BIOL 318 - Exam 4
Lecture 1: Urinary System – Chapter 23
This unit is about what the urinary system does, how the kidney is built, how the nephron works, and how blood and urine move through the kidney.
You are expected to:
Explain what the urinary system does beyond just making urine
Identify the major kidney and nephron structures
Explain what each nephron part does
Trace blood flow and urine flow
Already understand pressure, diffusion, osmosis, and transport mechanisms because they apply directly to kidney function
Functions of the Urinary System:
The kidneys are not just waste filters. They are full-blown regulators of internal balance. They:
Filter blood to remove wastes
Control blood volume and blood pressure
Control osmolarity (how concentrated your blood is)
Maintain electrolyte balance (Na+, K+, Ca2+, etc.)
Stimulate red blood cell production through erythropoietin
Help activate vitamin D (calcitriol) for bone health
Remove drugs, hormones, and toxins
Detoxify free radicals
Can make glucose from amino acids during extreme starvation
Kidney Location & Protective Layers:
The kidneys:
Sit against the back abdominal wall (retroperitoneal)
The right kidney is slightly lower because the liver pushes it down
They sit just below the diaphragm
They’re protected by three connective tissue layers:
Fibrous capsule → tough outer layer that protects the kidney itself
Perirenal fat capsule → cushions the kidney and holds it in place
Renal fascia → binds the kidney to the abdominal wall
Meaning: Kidneys are fragile but heavily protected because they’re essential.
Renal Circulation:
The kidneys are blood-hungry organs:
Receive 21% of cardiac output
Filter about 1.2 liters of blood per minute
Yet they only weigh 0.4% of body weight
Why this matters: The kidneys continuously monitor and correct your blood in real time.
Nephron Overview:
The nephron is:
The functional unit of the kidney
Each kidney has about 1.2 million nephrons
It has two major parts:
Renal corpuscle → filters blood
Renal tubule → turns filtrate into urine
If something damages nephrons, you lose kidney function permanently.
Nephron Structures (Order Matters):
You must know this sequence perfectly:
Glomerulus
Bowman’s Capsule
Proximal Convoluted Tubule (PCT)
Loop of Henle
Descending Limb
Ascending Limb
Distal Convoluted Tubule (DCT)
Collecting Duct
Renal Corpuscle:
The renal corpuscle → Glomerulus + Bowman’s Capsule. It’s only job:
Filter blood plasma
Push fluid and small solutes into Bowman’s capsule
This fluid is called filtrate
Big idea: Filtration happens here and only here.
Renal Tubule Functions:
Each section does something specific:
PCT
Simple cuboidal with microvilli
Major site of reabsorption
Loop of Henle
Creates concentration gradient
Allows urine to become concentrated
DCT
Simple cuboidal without microvilli
Secretion + fine control of ions
Collecting duct
Final urine concentration
Channels urine toward the renal pelvis
Many together form renal pyramids
Flow of Urine Through the Kidney:
Urine moves in this order:
Renal pyramid → Papilla → Minor calyx → Major calyx → Renal pelvis → Ureter → Bladder
Papilla:
The papilla is the tip of the renal pyramid. It’s where urine drips into the minor calyx.
Juxtaglomerular Apparatus (JGA):
This system regulates:
Blood pressure
Glomerular filtration rate (GFR)
It connects:
The DCT
The afferent arteriole
Key components:
Macula densa cells (in DCT)
Juxtaglomerular cells (in arteriole)
Macula Densa Function:
These cells detect Na+ concentration in the DCT:
High Na+ → High GFR
ATP released to mesangial cells
Afferent arteriole constricts
GFR decreases
This prevents over-filtration and fluid loss.
Juxtaglomerular Cells & Renin:
These cells:
Release renin when blood pressure drops
Renin activates:
Aldosterone
ADH
Vasoconstriction
Result: Blood pressure and volume go back up.
Renin Release Pathways:
Renin is triggered by three things:
Low renal blood pressure
Low Cl- in the DCT
Sympathetic nervous system activation
Meaning: Your kidneys respond directly to both circulation and nervous system control.
