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Y2 - CPT > Lecture 15 - NSAIDs > Flashcards

Lecture 15 - NSAIDs Flashcards

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1
Q

What are the different types of prostanoids?

A

Prostaglandins, prostacyclin and thromboxanes

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2
Q

Why type of production are prsotanoids done under?

A

Produced locally and on demand

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3
Q

What is the name of the prostanoid PGI2?

A

Prostacyclin

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4
Q

What is therapeutic benefit of prescribing NSAIDs?

A

They inhibit the down stream products of arachidonic acid

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5
Q

What types of acid is arachidonic acid mainly derived from?

A

Dietary linoleum acid

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6
Q

What are the half lives of prostanoids like?

A

Short half-life

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7
Q

What is the normal function of prostacyclin (PGI2)?

A

Inhibts platetl aggregation since PGI2 binds to. Platelet. Receptors increasing cAMP levels in platetls

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8
Q

How do Prostacylins (PGI2) and TXA2 (Thromboxane A2) typically affect the CVS?

A

PGI2 = cytoprotective ofCVS

TXA2 = bad for CVS

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9
Q

What does Thromboxane A2 do ?

A

Leads to platelet aggregation

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10
Q

Why is PGE2 and prostacyclin (PGI2) improtant to the GI tract?

A

PGE2 contributes to Regualtion of acid secretion in parietal cell

PGI2 contributes to maintenance of blood flow and mucosal repair

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11
Q

How are prostanoids signalled?

A

They have many receptors and differential expression in tissues and repsonse (Many GPCR)

Have fine local control

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12
Q

What substances often enhance the action of prostanoids?

A

Local autocoids like Bradykinin and HIstamine

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13
Q

What 2 types of prostanoids do we need to carefully balance and why?

A

PGI2 (prostacyclin) and Thromboxane A2

they have a posing vascular effects
Fine balance between haemodynamic and thrombogenic control

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14
Q

What do we increase risk of. If imbalance in TXA2 and PGI2?

A

Hypertension
MI
Stroke

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15
Q

What are the benefits of the Mediterranean diet?

A

More conversion of Thromboxane A3 to PGI3 which is a better prsotnatooid

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16
Q

What do NSAIDs inhibit?

A

Cyclooxygenase enzymes (COX enzymes)

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17
Q

Where are COX1 and COX2 located?

A

COX1 = across most tissues
COX2 = indibcle mostly in chronic inflammation in brain, kidney and bone

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18
Q

What are the main effects NSAIDs do?

A

Analgesia
Anti-inflammatory

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19
Q

What is the mechanism of action of NSAIDs?

What do they compete with?

A

Inhibition of COX enzymes leading to reduced prostaglandins (prostacylins and Thromboxane synthesis)

Compete with arachidonic acid for hydrophobic site of COX enzymes

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20
Q

What are some common NSAIDs?

A

Naproxen
Ibuprofen
Celecoxib

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21
Q

How do NSAIDs act as analgesics?

A

Reduces peripheral pain fibre sensitivity by BLockinng PGE2 (Prostaglandins)

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22
Q

What is the pathway for NSAIDs acting as analgesics?

A

Reduced PGE2 (prostaglandin) synthesis in dorsal horn of cord
Dec neurotransmitter release
Reduced excitability of neurons in pain relay pathway

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23
Q

How do NSAIDs act as antiflammtories and act against oedema?

A

Prostaglandins lead to vasodilation and oedema (NSAIDs reduce prostaglandins) so less vasodilation so less increased capillary permeability and less local swelling

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24
Q

Do NSAIIDss efffet the chronic condition?

A

No just symptomatic relief

25
Q

How do NSAIDs act as antipyretics?

A

PGE2 is key in the Thermoregulation centre in the thalamus

Inhibits hypothalamic COX2 where cytokine induced prostglandin synthesis is elevated results in reduction in temperature

26
Q

what are some examples of pyrogens (cytokine)?

A

IL-1
IL-6

27
Q

Why do selective COX2 inhibitors have fewer ADRs?

A

They have much greater selectivity than COX1 at therapeutic doses

28
Q

What are all of the NSAIDs in order from most COX2 selective to COX1 selective?

A

Etoricoxib
Celecoxib
Diclofenac
Naproxen
Ibuprofen
Aspirin (LOW DOSE)

29
Q

What is the suffix to NSAIDs that are specific to COX2?

A

-Coxib

Celecoxib
Etoricoxib

30
Q

What part of the body to NSAIDs most commonly cause ADRs in ?

A

GI system

31
Q

What are the ADRs for NSAIDs on the GI tract?

