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Phys pharm > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What was the first experiment that Langley designed?

A
  • Application of pilocarpine and atropine on an isolated frog heart
  • Application of pilocarpine and atropine on cat salivary glands
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2
Q

What is the active ingredient of Jaborandi?

A

Pilocarpine

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3
Q

What were the effects of pilocarpine in Langley’s experiment? (2)

A
  • Slows heart rate

- Increases saliva secretion

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4
Q

What were the effects of atropine in Langley’s experiment?

A

Blocks both actions of pilocarpine

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5
Q

What did Langley conclude from his first experiment?

A
  • There is some substance in the nerve endings or gland cells with which atropine and pilocarpine are capable of forming compounds
  • Dependant on concentration and affinity
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6
Q

What is affinity?

A

Tendency of a chemical/molecule to bind to a receptor

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7
Q

What was the second experiment that Langley designed?

A
  • Denervated skeletal muscle from chickens

- Applied nicotine and curare to observe whether they act on the nerve fibres or on the muscle itself

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8
Q

What was the effect of nicotine in Langley’s experiment?

A

Causes muscle contraction (mimics the effect of stimulating the nerve)

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9
Q

What was the effect of curare in Langley’s experiment? (2)

A
  • Blocks the effect of electrical stimulation of the nerve (no contraction)
  • Blocks the effect of nicotine (no contraction)
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10
Q

What was the effect of nicotine in denervated muscle?

A

Caused muscle contraction

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11
Q

What was the effect of applying curare with nicotine in denervated muscle?

A

No contraction (blocked the effect of nicotine)

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12
Q

What did Langley conclude from his second experiment?

A
  • The receptive substance for nicotine and curare is on the muscle itself
  • The nerve must release a nicotine-like substance when stimulated
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13
Q

What experiment did Ehrlich do?

A
  • Staining white blood cells
  • Different cell types were specific to different dyes
  • Must have different receptors
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14
Q

What are receptors? (2 definitions)

A
  • Macromolecular proteins which serve as recognition sites for chemicals used in cell-cell communication e.g. neurotransmitters, hormones etc.
  • Any protein of a cell that can bind a molecule/drug which then modulates some activity of the cell
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15
Q

What is signal transduction?

A

Conversion of an extracellular signal to an intracellular signal

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16
Q

What is a chemical mediator?

A

Extracellular signal molecules

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17
Q

What is cell signalling?

A

Detection of an extracellular signal by a receptor which generates intracellular signals that alter cell behaviour

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18
Q

What is endocrine signalling?

A

Chemical mediator is secreted into the bloodstream and distributed throughout the body so can act on various target cells

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19
Q

What is paracrine signalling?

A

Chemical mediator acts locally so acts on neighbouring cells (doesn’t enter the bloodstream)

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20
Q

What is autocrine signalling?

A

When paracrine signalling occurs between cells of the same type

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21
Q

What is neuronal signalling?

A
  • Faster and more specific than endocrine signalling

- Involves neurons and synapses

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22
Q

What is contact-dependent signalling?

A
  • The chemical mediator is not released into the extracellular space, anchored to the signalling cell
  • Direct interaction is required for the target cell to recognise the membrane-bound chemical mediator
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23
Q

Where is adrenaline secreted from?

A

Adrenal glands

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24
Q

Where are the adrenal glands located?

A

On top of both kidneys

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25
Q

What are the receptors for adrenaline?

A

Adrenergic receptors

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26
Q

What kind of signalling does adrenaline do?

A

Endocrine

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27
Q

What happens during an extreme allergic reaction to a wasp sting?

A
  • Mast cells in the skin release histamine

- Histamine causes dramatic drop in blood pressure and closing of airways

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28
Q

What is epinephrine?

A

Adrenaline

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29
Q

What chemical is in epi pens?

A

Epinephrine (adrenaline)

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30
Q

What are the effects of adrenaline/epinephrine?

A
  • Increases blood pressure
  • Increases heart rate
  • Increases metabolism
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31
Q

What kind of signalling does insulin do?

A

Endocrine

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32
Q

What kind of signalling does histamine do?

A

Paracrine

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33
Q

What kind of signalling does nitric oxide (NO) do?

A

Paracrine

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34
Q

How do over the counter allergy medicines work?

A
  • Block histamine receptors

- Anti-histamine (antagonist for histamine)

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35
Q

What is the effect of nitric oxide?

