Toxizität Flashcards

1
Q

Arsen

A

This patient most likely has chronic arsenic poisoning, which manifests with distal sensorimotor polyneuropathy, white bands across the nails (Mees lines), and hyperkeratosis. Workers in battery factories have an increased risk of being exposed to arsine, a highly toxic gaseous form of arsenic with a distinct garlic-like odor. Elevated arsenic levels in the urine confirm the diagnosis. Treatment consists of chelating agents dimercaprol or succimer (in children).

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2
Q

Blei

A

Chronic lead poisoning is an occupational hazard for battery factory workers and presents with polyneuropathy. However, lead poisoning does not cause hyperkeratosis and lead-induced polyneuropathy is mainly a motor neuropathy. Furthermore, sensory symptoms (e.g., paresthesias) are rare. Other features suggestive of lead poisoning such as intestinal colic, anemia, radial nerve palsy, and Burton line (a blackish‑blue line along the margins of the gums) are also absent in this patient.

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3
Q

Cadmium

A

Although this patient’s occupation puts him at risk of chronic cadmium toxicity, this diagnosis is unlikely because he does not present with typical features such as anosmia, yellowing of teeth, and kidney or lung disease (e.g., tubulointerstitial nephritis or emphysema).

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4
Q

Quecksilber

A

Chronic mercury poisoning is an occupational hazard for battery factory workers and manifests with polyneuropathy. However, mercury poisoning does not cause hyperkeratosis or white transverse lines across the nails. Mercury toxicity usually causes intention tremor, erethism, and bluish‑violet discoloration of the gums, which are features this patient does not have.

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5
Q

Betablocker

A

Intravenous glucagon is part of the initial treatment for symptomatic patients with beta-blocker overdose who do not respond to IV fluids and atropine alone. Excessive beta-adrenergic blockade most commonly manifests as bradycardia and hypotension. In severe cases, profound myocardial depression and cardiogenic shock can occur. Glucagon increases intracellular cAMP by activating adenylate cyclase, which improves cardiac contractility while bypassing the beta receptors.

ADDITIONAL INFORMATION
Additional treatment depends on the severity of symptoms and may include administration of vasopressors (to correct hypotension), intravenous calcium (to treat cardiogenic shock), high-dose insulin and glucose (to treat hypoglycemia) and intravenous lipid emulsion therapy (to prevent further absorption of beta-blocker)

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6
Q

Phencyclidine

A

Phencyclidine can cause visual hallucinations, paranoid delusions, agitation, tachycardia, and hypertension, all of which are seen here. However, dilated pupils and distorted time perception are not typical features of intoxication with this drug. Instead, patients usually present with miosis. Furthermore, phencyclidine intoxication typically manifests with nystagmus and aggressive behavior, neither of which are seen in this patient.

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7
Q

LSD

A

This patient has most likely used lysergic acid diethylamide (LSD), a hallucinogenic drug that primarily acts by activating 5-HT2A receptors and D2 receptors in the CNS. Vivid visual hallucinations and distorted time perception are characteristic features of LSD use, but patients can also experience anxiety, agitation, and paranoid delusions (a “bad trip”). In addition, LSD has sympathomimetic effects such as tachycardia, hypertension, and mydriasis. Treatment consists of supportive care, reassurance, and, if needed, antipsychotics for psychosis and benzodiazepines for anxiety.

Symptoms of hallucinogen intoxication typically resolve spontaneously after 6–12 hours. Long-term complications include persistent psychosis and hallucinogen persisting perception disorder.

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8
Q

Organophosphates

A

DUMBBELSS mnemonic for cholinergic intoxication: Diarrhea, Urination, Miosis/Muscle weakness, Bronchospasm, Bradycardia, Neuromuscular excitation, Lacrimation, Salivation, and Sweating.

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9
Q

Immunsuppressiva

A

MMF
• Panzytopenie
• Infektion: respiratorisch, gastrointestinal (CMV)
• Metabolisches Syndrom: Hyperglykämie, Hypercholesterinämie
• niedrige Neuro- und Nephrotoxizität
• periphere Ödeme

Tacrolimus
• Nephro- und Neurotoxizität (schwerer als bei Cyclosporin A)
• metabolisches Syndrom (schwerer als bei Cyclosporin A)
• Hyperurikämie, Transaminitis
• Haarverlust
• Kopfschmerzen
• Insomnie
• Elektrolyte: Hyperkaliämie, Hypophosphatämie, Hypomagnesiämie

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10
Q

MDMA

A
  • sense if closeness
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11
Q

Phencyclidin

A
  • Agressivität
  • Synästhesie
  • Miosis
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12
Q

Amphetamine

A
  • erhöhtes Libido
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13
Q

Kokain

A
  • taktile Halluzinationen
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14
Q

Cannabis

A
  • impaired reaction time
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