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Neurology - Sem 3 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q
  1. What are analgesics?
  2. What is used in step 1 of the WHO pain ladder?
  3. What is used in step 2 of the WHO pain ladder?
  4. What is used in step 3 of the WHO pain ladder?
A
  1. Drugs which provide relief from pain
  2. Non-opioid medication
  3. Weak opioid & Non-opioid
  4. Strong opioid & Non-opioid
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2
Q
  1. What are NSAID’s?
  2. What is their effect?
A
  1. Non-steroidal anti-inflammatory drugs
  2. Analgesic, antipyretic, anti-inflammatory
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3
Q
  1. What do NSAID’s block?
  2. Is it competitive or non-competitive? and is it reversible?
  3. What is the function of COX?
  4. What are examples of NSAID’s?
  5. What are the common side effects?
A
  1. Inhibitors of COX 1 and COX 2 (Cyclogenoxygenase)
  2. Competitive reversible
  3. Catalyse formation of prostaglandins, and thromoxane from Arachidonic acid
  4. Aspirin, Ibuprofen, Naproxen
  5. GI irritation, GI bleding, renal toxicity
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4
Q
  1. What do COX2 ihibitors do?
  2. What are some examples of these?
  3. Why are they better than NSAID’s?
  4. What is their major side effect?
A
  1. Inhibit COX 2 enzyme
  2. Rofecoxib, Etoricoxib etc.
  3. Less chance of GI bleeding
  4. Increase risk of CV events
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5
Q
  1. What is paracetamol used for?
  2. What is its mechanism of action?
  3. How do they specifically deal with pain?
  4. Why are they dangerous?
A
  1. Analgesic, fever
  2. Inhibits COX enzyme stops production of Prostaglandin H2
  3. Acts on TRPA1 receptor to supress signal transduction to dorsal horn, and inhibits Na+ channels
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6
Q
  1. What are opioids, what is their function?
  2. What is their mechanism of action?
  3. What do they do postynaptically
  4. What are examples of exogenous opioids?
  5. Examples of endogenous opioids?
A
  1. Drugs that act on opioid receptors, analgesic
  2. Reduce intracellular [cAMP] so decrease Ca+ influx inhibiting excitatory NT’s
  3. Cause hyperpolarisation of neuronal membrane - decrease AP probability
  4. Morphine, Codeine
  5. Endorphins, Dynorphins, etc.
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7
Q
  1. What is Co-codamol?
  2. What receptor does codeine bind to?
  3. What is the mechanism of action of Codeine?
A
  1. Codeine & Paracetamol
  2. Mu opiate receptor
  3. Decreases intracellular cAMP so inhibits release of nociceptive NT’s
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8
Q
  1. What are Tryclyclic Antidepressants? What are they used for?
  2. What are some examples?
  3. What is their mechanism of action?
  4. What are their side effects?
A
  1. Used to treat depression and neuropathic pain
  2. Imipramine, Amitryptyline, Nortripyline
  3. Block reuptake of monoamines by neurons, competitive inhbition of binding site. Inhibit NA and 5-HT reuptake
  4. Sedation, confusion due to effect on muscarinic and histamine receptors etc.
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9
Q
  1. What is Gabapentin?
  2. What is its mechanism of action?
  3. What are the side effects?
A
  1. Anticonvulsant drug to treat neuropathic pain
  2. Increases GABA synthesis, so inhibition of signals. And decreases Ca+ currents at voltage gated Ca+ channels
  3. GI disturbances, drowsiness
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10
Q
  1. What is Methylprednisolone?
  2. What is the mechanism of action?
  3. Where does it act?
A
  1. Corticosteroid
  2. Modifys transcription and protein synthesis, interfere with leukocyte infiltration & Inflammatory mediators
  3. Cytoplasmic receptors (In the cytoplasm)
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11
Q
  1. What is the action of interferons?
  2. What is Natalizumab?
  3. What is the risk with this drug?
A
  1. Interfere with T cell migration across the BBB