A
  • Generated by endothelial cells

- Causes smooth muscle relaxation and vasodilation

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36
Q

What is the function of Viagra?

A
  • Prevents breakdown of nitric oxide

- Prolongs the vasodilation of NO

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37
Q

What is the other name for eicosanoids?

A

Prostaglandins

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38
Q

What are eicosanoids?

A

Lipid mediators used in the immune system

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39
Q

What are endocannabinoids?

A

Lipid mediators synthesised in neurons

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40
Q

Which drugs interfere with eicosanoid signalling?

A

Over the counter pain medications e.g. paracetamol, aspirin

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41
Q

How do pain medications interfere with eicosanoid signalling?

A

Prevent their synthesis

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42
Q

How does cannabis work?

A

Mimics the effects of endocannabinoids

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43
Q

How might drugs acting on neurotransmission act?

A
  • Interfere with neurotransmitter synthesis, storage or release
  • Interfere with neurotransmitter receptors
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44
Q

Which drugs act on neurotransmitter receptors? (4)

A
  • Nicotine
  • Curare
  • Pilocarpine
  • Atropine
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45
Q

How does BoTox work?

A

Prevents vesicle fusion in neurotransmission

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46
Q

How do amphetamines work?

A

Interfere with the storage of neurotransmitter

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47
Q

What is an example of contact-dependent signalling?

A
  • Delta-Notch signalling in development

- T cell activation from an antigen-presenting cell

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48
Q

What are the 4 categories of cell-cell communication?

A
  • Endocrine
  • Paracrine
  • Neuronal
  • Contact-dependent
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49
Q

What is the effect of stimulating the vagus nerve on the heart?

A

Heart rate slows

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50
Q

What experiment did Loewi do?

A
  • Stimulated vagus nerve, collect media surrounding heart
  • Transfer media to a recipient heart
  • Heart rate slows
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51
Q

What did Loewi call the first neurotransmitter?

A

Vagusstoff

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52
Q

What is Vagusstoff?

A

Acetylcholine

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53
Q

What does the vagus nerve release?

A

Acetylcholine

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54
Q

What experiment did Dale do?

A
  • Proved that acetylcholine causes muscle contraction in the neuromuscular junction of leeches
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55
Q

Which receptors can acetylcholine act on? (2)

A
  • Nicotinic

- Muscarinic

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56
Q

How are nitric oxide and prostaglandins released from neurones? (lipid mediators)

A
  • Synthesised on demand and leave via constitutive secretion

- Rise in intracellular calcium activates the enzymes which produce them rather than cause their release

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57
Q

Which enzyme is involved in nitric oxide synthesis?

A

Nitric oxide synthase

58
Q

Which enzyme is involved in prostaglandin synthesis?

A

Phospholipase A2 (PLA2)

59
Q

What is synaptotagmin?

A

Calcium sensor protein on synaptic vesicles

60
Q

Which neurotransmitter is released by cholinergic neurones?

A

Acetylcholine

61
Q

Where is acetylcholinesterase found?

A

Anchored to the membrane of target cells

62
Q

What does acetylcholinesterase do?

A

Breaks down acetylcholine into choline (pre-cursor) which is taken up again by the presynaptic neuron to be recylced

63
Q

What are the 2 pathways of exocytosis?

A
  • Constitutive

- Regulated

64
Q

What is the constitutive pathway of exocytosis?

A

Diffusion of molecules across the membrane

65
Q

What is the regulated pathway of exocytosis?

A

Involves the storage of molecules in vesicles which fuse with the membrane in response to a signal

66
Q

What is Fluoxetine used to treat?

A
  • Depression

- AKA Prozac

67
Q

How does Fluoxetine work?

A

Inhibits the transporter responsible for reuptake of serotonin into presynaptic neurones

68
Q

How does amphetamine work?

A
  • Enters neurones via the noradrenaline transporter and enters synaptic vesicles instead of noradrenaline which causes NA to build up in the cytosol
  • Causes increased NA secretion via the NA transporter to act on postsynaptic receptors
  • NA reuptake is suppressed
69
Q

Which neurotransmitter do amphetamines affect?

A

Noradrenaline

70
Q

What side effects do opiates cause? (2)

A
  • Constipation

- Respiratory depression

71
Q

What are opioids used for?

