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Year II Pharmacology Term IV > Toxicology > Flashcards

Toxicology Flashcards

1
Q

Bioaccumulation

A

Increasing concentration of a substance in the environment resulting from environmental persistence and physical properties

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2
Q

Biomagnification

A

is the fold increase in concentration of a substance that occurs in a food chain as a consequence of bioaccumulation

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3
Q

Endocrine disruptors

A

Chemicals in the environment that have endocrine effects (estrogen/anti-androgen/thyroid). Potential cause of infertility, reproductive cancers or birth defects.

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4
Q

Environmental toxicology

A

EPA Environmental Protection Agency regulates toxicology and environmental exposure to chemicals

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5
Q

Acceptable daily intake (ADI)

A

Daily intake of chemical which during lifetime appears to be without appreciable risk.

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6
Q

Occupational toxicology

A

OSHA Occupational Safety and Health Agency regulates exposure of workers to chemicals

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7
Q

Threshold limit value (TLV)

A

Exposure limit to a specific agent for a stated period of time-(shorter time = higher level). Used for occupational control.

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8
Q

Carbon Monoxide Poisoning

Description of CO
Symptoms
Mechanism
Prevention
Treatment
A

Description of CO
- Odorless, colorless gas

Symptoms
- Headache, loss of judgement, dizziness, nausea, convulsion & death

Mechanism
- Competes avidly with oxygen for hemoglobin (200 fold greater affinity) -affinity for fetal hemoglobin even higher.

Diagnosis
A CO-oximeter must be used to determine carboxyhemoglobin (COHb) levels. A regular pulse oximeter will misrepresent carboxyhemoglobin for oxyhemoglobin

Treatment
- 100% oxygen and hyperbaric oxygen

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9
Q

Solvents–benzene and toluene

Source

Acute exposure symptoms

Chronic exposure symptoms

Inhaltion effects

A

Common – many consumer products, gasoline, manufacturing etc.
Acute exposure: CNS depression with ataxia and coma.
Chronic exposure: Neuro- and bone marrow toxicity, leukemia.
Inhalation can cause chemical pneumonitis.

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10
Q

Difference in lethal dose of gasoline/benzene when taken by lung or digestion

A

GIT needs larger LD 50 than lungs even in children so be careful of making patient who swallowed gasolone vomit since there is a risk they could aspirate it into his lungs

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11
Q

Name 2 classes of agents in pesticide toxicology

with examples

A

Chlorinated hydrocarbons (DTT, DDD, dioxin etc)

Cholinesterase inhibitors (carbamates-carbaryl, organophosphates-malathion, parathion)

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12
Q

Cholinesterase inhibitors (carbamates-carbaryl, organophosphates-malathion, parathion)

Mechanism
Side Effects
Treatment

A

Chlorine confers environmental stability

Moderately toxic, bioaccumulate, concerns about endocrine disruption, no specific treatment

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13
Q

Cholinesterase inhibitors (carbamates-carbaryl, organophosphates-malathion, parathion)

Mechanism
Symptoms
Treatment

A

Environmentally less stable than chlorinated pesticides

Muscarinic and nicotinic activators, SLUDGE (Salivation, Lacrimation, Urination, Defecation, GI upset, Emesis).

Treatment = Atropine blocks receptor activation + Pralidoxime to regenerate cholinesterase.

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14
Q

Name 3 agents in herbicide toxicology

A

Chlorophenoxy Acids (2,4-dichlorophenoxiacetic acid and 2,4,5-trichlorophenoxyacetic acid)

Glyphosate

Paraquat-bipyridyl herbicide.

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15
Q

Chlorophenoxy Acids (2,4-dichlorophenoxiacetic acid and 2,4,5-trichlorophenoxyacetic acid)

A

In Vietnam War, above combination code-named Agent Orange -associated with chronic disease- to date association inclusive

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16
Q

Glyphosate

A

Most widely used herbicide in the world. Causes eye and skin irritation. No specific treatment.

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17
Q

Paraquat-bipyridyl herbicide

A

Ingestion can be fatal. GI irritation, hematemesis and bloody stools. Within days pulmonary impairment can lead to pulmonary fibrosis and possibly death. Treatment supportive. Gastric lavage if recent ingestion and dialysis.

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18
Q

Common sources of CO

A 
Motor vehicle exhaust
Spillage from appliances
Building fires
Forklift trucks, snow blowers
Generators, heaters
Zamboni, (oh, yes!)
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19
Q

Clues of CO posining

A

More than one person affected
Pets affected
Temporal relation of symptoms and use of combustion appliances
Main indoor pollutant causing headaches is CO, but
Tobacco smoke, volatile organics

20
Q 
Lead
Age group at risk
Chronic exposure signs
Histological signs 
Treatment
A

Children - paint chip ingestion

Chronic exposure

  • peripheral neuropathy
  • wrist-drop)
  • anorexia
  • anemia
  • tremor
  • GI symptoms
  • children: growth delay, neurocognitive deficits, and developmental delay
  • Lead line seen in chronic lead poisoning on gums just above teeth in 50-70% patients.

Histoligical signs
- Basophilic stippling in red blood cells.

Treatment
- Oral succimer used as preferred chelator in children

21
Q

Arsenic

Acute poisoning
Chronic poisoning

A

Acute

  • severe GI discomfort
  • Rice water stools
  • Vomiting
  • Capillary damage with dehydration and shock (similar to typhoid and cholera)

Chronic

  • Groun water/private wells/soil
  • Skin changes
  • Hair loss
  • Bone marrow depression
  • Anemia
  • Nausea
  • GI distress
22
Q

Mee’s lines

A

Transverse white lines that run across the nail, following the shape of the nail moon.
Arsenic poisoning.

