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[Ther 201] 2nd Exam Transes > Introduction to Toxicology (Lynn R. Panganiban, MD) > Flashcards

Introduction to Toxicology (Lynn R. Panganiban, MD) Flashcards

1
Q

It is the science of adverse effects of chemical, physical and biological agents on living organisms.

A

Toxicology

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2
Q

What are the physical agents toxicology is concerned with?

A

Radiation and heat waves

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3
Q

What are the biological agents toxicology is concerned with?

A

Parasites and infectious disease etiologic agents

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4
Q

Define: Toxicity

A

Ability of a substance to cause harm in an organism

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5
Q

T/F: Toxicity is an innate property of the substance.

A

True

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6
Q

While we cannot control a drug’s toxicity, we can control its toxicity during (1).

A

Manufacture

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7
Q

Define: Toxicodynamics

A
  1. Mechanisms of actions of chemicals

2. Extension of definition of pharmacodynamics

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8
Q

Define: Toxicokinetics

A

ADME of substances in their toxic statess

i.e. changes from 1st order to 0 order

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9
Q

Define: Poison

A

Any agent capable of producing a deleterious effect leading to injury or death

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10
Q

What is the more medically acceptable term for “poison”?

A

Toxicant

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11
Q

T/F: Toxins are artificial substances.

A

False

They are naturally occurring substances of endogenous plant or animal origin.

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12
Q

What are used for substances that are synthetically manufactured?

A

Xenobiotics

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13
Q

What is the state of being overdosed on drugs, medicaments, chemicals and biological substances?

A

Poisoning

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14
Q

What is the difference between an adverse reaction and poisoning?

A

An adverse reaction always occurs within therapeutic doses.

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15
Q

Enumerate the factors affecting responses to toxic agents

A
  1. Physical & chemical properties
  2. Exposure situation
  3. Individual factors
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16
Q

Enumerate the important physical and chemical properties of toxic agents

A
  1. Physical state
  2. Solubility
  3. Vapor pressure
  4. Vapor density
  5. Reactivity
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17
Q

What physical state is most toxic to humans?

A

Gas

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18
Q

In terms of solubility, what toxicants are most harmful?

A

Fat-soluble, non-ionised substances

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19
Q

What values of vapour pressure are considered most toxic?

A

Greater than or equal to 1 mmHg

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20
Q

What values of vapour density are considered most toxic?

A

Greater than one (heavier than air)

Dangerous for people on the first floor!

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21
Q

Toxicants with (1) and (2) are more deleterious.

A

(1) Charged particles

(2) Reactive oxygen species

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22
Q

Define: Acute Exposure

A
  1. Exposure happens in less than 24 hours.
  2. Single dose
  3. Series of doses within 13hrs if administered orally
  4. Continuous for 4 hrs via inhalation
  5. Large volume of drugs
  6. Effects appear within 14 days
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23
Q

Define: Subacute Exposure

A
  1. Repeated daily exposure for 21 ways via specific route
  2. No need for high dosage
  3. SSx manifest within 21 days.
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24
Q

Define: Subchronic Exposure

A
  1. Repeated daily exposure for 90 days

2. Can be low dose

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25
Q

Define: Chronic Exposure

A
  1. Lifetime exposure
  2. Two years for rat and mice
  3. Seventy years for humans
  4. May result in transgenerational effects
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26
Q

What parameter is expressed in terms of exposures/time period?

A

Frequency

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27
Q

What parameter is critical to the concentration level of substance in biological fluids at the site?

A

Frequency

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28
Q

Enumerate the major routes by which toxic substances gain access to the body

A 
Ingestion
Inhalation
Dermal/Percutaneous
Parenteral
Mucosal
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29
Q

Rank the routes of entry in terms of descending effectiveness toxicity

A 
Parenteral
Inahalational
Intraperitoneal
Intramuscular
Subcutaneous
Intradermal
Oral & Dermal
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30
Q

What is the most critical factor determining whether the intrinsic property of a substance will be expressed?

A

Dosage

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31
Q

T/F: Dose should not be dependent on the weight of the individual.

A

False

It should be.

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32
Q

Which tenet may not necessarily apply in cases of toxicity?

A

The dose makes the poison

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33
Q

What are examples of endocrine disruptive agents?

A 
Bisphenol A (found in plastics and can affect reproductive development of children)
DDT (affects reproductive development)
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34
Q

What substances can induce their effects in picograms?

A

Dioxins

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35
Q

What is the mechanisms of action of carcinogenic or genotoxic substances?

A

Disrepair of components of the central dogma

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36
Q

Enumerate the individual factors that contribute to toxicity

A

Age
Sex (pregnant women > women reproductive age group)
Genetic Background (toxicogenomics; G6P deficiency bleeding from nitrates)
Nutritional Status (low protein/albumin)
General Health Status (liver, kidney or heart disease)
ADME

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37
Q

T/F: Toxic action of drug is an exaggeration of its therapeutic action.

