Path 7 Flashcards
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
rat bite erosions on x-ray
gout
What do you see on x-ray in gout?
rat bite erosions
What do you see on xray in pseudogout?
white lines of chondrocalcinosis
white lines of chondrocalcinosis on xray - diagnosis?
pseudogout
What is the management of gout acutely and long term?>
acute: colchicine, NSAIDs
long term: allopurinol
What group of conditions do gout and pseudogout belong to?
inflammatory crystal arthropathy
What groups of people are affected by gout and pseudogout?
gout: obese, middle aged men
pseudogout: >50yo women
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.
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.
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
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
MoA of colchicine
inhibits polymerization of tubulin to reduce motility of neutrophils
types of presentation in gout
acute monoarthritis
chronic tophaceous gout (polyarticular arthritis, tophi deposits behind ear lobes, fingers and elbows, urate kidney stones)
Aetiology of gout
hyperuricaemia due to
- increased intake (e.g. alcohol)
- increased production (e.g. TLS, inherited metabolic abnormalities)
- decreased excretion (e.g. diuretics)
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
