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2.3 T1: Immune system > T1 L14: Pharmacological aspects of immunology > Flashcards

T1 L14: Pharmacological aspects of immunology Flashcards

1
Q

What are some examples of NSAIDS?

A
  • Aspirin
  • Propionic acid derivatives: ibuprofen, naproxen
  • Arylalkonic acids: indometacin, diclofenac
  • Oxicams: piroxicam
  • Fenamic acids: mefanamic acid
  • Butazones: phenylbutazon
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2
Q

What is the mechanism behind NSAIDS?

A

They antagonise cyclo-oxygenase (COX) to prevent the production of prostaglandins

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3
Q

What does COX-1 do?

A

It’s expressed in all tissues

Its inhibition causes anti-platelet activity

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4
Q

What does COX-2 do?

A

It’s induced during inflammation (IL-1)

Its inhibition causes analgesia and anti-inflammatory actions

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5
Q

What does COX-3 do?

A

May be relevant to paracetamol

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6
Q

What is Reye’s syndrome?

A

Swelling of the brain and liver most often in children caused by viral infection or aspirin

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7
Q

What is fulminant hepatic failure in children?

A

In children, fulminant hepatic failure is a rare multisystem disorder in which severe impairment of liver function, with or without encephalopathy, occurs in association with hepatocellular necrosis in a patient with no recognized underlying chronic liver disease

(Reye’s syndrome)

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8
Q

What is aspirin used for?

A

Pain, inflammation, primary and secondary prevention of stroke and MI, treatment for acute MI and stroke

Limited by GI toxicity and tinnitus

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9
Q

What is tinnitus?

A

Hearing ringing that comes from inside the ear

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10
Q

What are the risk factors for GI bleeding due to NSAIDS?

A

Previous GI bleeding
Increasing age
Chronic disease Eg. rheumatoid arthritis
Steroids

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11
Q

How do NSAIDS cause nephrotoxicity?

A

They change glomerular blood flow

-They decrease GFR, cause sodium retention, hyperkalaemia, papillary necrosis

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12
Q

Why do asthmatics experience bronchospasm when using NSAIDS?

A

The inhibited prostaglandins prevent the production of leukotrienes which cause vasodilation

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13
Q

What is acetaminophen?

A

Paracetamol

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14
Q

How can paracetamol metabolism lead to liver necrosis?

A

In high does of paracetamol, the phase 1 reaction happens and produces NAPQI which causes hepatic necrosis

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15
Q

Which drug is used in paracetamol overdose?

A

N-acetylcysteine (glutathione precursor) which prevents the metabolism of NAPQI

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16
Q

What are coxibs?

A

COX-2 inhibitors used as anti-inflammatory and analgesic drugs

But the efficacy is not superior to non-selective NSAIDS. Only recommended in high risk patients and those who have had a cardiovascular assessment because the drugs seem to increase risk of MI

17
Q

What is mechanism of action of steroids?

A

They reduce immune activation by altering gene expression in certain cells

18
Q

What is hydrocortisone used for?

A

It has a low potency but high lipid solubility

Systemic use: replacement therapy
Topical use: skin, joints

19
Q

What is Prednisolone used for?

A

It has a medium potency and good lipid solubility

Systemic use: anti-inflammatory
Topical use: enemas

20
Q

What are enemas?

A

They’re injected into the GI tract to clear the tract to allow examination or to relieve constipation

21
Q

What is Beclomethasone used for?

A

It has medium potency and poor lipid solubility

Topical use: Asthma, Crohn’s

22
Q

What is Dexamethasone used for?

A

It has high potency and good lipid solubility

Systemic use: cerebral oedema

23
Q

What is Triaminiclone used for?

A

It’s a steroid
It has a high potency and poor lipid solubility

Topical use: skin, joints

24
Q

What are some early and later side-effects if using steroids?

A

Early

  • Weight gain
  • Glucose intolerance
  • Mood change (depression, anxiety, psychosis)
  • suppression of ACTH release

Later

  • Proximal muscle weakness
  • Osteoporosis
  • Skin changes
  • Body shape changes
  • Hypertension
  • Cataracts
  • Adrenal suppression
25
Q

What does DMARD’s stand for?

A

Disease-modifying anti-rheumatic drugs

26
Q

How does Methotrexate work?

A

A DMARD. It’s a competitive inhibitor of dihydrofolate reductase (DHR), so it has anti-folate action
-folate is needed for purine synthesis in DNA so this reduced T-cell activity and tumour synthesis

Indications: Rheumatoid arthritis, psoriasis, Crohn’s disease

Main toxicities: Hepatotoxicity, leukopenia, pulmonary fibrosis, teratogenic

27
Q

How does Azathioprine work?

A

A DMARD. It inhibits thiopurine S methyltransferase (TPMT), so it inhibits purine synthesis

Very similar to methotrexate in terms of indications and side-effects

28
Q

How does Ciclosporin work?

A

A DMARD. It inhibits calcineurin, which reduces T-cell activity

Used more in dermatology and transplantation

Main toxicities: nephrotoxic, hepatotoxic, gum hyperplasia, hirsutism

2.3 T1: Immune system (21 decks)

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