🧠Introduction to the Urinary System (pg. 572–573)
Main Function: Filters and removes waste products from blood (urea (most abundant nitrogenous waste), excess salts, etc.).
waste products- urea, creatinine, uric acid, ammonia
Organs Involved: 2 kidneys, 2 ureters, 1 bladder, 1 urethra.
Key Point: Helps maintain fluid, electrolyte, and acid–base balance.
Malfunction can cause uremia (dangerous waste buildup).
Location of the Kidneys (pg. 573)
Found under the muscles of the back in the retroperitoneal space.
The right kidney is lower than the left due to liver placement.
Protected by the lower ribs and a renal fat pad.
🧫Gross Structure of the Kidney (pg. 573–574)
External Anatomy
Hilum: Entry/exit point for arteries, veins, nerves, and ureter.
Covered by a fibrous capsule.
Internal Anatomy
Important structures you should recognize from Figure 20-2:
Renal cortex – outer layer.
Renal medulla – inner layer.
Renal pyramids – triangle sections in the medulla; makes most medullary tissue
Renal columns- connective tissue
Renal papilla – tip of pyramid; opens into calix, allowing urine to flow into the minor calyces before entering the major calyces.
Renal pelvis – collecting area that leads to ureter.
Calyx (calyces) – funnel-like areas that collect urine. (the plumbing system)
🔬 Microscopic Structure: The Nephron (pg. 574–575)
Each kidney has over 1 million nephrons!
Nephron components:
A. Renal Corpuscle
Glomerular capsule (Bowman capsule) – surrounds the glomerulus.
Glomerulus – capillary network where filtration begins, also part of circulatory system
B. Renal Tubule
Proximal Convoluted Tubule (PCT) – reabsorbs most of the filtered nutrients.
Nephron loop (Loop of Henle) – dips into medulla; has descending and ascending limbs. Important for concentrated or very diluted urine.
Distal Convoluted Tubule (DCT) – lead-s from loop to collecting duct.
Collecting Duct (CD) – collects from multiple nephrons, sends urine to calyces → renal pelvis → ureter.
🧠 Note the two nephron types:
Cortical nephrons: mostly in the cortex. makes up 85%
Juxtamedullary nephrons: loop dips deep into the medulla. important in concentrating urine
💧 Overview of Kidney Function (pg. 576–579)
🔄 Main Functions:
Maintain homeostasis by adjusting fluid, electrolytes, and acid–base levels.
Remove wastes (e.g., urea, ammonia, uric acid, and creatinine from the bloodstream through filtration.)
Regulate blood volume/pressure, electrolytes, and pH.
Produce erythropoietin (EPO) during low oxygen (stimulates RBC production).
💉 Juxtaglomerular (JG) Apparatus
JG cells monitor blood pressure.
When blood pressure or blood volume drops, they secrete renin, starting the renin–angiotensin–aldosterone system (RAAS) to raise BP.
constricts blood vessels
Also involved in secreting EPO when oxygen is low.
🔄 Urine Formation (pg. 577–579)
The nephron forms urine in 3 main steps
Filtration – Occurs only in renal corpuscle.
Blood pressure forces water/solutes through glomerular-capsular membrane into the capsule.
Called glomerular filtrate (~180 L/day) at a rate of 125ml/min
glomerulus → bowman capsule
Reabsorption – Occurs in tubules, mainly PCT
Water (by osmosis), glucose, ions are reclaimed back into blood.
99% of filtrate is reabsorbed!
when failed → glycosuria
Secretion – Occurs in DCT and CD.
Moves substances (e.g., drugs, H⁺, K⁺, NH₄⁺) from blood into tubule.
urine → blood
Key Concepts:
Countercurrent mechanisms: Loop of Henle and surrounding vessels help concentrate urine by making medulla salty (hyperosmotic).
Transport Maximum (Tm): Max amount of a substance the nephron can reabsorb. If too much (e.g., too much glucose), excess ends up in urine.
