Pharmacology Flashcards Preview

Module 204, Theme 1: Immunology > Pharmacology > Flashcards

Flashcards in Pharmacology Deck (18)
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1
Q

Aspirin

  • Indication
  • Toxicity
  • Replacements
A

Use

  • Antiplatelet [MI, IHD)
  • Analgesic
  • Inflammation

Toxicity

  • GI
  • Tinnitus
  • Reye’s syndrome
2
Q

Paracetamol

- Use

A

Analgesic
Antipyretic

Does not cause significant toxicity or anti-inflammation
- Doesn’t bind to COX 1/2

3
Q

Paracetamol overdose mechanism

A

Can be caused by 20/30 500mg tablets

Paracetamol metabolised Into NAPq1= hepatic necrosis
- When it can not undergo conjugation in the liver (Phase 2), so undergoes oxidation (Phase 1)

Can be overcome by
- methionine that shunts NAPQ1 into excretion

4
Q

NSAID GI toxicity

A

Inhibition of prostaglandins (which initially protects gut mucosa)

  • Irritation of GI
  • Ulcers (gastric and duodenal)
  • GI bleeding
  • Colitis

Risk of upper GI bleed

  • 4.7
  • Older NSAIDs= greater risk
  • Older, chronic disease
  • Steroids
  • Previous GI bleed.
5
Q

NSAID nephrotoxicity

A

Reduces glomerular blood flow

  • Decreases GFR
  • Na+ retention
  • Hyperkalaemia
  • Papillary necrosis

Acute renal failure

6
Q

NSAID and bronchoconstriction

A

Possibly shunting of Arachidonic acid down 5LPO to leukotrienes by COX2 inhibition= bronchoconstriction

7
Q

Main 4 NSAIDs

A

Further down= more side effects

Ibuprofen

Naproxen

Diclofenac

Indometacin

8
Q

Preventing NSAID toxicity

A

Consider alternative

  • Paracetamol
  • Weak opioids

Gastroprotective drug in co-administration
- PPIs

Avoid in renal failure

9
Q

Selective COX-2 inhibitors

A

Coxibs
- i.e Celecoxib

Safer than normal NSAIDs and comparable effects

However

  • Increases MI rates by by small amount
  • MI in first 3 months
  • May be due to the lack of anti-platelets effects

Only used when needed, i.e GI toxicity

10
Q

Hydrocortisone

A

Endogenous glucocorticoid
- Modulator of immune response at high doses

Mechanism

  • modulates gene expression in T, B and innate cells
  • Delay of onset, so much be taken regularly
11
Q

Immunomodulation by steroids

A

Cell trafficking

  • Reduces lymphocytes and monocytes
  • Increases neutrophils but with impaired function

Cell function

  • Decreases T and B cell responsiveness
  • Inhibits COX
  • Impairs phagocytes

Does not affect Ab levels of complement

12
Q

steroids uses

A

Inflammation

Graft rejection

replacement therapy

13
Q

Steroid preparation

A

Systemic

  • Oral
  • Injection

Topic

  • Skin
  • Joint injection
  • Inhaled
  • Enteric coated
  • Rectal
14
Q

Prednisolone

A

Main oral corticosteroid

  • Medium potency
  • Anti-inflammatory
15
Q

COX-1

  • Function
  • Effects of inhibition
A

Expressed in all tissues
- Esp. stomach, kidneys, platelet, vascular endothelium

  • Inhibition leads to anti-platelet activity
16
Q

COX-2

  • Function
  • Effects of inhibition
A

Induced in inflammation via IL-1
- i.e injury, infection, neoplasia

Inhibition
- Analgesia, anti-inflammatory

17
Q

COX 3

  • Function
  • Effects of inhibition
A

Expressed in CNS

- Inhibited by paracetamol= antipyretic and analgesic

18
Q

Side effects of corticosteroid drugs

A

Adrenal suppression when prolonged therapy
- Adrenal atrophy, can lead to adrenal crisis

Increased risk to infection

  • Phagycoytic defects: s.aureus, candida [earlier risks]
  • Cell mediated: TB, varicella, listeria, pneumocystis.