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What is Arthritis?
 There are 127 different kinds of
arthritis!
 Rheumatoid arthritis: Severe
inflammation that involves many
joints and moves beyond
musculoskeletal system.
 Gout: Very painful form of arthritis
characterized by the formation of uric
acid crystals and severe inflammation.
 Osteoarthritis: progressive
degeneration of joint cartilage. Minor
degree of inflammation.
GOUT
• Gout is a metabolic disorder of purine
metabolism, characterized by intermittent
attacks of acute pain, swelling and
inflammation.
• It always preceded by hyperuricaemia
Hyper uricaemia 6.8mg/dl
• Excessive amount of uric acid production
• Decreased excretion
• Or both
• Primary Hyperuricemia and
Gout
• Uricacid under excretion 80–90%
• Urate over production (10–20%)
• Purine intake shell fish , Red
meat
• Idiopathic
• PRPP synthetase over activity
Secondary Hyperuricemia and Gout
Identifiable Associated Condition
• develop during course of other diseases
(lymphomas, chemotherapy, CKD) cell death
• Some drug therapy (Thiazide diuretics,
furosamide, ethacrynic acid, Aspirin)
• Some disorders Diabetic ketoacidosis, lead
poison, Lymphoproliferative
diseases, Hemolytic anemias, psoriasis
• Dual mechanism
Obesity and hypo perfusion to joint
Uric acid production and excretion
RNA,DNA
PURINES
HYPOXANTHINES
XANTHINES
URIC ACID (low water soluble)
Uric acid freely filtrated through by glomerulus and
reabsorbed by tubular fluid
Xanthine oxidase
Xanthine oxidase
Probencid
PRPP
Hyperuricemia Gout Deposits of urate crystal
Gout
Pathophysiology of gout
Uricacid
Blood
React with sodium
Sodium crystals (tophi)
Deposited in soft tissues and joints
Inflammation(ry)
Infiltration of granulocytes that phagocytise the urate crystals
Generate free radicals
Free radical damage the tissue
Release of proteolytic enzyme glycoprotein
Release of lactic acid
More ppt of urate crystals
Indomethacin
Colchicine
Colchicine
ColchicineRelease of lysosomal enzymes
Destruction of joints
Symptoms
• Acute joint pain
• Swelling in the joints
• Skin may be in red colour and shiny appearance
• Formation of tyophi
Cause and risk factors
• Hereditary factors 40-50 age
• Consumption of alcohol spe..Beer
• Excessive consumption of red meat, internal organs
• Trauma to joints
Diagnosis
• Joint fluid aspiration
• Blood test (Serum uric acid levels)
• X-rays
Acute gout
• Painful arthritic attack of sudden onset.
• Usually occurring at night or in early morning
• Arthritic pain worsen progressively
• Generally involves one or few joints
• Most common site of initial attack metatarsophalangeal
joint.
• Other sites ankle, heel, knee, wrist, elbow and fingers.
Chronic gout
• Frequency of attacks increases, continuous
deposit leads to damage joints and chronic pain
• Patients may develop large subacutenous tophi (Stones)
in pinna of external ear, eyelids, nose and around joints
• The ureate crystals in kidney leads renal disease.
• Articular cartilage may be destroyed result in joint
deformities
GOUT - TREATMENT
1. terminate acute attack
2. provide rapid, safe pain/anti-inflammatory relief
3. prevent complications
• destructive arthropathy
• tophi
• renal stones
GOALS:
Classification of drugs used in gout CAPS
ACUTE GOUT :
1. Colchicine
2. Corticosteroids
3. NSAIDS
CHRONIC GOUT:
• Inhibit uric acid synthesis:- Allopurinol, febuxostate
(Urostatic)
• Increase uric acid excretion:- Probencid, Sulphinpyrazole
(Urosuric)
Colchicine
• Alkaloid from colchium autumnale. (1973)
• Neither analgesic nor anti inflammatory, but specific
for gouty inflammation.
• It is only effective in prophylaxis of acute gout
• It has no effect on synthesis or promote excretion
• MOA
• Colchicine binds to intracellular protein ‘Tubulin’ and
causes depolymerisation and disappearance of
microtubules in granulocytes & Inhibit granulocyte
migration so dec phagocytic activity
• Colchicine inhibit glycoprotein release
– Other actions-
- arrest of mitosis in metaphase “spindle poison”
- increases gut motility.
- Antipyretic , respiratory depressant
- Inhibit histamine , Insulin release
- hypertensive at high dose, Increase vasomotor tone
Uses
 Colchicine preferred in pts without confirmed diagnosis of
gout.
