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PHARM > Poisons/Toxicities > Flashcards

Poisons/Toxicities Flashcards

1
Q

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

A

Nonexertional heat stroke (NHS)

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2
Q

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

A

Anticholinergic (amitriptyline, scopolamine) inhibit sweat

sympathomimetics (amphetamines, cocaine) inhibit vasodilation

dopamine antagonists (chlorpromazine, haloperidol) disrupt hypothalamic thermoregulation

diuretics
beta blockers

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3
Q

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

A

ferrochelatase

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4
Q

elevated zinc protoporphyrin levels suggest

A

lead poisoning

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5
Q

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

A

thyroid

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

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6
Q

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

A

lead poisoning

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7
Q

Hypokalemia and hypercalcemia can present with

A

constipation

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8
Q

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

A

hypokalemia

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9
Q

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

A

hypercalcemia

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10
Q

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

A

venous return to the heart

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11
Q

can cause syncope and sudden cardiac death.

A

Left ventricular outflow obstruction (eg, hypertrophic cardiomyopathy)

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12
Q

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.

A

vasculature

epidermal

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13
Q

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)

A

Ionizing radiation

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14
Q

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 ___.

A

fresh frozen plasma

vitamin K

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15
Q

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

what is the antidote?

A

Cyproheptadine

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16
Q

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

what is the antidote?

A

Physostigmine

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17
Q

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

what is the antidote?

A

Flumazenil

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18
Q

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

what is the antidote?

A

Naloxone

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19
Q

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

A

opioids

*including prescription analgesics and heroin

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20
Q

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

A

Fomepizole

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21
Q

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

A

Ethylene glycol and methanol

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22
Q

Mathanol is converted to formaldehyde via

A

alcohol dehydrogenase

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23
Q

Formaldehyde is then turned into formic acid causing (2)

A

AKI

Blindness

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24
Q

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

A

alcohol dehydrogenase

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25
Q

Toxicity Clinical features:
Visual deficits
Altered mentation

Labs:
↑ Osmolar gap
↑ Anion gap metabolic acidosis

A

Methanol

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26
Q

Toxicity Clinical features:
Renal failure/flank pain
Altered mentation

Labs:
↑ Osmolar gap
↑ Anion gap metabolic acidosis
Calcium oxalate crystals in urine

A

Ethylene glycol

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27
Q

Toxicity Clinical features:
Altered mentation

Labs:
↑ Osmolar gap
No increased anion gap or metabolic acidosis

A

Isopropyl Alcohol

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28
Q

Toxicity Clinical features:
Altered mentation

Labs:
↑ Osmolar gap
↑ Anion gap metabolic acidosis (ketosis)

A

Ethanol

Ketoacidosis

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29
Q

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?

A

Seretonin Syndrome

Tryptophan converted to Seretonin

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30
Q

Mental status changes
(eg, anxiety, agitation, delirium)

Autonomic dysregulation
(eg, diaphoresis, hypertension, tachycardia, hyperthermia, vomiting, diarrhea)

Neuromuscular hyperactivity
(eg, tremor, myoclonus, hyperreflexia)

A

Seretonin Syndrome

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31
Q

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

A

Organophosphates

Cholinesterase Inhibitors

32
Q

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

A

pralidoxime

33
Q

a cholinesterase reactivating agent

A

pralidoxime

34
Q

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

A

anticholinergic

35
Q

___ 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).

A

Cyanide

36
Q

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 (_____).

A

hydroxocobalamin
sodium nitrite
sodium thiosulfate

37
Q

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

A

tricyclic antidepressant

38
Q

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

A

arsenic

*treat with Dimercaprol (chelating agent)

39
Q

Impairs celliular respiration

causes garlic odor breath

A

arsenic poisoning

40
Q

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

A

Methylene blue

41
Q 
act as competitive antagonists for endogenous catecholamines; therefore, toxicity presents with: 
delayed capillary refill 
hypotension 
bradycardia 
bronchospasm (+/- wheezing)
hypoglycemia.
A

Beta blockers

42
Q

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

A

Prazosin

alpha-1 adrenergic blocker

43
Q

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

A

redosing

44
Q

Benzodiazepine overdose does NOT cause

A

miosis

45
Q

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

A

acetylcholinesterase

46
Q

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

A

Pralidoxime

Give AFTER Atropine though

47
Q

Manifestations of Organophosphate poisoning

Cholinergic excess

A 
Muscarinic:
Diarrhea/diaphoresis
Urination
Miosis
Bronchospasms, bronchorrhea, bradycardia
Emesis
Lacrimation
Salivation

Nicotinic:
muscle weakness, paralysis, fasciculations

48
Q

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

A

atropine

49
Q

atropine a competitive inhibitor of ____ at the muscarinic receptor

A

acetylcholine

50
Q

Insecticides and contaminated water are common sources of

A

arsenic

51
Q

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

can cause

A

Methemoglobinemia

52
Q

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

A

methemoglobinemia

*functional anemia

53
Q

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

A

methemoglobinemia

54
Q

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

A

theophylline

55
Q

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

A

Iron

56
Q

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

A

Acute salicylate poisoning

57
Q

Acute _____ poisoning causes:

Direct medullary stimulation
(respiratory center, chemoreceptor trigger zone)

Impaired oxidative phosphorylation

Decreased prostaglandin synthesis

A

salicylate poisoning

58
Q

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

A

lipophilic

59
Q

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

A

protonated/uncharged

60
Q

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

A

Salicylate

61
Q

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

A

lipophobic

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

62
Q

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

A

traps salicylate in the blood

and increases its urinary excretion

63
Q

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

A

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

64
Q

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

A

charcoal

65
Q

Salicylate is metabolized mostly via hepatic ____

A

glucuronidation

66
Q

Normal pH
Very Low PaCO2 (alkalosis)
Very Low Bicarb (acidosis)

+ Hyperthermia, Tachypnea, Tinnitis

Diagnosis?

A

Acute salicylate poisoning

67
Q

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

A

alkalosis

*basic bitches hyperventilate

68
Q

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.

A

acidosis

69
Q

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

A

M3

70
Q

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

A

cyclic-GMP

71
Q

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

A

relaxation and vasodilation

72
Q

M3 activation causes smooth muscle

relaxation in ____ (1)

contraction in ____ (4)

A

peripheral vasculature

Lungs, bladder, eyes (miosis), GI tract

73
Q

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

A

RNA polymerase II

halting mRNA synthesis = apoptosis

74
Q

RNA Polymerase I makes

A

ribosomal RNA

75
Q

RNA Polymerase II makes

A

messenger RNA

76
Q

RNA Polymerase III makes

A

transfer RNA

77
Q

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.

A

amatoxin (mushroom)

PHARM (11 decks)

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