Kidney and GU Flashcards
(136 cards)
Describe the two types of kidney stones caused by hypercalcaemia
Calcium oxalate stones: black/ dark brown, radiopaque, form in acidic urine
Calcium phosphate: dirty white, radiopaque on x-ray, form in alkaline urine
Give 3 risk factors for calcium oxalate and calcium phosphate stones
Hypercalcaemia: Increased GI absorption/ hyperparathyroidism
Hypercalciuria: Impaired renal tubular reabsorption
Hyperoxaluria: Genetic defect causing increased oxalate excretion, defect in liver metabolism or diet heavy in oxalate-rich foods
Describe uric acid kidney stones
Red-brown
Radiolucent
Uric acid forms urate ion –> monosodium urate
Describe struvite kidney stones (infection stones)
Mg2+ Ammonium Phosphate Bacteria use urease to break urea down into carbon dioxide and ammonia (which makes urine more alkaline and favours precipitation) Dirty white/ radiopaque
Give 3 risk factors for struvite kidney stones
Urinary tract infections
Vasicoureteral reflux
Obstructive urpathies
Describe the pattern of pain with kidney stones
Dull/ localised flank pain in the mid-lower back
Renal colic
Pain due to dilation stretching and spasm, worse at uteropelvic pelvic junction
How would you diagnose kidney stones?
History and physical exam
Imaging: XR, CT, US
Urinalysis: microscopic/ gross haematuria
How would you treat kidney stones?
Hydration
Medication: analgesics, potassium citrate to reduce stone formation
Alpha adrenergic blockers/ CCB to help pass stones
Shockwave lithotripsy
Surgery/ stent placement
What is the usual BUN to creatinine ratio?
(5-20) : 1
Give 4 causes of absolute fluid loss leading to decreased blood flow in pre renal AKI
Haemorrhage
Vomiting
Diarrhoea
Severe burns
Give 2 causes of relative fluid loss leading to decreased blood flow in pre renal AKI
Distributive shock
Congestive HF
Give the equation for GFR
Blood filtered (ml) / minute
Describe the effect of reduced GFR in pre renal AKI
Less urea and creatinine filtered therefore more in the blood (azotemia)
Oliguria: low urine
RASS activated
Water and sodium reabsorption is tied to urea reabsorption therefore BUN: creatinine is >20:1
Give the percentage of sodium excreted compared to sodium filtered in pre-renal AKI
<1%
How is urine concentration affected in pre-renal AKI
More concentrated urine, Uosm >500 mOsm/ kg
Where is the damage in intrarenal AKI?
Tubules
How can the tubules become damaged causing intrarenal AKI?
Acute tubular necrosis (due to pre-renal AKI) Nephrotoxins: Aminoglycosides (Abx) Lead Myoglobin Ethylene glycol Radiocontrast dye
What is tumour lysis syndrome and how can it cause intrarenal AKI?
Uric acid is released during cancer treatment, excess uric acid damages the tubules
How would you treat intrarenal AKI?
Hydration (improves from)
Medications:
Allopurinol
Urate oxidase
How does the necrosis of cells in intrarenal AKI cause problems in the kidney?
Dead cells slough off and clog the tubules, increasing pressure
There is a decrease in GFR: oliguria, azotemia
Hyperkalaemia and metabolic acidosis since dead cells are not absorbing
Dead cells form a brown granular cast
How does glomerulonephritis cause intrarenal AKI?
Antigen-antibody complexes are deposited in tubules
Activates the complement system, other immune cells are attracted with lysosomal enzymes which cause damage
Increase the permeability of podocytes so large molecules can pass through
What is the effect of fluid leakage due to tubular damage in intrarenal AKI?
Reduced pressure difference, reduced GFR, causing: oedema, HTN, oliguria, azotemia
Describe acute interstitial nephritis including symptoms
Infiltration of immune cells (type I or IV hypersensitivity) causing oliguria, eosinophiluria, fever, rash
Give 3 causes of type I or Iv hypersensitivity in acute interstitial nephritis
NSAIDs
Penicillin
Diuretics