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Pharmacology: Exam 3 > Lecture 2: Toxicology II > Flashcards

Lecture 2: Toxicology II Flashcards

1
Q

List the Metals that can cause intoxication (6)

A
  • Lead (Pb)
  • Mercury (Hg)
  • Cadmium (Cd)
  • Arsenic (As)
  • Iron (Fe)
  • Copper (Cu)
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2
Q

List the Gases that can cause intoxication (2)

A
  • Carbon Monoxide (CO)
  • Hydrogen cyanide (HCN)
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3
Q

List the Inhaled Particles that can cause intoxication (2)

A
  • Silica
  • Asbestos
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4
Q

List the Drugs that can cause intoxication (6)

A
  • Methylenedioxymethamphetamine (MDMA)
  • Gamma-hydroxybutyrate (GHB)
  • Acetaminophen
  • Benzodiazepines
  • Opioids
  • Tricyclic antidepressants (TCA)
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5
Q

List the Antidotes & Treatments that treat intoxication (13)

A
  • N-acetylcysteine
  • Flumazenil
  • O2
  • Na Thiosulfate
  • Fomepizole
  • Succimer
  • DImercaprol
  • Naloxone
  • Atropine
  • Pralidoxime
  • Penicillamine
  • Deferoxamine
  • Charcoal
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6
Q

What ways can you be exposed to Arsenic (As)?

A
  • Drinking H2O in Ganges delta in India & Bangladesh (natural minerals)
  • Commerical applications in semiconductors, wood preservatives, ant bait
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7
Q

Explain the toxicodynamics of Arsenic

Toxicodynamics: effects of toxic on the organisms

A
  • Interfere with enzyme activity & cell signal transduction, oxidative stress, alter gene expression
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8
Q

What are the acute toxic effects of Arsenic (As)?

A
  • GI: N/V/D, abdominal pain, diffuse capillary leak & fluid loss→hypotension, shock,death
  • Cardiopulmonary: Pulmonary edema, ventricular arrhythmias (promptly or delay of several days), pancytopenia
  • CNS/PNS: Delirium, encephalopathy, coma, neuropathy (2-6 weeks onset)→proximal muscles & respiratory failure
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9
Q

What are the chronic toxic effects of Arsenic (As)?

A
  • Fatigue, weight loss, weakness
  • Anemia, GI complaints, peripheral neuropathy
  • Hyperpigmentation & hyperkeratoses of skin on hands & feet
  • Cancer: Lung, skin, liver
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10
Q

What is the treatment for Arsenic (As) toxicity?

A

Dimercaprol

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11
Q

For the Metal, Arsenic (As)

  • Exposure
  • Mechanism of Action
  • Physiological Effects
  • Treatment
A
  • Exposure: Drinking H2O, commerical applications, ant bait
  • MOA: Oxidative stress
  • Physiology Effects:
    1. Acute: Hypotension, shock, death (GI), Venticular arrhythmias (cardiopulmonary), encephalopathy (CNS/PNS)
    2. Chronic: Hyperpigmentation & Hyperkeratoses of skin on hands & feet
  • Treatment: Dimercaprol
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12
Q

In what ways can you be exposed to Iron (Fe)?

A
  • Ingesting of Fe tablets by young children ≥ 10 tablets can be lethal (acute toxicity)
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13
Q

What are the acute toxic effects of Fe?

A
  • Necrotizing gastroenteritis, Vomiting Abdominal pain, Bloody diarrhea
  • Followed by shock, lethargy, dyspnea
  • Subsequent improvement followed by severe metabolic acidosis, coma, death
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14
Q

What can cause chronic toxicity of Fe?

A
  • Pts w/ Excessive Fe absorption (inherited hemochromatosis)
  • Recieve many blood transfusions (thalassemia, sickle cell anemia, aplastic anemia)
  • Excess Fe deposits on heart,liver,pancreas (Can cause organ failure & death)
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15
Q

List the treatments for acute toxicity of Iron (Fe).

A
  • Whole bowel irrigation: Instillation of large volumes of polyethylene glycol (PO, NGT), Osmotically balanced electrolyte solution which prevents fluid & electrolyte shifts, Rapidly flush out unabsorbed Fe tablets
  • Deferoxamine (IV): Fe chelator for absorbed Fe which promotes excretion in urine & feces
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16
Q

What are the side effects of Deforxamine?

