Test 3: urinary Flashcards
parts of the kidney from out to inside
Capsule
* Cortex
* Medulla
* Renal papilla/crest
* Renal pelvis
* Hilus
what are some functions of the kidney
Eliminate metabolic waste, toxic substances, drugs
- Fluid (water), acid-base, electrolyte homeostasis
- Conserve nutrients (proteins, glucose)
- Endocrine
- Renin-angiotensin-aldosterone system
- Erythropoietin
- Vitamin D activation
- Prostaglandin production
valve between ureters and the bladder
Vesicoureteral valve
where are some common places for stones in a male
urethral process (tip of penis)
sigmoid flexure
urethral recess- ruminants
in fetal anatomy the umbilical — and — are near the bladder
artery
urachus
renal dysplasia
maldevelopment
Disorganized development of the renal parenchyma (in utero or neonatal period)
how to tell dysplasia from hypoplasia
dysplasia- will be lumpy bumby- Disorganized development of the renal parenchyma (in utero or neonatal period). histo will have Inappropriate structures for the stage of development
Persian cats and bull terriers have a — mutation that leads to Polycystic Kidney Disease
PKD1 gene mutation
Polycystic Kidney Disease causes
fluid filled cysts in the kidney
leading to chronic renal failure
inherited condition- persian cats and bull terrier
animals with Polycystic Kidney Disease can have cysts
kidney
liver
pancreas
renal cysts
can be incidental finding in pigs
can become inflamed/infected
congenital or acquired
renal cysts can be — or —
congenital or acquires
incidental or can become inflamed/infected
what are three type of urachal abnormalities
the main function of the glomerulus is
blood filtration
the main function of tubules are
Water homeostasis, electrolyte and acid-base balance
how to measure GFR
measure urea nitrogen, creatinine and SDMA in the blood
— in the kidney should stay the same despite systemic changes
GFR
— are sensors between the afferent and efferent arterioles in the glomerulus
Juxtaglomerular Apparatus (JGA)
macula densa- sense the change
JG cells produce renin
azotemia
increase in BUN and creatinine
how does RAAS work
— produce renin
JG cells
renin is produced when there is a decrease in GFR
will activate angiotensinogen into angiotensin 1, then ACE will activate that into angiotensin II
angiotensin II will stimulate pituitary to make ADH, adrenal glands to make aldosterone and will constrict arterioles in the kidney leading to INCREASED BLOOD PRESSURE
what does angiotensin II do to the pituitary
produce ADH (antidiuretic hormone)
ADH will cause collecting duct to increase water reabsorption
angiotensin II also stimulates adrenal gland to make aldosterone which will increase water retention by increasing sodium reabsorption
angiotensin II will also cause hypothalamus to stimulate thirst
increase blood pressure and volume to maintain constant GFR
what type of cells in the ureters and urinary bladder
Mucosa (transitional epithelium/urothelium)
Smooth muscle wall
* Bladder: detrusor muscle
Serosa/adventitia
what type of cells in the urethra
depends where in the urethra
Mucosa
* Urothelium (cranial)
* Stratified squamous epithelium (caudal - female)
Smooth muscle wall
* Internal urethral sphincter
* External urethral sphincter (urethralis muscle)
tubule rupture is also called
tubulorrhexis
what are some defense mechanisms of the urinary tract
Immune system
* Basement membranes
* Mesangial cells (phagocytic)
* Urine flow
* Urine pH & osmolality
* Mucus
what are four portals of entry to the urinary system
Ascending
* Example: bladder kidney
Hematogenous
* Example: sepsis with embolic inflammation
Descending
* Example: kidney bladder
Direct
* Example: direct-acting toxins
BUN stands for
blood urea nitrogen
— is a sensitive & early marker of decreased GFR (dogs & cats)
SDMA
uremia:
urine in blood (uremic toxins & others)
Isosthenuria:
the kidney is unable to
concentrate or dilute urine
* “fixed” USG: 1.008-1.012
Anuria:
kidneys are unable to
produce urine
Oliguria:
production of a small
volume of urine
Polyuria:
production of a large
volume of urine (often dilute)
Polydipsia:
increased thirst (water
consumption)
renal failure means
only 25% of kidney is still working
acute kidney injury is measured
graded I-V
chronic kidney disease is measured
stage 1-4
what are some clinical signs of acute kidney injury
Rapid onset
Vomiting, lethargy, diarrhea
* Decreased urine production
* Bloodwork changes:
* Azotemia (increased BUN, creatinine)
* +/- metabolic acidosis
what are some causes of acute kidney injury
toxin
ischemia
infection
obstruction
grossly what will an AKI kidney look like?
