Canine Flash Notes - Renal Physiology Flashcards
(118 cards)
what is azotemia? what are the different types & why is it important to characterize?
increase in BUN and/or creatinine
pre-renal, renal, & post-renal
important for accurate diagnosis, treatment, & prognosis
what is uremia?
clinical syndrome resulting from the accumulation of metabolic waste products due to renal failure
what is pre-renal azotemia? what is seen on lab values?
reduced renal perfusion - often caused by dehydration
increased BUN, creatinine, & USG over 1.030
what is renal azotemia? what is seen on lab values?
loss of 75% of nephrons
increased BUN, creatinine, & USG < 1.017
what is post-renal azotemia? what is seen on lab values?
blockage of urine outflow
increased BUN & creatinine, oliguria or anuria, & hyperkalemia
what is the pathophysiology of pre-renal azotemia? what happens if it remains uncorrected? sequela?
decreased renal perfusion causing a decrease in glomerular filtration of metabolites which results in an increase in BUN & creatinine while urine concentrating ability remains normal (normal tubular function)
renal ischemia & kidney destruction - renal disease or renal failure
what is the pathophysiology of renal azotemia?
GFR decreases due to loss of at least 75% of nephrons - renal disease results in azotemia, which eventually causes renal failure
acute renal failure - reversible or irreversible
chronic renal failure - irreversible
how do you treat pre-renal azotemia?
restore circulating fluid volume & renal perfusion, correct electrolyte abnormalities, & treat cause (dehydration, shock, addison’s, etc)
what is the prognosis of pre-renal azotemia?
usually, kidneys will resume normal function when re-perfusion is re-established if there is not prolonged ischemia
what are the 4 main causes of pre-renal azotemia?
- dehydration
- shock
- hypoadrenocorticism
- heart failure
what is the pathophysiology of post-renal azotemia?
blockage of urinary outflow & hyperkalemia develops as it can’t be eliminated
life threatening effects - cardiac conduction (bradycardia & death)
initially kidneys resume normal function if corrected, but too much time with obstruction can result in acute renal lesion (hydronephrosis)
what is the classic case presentation of a dog with renal azotemia? what lab changes are seen?
acute - anuric/oliguric, occasionally polyuric
chronic - pu/pd, gi signs (vomiting/diarrhea), & oral ulcers
increase in BUN/creatinine & low specific gravity
what are some causes of acute renal failure in dogs?
pre-renal ischemia from dehydration/hypovolemia, ethylene glycol toxicity, aminoglycoside toxicity, heavy metal toxicity, hypercalcemia, leptospirosis
chronic renal disease resulting in failure
how is renal azotemia treated?
acute - supportive care until it repairs itself (fluids, treat hyperkalemia, treat acidosis)
chronic - no cure, palliative care, fluids, & diet restricted proteins & phosphorus (hill’s k/d)
what is the classic presentation of an animal with post-renal azotemia? sequela?
oliguria, straining to urinate, abdominal discomfort
heart failure from hyperkalemia & hydronephrosis
what are the main causes of post-renal azotemia?
obstruction - calculi in renal pelvis/ureter/urethra, tumor block, entrapment of urinary tract from a hernia, trauma, stricture, or iatrogenic from surgery or catheterization
ruptured urinary tract
how is a diagnosis of post-renal azotemia made based off of lab changes?
increased BUN/creatinine, ECG shows bradycardia, spiked t waves, absent p waves
check creatinine of abdominal fluid if rupture is suspected
how is post-renal azotemia treated?
hyperkalemia addressed first!!!
unblock the animal - cystocentesis if you can’t immediately unblock
fluids - sodium bicarb 0.5-1.0 mmol/kg slow IV over 15 minutes, 20% dextrose 0.5-1.0 g/kg IV with </= 1 unit of regular insulin per 3 grams of dextrose, or 10% calcium gluconate up to 0.5-1.0 g/kg IV
what values designate an animal as being polyuric/polydipsic?
urine production > 25ml/lb/day (more than 50 ml/kg/day)
water consumption > 50 ml/lb/day (more than 100 ml/kg/day)
T/F: pu/pd is a manifestation of a disease & not a diagnosis
true
what is the mechanism of polydipsia?
low plasma osmolality stimulates chemoreceptors in the thirst center - posterior pituitary gland releases ADH
renal response to ADH is to concentrate urine requiring 1/3 functioning nephrons & a hypertonic renal medullary interstitium (2/3 non-functional nephrons for kidney not to concentrate urine causing polyuria)
what is the common presentation of an animal that is pu/pd?
nocturia, inappropriate urination, incontinence, pollakiuria, & polydipsia
what urine production metabolism rate is used for a caged animal?
urine volume 25-45 ml/kg/24 hours
if a pu/pd dog has a usg of 1.040, what do you think? what if it is less than 1.007? what if it is 1.025 or higher with pu/pd?
1.040 - unlikely to be polyuria
1.007 - hyposthenuria, tentative diagnosis of central diabetes insipidus, nephrogenic diabetes insipidus, or pituitary diabetes insipidus
1.025 - suggests hypoadrenocorticism, diabetes mellitus, or renal glucosuria