Deforxamine used as treatment for acute toxicity of Fe

A
  • Ocular & auditory disturbances (blurred vision, tinnitus)
  • Renal effects (↑ serum creatinine)
  • Acute respiratory distress syndrome (children)
  • Rapid infusion → histamine release → hypotension
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17
Q

List the treatments for chronic toxicity of Iron (Fe)

A
  • Intermittent phlebotomy: in the absence of anemia
  • DeFEroxamine (IM, SQ)
  • DeFErasirox (PO): Fe chelator for absorbed Fe which promotes excretion 1° in feces
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18
Q

What are the side effects of Deferasirox?

Deferasirox used for treatment for chronic toxicity of Fe

A
  • GI bleeding (elderly, fatal)
  • Nephrotoxic
  • Hepatotoxic
  • Rash
  • Pyrexia
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19
Q

For the Metal, Iron (Fe)

  • Exposure
  • Mechanism of Action
  • Physiological Effects
  • Treatment
A
  • Exposure
    1. Acute: Ingestion of Fe tablets
    2. Chronic: Excessive Fe absorption, many blood transfusions, Fe deposits on the heart, liver, and pancreas
  • MOA: N/A
  • Physiological Effects
    1. Acute: Necrotizing gastroenteritis, severe metabolic acidosis
    2. Chronic: Organ failure and death
  • Treatment:
    1. Acute: Whole bowel irrigation, DeFEroxamine
    2. Chronic: Intermittent phlebotomy, DeFEroxamine, DeFErasirox
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20
Q

What ways can you get acute toxic exposure to Cooper (Cu)?

A
  • Inhalation of Cu fumes or dust
  • Ingestion of Cu salts (sulfate)
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21
Q

What are the physiolgical effects of acute toxicity to Cu?

A
  • Severe cough, dyspnea, fever, leukocytosis, pulmonary infiltrates (Inhalation)
  • N/V (blue-green), GI bleeding, gastroenteritis, hepatotoxicity, shock (Ingestion)
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22
Q

List the treatments for acute toxicity caused by Cu?

A
  • Supportive treatment (O2)
  • Decontamination
  • Chelators:
    1. Dimercaprol
    2. Penicillamine
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23
Q

What are the side effects of Penicillamine?

Penicillamine used as treatment for acute toxicity of Cu

A
  • Myelosuppression
  • Proteinuria
  • Lupus-like syndrome
  • Neurologic worsening (10%)
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24
Q

What can cause chronic toxicity of Cooper (Cu)?

A
  • Bordeaux mixture: Cu salt, fungicide, vineyard workers
  • Wilson disease: Disorder of copper metabolism, ↑ concentration of Cu in CNS & viscera
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25
Q

What are the physiological effects of chronic toxicity to Cooper (Cu)?

A
  • Pulmonary fibrosis, lung cancer, cirrhosis, angiosarcoma, & portal hypertension (Bordeaux mixture)
  • Hepatic & neurologic dysfunction (e.g., tremor)(Wilson disease)
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26
Q

List the treatments for chronic toxicity to Cu

A
  • Penicillamine (PO, dimethylcysteine)
  • Trientine (PO)
  • Dietary Cu below 2 mg/d

Treatments for Wilison disease

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27
Q

What are the side effects of Trientine?

Low yield

Trientine used as a treatment for chronic toxicity to Cu

A
  • Anemia because Fe deficiency
  • Arthralgia
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28
Q

For the Metal, Cooper (Cu)

  • Exposure
  • Mechanism of Action
  • Physiological Effects
  • Treatment
A
  • Exposure
    1. Acute: Inhalation of Cu fumes or dust/Ingestion of Cu salts
    2. Chronic: Bordeaux mixture, Wilson disease
  • MOA
    1. Acute: N/A
    2. Chronic: ↑ Cu in CNS & viscera (Wilson disease)
  • Physiological Effects
    1. Acute: Dyspnea, Leukocytosis (Inhalation)
    2. Chronic: Pulmonary fibrosis (Bordeaux mixture); Hepatic and neurologic dysfunction (Wilson disease)
  • Treatment
    1. Acute: Dimercaprol, Penicillamine
    2. Chronic: Penicillamine, Trientine
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29
Q

Explain how gases (CO, HCN) affect the body systems

A

Inhaled gases travel to the alveoli, Distribute to the blood & other tissues

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30
Q

What are the chemical properties of Carbon monoxide (CO) and in what ways can you get exposed to it?