wet, swollen red
AKI stage is based on
creatinine level and clinical signs such as ultrasound
chronic or acute kidney disease will show anemia in the blood work
chronic
chronic kidney disease will present with
Vomiting, lethargy, diarrhea,
poor body condition
* PU/PD
Bloodwork changes:
* Azotemia, ANEMIA
* +/- metabolic acidosis
Tubular or lower urinary tract injury will cause what dysfunction
accumulate metabolic waste leading to azotemia, uremia, and uremic syndrome
tubular necrosis will cause —
Unable to maintain fluid, acid-base and electrolyte homeostasis
leading to dehydration, PU
metabolic acidosis
too much Na, K and Ca in the blood
damage to GBM will cause the loss of —
selective blood filtration leading to loss of glucose and protein in the urine
Interstitial necrosis,
inflammation, fibrosis will cause —
Endocrine alterations
leading to Decreased erythropoietin →anemia
decreased Vit D activation → secondary hyperparathyroidism
uremia is Multisystemic manifestation of circulating — due to
acute or chronic renal failure
uremic toxins
uremic toxins interfere with — and damage —
electrolyte, protein, and acid-base metabolism
endothelial & epithelial cells
where are common places for uremic lesions
stomach
left atrium
pleura
Uremic pneumonitis
* Alveolar walls & blood vessels mineralize
Uremic encephalopathy
* Reactive astrogliosis (horses, camelids)
how does renal failure cause hyperparathyroidism
kidney disease will cause —parathyroidism
hyper
decreased GFR will cause increased phosphous in the blood, body tries to correct Ca:P ratio by decreasing Vit D activation, and bone resorption
ischemia in the kidney usually caused by
renal artery infarct
renal papillary/crest necrosis
acute tubular injury
renal hemorrhage
caused by systemic disease
such as herpes, African swine fever
acute renal infarcts look
swollen, red (hemorrhage) to tan (necrosis)
chronic renal infarcts look
depressed, firm and tan (fibrosis)
what are some things that cause ischemia in the kidney
Thrombi/thromboemboli
* Valvular endocarditis
* Bacterial emboli
* Neoplastic emboli
toxins
vasculitis
renal crest necrosis
caused by NSAIDs, pyelitis/pyelonephritis, urolithiasis, amyloid
renal papillary necrosis is caused by
ischemia
NSAIDs, pyelitis/pyelonephritis, urolithiasis, amyloid
how does NSAIDs lead to renal crest necrosis?