A

False

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38
Q

What happens when a person overdoses on paracetamol?

A

Develops liver problems

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39
Q

What is the mechanism of action of isoniazid?

A

Attacks the ribosomes of Mycobacterium

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40
Q

How does isoniazid overdose manifest?

A

Inhibition of GABA synthesis resulting in seizures and B6 deficiency

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41
Q

T/F: One toxicant may exert several mechanisms of toxic actions.

A

True

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42
Q

Toxicity may also affect the (1) not just the CNS. Give an example.

A

blood; lead toxicity

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43
Q

What does lead toxicity do to the body?

A
  1. Breakdown of sulfhydryl molecules of myelin sheaths causing neuropathy
  2. Interference with haemoglobin production by enzyme inhibition leading to multi-organ system effects
    e. g. alcohol & tobacco
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44
Q

T/F: Toxic action can only be brought about by the parent compound.

A

False

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45
Q

What is a metabolite of diazepam that has the same potency as its parent compound?

A

Oxazepam

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46
Q

When metabolised, what is paracetamol converted to? Is it toxic?

A

NAPQI; yes

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47
Q

T/F: The mechanism of toxic action in acute exposure is no different from those in chronic exposure.

A

False

e.g. seizure as a result of acute exposure and cancer as a result of chronic exposure

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48
Q

What substances inhibit acetylcholinesterase?

A

Organophosphate

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49
Q

Enumerate the clinical signs of cholinergic manifestation

A

Salivation, diarrhoea, pupil dilation, sweating and bradycardia

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50
Q

Intensity of the toxic effect depends primarily on what properties of the ultimate toxicant?

A

Concentration and persistence

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51
Q

T/F: The effect of a chemical is dependent solely on the dose administered.

A

False.

It depends more on the concentration and disposition of the chemical in the target organ.

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52
Q

T/F: Drugs that are normally metabolised through first-order kinetics may change to zero-order kinetics during overdose.

A

True

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53
Q

Give examples of drugs that exhibit zero-order kinetics when overdosed.

A

Phenobarbital, theophylline and salicylate

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54
Q

T/F: During overdose, some drugs may change their volume of distribution

A

True

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55
Q

Enumerate the factors affecting kinetic processes.

A
  1. Duration and concentration at the portal of entry.
  2. Rate and amount of chemical absorbed
  3. Distribution of the toxicant within the body
  4. Efficiency of biotransformation and nature of metabolites
  5. Ability of the chemical or its metabolites to pass through cell membranes and come into contact with specific cell components
  6. Amount and duration of storage of the chemical or its metabolites in body tissues
  7. Rate and site of excretion
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56
Q

T/F: The higher the concentration of the chemical at the portal of entry, the greater the damage

A

True

e.g. concentrated HCl causes greater damaged than diluted HCl

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57
Q

In terms of rate and amount of chemical absorbed, when will toxicity be low?

A

Slow absorption and small amount of absorption

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58
Q

T/F: Slowly released products have a wide margin of safety.

A

True

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59
Q

Where are toxicants most highly concentrated?

A

Brain, heart and kidneys

60
Q

T/F: The organ where a chemical is most highly concentrated is where the most tissue damage occurs.

A

False

61
Q

Describe: Lead as Storage Depot

A

95% of lead is stored in the bones for years, where it may reach the brain and cause effects to the hematologic and nervous systems.

62
Q

Describe: DDT as Storage Depot

A

DDT is converted to DDE and stored in adipose tissue, bones, and plasma proteins for up to 8 years.

63
Q

What is the half-life of lead?

A

20 years

64
Q

T/F: A chemical may be converted into a metabolite that is more toxic than the parent compound.

A

True

65
Q

What drugs undergo Michaelis-Menten kinetics at toxic concentrations?

A
  1. Paracetamol

2. Alcohol (0 to begin with)

66
Q

In what conditions will the blood-brain barrier not work?

A

Hypoglycemia and acidosis

67
Q

T/F: Heavy metals can’t pass through the placenta.

A

False

Heck, even nicotine can (fetal tobacco syndrome)

68
Q

What is the half-life of DDT in the body? In the environment?

A

30; 100

69
Q

What is the relationship between rate of excretion and toxicity?

A

Greater rate, less toxicity

70
Q

What is responsible for delayed excretion of certain compounds via enterohepatic circulation?

A

Bacterial flora in distal ileum convert metabolites into lipophilic states

71
Q

What compounds are recovered via enterohepatic circulation?

A 
Carbamazepine (anti-convulsant)
Dapsone (anti-infective; leprosy)
Phenobarbital (anti-convulsant)
Quinine (for malaria)
Theophylline (asthma and lung problems)
72
Q

What compounds are ionised in alkaline urine? acidic urine?

