Brainscape's Knowledge GenomeTM

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


See full index

randomsmithchapters > Renal Diseases > Flashcards

Renal Diseases Flashcards

1
Q

Describe the progression of lesions associated with ulcerative posthitis and associated clinical signs?

A

-begins as a small ulcer near mucocutaneous junction of prepuce as a loss red scab cover that is painful to palpation
–>spreads to internal mucosal prepucial surface– dysuria, vocalization while urinating
–>fibrous adhesions within the prepuce– stricture, impaired breeding soundness, weight loss in chronic cases

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

What are differentials for ulcerative posthitis and describe differentiating features

A

–ulcerative dermatosis– lip & leg ulcer of sheep, lesions bleed readily (ulcerative posthitis lesions usually do not)
–contagious ecthyma (ORF)– raised proliferative scab that is thick and durable on face, lip, udder
–Urolithiasis– ddx for any dysuric male sm rum
–preputial trauma
–Caprine herpesvirus-1 (CHV-1)– penile, vulva & vaginal lesions
–Ovine herpesvirus-2 (OHV-2)– ulcers tset pos for herpesvirus

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

What bacteria is most commonly implicated in ulcerative posthitis/vulvitis?

A

Corynebacterium renale

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

What are the virulence factors that allow C. renale to cause disease?

A

Contain enzyme urease
–>high protein diet–> INC ammonia production in Rumen–> converted urea in liver
–>proliferation of C. renale–> urease hydrolyzes urea back to ammonia– causes chemical irritation & ulceration to the prepuce

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

What are risk factors for the development of ulcerative posthitis?

A

-excessive protein diet ( usu. >16%)– alfalfa, lush legume, etc.
-Rams, pet weathers, club/show lambs
–wool & fiber production animals
- INC plane of nutrition in males prior to breeding
–breeds w/ dense wool/hair (merino sheep, angora goats)

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

Why are production losses seenw ith ulcerative posthitis?

A

pain
incapacitation of breeding
loss of breeding soundness
deformation of external genitalia

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

What antibiotics is C. renale sensitive to?

A

penicillin
amplicillin
cephalosporins
oxytetracycline

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

With antibiotic treatment of C. renale ulcerative posthitis/vulvitis,what other treatments/management changes need to be made

A

-dec protein& NPN intake (incorporate grass hay into feeding)
isolation of infected animals
fl y control
wool & hair removal from prepuce
topical antibiotic treatment (mastitis treatment tubes)

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

Describe the pathogenesis of Acute renal failure in horses caused by aminoglycosides:

A

-accumulate in proximal tubular epithelial cells (via urine–glomerulus)
–reaches toxic levels
—disrupts normal cell function
—-cell swelling & cell death
—– sloughing into tubular lumen, releasing lysosomal enzymes, intracellular Ca accumulation

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

Pigment nephropathy can occur with what diseases?

A

Rhabdomyolysis– myoglobin pigment
DIC/severe hemolysis/toxins (red maple leaf toxicosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which form of vitamin K can cause renal damage

A

menadion sodium bisulfit– K3

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

How does vitamin K3 cause renal disease?

A

direct tubular damage d/t oxidative stress
and
pigment nephropathy d/t hemoglobinuria

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

NSAIDS cause kidney injury at what location?

A

medullary crest necorisis

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

Supplementation of what vitamin, or plants containing this vitamin can cause renal disease?

A

Vitamin D

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

List heavy metals that can cause renal disease:

A

mercury (also causes GI irritation)
cadmium
Zinc
Arsenic
Lead

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

What is the toxic principle of acorn toxicity?

A

tannin

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

Acorn toxicity manifests as what C/S/disease?

A

–erosive GI disease–> diarrhea, edema
–INC vascular permeability–> body cavity effusion
–uremia
SHOCK

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

List drugs (besides NSAIDs, aminoglycosides) that can cause renal disease

A

oxytetracycline
polymixin B
amphtericin B
imidocarb diproprionate (babesia equi tx)
ochratoxins
PA poisoning
Blister beetle/cantharidin toxicosis

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

What are risk factors for the development of vasomotor nephropathy?

