Urinary System Flashcards
Water only moves _______ in the kidney
Passively
Thick asending limb (loop of henle)
Impermeable to water and actively removes Na and Cl from urine
Distal tubule and collecting duct
Selectively permeable to water (vasopressin/ ADH opens pumps so water can be reabsorbed)
Urea in the kidney
In the collecting duct, recycled into the medulla passively down a concentration gradient (helps with concentration)
Acquired from diet (through liver)
How the kidney concentrates urine:
Glomerulus → proximal renal tubule→ Loop of Henle → collecting tubules
Glomerulus
Blood supply, filtration (small molecules) and supplies the kidney with nutrients
Normal SG
300 osmol= 1.008-1.012
Less than= dilute
Proximal renal tubule
Absorbs water and electrolytes (non-selectively)
Loop of Henle
Separates water from electrolytes : Na, Cl- pumps from ascending limb → renal interstitial
Dilutes urine
Dilution
Remove solutes in excess of water (urine less concentrated)
How does the renal medulla become hyperosmotic?
@ the Loop of Henle (ascending limb)
Na/Cl pumping electrolytes out of limb into the central medulla
Counter current multiplier
Forming a concentrated urine
Loop of henle generates an hyperosmotic medulla for separation of water an solutes
Requires energy, hairpin configuration and separation of water from solute
How is the hyperosmotic medulla maintained after water enters
Vasa recta: water moves in to dilute hyperosmotic medulla → collects water from medulla and brings it back to the urinary system circulation (prevents solute washout)
Vasa recta (counter current exchanger)
Blood supply to the medulla bringing nutrients and O2 and removing waste
OG from JG nephrons
Requirements for the counter current exchanger
Hairpin configuration
High permeability to water and solutes
Slow circulation to allow diffusion
What 2 things are required to form a concentrated urine?
Hyperosmotic renal medulla and ADH (vasopressin)
Water deficit
↑ extracellular osmolality, ADH secretion, plasma ADH, H2O and urea permeability, H2O and urea reabsorption and ↓ H2O excretion
done to conserve water
Water excess
↓extracellular osmolality, ADH secretion, plasma ADH, H2O and urea permeability, H2O and urea reabsorption and ↑H2O excretion
excreting water and diluting urine
Kidney function (maintaining homeostasis)
Filter our metabolic waste
Maintain hydration and electrolyte balance (P,K, Na)
Prevent plasma protein loss
Acid base and calcium balance
BP control
RBC production
33% kidney function
Concentrating function is impaired
<1.025-1.030 in dogs
<1.035 and 1.040 in cats
25% of kidney function
Impaired kidney function and azotemic
Primary Renal azotemia
Elevation or buildup of nitrogenous products (BUN< creatinine, SDMA) in the blood due to ↓ kidney function
Ex: acute and chronic kidney disease
Kidney failure
Failure to maintain homeostasis, destruction of 3/4 of functional mass of both kidneys
Creatinine >1.5 mg/dl or BUN >33mg/dl
SG: 1.008-1.030 (1.035 in cats)
T/F: When the creatinine is almost normal (little ↑), there’s a big drop in GFR
TRUE
important for kidney disease
T/F: Large reductions of high creatinine minimally affect GFR
TRUE
kidney function not affected much
Prerenal azotemia
↑ creatinine and BUN
SG adequate: >1.030 in dogs and >1.035 in cats
Renal Azotemia
↑ creatinine and BUN
SG inappropriate: 1.007-1.029 in dogs and 1.007-1.034 in cats
Kidney not functioning well
Postrenal azotemia
↑ creatinine and BUN
SG variable
Detection of urinary obstruction or rupture (clinically sick)
All manifestations of disease are the result of two processes:
- What the disease induces
- The body’s compensatory response
Disease induced → body’s response
Polyuria → polydipsia
Polydipsia → polyuria
Trauma → inflammation
Systemic infection → fever
Hypoxemia → tachypnea
If chronic kidney disease is driving PU/PD, what happens to serum sodium? (↓ 25% kidney function/ azotemia)
Primary polyuria
Serum [Na+] is higher because more water is urinated out first (hemoconcentrated)
If hyper-anxiety is driving PU/PD, what happens to the serum sodium?
Primary polydipsia
Diluting out the components in your blood
Serum [Na+] is lower because more water consumed
Proteinuria
Lab abnormality implying urine protein excretion in excess
Pre-renal proteinuria
Detected if ↑ concentration of small proteins in blood, functional (Hb, myoglobin)
When does pre-renal proteinuria happen?
Intravascular hemolysis
Myoglobinemia
Myeloma
Pre-renal proteinuria urinalysis
Red color
High protein (could be 2 or 3 +)
Renal proteinuria
Glomerular (can lead to renal failure, chronic)- albumin
Renal tubular disease and interesital disease (mild and not as common)
Renal proteinuria urinalysis
Protein in the urine (1+ …)
No RBCs and WBCs
Low SG
run urine protein creatinine ratio
Post-renal proteinuria
Ureter, bladder, urethra disease
Urinary obstruction or leakage in the body
Most common, doesn’t relate to kidney disease
Post-renal proteinuria urinalysis
Protein (norm)
Color: red
TNTC WBCs, RBCs, and epithelial cells
Tests for proteinuria
Urine dipstick (urinalysis- albumin)
Urine protein to creatinine ratio (renal proteinuria)
Sulfasalycyclic acid turbidity and electrophoresis)
Components to uroliths (urinary stones)
Nidus (Ca++ oxalate how stone formed)*
Stone
Shell
Surface crystals
Why stones form?
Precipitation crystallization**
Matrix nucleation
Crystallization inhibition
Homogenous or heterogenous nucleation
Homogenous or heterogenous nucleation
Homo: requires energy and forms initiation of crystal
Hetero: Something initiates it
Struvite stones
Magnesium amonium phosphate
pH causes stone to from (↑ urine alkalinity)
Acidify urine to reverse stones
What causes urolith formation?
Hepatic disease
UTI
Genetic abnormalities
Hypercalemic disorders
Altered pH
Vitamin and Mineral Excesses in Diet
Sequela to drug admin
Hypovolemic disorders