  2. Prevents lymphocyte migration across the BBB
  3. PML (Progressive multifocal leukocenphalopathy)
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12
Q
  1. What is Alemtuzamab?
  2. Are infusion reactions common?
  3. What is the side effect?
A
  1. Monoclonal antibody, targets B and T cells leading to cell lysis
  2. Yes
  3. Secondary autoimmune disease e.g. thyroid disease, immune thrombocytopenia
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13
Q
  1. What is Reserpine?
A
  1. Vascular monoamine transporter (VMAT) blocker - caused depression as it depleted Monoamines in the brain
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14
Q
  1. What drugs are given to patients with MDD? (4)
A
  1. SSRI’s
  2. Tricyclic antidepressants
  3. SNRI
  4. Noradrenaline reuptake inhibitors
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15
Q
  1. What are SSRI’s?
  2. What are examples of them?
  3. What are side effects?
A
  1. Selective inhibitors of 5-HT reuptake
  2. Sertraline, Fluocetine, Paroxetine
  3. Nausea, Insomnia, Diarrhoea
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16
Q
  1. What are SNRI’s?
  2. What are examples?
  3. What can overdose lead to?
A
  1. Non selective, Mixed 5-HT & Noradrenaline reuptake inhibitors
  2. Venlafaxine
  3. CNS depression, Serotonin toxicity etc.
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17
Q
  1. What are monoamine receptor antagonists?
A
  1. Non-selective and inhibit amine receptors such as A2 adrenoreceptors & 5HT2 receptors
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18
Q
  1. What is Mirtazapine?
  2. What is its mechanism of action?
  3. What is the net effect?
A
  1. a2 adrenergic receptor antagonist
  2. blocks negative feedback by which NA uses to switch itself off via a2 autoreceptors
  3. Increased NA release, and 5-HT release
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19
Q
  1. What are Monoamine oxidase inhibitors?
  2. What are examples of irreversible inhibitors?
  3. What are examples of selective MAO-A inhibitors?
  4. What is a major side effect of these drugs?
A
  1. Inhibit MAO-A and MAO-B enzymes which break down monoamines
  2. Phenelzine, Tranylcypromine
  3. Moclobromide
  4. Cheese reaction which can lead to hypertension and stroke due to inability to metabolise tyramine
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20
Q
  1. What are 3 other treatments for MDD?
A
  1. Electroconvulsive therapy
  2. Deep brain stimulation
  3. Vagus stimulation
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21
Q
  1. What does MAO-A break down?
  2. What does MAO-B break down?
A
  1. 5-HT
  2. Phenylthylamine & DA
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22
Q
  1. What is Diazepam?
  2. What is its mechanism?
  3. What are its side effects?
  4. How long is it prescribed for?
A
  1. Drug with anxiolytic, sedative, and relaxing effects
  2. Facilitates action of GABA, enhancing its effect - leading to hyperpolarisation of neurons
  3. Sedation, respiratory depression, dependence
  4. 4 weeks to prevent dependence
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23
Q
  1. What are beta blockers?
  2. What does this treat?
A
  1. B adrenoreceptor receptor antagonists which relax smooth muscle and tissues
  2. Used to treat physical symptoms of anxiety (SNS arousal)
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24
Q
  1. How many GABA molecules are required to bind to the GABA receptor?
  2. What is the GABA A receptor?
  3. What is the GABA B receptor?
A
  1. 2 GABA molecules
  2. Chloride ion channel - leads to hyperpolarisation of the neuron
  3. Coupled to K+ channel, which lets K+ out. inhibits cAMP production
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25
Q
  1. What are the 3 things that bind to GABA receptors?
  2. Which sub-units does GABA bind to?
  3. Which sub-units does Benzodiazepines bind to?
  4. Which sub-units does Barbituates bind to?
A
  1. GABA, Barbituates, and Benzodiazepines
  2. alpha sub-unit and beta 2 sub-unit
  3. alpha & gamma sub-units
  4. beta and gamma sub-units
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26