A

hemorrhagic shock
severe IV volume deficit
septic shock
coagulopathy
adverse drug rxns

***Lesion is ATN

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

what is the pathogenesis of acute glomerulopathy (which is rare)?

A

arteriolar microgangiopathy– distends glomerular capillaries–> fibrin thrombi & proteinacious debris (BOwmans Capsule)

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

Which species/serovar of leptospira have been a cause of interstitial nephritis in horses?

A

L. interrogens serovar pomona

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

How to diagnose leptospira interrogens serovar pomona as a cuase of interstitial nephritis in horses?

A

urine PCR
–> furosemide and getting 2nd voided sample will increase sensitivity
OR
rising serum titer or baseline >1:6400

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

What is the risk of performing a renal biopsy?

A

life threatening hemorrhage
- INC complication risk– L Kidney bx (go through spleen), neoplasia, low USG

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

Why are newborn foals often proteinuric the first couple of days of life?

A

proteinuria (1-2 d) d/t absorption of small molecular weight proteins in colostrum

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

Spurious hypercreatinemia in foals should decrease within what time period?

A

within 12 to 24 hours after birth

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

What form of acute renal failure is seen in foals? and through what pathologic mechanism?

A

Acute tubular necrosis
– post diarrhea
— d/t dehydration= poor perfusion (vasomotor nephropathy)

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

Why do foals have a greater dose of aminoglycosides than adults?

A

because of greater volume of distribution

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

Multifocal renal abscesses/infarcts are seen in foals, with what bacteria isolated most commonly?

A

Actinobacillus equilli
**usu die/euthanize before see ARF
**2-4 d old foals @ highest risk

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

What is the most common glomerular disease in horses?

A

proliferative glomerulonephritis

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

Describe the pathogenesis of proliferative glomerulonephritis.

A

circulating immune complexes along glomerular capillaries or in situ along basement membrane

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

Which immune complex is most commonly seen with proliferative glomerulonephritis?

A

IgG

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

What are common antigens seen to cause proliferative glomerulonephritis in horses?

A

–streptococcal antigen
–Equine infectious anemia virus

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

What is the most common cause of chronic renal failure in horses?

A

Chronic interstitial nephritis & fibrosis

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

Causes of chronic interstitial nephritis

A

ATN
nephrotoxins or vasomotor nephropathy
other etx: drug induced, urinary obstruction, pyelonpehritis, renal hypoplasia/dysplasia/papillary necrosis

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

What horses are at risk for the development of pyelonephritis (rare)?

A

-multiparous mares
-horses with bladder paralysis (d/t vesiculoureteral reflux)

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

What bacteria are commonly isolated in pyelonephritis (horses)?

A

staph
strep
corynbacterium

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

What are clinical signs of uremic encephalopathy?

A

obtundation
anxiety
head pressing
seizure

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

What are electrolyte abnormalities seen with CRF?

A

INC K
DEC Na
DEC Cl
+/- INC Ca
Dec PHOS (w/ inc Ca)

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

What is normal urine protein concentration?

A

100 mg/dL

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

What is normal urine protein to urine creatinine ratio?

A

1:1 (normal)

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

What is considered an abnormal urine protein to urine creatinine ratio?

A

> 2:1

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

What is the calculation for GFR?

A

{(Crea urine)/ (Crea serum)} X urine flow/ body weight (kgs)

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

What is considered a normal gfr and decreased GFR?

A

Normal: 1.5 to 3.0 ml/kg/min
Dec GFR: <1.0 ml/kg/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the cause of enzootic hematuria?

A

Chronic bracken fern ingestion

others: peteris spp,, chelarithes sieberi, onchyium contigium

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

Acute ingestion of bracken fern causes:

A

acute coaguloapthy or fulminant septicemic crisis (assoc with severe bone marrow suppression)

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

What are clinical signs of enzootic hematuria?

A

hematuria
chornic blood loss– tachycardia, pale mm, tachypnea, exercise interolance, pale mm
dysuria
pollakuria

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

what does the bladder palpate like with enzootic hematuria?

A

thickened bladder wall
bladder tumours
– rare we see obstruction of bladder trigone

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

What are potential ddx for enzootic hematuria

A

UTI
Malignant catarrhal fever
urolithaisis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the pathophysiologic consequences of bracken fern ingestion?