Dehydration Feedback Loop:
When you become dehydrated, the amount of water in your blood drops. Because there’s less water, the salt concentration in your blood becomes higher and your blood pressure falls.
When blood pressure drops, less blood is pushed into the kidneys, so the glomerular filtration rate (GFR) decreases. Since filtration is slower, less filtrate moves through the nephron.
Because filtrate is moving more slowly, the kidneys now have more time to reabsorb water and sodium back into the bloodstream. As this happens, the concentration of sodium reaching the DCT becomes low.
The macula densa in the DCT detects this low sodium level, which signals the juxtaglomerular cells to release renin.
Renin triggers the release of:
Aldosterone, which increases sodium and water reabsorption
ADH, which increases water reabsorption
It also causes vasoconstriction, which raises blood pressure
As a result of all of this: blood volume increases, blood osmolarity returns toward normal, and blood pressure rises back toward normal.
Lecture 2: Urinary System – Chapter 23
Glomerular Filtration – The Filtration Barrier
Your blood does not just freely pour into the nephron. It passes through three controlled layers that decide what gets filtered:
Fenestrated Endothelium → this is the inner wall of the glomerular capillaries. It is highly permeable and has pores that let water and small solutes through, but block blood cells.
Basement Membrane → this is a thick, negatively charged barrier made of proteoglycans. It repels negatively charged proteins and blocks molecules larger than 8 nanometers, such as albumin.
Your blood plasma is about 7% protein, but your filtrate is only 0.03% protein, which shows how selective this layer is.
Filtration Slits (Podocytes) → these are extensions of podocyte cells that wrap around capillaries. They create tiny slits that act as the final size and charge filter.
Together, these three layers ensure that only appropriate substances enter the filtrate.
What Actually Gets Filtered:
The primary filtrate contains:
Water, electrolytes, glucose, fatty acids, amino acids, nitrogenous wastes, and vitamins
Your kidneys filter the entire blood volume 50-60x per day.
Average filtration rates:
Females: 105 mL per minute (150 L per day)
Males: 125 mL per minute (180 L per day)
Even though this is an insane amount of fluid, 99% of it is reabsorbed, and only 1-2 liters become urine each day.
This shows that urine is what’s left over after selective reabsorption, not what was initially filtered.
Filtration Pressure (Why Filtration Happens):
Filtration depends on net filtration pressure (NFP).
It is determined by:
Blood hydrostatic pressure, which pushes fluid out of blood
Capsular pressure, which resists fluid entry
Colloid osmotic pressure, which pulls water back into blood due to proteins
The afferent arteriole is wide, the efferent arteriole is narrow, which maintains high pressure inside the glomerulus.
If blood pressure becomes too high, the glomerular capillaries can rupture, leading to kidney damage and failure.
Regulation of Filtration – Myogenic & Sympathetic Control:
Myogenic Mechanism:
When blood pressure rises, the smooth muscle of the afferent arteriole stretches and constricts.
This prevents sudden spikes in filtration and keeps GFR stable.
Sympathetic Control:
During stress or low blood volume:
Arterioles constrict
GFR can drop as low as 3 mL/min
Blood flow is prioritized to the heart and brain
ADH assists with water retention
This is your body choosing survival over filtration.
Renin-Angiotensin-Aldosterone System (RAAS):
When blood pressure drops:
Baroreceptors in the aorta and carotid arteries signal the brainstem
The kidneys release renin
Renin converts angiotensinogen from the liver into angiotensin I
Angiotensin I becomes angiotensin II in lung capillaries using ACE
Angiotensin II becomes angiotensin III
Angiotensin III stimulates secretion of aldosterone
Aldosterone causes:
Increased sodium and water reabsorption
Increased blood volume
Increased blood pressure
ACE inhibitors work by blocking this system to treat high blood pressure.
Proximal Convoluted Tubule (PCT) – Main Reabsorption Site
The PCT:
Is the longest and most coiled tubule
Reabsorbs about 65% of filtrate
Has microvilli for massive surface area
Moves water and solutes back into blood via peritubular capillaries
This is where most of the “good stuff” is recovered.
How Reabsorption Works in the PCT:
Transcellular Route:
Substances move through the cells using active transport. The Na+/K+ pump on the basal side drives this movement. Mitochondria are abundant because this is energy-intensive.
