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CMS - term 1 > Urinary > Flashcards

Urinary Flashcards

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1
Q

causes of hemoglobinuria - equine

A

RBC breakdown (intravascular)

red maple toxicity
infectious disease of hemaotpoeitic system
immune mediated disease

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2
Q

causes of myoglobinuria - quine

A

muscle damage/necrosis

rhabomylolysis
sycamore toxicity
stypical myopathy
trauma
polysaccharide storage myopathy
idiopathic

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3
Q

causes of hematuria - equine

A

blood from urinary, renal, bladder, repro

oak toxicity
urethral rents
urethritis
bacterial cystitis
urolithiasis
pyelonephritis
idiopathic
verminous nephritis
renal and vesicular neoplasia

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4
Q

discoloured urine - false

A

oxidation after exposure to air
darked after contact with snow
plant derived pigment - white clover
drug induced
- bright orange/red - rifampin/phenothiazine/nitazoxinade
- dark brown/black - doxycycline

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5
Q

urinalysis - red urine

A

dipstick - haem
spin - clear serum –> hameturia
ammonium sulphate 80% - hemaglobin will precipitate, myoglobin won’t
microscopy - cell types, crystals
endoscopy - neoplasia in bladder (Transitional cell carcinoma)
US - stones, bladder wall thickness
renal biopsy - indicated when azotemia in otherwise young healthy horse with acute renal failure

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6
Q

ddx PUPD - equine

A

PPID
Diabetes mellitus
Diabetes insipidus
kidney disease/renal failure
drug induced - alpha 2s, steroids, antibiotics, pychogenic polydipsia (bored)

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7
Q

polydipsia in horses - quantity

A

> 100ml/kg/day (>10% bodyweight)

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8
Q

polyuria in horses - quantity

A

> 50ml/kg/day

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9
Q

testing in PUPD - equine

A

watch to quantify/confirm PD - >70ml/kg/day

hematology - anemia, neutrophilia, ACTH/TRH stim

biochem - azotemia, glucose, calcium, liver parameters

urinalysis - USG (low not consistent with PUPD and suggests renal concentrating issue, medium consistant with chronic renal failure, high not consistent with PUPD and kidneys fine), glycosuria

water restriction trial - differentiate between diabetes insipidus and psychogenic

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10
Q

causes PUPD - dog

A

physiological - activity, weather, diet change
renal - CKD, pyelonephritis, AKI, fanconis
hepatic
cushings
diabetes
hypercalcemia
pyo
iatrogenic
psychogenic dolydipsia

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11
Q

causes PUPD - cat

A

physiological - diet change, activity, increased grooming, playing with water
renal - CKD, AKI, post obstructive diureses
diabetes
iatrogenic
hyperthyroidism

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12
Q

causes of PUPD - ferrets

A

renal
cushings
diabetes

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13
Q

causes of PUPD - rabbits

A

diet change - hay to grass in spring
renal - CKD
hepatic
pyo
metabolic
pregnancy toxemia
pain

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14
Q

causes of PUPD - birds

A

during egg laying
renal
hepatic
toxins
pituitary adenoma
stress/fear

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15
Q

clinical exam in PUPD

A

Neuro -
altered mentation - hepatic encephalopathy
hyperactivity - primary polydipsia or result of hyperthyroidism

ocular -
icterus - hepatic
cataracts - diabetes mellitus
retinal changes - hypertension secondary to CKD, AKI, hyperthyroidism

cervical palpation -
goitre - hyperthyroidism

oral -
mm -
icterus - heaptic
congested - systemic inflammatory
pale - anemia of chronic disease (CKD, neoplasia)
lingual ulceration/halitosis - advanced CKD

thoracic -
tahcycardia - hyperthryoidism, pheochromocytoma, sepsis
bradycardia - addisons
painting - cushings
tachypnoea - pulmonary neoplasai/mets

derm -
cushings - skin thinning, hair loss, pigment change
hepatocutaneous syndrome

repro -
egg laying - physiological polydipsia
pregnancy - toxemia, gestational diabetes
discharge - open pyo

plantigrade stance/struggling to jump - diabetic peripheral neuropathy

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16
Q

urinalysis - PUPD

A

USG - renal

dipstick -
glucose - diabetes or fanconis (or stress)
ketones - diabetes mellitus
blood - renal, pyo, contamination from repro
protein - renal, UTI, cushings

sediment -
protein:creatinine - renal, cushings
active sediment - pyo or UTI

culture - UTI, pyo, contaminated sample

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17
Q

blood testing - PUPD

A

renal -
increased urea and creatinine
+/- phosphate
non-regenerative anema

hepatic -
increased liver enzymes
decreased albumin

diabetes mellitus -
increased glucose
increased ALP, bilirubin and cholesterol
hypokalemia

cushings -
increased cholesterol, ALP and bile acids
decreased urea
stress leukogram

hyperthyroidism -
increased RBC
stress leukogram
increased glucose, renal enzymes, phosphate
decreased creatinine

hypercalcemia -
increased total and ionised calcium

pyo -
neutrophilia
mild anemia
increased globulins , liver and kidney enzymes
decreased glucose