A

irritant
mutagenic
carcinogenic
immunosuppressive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the toxic principle of bracken fern?

A

ptaguiolside

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is thought to have synergism with bovine pappilloma virus 2 responsible for bladder tumors?

A

ptaquiloside carcinogenic in bracken fern

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

How to stop the hematuria seen with bracken fern ingestion?

A

will d/c with brakcen feeding
**before onset of tumour formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are the most common bacteria that cause ascending UTI in ruminants?

A

C. renale
E coli

Others: Salmonella spp., T pyogenes, P aeruginosa, Strep spp, Staph spp, corynbacterium pseudotuberculosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Cystitis associated with UTI can lead to showing of what C/S?

A

dysuria
pollakuria
driblle urine
retained arched stance after voiding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What are the most common presenting C/S in ruminants with UTIs?

A

Dec feed intake and dec milk production

other C/S: fever, inc RR, dec skin trugor, renal enlargement, ruminal stasis, etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What are ddx for C/S of dysuria seen with urinary tract infections?

A

vaginitis
perivaginal abscess
pelvic entrapement of bladder
vulvar trauma
postparturient swelling vagina and vulva

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are ddx for C/S of hematuria seen with UTIs?

A

parturition
papillomas in UT
postparturient hemoglobinuria
enzootic hematuria (many animals affected)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Describe the pathogenesis of diarrhea seen with pyelonephritis:

A

D/t proteinuria
–> dec albumin
–> dec oncotic pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Describe the pathogenesis of anemia seen with pyelonephritis

A

d/t dec EPO production
blood loss in urine
**chronic disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How is uti definitively daignoses?

A

-midstream/end stream– most accurate urien sample

other sources of contam: mertirit, vaginitis, prostatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

UTI urine abnormalities

A

hematuria
proteinuria
bacteria
USG: 1005 to 1020
gram stain urine– prelim dx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Describe routes that lead to the itnro of pathoens that lead to development of UTI:

A

-urogenital trauma– calving
-obstetric manipulation
-abnormal vulvar confirmation
-urine retention conditions: baldder adhesions, uracha reminan infection, spinal cord dzes
-bladder catheterization
-urolithiasis
-urogenital pappilloma
-dec bladder function or ectopic ureters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Describe the pathogenesis behind the development of pyelonephritis after bacteria establish in urinary tract

A
  1. Dec bladder function or ectopic ureters
  2. vesiculourteral reflux– aid infection/development of infection
    3 papillary & tubular epithelium necrosis, accumulation of necrotic debri in renal pelvis
    (loss of nephron function, abscessation, necrosis & loss of kidney shape)
  3. struvit uroliths or other calculi form around debri
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is the most common cause of pyelonephritis in bovine spp?

A

C renale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is the most virulent bacterial spp to cause pyelonephritis in cattle?

A

C. cystidis
C. pilosum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

How does C. renale cause UTI/pyelonephritis?

A
  1. adheres to UT epithelium via pili (pH mediated)
  2. enhanced in alkaline conditions, Dec acidic (feed urine acidifying diet– improvement)
    –ureolysis and ammonium– maintain alkaline environment and INC colonization
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

UTI are seen more commonly in which gender & why?

A

Females more commonly d/t shorter urethra
– breeding/parturition trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Most pyelonpehritis cases are seen when in ruminants?

A

IN cattle– 90 d post-vacliving

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

In 7 out of 15 cows diagnoses with pyelonephritis, have what repro trat abnormalities?

A

pneumovagina
metritis
poor perineal conformation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Long term antibiotic treatment is recommended with what antibiotic for treatment of C. renale?

A

Penicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Which antibiotics in the treatment of C. renale reach higher serum and urinary concentrations, compared to PPG?

A

Na or K Penn: 22,000-44,000 IU/kg q6h
Na ampicillin: 10-50 mg/kg q8h

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What can be used as a prognostic indicator for cull rate d/t pyelonephritis in cattle?

A

marked azotemia & pylonephritis: BUN >100 mg/dL, CREA > 1.5 mg/dL are more likely to be culled than nonazotemic w/ pyelonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What are preventative measures that can be taken to prevent pyelonephritis?