A

Pain relief

72
Q

Which 4 classes of proteins are commonly targeted by drugs?

A
  • Enzymes
  • Transporters
  • Ion channels
  • Receptors
73
Q

What are the 4 classes of receptors?

A
  • Ligand-gated ion channels
  • G-protein coupled receptors
  • Kinase-linked receptors
  • Nuclear receptors
74
Q

What are ionotropic receptors?

A

Alternative name for ligand-gated ion channels

75
Q

What are metabotropic receptors?

A

Alternative name for G-protein coupled receptors

76
Q

What are the conserved features of ligand-gated ion channels? (3)

A
  • Extracellular binding site
  • Transmembrane domains
  • Forms an aqueous pore selective for ions
77
Q

What are the conserved features of G-protein coupled receptors? (3)

A
  • 7 transmembrane domains
  • Binding domain
  • Intracellular G-protein binding domain
78
Q

What are the conserved features of kinase-linked receptors? (3)

A
  • Single transmembrane domain
  • Extracellular binding site
  • Intracellular catalytic domain
79
Q

What are the conserved features of nuclear receptors?

A
  • No transmembrane domain
  • Found in the cytoplasm or nucleus
  • DNA binding motif for regulating gene transcription
  • Ligand must be able to cross plasma membrane
80
Q

What is an agonist?

A

Ligands which produce a response when they bind to a receptor

81
Q

What are examples of agonists? (4)

A
  • Pilocarpine
  • Nicotine
  • Acetylcholine
  • Morphine
82
Q

What is an antagonist?

A
  • Ligands which prevent/inhibit the action of an agonist

- May bind to the receptor but do not cause a response

83
Q

What are examples of antagonists? (2)

A
  • Atropine

- Curare

84
Q

What would injection of atropine cause in a whole body system?

A

Increase in heart rate

85
Q

How does atropine cause increase in heart rate?

A

Blocks the action of acetylcholine which slows the heart

86
Q

What is the effect of antagonists on isolated tissues?

A

Nothing

87
Q

Which receptor has the most rapid form of signal transduction?

A

Ligand-gated ion channels

88
Q

What class of receptor are nicotinic ACh receptors?

A

Ligand-gated ion channels (ionotropic)

89
Q

How long does signal transduction take with ligand-gated ion channels?

A

Milliseconds

90
Q

How long does signal transduction take with G-protein coupled receptors?

A

Seconds

91
Q

What class of receptor are muscarinic ACh receptors?

A

G-protein coupled receptors

92
Q

How long does signal transduction take with kinase-linked receptors?

A

Hours (usually involves activation of transcription/protein synthesis)

93
Q

What class of receptor are cytokine receptors?

A

Kinase-linked receptors

94
Q

How long does signal transduction take with nuclear receptors?

A

Hours (involves transcription/protein synthesis)

95
Q

What class of receptor are oestrogen receptors?

A

Nuclear receptors

96
Q

Which receptors are involved in synaptic transmission?

A

Ligand-gated ion channels (fastest)

97
Q

How many protein subunits do ligand-gated ion channels have?

A

3-5

98
Q

How many transmembrane domains do each subunit of ionotropic receptors have?

A

2-4

99
Q

What happens when an agonist binds to an ionotropic receptor?

A

Channel opens

100
Q

What does nAChR mean?

A

Nicotinic Acetylcholine Receptor

101
Q

What is curare an antagonist for?

A

Nicotinic ACh receptors (ionotropic)

102
Q

What is GABA an agonist for?

A

Ionotropic receptors on inhibitory neurones

103
Q

What is phenobarbitone?

A
  • Mimics action of GABA

- Used for euthanasia, inhibits CNS

104
Q

What is picrotoxin an antagonist for?

A

GABAa receptors

105
Q

What are GABAa receptors?

A

Ionotropic receptors for GABA

106
Q

How many subunits do nicotinic ACh receptors have?

A

5

107
Q

What disease results from malfunction of nicotinic receptors?

A

Myasthenia Gravis

108
Q

What causes Myasthenia Gravis

A

Autoimmune attack of nicotinic ACh receptors on skeletal muscle

109
Q

What are the symptoms of Myasthenia Gravis?

A

Muscle weakness

110
Q

Which drug blocks the action of acetylcholinesterase?

A

Neostigmine

111
Q

What does neostigmine do?

