Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ZUKU NAVLE PREP > Canine Flash Notes - Renal Physiology > Flashcards

Canine Flash Notes - Renal Physiology Flashcards

1
Q

what is azotemia? what are the different types & why is it important to characterize?

A

increase in BUN and/or creatinine

pre-renal, renal, & post-renal

important for accurate diagnosis, treatment, & prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is uremia?

A

clinical syndrome resulting from the accumulation of metabolic waste products due to renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is pre-renal azotemia? what is seen on lab values?

A

reduced renal perfusion - often caused by dehydration

increased BUN, creatinine, & USG over 1.030

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is renal azotemia? what is seen on lab values?

A

loss of 75% of nephrons

increased BUN, creatinine, & USG < 1.017

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is post-renal azotemia? what is seen on lab values?

A

blockage of urine outflow

increased BUN & creatinine, oliguria or anuria, & hyperkalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the pathophysiology of pre-renal azotemia? what happens if it remains uncorrected? sequela?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the pathophysiology of renal azotemia?

A

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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how do you treat pre-renal azotemia?

A

restore circulating fluid volume & renal perfusion, correct electrolyte abnormalities, & treat cause (dehydration, shock, addison’s, etc)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the prognosis of pre-renal azotemia?

A

usually, kidneys will resume normal function when re-perfusion is re-established if there is not prolonged ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are the 4 main causes of pre-renal azotemia?

A
  1. dehydration
  2. shock
  3. hypoadrenocorticism
  4. heart failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the pathophysiology of post-renal azotemia?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the classic case presentation of a dog with renal azotemia? what lab changes are seen?

A

acute - anuric/oliguric, occasionally polyuric

chronic - pu/pd, gi signs (vomiting/diarrhea), & oral ulcers

increase in BUN/creatinine & low specific gravity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are some causes of acute renal failure in dogs?

A

pre-renal ischemia from dehydration/hypovolemia, ethylene glycol toxicity, aminoglycoside toxicity, heavy metal toxicity, hypercalcemia, leptospirosis

chronic renal disease resulting in failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how is renal azotemia treated?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is the classic presentation of an animal with post-renal azotemia? sequela?

A

oliguria, straining to urinate, abdominal discomfort

heart failure from hyperkalemia & hydronephrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the main causes of post-renal azotemia?

A

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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how is a diagnosis of post-renal azotemia made based off of lab changes?

A

increased BUN/creatinine, ECG shows bradycardia, spiked t waves, absent p waves

check creatinine of abdominal fluid if rupture is suspected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

how is post-renal azotemia treated?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what values designate an animal as being polyuric/polydipsic?

A

urine production > 25ml/lb/day (more than 50 ml/kg/day)

water consumption > 50 ml/lb/day (more than 100 ml/kg/day)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

T/F: pu/pd is a manifestation of a disease & not a diagnosis

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is the mechanism of polydipsia?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is the common presentation of an animal that is pu/pd?

A

nocturia, inappropriate urination, incontinence, pollakiuria, & polydipsia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what urine production metabolism rate is used for a caged animal?

A

urine volume 25-45 ml/kg/24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

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?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

how is a water deprivation test used to diagnose disease in a pu/pd dog with no other signs of systemic disease?

A

if USG is over 1.025, suspect psychogenic polydipsia or cushing’s

if under 1.025, proceed with an ADH test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what tests are used to differentiate normal psychogenic polydipsia, hyperadrenocorticism, pituitary diabetes insipidus, nephrogenic diabetes insipidus, or medullary washout?

A

water deprivation tests, ADH test, gradual H2O test, & ADH + gradual H2O deprivation tests

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

how are results of an ADH test interpreted for an animal with pu/pd?

A

if USG is over 1.025 - pituitary diabetes insipidus, no ADH

if USG less than 1.025 - proceed with gradual H2O deprivation test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is the point of doing a gradual H2O test on a pu/pd dog?

A

correct possible medullary wash out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

how are results of an gradual H2O test interpreted for an animal with pu/pd?

A

if USG is higher than 1.025 - suspect psychogenic polydipsia or cushing’s

if USG is lower than 1.025 - proceed with ADH test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

how are results of an ADH + gradual H2O test interpreted for an animal with pu/pd?

A

if USG is less than 1.025 - kidney unresponsive to ADH

if USG is higher than 1.025 - pituitary diabetes insipidus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what are some differentials for a dog that is pu/pd?

A

diabetes mellitus, hypoadrenocorticism, primary renal disease, liver disease, pyometra, hypercalcemia, hyperparathyroidism, pituitary diabetes insipidus, & psychogenic polydipsia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what is isosthenuria?

