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Y2 - CPT > Lecture 15 - NSAIDs > Flashcards

Lecture 15 - NSAIDs Flashcards

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
How do NSAIDs act as antipyretics?
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
what are some examples of pyrogens (cytokine)?
IL-1 IL-6
27
Why do selective COX2 inhibitors have fewer ADRs?
They have much greater selectivity than COX1 at therapeutic doses
28
What are all of the NSAIDs in order from most COX2 selective to COX1 selective?
Etoricoxib Celecoxib Diclofenac Naproxen Ibuprofen Aspirin (LOW DOSE)
29
What is the suffix to NSAIDs that are specific to COX2?
-Coxib Celecoxib Etoricoxib
30
What part of the body to NSAIDs most commonly cause ADRs in ?
GI system
31
What are the ADRs for NSAIDs on the GI tract?
Dyspepsia Nausea Peptic ulceration Bleeding and perforation INC RISK OF GI BLEED
32
Why do NSAIDs often cause GI problems as ADRs like Peptic ulceration, bleeding and dyspepsia?
They decrease mucus and bicarbonate secretion leading to increased acid secretion Decreased mucosal blood flow leads to enhanced cytotoxicity and hypoxia
33
What are contradinnidcataions of NSAIDs?
Elderly (Bleeds) Prolonged use Smoking Alcohol Hx of peptic ulceration Helicobacter pylori infection (inc acid production)
34
What are the contraindications to NSAIDs?
Aspirin Glucocorticoid steroids Anticoagulants
35
What drug should also be prescribed with NSAIDs?
Proton Pump INhibtors (Omeprazole)
36
What are the renal adverse affects of NSAIDs?
Reversible reduced GFR and renal blood flow
37
What are the contraindications to NSAIDs when considering the kidneys?
CKD Heart failure So anytime theres greater reliance on prostaglandins for vasodilation and renal perfusion
38
Why are NSAIDs bad for the kidneys?
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
What are the drug tot drug interactions from NSAIDs whine considering the kidneys?
ACEi ARBs Diuretics
40
Why are ACEi and ARBs with NSAIDs bad?
NSAIDs = less prostaglandins so afferent arterial constricted ACEi and ARBs means efferent areteriole dilates
41
What is the danger of using selective COX2 inhibtors??
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
What are the 2 selective COX2 inhibtors?
Celecoxib Etoricoxib
43
Why do NSAIDs often affect the concentrations of other drugs in the body?
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
What drugs do NSAIDs increase the plasma concentration of?
Sulfonylurea Methotrexate Warfarin
45
What is the side effect of NSAIDs displacing sulfonylureas leading to their increased plasma concentration?
Hypoglycaemia
46
What is the side effect of NSAIDs displacing methotrexate leading to their increased plasma concentration?
Accumulation and hepatotoxicity
47
What is the side effect of NSAIDs displacing warfarin leading to their increased plasma concentration?
Increased risk of bleeding
48
What are some situations you should be careful of giving NSAIDs for?
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
What are the indications for using NSAIDs?
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
What is paracetamol used for?
Moderate analgesia Fever (Antipyretic)
51
Why does paracetamol have few affects on platelets and limited effect on GI?
Its selective to COX-2 in the CNS
52
What inactivates Paracetamol?
Conjugation in the liver
53
What is the toxic highly reactive metabolite of paracetamol?
NAPQI
54
What is the pathway of a paracetamol overdose?
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
What are the symptoms of a paracetamol overdose?
Nausea, vomiting and abdominal pain in the first 24h Mex liver damage at 3-4 days
56
What is the cure for a paracetamol overdose?
IV Acetylcysteine
57
How does IV Acetylcysteine work to cure a paracetamol overdose?
Replenishes Glutahione thione (GSH) so NAPQI can be Phase 2 metabolised to a safe product
58
Why cant you just give glutathione in a paracetamol overdose?
GSH cant get into hepatocytes but Acetylcysteine can

Y2 - CPT (30 decks)

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