Paracellular Route:
Substances move between cells due to leaky tight junctions. Water pulls dissolved solutes with it. This is called solvent drag.
What the PCT Reabsorbs:
About 65% of sodium and water are reabsorbed here. All glucose, amino acids, and lactate are reabsorbed.
Sodium-hydrogen antiporters:
Save sodium
Remove hydrogen ions
Angiotensin II increases sodium reabsorption.
About 50% of urea is also rebasorbed.
Calcium and magnesium follow through solvent drag.
Secretion in the PCT:
The sodium-hydrogen antiporter also allows for secretions of hydrogen ions, helping regulate blood pH.
Some drugs require multiple daily doses because they are secreted quickly by the PCT.
Saturation of Transport Proteins:
Transport proteins are limited in number. When all are occupied, excess solutes remain in the urine. This is why:
Glucose appears in urine in diabetes
Drugs show dose-dependent excretion
Anything that appears in urine after saturation suggests a disorder or overload.
Solvent Drag Explained:
Blood entering the glomerulus has low protein concentration in the filtrate, creating high colloid osmotic pressure in the capillaries.
This pressure pulls water back into the blood, and dissolved ions are pulled with it.
This movement of solutes carried by water is called solvent drag.
Distal Convoluted Tubule (DCT):
The DCT:
Has cuboidal cells
Has no microvilli
Contains many mitochondria
Receives about 20% of the original filtrate
Functions:
Regulates acid-base balance
Absorbs potassium
Secretes hydrogen ions
Regulates sodium, potassium, and bicarbonate
Cell Types:
Intercalated cells regulate acid and bicarbonate.
Principal cells absorb sodium and secrete potassium; water follows.
Aldosterone regulates sodium and potassium movement here.
Hormone Regulation in the DCT – ANP:
Atrial natriuretic peptide (ANP):
Increases sodium and water excretion
Increases GFR
Inhibits the sympathetic nervous system
Blocks renin, angiotensin II, and aldosterone
Inhibits the Na/K+ pump
Inhibits ADH
ANP is your body’s anti high blood pressure hormone.
Lecture 3: Urinary System – Chapter 23
This lecture explains:
How nephrons control how much water you excrete
How the loop of Henle builds concentration
How blood vessels preserve that concentration
How hormones control urine concentration and blood pressure
Comparative Physiology of Urine Concentration:
Animals in dry environments have longer nephron loops, which lets them concentrate urine much more.
Example: the kangaroo rat survives without drinking water because its kidneys are elite at saving water.
This proves that loop length determines concentration power.
Cortical vs Juxtamedullary Nephrons:
You have two types of nephrons:
Cortical Nephrons:
Short loops
Corpuscle in the outer cortex
Make up 85% of your nephrons
Poor at concentrating urine
Juxtamedullary Nephrons:
Long loops that dive deep into the medulla
Corpuscle near the medulla
Make up 15%
These are the ones that create the concentration gradient
Humans have both types, which is why we can make both dilute and concentrated urine.
Water Abundance vs Dehydration:
When you drink a lot of water:
Your collecting ducts become impermeable to water
You excrete large amounts of very dilute urine
Urine can be as low as 50 mOsm/L
When you are dehydrated:
Collecting ducts become permeable to water
Water is reabsorbed back into blood
Urine becomes highly concentrated
Can reach 1200 mOsm/L
Structure & Function of the Loop of Henle:
The loop has two limbs with opposite jobs.
Descending Limb:
Highly permeable to water
Impermeable to salt
Water leaves the tubule
Tubular fluid becomes more concentrated
Osmolarity rises from 300 to 1200 mOsm/L
Ascending Limb:
Impermeable to water
Actively pumps NaCl out
Salt leaves, but water cannot flow
Tubular fluid becomes dilute
Osmolarity falls from 1200 to about 100 mOsm/L
As salt is pumped into the surrounding tissue, the medulla becomes extremely salty, which is what later pulls water out of the collecting duct.
Countercurrent Multiplication (How the Gradient is Built):
Countercurrent means the fluid in the two limbs flows in opposite directions.
