URO Flashcards
what diseases cause a reduced renal repose to ADH
Addisons, Cushing, diuretics, high salt diet, post-obstruction, HyperT
how does osmotic dieresis cause PU and common electrolytes
Solute in urinary tubules pulls fluid out into urine
Glucose: DM, renal glucosuria, Fanconis syndrome (allow with lots of that electrolytes in small dog breeds)
Sodium: Addisons, diuretics, high salt diet, post-obstruction
What causes a loss of concentration gradient
low salt diet
medullary washout (e.g. prolonged PUPD, prolonged aggressive fluid therapy)
how does Phaeochromocytoma cause PU
(Catecholamine producing tumour of the adrenal gland i.e. adrenaline)
Adrenaline = Primary sign is hypertension = high GFR = polyuria
What electrolytes are high with renal disease
Phosphorus is GFR dependent so slow GFR = high phosphorus
Potassium should also be cleared by GFR so is high
what molecules are high in blood with renal failure
urea and creatinine
SDMA
what is lost with a PLN
albumin
safer alternative to water deprivation test
trying to differinate between central and nephrogenic DI, and psychogenic
just do vasopressin trial xxx don’t dehydrate dogs on purpose
threee categories of AKI
- Haemodynamic = redcued renal perfusion
- Intrinsic Renal i.e. actual damage to the kidneys (ischeamia, infectious, immune-mediated, sepsis, nephrotoxic drugs)
- Postrenal i.e. urethral obstruction, uretral obstruction or urine leakage
signs of lepto
AKI and liver damage and dyspnoea
SNAP test in all AKI patients!!! zoonotic!
Treat with doxycycline
two treatment options for an AKI
- IVFT: match losses and maintain fluid status using very high fluid rates (up to 10x maintenance but avoid volume overload)
- Dialysis if no response to IVFT> Peritoneal catheter => infusion of dialyse solution (glucose) => left for 20mins-hours => drained and repeated
signs of CRF
○ PU/PD
○ Anorexia
○ Weight loss
○ Dehydration
○ Pallor
○ Vomiting and diarrhoea (due to uraemia)
○ Mucosal ulcers
Uraemic breath
How does nephron loss cause further renal damage
Nephron loss > other nephrons GFRs increased to compensate> glomerular capillary wall damage and more plasma protein filtration > further glomerular and tubulointerstitial damage.
Nephron loss > reduced total GFR> build up of products normally excreted (e.g. urea)> uraemic crisis.
How can anaemia develop from CRF
Reduced renal function > reduced Erythropoietin (EPO) production > nonregenerative anaemia
What is iris staging
Guidelines for treatment
Stage 1-4 based on
- Creatinine OR SDMA
which is more specific: SDMA or creatnine
creatine can come from muscle mass too
excreted by kidney so high in renal failure with 75% nephron loss
SDMA is most expensive but high with 40% nephron lost and kidney specific
key principles in CKD management
Diet very important stage II onwards
Later stages - more emphasis on
- Treating 2ndary anaemia/acidosis/nausea
- Maintaining hydration
- Ensuring adequate nutrition
stage 1 treatment
- care with nephrotoxic drugs
- fresh water always
- Monitor SDMA and creatinine
- Treat hypertension and proteinuria
- Renal diet and phosphate binder
What is uraemic crisis
Build up of urea and other toxins usually excreted in kidneys to intolerable levels. Due to-
○ End stage Chronic Kidney Disease
○ Acute Kidney Injury
○ Acute on Chronic –AKI (e.g. ischemic or toxic insult) exacerbating existing CKD
uraemia crisis treatment
Work out if AKI, CKD or acute on chronic and treat as needed but in addition…
- IVFT- Hartmann’s to Replace dehydration + ongoing losses
- blood gases- assess for acidosis. Bicarb if pH <7.2
- Treat nausea, Antiemetics e.g. maropitant
- Treat GI ulceration: Omeprazole +/- H2 Blockers +/- sucralfate
- Nutritional support- Important! Appetite stimulants( Mirtazapine) and Feeding tubes (Nasogastric so don’t have to GA)
What renal and extra renal conditions predispose to CKD
- Renal diseases
○ Glomerular disease
○ Fanconi’s syndrome
○ Polycystic Kidney Disease
○ Pyelonephritis
○ Nephrotoxin exposure
○ Neoplasia
Extrarenal issues
○ Hypertension
○ Cardiac disease
○ Hyperthyroidism
○ Diabetes
○ Urolithiasis/ obstruction
○ Cystitis
○ Neoplasia
○ Hypercalcaemia
how to renal disease and hypertension drive eachother
- Renal injury stimulates sympathetic pathways
- Renin release and angiotensin conversion
- Vasoconstriction and aldosterone release so more sodium reabsorption
- This drives hypertension
This drives renal injury
treatment of renal hypertension
○ ACE inhibitors (ACEi) e.g. Benazepril, Enalapril
○ Angiotensin receptor blockers (ARB) e.g. Telmisartan, Spironolactone
○ Calcium Channel Blocker (CCB) stop vasonstriction e.g. Amlodipine