Urinary Tract Pathology

Front 1

What are the four major anatomic structures of the kidney that are susceptible to disease insult?

Back 1

- glomeruli
- tubules
- interstium
- vasculature

Front 2

Anuria

Back 2

lack of urine formation

Front 3

Azotemia

Back 3

increased non-protein nitrogenous compounds in the blood

- elevated BUN and/or serum creatinine

Front 4

Bactiuria

Back 4

bacteria in the urine

Front 5

BUN or SUN

Back 5

Blood/serum Urea nitrogen.

used as an indicator of glomerular filtration rate (GFR)

Front 6

Creatinine

Back 6

End product of creatine catabolism. Used as an indicator of glomerular filtration rate by virtue of its relatively constant rate of production from skeletal muscle, its complete filterability at the glomerulus, and its lack of tuburlar reabsorption

Front 7

Hematuria

Back 7

blood in the urine

Front 8

Hyposthenuria

Back 8

dilute urine (specific gravity <1.008)

Front 9

Isosthenuria

Back 9

a state in chronic renal failure in which the kidney cannot form urine with a higher or lower specific gravity than protein-free plasma

Specific gravity 1.012 - 1.008

Front 10

oliguria

Back 10

lower than normal urine production

Front 11

pollakiuria

Back 11

frequent urination, typically of small volumes, without an increase in renal output

Front 12

polydipsia

Back 12

increased and frequent water consumption

Front 13

polyuria

Back 13

frequent urination, usually of large volumes, with increased renal urine output

Front 14

proteinuria

Back 14

protein in the urine

Front 15

pyuria

Back 15

pus in urine

Front 16

stranguria

Back 16

difficulty in passing urine, often with evidence of pain and tenesmus

Front 17

Definition of syndrome

Back 17

The aggregate of signs (symptomes), clinical laboratory findings, and morphological changes associated with any morbid process that constitute together a distinct clinicopathological entity

Front 18

Chronic renal failure diseases all have one thing in common

Back 18

the progressive destruction of neprhons

Front 19

Chronic renal failure and compensation

Back 19

When there is nephron destruction, the remaining nephrons try to compensate and take over

- HYPERTROPHY to try handle an increased amount of filtration

Front 20

at what point can the gomeruli no longer compensate for the loss of nephrons

Back 20

at 1/3 of the nephrons remaining the neprhons can no longer compensate and increase their filtration rate to a rate that is necessary

Front 21

Azotemia occurs at what point in chronic renal failure

Back 21

1/3 of the nephrons working the effective glomerular filtration rate of the kidney begins to decrease

increase in blood urea nitrogen and serum creatinine concentrations

Front 22

Why does polyuria develop in chronic renal failure

Back 22

1). the few numbers of working nephrons are not adequate to maintain the medullary solute gradient and countercurrent exchange mechanism. No longer able to form concentrated urine

2). Solute diuresis occurs due to the fact that the few functional nephrons must handle an increase in solute load when the nephron's tubular transport mechanisms are overwelmed. Because of this the solutes that should that are normally removed from the tubular lumen are retained, which than retains water in the tubules

Front 23

when does uremia occur in chronic renal failure

Back 23

when only 1/4 of the nephrons work

Front 24

what is found in uremia

Back 24

- azotemia (increase BUN and crea)
- polyuria (frequent urination of large volumes and increased renal output)
- polydipsia
- metabolic acidosis
- electrolyte abnormalities
- metastatic mineralization
- oral and gastointestinal ulcers
- isostheruria
- non-regenerative anemia

Front 25

Why is there dehydration in Chronic renal failure

Back 25

- occurs due to impairment of renal concentration with consequent excretion of large volumes of water

vomiting

diarrhea

Front 26

Explain why salt and water is retained in Chronic renal failure

Back 26

- you get a volume depletion due to the dehydration which increases secretion of renin.

- renin is able to take angiotensinogen and make it into angiotensin I and then angiotensin II.