A

USG of 1.008-1.012 - same as plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is hyposthenuria?

A

USG < 1.007, inability to concentrate urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what are the minimal concentration ranges of USG in dogs & cats?

A

dogs: 1.013-1.030

cats: 1.013-1.035

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what is the point of doing a water deprivation test on a pu/pd animal? what are the contraindications to doing it?

A

determines if ADH is released in response to subclinical dehydration

if kidneys can respond to ADH & concentrate urine

contraindications - dehydration, azotemia (BUN, creatinine), or hypercalcemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

when do you terminate a water deprivation test?

A

urine concentration > 1.025, > 5% weight loss, azotemia develops, dehydration develops

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is the benefit of doing a gradual water deprivation test?

A

for animals with psychogenic polydipsia with medullary washout (animal can’t concentrate on abrupt test), so this allows the gradient to be re-established

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

how is a gradual water deprivation test done?

A

reduce water intake bt 5% daily

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what is a negative result for a gradual water deprivation test?

A

animal fails to concentrate without renal disease or lab abnormalities - indicates neurogenic or nephrogenic diabetes insipidus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

when is an ADH response test done?

A

done after abrupt or gradual water deprivation test if there is an inadequate concentration

tests renal tubular ability to concentrate urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

how is an ADH response test done? how are the results interpreted?

A

vasopressin is given IM & USG is measured at 30, 60, 90, & 120 minutes

negative water deprivation test + positive ADH concentration >1.025 - diagnostic for neurogenic diabetes insipidus

both negative water deprivation & ADH response tests - indicate nephrogenic diabetes insipidus or DDI if after abrupt H2O deprivation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what is a negative result of an abrupt H2O deprivation test?

A

failure to concentrate, USG < 1.025 without renal disease or other lab abnormalities - indicates neurogenic or nephrogenic diabetes insipidus and/or medullary washout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what are the 3 main types of diabetes insipidus & their basic pathophysiology?

A
  1. nephrogenic - partial or complete renal tubule insensitivity to ADH
  2. central - partial or complete primary deficiency of ADH
  3. dipsogenic/psychogenic - excessive water intake
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what are the main causes of nephrogenic diabetes insipidus?

A

acquired secondary - renal & metabolic disorders affecting renal tubules’ ability to respond to ADH (most acquired forms are reversible following correction of the cause)

primary causes - acute renal failure, hydronephrosis, chronic pyelonephritis, fanconi’s syndrome

secondary causes - pyometra, DM, liver disease, lymphoma, cushing’s, addison’s, hyperthyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what metabolic changes can result in nephrogenic diabetes insipidus?

A

hypercalcemia & hypokalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what drugs are implicated as causes of nephrogenic diabetes insipidus?

A

steroids, anticonvulsants, & diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

how is nephrogenic diabetes insipidus diagnosed?

A

negative H2O & ADH test - both tests have a USG result of < 1.025

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

how is acquired nephrogenic diabetes insipidus treated? what about congenital?

A

acquired - treat predisposing cause & provide unlimited water supply

congenital - unlimited water supply, low sodium/protein diet, & chlorothiazide diuretics to enhance proximal tubule reabsorption of Na, Cl, & H2O

49
Q

what are the main causes of central/pituitary diabetes insipidus?

A

idiopathic - most common

CNS trauma/infection, neoplasia, parasitic migration

50
Q

what is the pathophysiology of central diabetes insipidus?

A

ADH acts on the distal tubules & collecting ducts to increase reabsorption of water, but there is either a lack of ADH formation and/or release of ADH

so decreased ADH = water diuresis (polyuria)

51
Q

how is central diabetes insipidus diagnosed?

A

negative H2O test & positive ADH test

persistent hypernatremia, H2O test USG < 1.025, ADH test positive

52
Q

how is central diabetes insipidus treated?

A

unlimited water!!!!

desmopressin for ADH supplementation

for pituitary tumors - cobalt radiation

53
Q

what is the cause of psychogenic diabetes insipidus?

A

disorder of thirst centers resulting in primary psychogenic DI - behavior problem or from drugs (salt, diuretics, glucocorticoids, fluids, anticonvulsants)

secondary polyuria to rid the body of excessive H2O - large breed dogs, kidneys are usually functional, but causes medullary washout

54
Q

how is psychogenic DI diagnosed?

A

urinalysis shows a USG of 1.001-1.003

water deprivation test shows concentrated urine

abrupt water deprivation diagnoses about 2/3 of cases

gradual water deprivation done in other 3rd to eliminate medullary washout

55
Q

how is psychogenic DI treated?

