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Pharmacology Y2 > GORD > Flashcards

GORD Flashcards

1
Q

What drugs can be given to treat GORD?

A
  • PPIs

- Histamine receptor antagonists

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2
Q

How do NSAIDs work to alleviate pain?

A
  1. They inhibit the enzyme cyclo-oxygenase (COX) which is the rate-limiting step for the production of all prostanoids (prostaglandins & thromboxanes).
  2. This reduces the amount of Prostoglandins and thus alleviates pain.
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3
Q

How do prostaglandins work to induce pain?

A
  1. They sensitise peripheral nociceptive C fibres which lowers their threshold for electrical stimulation. This makes it easier to stimulate them and cause pain.
  2. They sensitise peripheral nociceptor mediators like bradykinin and histamine which causes pain.
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4
Q

Which prostaglandin is mainly involved in causing pain in inflamed tissues (e.g in arthritis)?

A

Prostaglandin E2

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5
Q

There are 2 forms of the COX enzyme. Inhibition of which one has an analgesic effect?

A

COX-2

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6
Q

Why are one of the main side effects of NSAIDs peptic ulcers/ gastric irritation?

A

Inhibition of COX-1, the other major form of COX.

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7
Q

Where is the COX-1 enzyme (which when inhibited leads to gastric injury) found?

A

Gastric mucosal cells

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8
Q

How does NSAID inhibition of COX-1 cause peptic ulcer disease?

A
  1. NSAID inhibits prostaglandin synthesis.
  2. In the stomach, prostaglandins are involved in protecting the gastric mucosa from acid. If reduced, the mucosa will be more vulnerable and inflammation-prone.
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9
Q

How do prostaglandins protect mucosal cells from acid?

A
  • increase bicarbonate release
  • increase mucus production
  • increase blood flow
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10
Q

Why is bad blood flow especially relevant in ulcer formation?

A

Tissue repair is dependent on good blood supply. Reduced blood flow means less tissue repair of ulcers in the stomach.

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11
Q

Except for gastric injury, what are other adverse side effects of NSAIDs?

A
  • Reduced creatinine clearance and possible nephritis
  • Prolonged use -> chronic renal failure
  • Skin rashes & other allergies - - Dizziness
  • Tinnitus.
  • Adverse cardiovascular effects in those at risk (hypertension, stroke, MI)
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12
Q

In young children, what has using Aspirin (an NSAID) been linked with?

A

A rare but serious post-viral encephalitis (Reye’s syndrome)

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13
Q

Name some NSAIDs.

A
  • naproxen
  • diclofenac
  • ibuprofen
    (-aspirin)
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14
Q

What are the main uses of NSAIDs?

A
  • analgesics (for the relief of mild to moderate pain)
  • anti-pyretics
  • anti-inflammatory drugs for chronic control of inflammatory diseases
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15
Q

How do PPIs work (Target, Location, Effect) ?

A

Irreversible inhibitors of H+/K+ ATPase on the apical membrane of gastric parietal cells which reduces the amount of gastric acid produced by parietal cells.

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16
Q

Why can their effect last for so long?

A

PPIs are weak bases and can accumulate in parietal cells which concentrates their actions.

17
Q

Name some PPIs.

A
  • omeprazole

- lansoprazole

18
Q

What are some of the adverse side effects of using PPIs?

A
  • headache
  • diarrhoea
  • bloating
  • abdominal pain
  • rashes
19
Q

The use of PPIs can mask signs of what condition?

A

Gastric cancer

20
Q

What drugs can PPIs interfere with?

A

Clopidogrel (anti-platelets) -> it reduces their activity

21
Q

How are PPIs administered?

A

Orally as pro-drugs, and degrade rapidly at low pH in the stomach.

22
Q

How do Histamine (H2) receptor antagonists work?

A
  1. They inhibit gastric acid secretion by inhibiting the stimulatory action of histamines secreted by Enterochromaffin-like (ECL) cells.
  2. This stops H2 driven increases in cAMP which would normally activate the proton pump on the apical side of the membrane.

They are not as good as PPIs.

23
Q

What cells do H2 receptor antagonists target?

A

H2 receptors on the basolateral side of gastric parietal cells.

24
Q

What are the adverse side effects of H2 receptor antagonists?

A
  • Diarrhoea
  • dizziness
  • muscle pains
  • transient rashes
25
Q

Name some H2 receptor anatagonists.

A
  • Ranitidine

- Cimetidine

26
Q

Why is bioavailability of ranitidine only 50%?

A

It undergoes first pass metabolism

27
Q

What does Paracetamol (acetaminophen) target (not known very well)?

A

COX-3 isoform on nervous tissue, involving interaction with cannabinoid receptors or the endogenous opioids or 5-HT.

28
Q

Paracetamol does not have many side effects at low doses. What can happen if you take too much (overdose)?

A

Serious hepatotoxicity

29
Q

What are the main uses of paracetamol?

A
  • analgesic (mild-to-moderate pain)

- antipyretic

30
Q

How does prolonged PPI usage increase the risk of fracture?

A

Since absorption of calcium salts is pH dependent, change in pH caused by PPIs might be responsible for a reduction in absorption and calcium availability in bone.

Pharmacology Y2 (9 decks)

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