A

Weakly acidic drugs; weakly basic drugs

73
Q

Enumerate the kinetic processes the body adapts to protect itself from toxicants.

A

Presystemic elimination
Distribution away from target site
Detoxification
Excretion

74
Q

What is the process that prevents formation of ultimate toxic metabolites and enhances its elimination?

A

Detoxification

75
Q

What agents are used in detoxification?

A

Antioxidants
Glutathione
Superoxide dismutase

76
Q

What are the modes of excretion?

A 
Liver
Kidney
Bile
GI tract
Breast milk
77
Q

Enumerate the potential stages in development of toxicity after clinical exposure

A
  1. Delivery
  2. Interaction with target molecule
  3. Cellular dysfunction & injury
  4. Dysrepair
78
Q

What are direct injuries usually caused by?

A

Caustic agents

79
Q

Ethylene glycol is converted to (1) by (2), which produces (3) and (4), causing damage to (5) and (6).

A

(1) oxalic acid (potential acute kidney and lung injury)
(2) oxidation
(3) acidosis
(4) hypercalcemia
(5) kidney
(6) GIT

80
Q

What are the two altered states of cell regulation? Of cell maintenance?

A

Dysregulation of gene expression
Dysregulation of ongoing cellular activity

Impaired internal maintenance
Impaired external maintenance

81
Q

What are the forms of interaction with the target molecule?

A

Non-covalent binding
Covalent binding
Electron transfer (i.e. snake venom)
Enzymatic reactions

82
Q

Which process is most affected by toxicity? What are its components?

A

Cellular regulation

Dysregulation of gene expression
Dysregulation of on-going cellular activity

83
Q

Common endocrine disruptors affect?

A

Reproductive genes
Thyroid
Obesity

84
Q

Give examples of compounds that produce transgenerational toxicity

A

Bisphenol A
DDT
Nonlyphenol

85
Q

What compounds mimic endogenous estradiol?

A

Bisphenol A
DDT
Phthalate

86
Q

What compounds produce inhibitory effect on the M2 and M3 receptors?

A

Atropine and atropine-like drugs

87
Q

What causes “Alice in Wonderland” toxidrome?

A

Datura metel (Angel’s trumpet plant or talampunay)

88
Q

What are the components of Datura metel?

A

Scopolamine, atropine, hyoscine and calcium oxalate

89
Q

Enumerate the manifestations of anticholinergic toxidrome present during the 1st to 6th hour

A 
Mydriasis
Decreased bowel sounds
Urinary retention
Dry mouth
Hallucinations/agitation
Flushed skin
Tachycardia
Hyperthermia
Blind as bat
90
Q

T/F: Exaggeration of benzodiazepine stimulation of GABA alpha-receptor leads to sedation and coma.

A

True

91
Q

Amphetamine and other sympathomimetic drugs lead to?

A

Increased release of neurotransmitters

92
Q

Differentiate anti-cholinergic and sympathomimetic

A

Sympathomimetic - no dryness of skin

Anti-cholinergic - dry and hot skin and very high-grade fever

93
Q

What compounds cause enzyme inhibition?

A

Lead
Organophosphate
Isoniazid

94
Q

Describe: Isoniazid overdose

A

It causes seizures and inhibits GABA synthesis.

95
Q

What enzymes does isoniazid inhibit?

A

Glutamic acid decarboxylase and pyridoxine phosphokinase

96
Q

Can you treat isoniazid overdose with benzodiazepine?

A

No. Seizures will not stop.

97
Q

What are examples of impaired internal maintenance?

A

Impaired ATP synthesis
Oxidative stress
Impaired membrane function

98
Q

What cases fall under impaired ATP synthesis?

A

Impaired H+ delivery to ECT (fluoroacetate)
Inhibition of electron transport complexes (cyanide)
Inhibition of O2 delivery to ETC
Inhibition of ADP phosphorylation

99
Q

Paracetamol undergoes (1) and (2) for metabolism and excretion.

A

(1) Glucuronidation

(2) Sulfation

100
Q

NAPQI is reduced to (1) by (2).

A

(1) Mercapturate

(2) Glutathione

101
Q

Paracetamol overdose manifests as…

A

Liver toxicity

102
Q

T/F: Ethanol and organic solvents increased cell membrane fluidity.

A

True

103
Q

T/F: Hydrocarbons destroy plasma membrane.

A

False

They destroy lysosomal membranes.

104
Q

Describe: Impaired external maintenance by coumarin

A

Inhibits hepatic synthesis of coagulation factors

105
Q

What are the different toxicity repair mechanisms?

A

Molecular (proteins, lipids and DNA)
Cellular
Tissue

106
Q

How long does it take liver tissue to regenerate?

