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PM2C Autumn Amy L > Drug Toxicology I > Flashcards

Drug Toxicology I Flashcards

1
Q

Define: Pharmacology

A

The study of the effect of drugs on the function of living systems

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2
Q

Define: Toxicology

A

The study of the effect of poisons on the function of living systems

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3
Q

Name 3 chemical agents that cause toxicity

A
  1. Drugs
  2. Insecticides/herbicides
  3. Plant toxins
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4
Q

Define: Adverse drug reaction

A

Noxious or unintended responses occurring at therapeutic doses

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5
Q

Explain Type A (augmented) ADRs

A
  • Related to known pharmacology but undesirable
  • Common, dose-related
  • Predictable
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6
Q

Give an example of a Type A (augmented) ADR

A

Haemorrhage with anticoagulants (e.g. warfarin)

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7
Q

Explain Type B (bizarre) ADRs

A
  • Unrelated to known pharmacology
  • Rare
  • Unpredictable
  • Often idiosyncratic (= peculiar, individual)
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8
Q

Give an example of a Type B (bizarre) ADR

A

Anaphylaxis with penicillin

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9
Q

Define: Toxicokinetics

A

The effects of the body on the poison

Relates to ADME

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10
Q

What information does toxicokinetics provide?

A

Makes it possible to predict concentration of toxin that has reached the site of injury and the resulting injury

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11
Q

Define: Detoxification

A

Compound rendered less toxic

Occurs during metabolism

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12
Q

Define: Toxification

A

Relatively inert compound converted into toxin

Occurs during metabolism

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13
Q

Name 2 ways that toxins are ‘absorbed’

A

Ingestion (salmonella) or inhalation (asbestos)

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14
Q

How many phases of metabolism of toxins are there?

A

2: Phase I and Phase II

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15
Q

What occurs during Phase I of metabolism of toxins?

A
  1. Oxidation
  2. Reduction
  3. Hydrolysis by cytochrome P450
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16
Q

What occurs during Phase II of metabolism of toxins?

A

Conjugation to allow excretion in urine and bile

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17
Q

Where may toxins be stored if they aren’t excreted?

A
  • Bone (e.g. lead)
  • Fat (e.g. DDE, a metabolite of the pesticide DDT)
  • The toxin may be slowly released into the body
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18
Q

Name a common form of ADR

A

Allergic reaction

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19
Q

How many clinical syndromes of allergic reaction are there?

A

4: Type I, II, III & IV

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20
Q

What is a Type I allergic reaction?

A
  • A hypersensitivity reaction
  • Mediated by IgE = an antibody
  • IgE causes degranulation of mast cells = release of histamine
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21
Q

What is a Type II allergic reaction

A
  • Antibody-mediated cytotoxic hypersensitivity
  • Involve haematological reactions = those pertaining to the blood cells and blood-forming organs
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22
Q

What is a Type III allergic reaction?

A

Immune complex-mediated hypersensitivity

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23
Q

What is a Type IV allergic reaction?

A

Delayed-type hypersensitivity

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24
Q

What can Type I hypersensitivity reactions trigger?

A

Anaphylaxis

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25
Q

What is a hapten?

A

A small molecule that binds to a bigger molecule which triggers an immune response

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26
Q

What is the molecular process of a Type I hypersensitivity reaction?

A
  1. Low MW allergen enters the body
  2. A hapten binds to the allergen to form an immunogenic conjugate
  3. IgE recognition of immunogenic complex causes degranulation of mast cells
  4. Massive histamine release
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27
Q

What does the release of histamine from the mast cells cause?

A
  • Bronchoconstriction
  • Vasodilation
  • Inflammation
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28
Q

What substance is used to treat allergic reactions?

A

Adrenaline (epipen)

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29
Q

What is the molecular process of a Type II hypersensitivity reaction? (Antibody-mediated cytotoxic hypersensitivity)

A
  • The toxin antigens bind to RBCs
  • Antibody IgE molecules trigger T cells
  • T cells begin lysis = cytotoxic T cell-mediated cell lysis
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30
Q

How can sulphonamides be toxic?

A

Can deplete red blood cells = haemolytic anaemia

Due to Type II hypersensitivity reaction

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31
Q

How can some NSAIDs be toxic?