Renal Threshold: Blood level beyond which the nephron cannot reabsorb all of a substance.
💡 Summary of Urine Formation (pg. 579)
Process | What Happens |
Filtration | Blood is filtered through glomerulus into the capsule. |
Reabsorption | Good substances (e.g., water, glucose) are reabsorbed back into blood. |
Secretion | Waste (e.g., drugs, H+, K+) is actively moved from blood into urine tubule. |
📊Table 20-1 – Nephron Function
Part of Nephron | Process in Urine Formation | Substances Moved |
Glomerulus & Glomerular Capsule | Filtration | Water, solutes (Na+, Cl-, K+), glucose, and other nutrients filtered out of blood. |
Proximal Convoluted Tubule (PCT) | Reabsorption & Secretion | Water, solutes (glucose, amino acids, Na+); also secretes nitrogenous wastes & drugs |
Nephron Loop (Loop of Henle) | Reabsorption | Sodium and chloride ions (Na+, Cl-) |
Distal Convoluted Tubule (DCT) & Collecting Duct (CD) | Reabsorption & Secretion | Water, sodium, and chloride ions reabsorbed; ammonia, H+, Ka+, drugs secreted |
🧠 Helpful Breakdown:
Filtration = Blood → Nephron
Happens ONLY in the glomerulus/capsule.
Reabsorption = Nephron → Blood
Major site: PCT (2/3 of all reabsorption happens here!). Water, glucose, ions return to blood.
Secretion = Blood → Nephron
Mostly occurs in DCT & CD. Actively removes extra ions (H⁺, K⁺), toxins, and drugs.
Tie This into the Big Picture:
The PCT is where the bulk of useful substances are reclaimed.
The Loop of Henle sets up the medullary salt gradient for water reabsorption.
The DCT & CD fine-tune urine concentration based on hormones like ADH and aldosterone.
Filtration happens just once—but reabsorption and secretion happen continuously to maintain homeostasis.
💧Regulation of Urine Volume (pg. 580–581)
🔑 Hormones Involved:
Antidiuretic Hormone (ADH)
Released from: Posterior pituitary
Action: Makes collecting ducts permeable to water.
Effect: Decreases urine volume by reabsorbing water.
“Water-retaining” or “urine-decreasing” hormone.
Aldosterone
Released from: Adrenal cortex
Action: Stimulates tubules to reabsorb sodium → water follows.
Effect: Decreases urine volume.
“Salt- and water-retaining” hormone.
Atrial Natriuretic Hormone (ANH)
Released from: Heart’s atrial wall
Action: Inhibits ADH/aldosterone → increases sodium and water loss.
Effect: Increases urine volume.
“Water-losing” or “salt-secreting” hormone.
🔁
Renin–Angiotensin–Aldosterone System (RAAS)
Stimulated by: Low blood pressure or low plasma volume
Sequence:
JG cells detect ↓ BP → release renin
Renin converts angiotensinogen → angiotensin I
ACE converts angiotensin I → angiotensin II → high BP
Angiotensin II causes:
Vasoconstriction
Aldosterone release
Aldosterone increases Na⁺/water reabsorption → ↑ blood volume & pressure
🔎Urine Volume Conditions
Anuria – No urine output
Oliguria – Low urine output
Polyuria – Excessive urine output
pyuria- pus in the urine
dysuria- painful urination
🚽 Elimination of Urine (Ureters, Bladder, Urethra) (pg. 581–583)
✏ Ureters
Muscular tubes that move urine from kidneys to bladder
Use peristalsis to move urine
Renal colic = pain from kidney stones traveling down ureter
🫙Urinary Bladder
Located behind pubic symphysis
Transitional epithelium stretches with filling
Rugae allow expansion when empty
Trigone: triangular area with smooth lining (between ureter and urethral openings)
🧻Urethra
Carries urine out of the body
Lined with mucous membrane
Female urethra ≈ 4 cm long (only urine)
Male urethra ≈ 20 cm long (urine + semen)
💥 Micturition (Urination Process) (pg. 583)
🧠 Controlled by:
Internal sphincter – involuntary smooth muscle
External sphincter – voluntary skeletal muscle
📈 Reflex Arc:
Bladder stretches → spinal reflex triggered → empties bladder unless overridden by brain
Voiding reflex occurs ~150–300 mL; strong urge ~400 mL
💉Urinary Catheterization
Insertion of sterile tube into urethra to drain urine
Used for retention, surgery, infection risk
Improper technique → risk for cystitis (bladder infection)
🚨 Abnormal Urine Output (pg. 583–584)
Urinary retention = bladder can’t empty (even though kidneys make urine)
treated by urinary catheterization, allowing for drainage of the bladder and relief of discomfort.
