renal failure Flashcards
what is chronic renal failure
when compensatory mechanisms of the diseased kidneys are no longer able to maintain the excretory, regulatory and endocrine functions of the kidneys - the resultant retention of nitrogenous sulutes, derangements of fluid and electrolyte and acid-base balance and failure of hormone production constitute CRF
what are the 3 levels of acute kidney injury
pre renal = blood supply
renal = kidney pathology
post renal = obstruction of the UT (leak or rupture)
what things might cause acute kidney injury at the level of the kidney
- drugs
- toxins (anti freeze)
- plants (lillies in cats)
acute kidney disease leads to
- kidneys suddenly cant function
- therefore excretion and homeostasis cant be achieved
- leads to azotemia, hyperkalemia and acidosis
when does AKI happen
- rare
- all species
- rapid deterioration of renal function
- in some cases reversible
- prognosis is poor
- aetiology and pathology often unknown
- URGENT
clinical findings of acute kidney injury
- rapid and progressive
- very sick
- lethargic
- depressed
- anorexic
- vomiting
- dehydration
- anuria or oliguria
- large painful bladder
- large painful kidneys
clinical history of a patient with chronic kidney disease
- PUPD
- vomiting (dogs)
- anorexia
- weight loss
- lethargy
- non specific signs
how do you differentiate CKD from AKI
- Hx of previous PUPD
- weight loss and porr hair coat
- renal size
- non-regenerative anemia
- parathyroid gland size on US
- hyperkalemia
clinical signs of CKD
- PUPD
- weight loss
- GI signs (incliding oral)
- small knobbly kidneys
- anemia (non-regenerative)
- poor hair coat
- oral lesions (most common in dogs)
- pallor of muscous membranes
- dehydration
- osteodystrophy
- ascited or oedema
- poor platelet function (bruising, petechiae)
clinical signs of CKD manifest due to
- inability to concentrate urine appropriately
- cant excrete nitrogenous waste
- leads to dehydration and azotaemia/uraemia
- uraemia impacts appetite
- electrolyte imbalance
what should you do with a patient in CKD
re profuse and re hydrate
why does nephron loss lead to hyperfiltration
- pregressive nephron loss leads to declining GFR
- compensatory rise in nephron GFR = hyperfiltration
- large functional reserve
- contributes to worsening of disease
outline the mechanism of renal secondary hyperparathyroidism
- low iCa drives increased PTH production to attemtp to preserve calcium, promote phosphate loss, promote uptake of calcium from gut via calcitriol and promote release of calcium stores from bone
- BUT the kidneys are damaged so they cant do the above
- ionised calcium may be low due to retained phosphate binding to iCa. PTH that monitors iCa not tCa cant recognize, urinary losses, lower dietary intake if not eating and less absorption from the gut
- calcitriol production therefor compromised as less tubular mass to do 1-alpha hydroxylation ADN anti-calcitriol effects of FGF-23 (trying to decrease PO4 which gets in via gut with Ca via calcitriol)
- FGF then high because trying to get rid of phosphate from blood. it is anti-calcitriol, PTH then overstimulated
weight loss and polydipsia best fits AKI or CKD
CKD
oliguria fits best with: AKI or CKD
AKI