NSAIDS inhibit COX
this leads to decrease in prostaglandins
decrease in vasodilation
which leads to local ischemia and coagulative necrosis
inflammation of renal pelvis +/- tubulointerstitium
PYELITIS/PYELONEPHRITIS
inflammation of tubules & interstitium
TUBULOINTERSTITIAL NEPHRITIS
inflammation of urinary bladder
cystitis
Tubulointerstitial Nephritis is injury to the — also impairs tubular function & eventually
— function
interstitium
glomerular
Tubulointerstitial Nephritis can be caused by
infectious and non infectious
ischemia
lepto
lyme disease
results in interstitial fibrosis and nephron loss
what are some causes
acute Tubulointerstitial Nephritis
possible cause: lepto, lyme, adenovirus, ischemia
pyelitis/pyelonephritis is usually caused by
ascending bacterial infection
Ecoli, corynebacterium
renal pelvis +/- tubulointerstitium inflammation
what are some predisposing factors for Pyelitis/Pyelonephritis
- Vesicoureteral reflux
- Urine stasis
- Short urethra (females)
usually caused by ascending bacterial infection such as ecoli
renal pelvis +/- tubulointerstitium inflammation
how to tell chronic pyelonephritis from chronic infarct
chronic pyelonephritis will have regression of the renal pelvis
embolic nephritis is usually caused by
fungi, bacteria from the blood →hematogenous infection
from Glomerular or peritubular/interstitial capillaries
what are some predisposing factors for embolic nephritis
Sepsis/septicemia
spread by blood
what are some causes of embolic nephritis
E. coli (calves)
* Actinobacillus equuli (foals)
* E. rhusiopathiae (swine)
* Disseminated fungal infections
embolic nephritis
Ecoli or fungal infection from blood
cystitis is usually caused by
bacteria or toxins
what are some predisposing factors for cystitis
Damage to the mucosa (ex: uroliths, trauma)
* Incomplete emptying of the bladder
* Diabetes mellitus (dog, cat) - emphysematous cystitis
pizzle rot is caused by
Corynebacterium renale
causes ulcerative urethritis/posthitis
Feline infectious peritonitis (FIP)
* Pyogranulomatous and necrotizing vasculitis
Dog – Dioctophyma renale “giant kidney worm”
Inflammation restricted to glomeruli
Glomerulitis
glomerulitis is often associated with
septicemia
Glomerulonephritis is often —
immune-mediated
what are the three layers of glomerular
endothelium (blood vessel)
glomerular basement membrane
Visceral epithelium with podocytes
glomerular dysfunction leads to
non selective filtration
proteinuria
loss of albumin in the urine will cause
edema
loss of antithrombin III in the urine will cause
hypercoaguable state
nephrotic syndrome leads to
proteinuria, hypoalbuminemia, edema, hypercholesterolemia
Dysfunction of the glomerular filtration
membrane will cause cells to form —
hypercellular tuft
Endothelial, epithelial or mesangial cell proliferation
Fibrosis/scarring of the glomerulus
Glomerulosclerosis
Glomerular obsolescence
Glomerulus is shrunken, hypocellular & sclerotic (fibrosis)
what causes glomerulonephritis
immune mediated
antigen-antibody complexes get stuck/ deposit into the glomerulus membrane
what can cause ICGN
any disease with prolonged antigenemia & IC formation
* Examples: dirofilariasis, Feline Leukemia Virus, pyometra, Systemic Lupus Erythematous
immune complex Glomerulonephritis
how to test for ICGN
hard to test for
* Clinical pathology
* Histochemical stains
* Transmission Electron Microscopy (TEM)
* Immunofluorescent antibodies (IFA)
* Immunohistochemistry (IHC)
immune complex Glomerulonephritis
kidney with amyloidosis will appear
waxy, firm, tan
congo red stain
what happens to the kidney during Nephrogenic diabetes insipidus
DCT & CD do not respond to ADH
- Congenital (foals) or acquired (pyometra)
what is filtered in the proximal tubular
Conserve glucose and protein (amino acids)
Excrete metabolic waste (UREA)
Electrolyte balance (Na, Cl, K, Ca, Phos, Mg)
what is filtered in the loop of henle
Water homeostasis (concentrate
or dilute urine)
NaCl in or out controls water
distal tubule controls filter of —
Acid-base homeostasis (retain bicarbonate & excrete acids)
renal tubules will filter
the main function of the renal tubules is
modify ultrafiltrate
major consequence of tubular dysfunction is
unmodified urine
