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4th yr- CMS- drugs and medication > Commonly prescribed analgesic > Flashcards

Commonly prescribed analgesic Flashcards

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Introductory Sommelier Exam (CMS) flashcards
1
Q

What are commonly prescribed analgesics Called

A

Non steroidal anti inflammatory drugs (NSAIDS)

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2
Q

What do we need to consider before prescribing NSAIDS

A
  1. Drug interactions

2. Patient factors

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3
Q

What is the major ode of action of NSAIDS

A

Inhibition of the cyclo-oxygenase enzymes 1 and 2 to reduced prostaglandin synthesis

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4
Q

Talk through the synthesis of prostaglandins

A 
1. Phospholipid 
(Phosphlipase)
2. Arachidonic acid
(Cyclic oxygenase COX1, COX2)
3. Cyclic endopeloxides PGG2
(Cyclo oxygenase)
4. prostaglandin
5. PGE2, PGD2, PGF2,
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5
Q

What do prostaglandins produce

A
  1. Analgesic actions
  2. Antipyretic action
    3Inflammatory actions
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6
Q

Name the 2 Cyclic oxygenase enzymes

A

COX1

COX2

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7
Q

Describe COX 1

A
  1. It is constitutionally active
  2. Expressed in many tissues eg kidneys, blood vessels, stomachs
  3. Unwanted/ adverse affects of NSAID are predominately down to COX 1
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8
Q

Describe COX 2

A

Is an inducible enzyme inducted by inflammatory cells

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9
Q

The unwanted effects of NSAIDS are due to which COX enzyme

A

COX1

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10
Q

What do several prostaglandin make

A

Nociceptors that response to mediators such as 5-HT, bradykinin

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11
Q

How are NSAIDS effective painkillers

A

They stop prostaglandin synthesis

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12
Q

Talk through the antipyretic effect of NSAIDS

A
  1. Bacteria leads to infection in a healthy body
  2. Bacterial toxin released
  3. Macrophages activated
  4. NSAIDS block COX2 metabolised PG synthesis
  5. This returns the body back to normal rather than pyrexia occurring
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13
Q

What is pyrexia

A

Body temperature greater than 38

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14
Q

What are the anti inflammatory effects of NSAIDS

A

COX-2 inhibition of prostaglandins synthesis leads to:

  1. Less vasodilaiton
  2. Less tissue oedema
  3. Less sensitisation of nociceptors
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15
Q

What does less vasodilation lead to

A

Reduced flushing and reduced redness of skin

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16
Q

What do we mean by less tissue oedema

A

Reduced swelling

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17
Q

What do we mean by less sensitisation of nociceptors

A

Analgesia

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18
Q

Name the most common NSAID agents

A
  1. Salicylates e.g. aspirin
  2. Paracetamol
  3. Proprionic acid derivatives EG ibuprofen, naproxen
  4. Selective COX-2 inhibitors
  5. Enoic acids
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19
Q

What is aspirin made of

A

acetylsalicylic acid

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20
Q

Give examples of Proprionic acid derivatives

A

Ibuprofen

Naproxen

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21
Q

What is the half life of ibuprofen

A

2 hours

22
Q

What is the half life of naproxen

A

14 hours

23
Q

why might we prefer Proprionic acid derivatives over aspirin

A

As Proprionic acid derivatives are better tolerated in regards to gastrointestinal effects

24
Q

Give examples of selective COX-2 inhibitors

A

etoricoxib,
celecoxib,
parecoxib

25
Q

When are selective COX-2 inhibitors used

A

most commonly prescribed in Rheumatology

26
Q

Give example of Enoic acids NSAIDS

A

piroxicam,
meloxicam,
ketorolac,
diclofenac

27
Q

Aspirin and ibuprofen selectively inhibit which form of COX

A

Weakly COX-1 Selective

28
Q

How does aspirin work

A

It binds irreversibly to COX-1 hence the effects outlasts presence of the drug

29
Q

Diclofenac selectively inhibit which form of COX

A

Weakly COX-2 selective

30
Q

Celecoxib selectively inhibit which form of COX

A

Moderately COX-2 selective

31
Q

Etoricoxib selectively inhibit which form of COX

A

Very COX-2 Selective

32
Q

How does paracetamol work

A

It is a reversible non competitive COX inhibitor

33
Q

What is paracetamol effective against

A

Pain relief and anti pyretic actions

34
Q

What are gastrointestinal effects of NSAIDS

A
  1. Dyspepsia
  2. Nausea
  3. Gastritis
  4. Intestinal damage
  5. Bleeding
  6. Oral ulcerations
35
Q

what are the bleeding risks of NSAIDS

A
  1. Anti platelets activity exacerbates gastrointestinal bleeding
  2. Increased risk of thrombotic effects eg MI or stroke
36
Q

What other side effects may NSAIDS have

A
  1. May have irritant effect on skin or mucosa
  2. Skin rashes
  3. Bronchospasm
  4. Nephritis and papillary necrosis
37
Q

What does aspirin overdose have an impact on

A

Acid base balance

38
Q

What can changes in acid base balance lead to

A

respiratory alkalosis or respiratory and metabolic acidosis

39
Q

What can overdose of aspirin cause

A
  1. Hyperpyrexia
  2. Nausea and vomiting
  3. Vertigo, tinnitus and haring impatient
40
Q

What is Hyperpyrexia

A

Body temperature of 40 plus

41
Q

What is reyes syndrome

A

A syndrome present in children given aspirin for viral infections to lower their high temper

42
Q

What is the mortality rate for reyes syndrome

A

20-40%

43
Q

How do we avoid reyes syndrome

A

Never prescribe aspirin for those under the age of 16

44
Q

Above what dose can paracetamol start causing problems

A

A dose of 10-15g

45
Q

What is the maximum dose of paracetamol for a Healthy adult

A

1g per day in 4 divided doses

46
Q

What are the major side effects of paracetamol overdose

A

Severe liver damage

47
Q

How does liver damage manifest as a consequence of paracetamol over dose

A

Hepatitis which can be severe enough to end in acute liver failure and death

48
Q

What is the toxic metabolite produced as a consequence of paracetamol overdose

A

N-acetyl-p-benzoquinone

49
Q

Why is N-acetyl-p-benzoquinone toxic

A

There is limited capacity for the body to remove this

50
Q

How is N-acetyl-p-benzoquinone toxic usually metabolised

A

In conjugation with GLUTATHIONE

51
Q

What are paracetamol overdose patients given

A

given IV N-acetylcysteine or PO methionine to increase glutathione production to mop up the excess toxic metabolite

4th yr- CMS- drugs and medication (4 decks)

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