A

gradual water restriction to restore renal hypertonic medullary interstitium

behavior modification - diazepam

56
Q

what is the number one urolith in dogs & cats?

A

struvite

57
Q

what are the main causes of urolithiasis in dogs?

A

UTI - commonly present with urease producing bacteria, resulting in alkaline urine precipitates

metabolic disorders - PSS causing urate crystals

calcium phosphate - hyperparathyroidism

58
Q

how do dietary factors influence the formation of uroliths?

A

high magnesium - alkalinizing diet, favors struvite formation

corn gluten or soybean hulls - silica

high calcium or phosphorus diets - calcium phosphate

59
Q

what breeds are predisposed to struvite crystal/urolith formation?

A

females > males - mini schnauzers, welsh corgis, dachshunds, poodles, pugs, pekingese, beagles, & scottish terriers

60
Q

what breeds are predisposed to oxalate crystal/urolith formation?

A

males!!

mini schnauzers, mini poodles, yorkies, lhasa apsos, shih tzus, & dalmatians

61
Q

what breeds are predisposed to urate crystal/urolith formation?

A

dalmatian!!!! 60% of all urate uroliths!!!!!

portosystemic shunt dogs - mini schnauzers, yorkies, & pekingese

62
Q

what breeds are predisposed to silica crystal/urolith formation?

A

german shepherds

63
Q

what breeds are predisposed to cystine crystal/urolith formation?

A

males!!!

dachshund, basset hounds, english bulldogs, yorkies, irish terriers, & chihuahuas

64
Q

how are struvite uroliths treated?

A

abx for 3-5 days for UTI/struvite

ampicillin if no culture or TMS

65
Q

medical dissolution of stones will not work on what type of urolith?

A

calcium oxalate!!!!

66
Q

what urolith types require surgical intervention?

A

oxalate, calcium-phosphate, & silica

obstructed animals

those that medical treatment doesn’t effect

67
Q

what is the urine pH of animals with struvite stones?

A

alkaline - urease bacteria!!!!

68
Q

what does FLUTD stand for?

A

feline lower urinary tract disease

69
Q

what are predisposing factors of FIC/FLUTD?

A

bacterial/viral infection, dirty litter boxes, alkaline urine, dry&raquo_space;> canned food

70
Q

what is the number one blockage site in cats with urinary obstructions?

A

penile urethra!

71
Q

why do an ecg on a blocked cat?

A

look for life threatening side effects from hyperkalemia - tall T waves & bradycardia

72
Q

what is post-obstructive diuresis?

A

often occurs following relief of urinary obstruction

kidneys shut down because they finally get a break

73
Q

what fluids should be used on a blocked cat with hyperkalemia & acidosis?

A

0.9% saline + unblocking will quickly drop potassium

if it doesn’t, glucose & insulin therapy

bicarbonate if acidotic (ph < 7.2) 1-2 mEq slowly IV

calcium gluconate if life threatening arrhythmia

74
Q

how do you prevent a cat from becoming blocked again?

A

low magnesium diet

canned food

encourage exercise & free choice water

clean litter box often

75
Q

T/F: if a cat blocks once, there is a 70% chance it will happen again

A

true

76
Q

what surgical option is available for a cat that continuously blocks?

A

penile urethrostomy

77
Q

what must you differentiate urinary incontinence from?

A

abnormal elimination due to behavior, inadequate house training, or other disease

78
Q

what is enuresis?

A

urinary incontinence while animal is asleep

79
Q

what are some non-neurogenic causes of incontinence?

A

hormone-responsive, stress incontinence, urethral incompetence, pelvic bladder, urachal remnant, ectopic ureters

80
Q

what are some neurogenic causes of incontinence?

A

low motor neuron bladder (atonic), upper motor neuron bladder (automatic bladder), detrusal-urethral disorders, urge incontinence, detrusor hyperreflexia

81
Q

what are the normal phases of micturition in a healthy bladder?

A

storage (filling) phase - sympathetic (ANS) relaxes bladder detrusor muscle & increases internal urethral sphincter tone

somatic - controls external urethral sphincter (urethralis muscle)

stretch of bladder wall - sensory fibers to reflex & brain

voiding (emptying phase) - parasympathetic (ANS), contraction of detrusor muscle & inhibition of sympathetic & somatic urethral sphincters

82
Q

what are the differences in clinical signs between urinary incontinence & abnormal micturition?