A

Blocks the action of acetylcholinesterase (therefore preventing breakdown of acetylcholine)

112
Q

How is Myasthenia Gravis treated? (2)

A
  • Anti-cholinesterase drugs

- Immunosuppressants

113
Q

How many subunits do G-proteins have?

A

3

114
Q

What proteins can be effectors in G-protein coupled receptors? (2)

A
  • Ion channels

- Enzymes

115
Q

How many types of G proteins exist?

A

Approx 20

116
Q

What are the 3 subunits of G proteins?

A
  • Alpha
  • Beta
  • Gamma
    (Referred to as beta-gamma subunit because they stay together)
117
Q

What is the structure of a G protein when it is inactive? (2)

A
  • Alpha subunit has GDP bound

- Alpha subunit has high affinity to beta-gamma subunit, forms complex

118
Q

What happens when an agonist binds to a G-protein coupled receptor? (6)

A
  • Causes a conformational change in the receptor which causes a conformational change in the G protein
  • Alpha subunit dissociates from GDP and replaces it with GTP (G protein now active)
  • G protein dissociates from the receptor
  • Alpha subunit separates from beta-gamma subunit
  • Separated subunits go on to regulate effectors
  • Receptor can continue to activate G proteins as long as the agonist remains bound
119
Q

How does a G protein become inactive?

A

Alpha subunit hydrolyses GTP to GDP and re-associates with the beta-gamma subunit

120
Q

What are the 3 types of G proteins?

A
  • Gs
  • Gi
  • Gq
121
Q

What does Gi/Gs/Gq refer to?

A

Which alpha subunit is in the G protein (alpha i/s/q)

122
Q

What does Gs do?

A
  • S=stimulatory
  • Stimulates adenylyl cyclase
  • Causes increased production of cAMP (second messenger)
123
Q

What does adenylyl cyclase do?

A

Converts ATP to cAMP

124
Q

What does Gi do?

A
  • I=inhibitory
  • Inhibits adenylyl cyclase
  • Causes decreased production of cAMP (second messenger)
125
Q

What does Gq do?

A
  • Activates Phospholipase C
  • Increased production of IP3 and DAG (second messengers)
  • IP3 causes increase of intracellular calcium
  • DAG causes activation of Protein Kinase C
126
Q

What is PLC?

A

Phospholipase C

127
Q

What is DAG?

A

Diacylglycerol

128
Q

What effectors do alpha subunits of G proteins regulate?

A

Enzymes

129
Q

What effectors do beta-gamma subunits of G proteins regulate?

A

Ion channels

130
Q

What are GIRKs?

A

Potassium channels

131
Q

How do beta-gamma subunits affect GIRKs?

A
  • Causes opening of GIRKs in neurones
  • Leads to hyperpolarisation
  • Prevents action potentials firing
132
Q

Which receptors does morphine bind to?

A

Opioid receptors

133
Q

Which G protein associates with opioid receptors?

A

Gi

134
Q

How does morphine reduce pain?

A
  • Binds to opioid receptor coupled to Gi protein

- Beta-gamma subunit opens GIRKs which reduces calcium influx, therefore reducing pain transmission in the CNS

135
Q

How do morphine/heroin cause addiction?

A
  • Binds to opioid receptor coupled to Gi protein
  • Alpha i subunit causes reduction of cAMP
  • Leads to changes in gene transcription associated with addiction
136
Q

Which enzyme breaks down cAMP?

A

cAMP phosphodiesterase

137
Q

What is cAMP broken down into?

A

5’-AMP (no signalling activity)

138
Q

What are 3 proteins which cAMP can regulate as a second messenger?

A
  • Protein Kinase A (PKA)
  • EPAC
  • CREB
139
Q

What is CREB?

A

Transcription factor

140
Q

How does cAMP regulate PKA?

A
  • Binds to regulatory subunits of PKA which causes them to dissociate
  • Frees catalytic subunits to phosphorylate targets
141
Q

How does IP3 cause increase of intracellular calcium?

A
  • Binds to IP3 receptors (ion channels) on the endoplasmic reticulum
  • Channels open and release calcium
142
Q

What causes smooth muscle contraction?

A
  • Agonists bind to receptors coupled to Gq proteins
  • Increased PLC activity leads to increased intracellular Ca2+
  • Ca2+ causes contraction

Phys pharm (11 decks)

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