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Titi Pipi > Tina Reed > Flashcards

Tina Reed Flashcards

1
Q

congenital anomalies of the urinary tract

A

uncommon

unilateral renal agenesis : 0,07% of the population

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2
Q

innervation of the kidney

A

predominantly sympathetic, because the kidneys appear to be poorly supplied by cholinergic nerves.

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3
Q

tubular sodium reabsorption and renin release is influenced by which nerve

A

sympathetic activation of α1-adrenoceptors.

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4
Q

3 most abundand receptors in renal vasculature

A

α- and β-adrenoceptors, dopaminergic adrenoceptors

specifically dopamine type 1 receptors, leads to increased perfusion of the outer renal medulla -

dopamine use indicated in acute renal injury

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5
Q

how does xylazine induce diuresis

A

dont know exact mechanism, maybe

  • drug binding to α2-adrenoceptors located on collecting duct epithelium.

Activation of these receptors can lead to antagonism of the effects of antidiuretic hormone on cortical collecting ducts, which results in diuresis.

OR

  • transient hyperglycemia induced by xyl
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6
Q

equine ureteral smooth muscle is influenced by which receptors?

A

smooth muscle contains α1- and β2-adrenoceptors, which induce contraction and relaxation, respectively, when activated by norepinephrine

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7
Q

Somatic innervation of the lower urinary tract is primarily to the striated muscle of the external urethral sphincter via

A

a branch of the pudendal nerve, which originates from the sacral cord segments (S1–S2).

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8
Q

what is renal agenesis?

A

failure of the metanephric duct to fuse with the metanephrogenic mesodermal tissue

frequency of unilateral renal agenesis in horses: 0,07%

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9
Q

Blood BUN-to-Cr ratio to differentiate acute from chronic renal failure

A

acute renal failure: Cr tends to increase proportionately more than BUN, <10:1.

chronic kidney disease often > 10:1

(Crea wieder niedriger)

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10
Q

What happens to Calcium in acute renal failure?

A

hypocalcemia and hyperphosphatemia are more common with acute renal failure.

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11
Q

Urine specific gravity is used to separate urine concentration into three categories:

A

(1) hyposthenuria: specific gravity < 1.008
(2) isosthenuria 1.008–1.014 (osmolality 260–300 mOsm/kg);
(3) hyper: > 1.014 and osmolality greater than 300 mOsm/ kg).

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12
Q

Does aciduria reflect metabolic acid base status?

A

Not really

typically has been attributed to metabolic acidosis, many patients actually may have hypochloremic metabolic alkalosis accompanied by paradoxic aciduria.

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13
Q

Which factors acidify urine?

A

Vigorous exercise

bacteriuria

normal in foals

neutral:

concentrate feeding (more towards neutral value)

very dilute urine → neutral

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14
Q

A positive result for blood on a urine reagent strip can reflect the presence of

A

hemoglobin, myoglobin, or intact erythrocytes in the urine sample

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15
Q

What are casts? what do they imply?

A

Casts are molds of Tamm-Horsfall glycoprotein and cells that form in tubules and subsequently pass into the bladder.

Casts are rare in normal equine urine but may be associated with inflammatory or infectious processes.

unstable in alkaline urine; thus, one should evaluate sediment as soon as possible after collection to ensure accurate assessment.

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16
Q

Which crystals do you see in the urine

A

NORMAL

li:

round: calcium carbonate (CaCO3)

länglich: Calcium phosphate

re:

Calcium oxalate

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17
Q

Which enzymes can be measured in horse urine

A

GGT: PROXimal tubular cells

ALP: PROX

NAG (higher in intact males): PROX

LDH (higher in intact males): DISTAL TUBULAR C.

kallikrein

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18
Q

medullary rim sign

A

distinct curvilinear hyperechoic bands in the outer renal medulla parallel to the corticomedullary junction with renal disease attributable to acute or chronic phenylbutazone toxicity.