A

They can deplete neutrophils = agranulocytosis

Due to Type II to hypersensitivity reaction

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32
Q

How can quinine an heparin be toxic?

A

They can deplete platelets = thrombocytopenia

Due to Type II hypersensitivity reaction

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33
Q

Define: Haemolytic anaemia

A

When the levels of RBCs are depleted (e.g. by sulphonamides)

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34
Q

Define: Agranulocytosis

A

When the levels of neutrophils are depleted (e.g. by some NSAIDs)

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35
Q

Define: Thrombocytopenia

A

When the levels of platelets are depleted (e.g. by quinine and heparin)

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36
Q

Name the 4 major superfamilies of receptor

A
  1. Ligand-gated ion channels (voltage-gated ion channels)
  2. GPCRs (metabotropic receptors)
  3. Enzyme-coupled receptors (tyrosine kinase activity)
  4. Nuclear receptors (regulate gene transcription)
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37
Q

Name 4 targets of toxins

A
  1. Receptors
  2. Enzymes (metabolic and catabolic pathways)
  3. Carriers (uptake/transport systems)
  4. Others e.g. proteins involved in vesicle release
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38
Q

What do animal toxins block?

A

Ion-conduction

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39
Q

What substance blocks voltage-gated K+ channels?

A

Dendrotoxins

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40
Q

What substance acts on Na+ channels?

A

Tetrodotoxin

41
Q

What effect does blocking the Na+ channels have?

A

Block action potentials

42
Q

What kind of toxin blocks ion conduction?

A

Animal toxins

43
Q

What do dendrotoxins block?

A

Voltage-gated K+ channels

44
Q

What does Tetrodotoxin act on?

A

Na+ channels

45
Q

List 4 symptoms of high quantities of acetylcholine

A
  1. Convulsions
  2. Bradycardia (= abnormally slow heart action)
  3. Bronchodilation
  4. Increased secretion (eyes watering, nose running)
46
Q

Name the enzyme that oximes reactivate

A

ACh-esterase

47
Q

Name the strong nucleophile that reactivates ACh-esterase

A

Oximes

48
Q

What does cyanide inhibit?

A

Cytochrome C oxidase

49
Q

What effect does inhibiting cytochrome C oxidase have?

A

Prevents cellular respiration

50
Q

Where is Cytochrome C oxidase found?

A

Mitochondria

51
Q

What effect does carbon monoxide have on haemoglobin and what does this cause?

A

It displaces the oxygen causing hypoxia = COHb

52
Q

Define: Hypoxia

A

Deficiency in the amount of oxygen reaching the tissues

53
Q

Name the 2 organs that are particularly susceptible to toxin damage

A

Liver and kidney

54
Q

Why are the liver and kidney more susceptible to toxin damage?

A

Their major role is excretion

55
Q

What is toxin damage of the liver called?

A

Hepatotoxicity

56
Q

What is hepatic necrosis caused by?

A

Paracetamol poisoning

57
Q

Define: hepatic necrosis

A

Death of liver tissue

58
Q

What is hepatitis?

A

Hepatic inflammation

59
Q

What can cause hepatitis?

A

Halothane (anaesthetic) can covalently bind to liver proteins to trigger an autoimmune response

60
Q

What is cirrhosis?

A

Chronic liver damage

61
Q

What can cause cirrhosis?

A

Long term alcohol (ethanol) abuse causes:

  • Toxicity
  • Inflammation
  • Malnutrition (ethanol becomes a food source)
62
Q

What effect can paracetamol poisoning have on the liver?

A

Hepatic necrosis = death of liver tissue

63
Q

What effect can halothane (anaesthetic) have on the liver?

A

Hepatitis

64
Q

What effect can long term alcohol abuse have on the liver?

A

Can cause cirrhosis = chronic liver damage

65
Q

What occurs in Phase II conjugation (metabolism) with regards to paracetamol?

A

90% of the paracetamol is safely conjugated with conjugating agents (e.g. sulphate)

66
Q

What occurs in Phase I metabolism of paracetamol?

A
  • 10% of the paracetamol undergoes Phase I reactions
  • This produces an intermediate species (NAPQI)
  • NAPQI = very toxic to the liver (binds to protein thiol groups)
  • = Hepatotoxicity
67
Q

Why is NAPQI very toxic to the liver?

