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Clinical Life Sciences 2 > Pharmacodynamics > Flashcards

Pharmacodynamics Flashcards

1
Q

What are the four main locations that drugs act on?

A
  1. Receptors
  2. On DNA
  3. Enzymes
  4. Membranes
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2
Q

What drugs stimulate receptors?

A

Agonists

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3
Q

What drugs prevent receptor stimulation?

A

Antagonists

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4
Q

What do receptors do?

A

They initiate cellular responses

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5
Q

What are receptors?

A

Proteins in or on cells?

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6
Q

What are the four main types of proteins that receptors are linked to?

A
  1. G-protein coupled receptors
  2. Ion channels
  3. Gene transcription
  4. Enzymes
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7
Q

Name a Beta2 adrenoceptor agonist

A

Salbutamol

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8
Q

Name a Beta2 receptor antagonist

A

Propanol

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9
Q

Name a H1+2 receptor agonist

A

Histamine

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10
Q

Name an opiate Mu receptor agonist

A

Morphine

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11
Q

Name an opiate Mu receptor antagonist

A

Naloxone

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12
Q

Name a M2 muscarinic agonist

A

Acetylcholine

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13
Q

Name a M2 muscarinic antagonist

A

Atropine

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14
Q

How do G protein coupled receptors interact with ion channels?

A

They cause confirmation changes which allow ion exchange

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15
Q

How to G protein coupled receptors affect enzymes?

A

They activate or inhibit enzymes which will result in second messengers being produced or inhibited

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16
Q

What are the two types of opioid analgesics?

A

1 - Morphine based

2 - Synthetic

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17
Q

What are the three main opioid receptors?

A

Delta, Kappa and Mu

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18
Q

What type of receptors do opioids act on?

A

G-Protein Coupled Receptors

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19
Q

What occurs after receptor binding of opioids?

A
  1. Inhibition of adenylate cyclise -> decreased intracellular cAMP
  2. Couple to K:Ca ion channels -> inhibition of transmitter release and postsynapse excitability
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20
Q

75% of presynapse receptors for opioids are….?

A

Mu receptors

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21
Q

By what 3 means do opioid analgesics work?

A
  1. Inhibits pain transmission in dorsal horn
  2. Activates descending pathways in grey matter inhibiting pain transmission (reduced GABA)
  3. Inhibits nociceptive afferents in tissues
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22
Q

How is pain transmission inhibited at the dorsal horn?

A

By inhibiting presynaptic afferent impulses

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23
Q

How are the descending pathways activated?

A

By inhibiting GABA release in periaqueductual grey matter (PAG)

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24
Q

Why does activating the descending pathways inhibit pain?

A

It inhibits the discharge of the Dorsal Horn

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25
Q

What does the dorsal horn project into?

A

The Thalamus

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26
Q

What does the thalamus project in to?

A

The Cortex

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27
Q

Why does respiratory depression occur when morphine is administered?

A

The activation of Mu receptors reduce the respiratory centres sensitivity to CO2

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28
Q

Why can nausea and vomiting occur when morphines administered?

A

Activation of the chemoreceptors trigger zone

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29
Q

Why can pupillary constriction occur when morphine is administered?

A

Activation of the kappa receptors leads to the stimulation of the oculomotor nucleus (parasympathetic NS)

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30
Q

Why is it important to be cautious when administering morphine to someone with asthma?

A

It can cause histamine release leading to bronchospasm and hypotension

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31
Q

What does tissue damage lead to the production of? Causing activation of nociceptive fibres?

A

Bradykinins
ATP
H ions
Prostaglandins

32
Q

What non analgesic effects to kappa opiod receptors have on the body? (3)

A

Decreased RR
Pupil miosis
Sedation

33
Q

What non analgesic effects to mu opiod receptors have on the body? (2)

A 
Resp depression (resp centre - medulla oblongata)
Euphoria
34
Q

What is histamine?

A

An inflammatory mediator

35
Q

What does IgE production in an allergic reaction lead to?

A

Mast cell degranulation and histamine release

36
Q

What are the main effects of H1 receptors? (3)

A

Vasodilation
Increased cap permeability
Bronchospasm

37
Q

What are the main effects of H2 receptors? (4)

A

CNS effects
Gastric acid production
Smooth muscle relaxation
T cell and Cytokine proliferation

38
Q

What actions does chloraphenamine have? (4)

A

Anti-allergic
Sedative
Anti-muscarinic
Anti-emetic

39
Q

What is chloraphenamine?