A
  • Chemical properties: colorless, odorless, tasteless
  • Exposure: combustion of carbonaceous material: cars, poorly vented furnaces, fireplaces, wood-burning stoves, kerosene space heaters, charcoal grills
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31
Q

Explain the mechanism of action of CO intoxication

A
  • CO avidly binds to hemoglobin → carboxyhemoglobin, more than O2
  • ↓ unloading of O2 to other tissues by ↑ O2 affinity to hemoglobin at other O2 binding sites
  • Further ↓ O2 delivery
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32
Q

What are the physiological effects caused by CO toxicity?

A
  • Hypoxia: CNS & heart especially sensitive
  • Clinical presentation: HA, dyspnea, drowsiness, lethargy, confusion, Higher doses can cause seizures, coma & death
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33
Q

What is the treatment for CO toxicity?

A
  • Promptly remove CO source
  • 100% O2 via non-rebreathing facemask or endotracheal tube
  • Hyperbaric chamber with severe intoxication
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34
Q

For the Gas, Carbon Monoxide (CO)

  • Exposure
  • Mechanism of Action
  • Physiological Effects
  • Treatment
A
  • Exposure: Cars (combustion of carbonaceous material)
  • MOA: CO binds to hemoglobin, ↓O2 delivery
  • Physiological Effects: Hypoxia
  • Treatment: Remove CO source, 100% O2, Hyperbaric chamber w/ severe intoxication
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35
Q

What ways can you be exposed to Hydrogen cyanide (HCN)?

A
  • Burning of plastics, wool
  • CN- (cyanide) salts in cassava, apple, peach, & apricot seeds

HCN has an almond-like odor

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36
Q

Explain the mechanism of action and side effects of HCN intoxication

A
  • Inhibits cytochrome a3 mediated electron transfer, which prevents energy production by oxidative phosphorylation
  • Death can occur quickly because of lack of ATP production
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37
Q

List the treatments for HCN toxicity (3)

A
  • Sodium nitrate
  • Sodium thiosulfate
  • Hydroxocobalamin
38
Q

What is the mechanism of action for the tx: sodium nitrate (or amyl mitrate)?

Sodium nitrate is used to treat HCN toxicity

A

Converts hemoglobin into methemoglobin which binds to cyanide with high affinity to produce cyanmethemoglobin

39
Q

What is the mechanism of action for the tx: sodium thiosulfate?

Sodium thiosulfate is used to treat HCN toxicity

A
  • Converts cyanide into less toxic thiocynate which is renally eliminated
40
Q

What type of patients should avoid sodium nitrate treatment?

A

Patients w/ additional smoke inhalation damage

41
Q

What is the mechanism of action of tx: Hydroxocobalamin (Vitamin B12)? and include side effects?

Hydroxocobalamin is used to treat HCN toxicity

A
  • (Alternative treatment) Converts CN → cyanocobalamin which is renally eliminated
  • Side effects: Discoloration of urine & skin, allergic reaction (urticaria), chest discomfort, pain at injection site
42
Q

For the Gas, Hydrogen cyanide (HCN)

  • Exposure
  • Mechanism of Action
  • Physiological Effects
  • Treatment
A
  • Exposure: Buring pf plastics, wools and in cassava, apple, peach and apricot seeds
  • MOA: Inhibits cytochrome a3 mediated electron transfer, prevents energy production by oxidative phosphorylation
  • Physiological Effects: Death (d/t lack of ATP)
  • Treatment: Sodium nitrate, Sodium thiosulfate, Hydroxocobalamin (vit B12)
43
Q

A 3-year-old boy ingests 30 ferrous sulfate tablets. Which of the following most likely will develop signs of acute toxicity?
A. Stomach
B. Liver
C. Kidney
D. Pancreas

A

A. Stomach (Necrotizing Gastroenteritis)

44
Q

What ways can you be exposed to Silica (inhaled particles)?

