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Pharmacology: Exam 3 > Lecture 1: Toxicology I > Flashcards

Lecture 1: Toxicology I Flashcards

1
Q

List the Halogenated Hydrocarbons that can cause intoxication

A
  • Carbon tetrachloride (CCl4)
  • Chloroform (CHCl3)
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2
Q

List the Aromatic Hydrocarbons that can cause intoxication

A
  • Benzene
  • Toluene
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3
Q

List the Alcohols that cause intoxication

A
  • Methanol
  • Ethylene glycol
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4
Q

List the Pesticides that cause intoxication

A
  • Organophosphates
  • Carbamates
  • Pyrethroids
  • Rotenone
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5
Q

List the Rodenticides that cause intoxication

A
  • Brodifacoum
  • Difenacoum
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6
Q

List the Metals that cause intoxication (6)

A
  • Lead (Pb)
  • Mercury (Hg)
  • Cadmium (Cd)
  • Arsenic (As)
  • Iron (Fe)
  • Copper (Cu)
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7
Q

List all the Antidotes and Treatments that treat different intoxications

A
  • N-acetylcysteine
  • Flumazenil
  • O2
  • Na Thiosulfate
  • Fomepizole
  • Succimer
  • Dimercaprol
  • Naloxane
  • Atropine
  • Pralidoxime
  • Penicillamine
  • Deferoxamine
  • Charcoal
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8
Q

Define Toxicology

A

Study of the adverse effects of xenobiotics (foreign bodies) on living systems

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9
Q

What differentiates a poison from a remedy?

A

Right dose

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10
Q

How many patients in the USA present with acute poisoning?

A

8 million patients; Accounting for 10-20% of hospital admissions

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11
Q

True or False. Chronic toxicity from low-dose toxicants may take years to develop a clinical presentation

A

True

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12
Q

What causes the highest poison exposure for all group w/ fatal outcomes?

A

Medications

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13
Q

What other substances can cause poison exposure in all age groups?

Low yield

A
  • Cosmetic, personal care items
  • Cleaning substances (fatal outcome)
  • Pesticides (fatal outcome)
  • Art & crafts, office supples
  • Alcohols (fatal outcome)
  • Food products
  • Plants
  • Gas, fumes, chemicals (fatal outcome)
  • Automotive products (fatal outcome)
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14
Q

What types of medications are most frequently involved in human poisoning exposures?

A

Analgesics (Aspirin, Ibuprofen, Acetaminophen)

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15
Q

What are the three ways to get exposed to a toxicant?

A
  1. Skin contact
  2. Ingestion
  3. Inhalation
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16
Q

What occurs in the body when exposed to a toxicant?

A

Distributed throughout the body, activated or inactivated, interacts with cells which can result in toxicity

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17
Q

What organ is affected by inhaled gases/particles?

A

Lungs

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18
Q

What organ(s) are affected by ingested chemicals? (4)

A
  • Liver (Bioactivation or inactivation)
  • Brain (Lipophilic)
  • Kidney
  • Heart (disruption of ion gradients)
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19
Q

Which compounds have selective toxicity?

A
  • Enzymes
  • Receptors (helps choose antibodies)
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20
Q

Which compounds have non-selective toxicity?

A
  • Acids
  • Bases
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21
Q

What outcome occurs with immediate toxicity?

A

Skin damage

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22
Q

What outcome occurs with delayed toxicity?

A

Cancer (Chronic exposure)

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23
Q

What method of toxicant exposure occurs with Halogenated hydrocarbons (CCl4 & CHCl3)?

Carbon tetrachloride (CCl4)
Chloroform (CHCl4)

A

Inhalation/Ingestion

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24
Q

True or False. Halogenated hydrocarbons (CCl4 & CHCl3) can penetrate the blood-brain barrier (BBB).