what are some sequelae of tubular dysfunction
what is a tubular cast
accumulation of dead cells that can obstruct the tubule
acute tubular injury is the — of tubular epithelial cells that will form downstream — and can —
necrosis and sloughing
casts
regeneration
hemoglobinuria is caused by
ischemia and cytotoxicity
RBC are being broken down- hemolysis
Copper toxicity (sheep and goats), Red maple (Acer rubrum) toxicity (horses), babesiosis (cattle), immune-mediated hemolytic anemia (dogs)
myoglobinuria is caused by
Causes of extensive muscle necrosis (rhabdomyolysis):
Trauma, exertional rhabdomyolysis (horses), capture myopathy (wildlife), other myopathies
another name for red-brown urine
pigmenturia
hemoglobinuria
hemolysis from copper toxicosis
ethylene glycol toxicosis is caused by ingestion of
antifreeze
Ethylene Glycol Toxicosis will cause the formation of
calcium oxalate crystals
will obstruct tubules and damage epithelial cells
can also deposit in the brain and cause pulmonary edema
stones are also called
Urolithiasis
sequelae of lower urinary tract dysfunction
retained urine
Retain K+: hyperkalemia
Retain acids: metabolic acidosis
Retain waste: azotemia, uremia
Hyperkalemia: can cause acute cardiac arrhythmias or arrest
Sabulous urolithiasis are — and made of —
Masses of sandy sludge
Organic matrix
*urethral plugs (cat), neurogenic (horse)
what are some factors that are involved in urolith formation
urine pH, hydration status,
infection, diet, breed
obstruction in the lower urinary tract can lead to
hydronephrosis caused by obstruction that lead to distention and pressure atrophy of the renal pelvis
feline lower urinary tract disease presents in — cats
Young-middle age, overweight male
what are some causes of feline lower urinary tract disease
Urolithiasis (urethra)
* Urethral plugs (common)
* Strictures, developmental anomalies
* Bacterial cystitis
* Feline Interstitial Cystitis (neurogenic)
* Idiopathic (common)
urate crystal deposition in birds and reptiles are called
urate tophi
caused by renal disease, too much uric acid and dehydration
most common neoplasia of the epithelial cells in the kidney
renal cell carcinoma
Adenoma (uncommon)
Urothelial cell (transitional cell) carcinoma
most common neoplasia of the mesenchymal cells in the kidney
Lymphoma
Hemangioma/sarcoma
Nephroblastoma (swine, chickens, dogs)
metastatic cancers of the kidney
Lymphoma, hemangiosarcoma
cancers of the epithelial cells of the lower urinary tract
Urothelial cell (transitional cell) carcinoma
Squamous cell carcinoma
Papilloma
cancers of the mesenchymal cells of the lower urinary tract
Lymphoma
Hemangioma/sarcoma
Leiomyoma/sarcoma
Rhabdomyosarcoma (young dogs)
pig
nephroblastoma
cancer of the mesenchymal cells of the kidney
in dogs can occur ectopically in the spinal canal
bovine lymphoma
big,white, soft, bulging
bladder
urothelial cell (transitional cell) carcinoma
bladder
bovine hemangiosarcoma
Urinary bladder neoplasia associated with Bracken Fern & Bovine Papilloma Virus-2
GFR — with declining renal function. The — is an important mechanism that helps the kidney maintain a constant GFR despite systemic changes in blood flow.
decreases
renin-angiotensin-aldosterone-system (RAAS)
Tubules are lined by a single layer of epithelium along a basement membrane. They are surrounded by an intricate network of capillaries, called the —
vasa recta
Interstitial cells in the renal medulla produce prostaglandins that act — on interstitial blood vessels.
locally
(act as vasodilator)
The proximal convoluted tubules have 1-alpha-hydroxylase, which convert inactive vitamin D to the active form. Cells within the interstitium also make —, which stimulates red blood cell production.
erythropoietin
how does RAAS work?
decreased renal blood flow cause Lower levels of Na and Cl arrive at the macula densa in the distal convoluted tubule.
this triggers the juxaglomerular cells to produce renin, which then activates angiotensinogen
Angiotensinogen II travels to the adrenal glands (release aldosterone), pituitary gland (release ADH), and back to the kidney to increase blood pressure in the glomerulus and increase water reabsorption in the tubules and collecting duct.