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18
Q

targeted disease testing - PUPD

A

SDMA - renal
bile acid stim - hepatic
fructosamine - diabetes mellitus
ACTH stim/low dose dexmethasone suppression - cushings
total/free T4 - hyperthyroidism

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19
Q

pre renal AKI

A

before kidney - vasculature
decrease in perfusion to kidneys
reduction in GFR –> increase in SDMA/urea/creatinine
reduced perfusion due to hypotension, hypovolemia, shock
–> ishemia
efferent venous drainage issues - cirrhotic liver disease, right sided heart failure, fluid overload
usually milder increases in creatinine than other types of SKI
can lead to intrinsic AKI if not treated

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20
Q

AKI vs CKD

A

AKI can return to normal if treated
AKI on CKD - can only return to previous CKD state, usually to a worse state than before teh AKI
CKD - at least 3 months

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21
Q

intrinsic AKI

A

primary - AKI is the main presenting sign
secondary - AKI secondary to larger constellation of conditions

non specific signs -
lethargy
hypo/anorexia
nausea/vomiting/diarrhoea
PUPD
uremic breath

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22
Q

post renal AKI

A

urine not able to leave kidneys properly
obstruction of urinary tract
back up of urine –> increased tubular pressure –> reduction in GFR –> increase SDMA/creatinine/urea
urethral or ureteral obstructions or urinary tract rupture
mroe likely to be hyperkalemic - look for obstructions if see this

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23
Q

causes of AKI requiring immediate treatment (within hours)

A

infectious - pyelonephritis, pyelonephrosis
obstructive - rethral or ureteral
addisons (dogs)

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24
Q

causes of AKI requiring immediate treatment (within days)

A

neoplasia - usually present as CKD
glomerulanephritis

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25
Q

infectious AKI

A

pyelonephritis - infection of kidneys - usually e coli
pyelonephrosis - dilation of renal pelvis with pus

more common in acute on chronic

risk factors -
obstruction
diabetes
renal and non renal neoplasia

signs -
pyrexia
neutrophilia
renal pain
renal pelvic/uretal dilation or free fluid on ultrasound

diagnosis - cystocentesis - culture

treatment -
antibiotics with good renal perfusion
lepto - doxy or amoxyclav
sepsis - amoyclav
surgical drainage

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26
Q

AKI - addisons in dogs

A

hypovolemia and distrubutive shock –> marked pre renal azotemia
hyperkalemia and hyperphosphatemia
looks like AKI - check basal cortisol to rule out addisonian crisis
if high suspicion then ACTH stim and treat preemptively

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27
Q

treatment AKI

A

supportive care
maintain hydration
maintain calorie intake
assessing and treating systemic hypertension
address electrolyte and acid base imbalance
discontinue nephrotoxic drugs

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28
Q

supportive care for AKI

A

fluids
electrolytes
feeding tube/assisted feeding

29
Q

maintaining hydration in AKI

A

stages of fluid therapy -
resuscitation - replacing intravascular deficits, only needed if signs of shock
optimisation - rehydration of total body deficits - based on % dehydration signs and monitored
stabilisation - maintenance water requirements - if not able to do themselves, consider ins and outs
evacutation - de escalation - reduce until drinking on its own with regular hydration assessments

lactated ringers
potassium supplementation if needed
creatinine will go up when stop - removing dilution effect
note oliguria and anuria - ins and outs approach

30
Q

maintaining calorie intake AKI

A

uremia –> nausea –> anorexia
oral ulceration - pain

medications - anti nausea (maropitant), appetite stimulants

if can’t eat 75% required intake by 48 hours - tube

31
Q

treating hypertension in AKI

A

lots of animals with AKI get hypertension
some antihypertensive medications are nephrotoxic

amlopidine

RAAS inhibitors can worsen AKI, can use in CKD so when reclassified at 3 months can reevaluate

32
Q

addressing acid base and electrolyte imbalances in AKI

A

hyperkalemia - in obstructive AKI - IV or oral supplements
hyperphosphatemia - always present in AKI
hypernatremia - usually resolves with rehydration

