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CPT (My own) > NSAIDs > Flashcards

NSAIDs Flashcards

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1
Q

Briefly describe the process of eicasanoid synthesis

A

Phospholipids–>Arachidonic acid–>Prostanoids

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2
Q

What are some of the enzymes involved in the eicosanoid synthesis?

A

COX enzymes

Cell specific syntheses/isomerase

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3
Q

Give examples of prostanoids

A 
PGE2
PGF2
PGD2
PGI2- prostacyclin
TXA2- thromboxane
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4
Q

What are some features of prostanoids?

A

Produced locally on demand

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5
Q

What are some features of the enzymes involved in prostanoid synthesis?

A

Short half life and fine control

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6
Q

What do the therapeutic benefits of prescribing NSADIs come from?

A

From inhibition of down stream products of arachidonic acid

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7
Q

Why do adverse effects form?

A

Also from the inhibition of the downstream pathway

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8
Q

Where is arachidonic acid derived from?

A

Primarily from linoleum acid- vegetable oils

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9
Q

How is linoleum acid converted to arachidonic acid?

A

Hepatically converted to arachidonic acid and then incorporated into phospholipids

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10
Q

Where is arachidonic acid found in the body?

A

Everywhere, in particular muscle, brain and liver

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11
Q

What are the functions of proastacyclin?

A 
Inhibits platelet aggregation
Vasodilator 
Endothelium
Kidney
Brain
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12
Q

What is the overall effect go prostacyclin on CVS?

A

Cytoprotective

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13
Q

What are the functions of thromboxane?

A

Platelet aggregation
Vasoconstictor
Macrophages
Kidney

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14
Q

What is the importance of interactions between prostacyclin and thromboxane?

A

Have a fine balance for vascular tone and platelet aggregation
Fine balance between haemodynamic and thrombogenic control

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15
Q

What are the two functional forms of cyclooxygenase enzymes?

A

COX-1

COX-2

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16
Q

What is the predominant COX enzyme?

A

COX-1, constitutively active across most tissues

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17
Q

Where is COX-2 inducible?

A

Mostly in chronic inflammation, constitutively in brain, kidney and bone

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18
Q

Give some examples of the homeostatic functions of COX-1

A

GI protection
Platelet aggregation
Vascular resistance

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19
Q

Give some examples of the homeostatic functions of COX-2

A

Renal homeostasis
Tissue repair and healing
Reproduction
Inhibition of platelet aggregation

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20
Q

Give some examples of the pathological functions of COX-1

A

Chronic inflammation
Chronic pain
Raised blood pressure

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21
Q

Give some examples of the pathological functions of COX-2

A 
Chronic inflammation
Chronic pain
Fever
Blood vessel permeability
Tumour cell growth
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22
Q

How can drugs be targeted to just one type of COX enzyme?

A

COX 2 has a larger more flexible substrate channel than COX 1 and a larger space at the site of inhibitor binding which can be used as a target

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23
Q

What do prostanoids signal through?

A

Locally via GPCRs which are expressed in different amounts in different parts of the body

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24
Q

What does the specific action on the prostanoids depend on?

A

Depends on the receptor subtype and location

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25
Q

What can enhance the action of prostanoids?

A

Local autocoids

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26
Q

What are some examples of local autocoids?

A

Bradykinin
Histamine
Seratonin

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27
Q

What is the imbalance between thromboxane and prostacyclin?

A

Imbalance has a role in hypertension, MI and stroke

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28
Q

What are some examples of better prostanoids?

A

TXA3 and PGI3

Diet rich in fish oils

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29
Q

What foods can TXA3 and PGI3 be found in?

A

Mediterranean foods

30
Q

What are the predominant uses of NSAIDs?

A

Analgesic and anti-inflammatory effects

31
Q

What is the single common mode of action of NSAIDs

A

`inhibition of COX–> decrease in prostanoid synthesis

32
Q

How do COX inhibitors work?

A

Compete with arachidonic acid for hydrophobic site for COX

33
Q

How do NSAIDs have an analgesic effect peripherally?

A

Inhibition reduces peripheral pain fibre sensitivity by blocking PGE2 in the dorsal horn

34
Q

How do NSAIDs have an analgesic effect centrally?

A

The central component is associated with PGE2 synthesis in dorsal horn–>Decreased NT release–>Decreased excitability of neurones in pain relay pathway to higher centres

35
Q

Which dose is most efficacious?

A

First dose has efficacy but full analgesia after several dosing

36
Q

How do NSAIDs have an anti-inflammatory effect?

A

NSAIDs inhibit vasodilation in post capillary venues to increase permeability and local swelling
Also reduce production go prostaglandins released during injury

37
Q

What is important to consider with NSAIDs and their anti-inflammatory effects?

A

Just symptomatic relief but COX inhibition

38
Q

Describe the mechanism of pyrexia

A

Pyrogen–>Prostaglandins–? thermoregulatory centres–> Increases the set point f temoerature–> Patient is febrile

39
Q

Where is the location of the thermoregulatory centre?

