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Stage 3 - Case 3 (Musculoskeletal) > Lecture 2 & 3: Pathophysiology and Pharmaceutical Care of Hyperuricaemia and Gout > Flashcards

Lecture 2 & 3: Pathophysiology and Pharmaceutical Care of Hyperuricaemia and Gout Flashcards

1
Q

What is Hyperuricaemia and what can cause this?

A
  • Elevated uric acid levels. Purines breakdown into uric acid
  • Due to increased purine breakdown from diet and impaired excretion from kidneys
  • Diuretics (compensation mechanism) and low-dose aspirin can increase uric acid levels
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2
Q

What is gout?

A
  • Form of inflammatory arthritis
  • Crystal arthropathy (joint disease)
    Deposition of monosodium crystals in joints and tissues which causes joint pain and swelling
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3
Q

What are the most common areas for gout?

A
  • Metatarso-phalangeal joint of big toe
  • Fingers, toes, ankles, wrists
  • Metatarsi in foot, meta carpals in hands
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4
Q

How does a lack of uricase lead to gout?

A
  • Uricase converts uric acid into allantoin which is more soluble and excretable
  • Uric acid is a weak acid and is urate at physiological pH
    More urate = risk of gout
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5
Q

What are the mechanisms of hyperuricaemia?

A
  • Overproduction of urate through purine degradation
  • Under excretion of urate
  • Urate transportasomes in proximal tubules -> reuptake transporters of urate through urine
  • Variants in multi-drug transporters which blocks excretion
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6
Q

What are the factors that cause precipitation of urate into joints?

A
  • Low temperature: reduced solubility
  • lower pH
  • Cation concentration: Na+ combined cause crystals to form, K+ as well but they are more soluble
  • Articular dehydration: Less fluid concentrates urate ions = formation
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7
Q

What is the pathogenesis of acute gout?

A
  • MSU crystals formed by hyperuricaemia
  • Recognised by phagocytes and are ingested
  • Causes Na+ conc in phagocytes to increase cause they are in the crystals
  • Hyperosmolarity causes water influx (compensation) - swelling
  • Causes K+ efflux = less
  • K+ too low which induces inflammasome production (NLRP3) of Il-. Inflammation process, neutrophil recruitment. Requires 2nd signal through toll-like receptors which activate inflammasome - Acute gout (resolves quickly)
  • Flare resolution involves neutrophil extracellular trap (NET) which binds to MSU crystals
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8
Q

What is the cycle of gout?

A
  • Inflammasome activation phase
  • Amplification phase: Tissue damage, mediators, prostaglandins
  • Resolution: -> Pain and swelling Subsides
    Intercritical Gout (quiscent phase): After resolution there is a period of remission (asymptomatic)
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9
Q

What is the difference between primary and sceondary gout?

A
  • Primary: Triggers arent identifiable, caused by intrinsic factors: genetic abnormality, hormones. Cause isnt known
  • Secondary: Develops from disorder (renal failure) or consequence of drug.
  • Diuretics and low dose aspirin = inc urate. Vit D and ascorbic acid = decr urate
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10
Q

What are some characteristics of gouty arthritis?

A
  • Hot swollen and painful distal joints
  • Sudden onset
  • Usually mono-articular
  • Recurrent episodes
  • Chronic gout: subcutaneous gouty tophi: skin nodules of deposited crystals in hands, elbow, ears. Swollen
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11
Q

What are some risk factors for gout?

A
  • Middle aged men
  • Obesity
  • Genetic
  • Conditions: Diabetes, hypertension
  • Certain meds
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12
Q

What are some environmental causes of gout?

A
  • Diet: Purine diet
  • Alcohol: Causes uric acid increase by net ATP degradation to AMP, Urinary excretion decreased from dehydration and metabolic acidosis
  • Adiposity and Insulin resistance: Obesity, Insulin causes decreased renal excretion of urate
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13
Q

What is the natural cause of Gout?

A
  • Genetic risk of hyperuricaemia
  • Polymorphisms in GLUT9 gene (renal urate transporter) and URAT1 (regulates blood urate levels)
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14
Q

What are some questions that need to be asked on consultation about Gout?

A
  • Symptoms (hot?, swollen?), severity, onset
  • Any injury or recent infection
  • Have you tried anything?
  • Frequency and duration of attacks?
  • Co-morbidities
  • Diet
  • Impact and Family history
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15
Q

What symptoms suggest of gout and what test should be done?

A
  • Rapid onset with redness and swelling
  • Normally found in 1 or 2 metatarsophalangeal joints
  • Tophi
  • Serum urate levels tested. Over 360 = diagnose
  • Can do joint aspiration, microscopy
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16
Q

What is Podagra?

A
  • Podagra is a type of gout that causes pain and inflammation in the big toe joint.
  • Also seen in pseudogout, psoriatic arthritis and reactive arthritis
17
Q

What are some differential diagnosis for gout?

A
  • Osteoarthritis: weakening of tissues of joints. Worn away
  • Pseudogout: accumulation of calcium pyrophosphate dihydrate crystals in the joints. Trigger inflammation, pain, swelling
  • Bursitis: inflammation of bursur, fluid filles sac around knee
  • RA: Chronic autoimmune. Fighting own cells
  • Psoriatic arthritis: Arthritis that damages skin
  • Septic arthritis: Unwell w/ swollen joint. Usually from surgery or trauma + can be fatal
18
Q

What are the 3 phases of gout?

A
    1. First attack aymptomatic hyperuricameia
    1. Acute attacks with intervals (recurrent)
    1. Chronic tophaceus gout
19
Q

What are the differences between gout and pseudogout?

A
  • Pain: G: Severe, P: Moderate
  • Sites: G: small joints, P: large joints (knee)
  • Age: G: 40yro, P: Elderly
  • Crystal deposition: G: Uric acid, P: Calcium pyrophosphate
    Treatment: G: NSAIDs, allipurinol. P: Joint aspiration, NSAIDs
20
Q

What are some non-pharmacological management strategies for Gout?

A
  • Attack: Rest and ice
  • Review meds: diuretics
    Prevention: Hydration (avoid kidney stones), address obesity and manage diabetes, alcohol and diet
21
Q

What are some pharmacological management strategies for gout?

A
  • Colchicine
  • NSAIDs
  • IV Uricase
  • Xanthine Oxidase Inhibitors
  • Steroid Injections
  • New: Biologics (Canakinumab)
22
Q

What is Colchicine used for and what does it do?

A
  • Prevention (prophylaxis) of gout used in initiation of urate lowering therapy
  • Reduces frequency and severity and has narrow therapeutic index. Interacts w/ CYP450 (dose changes)
  • Inhibits recruitment of neutrophils and pro-inflammatory TNFa. Inhibits chemotaxin production (not analgesic)
  • Main risk: Blood disorders (anemia) refer. Also affects GI
23
Q

?

A
24
Q

Name some Xanthine Oxidase inhibitors?

A
  • Allopurinol
  • Febuxostat
25
Q

What does Allopurinol do and how does it help?

A
  • Purine->Hypoxanthine->Xanthine->Uric acid
  • Inhibits last 2 conversions
  • Lowers serum uric acid
  • Can cause GI upset and hypersensitivity
26
Q

What are the differences between allopurinol and febuxostat?

A
  • Unlike allopurinol it isnt a purine analogue
  • slightly higher risk of cardiovascular events
  • Not recommended for acute gout attacks

Stage 3 - Case 3 (Musculoskeletal) (4 decks)

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