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