Path 7 Flashcards by Justyna Gromala

What crystals are seen in gout and pseudogout and how are they under polarised light?

Gout: needle shaped (MSU - monosodium urate crystals) negative birefringence

Pseudogout: rhomboid shaped calcium pyrophosphate crystals) positive birefringence

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rat bite erosions on x-ray

gout

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What do you see on x-ray in gout?

rat bite erosions

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What do you see on xray in pseudogout?

white lines of chondrocalcinosis

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white lines of chondrocalcinosis on xray - diagnosis?

pseudogout

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What is the management of gout acutely and long term?>

acute: colchicine, NSAIDs

long term: allopurinol

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What group of conditions do gout and pseudogout belong to?

inflammatory crystal arthropathy

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What groups of people are affected by gout and pseudogout?

gout: obese, middle aged men

pseudogout: >50yo women

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What monoclonal antibody can be used in the management of gout?

IL-1 blockade

do not prescribe routinely, are prescribed by rheumatologists

can be used to treat acute gout flares in patients if NSAIDs and colchicine are contraindicted, not tolerated or ineffective.

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management of gout - acute flare and long term

acute: colchicine and NSAID (+ice pack cooling, +/- PPI)
intramuscular or intraarticular steroid injectoins can also be considered. IL-1 blockade can also be considered.

chronic: allopurinol (urate lowering therapy, XO inhibitor); probenecid is second line (inhibits uric acid reabsorption along the renal tubules)

conservative measures: decrease alcohol intake and purine intake (e.g. in sardines, liver, port wine); weight loss if overweight. sufficient fluid intake is recommended.

review medications in case something is causing it.

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MoA of probenecid

inhibits uric acid reabsorption along the renal tubules and therefore decreases uric acid levels and can be used as urate lowering therapy in the long term management of gout

increases fractional excretion of uric acid

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Why should you administer anti-inflammatory prophylaxis before initiating ULT (urate lowering therapy?

because ULT may trigger, prolong or worsen an acute flare. this is because it causes preexisting urate crystal deposits to dissolve and become mobile

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MoA of colchicine

inhibits polymerization of tubulin to reduce motility of neutrophils

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types of presentation in gout

acute monoarthritis
chronic tophaceous gout (polyarticular arthritis, tophi deposits behind ear lobes, fingers and elbows, urate kidney stones)

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Aetiology of gout

hyperuricaemia due to
- increased intake (e.g. alcohol)
- increased production (e.g. TLS, inherited metabolic abnormalities)
- decreased excretion (e.g. diuretics)

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What is the aetiology of pseudogout?

idiopathic
electrolytes (hyperPTH, hypoPO4, hypoMg)
metabolic (DM, hypothyroid, Wilson’s, haemochromatosis)

What joints are affected in pseudogout?

knee
wrist

shoulder
can also affect hips, ankles

How does pseudogout present?

hot, swollen joint with effusion

chondrocalcinosis on X-ray

What is the management of pseudogout?

NSAIDs or intraarticular steroids

What are the features seen on X-ray in OA?

Loss of joint spaces
Osteophytes
Subchondral cysts
Subchondral sclerosis

Which joints are affected by osteoarthritis?

vertebrae
hips
knees

hand features in OA

heberden’s nodes (DIPJ)
bouchards nodes (PIPJ)

Heberdens and Bouchards nodes - where found?

Heberden’s - DIPJ

Bouchard’s - PIPJ

What are the steps of fracture repair?

organisation of haematoma (pro-callus)
formation of fibrocartilagenous callus
mineralisation of firicartilagenous callus
remodelling of bone along the weight lines

Which factors influence how a # heals?

fracture type patient age neoplasm metabolic disorder drugs vitamin deficiency infection

Name and describe 5 main # types

simple (straight across bone, transverse break, 2 bone fragments - proximal and distal) compound (skin pierced?) greenstick (not complete through bone, seen in children) comminuted (multiple (>2) fragments of bone; the bone is broken in more than 1 places) impacted (shortening) -> see image on meded page 228

What type of infection is leishmaniasis

protozoan disease spread by sandflies

Where in the body do leishmania parasites multiply?

in macrophages

What are the 3 main forms of leishmaniasis?

cutaneous (skin infection at the site of the bite, poor healing, taking up to a year and often resolving in scars) -> can also have difuse cutaneous in patients with immunodeficiency, they get nodular skin lesions but do not ulcerate.. mucocutaenous (causes skin and mucosal ulcers of the nose and mouth) visceral aka black fever (parasite migrates to the liver, spleen and BM; massive splenomegaly, hepatomegaly, fever, weight loss, lethargy, anaemia, rarely hyperpigmentation)

What are the features seen in aport syndrome and what is the inheritance pattern?

glomerulonephritis + sensorineural hearing loss +/- ocular abnormalities X-linked recessive

What is the drug of choice in the management of mucormycosis?

IV amphotericin B or isavuconazole + surgical debridement

What is the most common parastitic cause of small intestine malabsorption?

giardia lamblia

what is the underlying pathology in Goodpasture's syndrome and what type of hypersensitivity disorder is it?

Type 2 HS d/o there are antibodies against collagen type IV in the basement membrane / anti-GBM antibodies this causes glomerulonephritis, pulmonary haemorrhage

How do you manage Goodpasture syndrome?

corticosteroids and immunosuppression

Which antidepressant is most assocaited with hyponatraemia?

citalopram (SSRI)

What lung tumour is associated with non-smoking women?

Adenocarcinoma

Pathogens seen in pts with CF - why they should not be in close proximity

Burkholderia cepacia complex (BCC), Pseudomonas aeruginosa, and methicillin resistant Staphylococcus aureus BCC, PA, MRSA -> Double check this