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Practical - Y2B2 - (Musculoskeletal) 📗 > Pharmacology 💊 > Flashcards

Pharmacology 💊 Flashcards

1
Q

what is the definition of hyperuricemia?

A

Is a plasma uric acid concentration > 6.8mg/dL.

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2
Q

what are the causes of hyperuricemia?

A
  • Underexcretion: 80 % of cases.
  • Over-production: 20 % of cases
  • Both
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3
Q

causes of underexcretion in hyperuricemia

A

decreased secretion or increased reabsorption

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4
Q

causes of overproduction in hyperuricemia

A
  • High purine diet
  • Tumor lysis syndrome
  • Enzymatic defects in purine biosynthesis ( Lesch - Nyhan syndrome) (small % of cases)
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5
Q

what are the medications that increase uric acid levels?

A
  • Loop & thiazide diuretics
  • Low dose aspirin
  • Cyclosporine
  • Niacin
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6
Q

what is the clinical presentation of gout?

A
  • Deposition of urate crystals in joints →an inflammatory process
  • Acute flares (acute attacks) usually present as pain, swelling, tenderness & redness in the affected joints (big toe mainly).
  • Subcutaneous tophi
  • Urate renal stones
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7
Q

lifestyle modification to manage gout

A
  1. Limiting high purine intake (Coffee, tea, meat, egg)
  2. Weight reduction
  3. Stop alcohol
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8
Q

what are anti-gout drugs?

A
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9
Q

what are xanthine oxidase inhibitors?

A
  • Allopurinol
  • Febuxostat
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10
Q

what is the mechanism of action of allopurinol?

A

A purine analog → competitively inhibit xanthine oxidase → decrease uric acid production

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11
Q

what causes the long duration of allopurinol?

A

due to conversion to active metabolite, oxypurinol (alloxanthine)

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12
Q

Dose of allopurinol

A

Once /day

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13
Q

what are the uses of allopurinol?

A
  1. Chronic gout
  2. Secondary hyperuricemia to : hematologic malignancies (large amounts of purines are produced, after chemotherapy tumor lysis syndrome) or in renal disease.
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14
Q

what are the side effects of allopurinol?

A
  • Hypersensitivity reactions, Skin rash
  • Precipitation of acute attack of gout at the start of therapy
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15
Q

what causes precipitation of acute attack of gout under intake of allopurinol?

A

mobilization of the deposited uric acid crystals.

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16
Q

how to manage acute attack of gout?

A
  • By the use of anti-inflammatory drugs
17
Q

why should Dose of 6-Mercaptopurine and azathioprine should be decreased when given with allopurinol?

A

because the enzyme used for their metabolism is deficient

18
Q

what are the characteristics of Febuxostat?

A

Comared to allopurinol:

  • A non-purine structure
  • Lower risk for rash and hypersensitivity reactions
  • Lesser degree of renal elimination → thus requires less adjustment in those with reduced renal function.
  • Greater risk of heart disease or stroke→Febuxostat should be
    used with caution in patients with a history of heart disease or
    stroke
19
Q

what are Uricosuric drugs?

A

Probencid

20
Q

what is the mechanism of action of probencid?

A

Biphasic action:

Low doses: ↓ secretion of uric acid (&other acidic drugs) by the renal PCT.

Therapeutic doses:↓ Uric acid reabsorption from renal PCT.

21
Q

what are the therapeutic uses of Probencid?

A
  • Chronic gout.
  • To prolong the half-life of some acidic drugs e.g. penicillins and rifampicin by inhibiting their renal tubular secretion .
22
Q

what are the side effects of Probencid?

A

GIT disturbance, skin rash, rarely anaphylactic reactions & aplastic anemia.

23
Q

Precautions during the use of uricosuric drugs

A
  • Should not be used during acute attack of gout & started 2-3 weeks after the acute attack
  • Maintain large volume of alkaline urine to avoid stone formation.
  • Should be avoided in patients with gouty nephropathy.
24
Q

why shouldn’t probencid be used during acute attack of gout & started 2-3 weeks after the acute attack?

A

because the biphasic action on uric acid excretion during the acute attack may aggravate the condition at initial phase of therapy

25
Q

what are drugs that increase uric acid metabolism?

A

Rasburicase & Pegloticase

26
Q

what is the mechanism of action of Rasburicase & Pegloticase?

A
  • Recombinant form of the uricase enzyme → converts uric acid to allantoin, a water-soluble nontoxic metabolite → excreted primarily by the kidneys.
27
Q

when are Rasburicase & Pegloticase used?

A

Indicated for gout patients who fail treatment with standard therapies

28
Q

method of administration of Rasburicase & Pegloticase

A

IV infusion/2 weeks (pegloticase)

29
Q

what are adverse effects of Rasburicase & Pegloticase? And how are they managed?

A
  • Infusion-related reactions and anaphylaxis may occur with
    pegloticase.
  • management: patients should be pretreated with antihistamines and corticosteroids
30
Q

what are NSAIDs used during acute attack of gout?

A

Indomethacin, ibuprofen, Naproxen

31
Q

what is the mechanism of action of NSAIDs?

A
  • Reversible inhibition of COX enzymes →decreasing synthesis of PGs resulting in decrease inflammation and pain
  • Indomethacin is the NSAID of choice, although all NSAIDs are effective.
32
Q

what NSAID should be avoided during treatment of acute attack of gout?

A

Don’t use aspirin → competes with uric acid for excretion.

33
Q

what is the mechanism of action of colchicine?

A
  • It binds to tubulin → inhibits polymerization of intra-cellular microtubular system and inhibit the motility of leukocyte, phagocytosis→ reduce leukocyte migration and inflammatory functions
  • It inhibits mitotic spindle and cell division (mitotic block).
34
Q

what are the uses of colchicine?

A
  • Acute attacks of gout
  • Familial Mediterranean fever (FMF)
  • liver cirrhosis
35
Q

Dose of colchicine

A

1.2 mg orally initially followed by 0.6 mg/ 12 hour until the attack resolves.

36
Q

disadvantages of colchicine

A

slow onset and high toxicity→it is not a first-choice drug in acute gouty arthritis.

37
Q

Side effects of colchicine

A

The most common:
- GIT toxicity→Diarrhea (severe), nausea, vomiting & abdominal cramps

The most serious:
- Bone marrow depression (onset in days)→ aplastic anemia and agranulocytosis.

The most rare:
- Alopecia, CV toxicity, Hepatotoxicity.

38
Q

how does colchicine cause diarrhea?

A
  • Colchicine is excreted unchanged in bile→inhibits the continuous renewal of GIT epithelium (mitotic block)→accumulation of toxins and bacterial products→diarrhea.

Practical - Y2B2 - (Musculoskeletal) 📗 (7 decks)

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