Multiplication means salt keeps getting added to the medulla over and over with every cycle of filtrate.
The ascending limb repeatedly pumps salt into the tissue.
The descending limb repeated loses water to that salty tissue.
Each pass makes the medulla more and more concentrated.
By the end, the medulla forms a strong 300 → 1200 mOsm gradient, which is what allows extreme water reabsorption later.
Without this system, concentrated urine would be impossible.
Urea’s Role in Urine Concentration:
Urea is not just waste. It actually helps build the medullary gradient
When ADH is present, the lower collecting duct becomes permeable to urea. Urea leaves the duct and enters the medulla, raising osmolarity even more. Urea then cycles back into the nephron loop and returns to the collecting duct.
When ADH is high, urea contributes about 50% of the medulla’s osmolarity.
Urea is a recycled osmotic weapon
Aldosterone:
Aldosterone is released when:
Blood sodium is low
Blood potassium is high
Blood pressure is low
Angiotensin II is present
It acts on:
Thick ascending loop
DCT
Collecting duct
It effects:
Increases sodium reabsorption into blood
Increases potassium secretion into urine
Water follows sodium
Blood volume and blood pressure rise
Aldosterone is your sodium-saving hormone.
ADH and Aquaporins:
ADH is released when:
Blood osmolarity is high
Blood pressure is low
Angiotensin II is present
It causes:
Aquaporin water channels to be inserted into collecting duct membranes
Water to move from urine into blood
Urine to become concentrated
Blood volume to increase
This happens fast, without making new proteins at first. Long-term high ADH causes new aquaporins to be produced. ADH is your water-saving hormone.
Natriuretic Peptides (ANP):
ANP is released when blood pressure is too high. Its job is to lower pressure by dumping sodium and water. It does this by:
Dilating afferent arterioles to increase filtration
Inhibiting aldosterone
Inhibiting ADH
Blocking sodium reabsorption in collecting ducts
ANP is the anti-aldosterone, anti-ADH hormone.
AQP2 Recycling:
Aquaporins can be:
Inserted into the membrane for water reabsorption
Removed and degraded when ADH drops
Recycled or broken down in lysosomes
This allows minute-by-minute control of water balance.
Both Nephron Types Work Together:
Cortical nephrons handle most filtration. Juxtamedullary nephrons create the medullary gradient. All filtrate eventually enters the same collecting ducts and is exposed to the gradient. That is why every drop of urine can be controlled for concentration.
Drinking Saltwater:
Drinking ocean water is dangerous because:
Ocean water is ~1000 mOsm/kg
Blood is only ~300 mOsm/kg
Kidneys must excrete excess salt
To remove the salt, you lose more water than you drank
You become more dehydrated
Only animals with extreme juxtamedullary systems could survive it.
Lecture 4: Urinary System – Chapter 23
Buffer Systems & pH Control:
Your blood pH has to stay in a very tight range or your enzymes stop working correctly. Your body uses five buffer systems to control pH:
Bicarbonate
Phosphate
Respiratory
Metabolic
Renal (kidneys)
The kidneys are the long-term pH regulators:
If blood pH is too low (acidic), the kidneys excrete hydrogen ions (H+)
If blood pH is too high (basic), the kidneys excrete bicarbonate (HCO3-)
So your kidneys literally decide whether to dump acid or dump base to stabilize your blood.
pH Control in the PCT:
The proximal convoluted tubule (PCT) helps regulate pH by handling hydrogen and bicarbonate:
Hydrogen Secretion:
Sodium/Hydrogen antiporter pushes H+ into the tubule
H+-ATPase pumps hydrogen out directly
Bicarbonate Reabsorption:
Carbonic anhydrase on the tubule surface forms carbonic acid
Carbonic acid splits into water and CO2
These enter the cell and are converted back into bicarbonate
Bicarbonate leaves the cell and reenters the blood
Translation: The PCT gets acid out of urine and puts base back into the blood to stabilize pH.
Collecting Duct & Intercalated Cells:
The collecting duct has specialized pH-control cells called intercalated cells.
