urinary system notes pt 4 Flashcards

1
Q

The primary functions of the kidneys include:

A
  • excretion of waste products
  • maintenance of normal salt and water concentrations
  • acid-base regulation
  • production of hormones (renin, erythropoietin, prostaglandins)
  • conversion of Vitamin D to the active form - calcitriol (1,25- dihydroxycholecalciferol)
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2
Q

3 things the kidneys need to perform their functions

A
  • adequate perfusion (normal renal blood flow is up to 25 % of cardiac output)
  • sufficient functional tissue mass (sufficient functional glomerular filtration rate)
  • functional (unobstructed) normal outflow of urine
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2
Q

Renal failure results in what? usually assessed how?
kidney failure leads to what?

A
  • accumulation of waste, salt/water imbalances, acid-base imbalances, and decreased production of hormones
  • commonly assessed by measuring urea, a relatively harmless molecule
  • Failure of the kidney to perform its normal functions leads to uremia, a clinical syndrome with fairly consistent lesions and clinical signs
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3
Q

general patterns of renal disease

A
  • multifocal (embolic)
  • segmental or wedge shape lesion of infarcts and pyelonephritis
  • diffuse distribution of tubulointerstitial disease
  • glomerular, cortical, and medullary patterns of injury
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4
Q

major developmental abnormalities of the kidneys

A
  • aplasia/hypoplasia
  • juvenile nephropathy
  • renal dysplasia
  • renal cysts
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5
Q

Aplastic/hypoplastic kidneys - can they be compatible with life?

A
  • can be compatible with normal life as long as more than 50 % of renal tissue develops
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6
Q

familial patterns in renal aplasia have been reported in what breeds?

A

Doberman pinschers and beagles

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7
Q

Ectopic kidneys - risks of what?

A
  • risk of obstruction due to the altered positioning of the ureters
  • It is most commonly seen in pigs and dogs.
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8
Q

Progressive juvenile nephropathy
- what is it?
- breeds?
- onset and signs?
- character of disease / lesions?

A
  • broad term for many non-inflammatory, degenerative, and developmental diseases in young animals
  • usually a congenital disease that may be inherited > if mode of inheritance is known = familial or hereditary nephropathy
  • Lhaso Apsos, Shit Tzus, and golden retrievers
    <><>
  • often develop uremia at 6-9 months (but can be late onset)
  • changes are typical of glomerulonephritis
    > Glomeruli tend to be diffusely involved, with secondary tubular/interstitial changes
    <><><><>
    <><><><>
  • Samoyed hereditary glomerulopathy
  • familial glomerulonephritis of Doberman pinschers
  • familial renal fibrosis of Norwegian elkhounds
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9
Q

Renal dysplasia
- what is it?
- causes?
<><><>
- categories?
- gross appearance?
- clinical signs?

A
  • disorganized development of the renal parenchyma due to anomalous differentiation
  • usually congenital
    > in some species (dog, cat, pig), kidneys continue to develop after birth so some perinatal diseases can lead to the same lesions
    <><><>
    Types:
  • development of anomalous structures
  • the presence of structures that are inappropriate for the animal’s current stage of development
    <><>
  • Grossly, the kidneys can be essentially normal, or be small, misshapen, and fibrotic.
  • Animals with gross lesions of renal dysplasia usually develop uremia
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10
Q

renal cysts
- significance
- mechanisms for development

A
  • Single renal cysts are usually incidental lesions of no consequence
    <><><><>
    Mechanisms for developmment:
  • obstructive lesions
  • lesions in the tubular ECM matrix/basement membrane
  • focal hyperplastic epithelial lesions
    > all of these result in an imbalance between the intratubular pressure and the strength of the tubule wall
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11
Q

Polycystic kidney disease (PKD)
- etiology, forms, outcomes

A
  • inherited polycystic disease described in many species/breeds
    <><><><>
    occurs in 3 forms:
  • autosomal dominant form (ADPKD) occurs in Persian cats, bull terriers, pigs, and lambs
    > often concurrent hepatic and pancreatic cysts, sometimes with fibrosis
    > tend to be bilateral, arise in the convoluted tubules, progressively enlarge through life compressing adjacent normal parenchyma, and eventually result in renal failure with lesions of chronic tubulointerstitial nephritis
    <><>
  • autosomal recessive form has been reported in Cairn terriers, West Highland white terriers, Persians, and sheep
    > biliary cysts occasionally occur in this form
    <><>
  • congenital form of PKD (CPKD) has been described in pigs, lambs, goat kids, puppies, kittens, and foals
    > unknown mode of inheritance
    > hepatic and pancreatic cysts can also be present
    > often results in stillbirths or fatal renal failure in the first weeks of life
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12
Q

renal infarction
- often arise how?
- possible sequelae?
- outcomes?

A
  • They arise from thrombi or emboli in the renal artery or one of its branches, and often are secondary to valvular thrombosis / endocarditis
    <><>
  • Septic thrombi result in abscesses which can resolve, become sequestered or drain into the renal pelvis
  • Non-septic or bland thrombi produce the more classically described renal infarcts
    <><>
  • Thrombosis of the renal artery will essentially cause necrosis of the entire kidney (there can be minimal collateral circulation from the capsular and perihilar vasculature)
  • Involvement of the interlobar artery would give subtotal necrosis
  • involvement of the arcuate or interlobular arteries gives the more common wedge-shaped lesion
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13
Q

infarcted kidney - gross appearance and progression

A
  • Initially affected tissue swells and is cyanotic with congestion due to blood oozing in from unaffected collateral vessels, which results in a poorly demarcated border between affected and unaffected tissue
  • At the periphery, red cells survive resulting in a red rim (not truly hyperemia)
    > This lesion persists for 2-3 days, during which time normal circulation can be re- established
  • After dehemoglobinization of the lesion (2-3 d) the infarcted region becomes pale in colour
    <><><><>
  • Revascularization can occur in the peripheral areas, but the areas of complete necrosis undergo progressive fibrosis, becoming the pale white-tan-grey, sunken fibrotic lesions classically described in renal infarction
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14
Q

Renal hemorrhage - how common? associated with what?

A
  • frequent finding
  • Petechiae with:
    > disseminated bacterial disease
    > viral disease
    > coagulation disorders
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15
Q

hydronephrosis
- common?
- causes
- what typifies this condition
- outcomes / lesions?
- most severe forms are from what?

A
  • common
  • anything that occludes the ureters or urethra > can result in sufficient back pressure to cause the characteristics that typify this condition:
    > pelvic dilation
    > high fluid pressure of urine
    > renal compression and parenchymal loss
    <><><><>
  • Back pressure and a nonexpansile capsule cause intrarenal pressure to increase, leading to ischemic lesions
    > Pressure and ischemia cause increased apoptosis of renal epithelial cells so that the cortex and medulla become reduced in size and the pelvis dilates
    <><><><>
  • The most severe forms of hydronephrosis arise from unilateral incomplete obstruction
16
Q

general response of the inner renal medulla to ischemic insults
- when is this most seen?
- other possibilities?
- outcomes?

A
  • Necrosis of the medullary crest or papillae
    (papillary necrosis)
  • horses > administration of (NSAIDS) impairs prostaglandin production > juxtamedullary glomeruli cannot continue to supply blood to the medulla when required
    > prevents the protective effect of
    prostaglandin E2 on the medullary tubules and prevents the prostaglandin-based maintenance of medullary blood flow in situations of reduced renal blood flow such as in dehydration
    <><><>
  • Similar disease can occur in cats and dogs with treatment or accidental ingestion of drugs such as ibuprofen or acetaminophen
    <><><><>
  • generally, other conditions that cause reduction of blood flow to the area or direct compression can cause medullary crest/papillary necrosis
    > glomerular lesions (remembering that medullary flow comes from glomerular efferent arteries)
    > interstitial diseases such as fibrosis, interstitial inflammation, and edema, or amyloid that compress the vasa recta
    > compressive lesions like pelvic calculi or other causes of lower urinary tract obstruction.
    <><><><>
    Many instances of papillary necrosis are ‘incidental’ – few lead to clinical disease
17
Q

gross appearance of renal medullary necrosis?
possible sequelae?

A
  • coagulation necrosis
    > well-demarcated area of yellow-green to grey to pink tissue
    > The necrotic tissue can slough, and, if large enough, can cause obstructions
18
Q

Medullary degeneration and necrosis
- when does it occur
- what are the body’s mechanisms to prevent this in situations of acute reduction in renal blood flow

A
  • can occur due to prolonged dehydration
    <><><>
    Protective mechanisms
  • effects PGE and nitric oxide in maintaining medullary blood flow
  • reduction in metabolism of medullary epithelial cells in excessively hypoxic conditions
19
Q

end stage kidney - lesions, progression

A
  • end result of all of the major diseases is renal fibrosis
    > follows pattern of initiating disease
    > a progressive and self-perpetuating lesion > restrictions of blood flow or the flow of filtrate soon result in secondary changes that exacerbate the fibrosis
20
Q

changes in the kidney associated with aging
- structural, functional, signs?

A
  • decline in number of viable glomeruli
  • increase in glomerulosclerosis
  • increased interstitial fibrosis
  • atrophic changes in tubules
  • thickening of basement membranes
    > combine to result in reduced renal function
    <><><><>
  • Kidney volume and weight can also decline, usually associated with thinning of the cortex
  • Functionally:
    > reduced GFR
    > increased risk for/occurrence of hypertension
    > decreased ability to concentrate the urine
    > increase in vascular resistance
    <><><><>
  • usually no clinically apparent disease, but can predispose to clinical problems of other disease (urinary or systemic)
21
Q

renal neoplasia
- usually primary or metastatic?
- species differences?

A
  • usually metastatic
  • horses: adenoma (benign) or carcinoma
  • cats and dogs: renal carcinomas (metastatic)
  • cats: renal lymphoma (malignant)
  • pigs: nephroblastomas (benign usually)
22
Q

renal adenoma
- common?
- species?
- significance?

A
  • rare
    > occasional finding in horses and cattle, less so in dogs
  • usually incidental
  • arise from the epithelium of the proximal convoluted tubules
23
Q

Renal carcinomas
- frequency? species?
- age? sex?

A
  • cows, horses, and dogs: renal carcinomas are the most frequently observed primary renal tumour
  • rare in cats, sheep, pigs
  • older animals, male (except cattle > female, but more aged cows vs bulls…)
24
Q

clinical signs of renal carcinomas

A
  • hematuria, weight loss, and palpable abdominal masses
  • occasionally, paraneoplastic syndromes
25
Q

renal carcinomas, gross appearance? metastasis?

A
  • ovoid to spherical
  • unilateral
  • often found at one pole of the kidney
  • often grey to yellow with significant areas of hemorrhage and necrosis and can grow to be larger than the kidney it arose from
  • neoplastic tissue is usually well demarcated from normal renal tissue
    <><>
  • tumours often invade renal veins and lymphatics, and metastasis is common, often present at time of diagnosis
26
Q

Renal cystadenocarcinomas
- breeds?
- concurrent conditions?
- malignant?
- etiology

A
  • Older German shepherd dogs
  • in combination with nodular dermatofibrosis
  • generally bilateral
  • malignant forms often metastasizing to lymph nodes, liver, spleen, lung, and bone
  • Females often have concurrent uterine leiomyomas
  • autosomal dominant inheritance
27
Q

Nephroblastoma
- common for who?
- etiology
- appearance
- metastasis?

A
  • AKA embryonal nephromas or Wilms’ tumour
  • most common primary renal tumour in pigs and chickens
  • arise from the primitive nephrogenic tissue and as such are usually seen in animals under 2 years of age but can arise in foci of renal dysplasia
    <><><><>
  • often bilateral and multiple within affected kidneys,
  • grow to enormous sizes leading to abdominal distension
  • often contain tissue components not normally found in renal tissue such as cartilage, bone, collagen, adipose tissue, and skeletal muscle
  • metastasis rare in pigs, does occur in affected cats and dogs