 Acute gout-1mg orally followed by 0.25 mg 3 hrly till control.
 EHC 3-7days
 With safer alternatives NSAIDs use of Colchicine have declined
ADR:- diarrhoea, vomiting, abdominal pain.
 Acute toxicity - bloody diarrhoea, throat pain, respiratory
depression, haematuria.
 Chornic toxicity- agranulocytosis, peripheral neuritis and
myopathy, renal tubular necrosis.
NSAIDs
• Strong anti inflammatory drugs
• Use in patients without contraindication
• Use maximum dose/potent NSAID
e.g., Indomethacin 50 mg po t.i.d.
Diclofenac 50 mg po t.i.d.
Ketorolac 10 mg q4-6hrsr,
Napoxen, Piroxicam
• continue until pain/inflammation absent for 48 hours
• MOA: inhibit urate crystal phagocytosis and chemotatic
migration of leukocytes into inflammed joints.
• NSAIDs are not recommended for long term.
• (Salicylates are not used , have tendency to raise uric acid)
Corticosteroid
Use when NSAIDS/Cholchicine risky or contraindicated
e.g.,: elderly
hypertensive
peptic ulcer disease
renal impairment
liver impairment
use when • NSAIDS ineffective
Mode of administration –
• intra articular - Depomedrol 40-80 mg with lidocaine.
• Oral Prednisone 30-40 mg qd for 3-4 days, taper by 5 mg
every 2-3 days & stop over 1-2 wks
Drugs for chronic gout
• Uric acid synthesis inhibitors:- Allopurinol
(Xanthine oxidase inhibitor)
• Hypoxanthine Xanthine Uric acid
Xanthine oxidase
-
Allopurinol
• Allopurinol prevents the synthesis of uric acid
by inhibiting the enzyme Xanthine oxidase,
result reduce plasma ureate levels.
• Inc. xanthine, hypoxanthines are excreted
through urine
• Allopurinol short acting competitive inhibitor
• Metabolite alloxanthine is long acting t1/2 24hr.
• Start low 50-100 mg qd
• Increase by 50-100mg every 2-3 weeks according to
symptoms
– “Average” dose 300 mg daily
– lower dose if renal/hepatic insufficiency
– higher dose in non-responders
– prophylactic colchicine until allopurinol dose stable
• Indications:
• Chronic gout
• In patients 24 hrs urinary acid excretion exceeds 1.1g
• For recurrent renal ureate stones.
Allopurinol side effects
• GI upset, alopecia, cataract.
• Allopurinol Hypersensitivity:
Pruritic papular skin rash, fever, hepatitis,
eosinophilia, renal impairment
• CI:-
– Chidrens
– Elderly patients
– Pregnancy
– Lactation
– Liver and kidney diseases.
Allopurinol drug interactions
• Allopurinol prolong ½ life of Vidarabine, Cyclosporin
drugs and increase toxicity
• Dec. metabolism of 6-mercaptopurine, Azothiaprine
inc. its effects.
• Interferes with the mobilization of hepatic iron stores -
heamtonic should be avoided during allopurinol
therapy.
Uricosuric drugs: (probencid)
•Highly lipid soluble benzoic acid.
•It blocks reabsorption of urate in proximal tubule by
blocking transport (Bidirectional transport)
•PK: Dose dependent t1/2 life
•Dose -250- 500mg b.d. with plenty of fluids, alkalinization
of urine.
Uses :
chronic gout along with NSAIDs / colchicine for
initial 1-2 months.
Sulfinpyrazone
• It is a Pyrazolone derivaties related to
Phenylbutazone.
• Inhibits tubular reabsorption of uric acid at
therapeutic doses.
• Its action is additive with probenecid.
• Use -chronic gout
• Dose :100-200mg BD gradually increase
according to the response.
• It is newer and more potent uricosuric drug
• Used in patients allergic to probenecid or sulfinpyrazone
• It is reversible inhibitor of tubuler reabsorption
• Effective dose 60-80mg/day
• With allopurinol more effective
Benzbromarone
• A 56yrs old male awake in the night with sudden
severe pain in his first metatarsophalangeal joint
which lasted for a week. Over the next few months,
he had similar acute episode of pain in his ankles and
knees, as well as his big toe. The GP suspected gout
and referred him to specialist
• What treatment should be GP institute for the
acute attacks prior to the specialist diagnosis?
• what test could the rheumatologist do to
confirm the suspected diagnosis?
• What is the cause of gout?
• Which drugs act for acute attacks?