33
Q

renal amyloidosis

A

rare
synthesis and deposition of misfolded proteins in tissues

profuse diarrhoea - fibrin deposition in intestinal mucosa
enlarged kidney - palpable per rectum
subcutaneous oedema
weight loss
protein losing nephropathy - foamy urine
amyloid deposition in renal glomeruli

euthanasia, condemned at slaughter

34
Q

pyelonephritis

A

cattle and pigs
bacterial infection - renal pelvis
actinobacterium suis or e coli in pigs
range of bacteria in cattle
pus in ureters at pm

35
Q

actinobacterium suis - pyelonephritis

A

pigs
in prepuce and preputial diverticulum of boars
infection through natural service

pus
abscesses
cystitis - common reason for culling
pain (hunched back)
anorexia
polydipsia
loss of condition
vulval discharge
hematuria
may die suddenly

urine test - bacteriology
treatment - antibiotics (success dependent on stage of infection)

36
Q

e coli - pyelonephritis

A

pyelonephritis in sows that are AI’d
ascending infection from fecal contamination of vulva
predisposed by restricted water (not flushing out enougyh)

cystitis
pyelonephritis
increased urine frequency - little and often
pus/blood in urine

treatment - antibiotics, renal damage may be permanent if pyelonephritis set in
prevention - hygiene and unrestricted water access

37
Q

pyelonephritis - cattle

A

more in older beef cattle
range of bacteria
acute - pain, dullness, frequent urination, coloured urine, pyrexia, enlarged kidney
chronic - loss of condition, drop in yield, urination little and often

treatment - antibiotics probably won’t work
condemnation of carcass at salughter if systemic infection

38
Q

acute tubular necrosis

A

ruminants
nephrotoxins - oak, oxalates, heavy metals, aminoglycosides, tetracyclines
renal ischemia - caused by mastitis, metritis, abomasal torsion, salmonellosis

depression
inappetance
mild bloat
diarrhoea

treatment, supportive care, remove toxin

39
Q

nephrosis

A

lambs up to 4 months

dull
anorexia
weight loss
death

swollen pale kidneys at PM

usually following coccicia, menatodirus or crypto infection

40
Q

black disease

A

Clostridium Novyi B
necrotic liver damage

41
Q

blackleg

A

Clostridium chauvoei
muscle tissue damage

42
Q

botulism

A

clostridium botulinum
nervous, flaccid paralysis

43
Q

tetanus

A

clostridium tetani
nervous, after open wounds, rigidity

44
Q

pulpy kidney

A

clostridium perfringens D
4-10 week old lambs - unvaccinated dam
older weaned lambs that aren’t vaccinated
often triggered by move onto better pasture or supplemental feeding

sudden death
enterotexmia - from clostridial toxins, not from kidney disease
convulsion
pulmonary oedema

friable kidneys at PM

prevent - vaccinate pregnant ewes, vaccinate lambs twice before weaning

45
Q

leptospirosis

A

zoonosis - abortion material and urine splash high risk for humans
abortion, still birth, weak calves, infertility
milk drop

colonises renal tubules and intermittently excreted in urine - infected waterways

serology for diagnosis
vaccination available

46
Q

redwater fever (babesiosis)

A

coffee coloured hematuria
ixodes ricinus - heather, fern, tall grass, hilly regions - peak in spring and autumn

zoonosis - rare but serious

signs -
dullness
inappetence
pyrexia
loud heart sounds
hematuria
pipe stem feces –> constipation
young animals usually have no signs
early exposure - immunity in endemic areas

prevention - tick control
treatment - imidocarb (long withdrawal), blood transfusion, symptomatic treatment (laxative for constipation)

47
Q

AKI - horse - signs

A

NB often due to predisposing disease, common in hospitalised horses

uremia –> anorexia
colic signs
uremic encephalopathy - nervous signs
attempting to urinate and showing discomfort (obstruction)
pyrexia - acute septic nephritis (rare)

signs often masked by primary condition

48
Q

AKI - horse - diagnosis

A

history, signs
azotemia
isosthenuria

electrolyte abnormalities -
variable potassium (reduced excretion but diet can compensate)
serum magnesium - high in renal or pre renal
calcium - elevated in Chronic renal failure

minimal proteinuria
bacteremia rare
USG - differentiate pre ranl azotemia from kidney disease

49
Q

AKI - horse - treatment

A

treat underlying disease
correct dehydration and hypertension
avoid nephrotoxic drugs
surgery - remove obstructions

50
Q

chronic renal failure - horse

A

irreversible
greater than 3 months
less common than acute

51
Q

chonic renal failure - horse - signs

A

non specific
wight loss
dull
PUPD
peripheral oedema
dull coat
anemia
inappetence
change in mentation
mild diarrhoea
uremic encephalopathy