H+ Secreting Intercalated Cells:
Pump hydrogen into urine
Reabsorb bicarbonate back into blood
Used when blood is too acidic
HCO3- Secreting Intercalated Cells:
Pump bicarbonate into urine
Retain hydrogen in the body
Used when blood is too basic
This is the final fine-tuning of blood pH before urine leaves the kidney.
Titratable Acid (TA):
When hydrogen ions are secreted into urine, they don’t float freely because they would make urine dangerously acidic.
Instead, H+ binds to buffers inside the tubular fluid, mainly phosphate and bicarbonate
This binding is called titratable acid excretion and it reduces the acidity of urine and allows the kidneys to safely eliminate acid without damaging tissue.
Bladder Structure:
The bladder is a stretchable storage organ. Key features:
Lined with transitional epithelium (urothelium)
Surface cells called umbrella cells protect against:
Acidic urine
Hypertonic urine
Has the detrusor muscle, made of 3 layers of smooth muscle
Bladder wall changes with filling:
Empty bladder: thick, folded wall with rugae (5-6 cell layers)
Full bladder: stretched thin (2-3 cell layers)
This lets the bladder store urine without tearing.
Urethra – Male vs Female:
Female Urethra:
3-4 cm long
Anterior to the vaginal tract
Short length increases risk of UTIs
Male Urethra (~18 cm long):
Prostatic urethra (through prostate)
Membranous urethra (through pelvic floor)
Spongy urethra (through penis)
Male urethra is longer because it also carries semen.
Neural Targets of Micturition:
Three muscles are controlled during urination:
Detrusor muscle (bladder wall)
Internal urethral sphincter (smooth muscle)
External urethral sphincter (skeletal muscle)
Urination depends on who is contracting and who is relaxing at the right time.
Between Voiding Acts (Fill Mode):
When you are not urinating:
Detrusor muscle is relaxed (sympathetic control)
Internal sphincter is contracted (sympathetic control)
External sphincter is contracted (somatic motor control)
This keeps urine stored safely in the bladder.
Involuntary Micturition (Automatic Reflex):
When the bladder fills:
Stretch receptors in the bladder wall activate
Signals go to the spinal cord
Parasympathetic nerves activate through the pelvic nerve
Detrusor muscle contracts
Internal sphincter relaxes
If not consciously suppressed, urination will occur automatically. This is the reflex infants use.
Voluntary Micturition (Conscious Control):
The pons in the brainstem acts as the control center.
When it is appropriate to urinate:
Signals from stretch receptors and the cerebrum are processed
Pons sends signals through the spinal cord
Detrusor contracts
Internal sphincter relaxes
External sphincter relaxes via corticospinal tracts
Urine is released voluntarily
When it is not appropriate:
The brain inhibits parasympathetic activity
External sphincter remains contracted
Urination is delayed
Neural Control Overview:
Spinal cords run the reflex
Brain centers decide whether to allow or block it
Parasympathic = urinate
Sympathetic = store urine
Somatic = conscious control of external sphincter
Delaying Urination:
If you hold urine:
Stretch receptors temporarily adapt and fire less
The urge may briefly fade
But signals return stronger later as filling continues
If the bladder isn’t full but you try to urinate anyway:
You can use the Valsalva maneuver (abdominal pressure)
This activates stretch receptors manually
Sex Differences in Voiding:
Males:
Bulbocavernosus muscle forces out the last drops of urine
Prevents urine from being trapped in the long urethra
Females:
No internal urethral sphincter
Rely heavily on pelvic floor muscles
Higher risk of urinary incontinence
Risk increases with pregnancy obesity, and pressure changes
Lecture 5: Chapter 23 – Urinary System
Urine Appearance (Color & What It Means):
Normal urine color ranges from yellow to colorless. That yellow color comes from urochrome, which is a pigment produced from the normal breakdown of hemoglobin.
