged QRS interval. These clinical features suggest ?

tricyclic antidepressant (TCA) poisoning Management of TCA poisoning includes supportive care, telemonitoring, intravenous fluids, and benzodiazepines if seizure occurs. In addition, when the QRS interval >100 msec, intravenous sodium bicarbonateshould be given to shorten the QRS interval and reduce the risk of fatal arrhythmias

can antihistamines such as diphenhydramine cause anticholinergic toxicity?

yes Confusion and visual hallucinations (eg, picking at imaginary objects) ("mad as a hatter") Blurry vision, likely due to mydriasis ("blind as a bat") Hyperthermia from impaired heat dissipation ("hot as a hare") Dry mucous membranes ("dry as a bone") Urinary retention ("full as a flask")

does TCA overdose cause hyperthermia?

yes. TCA overdose causes hyperthermia via its anticholinergic effect (ie, muscarinic receptor inhibition) on sweat glands, which decreases sweating and heat dissipation.