A

It binds to the protein thiol groups = hepatotoxicity

68
Q

Name the process that NAPQI undergoes

A

Phase II conjugation with glutathione = makes NAPQI non-toxic and it is therefore safely excreted

69
Q

Why is it more difficult to get rid of NAPQI after a paracetamol overdose?

A
  1. Large quantities of NAPQI produced
  2. Enzymes are saturated
  3. Levels of glutathione are quickly depleted
70
Q

Name 2 treatments for paracetamol overdose

A

Acetylcysteine and Methionine

71
Q

Why are acetylcysteine and methionine used to treat paracetamol overdose?

A

Both are glutathione precursors = more glutathione and excess NAPQI is excreted

72
Q

Define: Nephrotoxicity

A

Poisonous effects of some substances on the kidney

73
Q

What effect does altering the blood flow have on the kidney?

A

Causes changes in glomerular filtration rate (GFR)

74
Q

Name 2 types of drug that can cause changes in the GFR due to altering blood flow

A
  • NSAIDs (e.g. aspirin) - reduce prostaglandins (prevent arachidonic acid binding to cyclooxygenases) which in turn reduces blood flow/GFR
  • ACE inhibitors (e.g. ramipril) - increase blood flow/GFR
75
Q

How do NSAIDs affect the GFR?

A

NSAIDs reduce the GFR as they lower the number of prostaglandins which reduces blood flow

76
Q

How do ACE inhibitors affect the GFR?

A

ACE inhibitors increase blood flow and so increase the GFR

77
Q

Why can lowering the GFR have dangerous consequences?

A

Makes it more difficult to excrete toxic compounds

78
Q

Define: Allergic nephritis

A

Inflammation of kidney due to allergic reaction

79
Q

Give 2 examples of substances that can cause allergic nephritis

A
  1. NSAIDs (fenoprofen)
  2. Antibiotics (e.g. metacillin)
80
Q

Name 2 drugs that can cause chronic nephritis

A

Long term NSAID and paracetamol use

81
Q

Define: Mutagen

A
  • A physical or chemical agent
  • That causes changes to the DNA
  • Increasing the frequency of mutation above the natural background level
  • The mutations are passed on when the cell divides
82
Q

Define: Carcinogen

A

A mutagen that capable of causing cancer

83
Q

Name the 2 major classes of gene that are involved in carcinogenesis

A
  1. Proto-oncogenes
  2. Tumour-suppressor genes
84
Q

What is the role of proto-oncogenes?

A

Promote cell progression

85
Q

Define: neoplasm/neoplastic cell

A
  • An abnormal mass of tissue
  • Results when cells divide more than they should or do not die when they should (due to a mutation)
  • May be benign or malignant (cancerous)
86
Q

What is the role of tumour-suppressor genes?

A

Inhibit cell cycle progression

87
Q

Define: Teratogenicity

A

The property or capability of producing congenital malformations

88
Q

Define: Teratogenesis

A

The creation of birth defects during foetal development

89
Q

Define: Teratogens

A

Substances that induce birth defects

90
Q

Name a teratogen

A

Thalidomide (S)

91
Q

How was thalidomide able to cause birth defects?

A

The (R)-enantiomer was a sedative but the (S)-enantiomer was a teratogen

92
Q

What was thalidomide marketed to treat?

A

Marketed as an anti-emetic to treat morning sickness in pregnant women

And as a sleeping pill (sedative)

93
Q

Name the cellular process that occurs during blastocyst formation

A

Cell division

94
Q

What substances affect blastocyst formation?

A
  1. Alcohol
  2. Cytotoxic drugs (toxic to cells)
95
Q

What are the 3 stages of foetal development?

A
  1. Blastocyst formation
  2. Organogenesis
  3. Maturation
96
Q

Name the cellular processes that occur during organogenesis

A
  1. Division
  2. Migration
  3. Differentiation
  4. Death
97
Q

What substances affect organogenesis?

A

Teratogens = thalidomide, retinoids, antiepileptics, warfarin

98
Q

Name the cellular processes that occur during maturation

A
  1. Division
  2. Migration
  3. Differentiation
  4. Death
99
Q

What substances affect maturation?

A
  1. Alcohol
  2. Nicotine
  3. ACE inhibitors (e.g. Ramipril)
  4. Steroids

PM2C Autumn Amy L (16 decks)

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