A
  • Mines
  • Foundries
  • Construction sites
  • Stone cutters

All increase the risk for silicosis

45
Q

What disease is caused by Silica intoxication?

A

Silicosis: progressive lung disease that results in fibrosis & often emphysema

46
Q

What is the prevention of Silica toxicity?

A

Minimize exposure

47
Q

For the Inhaled Particles, Silica

  • Exposure
  • Mechanism of Action
  • Physiological Effects
  • Treatment
A
  • Exposure: Mines, foundries, construction sites
  • MOA: N/A
  • Physiological Effects: Silicosis (lung disease)
  • Treatment: Minimize exposure
48
Q

What ways can you be exposed to Asbestos (inhaled particles)?

A

Inhalation of the fibers damages the lungs

49
Q

What diease(s) are caused by Asbestos?

A
  • Asbestosis
  • Mesothelioma
  • Other cancers (lung, colon)
  • Clinical presentation of lung disease may take 15 to 30 years after exposure
50
Q

Explain Abestosis, including the symptoms and treatment.

Disease caused by Abestosis toxicity

A
  • Interstitial & pleural fibrosis & calcification
  • Symptoms: of initial shortness of breath followed by severe cough & chest pains, Progressive disease
  • Treatment: NO specific treatment, Can be fatal
51
Q

Explain Mesothelioma, including the symptoms and treatment.

Disease caused by Abestosis toxicity

A
  • Rare cancer of the chest wall or peritoneum
  • Symptoms: Dyspnea & cough; Survival rate of < 2 years after diagnosis
  • Treatment: Prevention, Supportive treatment
52
Q

For the Inhaled Particles, Asbestos

  • Exposure
  • Mechanism of Action
  • Physiological Effects
  • Treatment
A
  • Exposure: Inhalation of fibers
  • MOA: N/A
  • Physiological Effects: Damage in lungs, Absestosis, Mesothelioma, & other cancer (lungs, cancer)
  • Treatment: Supportive treatment
53
Q

What ways can you be exposed to the drug Methylenedioxymethamphetamine (MDMA)?

A
  • Illegal drugs, Designer or street drugs (Psychoactive properties)
  • Amphetamine analog, Ecstasy (Rave parties, dance clubs, rock concerts)
54
Q

Explain the Mechanism of action of MDMA

A
  • Causes the release of serotonin (5-HT) & inhibits the reuptake & synthesis of 5-HT (↑5-HT in the synaptic cleft)
55
Q

How long does it take for the drug MDMA to take effect?

A

Effects start within 1 hour of ingestion & last about 3 to 6 hours

56
Q

What are the cardiopulmonary effects caused by MDMA toxicity?

A
  • Tachycardia
  • Tachypnea
  • Hypertension
  • Vasospasm
  • Pulmonary hypertension
  • Arrhythmias
  • Valvular disease
  • Myocardial infarction
57
Q

What are the neurologic effects caused by MDMA toxicity?

A
  • Mydriasis
  • Nystagmus
  • Head jerking
  • Hyperthermia
  • Sexual dysfunction
  • Seizures
  • Cerebral infarction
  • Neuronal destruction (5-HT depletion)
  • 5-HT syndrome (with other drugs)
58
Q

What are the psychologic effects caused by MDMA toxicity?

A
  • Euphoria
  • Empathy
  • Agitation
  • Hallucinations
  • Anxiety
  • Psychosis
  • Obsessive-compulsive behavior with chronic abuse
59
Q

What are the musculoskeletal effects caused by MDMA toxicity?

A
  • Teeth grinding
  • Jaw clenching, cramping
  • Rhabdomyolysis because ↑ muscle activity
60
Q

What are other physiogical effects caused by MDMA toxicity?