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19
Q

When to do Water Deprivation test

A

to determine whether hyposthenuric polyuria is caused by a behavior problem such as

primary (psychogenic) polydipsia or

central or nephrogenic diabetes insipidus

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20
Q

When to stop water deprivation test

A

one can stop the test when urine specific gravity reaches 1.025 or greater.

the test should be stopped if more than 5% of body weight is lost or clinical evidence of dehydration becomes apparent.

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21
Q

water deprivation test with long standing primary polydipsia

A

normal: >1.045 in response to water deprivation within 24 to 72 hours

With long-standing primary polydipsia: may not be able to concentrate urine fully (to a specific gravity greater than 1.025) because of partial washout of the medullary interstitial osmotic gradient.

=> modified water deprivation test

during which daily water intake is restricted to 40 mL/kg for several days, which should allow time for restoration of the medullary interstitial osmotic gradient.

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22
Q

Water deprivation test: urine isostenuric

What now?

A

assume central or peripheral diabetes insipidus

administer Vasopressin/ADH:

if >1020 after 1.5h=> central diab insipidus

failure to concentrate => nephrogenic

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23
Q

Tests to differentiate between central and peripheral diabetes insipidus

A

administer ADH/Vasopressin

administer desmopressin

Hickey-Hare test: IV challenge with hypertonic saline

The goal is to produce an increase in plasma osmolality, which should trigger release of endogenous vasopressin

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24
Q

possible outcomes of Hickey Hare test

A

normal response: expected in horses with primary polydipsia: concurrent increases in plasma vasopressin concentration and urine specific gravity. .

if urine specific gravity does not increase:

DIABETES INSIPIDUS

nephrogenic diabetes insipidus: increased plasma vasopressin concentration;

neurogenic diabetes insipidus no increase

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25
Q

early tests for renal dysfunction

A

measure GFR: by inulin clearance or endogenous Creatinine clearance (Cr usually under- or overestimates GFR)

urinary sediment

urinary enzymes: GGT,…

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26
Q

Generally, the parenchymal lesion associated with NSAID toxicity is

A

medullary crest or papillary necrosis.

Such lesions develop because the renal medulla normally receives much less blood flow than the renal cortex and consequently is much more susceptible to NSAID-induced changes in renal blood flow

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27
Q

intrinsic renal failure recognized most often in horses

A

Acute tubular necrosis (ATN)

(interstitial and primary glomerular disease being recognized occasionally and vascular disease almost never).

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28
Q

Most common causes of acute tubular necrosis

A

Ischemia, especially when associated with microvascular coagulation (which often leads to irreversible cortical necrosis), and

nephrotoxins (Genta, NSAIDS, pigmenturia, VIT D or K)

29
Q

Causes of intravascular hemolysis and hemoglobinuria include

A

incompatible blood transfusions,

immune-mediated hemolytic anemia,

fulminant hepatic failure, and

toxicosis from ingesting onions (Allium spp.) or withered red maple leaves (Acer rubrum)

30
Q

Acute interstitial nephritis often is not recognized but is believed usually to result from

A

an allergic reaction to drugs such as β-lactam and sulfonamide antibiotics.

Immunemediated and embolic or ascending bacterial infections also may be associated with the condition, which is characterized by edema and inflammatory cell infiltration of the interstitium

31
Q

Glomerulonephritis often is identified postmortem in aged horses and apparently is most often

A

immune mediated.

. Although the condition is theoretically reversible with immunosuppressive agents, in horses such undertakings are usually impractical and rarely are tried for long

32
Q

whats worse for the kidney:

frequent genta administration of lower conc or

infrequent but high dosing?

A

High trough concentrations are more nephrotoxic than high peak concentrations because tubule cells are exposed to higher aminoglycoside concentrations over a longer period of time. As a result, once-daily dosing may attenuate the risk of nephrotoxicosis while maintaining or improving therapeutic efficacy

33
Q

how to prevent renal aminoglycoside toxicity

A

both intravenous calcium supplementation (calcium gluconate 20 mg/kg q 12 h)409 and increased dietary calcium intake through alfalfa hay

34
Q

Which ABs are toxic for the kidney?