A

Dyspepsia
Nausea
Peptic ulceration
Bleeding and perforation

INC RISK OF GI BLEED

32
Q

Why do NSAIDs often cause GI problems as ADRs like Peptic ulceration, bleeding and dyspepsia?

A

They decrease mucus and bicarbonate secretion leading to increased acid secretion

Decreased mucosal blood flow leads to enhanced cytotoxicity and hypoxia

33
Q

What are contradinnidcataions of NSAIDs?

A

Elderly (Bleeds)
Prolonged use
Smoking
Alcohol
Hx of peptic ulceration
Helicobacter pylori infection (inc acid production)

34
Q

What are the contraindications to NSAIDs?

A

Aspirin
Glucocorticoid steroids
Anticoagulants

35
Q

What drug should also be prescribed with NSAIDs?

A

Proton Pump INhibtors (Omeprazole)

36
Q

What are the renal adverse affects of NSAIDs?

A

Reversible reduced GFR and renal blood flow

37
Q

What are the contraindications to NSAIDs when considering the kidneys?

A

CKD
Heart failure

So anytime theres greater reliance on prostaglandins for vasodilation and renal perfusion

38
Q

Why are NSAIDs bad for the kidneys?

A

Prostaglandins vasodilates the afferent Arterioles so inhibiting prostaglandins means reduced GFR leading to increased H20 Na+ and therefore BP in the body
Prostaglandins inhibit sodium absorption

39
Q

What are the drug tot drug interactions from NSAIDs whine considering the kidneys?

A

ACEi
ARBs
Diuretics

40
Q

Why are ACEi and ARBs with NSAIDs bad?

A

NSAIDs = less prostaglandins so afferent arterial constricted

ACEi and ARBs means efferent areteriole dilates

41
Q

What is the danger of using selective COX2 inhibtors??

A

Inhibit PGI2 so doesn’t have antiplatelt action

So the balance between levels of TXA2 and PGI2 lost, More TXA2 made by COX1 so more platelet aggregation

ALL NSAIDS INCREASE risk of MI

42
Q

What are the 2 selective COX2 inhibtors?

A

Celecoxib
Etoricoxib

43
Q

Why do NSAIDs often affect the concentrations of other drugs in the body?

A

Have a very high affinity for transport proteins so displace most other drugs leading to the free concentration of that dis[placed drug increasing

44
Q

What drugs do NSAIDs increase the plasma concentration of?

A

Sulfonylurea
Methotrexate
Warfarin

45
Q

What is the side effect of NSAIDs displacing sulfonylureas leading to their increased plasma concentration?

A

Hypoglycaemia

46
Q

What is the side effect of NSAIDs displacing methotrexate leading to their increased plasma concentration?

A

Accumulation and hepatotoxicity

47
Q

What is the side effect of NSAIDs displacing warfarin leading to their increased plasma concentration?

A

Increased risk of bleeding

48
Q

What are some situations you should be careful of giving NSAIDs for?

A

Cardiovascular disease risk
Renal function
GI disease
ACEi, ARBs, Diureitcs, methotrexate and warfarin
Third trimester of. Pregnancy (early closure of ductus arteriosus and delayed labour)

49
Q

What are the indications for using NSAIDs?

A

Inflammatory conditions
Osteoarthritis
Postoperative pain
Topical use of cornea
Menorrhagia
Low o dose aspirin for platelet aggregation inhibition
Opioid sparing when used in combination

50
Q

What is paracetamol used for?

A

Moderate analgesia
Fever (Antipyretic)

51
Q

Why does paracetamol have few affects on platelets and limited effect on GI?

A

Its selective to COX-2 in the CNS

52
Q

What inactivates Paracetamol?

A

Conjugation in the liver

53
Q

What is the toxic highly reactive metabolite of paracetamol?

A

NAPQI

54
Q

What is the pathway of a paracetamol overdose?

A

GSH needed to convert NAPQI into its safe metabolite in Phase 2 liver metabolism

Eventually GSH depleted and NAPQI builds up leading to cell necrosis (NAPQI nucleophilic)

55
Q

What are the symptoms of a paracetamol overdose?

A

Nausea, vomiting and abdominal pain in the first 24h

Mex liver damage at 3-4 days

56
Q

What is the cure for a paracetamol overdose?

A

IV Acetylcysteine

57
Q

How does IV Acetylcysteine work to cure a paracetamol overdose?

A

Replenishes Glutahione thione (GSH) so NAPQI can be Phase 2 metabolised to a safe product

58
Q

Why cant you just give glutathione in a paracetamol overdose?

A

GSH cant get into hepatocytes but Acetylcysteine can

Y2 - CPT (30 decks)

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