nephrology Flashcards
what does the RAAS system control?
regulates blood pressure
what controls RAAS?
Juxtaglomerular apparatus
what is the pathway of RAAS?
JG cells -> renin
liver ->angiotensinogen
renin causes angiotensinogen to become Angiotensin I
lungs -> ACE
ACE causes angiotensin I to II (vasoconstrictor)
angiotensin II cause aldosterone release from the adrenal glans (increases resorption)
what is ADH?
also known as vasopressin
produced by the hypothalamus and secreted by posterior pituitary
acts on the medullary collecting ducts and makes them more permeable to water -> increases synthesis of aquaporins
what produces BNP?
released in ventricles in response to stretching- dilates afferent and constricts efferent arteriole which increases GFR -> lowers BP
how do loop diuretics work?
act on thick descending loop of henle
prevent Na/K/Cl channels from functioning
how do thiazide diuretics work?
e.g. bendroflumethaside
acts on sodium/chloride transports and decreases reabsorption
SE- hypokalaemia, glucose intolerance, hypercalcaemia
how do potassium-sparing diuretics work?
e.g. spironolactone
blocks aldosterone receptors
sodium is lost and potassium is spared
can prevent formation of ascites in patients with chronic liver disease
where do renal stones commonly obstruct?
- vesico-ureteric junction
- mid-ureter where the ureter crosses the iliac vessels
- pelvi-ureteric junction
types of renal stones?
- calcium oxalate- stones are radio-opaque (85% of all stones)
- cystine- relatively radiodense
- uric acid- radiolucent
- calcium phosphate- radio-opaque
- struvite
RFs of renal stones?
dehydration
hypercalcaemia, hyperparathyroidism, hypercalciuria
cystinuria
high dietary oxalate
renal tubular acidosis
medullary sponge kidney, PKD
drugs- loop diuretics, steroids, acetazolamide
features of renal stones?
lion pain, intermittent 'colicky' pain N&V haematuria dysuria secondary infection may cause fever
Ix of renal stones?
urine dipstick and culture Ca and urate U&Es FBC/CRP *non-contrast CT KUB gold standard within 14 hours*
differentials of renal stones?
AAA pancreatitis gallstones MSK pain pyelonephritis
mx of renal stones?
NSAIDs e.g. diclofenac
stones <6mm typically pass on their own within 4 weeks
if emergency- nephrostomy tube, ureteric catheters, ureteric stent
if non-emergency- shock wave lithotripsy, percutaneous nephrolithotomy, ureteroscopy
prevention of renal stones?
prevent hypercalcaemia- high fluid intake, low animal protein, low salt diet, thiazide diuretics
prevent urinary acid secretion- cholestyramide, pyridoxine
prevent uric acid stones- allopurinol, urinary alkalinisation
what is nephritic syndrome?
a type of GN
haematuria with red cell casts. proteinuria, hypertension, oliguria
causes of nephritic syndrome?
rapidly progressive glomerulonephritis
IgA nephropathy
post-strep GN
what is rapidly progressive GN
rapid loss of renal function associated with the formation of epithelial crescents in the majority of glomeruli
causes of rapidly progressive GN
goodpastures syndrome- associated haemopytysis
Wegener’s granulomatosis
SLE
Ix of rapidly progressive GN
renal biopsy- crescenteric GN
bloods- U&E, ESR/CRP, complement, autoantibodies, urine, CXR, renal USS
mx of rapidly progressive GN
aggressive immunosuppression e.g. ciclosporin, corticosteroids, cyclophosphamide
features of IgA nephropathy?
mesangial deposition of IgA immune complexes
young male, recurrent episodes of macroscopic haematuria
develops 1-2 days after URTI
what is post-streptococcal GN?
typically occurs 7-14 days following a group A beta-haemolytic streptococcal infection
immune complexes deposit in glomeruli
young children most commonly affected