A

aminoglycosides

SOME cephalosporines such as cephaloridine

Polymyxin B

35
Q

clinical differentiation of prerenal or renal failure

A

In prerenal failure, volume repletion also should restore renal function, with the result that the magnitude of azotemia should decrease by 50% or more during the first day of therapy.

36
Q

Eosinophiluria generally seems to be limited to

A

renal interstitial disease

37
Q

Blood and urine characteristics of ATN

A

specific gravities usually less than 1.020

Reduction of GFR

Granular casts

Plasma sodium and chloride low.

slight to moderate proteinuria

(Prominent Enzymuria and phosphaturia early )

(Plasma concentrations of calcium and inorganic phosphate vary greatly)

38
Q

differentiate ARF caused by acute glomerulonephritis from that caused by hypoperfusion

A

glomerulonephritis:

significant proteinuria and red blood cell numbers

39
Q

why can ARF cause anemia?

A

Severe uremia

→ decreases erythrocyte life span and

→ induces platelet dysfunction.

=> anemia (possibly also caused by decreased production of EPO) and bleeding tendencies may be associated with ARF.

40
Q

In the event that the horse remains oliguric 10 to 12 hours after starting fluid therapy in ARF…

A

administration of dopamine in 5% dextrose slowly (3–5 μg/kg/min) may improve renal blood flow and urine output.

Administration of dopamine should be discontinued if blood pressure starts to rise.

41
Q

Diagnosis in chronic renal failure (in cases of non-congenital disease)

A

⅓ glomerulonephr

⅓ intersitial

42
Q

Abnormal Laboratory Values Reported for Horses with Chronic Renal Failure

4 häufigste?

A

BUN/Cr >10 85%

BUN/Cr >15 50%

Anemia <30% 40%

Hypoalbuminemia <2.5 g/dL 86% Hypoalbuminemia <2.0 g/dL 50%

Hyponatremia <135 65%

Hyperkalemia >5.0 mEq/L 56%

Hypochloremia Cl− <95 46%

Hypercalcemia >13.5 mg/dL 67% Hypophosphatemia (P <1.5 mg/dL) 47%

Acidosis pH <7.35 60%

43
Q

protein on the urinary strip: how can you know if this is significant?

A

measure urine protein-to-Cr ratio

> 2.0:1 likely supports significant proteinuria

44
Q

which values on the urine strip might be influenced by heavy proteinuria?

A

heavy proteinuria (more than 200 mg/kg/day)

can increase urine specific gravity to 1.020 or greater

45
Q

relation between blood crea and GFR in disease

A

doubling of creatinine roughly correlates to a 50% decline in GFR

46
Q

which hay in CKD

which nutritional requirements of feed?

A

grass hay

provide adequate but not excessive amount of protein (less than 10% crude protein), which should maintain the BUNto-Cr ratio in a target range between 10:1 and 15:1

47
Q

primary cystitis

A

uncommon in horses,

Bacterial cystitis is usually a secondary problem that may accompany alterations in urine flow caused by urolithiasis, bladder neoplasia, bladder paralysis, an anatomic defect of the bladder or urethra, or entry into the urinary tract (e.g., catheterization, endoscopy).*

48
Q

Definitive diagnosis of bacterial cystits requires…

A

quantitative culture results exceeding 10,000 colony-forming units (CFUs) per milliliter

in a urine sample collected by midstream catch or urethral catheterization.

49
Q

Pyelonephritis in horses has been described in association with

A

urolithiasis,

recurrent cystitis, and

bladder paralysis.

SELTEN!

50
Q

which bacteria can cause hematogenous septic nephritis

A

Actinobacillus equuli,

Streptococcus equi subsp. equi,

Rhodococcus equi, or

Salmonella spp.

51
Q

Horses develop two basic forms of uroliths,

A

both are composed primarily of CaCO3.

