Exam 4 - Polyuria/Polydipsia Flashcards

1
Q

what is polyuria for a dog?

A

urine production > 50 ml/kg/day

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2
Q

what is polydipsia for a dog?

A

water intake > 100 mg/kg/day

owner may mistake polyuria for pollakiuria, but most owners can measure water intake

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3
Q

what is isosthenuria?

A

usg 1.008-1.012

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4
Q

what is hyposthenuria?

A

usg 1.001-1.007

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5
Q

what represents minimally concentrated urine in dogs & cats?

A

dogs - usg <1.030

cats - usg <1.035

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6
Q

thirst is mainly controlled by what? what else can cause thirst?

A

mainly controlled by dehydration of osmoreceptors

non-osmotic factors such as decreased arterial blood pressure & increased body temperature can stimulate thirst

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7
Q

T/F: thirst is abnormally stimulated in patients with primary polydipsia

A

true

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8
Q

what is required of the body to be able to form concentrated urine?

A

body must produce ADH & renal tubules must respond to ADH

requires that the renal medullary interstitium be hypertonic & that at least 1/3 of the total nephron population be functional

so that in the presence of ADH, the distal portion of the distal convoluted tubule & collecting duct to become permeable to water where water is reabsorbed from the tubular lumen

hypertonicity of the renal medullary interstitium produces osmotic pressure that drives the water resorption & the kidneys maintain body fluid composition & volume

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9
Q

what is the mechanism causing pu/pd in a patient with diabetes mellitus? what diagnostics can you use to prove this?

A

osmotic diuresis due to glucosuria

blood glucose levels & measure urine glucose

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10
Q

what is the mechanism causing pu/pd in a patient with renal failure? what diagnostics can you use to prove this?

A

osmotic diuresis of remnant nephrons & structural disruption of medullary concentration gradient

measure BUN, creatinine, SDMA, & do a urinalysis

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11
Q

what is the mechanism causing pu/pd in a patient with bacterial pyelonephritis? what diagnostics can you use to prove this?

A

renal parenchymal damage + e. coli endotoxin competes with ADH on renal tubules

do a urine culture, abdominal ultrasound, & excretory urogram

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12
Q

what is the mechanism causing pu/pd in a patient with hypercalcemia? what diagnostics can you use to prove this?

A

inhibits binding of ADH to receptors on renal tubules

measure serum or plasma calcium

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13
Q

what is the mechanism causing pu/pd in a patient with hyperadrenocorticism? what diagnostics can you use to prove this?

A

glucocorticoids inhibit ADH release & inhibit the effects of ADH on renal tubules

do a LDDST, ACT stim test, or urine cortisol:creatinine ratio

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14
Q

what is the mechanism causing pu/pd in a patient with hyperthyroidism? what diagnostics can you use to prove this?

A

increased medullary blood flow & psychogenic

run a serum T4

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15
Q

what is the mechanism causing pu/pd in a patient with hepatic insufficiency? what diagnostics can you use to prove this?

A

loss of medullary concentrating gradient (low urea)

possibly psychogenic

do a chemistry panel, bile acids, blood ammonia, & abdominal imaging

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16
Q

what is the mechanism causing pu/pd in a patient with a pyometra & e. coli septicemia? what diagnostics can you use to prove this?

A

endotoxin competes with ADH binding sites on renal tubules

good history, cbc, abdominal imaging, & cultures

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17
Q

what is the mechanism causing pu/pd in a patient with post-obstructive diuresis? what diagnostics can you use to prove this?

A

osmotic diuresis due to retained solutes (especially urea)

take a good history & look at patient urine output

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18
Q

what is the mechanism causing pu/pd in a patient with hypoadrenocorticism? what diagnostics can you use to prove this?

A

mineralocorticoid deficiency results in sodium loss & renal medullary wash out

measure serum Na, K, & do an acth stim test

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19
Q

what is the mechanism causing pu/pd in a patient with diabetes insipidus? what diagnostics can you use to prove this?

A

primary - decreased ADH production

nephrogenic - defect in renal response to ADH

do a modified water deprivation test (diagnosis of exclusion)

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20
Q

what is the mechanism causing pu/pd in a patient with psychogenic issues? what diagnostics can you use to prove this?

A

primary - unexplained increase in water intake + renal medullary washout

do a modified water deprivation test (diagnosis of exclusion)

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21
Q

what is the mechanism causing pu/pd in a patient with an iatrogenic cause? what diagnostics can you use to prove this?

A

take a good history & look at fluid therapy

22
Q

what is the mechanism causing pu/pd in a patient with primary hyperaldosteronism? what diagnostics can you use to prove this?

A

resistance to the effects of ADH in renal tubules & disturbed regulation of ADH release

measure serum Na/K, take blood pressure measurements, do an abdominal ultrasound, & acth stim test (aldosterone)

23
Q

what is the mechanism causing pu/pd in a patient with acromegaly? what diagnostics can you use to prove this?

A

results in diabetes mellitus causing pu/pd

measure IGF-1 levels & do a ct scan

24
Q

what is the mechanism causing pu/pd in a patient with renal glucosuria? what diagnostics can you use to prove this?