A

6 - 8 weeks

107
Q

Give an example of a chemical allergy

A

Pyrethroids - insecticides

108
Q

Refers to a genetically determined abnormal reactivity to a chemical

A

Chemical idiosyncrasy

109
Q

Deficiency in NADH-methemoglobin reductase may lead to?

A

Cyanosis, CNS and GI effects

110
Q

T/F: Immediate toxicity is acute toxicity, while delayed toxicity is chronic/subchronic toxicity

A

True

111
Q

T/F: Neurotoxicity is an example of immediate toxicity caused by organophosphates.

A

False

Delayed!

112
Q

Give examples of reversible and irreversible toxicity

A

Reversible - paracetamol injury

Irreversible - alcoholic binge (2 million neurons lost!)

113
Q

Give examples of systemic toxicity

A

Phenol a.k.a. lysol leading to kidney damage

Oxalic acid leading to liver damage

114
Q

What compound is capable of interrupting formation of NAPQI from paracetamol?

A

N-acetylcysteine (precursor of glutathione)

115
Q

What is the antidote for isoniazid overdose?

A

GABA and exogenous vitamin B6

116
Q

What are clinical applications in cases of toxicity?

A

Choose antidotal therapy
Determine magnitude and extent of toxicity
Make effective/adequate treatment plan to address kinetic & dynamic properties
Predict plasma drug concentration

117
Q

What are the modifications in clinical responses of individual drugs with concurrent use of 2 or more drugs?

A 
Adverse interaction (loss of efficacy)
Beneficial interaction (enhancement of efficacy)
118
Q

T/F: Many drug interactions can be predicted by knowledge of pharmacokinetic & pharmacodynamic properties of the drugs.

A

True

119
Q

T/F: Altered pharmacokinetics, pharmacodynamic, drug-induced disease or change in fluids and electrolyte balance may modify response to another drug.

A

True

120
Q

T/F: Interactions demonstrated with certain drugs can be extrapolated to closely related drugs.

A

False

121
Q

Give examples of drugs with a low therapeutic margin

A 
Oral anticoagulants
Hypoglycemics
Cardiac glycosides
Anti-convulsants
Anti-cancer
Anti-hypertensives
122
Q

T/F: Pharmaceutical drug interactions are typically in vitro.

A

True

123
Q

T/F: IV fluid does not need to suit the drug.

A

False

124
Q

T/F: Certain drugs may be broken down by polyvinyl chloride plastics.

A

True

125
Q

T/F: Isoniazid can be converted to toxic forms if stored improperly.

A

True

126
Q

When do pharmacodynamic drug interactions occur?

A

When interactant drug alters effect of object drug at site of action

127
Q

What is the antidote for opiate overdose? What is the mechanism of action?

A

Naloxone; antagonism

128
Q

T/F: Flumazenil and benzodiazepine exhibit antagonism.

A

True

129
Q

What substances are used for potentiation of sedation?

A

Ethanol and CNS depressants

130
Q

T/F: An antihistamine can enhance the hypotensive effect of an anti-hypertensive.

A

True

131
Q

In indirect pharmacodynamic interactions, it is the (1) that interacts with the main drug.

A

Side effect

132
Q

Enumerate drugs that cause potassium depletion

A

Diuretics
Amphotericin
Ampicillin
Carbenicillin

133
Q

T/F: Furosemide can produce hypokalemia.

A

True

134
Q

Give an example of an indirect pharmacodynamic interaction

A

Cardiac glycosides and potassium-depleting drugs

135
Q

Define: Pharmacokinetic Drug Interaction

A

ADME is altered by the interactant drug

136
Q

Antimuscarinic drugs (1) gastrointestinal motility.

A

(1) decrease

137
Q

T/F: Food + isoniazid/penicillin/rifampicin would lead to increased absorption of the drugs.

A

False

Decreased!

138
Q

What are the three factors affecting distribution?

A

Concentration in drug plasma
Relative binding affinity of the drug
Volume of distribution

139
Q

T/F: Most drug interactions involving inhibition of metabolism occur in liver and are due to competitive inhibition.

A

True

140
Q

List potent inducers of the microsomal enzyme system

A 
Barbiturates
Imipramine
Phenytoin
Haloperidol
Carbamazpine
Rifampicin
141
Q

List potent inhibitors of the microsomal enzyme system

A 
Cimetidine
Isoniazid
Phenothiazines
Chloramphenicol
Metronidazole
TCADs
142
Q

What are the factors involved in excretion drug interactions?

A

Competition for tubular secretion

Change in urine pH

143
Q

Define: Object Drugs

A

Narrow margin of safety

144
Q

Define: Precipitant Drugs

A

Highly protein bound and affects metabolism of other drugs

145
Q

What is the major limitation in interventions?

A

Cost

[Ther 201] 2nd Exam Transes (5 decks)

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