A

isolation, esp with C. renale
clean & disinfect contam. reas
aseptic technica to prevent iatrogenic spread
-venereal transmission– prevent with AI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Define pyuria

A

> 5-10 WBC/HPF of urine
bacteria >20 per HPF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

List antibiotics that get good concentrations in the lower urinary tract?

A

penicillin
ampicillin
cefiotiofur
fluoncazole
gentamicin
amikacin
**Tx 7 to 14 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is the drug of choice for treatment of candida spp involves in lower UTI?

A

fluconazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What antibiotics of choice in UPper UTI ?

A

TMS
ceftiofur
penicillin
ampicillin
**2 to 3 weeks of treatment

78
Q

What are the most common organs of amyloid deposition in horses?

A

kidney
liver
spleen

79
Q

Describe the pathogenesis of amyloidosis in cattle

A

-long standing inflammatories dzes (TRP, metritis)
– lead tos ecdonary renal amyloidosis – sustained heavy proteinuria

**signs of chronic wasting disease, chronic diarrhea

80
Q

On rectal palpation of the kidneys in cattle, what is felt with amyloidosis?

A

enlarged kidney, that is not painful and has normal architecture

81
Q

Amyloid is what ind of protein?

A

Beta pleated sheets of amyloid proteins that are highly resistant to proteasomes or macrophages

82
Q

What are consistent signs of amyloidosis?

A

proteinuria
hypoalbuminemia

83
Q

What test can confirm protein levels in urine, for diagnosis of amyloidosis?

A

sulfasalicyclic acid precipitation test

84
Q

What are DDx for renal amyloidosis?

A

Other causes of chornic diarrhea/hypoproteinemia/wt loss/poor productivity: GI parsitism, BLV, Glomerular nephritis
-johnes dz
-cu deficiency
-salmonellosis
-BVD

85
Q

Describe the findings of amyloidosis of the kidneys and how to confirm that diagnosis

A

INC kidney size
yelllow-tan-white discoloration
waxy renal parenchyma on cut surface
generalized edema
***amyloid deposits stained with congo red– bright green birefringence with polarized light

86
Q

Glomerulonephritis is an example of what time of hypersensitivty reaction?

A

type III hypersensitivity
**vasculitis reaction

87
Q

There are many causes of tubular necrosis, ultimately the main cause in the development of TN is:

A

impaired renal perfusion
— infarction of renal cortex (endotoxemia)
— renal vein thrombosis ( lambs w/ heat stress injury)
– mechanical obstruction of renal vasculature (severe rumen distention, rumen acidosis, etc)

88
Q

LIst nephrotoxic plants

A

Amaranthus retroflexus (pig weed)
Lilium spp (easter lily)
Wuercus spp (oaks)
Philodendron spp (philodendron)
Pinus ponderosa (nephrosis occurs win ocnjunction iwth hepatocellular damage & abortion)
Xanthium spp (cocklebur)
Cestrum diurnum (day-blooming jasmine)
Oxalate containing plants

89
Q

How does dehydration lead to tubular injury?

A

Blood flow to kidneys
– renal tubular epithelial cells have high metabolic demands– toxins disrupt cellular enzymes
— dehydration
– concentrates toxins in tubular filtrate
–slows toxin clearance
–dec renal perfusion

90
Q

Describe how sulfonamides can cause renal tubular injury?

A

deposition of insoluble precipitates in renal tubules & block excretion of creatinine

91
Q

Describe how NSAIDS cause renal tubular injury

A

block effect of prostaglandins– which maintain renal blood work

prolonged administration & dehydration

medullary crest necrosis

92
Q

What are treatments that can restore urine production in TN?