Urinary suppression = kidneys don’t produce urine
Incontinence Types:
Stress – laughing/coughing
Urge – strong sudden urge
Overflow – bladder doesn’t empty completely
urinary retention and over distended bladder
men with enlarged prostate gland
Reflex – from neurological damage (e.g., spinal cord injury)
common in nervous system; stroke, parkinsonism, or spinal cord injury
Urinalysis (pg. 584–585)
🧪 Includes:
Routine urinalysis – color, pH, odor, specific gravity
Microscopic urinalysis – WBCs, bacteria, casts, crystals
⚖ Table 20-2 – Characteristics of Urine
Normal | Abnormal |
Color: Light to dark yellow | Red (RBCs), green (infection), brown/orange (bile), cloudy (UTI), orange/ yellow (gallstones) Beets (red), Carrots (dark yellow), B vitamins (bright yellow), Rhubarb (red), Spinach (dark green), Blueberries (blue) |
Clarity: Clear | Cloudy from WBCs (UTI), protein, bacteria |
Odor: Slight aromatic | Fruity (DM), foul (UTI), musty (PKU) |
pH: 4.6-8.0 | High = alkalosis; Low = acidosis |
Specific Gravity: 1.005- 1.030 | High = dehydration; Low = renal disease |
Compounds in Normal Urine:
Na⁺, Cl⁻, K⁺
Urea, creatinine, uric acid
Urochrome (yellow pigment from bilirubin metabolism)
🔬Proteinuria After Exercise
Proteinuria is the presence of plasma proteins—especially albumin—in urine. Normally, proteins are too large to pass through the nephron’s filtration membrane. However:
After intense exercise, some temporary proteinuria can occur, even in healthy individuals.
This postexercise proteinuria is not necessarily due to kidney damage.
One theory is that hormonal changes during exercise increase permeability of the nephron’s filter.
It typically resolves shortly after exercise and is considered acceptable unless persistent.
💡 Key Concept: While protein in the urine usually indicates kidney disease, short-term proteinuria after exercise can be normal and not a sign of pathology.
💢 Renal and Urinary Conditions
These are problems that disrupt the normal flow or function of the urinary system. Some are life-threatening, while others are chronic or obstructive.
🚫Obstructive Conditions
These block normal urine flow, causing urine backup and damaging the kidney.
Hydronephrosis
Swelling of renal pelvis and calyces from urine buildup.
Caused by stones, tumors, inflammation, or structural problems.
If untreated, leads to permanent kidney damage.
Renal Calculi (Kidney Stones)
Made of crystallized minerals (e.g., calcium, uric acid).
Staghorn calculi are large and branched stones.
Can cause renal colic—severe pain due to rhythmic ureter contractions.
Small stones pass in urine; large stones may block flow and need removal
🦠Tumors
Kidney and bladder tumors can block urine.
Most kidney tumors are renal cell carcinomas (often in 1 kidney).
Bladder cancers occur nearly as often.
Can cause hematuria (blood in urine), pain, and urinary blockage.
Diagnosed via cystoscopy—a procedure using a scope through the urethra.
📊 Clinical Application:
Removal of Kidney Stones with Ultrasound
1 in 1,000 people in the U.S. gets kidney stones.
