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(Physio) Health Sciences > Applied pharmacology > Flashcards

Applied pharmacology Flashcards

1
Q

What are the two classes of opioid receptors

A

µ / ð and k

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2
Q

Define opioids

A

‘A compound resembling opium in its physiological effects’

1 .Bind to specific opioid receptors

  1. ‘Mimic the action of endogenous peptide neurotransmitters

(for example, endorphins, enkephalins, and dynorphins)’

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3
Q

How do opioids work centrally?

A
  • Opiates reduced inhibition of the descending pain pathway by increasing its activity.
  • This increases the release of seretonin.
  • This increases release of endogenous opiates

•Nociceptin receptors – descending control

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4
Q

Describe the steps in the arachidonic acid cascade

A
  1. Phospholipase A2 produces Arachidonic acid (AA) from fatty acids
  2. COX enzymes convert AA into intermediates
  3. Other enzymes convert intermediates into prostanoids- prostaglandin or thromboxanes
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5
Q

State 3 side effects of strong opioids such as morphine

A
  • Constipation
  • Depression of cough reflex
  • Respiratory depression
  • Nausea & vomiting (central / enteric)
  • Tolerance effects (adaptation of 2nd messenger cascade)
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6
Q

Why is paracetamol a sort of NSAID

A

Non-opioid – not strictly an NSAID

Targets COX2 (maybe cox-3) in CNS

Poor peripheral COX1/2 inhibition

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7
Q

How do NSAIDs effects platlet aggregation

A

COX-1 inhibition reduces thromboxane A2 production, which prevents the haemolytic cascade

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8
Q

Describe effects of tramadol

A
  • Racemic mixture
  • Multiple therapeutic targets
  • Acts at µ opioid receptors
  • Serotonin / norepinephrine reuptake inhibitor

Less potential for-

respiratory depression

GI effects

(low dependency risk also)

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9
Q

How do gabapentin/pregablin (anticonvulsants) work for pain relief?

A

They antagonise thrombospondin

(secreted by astrocytes and agonist at VG ca2+ channels)

Thrombospondin promotes synaptogenesis- which can be linked to maintenance of central chronic pain

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10
Q

What are 2 effects of long term use of strong opioids

A
  • Possible immune suppression (downregulation of t-killer and macrophages)
  • Decreased sex hormone production
  • Opiate induced hyperalgesia - have effects on astrocytes/microglia to drive release pro-inflam cytokines which driver peripheral/central sensitisation
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11
Q

How do NSAIDs negatively impact the kidneys

A
  • prostaglandins cause vasodilation in the kidney
  • NSAIDs reduce renal filtration, and reduce sodium retention
  • Leads to physical damage to the nephron
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12
Q

How can antidepressants i.e. fluoxetine reduce pain?

A

•Selective serotonin reuptake inhibitors e.g. fluoxetine

  • Reduces reuptake of seretonin
  • greater activation of enkephalin containing interneurons in dorsal horn

Also involved in:

  • Sodium channel blockade i.e. neuronal excitability
  • NMDA receptor antagonism i.e. reduced central sensitisation
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13
Q

How do NSAIDs have antipyretic effects

A

NSAIDS reduce PGE2 production by binding to COX-2

Pyrogens – stimulate PGE2 in hypothalamus

PGE2 – inhibits temperature sensitive neurons making us think we’re cold = shiver = increased temperature

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14
Q

Finish this table:

Receptor: µ / ð

  • Analgesia
  • Respiratory depression
  • Pupils
  • GI motility
  • Smooth muscle spasm
  • Behaviour
  • Dependence
A
  • Analgesia- supraspinal / spinal / peripheral
  • Respiratory depression ++
  • Pupils- constriction
  • GI motility- reduced
  • Smooth muscle spasm- ++
  • Behaviour- euphoria ++ and sedation ++
  • Dependence- ++
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15
Q

How do opioid receptors cause a reduction in pain signals

A
  • opioid receptors are a type of g-protien coupled receptor
  • they are involved in the downregulation of cell excitability by blocking:
    • dorsal horn pre-synpase (reduced Ca2+)
    • dorsal horn post-synpase (K+ channel leak)
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16
Q

What is the site of action, and function of COX 2 enzymes?

A
  • Mast cells, fibroblasts, macrophages
  • Endothelial cells,
  • More in nuclear membrane
  • Inflammation
  • Pain
  • Fever
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17
Q

Describe what happens to codiene in the liver, and its side effects

A

codiene is converted to morphine by cytochrome p450

side effects include: respiratory depression and GI motility

18
Q

How does capsaicin work?