A

A potent H1 antihistamine

40
Q

What are the main two things chloraphenamine reduces?

A

Urticaria and Bronchoconstriction

41
Q

What are receptors that regulate gene transcription called?

A

Nuclear receptors

42
Q

Where are nuclear receptors located?

A

The cytosol

43
Q

Name some glucocorticoids (4)

A

Oestrogen
Progesterone
Steroid hormones
Thyroid hormones

44
Q

How are inflammatory mediators produced by glucocorticoids

A

Glucocorticoid > nuclear receptor > conformation change > binds to DNA > gene expression (transcription, translation and mRNA synthesis > production and release of inflammatory mediators

45
Q

What are enzymes?

A

Proteins that catalyse chemical reactions in the body

46
Q

True or False enzymes have specific binding sites for substrates?

A

True

47
Q

What is aspirin?

A

An enzyme inhibitor

48
Q

How does aspirin work?

A

Irreversibly inactivates COX

49
Q

What does inactivation of COX by aspirin lead to?

A

Reduction in prostaglandin and thromboxane production

50
Q

Do most other NSAIDs and COXIBs bind irreversibly or reversibly?

A

Reversibly

51
Q

Low doses of aspirin irreversibly block TXA2 formation in platelets… what effect does this have?

A

It has an antithrombotic effect and helps reduce heart attack risk

52
Q

What drugs act on non mammalian cell targets? (4)

A

Anti-virals
Anti-biotics
Anti-parasitics
Anti-fungals

53
Q

What class of antibiotic is penicillin?

A

A beta-lactam antibiotic (bacteriocidal)

54
Q

What do bacteriocidal antibiotics do?

A

Lead to cell lysis and death

55
Q

What does penicillin bind to?

A

Penicillin binding protein (DD-transpeptidase)

56
Q

What does pencillin binding to a bacterium result in?

A

Inability to cross link peptidoglycan in cell wall which leads to cell wall degredation, cell lysis and death

57
Q

Why does penicillin usually have minimal side effects?

A

As it acts on bacterial proteins (little effect on host) - selective toxicity

58
Q

What does the ABCDE of adverse drug reactions (ADR) stand for?

A 
Augmented 
Bizzare 
Chronic 
Delayed 
End of Use
59
Q

Name an augmented ADR

A

Decreased RR with morphin (predictable, common, dose dependent)

60
Q

Name a bizzare ADR

A

Anaphylaxis (unpredictable, uncommon, cure=stop use)

61
Q

Name a chronic ADR

A

Growth retardation with corticosteroid therapy

62
Q

Name a delayed ADR

A

Teratogenic drugs (thalidomide)

63
Q

Name an end of use ADR

A

Withdrawal from benzodiazipines

64
Q

How does paracetamol act?

A

Selectively inhbits COX and weakly inhibits prostaglandins

65
Q

What are the parasympathetic spinal cord outputs?

A

Craniosacral

66
Q

What are the sympathetic spinal cord outputs?

A

Thoracolumbar

67
Q

What the two main alpha receptor agonists?

A

Adrenaline and Noradrenaline

68
Q

What 3 main effects does beta1 receptor stimulation have on the heart?

A

changes…
Rate
Force
Contractility

69
Q

What effect does beta2 receptor stimulation have on the lungs?

A

Smooth muscle dilation

70
Q

How does ipatropium bromide function?

A

It ‘deactivates’ parasympathetic influence stopping bronchial smooth muscle contraction

71
Q

What kind of antagonist is ipatropium bromide?

A

A cholinergic antagonist

72
Q

What do pumps and carriers on cell membranes allow?

A

A cell to regulate it’s internal environment

73
Q

List some drugs that act on pumps and carriers

A
  • Diuretics
  • Digoxin
  • Anaesthetics
74
Q

What are voltage-operated channels?

A

Channels in a cell membrane that are activated by electrical membrance changes

75
Q

How does tetracaine work?

A

It blocks sodium channels

76
Q

True or False sodium must ionise and enter the intracellular axon to function?

A

True

77
Q

What are chelating agents?

A

Chemical compounds that react with metal ions to form a stable water soluble complex

Clinical Life Sciences 2 (7 decks)

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