Abnormal colors and what they usually mean:
Pink: blood in urine or foods with magenta pigment
Orange: dehydration or bile in the blood
Green: food dyes or a Pseudomonas bacterial infection
Brown: severe dehydration or certain drugs (like chloroquine)
Black: a rare genetic disorder called alkaptonuria
Important clinical terms:
Pyuria → pus in the urine, usually from a kidney infection
Hematuria → blood in the urine, seen with UTIs, trauma, or kidney stones
Urine Odor, Osmolarity & Chemical Properties:
Odor:
If urine sits in air, bacteria turn urea into ammonia, causing strong odor
Sweet or fruity smell → diabetic ketoacidosis (ketones)
Rotten smell → urinary tract infection
Osmolarity:
Urine osmolarity ranges from 50 to 1200 mOsm/L
Blood is about 300 mOsm/L
Urine can be hypotonic (dilute) or hypertonic (concentrated) depending on hydration
pH:
Normal urine pH is about 6.0
Range: 4.8 to 8.2
Normal Composition:
Urine is 95% water and 5% solutes. Solutes are mainly urea, sodium chloride, potassium chloride, bicarbonate, titratable acids, and calcium.
Abnormal Components (ALWAYS Pathologic):
Glucose, free hemoglobin, albumin (protein), ketones, and bile pigments
If you see glucose or protein in urine, something is wrong clinically
Kidney Stones – What They Are & Why They Form:
Kidney stones form when minerals and salts crystallize because urine becomes too concentrated. Most common stone-forming substances are calcium, oxalate, and uric acid. They form when the urine can’t dilute these substances enough.
Types of Kidney Stones:
Calcium Stones (Most Common)
From hypercalciuria (too much calcium in urine)
Two types: calcium oxalate and calcium phosphate
Oxalate comes from: diet and liver metabolism
Uric Acid Stones
Caused by not drinking enough water and/or a high-protein diet
Form in acidic urine
Related to purine breakdown
Cystine Stones
Hereditary
Kidneys excrete too many amino acids
Very rare, but very severe
Renal Clearance (How Fast a Substance is Removed from Blood):
Renal clearance is the volume of plasma cleared of a waste in one minute.
The formula is: Clearance = (Urine concentration x Urine flow rate) / Plasma concentration
This tells you how efficiently the kidneys remove a substance.
Examples:
Urea in urine = 6.0 mg/mL
Urea in plasma = 0.2 mg/mL
Urine output = 2 mL/min
The kidneys clear 60 mL of plasma of urea per minute.
GFR Measurement:
Glomerular filtration rate (GFR) is hard to measure using natural solutes, because most substances are reabsorbed or secreted.
So we use: creatine (small error but acceptable) and/or inulin (gold standard research marker)
For inulin:
It is filtered but not reabsorbed or secreted
So renal clearance = GFR
Normal GFR = approx. 120 mL/min
Hemodialysis – Why It’s Needed
Hemodialysis is required when:
75-90% of kidney function is lost
About 75% of nephrons are destroyed
Urine output drops to about 30 mL/hr (normal is 50-60)
At this point, the body cannot maintain homeostasis, leading to:
Acidosis (blood too acidic), Azotemia (nitrogen wastes in blood), Uremia (toxic waste buildup), and/or Anemia
How Hemodialysis Works:
Blood is taken from the radial artery
Blood flows through a tube with a semipermeable membrane
Dialysis fluid outside the tube has low solute concentration
Wastes diffuse out of the blood into the dialysis fluid
Cleaned blood is returned through the radial vein
This mimics glomerular filtration using diffusion, not pressure.
What Can Be Added During Dialysis:
Dialysis fluid can be customized to include glucose, electrolytes, drugs, erythropoietin (EPO), and/or heparin. This allows providers to both remove toxins and deliver needed blood components at the same time.
Lecture 6: Reproductive System – Chapters 27 & 28
Testes – Structure & Function
The testes have two jobs:
Endocrine → make hormones
Exocrine → make sperm
Inside the testes:
Divided into lobules
Each lobule contains seminiferous tubules where sperm are formed
Nurse cells (Sertoli cells) support and nourish developing sperm
Spermatogonia are the stem cells that become sperm
Blood-Testis Barrier:
Formed by tight junctions between nurse cells
Protects developing sperm from the immune system
Important because sperm have different DNA than the rest of the body
Interstitial (Leydig) Cells:
Located between seminiferous tubules
Stimulated by luteinizing hormone (LH)
Produce testosterone
Scrotum – Temperature Control System:
Humans evolved to make sperm at a lower temperature than core body temperature, so the testes must stay outside the abdominal cavity. There are four main temperature control mechanisms:
Cremaster Muscle
Skeletal muscle from the abdominal wall
Pulls testes closer to body when it’s cold
Dartos Muscle
Smooth muscle in scrotal skin
Wrinkles the scrotum when cold to reduce heat loss
Pampiniform Plexus
Network of veins that cool incoming arterial blood
Act as a heat exchanger
Purpose: Keep testes at the optimal temperature for sperm production.
