Ophthalmology Flashcards
Epidemiology of anterior uveitis
Associated with HLA-B27 protein
Associated w/ conditions including IBD, reactive arthritis, ankylosing spondylitis, sarcoidosis and Behcet’s disease
What is anterior uveitis?
Inflammation of the iris and ciliary body
Symptoms of anterior uveitis
Red eye
Acute onset eye pain
Small irregular pupils
Stages of Chronic Kidney Disease
CKD 1 = eGFR >90; normal function
CKD 2 = eGFR 60-89; mild reduction
CKD 3a = eGFR 45-59; mild-moderate reduction
CKD 3b = eGFR 30-44; mod-severe reduction
CKD 4 = eGFR 15-29; severe reduction
CKD 5 = eGFR <15; kidney failure
First line treatment CKD
ACEi/ARB
- need to have baseline eGFR and potassium, discontinue if dropping
- should not be combined due to risk of hyperkalaemia
What is Acute Kidney Injury (AKI)?
Sudden decrease of kidney function
rise in creatinine and urea, fall in eGFR and urine output
Pre-renal causes of AKI
Volume loss (haemorrhage, V+D, dehydration, etc)
Hypotension (sepsis, shock)
Decreased effective arterial volume
Renal artery stenosis
Medications: NSAIDs. ACEi, Cyclosporine and tacrolimus
Intra-renal causes of AKI
Acute tubular necrosis
Nephrotoxic agents
Intratubular obstruction
Pyelonephritis
Thrombotic Microangiopathies
Glomerulonephritis:
–> Nephritic syndrome (IgA nephropathy, post-strep, vasculitis)
–> Nephrotic syndrome (MCD, Membranous, Amyloid, Diabetic)
What is acute tubular necrosis?
Damage to the tubular epithelial cells within the renal tubules of the kidney due to either ischaemia or direct toxicity
Causes of acute tubular necrosis
Ischaemia
–> hypotension, shock, direct vascular injury
Nephrotoxicity
–> contrast
–> drugs e.g. aminoglycosides (gentamicin), cisplatin (& other chemos), methotrexate, NSAIDs, ACEi. ARBs, statins
Presentation of acute tubular necrosis
Oliguria (reduced urine output)
Uraemia (build up of toxins in blood)
Electrolyte imbalance
Brown urine
Urine microscopy shows muddy brown casts
Management for acute tubular necrosis
correction of underlying cause (e.g. fluid resus)
removal of nephrotoxins
may require haemofiltration or haemodialysis
What is acute interstitial nephritis?
Inflammation of the extra-glomerular tissue, thought to be mediated by an interstitial hypersensitivity reaction
Presentation of acute interstitial nephritis
Typically delayed presentation (2-40 days) after triggering medication
Rash, fever, AKI (oliguria, uraemia, EI), and eosinophilia
High Eosinophils
Causes of acute interstitial nephritis
Abx: rifampicin, penicillins, cephalosporins, quinolones
NSAIDs
Diuretics
PPIs
Acyclovir
Methotrexate
Infections (strep, mycoplasma, EBV, CMV, TB, Legionella)
Autoimmunity
SLE
Cause of IgA Nephropathy
IgA complexes deposit in the glomerulus
–> inflammation (type 3 hypersensitivity reaction)
Presentation of IgA nephropathy
recurrent haematuria 1-2 days after an URTI/GI infection/strenuous exercise
Sometimes mild proteinuria
Ix for IgA nephropathy
Urinalysis: +ve for blood +/- protein
Urine microscopy, culture & sensitivities (MC&S): RBCs (normally dysmorphic suggesting bleeding from glomerulus), WBCs
Gold standard = renal biopsy
–> shows IgA deposits within the mesangium (sub-endothelium) causing proliferation and inflammation
Management of IgA nephropathy
Symptom control
Optimising and monitoring fluid balance
Steroids if renal function starts deteriorating
Indications for dialysis (AKI)
AEIOU
Acidosis: severe pH<7.20
Electrolyte imbalance: persistent hyperkalaemia of >7mmol)
Intoxication: poisoning
Oedema: refractory pulmonary oedema
Uraemia: encephalopathy or pericarditis
Stages of AKI
Stage 1: creatinine rise of 1.5x compared to baseline or urine output <0.5 ml/kg/hour for 6 hours.
Stage 2: creatinine rise of 2x compared to baseline or urine output <0.5 ml/kg/hour for 12 hours.
Stage 3: creatinine rise of 3x compared to baseline or urine output <0.3 ml/kg/hour for 24 hours (or anuria for 12 hours) or serum creatinine >354umol/dl