kidney maintains normal GFR despite systemic hypotension
BUN increases or decreases with decreased GFR
increases
BUN (blood urea nitrogen): byproduct of protein metabolism that is excreted by the kidneys
Azotemia: excess urea (BUN) & creatinine in blood
Can be Pre-renal (ex: —)
Renal (due to —)
Post-renal (ex: —)
dehydration or hypovolemia
kidney disease
lower urinary tract obstruction
Severe —kalemia can cause cardiac arrhythmias or arrest
hyper
how do NSAIDs cause renal crest necrosis
Administration of systemic NSAIDs results in inhibition of COX enzymes throughout the body. One side effect of this is decreased production of prostaglandins (PGE2) by the medullary interstitial cells in the kidney. The production of PGE2 in the inner medulla is important for regulating blood flow in that area. Without PGE2, interstitial blood vessels in the renal papilla do not dilate and there is regional ischemia, followed by necrosis
ascular injury in the kidney is common. All of the following are TRUE except:
Renal vasculature is complex with multiple sharp turns
Hemorrhage is typically a manifestation of systemic disease
The kidney receives a large (20-25%) proportion of cardiac output
Chronic infarcts are easy to tell apart from chronic pyelonephritis
Chronic infarcts are easy to tell apart from chronic pyelonephritis
Kidney from a pig. The part of the kidney most severely affected is the ___. The name (morphologic diagnosis or condition) of this lesion is ___
renal papilla
renal papillary necrosis
secondary to NSAID
— is a term commonly used in pathology when describing chronic kidney disease of uncertain etiology (cause).
Tubulointerstitial nephritis
PYELITIS or PYELONEPHRITIS are terms used to describe inflammation of the renal —
renal papilla
The pathogenesis of pyelonephritis most commonly includes a — bacterial infection that begins in the lower urinary tract.
ASCENDING
EMBOLIC NEPHRITIS is usually the result of a HEMATOGENOUS infection and is secondary to —
septicemia/bacteremia
this is a kidney from a cow. Neutrophils and necrotic debris (suppurative inflammation) fill the renal pelvis and extends into the medulla. The term that best describes this lesion/condition is
pyelonephritis
— is the term used for disease that primarily targets the glomerulus, but may also affect the tubulointerstitial compartment.
Glomerulonephritis (GN)
3 parts of filtration membrane of glomerulus
he capillary endothelial cells
the basement membrane
the visceral epithelial cells (Podocytes)
Damage to any of the three filtration membrane components will result in — of particles from the blood into the urine ultrafiltrate
NON-SELECTIVE FILTRATION
When the filtration membrane is damaged, — is able to cross the membrane and enter the urine, resulting in proteinuria and — (low protein in the blood).
albumin
hypoproteinemia
The sequela of hypoproteinemia is EDEMA due to decreased —
plasma colloid oncotic pressure.
In animals (especially dogs & cats), glomerulonephritis is most often a — disease.
immune-mediated
The most common type of immune-mediated GN in animals is due to the deposition of — in the glomerulus.
IMMUNE COMPLEXES (IC)
Prolonged — can stimulate the production of IC, which typically consist of an antibody-antigen complex and sometimes incorporate complement proteins.
antigenemia
FLV, heartworm, lupus
The glomerulus can respond to this injury with proliferation of the endothelial, epithelial or mesangial cells, creating a —. This is characterized as —
hypercellular glomerular tuft
proliferative Glomerulonephritis
In addition to albumin, — is another important molecule that can be “lost” into the urine when there is damage to the filtration membrane. What are the sequela to loss of this molecule?
antithrombin III,
Antithrombin III (AT III) is normally selectively filtered by the glomerulus. AT III helps to balance the coagulation cascade and prevent excessive clot formation. When AT III is “lost” into the urine, the body is in a hypercoaguable state. Remembering back to General Pathology, hypercoagulability is one component of Virchow’s triad, which can lead to thrombosis.
In dogs and cats, glomerulonephritis is most often immune-mediated. What is the pathogenesis for this disease?
prolonged antigenemia
production of IC
IC deposited in the glomerular filtration membrane (anywhere)
flattening of the endothelial cells, thickening of the basement membrane, and effacement (loss) of the epithelial foot processes (filtration membrane damage)
glomerulus undergoes proliferation of the endothelial, epithelial or mesangial cells, thickening of the basement, or a combination
glomerulonephritis and glomerular dysfunction
As the epithelial cells are the “workhorse” of the renal tubules, this is a very meaningful finding. Necrotic cells will “slough” or fall off of the basement membrane and into the tubular lumen. Here, they can mix with mucoproteins or other debris and form
casts
The tubular segments have a multitude of specialized functions, but the overarching goal of the tubules is to —
modify the ultrafiltrate that the glomeruli produce into urine
the tubules perform numerous important functions to maintain water balance in the body (— or — urine), maintain acid-base homeostasis (retain — and excrete acid), maintain electrolyte homeostasis (balance — and others), excrete metabolic waste in the form of urea, and conserve nutrients (amino acids, glucose)
dilute or concentrate
bicarbonate
Na, Cl, K
Two common causes of acute tubular necrosis in animals are —
toxins and ischemia
Ethylene glycol is metabolized by the liver, but predominately causes lesions in the kidney due to the formation of numerous —
Calcium Oxalate crystals
— is released into the blood when there is extensive muscle damage.