Sperm Transport from the Testes:
Pathway inside the testes:
Seminiferous tubules → rete testis
Sperm are partially mature here
Then move into efferent ductules → epididymis
Final maturation occurs in the epididymis
Important details:
Nurse cells provide fluid
Cilia help move fluid
Sperm do not swim in the male tract because blood pressure is low and there is no pulse in the spermatic artery
Sperm have large mitochondria to survive low oxygen (hypoxia)
Spermatogenesis – How Sperm Are Made:
Sperm production occurs in stages and takes about 70 days.
Spermatogonia divide by mitosis
One daughter cell moves inward and enlarges
Meiosis I creates haploid spermatocytes
Meiosis II creates haploid spermatids
Spermiogenesis reshapes spermatids into sperm with flagella
Humans produce about 400 million sperm per day.
Spermatic Duct Pathway:
The exact flow of sperm:
Seminiferous tubules → Rete testis → Efferent ductules → Duct of epididymis → Vas deferens → Ejaculatory duct
Accessory Glands (Add Fluid & Function to Semen):
Seminal Vesicles
Located behind the bladder
Their ducts merge with the vas deferens
Produce most of the semen volume
Secrete fructose (energy for sperm), citrate, calcium, and prostaglandins (stimulate uterine contractions)
Prostate Gland
Surrounds urethra below the bladder
Secretes milky fluid that activates sperm
Makes semen clot initially, then enzymes liquify it
Neutralizes vaginal acidity from pH 3.5 to about 7.5
Bulbourethral (Cowper’s) Glands
Below prostate
Produce pre-ejaculate
Lubricates the urethra
Provides alkaline buffering
Normal sperm count: 50-120 million sperm per milliliter of semen.
Penis – Structure:
The penis has a root (internal); a shaft and glans (external). It contains three erectile tissue columns:
Corpus Spongiosum → surrounds the urethra; forms the glans
Two Corpora Cavernosa → located dorsally; responsible for most of the erection
During erection, blood fills small vascular spaces called lacunae.
Ovaries – Structure & Function:
Ovaries → produce egg cells and hormones
Internal regions:
Medulla contains blood vessels and connective tissue
Cortex contains developing follicles
Follicles → fluid-filled; each contains one oocyte
Ovary appearance → smooth in childhood, bumpy during reproductive years, small and scarred after menopause.
Oogenesis – How Eggs Are Made:
Oogenesis begins before birth.
Before Birth:
Oogonia form at 5-6 weeks of development
Increase to 6-7 million by month 5
Development halts before birth
By puberty, only ~200,000 remain
Most die by atresia
From Puberty to Menopause:
About two dozen follicles start maturing each month
Only one ovulates
Meiosis I finishes at ovulation
Produces one secondary oocyte and one polar body
If fertilization occurs, meiosis II finishes and produces one ovum and one additional polar body
Eggs are large because they contain nutrients to support early embryonic development.
Fallopian Tubes (Oviducts):
These tubes transport the ovulated egg to the uterus. Key features:
Funnel-shaped opening near ovary called the infundibulum
Finger-like fimbriae sweep the egg inside
Smooth muscle moves the egg
Lined with ciliated and secretory cells
Fertilization normally occurs in the fallopian tube.
Uterus – Structure:
The uterus is thick and muscular. It supports and nourishes the fetus. Regions:
Fundus → upper curved portion
Body → main portion
Cervix → inferior portion opening into vagina
The cervix contains glands that produce protective mucus.