Carbon tetrachloride (CCl4)
Chloroform (CHCl4)

A

True.
b/c lipid soluble

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25
How do most Halogenated hydrocarbons (CCl4 & CHCl3) affect the CNS? ## Footnote Carbon tetrachloride (CCl4) Chloroform (CHCl4)
* Depress the CNS w/ acute high exposure
26
What is the treatment for Halogenated hydrocarbons (CCl4 & CHCl3)? ## Footnote Carbon tetrachloride (CCl4) Chloroform (CHCl4)
* Support treatment for acute intoxication * Support tx (ABCD): Airway, Blood Pressure, Circulation, Decontamination
27
What is Support Treatment for toxicity? ## Footnote Support tx: ABCD
Maintainance of the Airway, Blood Pressure, Circulation and Decontamination of the patient
28
How can you get exposed to Carbon Tetrachloride (CCl4)? ## Footnote Halogenated hydrocarbons
Contaminated drinking H2O
29
What side effects does CCl4 have at low concentrations? high concentrations?
Low concentrations * Irritating to **eyes & respiratory system** High concentrations * Nausea, Vomiting, **Stupor, Seizures,Coma, Death** (CNS depression)
30
How is CCl4 bioactivated?
By **cytochrome P450 (CYP)** which produces **free radicals** that can cause damage to macromolecules, e.g., **lipid peroxidation**
31
What are the side effects of **acute nonlethal exposure** to CCl4?
* Produce **liver and kidney damage** * Can occur in several hours to days
32
What side effects occur when exposed to Chloroform (CHCl3)?
* Similar to CCl4 * Dizziness, Headaches, **Facilitated catecholamine-induced arrhythmias**
33
Describe the normal pathway for CHCl3 detoxification. And what occurs to cause toxicity?
Normal Pathway * CHCl3 (cholorform) →**CYP2E1** (biotransformation)→**Phosgene** (Reactive metabolite)→**GSH-Glutathione Transferase** (protects organ damage)→Detoxified product Toxicity * **GSH gets saturated** and can **NO longer inactive Phosgene** →**Hepatotoxicity**
34
How can you get exposed to Aromatic Hydrocarbons? ## Footnote Benzene, Toluene
Inhalation/Ingestion
35
What side effects occur with high **acute exposure** to Aromatic Hydrocarbons? ## Footnote Benzene, Toluene
* **CNS depression** * **Catecholamine-induced arrhythmias**
36
What is the treatment for Aromatic hydrocarbons? ## Footnote Benzene, Toluene
**Support treatment (ABCD)** for acute intoxication
37
What ways can you be exposed to Benzene ## Footnote Aromatic hydrocarbons
* 1/2 national exposure via **tobacco smoke** * Combustion of **fossil fuels/contaminated H2O**
38
What diseases can chronic exposure to Benzene cause? ## Footnote Aromatic hydrocarbons
Hematopoietic toxicity: * **Agranulocytosis** * **Leukemia (AML)** ## Footnote Note: AML= * M3 subtype: Promyelocytic leukemia * M5 subtype: Monocytic leukemia
39
In what ways can you be exposed to Toluene? ## Footnote Aromatic hydrocarbons
* **Gasoline (1°)** * Degreasers * **Paint** * **Furniture polish** * Abuse: Bagging/huffing **feeling Euphoric**
40
What side effects does exposure to Toluene cause? | Aromatic Hydrocarbons
* **CNS depression**→drowsiness, ataxia, tremors, impaired speech, hearing loss * Chronic exposure-**Liver and kidney damage** * High concentrations- **Death**
41
Hydrocarbons * Toxicant exposure * Physiological Effect * Treatment ## Footnote Halogenated and Aromatic
* Inhaled/Ingested * Depress CNS * Treatment is Supportive
42
List characteristics that you need to know for Halogenated hydrocarbons 1. CHCl3 2. CCl4
* Both penetrate BBB 1. CHCl3 (Choloform): * CYP2E1 bioactivated, Phosgene toxic metabolite 2. CCl4 (Carbon tetrachloride): * Contaminated H2O * Eye irritant, resp. decrease * Depress CNS * CYP450 bioactivated
43
For Aromatic hydrocarbons: (Benzene, Toluene) explain: * Way of exposure * Physiological effects
1. Benzene * Tobacco smoke, fossil fuels, contaminated H2O * AML (Leukemia) 2. Toluene * Gas/Paint/Polish * Acute: decrease CNS, Chronic: liver and kidney damage→death
44