52
Q

chronic renal failure - horse - test

A

azotemia
mild anemia
low albumin
hyperkalemia - distinct feature
urinalysis - renal casts, WBCs, proteinuria (more often in AKI)
Ultrasound - more useful in chronic than acute
biopsy - not that useful, can cause haemorrhage

53
Q

chronic renal failure - horse - treatment

A

progressive and irreversible
symptomatic treatment

steroids
avoid dehydration
avoid nephrotpxic drugs
vegetable oil - increase calorie intake
high energy low calcium diet
stone removal - probably won’t bother

poor prognosis long term

54
Q

azotemia

A

increase in creatinine and/or urea

55
Q

uremia

A

clinical signs associated with azotemia

56
Q

mechanisms of CKD

A

normal - gradual inflammation and destruction of kidney functional units, 2/3 gone to signs

acute kidney insult - causing long lasting inflammation and damage –> follows normal pattern

acute on chronic - acute attack with existing CKD, once acute attack over then return to CKD state, usually worse off

neoplasia - grows and reduces function

degenerative (eg polycystic kidney disease) - cysts spread in increase in size –> reduced function

juvenile onset CKD - start reducing function, over time clinical

glomerular disease - marked proteinuria, excess protein, reduction in function

tubulo-interstitial nephritis most common cause

57
Q

markers of GFR

A

Creatinine -
produced in muscles
filtered by kidneys
main parameter
no increase until 75% loss
also affected by muscle mass, hydration state and hyper thryoidism

urea -
produced by liver
filtered by kidneys
more variable than creatinine
less reliable

SDMA -
produced by most cells
filtered by kidneys
less affected by external factors
earlier diagnosis
not affected by muscle mass
less good for monitoring progression -m normal day to day variation

USG -
urine concentrating ability

phosphates -
disurption of phosphate calcium vitamin D cycle
higher may mean more discomfort

anemia -
anemia of chronic disease
reduced erythropoietin production

pH -
metabolic acidemia in very advanced CKD

FGF-23 -
novel biomarker for CKD
only in cats currently
early indication of phosphate increases

58
Q

CKD signs

A

uremia - weight loss, halitosis, dullness, anorexia, nausea, mouth ulcers, muscle and condition loss

signs relating to underlying cause

different sized kidneys

signs vary a lot with degree of azotemia

59
Q

management of nutrition and hydration - CKD

A

renal diet - adequate calorie, digestible, good quality protein, supplements
slow transition onto new diet

assisted feeding

appetite stimulants - metazopine, capromorelin

anti nausea - ondansetron, metazpoine
(don’t use metazopine and ondansetron together)

gastroprotectants - omeprazole (only if ulceration)

readily available water, water falvour enhancer

early renal diets - low phosphate and restricted protein

fluids

60
Q

management of hyperphosphatemia - CKD

A

target lower than range interval

dietary restriction

phosphate binders - given with foodm calcium or aluminium based

monitor with FGF-23

61
Q

management of proteinuria - CKD

A

protein restricted diet

monitor

RAAS inhibitors - dogs angiotension receptor blocks, cats ace inhibitors

62
Q

management anemia - CKD

A

treat at PCV <0.2

erythropoeitin and iron supplements

may need transfusion

63
Q

management of hypertension - CKD

A

can lead to issues with other organs and seizures

reliable BP measurements

dogs - ace inhibitor
cat - amlodipine or angiotension receptor blocker

64
Q

other management considerations - CKD

A

nephrotoxic drugs - NSAIDs - discontinue

positive urine cultures - treat as pyelpnephritis

hypokalemia - seen in advanced cases, lethary anorexia and muscle weakness, supplement oral potassium

hypercalcemia - complicated

acidemia - muscle wastage and anorexia, can supplement potassium cirtate or sodium bicarbonate but can put them off food

65
Q

monitoring CKD

A

iris 1 - every 6 months
iris 2 - 3-6 months
iris 3 - 1-3 months
iris 4 - 1-2 months

starved sample - blood/urine
BCS
muscle condition
hydration
creatinine (and urea but not as important)
phosphates
urine protein:creatinine
BP - doppler
PCV - anemia of chronic disease

optional - acid:base, ionised calcium, FGF-23

cysto centesis - if suspicious of pyelonephritis

66
Q

SDMA

A

glomerular filtration marker
increases earlier in damage
still affected by pre- and post-renal causes
day-to-day variation so not as good for tracking progress as creatinine
not affected by muscle mass
will definitely be up if creatinine already increased

67
Q

FGF-23

A

only in cats
indicator of phosphate levels - assessment of whether phosphate restriction working
assess need for early renal diet in early stages

68
Q
A

CMS - term 1 (15 decks)

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