MSK 09 Flashcards
What is Gout?
Caused by deposition of uric acid crystals in joint species and surrounding tissue
An acute attack lasts for 7-10 days but it is a chronic disease. if not treated damages kidney and joints
Which cites are most prone of Gout attack?
Metatarsophalangeal joint most common
Ankle knee and elbow
What are the causes of developing Goat?
Uric acid produce in our body naturally and they are the waste product of our purine breakdown which excreted by the kidney but why they cannot excreted or reabsorbed by (proximal tubule)then they cause increase of uric acid in our blood which cause hyperuricemia or Gout.
What is the parameter when we call hyperuricaemia?
> 0.36 mmol/L in women
>0.42 mmol/L in Men
How you diagnose Gout?
If Serum uric level is higher than 0.36mmol/L patient will experience red pain and inflammation.
Uric acid balance depends on which factors?
Diet: Red meat, fish Alcohol, bear they increase uric acid
Ethnicity: Maori Man around 12 % prone to gout.
Q: Acute gout attack occurs when?
MSU crystal comes in particular joint space
Release of pro inflammatory mediator’s TNF and IL-1 IL-8
Phagocytosis of MSU crystal by neutrophils
Gout is characterized by?
Severe pain and inflammation
What are the side effects of NSAIDs?
(Formula GIMIRI)
GI bleeding
MI Myocardial infection
RI Renal impairment
Q: Gout is usually a mono or poly articular disease?
Mono articular disease
because we have seen that this disease 90% occur in Metatarsophalangeal joint.
Side effects of Colchicine?
Its Therapeutic index is very narrow
Colchicine early toxicity is, GI toxicity like Nausea, vomiting, pain, diarrhoea.
Cardiac damage, corneal ulcer, Vit B12 absorption decreases
Colchicine drug interaction?
This drug is metabolised by CYP450 & 3A4 & P-gp
They interact with azole, statin, Macrolides grapefruits as a result the level of colchicine will increase in the blood serum and will cause toxicity. Refer to hospital immediately.
Colchicine can be toxic with camotherapeutic agent it gives?
Additive effects on cell division
What is the mechanism of Glucocoticosteroids?
It decreases arachidonic acid formation by inhibiting Phospholipase A2 resulting decreased prostaglandin synthesis. Decrease transcription of pro-inflammatory genes result decreased production of cytokines reduces inflammation
Side effects of Glucocorticoids?
Osteoporosis may develop with long term use of glucocorticoids.
Cardiovascular risk
GI bleeding
Infection
What is the Long-term prevention of GOUT or urate lowering therapy?
- Xantine-Oxidase inhibitors i.e.: allopurinol, Febuxostat
2. Uricosurics i.e. probenecid
The primary site of reabsorption of uric acid in our kidney is?
URAT1 if we block this than uric acid reabsorption will decrease, and excretion will increase.
Which criteria will make a patient to take urate lowering therapy?
If it causes more than 2 gout attacks in a year.
Chronic kidney disease
If Tophi appears (Deposition of uric crystal)
Urolithiasis (kidney stone)
What is your target Uric acid level in blood if you start ULT?
So, when we start ULT therapy our target serum uric acid level is Less than 0.36 mmol/L when tophi are present.
What is Allopurinol?
Xanthine oxidase inhibitor
Start with a low dose as it might leads to Allopurinol hypersensitivity syndrome
To check Allopurinol hypersensitivity syndrome a test is required that is?
HLA-B 5801
What is Allopurinol hypersensitivity syndrome?
It is called DRESS =Drug Rash Eosinophilia and Systemic Symptoms
So, the symptoms are: Rash, Fever, Eosinophilia etc
Around 25% who develop DRESS die
DRESS may start withing 2-6 weeks after taking allopurinol so strict monitoring is required for this treatment.
So, allopurinol treatment is not recommended for Asymptomatic GOUT until it reaches last stage of the crystallisation.
What is Febuxostat?
Second line xanthine oxidase inhibitor
What are the side effects of Febuxostat?
Serious hypersensitivity reaction
Stevens Johnson syndrome
Cardiovascular effects
