renal conditions Flashcards
criteria for AKI
<48hrs reduction in kidney function -
increase in creatinine >26.4
or increase in creatinine by >50%
or reduction in urine output
cause of prerenal AKI
inadequate blood supply to kidneys reducing filtration of blood hypovolaemia dehydration hypotension heart failure
causes of prerenal AKI
inadequate blood supply hypovolaemia - haemorrhage, burns renal hypoperfusions - NSAIDs dehydration - D+V hypotension (shock) heart failure
renal causes of AKI
vasculitis glomerulonephritis infection systemic conditions acute tubular necrosis gentamicin rhabdomyloysis
post renal AKI causes
obstruction to outflow, back pressure to kidney reducing function
kidney stones
ureter strictures
medication to avoid in patients with AKI
NSAIDs ACEi/ARB diuretics gentamicin contrast trimethoprim potassium sparing diuretic
acute tubular necrosis
damage + death to epithelial cells of renal tubules
–> damage occurs due to ischaemia or toxins
commonest cause of AKI
is acute tubular necrosis reversible
yes, epithelial cells have the ability to regenerate
takes approx 7-21 days to recover
muddy brown casts on urinalysis
acute tubular necrosis
–>renal tubular epithelial cells in urine
complications of acute tubular necrosis
hyperkalaemia !!
fluid overload - heart failure, pulmonary oedema
metabolic acidosis pH<7.15
uraemia >40 - can lead to encephalopathy or pericarditis
causes of hyperkalaemia
AKI, CKD
rhabdomyolysis
adrenal insufficiency - addisons
spironolactone
ACEi/ARB
NSAIDs
hyperkalaemia ECG
tall, tented T waces
flattening or absence of P waves
broad QRS complex
higher it gets progressively bradycardic
effect of hyperkalaemia on muscles
muscle weakness - patient complains of jelly legs
immediate management of hyperkalaemia
10mls of 10% calcium gluconate (wont lower potassium but will normalise ECG)
insulin with 50mls 50% dextrose
nebulised salbutamol
what would you give a acidotic hyperkalaemic patient
sodium bicarbonate (on top of hyperkal tx)
urgent indications for haemodialysis
hyperkalaemia - 7/>6.5 unresponsive to treatment
severe acidosis <7.15
fluid overload
urea >40 - pericardialrub/effusion
rhabdomyolysis
skeletal muscle tissue breaks down + releases breakdown products into the blood
usually triggered by an event that causes muscle to break down
–> extreme underuse, overuse or traumatic injury
presentation of rhabdomyolysis
muscle aches + pain oedema fatigue confusion - elderly frail patients red brown urine
rhabdomyolysis investigation
creatine kinase high
myoglobin in urine - gives red-brown colour
hyperkalaemia
–> ECG
rhabdomylosis management
IV fluids
IV sodium bicarbonate
IV mannitol - increases GFR
loss of which hormone in CKD leads to anaemia
erythropioetin = hormone that produces RBC
management of anaemia of CKD
exogenous eythropoietin blood transfusion (allosensitisation)
Xray changes seen in renal bone disease
sclerosis at both ends of vertebrae (denser white)
osteomalacia in centre (less white)
“ruger jersey” appearance (stripes found on rugby top)
management of renal bone disease
alfacalcidol/calcitriol = active forms of vit D
low phosphate diet
bisphosphonates for osteoporosis
diagnosis of polycystic kidney disease
US of kidney + genetic testing
–> bilateral cysts
genes involved in autosomal dominant PKD
PKD-1 - chromosome 16 (85%)
PKD-2 - chromosome 4 (15%)
extrarenal manifestations of polycystic kidney disease
cerebral (intracranial) aneurysms
hepatic, splenic cysts
cardiac valve disease - mitral/aorta regurgitation
colonic diverticula
aortic root dilatation
hernias
management of ADPKD
tolvaptain - vasopressin receptor antagonist
–> slows development of cysts + progression to renal failure
(ESRF mean age = 50yrs)
cysts may rupture -> haematuria, resolves
classic presentation of autosomal recessive PKD
young kids, assoc with hepatic lesions presents in pregnancy as oligohydramnios (low amniotics fluid during pregnancy, fetus not producing enough urine) resp failure at birth underdeveloped ear cartilage low set ears flat nasal bridge
amyloidosis
deposition of extracellular amyloid (insoluble protein fibrils) in tissues or organs
occurs due to abnormal folding of proteins which then aggregate + become insoluble
diagnosis of renal amyloidosis
renal biopsy = congo red staining, apple green birefringence under polarised light
serum amyloid precursor (SAP) scan (PET scan vibes)
types of amyloidosis
AL = production of abnormal immunoglobulin light chains from plasma cells
AM = production of acute phase protein (serum amyloid A protein (SAA))
–> assoc with systemic inflammation
amyloidosis treatment
AL = immunosuppresion - steriods, stem cell transplant
AA = treat underlying condition
what are the diffrent types of ANCA + what conditions they indicate?
p-ANCA (MPO) = microscopic polyangiitis + churg-strauss (eosinophilic)
c-ANCA(PR3) = granulomatosis with polyangitis (wegners)
henoch-schonlein purpura
IgA vasculitis
kids
purpuric rash on bum + legs
post URT 1-3 weeks
IgA nephritis in 50%
granulomatosis with polyangiitis (Wegners)
nose bleeds, crusty nasal secretions, HEARING LOSS, sinusitis
haemoptysis
cough, wheeze
saddle shaped nose
rapidly progressing glomerulonephritis
types of kiney stones
calcium based - oxalte, phosphate
uric acid - no on XRay
struvite - bacteria, stag horn
cystine - autosomal recessive disease
stone responsible for staghorn calculus
struvite
recurrent UTIs, bacteria can hydrolyse urea to ammonia
kidney stone investigation of choice
CT KUB
abdo xray shows calcium
pharmacological management of kidney stones
tamsulosin
alpha blocker, aids spontaneous passage
key difference between haemodialysis + haemodiafiltration
replacement of extra-convective ultrafiltrate throught the dialysis period in HDF
gold standard dialysis vascular access
arteriovenous fistula
artery + vein surgically connected - bypass capillary system, flows high pressure from artery to vein