A

osmotic diuresis due to glucosuria

measure bg & urine glucose

25
Q

what is the mechanism causing pu/pd in a patient with hypokalemia? what diagnostics can you use to prove this?

A

nephrons are less responsive to ADH

measure blood K

26
Q

what are some history clues that lead to a suspicion of pu/pd in companion animals?

A

litterbox needs to be changed more often

dog needs to go outside to urinate more often/has accidents in the house

water bowl needs to be refilled more often or pet is seeking more water sources

last estrus cycle!!!

27
Q

T/F: water intake can usually be measured but urine output is more difficult to measure

A

true

28
Q

what should you look for on physical exam when working a patient up for pu/pd? what are some common findings?

A

palpate the liver & kidneys

endocrine alopecia and/or pendulous abdomen may suggest hyperadrenocorticism

palpate the thyroid glands

lymphadenopathy

anal sac mass

recent onset cataracts suggesting diabetes mellitus

29
Q

T/F: if a patient presents for pu/pd & has a usg < 1.030, it is reasonable to evaluate for causes

A

true

30
Q

what is commonly seen on a cbc of a patient with pu/pd?

A

stress leukogram - absence may support hypoadrenocorticism

evaluate for inflammatory leukogram - may support pyelonephritis

polycythemia

31
Q

what is commonly seen on chemistry panels of patients with pu/pd?

A

BUN, creatinine, SDMA - low urea disrupts medullary concentration gradient, so you need to evaluate for azotemia and/or elevated SDMA

liver enzymes - may be elevated with liver disease or cushings/feline hyperthyroidism

calcium - high levels can cause pu/pd

hyperglycemia - diabetes mellitus or euglycemia with primary renal glucosuria

albumin - may be decreased with liver disease, addison’s & some renal diseases or can be increased with dehydration

32
Q

why may you have a hyposthenuric usg in a pu/pd patient?

A

psychogenic polydipsia or absent ADH/abnormal response to ADH

33
Q

if you have a usg that is less than or equal to 1.007, what does that exclude as a cause of pu/pd?

A

generalized renal dysfunction is excluded

34
Q

what is the preferred collection method for urine culture for a patient that is pu/pd?

A

cystocentesis

35
Q

T/F: lower urinary tract infections are not expected to cause polyuria but do cause pollakiuria

A

true

36
Q

how can an owner monitor the pet at home for polydipsia?

A

measure water intake at home for 2-3 days by measuring the amount of water put in the bowl & the amount left at the end of the day while isolating other pets & home & restricting other water sources

37
Q

what is normal water intake a day for a dog? what classifies them as polydipsic?

A

<60 ml/kg/day is normal

> 100 ml/kg/day is abnormal

38
Q

what is the mechanism of thirst from decreased blood volume caused by?

A

angiotensin II stimulates thirst

39
Q

what is required for the body to have normal urine concentrating ability?

A

adequate renal tubular function

hypertonic renal medullary interstitium (urea & Na)

ADH from the hypothalamus

renal tubular response to ADH

40
Q

what is the autoregulatory system in the kidneys?

A

made up by the macula densa cells in the walls of the late distal tubules that maintains gfr despite changes in arterial blood pressure

41
Q

what happens to the autoregulatory system if filtrate is flowing too slowly?

A

vasodilation of the afferent arterioles occurs & there is an increase in gfr

42
Q

what happens to the autoregulatory system if filtrate is flowing too rapidly?

A

vasoconstriction of the afferent arterioles occurs & there is a decrease in gfr

43
Q

what is gfr?

A

amount of fluid filtered from the blood into the capsule each minute

44
Q

what is net filtration pressure in the nephron?

A

result of forces that push fluids into bowman’s capsule against those that push fluids out

45
Q

what makes up the process of urine formation in the nephrons?

A

begins with glomerular filtration - hydrostatic pressures forces fluids & solutes through the membrane

net filtration pressure - result of forces that push fluids into bowman’s capsule against those that push fluids out

gfr - amount of fluid filtered from the blood into the capsule each minute

46
Q

what is included in active tubular resorption in nephrons?

A

glucose, amino acids, vitamins, & most ions are transported with Na on carrier molecules

47
Q

what is included in passive tubular resorption in nephrons?

A

sodium movement by active transport establishes a strong osmotic gradient - water moves by osmosis out of the filtrate

other substances follow the concentration gradient out of the filtrate (solvent drag)

48
Q

what resorption is happening in the descending loop of henle?

A

impermeable to sodium & freely permeable to water

sodium outside of the tubule causes water to leave the tubule & sodium concentration inside the tubule increases

49
Q

what resorption is happening in the ascending thin loop of henle?

A

permeable to sodium & impermeable to water - sodium leaves the tubule by diffusion so that the contents become more dilute

50
Q

what resorption is happening in the ascending thick loop of henle?

A

sodium actively transported out by the Na-K-Cl cotransporter

51
Q

when is ADH released?

A

released in response to plasma osmolality (excess water loss) or reduced blood volume (detected by baroreceptors)

52
Q

what is the action of ADH?

A

increases water resorption in the collecting ducts - acts on the distal & collecting tubules making them permeable to water so that water is resorbed into the interstitial space (blood stream) & urine is more concentrated