A

incontinence - dribbling of urine, loss of voluntary control, & urine-scald dermatitis

abnormal micturition - inability to urinate, disruption of urine stream (dyssynergia), stranguria/dysuria, & abdominal pain/discomfort

83
Q

what is the first & most important step in working to diagnose urinary incontinence?

A

history questions!!!!

84
Q

what are important parts of your physical exam on a patient you suspect has urinary incontinence?

A

physical exam - look for urine scalding, palpate bladder before & after urination

distended bladder = increased urethral resistance or decreased bladder contractility

neuro exam - check sacral reflex arc (pudendal nerve - sensory & motor)

perineal reflex - pinch perineum & look for contraction of anal sphincter & ventroflexion of tail

bulbospongiosus reflex - squeeze distal penis/vulva & look for constriction of anus

85
Q

what diagnostics should be done for an animal you’re working up for incontinence?

A

blood values - renal values

urinalysis & culture

radiographs - look for obvious abnormalities, excretory urogram, positive contrast vaginogram, or retrograde urethrography

86
Q

how are ectopic ureters in dogs diagnosed?

A

vaginoscopy with or without new methylene blue dye to use visualization of contrast for ectopic ureters - also check for urachal diverticulum, bladder wall thickening, calculi, prostatic enlargement, urethral strictures, & pelvic bone abnormalities

87
Q

how are urodynamic studies used for diagnosing micturition disorders?

A

cystometrogram - checks bladder tone & volume & detrusor reflex

urethral pressure profile - looks at intra-urethral resistance

88
Q

what is the purpose of using electromyography in an animal you suspect is incontinent?

A

looks at coordination of detrusor & urethral sphincter by checking anal sphincter

89
Q

if a female adult animal presents with suspected incontinence, has reflexes present, & a small bladder, what two things are you mainly considering as differentials?

A

hormone responsive urinary incontinence or urinary tract infection

90
Q

if a female adult animal presents with suspected incontinence, has reflexes present, a small bladder, and signs of a UTI, how do you treat? what do you do if the animal doesn’t respond?

A

treat UTI or FIC - if it stops, it was urge incontinence from the UTI/FIC

if incontinence continues - need to rule out neoplasia, chronic cystitis, polyps, uroliths, or urachal remnant

91
Q

if a young adult animal presents with suspected incontinence, has reflexes present, & a small bladder, what three things are you mainly considering as differentials? how would you diagnose?

A

patent urachus - physical exam, see urine coming from the umbilicus

ectopic ureter - contrast urogram

vaginal stricture - digital vaginal exam, vaginoscopy, & contrast vaginography

92
Q

if an adult animal presents with suspected incontinence, has reflexes present, & a large bladder that is difficult to express, what three things are you mainly considering as differentials? how would you diagnosis it?

A

obstruction due to calculi - urogram

upper motor neuron bladder - physical exam finding of spastic paresis in hind limbs

reflex dyssynergia - clinical signs show animal stop/start during urine stream

93
Q

if an adult animal presents with suspected incontinence, has reflexes present, & a large bladder that is easy to express, what three things are you mainly considering as differentials? how would you diagnosis it?

A

lower motor neuron bladder - physical exam shows flaccid paralysis in the hind limbs

94
Q

what clinical signs are seen with reflex dyssynergia? how is it diagnosed? how is it treated?

A

start & abrupt stop of urination with stranguria that is voluntary

dx - clinical signs, perineal reflex intact, large, non-expressible bladder that is easily catheterized

tx - decrease alpha sympathetic tone with phenoxybenzamine or bethanechol

95
Q

what clinical signs are seen with LMN atonic bladder? how is it diagnosed? how is it treated?

A

continuous involuntary dribbling of urine & hindlimb flaccid paralysis

dx - no perineal reflex & large expressible bladder

tx - no effective treatment, manually express three times a day, & may try bethanechol/abx

96
Q

what clinical signs are seen with UMN automatic bladder? how is it diagnosed? how is it treated?

A

intermittent involuntary incontinence & hindlimb spastic paralysis

dx - hyperactive perineal reflex & large turgid non-expressible bladder

tx - intermittent catheterization

97
Q

what animals are usually affected by hormone-responsive incontinence?

A

older, spayed females

98
Q

what clinical signs are seen with hormone-responsive incontinence? how is it diagnosed? how is it treated?

A

voluntary control of urine with intermittent dribbling

dx - normal reflexes/bladder, & positive response to treatment

tx - diethylstilbestrol +/- phenylpropanolamine

99
Q

what clinical signs are seen with urethral incompetence? how is it diagnosed? how is it treated?