A 55-year-old man who has worked in a chemical plant for 25 years has been chronically exposed to benzene. Which of the following is the most likely toxicity of chronic benzene exposure? A. Hepatotoxicity B. Nephrotoxicity C. Leukemia D. Parkinson disease
c. Leukemia
45
What are common side effects caused by the toxicity of alcohol? ## Footnote Methanol (wood alcohol) Ethylene glycol (in antifreeze)
* **CNS sedation** * **Oxidized to toxic metabolites**→can cause **coma, seizure, hyperpnea & hypertension→(Sedation)**
46
What side effects occur due to Methanol toxicity? ## Footnote Methanol (wood alcohol)
Methanol →Formic acid→**Retinal injury/blindness**
47
What side effects occur due to Ethylene glycol toxicity? ## Footnote Ethylene glycol (in antifreeze)
Ethylene glycol→**Renal failure**
48
What is the treatment for Alcohol toxicity? ## Footnote Methanol Ethylene glycol
**Fomepizole**
49
What is the mechanism of Fomepizole (tx for alcohol toxicity) and the side effects?
* **Inhibits alcohol dehydrogenase** * **Renal elimination** of parent compounds * Side effects: burning at injection site, nausea, headache, dizziness
50
Explain how Fomepizole stops the oxidation of the toxic metabolite of Methanol
Normal Pathway of Methanol toxicity * Methanol→alcohol dehydrogenase→Formaldehyde→aldehyde dehydrogenase→**Formic acid →Retinal injury/permanent blindness** Pathway with Tx: Fomepizole * Methanol→**Fomepizole inhibts alcohol dehydrogenase**= Formic acid never formed
51
Explain how Fomepizole stops the oxidation of the toxic metabolite of Ethylene glycol
Normal Pathway of Ethylene glycol toxicity * Ethylene glycol→alcohol dehydrogenase→Glycoladehyde→aldehyde dehydrogenase→**Glycolate**→glycolate oxidase→**Glyoxylate**→glycolate oxidase→**Calcium oxate crystals→Renal failure** Pathway with Tx: Fomepizole * Ethylene glycol→**Fomepizole inhibts alcohol dehydrogenase**= calcium oxalate crystals never form
52
List characteristics (side effects, MOA, tx, etc) that you need to know about: 1. Methanol 2. Ethylene glycol
1. Methanol * CNS sedation * Toxic metabolite: Formic acid * Retinal injury/blindness * Tx: Fomepizole 2. Ethylene glycol * CNS Sedation * Toxic metabolite: Calcium oxalate crystals * Renal failure * Tx: Fomepizole
53
What do the **Organophosphate** and carbamate insecticides inhibit? ## Footnote Pesticides
* Inhibit **Acetylcholinesterase→increase acetylcholine**
54
What side effects do **Organophosphate** and carbamate insecticides toxicity cause?
* Salivation * Lacrimation * Perspiration * Miosis * Nausea, Vomitng * Bronchospasm * Seizures * Coma
55
What is the treatment(s) for **Organophosphate** and carbamate insectides toxicity?
* Supportive (breathing) * Decontamination * **Pralidoxime** * **Atropine**
56
Explain the mechanism of Pralidoxime and Atropine ## Footnote Treatmenf for **Organophosphate** and carbamate insectides toxicity
* **Pralidoxime: reactivates cholinesterase**, usually for **organphosphates**, side effects: muscle paralysis/spasm * **Atropine**: Muscarinic receptor antagonist ## Footnote Pralidoxime side effects may be due to rapid infusion
57
For Pesticides: **Organophosphates** & carbamata insecticides * Mechanism of action * Treatment
* MOA: Inhibit acetylcholinesterase →↑ acetylcholine * Treatment: Atropine, Pralidoxime
58
For the pesticide: **Pyrethroids**: * Mechanism of action * Physiological effects * Treatment | LOW yield ## Footnote Pyrethroids (chrysanthematic, pyrethric acids)
* MOA: Extend the **opening time of sodium channels in the CNS and PNS** * Physiological effects: Loss of coordination, seizures, burning/itching sensation, contact dermatitis, asthma-like symptoms * **Supportive treatment** for acute intoxication
59
For the pesticide, **Rotenone** explain the mechanism of action | HIGH yield
* MOA: Inhibits **NADH-coenzyme Q reductase (complex 1)→stops oxidative phosphorylation** ## Footnote FYI: CO is toxic to cytochromes but the amount required is 1000X the lethal dose & thus plays no role in clinical poisoning
60
For the pesticide, **Rotenone** explains the side effects and treatments | HIGH yield