A

furosemide: work at the LOH, 1 mg/kg IV or IM, repeat q1-2 h until urien produced, monitor serum NA & K concen b/c K wasting

Mannitol: 0.25 to 1 g/kg IV bolus, osmotic diuresis

93
Q

List DDx for neurologic diseases that cause urinary incontinence (equine)

A

EHV-1
cauda eqiuina neuritis
polyneuritis equi
sorghum tox
aberrant larval migrans (haliceophalobus ginigvalis)
EPM

94
Q

Bethanechol in the treatmetn or urinary incontinence

A

0.03 to 0.04 mg/kg Sc or IV q6-8h
improves detrusor tone and strength of contraction

95
Q

The use of phenoxybenazmine with bethanechol is used for the treatment of urinary incontinence for:

A

is an alpha adrenerigc block to decrease urethral sphincter tone

4 mg/kg PO q6h

96
Q

Cattle is the primary maintenance horse of what lepto sppecies

A

L. interrogens serovar hardjo type hardjo (UK)
L. borgpetersenii serovar ahrdjo type hardjobovis (worldwide)

97
Q

Cattle are the incidental host for what lepto species?

A

L interrogens serovar pomona
L interrogens serovar grippotyphosa

98
Q

What serovars of lepto cause renal infection in cattle?

A

L interrogens serovars jardjo and pomona rippotyhposa

99
Q

Which serovar is host adapted in cattle causing persistent latent urogenital infection?

A

serovar hardjo

100
Q

L interrogens serovards hardjo cause what reproductive abnormalities in cows?

A

infertillity
stillbirth
abortion
birth of weak calves (PI)
milk drop syndrome or flabby udder (fever, agalactia, mastitis, soft udder, milk yellow to red tinged)

101
Q

in non host adapted lepto serovars cause what C?S

A

severe systemic dz
hemolytic anemia
hepatitis
interstital nephrtis
tubular nephrosis (calves > adults)
menintis (rare)
agalactia, mastitis– lactating cows
abortion– pregnant cows

102
Q

Leptospira pomona causes produces what that causes acute IV hemolysis and anemia?

A

hemolysins

103
Q

IN the non-symptomatic, convalescent phase of Leptospirosis in cattle, lepto localizes to what organs?

A

mammary gland
kidney
genital tract
**chronic renal infection

104
Q

Once lepto organisms localize to specific organs, it is shed and transmitted via what routes?

A

urine
uterine & vaginal secretions
placenta
fetal tissues
semen

105
Q

Where is leptospira protected from macrophages and humoral antibodies?

A

within the lumen of renal proximal convoluted tubule

106
Q

What are virulence factors of leptospira?

A
  1. LPS toxin & outer membrane proteins– interstitial nephritis
  2. adhesion to cells & extracellular matrix (fibrinectin binding proteins, lig A, B & C)
  3. bact motility
  4. hemolysis: sphingomyelinase C & H, hemolysis assoc protein 1 (HAP-1)
  5. Iron sequestration
107
Q

What diagnostic tests are commonly used to diagnose lepto?

A

Floursecent ab test
PCR
immunoblot
***inc sensitivity in testing by doing 2 tests on one sample

108
Q

What is the best urine sample for diagnosis of lepto?

A

2nd voiding urine samples after furosemid administration

109
Q

How is lepto diagnosed on histology

A

Wartharin starry silver stains
immunoperioxidase stain– more sensitive

110
Q

Serum titer of what value, is indicative of leptospira infection as a cause of acutre renal failure in horses?

A

> 1: 6400

111
Q

Proteinuria indicative of glomerular injury at what diagnostic value?

A

urine protein: creatinine ratio >2:1

112
Q

What it the most accurate assessment of renal function?

A

glomerular filtration rate
**inulin or radiolabelled substances

113
Q

define oliguria

A

fail to produce urine w/in 12 to 24 hours of IV fluid therapy

114
Q

In oliguric renal failure of >12 to 24 hours, what treatment can be pursued:

A

-furosemide (max of 4 doses)
-dopamine
-dobutamine (do not use with furosemide)
-mannitol

**no improvement in 72 hours, then hemodialysis or continuous flow peritoneal dialysis

115
Q

Which ruminants are at highest risk in developing urolithiasis?

A

castrated small ruminants
dietary and environmental factors inc risk

116
Q

What are common disorders results from urolithiasis?

A
  1. urethral obstruction
  2. chronic urethral obstruction
  3. urethra rupture
  4. urinary bladder rupture
117
Q

What differentials come to mind with proteinuria and hematuria on dipstick?

