Lecture 98 - Gout and other mineral deposits Flashcards

1
Q

what is gout

what is the precursor

A

chronic inflammatory arthritis that results from monosodium urate (MSU) crystal deposition in tissues or joints resulting from supersaturation of uric acid in extracellular fluids

Precursor: Hyperuricemia –

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2
Q

what is gout

what is the precursor

A

chronic inflammatory arthritis that results from monosodium urate (MSU) crystal deposition in tissues or joints resulting from supersaturation of uric acid in extracellular fluids

Precursor: Hyperuricemia –

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3
Q

Causes of hyerpuricemia:

A

Decreased Uric Acid Excretion through the kidey

Increased Uric Acid Production

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4
Q

what can lead to increased uric acid production

A

Tumor lysis syndrome, Luekmia, myeloproliferation

Lesch Nyan Syndrome

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5
Q

Risk factors for Gout:

modifiable (drugs, lifetyle, Comorbidities)
non modifiable

A

Age – older men
Meds – Thiazides, furosemide, low dose ASA, Cyclsporin

Life style –obesity,, high meat diet, binge drinking

Comorbdities – HTN, CVD, DM, CKD, HLD

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6
Q

Per lecture – describe the pathogenesis of gout

A

Uric Acid Burden - Super saturation –> Crystals –> Deposition into tissues –> Bound by Antibodies + Phagocytosis of PMNs –> Inflammatory Mediators (IL-1, IL-6, TNF) –> ROS, Complemen t

The inflammasome

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7
Q

what are the 4 stages of gout

A

asymptomatic hyperuricemia

Acute intermittent Gout – acute flair – Rapid onset and monoarticular

Inter-critical gout – asymptomatic between flaires, but uric acid crystals still present in the joint –> chronic low grade inflammation –>high risk of attacks and thopi

advanced gout – lng standing gout; intercritical periods are no long pain free

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8
Q

eval of synovial fluid under polarized light =

what other tests of the synovial fluid should be run to rule out disease proceses

A

Intracelluar Needle Shaped Rods with Negative Biferengence under polarized light (yellow under parallel light, blue under perpendicular)

– also do gram stain to check for prescence of bacteria;
DDx - septic arthritis

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9
Q

classical radiographic finding of advanced gout

A

Rat bite

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10
Q

Clinical manifestations of gout

A

Gouty Arthritis – recurrent attacks of articular and periarticular inflammation
Tophus – Accumulation of MSU deposits in joints, bones, soft tissue
Gout Nephrolithiasis – uric acid calculi
Gout Nephropathy –

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11
Q

what drugs/exposures also known to cause gout

A

Cyclosporin– can interfere with uric acid exceretion

Lead Poisoning
Moonshine /
Occupational – Painter, Plumber, Pipefitters, mechanics, battery, steel workers

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12
Q

what is the goal level of uric acid in the serum?

A
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13
Q

treatments for acute gout

A

NSAIDs – first line for attacks,
Colchicine
Il-1RA = Anakinra (Kineret)

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14
Q

treatment for chronic gout

A

Colchicine
Allopurinol
Febuxostat
Probenacid

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15
Q

Mechanism of Colchicine

A

Microtubulin formation inhibition

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16
Q

mechanism of allopurinol and febuxostat

contraindicated with what drugs

side effects of each

A

Xanthine Oxidase inhibitin – prevents formation of Uric acid

ccontraindicated with Azathriprine and 6MP which require XO for metabolsim

Allopurinol –
DRESS SYNDROME – Drug Rxn, Eosino, Systemic Symptoms
Hypersensitivity, Steven Johnson Syndrome,

Febuxostat – Hepatic impairment

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17
Q

maintenacne therapy for Gout

what is the mechanism

A

Pegloticase –

Facilitates the conversion of Uric acid to Allantoin (water soluble and renally excreted)

18
Q

what joint is classically affected with Gout

A

MTP of the big toe – (podagra)

19
Q

what is pseudogout

A

Calcium Pyrophosphate Dihydrate Deposition Disease (CPPD)

20
Q

what is pseudogout

what joints are affected?

what is seen under polarized light

what might been seen on imaging?

Treatment:

A

Calcium Pyrophosphate Dihydrate Deposition Disease (CPPD)

Joints – Knee, Wrist, Pubis, hip,

Polarized light: weakly birefringement (blue when parallel); rhomboid shaped

Imaging: chondrocalcinosis

Treat: NSAIDs, colchicine, STeroids

21
Q

Milwaukee Shoulder Syndrome –

what is the crystal deposition?
who does it effect?
what is seen on imaging?