* Physiological effects: Nausea/Vomitting, Seziures, Death @ at very high doses * Treatment: **Supportive treatment** for acute intoxication
61
What are Rodenticides structurally similar to? ## Footnote Brodifa**coum** Difena**coum**
* Structurally similar to warfin (More lipophilic) * Can have longer half-life (effects clotting factors: 2,7,9, 10)
62
For Rodenticides: Brodifa**coum**, Difena**coum**: * Ingestion: * Toxicity effects: * Treatment:
* Ingestion: **Can occur w/ intentional poisoning & suicide** * Toxicity effects: **Bleeding** * Treatment: Fresh frozen **plasma & phytonadione (VIT K)**
63
Which metals are Heavy metals?
* Lead (Pb) * Mercury (Hg) * Cadmium (Cd)
64
For Heavy metals; Pb, Hg, Cd * Explain exposure * Treatment
* Public health concern; Chronic low dose exposure (a concern) * Tx: Chelators
65
Treatment for Lead (Pb) poisoning ## Footnote Chelators
* **CaNa2 EDTA**: Ca2+ will be replace with Lead
66
What poisoning does **Succimer** treat? ## Footnote Chelators
Tx for Lead (Pb) and Mercury (Hg) poisoning
67
What poisoning does **Dimercaprol** treat? ## Footnote Chelators
Tx for Lead (Pb), Mercury (Hg), Arsenic (As) and Copper (Cu)
68
What poisoning does **Penicillamine** treat?
Tx for Copper (Cu) poisoning
69
What metal is a contraindication to all the chelator treatment?
Cadmium (Cd)
70
What ways can you be exposed Lead (Pb)?
Ubiquitous in environment * **Old paint** * **Drinking water** (lead paint) * Industrial pollution * Food * Dust ## Footnote Elimination from gasoline and paint in the late→↓Pb exposure in the USA
71
Who absorbs more of the ingested dose of Pb, Adults or Children?
* **Children absorbed 40%** of ingested dose * Adults absorb 10%
72
Where in the body is Inorganic Pb distributed?
* Initially distributes to soft tissues * **Redistributes to bone (MAINLY), teeth and hair** (can be detected by X-ray)
73
How long does Pb stay in blood and bone?
* Blood: t1/2 about 1-2 months * **Bone: t1/2 about 20-30 years** ## Footnote t1/2=half life
74
What are the Physiological effects of Pb toxicity?
* **CNS toxicity or Pb encephalopathy**: HA, confusion, clumisness, insomnia, fatigue and impaired concentration ## Footnote Enpathalopathy: Disrupts Ca2+ homeostasis which disrupts neurotransmitters
75
Who is more susceptible to CNS toxicity caused by Pb and what are the effects?
* Children which can lower IQ (estimated 9% of children may have blood conc. more than 10 μg/dL)
76
What are symptoms of Gastrointestinal (GI) toxicity caused by Pb exposure?
* Sx: Discomfort, constipation, or diarrhea * Higher doses can cause painful intestinal spasms which can be **treated with IV calcium gluconate**
77
What are the effects of Blood toxicity caused by Pb exposure?
* **Disrupts heme synthesis→shortens RBC life span, Hypochromic, microcytic anemia** * **↑ δ-aminolevulinic acid (ALA) & protoporphyrin IX** blood concentration by **inhibition of δ-aminolevulinic acid dehydratase & ferrochetalase** * Blood concentration>**25 μg/dL, Diagnostic for Pb intoxication**
78
Explain the function and side effects of the **tx: Dimercaprol** for Pb toxicity
* **Antidote w/ edatate calcium disodium** * **Chelator** which forms a coordinated bond w/ cationic metal & the complex **renally excerted** * Side effecs: ↑ blood pressure & heart rate ## Footnote Developed during WWII as an antidote to arsenical war gas or Lewisite
79
Which two chelators are a treatment for high Pb toxicity?
Dimercaprol + EDTA (Prevents Pb from entering CNS)
80
Explain the function and side effects of **tx: Succimer** for Pb toxicity
* Antidote for Pb including children * Side effects: ↑ hepatic enzymes, nausea/vomiting/diarrhea (N/V/D), loss of appetite
81
Explain the function and side effects of **tx: Edetate calcium disodium (EDTA)** for Pb toxicity
* Antidote for Pb * Can be combined w/ Dimpercaprol * Side Effects: nephrotoxicity
82
What treatment is used for Pb toxicity based on the conentration of Pb listed below: * 45-54 μg/dL= * 55-69 μg/dL= * 70-100 μg/dL=