A
  • Massive activation of TRPV1 receptors (temp sensitive, nociceptor)
  • Release of Substance P
  • Leads to depletion of substance P
19
Q

Describe the pharmacokinetics of NSAIDs

A
  • Absorption from stomach & small intestine
  • Significant plasma binding (albumin)
  • Hepatic metabolism
  • Some NSAIDs enter enterohepatic circulation
20
Q

Different NSAIDs have different binding selectivities. What does this mean in relation to COX enzymes

A

Some NSAIDS will act more on COX 1 or 2- affect different tissues, having different therapeutic effects

21
Q

Benefits of COX-2 selective NSAIDS?

A
  • Fewer gastric complications
  • Reduced effect of platelet aggregation
22
Q

What is the site of action, and function of COX 1 Enzymes?

A
  • Most tissues / cells
  • Mainly endoplasmic reticulum
  • Gastric protection
  • Blood flow
  • Platelet aggregation
23
Q

What are the 4 main therapeutic effects of NSAIDs

A
  1. Anti-inflammatory
  2. Analgesic
  3. Antipyretic
  4. Platelet aggregation
24
Q

How do NSAIDs have analgesic effects

A
  • Inhibition of COX-2 derived prostaglandins
  • Reduced sensitisation of free nerve endings
25
Q

How do NSAIDs negatively affects the GI tract

A
  • prostaglandins promote bicarbonate containing muscus in the stomach (protective)
  • NSAIDs reduce prostaglandin production
  • over time could lead to stomach ulceration
26
Q

How do NSAIDs have antiinflammatory properties

A
  • Inhibition of COX-2 derived prostaglandins
  • Which are powerful vasodilators
  • Promote release of other vasodilators
  • e.g. substance P and histamine

=

  • Reduced oedema
  • Reduced swelling
  • Reduced redness
27
Q

What are the 3 main mechanisms of anticonvulsants as a painkiller

A
  • Enhancement of GABA action
  • Inhibition of voltage-dependent sodium channels
  • Inhibition of T-type calcium channels
28
Q

What are NSAIDS

A

non-steroidal anti-inflammatory drugs i.e. ibuprofen

29
Q

How can an overdose of paracetamol cause liver damage

A
  • drug detoxified by liver
  • processed by cytochrome p450
  • converted into NAPQI (v harmful to liver tissue)
  • NAPQI immediately conjugated with glutathione
  • but there is a limited supply of glutathione
  • So if NAPQI builds up, causing irreversible liver damage
30
Q

How do NSAIDs negatively impact the respiratory system

A
  • They can cause ‘aspirin induced asthma’
  • Where the blocking of COX enzymes mean more lipoxygenase production (from Arachinodonic acid)
  • Lipoxygenase increases production of leukotrienes (prominant bronchoconstrictors)
  • This can exacerbate asthma symptoms
31
Q

How do NSAIDS disrupt the arachidonic acid cascade?

A

NSAIDS block the action of the COX enzymes, thus reducing prostaglandin/thromboxane production

32
Q

What does activation of µ-opioid receptors do

A
  • located on free nerve endings
  • reduces 1st order nociceptor sensitivity
33
Q

Purpose of analgesics?

A

To control symptoms and improve QoL by reducing pain/perception of pain

34
Q

State 2 ways in which NSAIDs may cause liver damage

A
  1. Retention of bile (cholestasis)
  2. Mitochondrial damage
  3. Inhibition of prostaglandin E2 production
  4. Reactive metabolites
35
Q

What is the WHO ladder of opioids

A

3 steps meant to promote a better use of stronger analgesics

Step 1- non opioids i.e. paracetamol

Step 2- mild opioids i.e. codiene

Step 3- strong opioids i.e. morphine

36
Q

Finish this table:

Opioid receptor: K

  • Analgesia
  • Respiratory depression
  • Pupils
  • GI motility
  • Smooth muscle spasm
  • Behaviour
  • Dependence
A
  • Analgesia- spinal
  • Respiratory depression- +
  • Pupils- no effect
  • GI motility- no effect
  • Smooth muscle spasm- no effect
  • Behaviour- dysphoria + sedation +
  • Dependence +
37
Q

What systems have common side effects of NSAIDs

A

•Gastrointestinal/renal/respiratory

38
Q

State 3 pharmacological approaches to pain management

A
  1. analgesics
  2. nerve block/transmission
  3. complementary therapies i.e. accupuncture
39
Q

How do NSAIDs affect pain central sensitisation

A
  • COX inhibition in dorsal horn-
  • Reduced prostaglandin production
  • Reduced transmitter release
  • Reduced 2nd order neuron sensitivity
40
Q

What are the three classes of opioids

A
  1. natural
  2. semi-synthetic
  3. synthetic

(Physio) Health Sciences (10 decks)

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