Q
  1. What is the effect if all 3 drugs bind to the GABA receptor?
  2. What is the function of BDZ when bound?
A
  1. Additive effect, which can be deadly
  2. Potentiates GABA and increases Cl- influx
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27
Q
  1. What is Tissue plasminogen factor (tPA)?
  2. When must it be used?
  3. Can it be given to patients with haemorrhagic stroke?
A
  1. Clot busting drug which lyses and reperfuses the brain after stroke
  2. In the first 3 hours of a stroke
  3. No, can cause further haemorrhage
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28
Q
  1. What is Aspirin?
  2. How is this helpful?
  3. What is its effect on platelets?
A
  1. Inhibition of COX1 enzyme so stops formation of thromboxane A2 & Prostaglandins
  2. It is an antithrombotic, so stops thombosis (Clotting)
  3. Lasts the lifetime of platelets as they cant regenerate the proteins
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29
Q
  1. What drug is used for thrombolysis?
  2. What is the side effect?
A
  1. Atelplase via IV
  2. Can lead to haemorrhage
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30
Q
  1. What are statins?
  2. What does this do?
  3. What is the knock on effect?
A
  1. Competitive inhibitors of HMG CoA- reductase
  2. Prevents synthesis of cholesterol in the liver
  3. Cells synthesise more LDL receptors on the cell surface so more uptake of cholesterol from serum
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31
Q
  1. What do thiazide diuretics do?
  2. What do they also do?
A
  1. Inhibit reabsorption of Na+ and Cl- in distal tubules
  2. Increase K+ and Bicarbonate excretion
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32
Q
  1. What are loop diuretics?
A
  1. Act on the loop of Henle, inhibit reabsorption of Na+ and Cl-
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33
Q
  1. What are K+ sparing diuretics?
A
  1. Interfere with Na+ reabsorption at distal tubules, but decrease K+ secretion
  2. Weak diuretic effect
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34
Q
  1. What do ACE inhibitors do?
  2. What is the result of blocking the conversion?
A
  1. Suppression of the Renin-Angiotensin-Alosterone system, preventing conversion of AT 1 to AT2
  2. Blocks bradykinin degradation by inhibiting ACE
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35
Q
  1. What do Angiotensin receptor blockers do?
  2. Why are they used?
A
  1. Competively block binding of AT1 to receptors so reduce effect of AT2 vasoconstriction, Na+ retention and Alodsterone release
  2. For people who cant tolerate ACE inhibitors
36
Q
  1. What drug is used for the following:
  • IV anaesthetic for rapid induction?
  • Inhalation anaesthetic to maintain anesthesia
A
  • Propofol
  • Isoflourane
37
Q
  1. What drug is used for the following:
  • Opioid analgesic
  • Neuromuscular blocking agent - for muscle relaxation
A
  • Fentanyl
  • Atracurium or Suxamethonium
38
Q
  1. What drug is used for the following:
  • Muscarinic antagonist to prevent bronchial and salivary secretions, or treat bradycardia
  • Anticholinesterase agent - reverse neuromuscular blockage
A
  • Atropine & Glycopyrrolate
  • Neostigmine
39
Q
  1. What effect do GABA A receptors have?
  2. What do anaesthetics do?
A
  1. Inhibitory (Cl- ion channels)
  2. Potentiate the action of GABA at the GABA A receptor
40
Q
  1. What do inhalation agents work on?
  2. What effect do they have on these receptors?
A
  1. Two pore domain K+ Channels
  2. Activate the channels causing hyperpolarisation, by reducing K+ concentration in the cell (Decrease membrane excitability)
41
Q
  1. Inhibition of which regions leads to unconsciousness and analgesia? (3)
  2. At high doses what can general anaesthesia do? (2)
A
  1. Midbrain, thalamus, parts of the cortex
  2. Loss of cardiovascular reflexes and respiratory paralysis
42
Q
  1. What are the 2 factors that determine the speed of induction & recovery?
  2. What are the 2 physiological factors?
A
  1. Blood:Gas parition coefficient (Solubility in blood) & Oil:Gas partition coefficient (Solubility in fat)