- angiotensin II causes vasoconstriction and hypertension

- the hypertension causes an increase of aldosterone

- aldosterone activated sodium retion and also water by the kidney

Front 27

In the end what does the salt and water retaining cause

Back 27

oliguria

Front 28

Why does metabolic acidosis occur in Chronic renal failure

Back 28

occurs due to the reduced total renal ammonia production and decrease bicarbonate up take

- reduced net excretion of phosphate

Front 29

what happens to phosphate in chronic renal failure

Back 29

hyperphosphotemia

- when the GFR falls below 25%, the phosphate is not excreted by the renal epithelium, which causes an increase in serum phosphate

Front 30

What happens to calcium in chronic renal failure

Back 30

Hypocalcemia

- due to the increase serum phosphate calcium is pushed into tissue

- also with renal impairment, hyperphosphatemia there is a reduced absorption of calcium from the GI system

Front 31

What happens with parathyroid hormone in chronic renal failure

Back 31

parathyroid hyperplasia

- due to the hypocalcemia there is an increase in PTH

Front 32

parathyroid hyperplasia causes

Back 32

secondary renal hyperparathryoidism

Front 33

What happens with bone metabolism in chronic renal failure

Back 33

renal osteodystrophy (rubber jaw)

- increase PTH causes demineralization of bone and medullary/myelo fibrosis

Front 34

metastatic mineralization in chronic renal failure

Back 34

abnormal calcium and phosphate levels can cause metastatic mineralization of many tissues such as the lungs, blood vessels, and gastrointestinal mucosa

Front 35

Non-regenerative anemia in chronic renal failure

Back 35

normocytic, normochromic anemia

- due to decreased renal production of erythropoietin

- also due to the increased fragility and decreased lifespan of the erythrocytes due to the uremic toxins

Front 36

What is the point of no return for end-stage renal failure

Back 36

GFR drops below 30-50% of normal

Front 37

What always happens to all the compensentory nephrons at the end, when they can no longer compensate

Back 37

sclerosis

Front 38

How does glomerular hypertension happen

Back 38

there is hyperprofusion to the glomerulus and because the afferent arteriole into the glomerulus is larger than the efferent you get a glomerular hypertenstion

Front 39

what is the importance of glomerular hypertension

Back 39

it causes damage to the epithelial and endothelial cells that then can cause an increase permeability to macromolecules

Front 40

What does the protenuria due

Back 40

- increases the capillary wall tension which causes stress and stretching of the capillary wall and mesangium

- podocytes have lesser capacity for proliferation so you get gaps in surface coverage and the protein can escape

Front 41

which cells produce matrix and proliferate leading to the collapse of the capillary and ultimately sclerosis

Back 41

mesangial cells

Front 42

proteinuria and tubolointerstitial damage

Back 42

proteins in ultrafiltrate - tubular epithelial cells secrete cytokines - the cytokines activate macrophages and directly stimulate fibroblast - interstitial damage and fibrosis

Front 43

Role of increased tubular NH3 in tubulointerstitial damage

Back 43

increased NH3 production - activation of alternate complement cascae - release proinflammatory cytokines from leukocytes - interstitial fibrosis

Front 44

What features would describe a chronic renal failure

Back 44

months or years
non-regenerative anemia
polyuria
small kidneys

Front 45

what features would describe an acute renal failure

Back 45

days
oliguria or anuria
normal to symmetrically enlarged kidneys

Front 46

Causes of Acute renal failure

Back 46

- acute tubular necrosis (ATN)
- acute glomerulonephritis
- acute massive renal infarction
- complete bilateral urinary tract outflow obstruction

Front 47

Two etiologies for acute tubular necrosis

Back 47

- ischemia

- toxic

Front 48

Morph of a kidney with ischemic acute tubular necrosis

Back 48

- multifocal or patchy necrosis along the neprons
- proximal tubules are especially vulnerable, but distal tubules are also affected
- basement membranes are often ruptured

Front 49

morph of a kidney with toxic acute tubular necrosis

Back 49

- kidneys are grossly swollen and pale
- may have perirenal edema
- proximal tubules are diffusly involved and distal tubule are normally shared
- in eythylene glycol there may be some calcium oxylate crystals in the proximal tubules

Front 50

If the animal survives the actue tubular necrosis which of the two etiologies does the kidney stand a chance of tubular regeneration

Back 50

toxic

Front 51

why are epithelial cells very vulnerable to ischemic and toxic injury

Back 51

- highly metabolically active and therefore have a high energy and O2 demand

- highly charged surface area and active transport systems to normally absorb ions

- effectively concentrate toxins intracellularly