* 45-54 μg/dL= Succimer * 55-69 μg/dL= EDTA * 70-100 μg/dL= EDTA + Dimercaprol
83
For Heavy Metal: **Lead (Pb)** * Exposure * Mechanism of action * Physiological effects * Treatment
* Exposure: Old paint, drinking water * MOA: Blocks heme synthesis * Physiological effects: CNS toxicity, Pb encephalopathy, GI toxicity, Blood toxicity * Treatment: Dimercaprol, Succimer, EDTA
84
List the three ways Mercury (Hg) can exist as toxin
* Elemental Hg * Inorganic Hg (mercuric chloride) * Organic Hg ( methyl mercury)
85
Explain exposure and side effects of Elemental Hg toxicity
* Exposure: Inhaled vapors * SE: **Tremors, depression, memory loss**, ↓verbal skills, renal inflammation * High concentration →**Corrosive to lungs**
86
What are the clinical presentations of Inorganic Hg (mercuric chloride)?
Corrosive: mucosal mouth damage, renal damage
87
Explain the chemical properties and exposure of Organic Hg ( methyl mercury)
* Chemical properties: **Very lipid solubility and less corrosive than inorganic Hg** * Exposure: Contaminated **fish**
88
What are the neurological symptoms of Organic Hg toxicity?
* Visual disturbances * Parasthesia * Ataxia * Hearing loss * Mental deterioration * Muscle tremors * Movement disorders
89
What occurs at very high doses of Organic Hg?
* Paralysis and death (especially toxic to the unborn child) * Misdiagnosed Alzheimers or Parkinson disease in elderly
90
What are the treatments for Mercury (Hg) toxicity?
* Dimercaprol * Succimer ## Footnote Chelating agents
91
For Hard Metal: **Mercury (Hg)** * Exposure * Physiological effects * Treatment
Exposure: * Inhaled vapors (Elemental Hg) * Contaminated fish (Organic Hg) Physiological effects: * Tremors,depression,memory loss (Elemental Hg) * Corrosive (Inorganic Hg) * Neurological symptoms (Organic Hg) Treatment: * Dimercaprol, Succimer (for All types)
92
How can you get exposed to the heavy metal, Cadmium (Cd)?
* **Ingestion or inhalation** * **Contaminated plants** * **Cigarrette smoke** * **Burning of fossil fuels** * **Industrial exposure,e.g., welding, smelting** * Greater absorption with inhalation
93
Where is Cd mainly distributed? and the half life?
* To the **liver and kidney** by binding to **metallothionein** * **t1/2=10-30 years**
94
What organ(s) is Cd especially toxic to?
Kidney and liver, also carcinogenic
95
What is the treatment for Cadmium (Cd)?
* Supportive tx for acute intoxication * **No evidence of chelation therapy effectiveness** * **Dimercaprol, penicillamine & EDTA contraindicated→↑risk of nephrotoxicity (kidney toxicity)**
96
A MSP3 student who plans on applying to medical school or pharmacy school is studying the effects of toxicants on human cell lines at the MCOM. Which of the following most likely disrupts electron transfer during oxidative phosphorylation? A. Chloroform B. Lead C. Rotenone D. Brodifacoum
C. Rotenone
97
1. Which of the following is NOT treated by supported treatment? a. Carbon tetrachloride b. Chloroform c. Toluene d. Ethylene Glycol
d. Ethylene Glycol
98
2. A patient comes to the ER after ingesting the rodenticide: Brodifacoum. Which of the following would be administered to the patient due to the toxicity? a. Penicillamine b. Phytonadione c. Pralidoxime d. Atropine
b. Phytonadione (Vit K)
99
3. Which of the following is NOT a metal that is a public health concern? a. Arsenic b. Lead c. Mercury d. Cadmium
a. Arsenic
100
4. A child has been experiencing headaches, confusion, and struggling with schoolwork. When reviewing his labs, you note that the urine sample contained high amounts of ALA and protoporphyrin. Which of the following would be a possible treatment? a. Succimer b. Penicillamine c. Phytonadione d. Fomepizole
a. Succimer
101
5. Which of the following can present as symptoms of Parkinson’s when exposed to a toxic dose? a. Toluene b. Methanol c. Lead d. Mercury
d. Mercury (Hg)

Pharmacology: Exam 3 (8 decks)

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