  2. Alveolar ventilation rate, cardiac output
43
Q
  1. What determines the speed of induction/recovery?
  2. What determines the potency of general anaesthesia?
A
  1. Blood:Gas partition coefficient (Solubility in blood)
  2. Oil:Gas partition coeficient (Solubility in fat)
44
Q
  1. What is the MAC (Minimal alveolar concentration)?
A
  1. Anaesthetic potency
45
Q
  1. What is propofol? What is it used for?
  2. What is the recovery time?
A
  1. IV anaesthetic agent, Induction of GA
  2. rapid induction & rapid recovery
46
Q
  1. What is the mechanism of action of propfol?
  2. What are the major side effects? (3)
A
  1. Potentiation of the GABA A receptor - inhibition all round
  2. Hypotension, respiratory depression, and nausea & vomiting
47
Q
  1. Can propofol be used to maintain anaesthesia?
48
Q
  1. What is Isoflourane? What is it used for?
  2. What is it administered with? (2)
A
  1. Volatile anaesthesia, Inhalation inducing agent
  2. O2 & Nitric oxide
49
Q
  1. What is the mechanism of action of Isoflourane?
  2. What are the side effects? (3)
A
  1. Binds to GABA, Glutamate NMDA and Glycine receptors
  2. Hypotension, Vasodilation, Respiratory suppression
50
Q
  1. What is Fentanyl? What is its function?
  2. What is its mechanism of action?
  3. What enzyme does it inhibit?
A
  1. Opioid analgesic, Pain suppression/Relief
  2. Strong agonist of Mu opioid receptor
  3. Adenylyl cyclase
51
Q
  1. What are the 2 ways that neuromuscular blocking drugs work?
A
  1. Blocking ACh receptors, or Activating ACh receptors and causes persistent depolarisation (Sensitisation)
52
Q
  1. What is the mechanism of action of non-depolarising neuromuscular blocking drugs?
  2. What other receptors do they block?
A
  1. Competitive antagonists at ACh receptors of motor end plate
  2. Facilitatory presynaptic autoreceptors, and inhibit release of ACh during repetitive stimulation of motor nerve
53
Q
  1. What are the side effects of non-depolarising neuromuscular blocking agents? (3)
A
  1. Hypotension, Bronchospasm, and Ganglion block
54
Q
  1. What is Atacurium?
  2. What conditions slow down the elimination of the drug?
A
  1. Non-depolarising neuromuscular blocking agent
  2. Low pH (Acidosis) and high temperature
55
Q
  1. What is the mechanism of action of Depolarising neuromuscular blocking agents?
  2. What is it hydrolysed by?
A
  1. Mimick the effect of ACh but not hydrolysed by AChE, leading to constant depolarisation so cell cannot repolarise
  2. Plasma cholinesterase (BuChE)
56
Q
  1. What is Suxamethonium?
  2. What are its main side effects? (3)
A
  1. Depolarising neuromuscular blocking agent
  2. Bradycardia, Hyperkalemia, increased intraoccular pressure
57
Q
  1. What is Neostigmine?
  2. What are its side effects?
  3. What is neostigmine used for?
A
  1. Cholinesterase inhibiting drug, so stops breakdown of cholinesterase and activates ACh receptors increasing muscle contraction (Can move)
  2. Bradycardia, hypotension, muscle fasciculation
  3. Reverse effects of muscle relaxants
58
Q
  1. What are Atropine & Glycopyrolate?
  2. What is the difference between the 2 drugs?
A
  1. Antagonist to muscarinic receptors to inhibit cholinergic transmission
  2. Atropine can cross BBB
59
Q
  1. Why are Atropine & Glycopyrolate used?
A
  1. To limit the PNS effects of neostigmine e.g. Bradycardia
60
Q
  1. What is an osmotic diuretic?
  2. What is the overall effect of this?
A
  1. Used to reduce intracranial pressure, by increasing solute content of fluid in proximal and collecting tubule so draws fluid from the body into the proximal tubule
  2. Less water is reabsorbed and there is a decrease in the ECF volume
61
Q
  1. What is Mannitol?
  2. What is it used for?
A
  1. Osmotic diuretic, increases flow of water from tissues into interstitial fluid and plasma
  2. To decrease intracranial pressure
62
Q
  1. What is pregabalin?
  2. What is its mechanism of action?
A
  1. Anxiolytic used when BDZ’s and SSRI’s not effective
  2. Binds to voltage sensitive Na+ channel in CNS and decreases stimulatory NT’s such as glutamate and NA
63
Q