myoglobin
What are some important sequelae to drinking antifreeze?
metabolic acidosis
uremia
azotemia
anuria
hyperkalemia
calcium oxalate crystal formation
What are some important sequelae to this severe, acute tubular dysfunction? secondary to copper toxicosis
hemoglobin
The most severe manifestation of urolithiasis is —
obstructive urolithiasis
If the obstruction causes damage to the mucosa/wall, but is removed, the tissue may heal by fibrosis (scarring). As the scar tissue contracts, narrowing of the lumen may occur. This is called a —
stricture
n cases of more chronic disease (typically partial or incomplete obstruction), distension of the proximal urinary tract may occur. The term for dilation of the renal pelvis is —
hydronephrosis
This is the lower urinary tract (and 1 kidney) from a cat. The bladder is distended with urine and dark red. At the tip of the urethra, a small plug of debris is obstructing the lumen. The name of this clinical syndrome in cats is
feline lower urinary tract disease FLUTD
caused by an urethral obstruction. This syndrome is often diagnosed in male cats that are young to middle-aged, overweight and indoor-only. Urethral obstruction is one cause of this syndrome.
The term for dilation of the renal pelvis is:
Hydronephrosis
The most common primary renal neoplasm is dogs is —
renal cell carcinoma
The most common primary renal neoplasm in cats is –
lymphoma
A unique primary neoplasm of the kidney is —. This is a tumor of embryonic origin and is commonly found in young animals. In dogs, this tumor can also form next to the —
nephroblastoma
spinal cord (ectopic neoplasm)
In cattle, an association has been identified between chronic — and —, and the development of urinary bladder neoplasia.
Bracken Fern toxicosis, Bovine Papillomavirus-2 infection
type of tumor in a bladder
hemangiosarcoma
squamous cell carcinoma
urothelial/transitional cell carcinoma
Rhabdomyosarcoma (young dog)
and others
One of the most common primary urinary bladder tumors in dogs and cats is —
UROTHELIAL CELL CARCINOMA.
malignant
urothelial cell carcinoma are also called
transitional cell carcinoma
malignant
transitional cell carcinoma benign or malignant?
This neoplasm is malignant, can be locally aggressive (regional invasion) and metastasizes to lymph nodes, lung, skin, bone, and other organs.
kidney what are some differentials
Renal cell carcinoma
Nephroblastoma
Urothelial cell carcinoma
Lymphoma
Hemangiosarcoma
AZOTEMIA is defined as a(n) — in Blood Urea Nitrogen (BUN) and a(n) — in creatinine concentration in the blood.
increase
increase
The main function of the glomerulus is non-selective filtration of blood.
true or false
false
main function in selective filtration
when it goes wrong allows protein and sugar to leave
All of the following statements are correct, EXCEPT:
Renal Failure is defined as the loss of >75% of renal function.
Injury to one part of the nephron results in eventual loss of the entire nephron.
The kidney can respond to vascular injury by making more nephrons.
Hyperkalemia is an important sequela of obstructive urolithiasis.
The kidney can respond to vascular injury by making more nephrons.
PYELONEPHRITIS is typically the result of a(n) — infection, while EMBOLIC NEPHRITIS is typically the result of a(n) — infection.
ascending
hematogenous
Acute Kidney Injury (AKI) is an irreversible change that is always due to Acute Tubular Injury (ATI) and results in renal failure.
true or false
false
can recover
caused by toxins, ischemia, infection, obstruction
grade I-V
cause azotemia +/- acidosis
CKD is irreversible and causes anemia from decreased erythropoietin