Ultrasound technique = lithotripsy.
Breaks stones into fragments without surgery.
Less risk, less pain, and faster recovery.
🧫
Urinalysis
A lab test that checks:
Physical properties: color, clarity, smell.
Chemical properties: pH, glucose, proteins.
Microscopic elements: cells, bacteria, crystals.
Proteinuria detected here can suggest kidney damage but must be interpreted carefully (as above).
🧪 Health & Well-Being Tip Summary
Proteinuria is not always bad.
Can result from exercise, not necessarily disease.
Must differentiate between transient and pathologic proteinuria.
🌡 Urinary Tract Infections (UTIs)
Most UTIs are caused by gram-negative bacteria, especially E. coli.
🦠Common Types of UTIs
➤Urethritis
Inflammation of the urethra.
Often caused by STIs like gonorrhea or chlamydia.
Infant boys more likely to get it than older boys/men.
➤Cystitis
Bladder infection
Common in women due to shorter urethra
Causes: Bacteria, stones, tumors
Symptoms: Pelvic pain, urgency, dysuria (painful urination), hematuria
Can become ulcerated or spread to kidneys if untreated
➤Urethral Syndrome (nonbacterial cystitis)
Most common in young women
Symptoms: Dysuria, frequency, no bacteria in urine
Possibly autoimmune, related to lupus
➤Overactive Bladder
Frequent urination of small amounts
Involves urgency, dysuria
Treated with nervous system drugs
➤ Interstitial Cystitis
Chronic bladder pain without infection
Treated with bladder irrigation and drugs to expand capacity
🧬 Pyelonephritis
Type of nephritis (inflammation of the kidney)
renal pelvis nephritis
Usually caused by bacterial infection (can also be fungal or viral)
🧯Acute Pyelonephritis
Sudden onset: Fever, flank pain, nausea, urgency
Bacteria enter via urethra or bloodstream
🕰 Chronic Pyelonephritis
Long-term damage
May be from autoimmune cause
Often asymptomatic early, but leads to scarring & renal failure
🧫 Glomerular Conditions
🔥Glomerulonephritis
Inflammation of glomeruli
Caused by autoimmunity, infection, or heredity
Damages filtration membrane → leads to proteinuria, hematuria
ACUTE → DELAYED IMMUNE RESPONSE TO A STRETOCOCCAL IN
CHRONIC→ LEADS TO RENAL FAILURE
💧 Nephrotic Syndrome
Collection of signs from glomerular damage:
Proteinuria – Albumin leaks into urine
Hypoalbuminemia – ↓ Albumin in blood
Edema – Water shifts into tissues due to low osmotic pressure
🧠 Albumin: Most abundant plasma protein; keeps water in vessels
🛑 Kidney Failure
🔴Acute Renal Failure (ARF)
Sudden ↓ in kidney function
Causes: Severe infection, glomerulonephritis, hypotension, hemorrhage, severe burns, obstruction of the lower urinary tract
Symptoms: Oliguria, high BUN (blood urea nitrogen)
Treat the cause → kidney function may fully recover
🟡Chronic Renal Failure (CRF)
Slow, irreversible decline in kidney function
Caused by: Diabetes, hypertension, glomerulonephritis, PKD
Progresses in stages → leads to uremia
🔴Stages of Chronic Renal Failure
📊 Refer to Figure 20–16 (GFR & BUN changes):
Stage 1: Compensated
Nephrons enlarge to take over lost ones
Function preserved for years
Stage 2: Renal Insufficiency
Kidneys can’t keep up
BUN rises, kidneys can’t concentrate urine
Polyuria and dehydration may occur
Stage 3: Uremia
Massive nephron loss
Waste buildup in blood
Requires dialysis or transplant
🧬 Polycystic Kidney Disease (PKD)
Inherited; appears ~40 y/o
Kidneys fill with fluid-filled cysts
S/S: Flank pain, hematuria
Cysts grow → kidney tissue destroyed → renal failure