What are Valproate & Lithium used for?

A

Treatment of bipolar disorder (Mania) — Mood stabiliser

64
Q

Taking which drug leads to the production of NAPQI?

What does this cause?

A

Paracetamol

Overdose symptoms

65
Q

What class of drugs are these?

Paracetamol

Morphine

Pregabalin

Gabapentin

Ibuprofen

Co-Codamol

A

Analgesics

66
Q

What class of drugs do these also act as?

Ibuprofen

Paracetamol

Aspirin

A

Antipyretics & Anti-inflammatory

67
Q

What drugs are these?

Phenelzine

Trancyclpromine

SSRI

SNRI’s

MAOI

TCA’s

A

Anti-depressants

68
Q

What drugs are these?

Phenelzine

Trancyclpromine

Moclobromide

A

Monoamine Oxidase Inhibitors - Increase MA

69
Q

What type of drug is this?

Venlefaxine

70
Q

What are these drugs used to treat?

Benzodiazepines (BDZ)

Barbituates

Beta blockers

Busiprone

Mirtazipine

71
Q

What is this drug used to treat?

Atelplase IV

A

Used for thrombolysis - during ischaemic stroke

72
Q

What are the following drugs?

Cortisone

Methyprednisolone

A

Corticosteroids

73
Q

What are these used for?

Oral Charcoal

N-Acetylcysteine

A

Paracetamol overdose

74
Q

What condition are these used to treat?

Natalizumab

Aletuzamab

Interferons

A

Multiple Sclerosis

75
Q

What are these drugs used to treat?

Selegeline

Rasagiline

Co-beneldopa

Pramipexole

Ropinrole

Amaltidine

A

Parkinson’s disease

76
Q

What are these drugs used to treat?

Busiprone

Sarizotan

A

Levadopa induced dyskinesia

77
Q

What are these drugs used to treat?

Risperidone

Olanzipine

Clozapine

Quetipine

A

Schizophrenia - Antipsychotics

78
Q

What are these drugs used for?

Propofol

Ketamine

Sodium thiopental

Etiomidate

A

Induction phase of anaesthesia

79
Q

What are these drugs used for?

Isoflourane

Seroflourane

Propofol

A

Maintenance phase of anaesthesia (Inhalation agents)

80
Q

What are these drugs used for?

Fentanyl

Morphine

A

Analgesics during anaesthesia

81
Q

What are these drugs?

Atacurium

Pancuronium

A

Neuromuscular blocking agents - non depolarising

82
Q

What is this drug used for?

Suxamethonium

A

Depolarising neuromuscular blocking agent

83
Q

What are these drugs used for?

BuChE

Neostigmine

Glycopyrollate

Atropine

A

Cholinesterase inhibiting drugs - to reverse muscle blocks

84
Q

What are these drugs?

Mannitol

A

Osmotic diuretic

85
Q

What are these drugs?

Sertraline

Fluocetine

Panxetine

A

SSRI’s - Antidepressants

86
Q

What are these drugs?

Imipramine

Amytrptaline

Nortryptaline

A

Trycylic antidepressants

87
Q

What are these drugs?

Phenelzine

Tranylcypromine

Moclobromide

A

Monoamine Oxidase inhibitors

Neurology - Sem 3 (15 decks)

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