• What would you prescribe for prophylaxis to
reduce recurrent attacks ?
360umol/L or 6mg/dl

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AUTONOMIC NERVOUS SYSTEM organization and functions
 

Gout

  • 1. 1 What is Arthritis?  There are 127 different kinds of arthritis!  Rheumatoid arthritis: Severe inflammation that involves many joints and moves beyond musculoskeletal system.  Gout: Very painful form of arthritis characterized by the formation of uric acid crystals and severe inflammation.  Osteoarthritis: progressive degeneration of joint cartilage. Minor degree of inflammation.
  • 3. • Gout is a metabolic disorder of purine metabolism, characterized by intermittent attacks of acute pain, swelling and inflammation. • It always preceded by hyperuricaemia
  • 4. Hyper uricaemia 6.8mg/dl • Excessive amount of uric acid production • Decreased excretion • Or both
  • 5. • Primary Hyperuricemia and Gout • Uricacid under excretion 80–90% • Urate over production (10–20%) • Purine intake shell fish , Red meat • Idiopathic • PRPP synthetase over activity Secondary Hyperuricemia and Gout Identifiable Associated Condition • develop during course of other diseases (lymphomas, chemotherapy, CKD) cell death • Some drug therapy (Thiazide diuretics, furosamide, ethacrynic acid, Aspirin) • Some disorders Diabetic ketoacidosis, lead poison, Lymphoproliferative diseases, Hemolytic anemias, psoriasis • Dual mechanism Obesity and hypo perfusion to joint
  • 6. Uric acid production and excretion RNA,DNA PURINES HYPOXANTHINES XANTHINES URIC ACID (low water soluble) Uric acid freely filtrated through by glomerulus and reabsorbed by tubular fluid Xanthine oxidase Xanthine oxidase Probencid PRPP Hyperuricemia Gout Deposits of urate crystal
  • 8. Pathophysiology of gout Uricacid Blood React with sodium Sodium crystals (tophi) Deposited in soft tissues and joints Inflammation(ry) Infiltration of granulocytes that phagocytise the urate crystals Generate free radicals Free radical damage the tissue Release of proteolytic enzyme glycoprotein Release of lactic acid More ppt of urate crystals Indomethacin Colchicine Colchicine ColchicineRelease of lysosomal enzymes Destruction of joints
  • 9. Symptoms • Acute joint pain • Swelling in the joints • Skin may be in red colour and shiny appearance • Formation of tyophi
  • 10. Cause and risk factors • Hereditary factors 40-50 age • Consumption of alcohol spe..Beer • Excessive consumption of red meat, internal organs • Trauma to joints
  • 11. Diagnosis • Joint fluid aspiration • Blood test (Serum uric acid levels) • X-rays
  • 12. Acute gout • Painful arthritic attack of sudden onset. • Usually occurring at night or in early morning • Arthritic pain worsen progressively • Generally involves one or few joints • Most common site of initial attack metatarsophalangeal joint. • Other sites ankle, heel, knee, wrist, elbow and fingers.
  • 13. Chronic gout • Frequency of attacks increases, continuous deposit leads to damage joints and chronic pain • Patients may develop large subacutenous tophi (Stones) in pinna of external ear, eyelids, nose and around joints • The ureate crystals in kidney leads renal disease. • Articular cartilage may be destroyed result in joint deformities
  • 14. GOUT - TREATMENT 1. terminate acute attack 2. provide rapid, safe pain/anti-inflammatory relief 3. prevent complications • destructive arthropathy • tophi • renal stones GOALS:
  • 15. Classification of drugs used in gout CAPS ACUTE GOUT : 1. Colchicine 2. Corticosteroids 3. NSAIDS CHRONIC GOUT: • Inhibit uric acid synthesis:- Allopurinol, febuxostate (Urostatic) • Increase uric acid excretion:- Probencid, Sulphinpyrazole (Urosuric)
  • 16. Colchicine • Alkaloid from colchium autumnale. (1973) • Neither analgesic nor anti inflammatory, but specific for gouty inflammation. • It is only effective in prophylaxis of acute gout • It has no effect on synthesis or promote excretion • MOA • Colchicine binds to intracellular protein ‘Tubulin’ and causes depolymerisation and disappearance of microtubules in granulocytes & Inhibit granulocyte migration so dec phagocytic activity
  • 17. • Colchicine inhibit glycoprotein release – Other actions- - arrest of mitosis in metaphase “spindle poison” - increases gut motility. - Antipyretic , respiratory depressant - Inhibit histamine , Insulin release - hypertensive at high dose, Increase vasomotor tone
  • 18. Uses  Colchicine preferred in pts without confirmed diagnosis of gout.  Acute gout-1mg orally followed by 0.25 mg 3 hrly till control.  EHC 3-7days  With safer alternatives NSAIDs use of Colchicine have declined ADR:- diarrhoea, vomiting, abdominal pain.  Acute toxicity - bloody diarrhoea, throat pain, respiratory depression, haematuria.  Chornic toxicity- agranulocytosis, peripheral neuritis and myopathy, renal tubular necrosis.