A
  • Dehydration
  • Hyperglycemia
  • Metabolic acidosis → chronic use & overdose
  • Hyponatremia → ↑ fluid uptake & antidiuretic hormone antagonism → seizures & cerebral edema
61
Q

List the different treatments of MDMA intoxication and the specific disease it treats

A
  • Fluid restriction→Hyponatremia
  • Nitroprusside or phentolamine→Refractory hypertension
  • Aggessive external cooling w/ ice H2O, mist & fans→ Hyperthermia
  • Diazepam→Anxiety, agitation & seizures
62
Q

For the Drug, Methylenedioxymethamphetamine (MDMA)

  • Exposure
  • Mechanism of Action
  • Physiological Effects
  • Treatment
A
  • Exposure: Illegal drugs, designer or street drugs, ecstasy
  • MOA: Causes the release of serotonin (5-HT) & inhibits the reuptake & synthesis of 5-HT
  • Physiological Effects: Tachycardia, hypertension (cardiopulmonary); hyperthermia, seizures (neurologic); euphoria, anxiety (psychologic); dehydration, hyponatremia
  • Treatment: fluid restriction (hyponatremia), nitroprusside/phentolamine (refractory HTN), agressive external cooling (hyperthermia), diazepam (anxiety, agitation & seizures)
63
Q

Whay ways can you be exposed to the drug, Gamma-hydroxybutyrate (GHB)?

A
  • Date rape drug, amnesia (Dance, rave clubs, rapidly produced euphoria)
  • Therapeutic use for narcolepsy
64
Q

Explain the mechanism of action of GHB toxicity

A

GABA(B) receptor agonist, ↑ dopaminergic activity

65
Q

What are the cardiopulmonary effects caused by GHB toxicity?

A
  • Hypoxia
  • Bradycardia
  • Hypotension
  • Bradypnea
  • Arrhythmia with chronic use
66
Q

What are the CNS effects caused by GHB toxicity?

A
  • Euphoria (low dose)
  • Deep sleep (moderate dose)
  • Coma (high dose)
  • Amnesia
  • Loss of sexual inhibition
  • Hallucinations
  • Myoclonus
  • Slurred speech
67
Q

List the treatment(s) for GHB toxicity?

A
  • Tx: Overdose, significant CNS depression- Supportive, intubation to prevent aspiration pneumonia
  • Bradycardia treatment with atropine
  • Severe withdrawal treatment with pentobarbital
68
Q

For the Drug, Gamma-hydroxybutyrate (GHB)

  • Exposure
  • Mechanism of Action
  • Physiological Effects
  • Treatment
A
  • Exposure: Date rape drug
  • MOA: GABAB receptor agonist, ↑ dopaminergic activity
  • Physiological Effects: Cardiopulmonary effects, CNS effects
  • Treatment: Supportive tx (overdose), Atropine (bradycardia)
69
Q

Explain the mechanism of action for the drug, Acetaminophen

Generic name: Tylenol

A

Liver damage by CYP-mediated bioactivation

70
Q

What is the treatment for Acetaminophen?

A

N-acetylcysteine

71
Q

Explain the mechanism of N-acetylcysteine

Tx for aceraminophen

A
  • Antidote for acetaminophen overdose
  • Administer within 8-10 hours
  • Can bind directly to NAPQI and eliminate it or act as precursor to create more GSH and sulfate
    (Glucuronidation, GSH, and sulfation of acetaminophen cause nontoxic metabolites)
72
Q

What is the max dose of Acetaminophen?

A

4000 mg

73
Q

For the Drug, Acetaminophen

  • Exposure
  • Mechanism of Action
  • Physiological Effects
  • Treatment
A
  • Exposure: Tylenol
  • MOA: CYP-mediated biactivation
  • Physiological Effects: Liver damage
  • Treatment: N-acetylcysteine
74
Q

Explain the mechanism of action of Benzodiazepines toxicity?

Generic name(s): Diazepam (Valium®), Chlordiazepoxide

A

↑ GABA activity at the GABAA receptor which can lead to CNS depression

75
Q

What are the physiological effects of Benzodiazepine toxicity?

A
  • (CNS Depression) respiratory depression, coma
  • Death is rare, increased toxicity with Alcohol and opioids
76
Q

What increases toxicity of Benzodiazepines?