23
Q

Mercury

Acute poisoning
Chronic poisoning
Organic mercury
Treatment

A

Acute Poisoning
- Acute poisoning causes chest pain shortness of breath, nausea, vomiting, kidney damage, gastroenteritis and CNS damage.

Chronic Poisoning
- Neurological and behavioral changes

Organic Mercury
- Anti-fungal agent and has high potential to bioaccumulate. Generally, more toxic than ionic or metallic mercury compounds. Highly fetal toxic.

Treatment
Succimer or IM dimercaprol

24
Q

Fe

Acute (Early and Late)
Treatment

A

Acute
Early
- GI bleeding, lethargy and grey cyanosis

Late
- GI necrosis can occur, pneumonitis, jaundice, seizures and coma

Treatment

  1. Deferoxamine
  2. Charcoal does not bind iron therefore use gastric lavage if within 60 minutes, if longer than an hour use whole bowel irrigation(Polyethylene glycol bowel prep (GoLYTELY, Colyte))
25
Q

CHelators mechanism of action

A

Have 2 (bidentate) or more (polydentate) electronegative groups to complex with cationic metal atoms.

26
Q

2 limitations of chelators

A

1) Organometals not chelated e.g. lead additive in gas, organic mercury through bioaccumulation (e.g. fish).
2) Chelators cannot reverse damage only prevent further damage caused by heavy metals.

27
Q

Acetaminophen

Treatment and treatment mechanism

When should it be given?

Other items that can be given

A

N-acetylcysteine

When acetaminophen is taken n overdose it is metabolized by the liver into a toxic metabolite

  1. N-acetylcysteine increases glutathione stores
  2. Combines directly with acetaminophen’s reactive metabolite as a glutathione substitute
  3. Enhances sulfate conjugation
  • Within 1-2 hours after ingestion of acetaminophen
  • Activated chacoal
  • Supportive therapy: IV fluids, oxygen, and cardiac monitor.
28
Q

Aspirin

Mechanism of toxicity
Symptoms
Treatment

A

Mechanism of toxicity

  • uncoupling of oxidative phosphorylation
  • increased oxygen consumption
  • Increased carbon dioxide production
  • Accelerated activity of the glycolytic and lipolytic pathways
  • Depletion of hepatic glycogen
  • Hyperpyrexia

Symptoms

  • Respitory alkalosis with anion gap metabolic acidos
  • Tinnitus
  • Hyperthermia
  • Hypernea

Treatment

  • Less than 60 minutes: Gastric lavage
  • More than 60 minutes:
  • activated charcoal
  • Alkanalize urine to encourage secretion
  • Furosemide (supplement K lost)
  • Hemodialysis
  • Whole bowel irrigation if a large mass of pills is ingested
29
Q

Benzodiazapine

Treatement

A

Flumazenil

Flumazenil blocks site of benzodiazepine action. Avoid in patients with seizures, benzodiazepine dependence or tricyclic overdose

30
Q

Methanol, ethylene glycol

Treatment

A

Fomepizole

To reduce production of toxic metabolites this drug competes for alcohol dehydrogenase. Methanol causes severe vision disturbances.

31
Q

Beta-blockers

A

Glucagon

Acts on cardiac cells to raise intracellular cAMP independently of β adrenoceptors.

32
Q

Cholinesterase inhibitors-Organophosphates, carbamates, malathion

Treatment

A

Atropine and pralidoxime (2-PAM)

Atropine competes for muscarinic receptors and 2-PAM given early can regenerate cholinesterase activity

33
Q

Acetaminphen

Treatment

A

N-acetylcysteine (NAC)

Give within 8-10 hours, follow liver function tests and drug levels. NAC acts as a glutathione substitute and binds hepatotoxic metabolite as it is made.

34
Q

Asprin

Treatment

A

IV Na bicarbonate

Respiratory alkalosis followed by metabolic acidosis. For moderate cases IV sodium bicarbonate alkalizes urine promoting salicylate excretion. Severe cases: hemodialysis

35
Q

Hypertension and tachycardia

A

Amphetamines, cocaine and anticholinergics

36
Q

Hypotension and bradycardia

A

Calcium channel blockers, beta-blockers, clonidine and sedative hypnotics

37
Q

Hypotension and tachycardia

A

Tricyclic antidepressants, vasodilators and beta-agonists

38
Q

Rapid respiration

A

Salicylates, carbon monoxide, other toxins that cause metabolic acidosis or cellular asphyxia.

39
Q

Hyperthermia

A

sympathomimetics, anticholinergics, salicylates, and drugs producing seizures or muscular rigidity

40
Q

Hypothermia

A

Any CNS-depressant drug, especially when accompanied by exposure to a cold environment

41
Q

Widening of the QRS complex duration

A

tricyclic antidepressant and quinidine

42
Q

QTc interval prolonged

A

quinidine, antidepressants and antipsychotics, lithium, and arsenic

43
Q

Variable atrioventricular (AV) block plus atrial and ventricular arrhythmias

A

digoxin and other cardiac glycosides

44
Q

Ischemic changes

A

Hypoxemia due to carbon monoxide

45
Q

Which drugs to focus on for this lecture

A
  • Carbon monoxide
  • Organophosphate (carbamyl/malathion/parathion)
  • Iron
  • Lead
  • Arsenic
  • Acetaminophen
  • Aspirin
  • Benzodiazepines
  • Methanol. ethylene glycol

Year II Pharmacology Term IV (5 decks)

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