  • 19. NSAIDs • Strong anti inflammatory drugs • Use in patients without contraindication • Use maximum dose/potent NSAID e.g., Indomethacin 50 mg po t.i.d. Diclofenac 50 mg po t.i.d. Ketorolac 10 mg q4-6hrsr, Napoxen, Piroxicam • continue until pain/inflammation absent for 48 hours • MOA: inhibit urate crystal phagocytosis and chemotatic migration of leukocytes into inflammed joints. • NSAIDs are not recommended for long term. • (Salicylates are not used , have tendency to raise uric acid)
  • 20. Corticosteroid Use when NSAIDS/Cholchicine risky or contraindicated e.g.,: elderly hypertensive peptic ulcer disease renal impairment liver impairment use when • NSAIDS ineffective Mode of administration – • intra articular - Depomedrol 40-80 mg with lidocaine. • Oral Prednisone 30-40 mg qd for 3-4 days, taper by 5 mg every 2-3 days & stop over 1-2 wks
  • 21. Drugs for chronic gout • Uric acid synthesis inhibitors:- Allopurinol (Xanthine oxidase inhibitor) • Hypoxanthine Xanthine Uric acid Xanthine oxidase - Allopurinol
  • 22. • Allopurinol prevents the synthesis of uric acid by inhibiting the enzyme Xanthine oxidase, result reduce plasma ureate levels. • Inc. xanthine, hypoxanthines are excreted through urine • Allopurinol short acting competitive inhibitor • Metabolite alloxanthine is long acting t1/2 24hr.
  • 23. • Start low 50-100 mg qd • Increase by 50-100mg every 2-3 weeks according to symptoms – “Average” dose 300 mg daily – lower dose if renal/hepatic insufficiency – higher dose in non-responders – prophylactic colchicine until allopurinol dose stable • Indications: • Chronic gout • In patients 24 hrs urinary acid excretion exceeds 1.1g • For recurrent renal ureate stones.
  • 24. Allopurinol side effects • GI upset, alopecia, cataract. • Allopurinol Hypersensitivity: Pruritic papular skin rash, fever, hepatitis, eosinophilia, renal impairment • CI:- – Chidrens – Elderly patients – Pregnancy – Lactation – Liver and kidney diseases.
  • 25. Allopurinol drug interactions • Allopurinol prolong ½ life of Vidarabine, Cyclosporin drugs and increase toxicity • Dec. metabolism of 6-mercaptopurine, Azothiaprine inc. its effects. • Interferes with the mobilization of hepatic iron stores - heamtonic should be avoided during allopurinol therapy.
  • 26. Uricosuric drugs: (probencid) •Highly lipid soluble benzoic acid. •It blocks reabsorption of urate in proximal tubule by blocking transport (Bidirectional transport) •PK: Dose dependent t1/2 life •Dose -250- 500mg b.d. with plenty of fluids, alkalinization of urine. Uses : chronic gout along with NSAIDs / colchicine for initial 1-2 months.
  • 27. Sulfinpyrazone • It is a Pyrazolone derivaties related to Phenylbutazone. • Inhibits tubular reabsorption of uric acid at therapeutic doses. • Its action is additive with probenecid. • Use -chronic gout • Dose :100-200mg BD gradually increase according to the response.
  • 28. • It is newer and more potent uricosuric drug • Used in patients allergic to probenecid or sulfinpyrazone • It is reversible inhibitor of tubuler reabsorption • Effective dose 60-80mg/day • With allopurinol more effective Benzbromarone
  • 29. • A 56yrs old male awake in the night with sudden severe pain in his first metatarsophalangeal joint which lasted for a week. Over the next few months, he had similar acute episode of pain in his ankles and knees, as well as his big toe. The GP suspected gout and referred him to specialist • What treatment should be GP institute for the acute attacks prior to the specialist diagnosis?
  • 30. • what test could the rheumatologist do to confirm the suspected diagnosis? • What is the cause of gout? • Which drugs act for acute attacks? • What would you prescribe for prophylaxis to reduce recurrent attacks ?