A

Alcohol and Opioids

77
Q

List the different treatments for Benzodiazepine(s) toxicity

A
  • Supportive care: Breathing
  • Flumazenil: GABA(A) receptor antagonist
    Side effects → seizures, withdrawal, Shorter t1/2
  • Activated charcoal: Absorption, large surface area (For drug to bind to), Ingestion within 30-60 minutes
    Side effects → N/V/D
78
Q

For the Drug, Benzodiazepines

  • Exposure
  • Mechanism of Action
  • Physiological Effects
  • Treatment
A
  • Exposure: Diazepam, Chlordiazepoxide
  • MOA: ↑ GABA activity at the GABAA receptor
  • Physiological Effects: CNS depression
  • Treatment: Supportive care, Flumazenil, Activated characoal
79
Q

List the different type of Opioids

A
  • Morphine
  • Heroin
  • Oxycodone
  • Fentanyl
  • Carfentanil
80
Q

Explain the mechanism of action of Opioids

Morphine, Heroin, Oxycodone, Fentanyl, Carfentanil

A

μ receptor agonist, CNS depression

81
Q

What the physiological effects of Opioid toxicity?

A
  • Respiratory depression
  • Coma
  • Hypotension
82
Q

List the different treatments for Opioid toxicity

A
  • Supportive care: Breathing, blood pressure
  • Naloxone or Naltrexone: μ receptor antagonist
    Side effects → Vomiting, sweating, tachycardia, hypertension, Shorter t1/2
  • Activated charcoal
  • Whole-bowel irrigation for sustained release products
83
Q

For the Drug, Opioids

  • Exposure
  • Mechanism of Action
  • Physiological Effects
  • Treatment
A
  • Exposure: Morphine, Heroin, Oxycodone, Fentanyl
  • MOA: μ receptor agonist
  • Physiological Effects: CNS depression → respiratory depression, coma, hypotension
  • Treatment: Naloxone/Naltrexone, Activated charcoal
84
Q

Explain the mechanism of action of Tricyclic antidepressants (TCA)

Amitriptyline, Desipramine

A

↑ norepinephrine & serotonin concentrations in the synaptic cleft, also muscurinic, ⍺ receptor antagonist & Na+ channel blocker

85
Q

What are the physiological effects of TCA toxicity?

A
  • Tachycardia
  • Seizures
  • Hypotension
  • Arrhythmia
86
Q

List the different treatments of TCA toxicity?

A
  • Supportive care: Blood pressure
  • Sodium bicarbonate: Reverse sodium channel blockade
    Side effects → Hypernatremia, metabolic alkalosis, Tissue necrosis (extravasation)
  • Activated charcoal
87
Q

For the Drug, Tricylic Antidepressants (TCA)

  • Exposure
  • Mechanism of Action
  • Physiological Effects
  • Treatment
A
  • Exposure: Amitriptyline, Desipramine
  • MOA: ↑ norepinephrine & serotonin concentrations; muscurinic, α receptor antagonist & Na+ channel blocker
  • Physiological Effects: Tachycardia, seizures, hypotension, arrhythmia
  • Treatment: Supportive care, Sodium bicarbonate, activated charcoal
88
Q

A MSP3 student who began interviewing at several prestigious medical schools is studying the effects of toxicants on human neuronal cell lines at the MCOM. Which of the following neurotransmitters does methylenedioxymethamphetamine increase the most?
A. Glutamate
B. GABA
C. Serotonin
D. Dopamine

A

C. Serotonin

89
Q
  1. A subject present with hepatic and neurological sx. After many tests, the patient is diagnosed with Wilsons disease. Which of the following could possibly be a treatment?
    a. Dimercaprol
    b. Trientine
    c. Deferasirox
    d. Flumazenil
A

b. Trientine

90
Q
  1. Which of the following is an acute toxic symptom of Arsenic?
    a. Arrhythmias
    b. Anemia
    c. Hyperkeratosis
    d. Cancer
A

a. Arrhythmias

91
Q
  1. Mesothelioma is a severe cancer with low prognosis. Which of the following can cause this cancer if exposed chronically?
    a. Silica
    b. HCN
    c. Fe
    d. Asbestos
A

d. Asbestos

92
Q

Match the following with the correct MOA:
a. GHB
b. MDMA
c. Morphine (Opioid)
d. TCA
e. Diazepam (Benziopines)
MOA:
1. Releases serotonin
2. μ receptor agonist
3. GABA a Agonist
4. Increase NE and serotonin/NA antagonist
5. GABA b agonist

A
  • a=5
  • b=1
  • c=2
  • d=4
  • e=3

Pharmacology: Exam 3 (8 decks)

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