A

Glomerulonephritis & ruminant urolithiasis

118
Q

On rectal what is appreciated in small ruminants with urolithiasis?

A

pulsation of urethra

119
Q

What are the most common sites of obstruction of urolithiasis in cattle, sheep & goats?

A

cattle: distal aspect of sigmoid flexure

sheep & goats-urethral process

120
Q

What are DDx for congenital abnormalities for urolithiasis?

A

ectopic ureter
pelvic displacement of urinary bladder
urethral duplication

121
Q

List differentials for urine dribbling seen in chronic urethral obstruction:

A

neuro dz
previous urethral trauma (Stricture)
congenital anomalies
infection
neoplasia (rare, slow progression)
ulcerative posthitis

122
Q

What is a diagnostic that can be performed to diagnose strictures in the urethra?

A

contrast urethrography

123
Q

Urethral rupture is most commonly seen in what species with what C/S

A

feed lot steers
**water belly

124
Q

Pressure necrosis leading ot urethral rupture manifests as what C/S

A

cellulitis
penile adhesions
urethral fistula formation
urethral stircture
eretion fialiure
depression
inappetance
bilateral symm pitting edema

125
Q

Bladder rupture most commonly occurs in what spp?

A

bulls– testosterone b/c high mm pressure

126
Q

What electrolyte abnormalities are seen on peripheral bloodwork with urine in the abdomen?

A

LOW Na, CL, PHos
uremia & hemoconcentration

127
Q

With a bladder rupture, the creatinine in abdominal fluid compared to serum is:

A

abdom fluid 2: 1 serum

indicative of uroperitoneum

128
Q

Which stones form in alkaline urine?

A

struvite (magenesium ammonium phosphate)
Calcium phosphate
Ca carbonate

129
Q

What stones are not affected by urine pH

A

Calcium oxalate

130
Q

How is vitamin A deficiency implicated in urolithiasis?

A

Metaplasia of UT epithelium
–> nidus
–> desquamation of cells/altered cells surface

131
Q

What diet predisposes to the deveopment of phosphate calculi?

A

High phosphate rations– grain based

132
Q

What diets prevent phosphate calculi?

A

High Ca: phosphate ratio will help prevent

133
Q

In what location of US are ruminants predisposed to development of silica calculi?

A

native rangeland grasses of western N america
**silica fraction in these grasses inc with maturity

134
Q

What diet predisposes ruminants to the development of calcium based stones?

A

alfalfa hay: INC Ca, low Phosph, Low Mg, INC oxalate

**common in ruminants on lush clover pastures

135
Q

What is the risk of passing a catheter & retrograde flushing utheral stones?

A

can rupture urethera & rarely successful clearance of obstruction acheived

136
Q

What are surgical options for treatment of urolithiasis and obstruction?

A

urethral process amputation
penectomy
perineal urthrostomy
prepubic urethrostomy
urethrotomy
cystotomy
tub cystotomy
bladder marsupilization

137
Q

What are the most common form of ureteral calculi that form in horses?

A

calcium carbonate

138
Q

Is hematuria typically seen with cystic calculi in horses?

A

No– hematuria is typically seen after exercise, with bleeding visualized at the beginni go fstream

139
Q

Cystic calculi should be differentiated from:

A

soft tissue masses (neoplasia)
sabulous urolithiasis

140
Q

What is sabulous urolithiasis?

A

accumulation of urine sediment in ventral aspect of the bladder

141
Q

What are options for treatment options for cystic calculi?

A

perineal urthretomy
laparocystotomy
Gokel cystotomy
laxer or shockwave lithotripsy

142
Q

What can be administered to acidify urine in horses?

A

ammonium chloride
ammonium sulfate
change legum to grass hay diet
sodium chloride (25-50 g) to promote diuresis

143
Q

Urethral obstruction in horses most commonly occurs where?

A

males– located at ischial arch where urethra is its narrowest

144
Q

Idiopathic renal hematuria C/S

A

sudden onset gross, life threatening hematuria of one or both kidneys

145
Q

What is seen on endoscopy of bladder with idiopathic renal hematuria?

