Glucocorticoids & Drugs Against Gout Flashcards Preview

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Flashcards in Glucocorticoids & Drugs Against Gout Deck (21)
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1
Q

How is uric acid synthesized?

A

Hypoxanthine is converted to xanthine via xanthine oxidase

Xanthine is converted to uric acid via xanthine oxidase

2
Q

What is an acute gouty attack?

A

When synoviocytes engulf crystallized uric acid, causing inflammation and severe pain

3
Q

What is the mechanism of action of Colchicine?

A

Binds to tubulin in amine cells and reduces their mobility and ability to conduct phagocytosis (interferes with microtubules)

4
Q

When is colchicine used? What is the most common side effect?

A

When acute gouty attacks are not controlled via NSAIDs (standard treatment), it may be used to relieve this

Most common side effect is diarrhea

5
Q

What is the mechanism of action of allopurinol?

A

Inhibits xanthine oxidase, allowing more xanthine and hypoxanthine to build up, and all three dissolve better together.

6
Q

What should allopurinol be used for?

A

Only in the chronic treatment of group -> acute treatment may result in exacerbation due to dissolution and reformation of crystals

7
Q

What drug must not be given with allopurinol?

A

6-mercaptopurine (Azathioprine) -> metabolized by xanthine oxidase. Leads to toxic bone marrow suppression

8
Q

What is the newest xanthine oxidase inhibitor and when is it used?

A

Febuxostat

It s a non-purine, non-competitive inhibitor of xanthine oxidase.

Used when patients are allergic to allopurinol (3%)

9
Q

What is the last class (other than NSAIDs and colchicine) which can be used in the acute treatment of gout, their mechanism of action, and give an example.

A

Uricosurics - urate is excreted and reabsorbed, these drugs favor the excretion

Example: probenecid

10
Q

What drugs can precipitate gout?

A

Thiazide and loop diuretics

Aspirin

11
Q

What is the mechanism of action of probenecid?

A

Blocks the reabsorption of urate by preferentially binding the organic anion transporter (OAT) which is used to reabsorb urate

12
Q

What is pegloticase? When is it used?

A

A pegylated (polyethylene glycol) form of uricase which converts uric acid to allantoin, which is more soluble

Since you develop antibodies to the protein, it is only used in otherwise uncontrolled gout

13
Q

What are the three classes of effects from glucocorticoids?

A
  1. Metabolic
  2. Anti-inflammatory
  3. Sodium-retentive (aldosterone-like)
14
Q

Why do glucocorticoids have so many side effects if they occur naturally?

A

The anti-inflammatory effects are only seen at many times the physiological does (100x higher)

15
Q

Why should you not rapidly stop taking glucocorticoids?

A

Atrophy of adrenal gland due to lack of stimulation via ACTH (high cortisol levels already). Can lead to an addison’s-like syndrome. Need to taper

16
Q

What is the most potent antiinflammatory glucocorticoid, which has much less sodium retention effects?

A

Dexamethasone - 30 times more potent than cortisol

17
Q

In what situations are low doses of corticosteroids administered chronically?

A

Serious inflammatory disease -> lupus erythematosus

18
Q

When are GC’s used in cancer?

A

It has certain anti-leukemic effects -> Acute Leukemia, Lymphoma, Myeloma, and some breast cancers

19
Q

How do glucocorticoids influence lung development?

A

They stimulate the production of pulmonary surfactant which is required for breathing (DPPC)

20
Q

What corticosteroid drug is given for infants who will be delivered prematurely and why?

A

Betamethasone - better crosses the placenta and is not bound by mother’s protein as much -> more gets to fetus to start pulmonary surfactant production

This reduces the incidence of respiratory distress syndrome

21
Q

Why do GC’s cause peptic ulcers?

A

At pharmacological doses, they inhibit COX production. Can be be bad if you are taking NSAIDs already.