A

deposition of Hydroxyapatite Crystals leading to activation of enzymse that lead to joint destruction

women of 5th-6th decade

XR erosion of humoral head, cartilage, capsule, bursae

22
Q

Causes of hyerpuricemia:

A

Decreased Uric Acid Excretion through the kidey

Increased Uric Acid Production

23
Q

what can lead to increased uric acid production

A

Tumor lysis syndrome, Luekmia, myeloproliferation

Lesch Nyan Syndrome

24
Q

Risk factors for Gout:

modifiable (drugs, lifetyle, Comorbidities)
non modifiable

A

Age – older men
Meds – Thiazides, furosemide, low dose ASA, Cyclsporin

Life style –obesity,, high meat diet, binge drinking

Comorbdities – HTN, CVD, DM, CKD, HLD

25
Q

Per lecture – describe the pathogenesis of gout

A

Uric Acid Burden - Super saturation –> Crystals –> Deposition into tissues –> Bound by Antibodies + Phagocytosis of PMNs –> Inflammatory Mediators (IL-1, IL-6, TNF) –> ROS, Complemen t

The inflammasome

26
Q

what are the 4 stages of gout

A

asymptomatic hyperuricemia

Acute intermittent Gout – acute flair – Rapid onset and monoarticular

Inter-critical gout – asymptomatic between flaires, but uric acid crystals still present in the joint –> chronic low grade inflammation –>high risk of attacks and thopi

advanced gout – lng standing gout; intercritical periods are no long pain free

27
Q

eval of synovial fluid under polarized light =

what other tests of the synovial fluid should be run to rule out disease proceses

A

Intracelluar Needle Shaped Rods with Negative Biferengence under polarized light (yellow under parallel light, blue under perpendicular)

– also do gram stain to check for prescence of bacteria;
DDx - septic arthritis

28
Q

classical radiographic finding of advanced gout

A

Rat bite

29
Q

Clinical manifestations of gout

A

Gouty Arthritis – recurrent attacks of articular and periarticular inflammation
Tophus – Accumulation of MSU deposits in joints, bones, soft tissue
Gout Nephrolithiasis – uric acid calculi
Gout Nephropathy –

30
Q

what drugs/exposures also known to cause gout

A

Cyclosporin– can interfere with uric acid exceretion

Lead Poisoning
Moonshine /
Occupational – Painter, Plumber, Pipefitters, mechanics, battery, steel workers

31
Q

what is the goal level of uric acid in the serum?

A

goal level is

32
Q

treatments for acute gout

A

NSAIDs – first line for attacks,
Colchicine
Il-1RA = Anakinra (Kineret)

33
Q

treatment for chronic gout

A

Colchicine
Allopurinol
Febuxostat
Probenacid

34
Q

Mechanism of Colchicine

A

Microtubulin formation inhibition

35
Q

mechanism of allopurinol and febuxostat

contraindicated with what drugs

side effects of each

A

Xanthine Oxidase inhibitin – prevents formation of Uric acid

ccontraindicated with Azathriprine and 6MP which require XO for metabolsim

Allopurinol –
DRESS SYNDROME – Drug Rxn, Eosino, Systemic Symptoms
Hypersensitivity, Steven Johnson Syndrome,

Febuxostat – Hepatic impairment

36
Q

maintenacne therapy for Gout

what is the mechanism

A

Pegloticase –

Facilitates the conversion of Uric acid to Allantoin (water soluble and renally excreted)

37
Q

what joint is classically affected with Gout

A

MTP of the big toe – (podagra)

38
Q

what is pseudogout

A

Calcium Pyrophosphate Dihydrate Deposition Disease (CPPD)

39
Q

what is pseudogout

what joints are affected?

what is seen under polarized light

what might been seen on imaging?

Treatment:

A

Calcium Pyrophosphate Dihydrate Deposition Disease (CPPD)

Joints – Knee, Wrist, Pubis, hip,

Polarized light: weakly birefringement (blue when parallel); rhomboid shaped

Imaging: chondrocalcinosis

Treat: NSAIDs, colchicine, STeroids

40
Q

Milwaukee Shoulder Syndrome –

what is the crystal deposition?
who does it effect?
what is seen on imaging?

A

deposition of Hydroxyapatite Crystals leading to activation of enzymse that lead to joint destruction

women of 5th-6th decade

XR erosion of humoral head, cartilage, capsule, bursae