A

no abnormalities in urethra or bladder
**+/- blood clots exiting ureters

146
Q

What breeds have been seen with idiopathic renal hematuria?

A

several breeds (donkeys & mules)
–Arabians overrepresented >50%

147
Q

With urethral hemorrhage when is hematuria seen?

A

AT the end of urination (with urethral contraction)

148
Q

What is seen on endoscopy with urethral hemorrhage/ at what most common location?

A

dorsocaudal aspect of urethra at the level of ischial arch
** can find location with external digital palpation

149
Q

What ist he pathology of urethral hemorrhage?

A

suspect d/t “blow out” corpus spongiosum” of penis
– inc ejaculation pressure
**urination = contraction at end of urination to empty urethra

150
Q

What are common and uncommon causes of pu/pd in horses?

A

Common: CRF, PPID, primary/ psychogenic polydipsia

Less common: excessive salt consumption, central & nephrogenic diabetes insipidus, diabetes mellitus, sepsis/SIRS, iatrogenic (corticosteroids, diuretics, alpha 2s)

151
Q

What is the mechanism of PU/PD with PPID?

A
  1. osmotic diuresis
    – renal threshold of glucose ~170 to 175 mg/dl
    +/- concurrent EMS
  2. Antagonism of antidiuretic hormone (ADH) on collecting ducts via cortisol
  3. Central DI
    –growth of pituitary adenoma leading to impingement oon other areas of brain (posterior pitutiary & hypothalamus– storage and production of adh)
  4. excessive sweating & hirsuitism
152
Q

How is the diagnosis of primary psychogenic polydipsia made?

A

Dx of exclusion:
-renal failure
-PPID
-Diabetes insipidus
-chornic, persisten hyperglycemia
other factors: med administration, salt

153
Q

What is a diagnostic that can be performed to diagnosis primary psychogenic polydipsia?

A

water deprivation test: fail to concentrate urine (USG 1020)

154
Q

What are the types of diabetes insipidus?

A
  1. inadquate secretion ADH (neurogenic/central DI)
  2. Dec sensitivity of renal epithelial cells of collecting ducts to circulatingAD or loss of ADH receptors on these cells
155
Q

How do animals with diabetes insipidus respond to a water deprivation test?

A

animals fail to concentrate urine

156
Q

What is sued to treat nephrogenic diabetes insipidus?

A

thiazide diuretics (unknown mech)
NSAIDS/prostglandin inhibitors
Amiloride (Na ch. blocker)

157
Q

What it the mechanism that Diabetes mellitus causes PU/PD?

A

chronic hyperglycemia & glucosuria
–> PPID- INC ACTH & cortisol–> INC glucose levels
–> EMS– peripheral insulin resistance

–islet cell exhaustion (B cell)- inadequate insulin production with persistent hyperglycemia

158
Q

Renal tubular acidosis is characterized by:

A

improper functioning of renal tubules: characterized by: hyperchloremia, metabolic acidosis and normal anion gap

159
Q

Causes of renal tubular acidosis:

A

Primary dz
genetic
idiopathic
secondary to underlying dz
drug induces (suggest mechanism)
others: pyelonephritis, hyperparathryoidism, hypervitaminosis D

160
Q

What is type 1 renal tubular acidosis?

A

distal tubular excretion of H ions is compromised

**patients unable to produce acidic urine, so patients develop severe acidosis and patients develop hypokalemia (K ions excreted in exchange)

161
Q

What is type 2 renal tubular acidosis?

A

decreased proximal tubular bicarb resorption and subsequent urinary loss of bicarb
**normal excreted when bicarb reabsorbed in PCT
–hyperchloremia d/t inc renal absorption of CL in subseq bicarb loss

162
Q

Differentiation between T 1 and T2 renal tubular acidosis

A

T1: hypokalemia
T2: hyperchloremia

163
Q

What is fanconi syndrome?

A

defective resorption: glucose, aa, phosph, K, Na, Ca, Mg, Uric acid & other orhganic acids
-inherited/primary
-secondary renal me ror autoimmune

164
Q

ON chemistry what is seen with renal tubular acidosis?

A

metabolic acidosis ,low bicarb, high chloride

**compensatory: low PCO2, +/- Low K

165
Q

What is urine pH with renal tubular acidosis?