A

voluntary control + stressful incontinence

dx - normal reflexes/bladder & positive response to treatment

tx - increase alpha sympathetic urethral tone, phenylpropanolamine

100
Q

what clinical signs are seen with urge incontinence? how is it diagnosed? how is it treated?

A

frequent small urinations, urine spraying, stranguria

dx - UTI/VIC, hyperreflexive detrusor, normal bladder, & response to treatment

tx - treat UTI/FIC, inhibit detrusor with propantheline

101
Q

what clinical signs are seen with bladder atony/overdistension? how is it diagnosed? how is it treated?

A

long continuous involuntary dribbling of urine

dx - large flaccid bladder with large residual volume, difficult catheterization

tx - remove obstruction, place an indwelling catheter, & start bethanechol

102
Q

what clinical signs are seen with paradoxical incontinence? how is it diagnosed? how is it treated?

A

short continuous involuntary dribbling of urine

dx - large turgid bladder (non-expressible) with normal reflexes

tx - remove obstruction & place indwelling catheter

103
Q

what clinical signs are seen with ectopic ureters? how is it diagnosed? how is it treated?

A

voluntary urination & continuous dribbling of urine

dx - clinical signs (young animal), normal bladder reflexes

tx - ureteral transposition + phenylpropanolamine

104
Q

what is the hallmark sign of glomerulopathies? what is the main cause?

A

proteinuria in absence of urinary tract inflammation

immune complexes found in glomerulus in most - but most cases, the exact cause is unknown

105
Q

what are some examples of infectious causes of glomerulopathies?

A

bacterial endocarditis, infectious canine hepatitis, brucellosis, pyometra, heart worms, FIP, FeLV, lyme disease, & ehrlichiosis

106
Q

what are some examples of neoplastic causes of glomerulopathies?

A

lymphoma & mast cell

107
Q

what are some examples of inflammatory/immune-mediated causes of glomerulopathies?

A

systemic lupus erythematous, chronic pancreatitis, chronic pyoderma, & polyarthritis

108
Q

what are the main sequela of glomerulopathies that can be life threatening?

A

uremia if more than 75% of nephrons are affected

pulmonary thromboembolism - hypercoagulable state due to loss of antithrombin III

nephrotic syndrome - from prolonged proteinuria & hypoalbuminemia with edema & ascites

109
Q

how are glomerulopathies diagnosed?

A

blood values - non-regenerative anemia, hypoalbuminemia

UA - persistent proteinuria, use UPC to assess magnitude (1-5 = chronic interstitial nephritis, 3-40 = glomerulonephritis, & 10-40 = amyloidosis)

110
Q

what is the only diagnostic test that can differentiate between amyloidosis & glomerulonephritis?

A

renal biopsy

111
Q

what is the pathophysiology of glomerulonephritis? what is the prognosis?

A

deposition of antigen-antibody complexes in glomeruli - these immune complexes change the permeability of glomerulus leading to proteinuria & hypoproteinemia

guarded

112
Q

what is the pathophysiology of amyloidosis? what is the prognosis?

A

disposition of fibrillar glycoprotein in organs

dogs - disposition primarily in glomeruli resulting in PLN

cats - disposition primarily in renal medullary interstitium resulting in chronic renal failure

poor prognosis

113
Q

what are the suggested causes of amyloidosis?

A

idiopathic

secondary to inflammation & neoplastic processes - tissue injuries stimulates liver amyloid precursors (liver, spleen, & kidney primarily affected) leading to progressive kidney dysfunction

familial form in shar pei, abyssinians, & beagles

114
Q

T/F: nephrotic syndrome is a descriptive term & not a diagnosis

A

true

115
Q

nephrotic syndrome means what things are present?

A

edema, ascites, proteinuria, hypoalbuminemia, hypercholesterolemia, & edema

proteinuria of sufficient magnitude to cause hypoalbuminemia (decreased oncotic pressure = edema)

hypercoagulability - loss of antithrombin III (thromboembolism & compromised immune system)

116
Q

what causes nephrotic syndrome in dogs & cats?

A

glomerulonephritis & amyloidosis

most patients with glomerular disease don’t develop nephrotic syndrome

117
Q

what treatment is used for glomerulonephritis & nephrotic syndrome?

A

treat underlying cause if found

diet - sodium/protein restricted diet

enalapril, anticoagulants

vitamin B & C, free choice water

118
Q

what treatment is used for amyloidosis?

A

no specific treatment proven effective - most animals are terminal

ZUKU NAVLE PREP (178 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions