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)
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
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
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
4
Q
major developmental abnormalities of the kidneys
A
- aplasia/hypoplasia
- juvenile nephropathy
- renal dysplasia
- renal cysts
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
6
Q
familial patterns in renal aplasia have been reported in what breeds?
A
Doberman pinschers and beagles
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.
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
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
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
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
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
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
14
Q
Renal hemorrhage - how common? associated with what?
A
- frequent finding
- Petechiae with:
> disseminated bacterial disease
> viral disease
> coagulation disorders
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