A

neural/alkaline

166
Q

What is the primary treatment in renal tubular acidosis?

A

IV/oral Na bicarbonate: replace 1/2 or 6 to 12 hours
– initial tx promotes kaliuresis (exacerbating low K)
–IV/oral KCL may be necessary

167
Q

What is the prognosis for treatment of renal tubular acidosis?

A

short term: good
– may require month long bicarb supplementation

168
Q

Bladder rupture is uncommon in adult horses, however what are the most common causes for bladder rupture males vs females?

A

Males: urolithiasis
females: foaling

169
Q

What are common primary kidney neoplasms?

A

renal cell carcinoma
adenoma (most common in older horses)
nephroblastoma- young horses
**Squamous cell carcinoma– most common bladder tumor in horses

170
Q

Bladder neoplasias are rare in ruminants, except for

A

Those caused by bracken fern

171
Q

Pelvic entrapment of the bladder is seen in ruminants, associated with:

A

postpartum straining
perineal hernia
vaginal prolapse
vaginal irritation
secondary displacement from trauma

172
Q

Urinary bladder eversion and prolapse is rarely seen, however is most common aseen with

A

dystocia d/t forceful straining that moves the bladder fundus caduall, +/- then forced out urthral orifice (bladder rolapse)

173
Q

What is the most common bacteria isolated, with septic foals leading to bladder necrosis

A

E coli is the most common isolate

174
Q

Uroperitoneum in foals is commonly mininterpreted as:

A

tenesmus in meconium impaction

175
Q

What is administered pre-operatively to correct hyperkalemia in uroperitoneumi n foals?

A

1-3 L of 0.9% NaCL with 5% glucose solution
**drain urine from abdomen

176
Q

How are ureteral defects diagnosed in foals?

A

US: retroperitoneal fluid around kidney on affected side
CT: find where abnormality is

177
Q

What is the most common cause of cystitis in down, recumbent foals?

A

candida spp common

178
Q

what is the treatment of candida cystitis?

A

fluconazole

179
Q

What is the most frequently reported developmental anomaly of the urinary tract in horses?

A

ectopic ureter

180
Q

what spp are predisposed to developing a patent urachus?

A

cloned calves

181
Q

What are pseudocysts?

A

outpocketings of renal capsule

182
Q

Why do pseudocysts develop?

A

d/t renal trauma, urinary tract obstruction or vascular or lymphatic anomalies

183
Q

What is renal oxalosis

A

metabolic dz, suspected to be inherited abnormality of glycine or glycoxalate metabolism (high levels of endogenous oxolate)
–> calcium oxalate cyrstals accumulate in renal tubules
–> obstruction of tubular outflow

184
Q

What disease should be ruled out with calclium oxalate crystals seen in urine?

A

exposure to xolate contianing plants or ehtylene glycol

185
Q

What are common sites of terminating ectopic ureters: Males

A

urethra
vas deferens
seminal vesicles

186
Q

What are common sites of terminating ectopic ureters: Females

A

urethra
vagina
cervix
ca bladder trigone

187
Q

What is the most common C/S of ectopic ureter?

A

urinary incontinence

188
Q

What is the triad of C/S/ consequences of EHEC that are characteristic of hemolytic uremic syndrome?

A

mciroangiopathic hemolytic anemia
thrombocytopenia
renal fialure

189
Q

What red cell abnormality is seen with hemolytic uremic syndrome?

A

shistocytes

190
Q

What is the difference between the typical and atypical form of hemolytic uremic syndrome in humans?

A

typical form: major cause of ARF yong children assoc with food/water consumption contam with shiga toxin–producing bact **enterohemorrhagic E. Coli (EHEC)

Atypical form: inheritated mutations of complement regulatory proteins & diverse acuases of enodthelial injry, including antiphospholipid abs, pregnancy, etc.

191
Q

What are the major pathogenesis hallmarks of hemolytic uremic syndrome?

A
  1. endothelial injury & activation leading to IV thrombosis
  2. plt aggregation
192
Q

What are sources of EHEC?

A

cattle are major source
** also isolated from humans

randomsmithchapters (15 decks)

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