> 90% are yellow-green spiculated stones that easily fragment (type I urolith)

Less commonly, uroliths are gray-white smooth stones that are more resistant to fragmentation (type II urolith)

52
Q

Common differential diagnoses for bladder paresis or paralysis include

A

equine herpesvirus–1,

polyneuritis equi,

illicit tail block,

equine protozoal myeloencephalitis, and

sacral fracture or osteomyelitis.

53
Q

idiopathic renal hematuria

which breed and treatment?

A

more than 50% of animals with idiopathic renal hematuria have been Arabians.

supportive: fe blood transfusions and aminocarpoic acid…

54
Q

definition of polyuria and polydipsia

A

For small animals, polyuria and polydipsia have been defined as urine output exceeding 50 mL/kg/day and fluid intake of more than 100 mL/kg/day.696,697 These values would equate to 25 L of urine production and 50 L of water consumption for a 500-kg horse.

55
Q

Vasopressin:

Excessive water consumption leads to…

A

suppression of vasopressin release.

56
Q

vassopressin in stressed horses

A

goes up

vasopressin also appears to be a “stress hormone” in horses because substantially greater concentrations (tenfold higher than those induced by water deprivation) have been measured after application of a nose twitch, nasogastric intubation, or exercise.

57
Q

treatment of diabetes insipidus

A

central: desmopressin (vasopressin analog)

nephrogenic: restrict sodium and water intake or to administer thiazide diuretics.

58
Q

acid-base in acute or chronic kidney disease

A

frequently acidotic.

almost invariably azotemic,

hypochloremic, and

normokalemic or hyperkalemic

59
Q

cause of RTA

A

most of the times idiopathic

60
Q

When should RTA be suspected?

A

whenever a horse has a severe hyperchloremic metabolic acidosis

in the absence of any obvious cause of extrarenal hypovolemia such as diarrhea or small intestinal ileus.

anion gap = NORMAL in RTA

61
Q

blood hallmarks in RTA

A

combination of

hyperchloremia,

acidosis

normo- or hypokalemia, and a

normal plasma anion gap.

62
Q

The most commonly reported and best-described renal tumor in the horse is

A

renal cell carcinoma or adenocarcinoma

(primary renal neoplasms <1% of all horse neoplasms)

63
Q

Much of the normal anion gap is determined by

A

presence of albumin

64
Q

Treatment of RTA?

Prognosis?

A

Supplementation of K and HCO3-→ normally improvement over 48hrs

on the long term good hay for K and oral Bicarb supplementation are needed

Prognosis: favorable except if there is underlying kidney disease

65
Q

Types of RTA and their features?

acidosis , hypokalemia , glucosuria/proteinuria , urine pH during moderate/during severe acidosis

A

TYPE 1: DISTAL/CLASSIC: Failure of H+ excretion

TYPE 2: PROX: Failure of HCO3 Resorption

66
Q

Which tumor reacts to COX 2 inhibitors

A

some SCC - use piroxicam

67
Q

Three categories of micturition problems

A

(1) the reflex or upper motor neuron (UMN) bladder (also known as spastic or autonomic bladder) -→ associated with broad deep spinal lesions -→ can lead to secondary atonia bc of overstretching of the detrusor muscle

(2) paralytic or lower motor neuron (LMN) bladder

  • → EHV 1
  • → cauda equina neuritis
  • → lumbosacral trauma

(3) the myogenic or nonneurogenic bladder → idiopathic

Either of the last two conditions can be associated with the atonic bladder syndrome,

68
Q

Tx of bladder incontinence and success rates

A

one study: Only 21% of cases successfully treated, and

approximately 50% were eventually euthanized because of incontinence.

  1. α-adrenergic blocker phenoxybenzamine to eliminate any urethral resistance
  2. Bethanechol chloride is a parasympathomimetic agent resistant to the action of acetylcholinesterase and apparently has a selective effect on the smooth muscle of the gastrointestinal tract and bladder

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