A

Preoptic area of the hypothalamus

40
Q

What are some examples of pyrogens?

A

Cytokines

Interleukins e.g. IL-1 and IL-6

41
Q

How do NSAIDs have anti-pyrexic effects?

A

Inhibits hypothalamic COX-2 where cytokine induces prostaglandin synthesis election results in reduction of temperature

42
Q

What do neither COX inhibitors have?

A

Neither have direct action on leukotrienes but do have indirect action through PGE2

43
Q

State a list of COX inhibitors

A 
Aspirin
Ibuprofen
Naproxen
DIclofenac
Celecoxib
Etoricoxib
44
Q

What are some example pf the most COX-1 selective drugs?

A

Aspirin
Ibuprofen
Naproxen

45
Q

What are some example pf the most COX-2 selective drugs?

A

Etoricoxib

Celecoxib

46
Q

What are the most common ADR’s of NSAID’s?

A

GI including

Dyspepsia, nausea, peptic ulceration, bleeding and perforation

47
Q

What is the mechanism of action that NSAIDs have on GI

A

Decreased mucus and bicarbonate secretion–> Increased acid secretion
Decreased mucus blood flow–> enhances cytotoxicity and hypoxia

48
Q

What should you be cautious of in terms of GI ADRS

A 
Elderly
Prolonged use
Glucocorticoid steroids
Anticoagulants
Smoking
Alcohol
History of peptic ulceration
H. Pylori
49
Q

Which of the 2 COX inhibitors has lower GI risks?

A

COX-2

50
Q

What effect does NSAIDs have on the kidney

A

Decreased GFR, decreased renal blood flow

51
Q

Who is most affected by NSAID renal ADRs?

A

People with underlying CKD or HF where there is a greater reliance on prostaglandins for vasodilation and renal perfusion
Very young and elderly

52
Q

How do NSAID’s affect the arterioles?

A

NSAIDs prevent afferent vasodilation by inhibiting PGE2 and PGI2 therefore doesn’t attain the back pressure needed for renal function

53
Q

How do prostaglandins affect absorption?

A

Prostaglandins inhibit Na absorption in the collecting duc- natriuresis- NSAIDs inhibit this acton- Increase Na, H20 and thus increase BP

54
Q

Give examples of COX2 inhibitors?

A

Celecoxib

Etoricoxib

55
Q

What was the initial intention of COX 2 inhibitors?

A

To avoid inhibition of homeostatic actions mediated by COX-1 with greater selectivity

56
Q

What is the ADR profile of COX 2 inhibitors?

A

Less GI ADR
Similar renal ADR
Potential unopposed aggregator effects

57
Q

Why are there COX 2 inhibitor potential unopposed aggregatory effects?

A

Do not share anti=plataelt action but impair PGI2 potentially

58
Q

What effect does NSAIDs have on other drugs?

A

Displace other bound drugs, increasing free drug concentration that can have effects

59
Q

What are the particular DDI’s to be aware of and its effects?

A

SUlfomylurea- hypoglycaemia
Methotrexate- accumulation and hepatotoxicity, leukopenia and rheumatoid arthritis
Warfarin- Increased risk of bleeding

60
Q

What is the displacement of bound drugs by NSAIDs known as?

A

Competitive displacement

61
Q

What are the pharmacological implications of competitive displacement?

A

Like dose adjustment needed

62
Q

Extra considerations and indications for NSAID use

A 
Inflammatory conditions
Osteoarthritis
Postoperative
Post-opertaive pain
Topical use on cornea
Menorrhagia
Low dose aspirin for platelet aggregation inhibition
Opioid sparing when used in contraindications
63
Q

What are the uses of Paracetamol?

A

For mild to moderate analgesia and fever

64
Q

What are the pharmacodynamics of paracetamol including the absorption and excretion?

A

Well absorbed from GI- t1/2 2 hrs

Predominantly inactivated by conjugation in the liver

65
Q

What is NAPQI?

A

Highly reactive metabolites

66
Q

How is NAPQI rendered harmless physiologically?

A

Glutathione conjugation

67
Q

What is the problem with hepatic glutathione?

A

Hepatic glutathione is limited

68
Q

What are the negative effects of NAPQI?

A

Highly nucleophilic- oxidising key metabolic enzymes which lead to cell death- necrosis and apoptosis

69
Q

What dose of Paracetamol is enough to cause irreversible damage?

A

150mg/kg

70
Q

What is the antidote for NAPQI accumulation?

A

N-acetylcysteine

Activated charcoal

71
Q

What are the side effects of paracetamol overdose?
First 24 hrs?
3-4 days later?

A

24 hrs- nausea, vomiting and abdominal pain

3-4 days- maximal liver damage

72
Q

What is the mechanism of action of N-acetylcysteine?

A

Replaces glutathione

CPT (My own) (6 decks)

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