Uterine Wall Layers:
The uterus has three layers:
Perimetrium → outer serous layer; protection
Myometrium → thick smooth muscle layer; responsible for contractions; strongest near the cervix
Endometrium → inner mucosal layer, contains glands and blood supply; top functional layer is shed during menstruation; basal layer stays and regenerates the lining
Lecture 7: Reproductive System – Chapters 27 & 28
Hormonal Control of the Male Reproductive System:
The male reproductive system is controlled by the hypothalamic-pituitary-gonadal (HPG) axis. Here’s the control chain in words:
The hypothalamus releases GnRH
GnRH tells the anterior pituitary to release LH and FSH
LH goes to the testes and stimulates Leydig (interstitial) cells to produce testosterone
Testosterone → promotes sperm production, causes development of male secondary sex characteristics, and acts on peripheral target tissues.
FSH, ABP, and Estradiol in Males:
FSH acts on the nurse (Sertoli) cells in the seminiferous tubules.
What FSH makes nurse cells do:
Secrete androgen-binding protein (ABP)
ABP binds testosterone and keeps it concentrated inside the seminiferous tubules
High testosterone inside tubules is required for normal spermatogenesis
Some testosterone is also converted into estradiol using the enzyme aromatase.
Estradiol helps coordinate sperm development
So yes, males make estrogen too, just in smaller amounts
Inhibin – The Male Feedback Brake
Inhibin is:
Released by nurse (Sertoli) cells
Its job is to suppress FSH release from the pituitary
This is a negative-feedback loop:
High sperm production → more inhibin → less FSH → sperm production slows
Low sperm production → less inhibin → more FSH → sperm production increases
This keeps sperm output stable instead of excessive.
Ovarian Cycle – Follicular Phase & Ovulation
Follicular Phase (Days 1-14):
This phase runs from the start of menstruation until ovulation. Key events:
FSH stimulates about two dozen follicles to begin developing
Developing follicles release estradiol (estrogen)
Estradiol causes one follicle to become dominant; causes that follicle to grow extra LH and FSH receptors
Rising estradiol initially inhibits GnRH
Then it suddenly causes a large LH surge
This LH surge triggers ovulation around day 14
Ovulation:
The dominant follicle ruptures and the oocyte is released into the uterine tube
Luteal Phase (Days 15-28):
After ovulation the ruptured follicle becomes the corpus luteum. LH keeps the corpus luteum active. It secretes progesterone (large amount) and estradiol (small amount). These hormones:
Maintain the uterine lining for possible pregnancy
Have negative feedback on the pituitary
Cause FSH and LH levels to drop
If no pregnancy occurs:
The corpus luteum shrinks after ~8 days
It becomes the corpus albicans
Progesterone levels fall → menstruation begins
Follicles are Activated Months in Advance:
The egg that ovulates this month actually started developing about 290 days earlier. Follicles develop in overlapping cohorts:
A new group starts every 28 days
Only one from each group becomes dominant and ovulates
The rest undergo atresia (degeneration)
This means the ovaries are always working almost a year ahead of time.
Menstrual Cycle – Proliferative & Secretory Phases:
Proliferative Phase (Days 5-14):
This happens after menstruation stops. Estradiol from developing follicles causes:
Rapid mitosis of the endometrium
Growth of new uterine lining
Formation of progesterone receptors
Secretory Phase (Days 15-26):
This occurs after ovulation. Progesterone is now dominant. The endometrium:
Thickens with fluid (not cell division)
Glands grow
Glands secrete glycogen
The uterus is now fully prepared for implantation.
Premenstrual & Menstrual Phases:
Premenstrual Phase (Last 2 Days of Cycle):
If fertilization did not occur:
Corpus luteum shrinks
Progesterone levels drop
Blood vessels in the uterus spasm
Blood supply is cut off
Endometrial tissue breaks down
Menstrual Phase (Days 1-5):
The broken endometrial tissue, blood, and fluid are discharged
Menstrual fluid contains fibrinolysin, which prevents clotting.
This is the physical reset of the uterine lining.
Erectile Dysfunction (ED):
Normal erection pathway:
Nitric oxide is released
It activated a second-messenger system
cGMP increases
Blood vessels dilate
Blood fills erectile tissue → erection occurs
Problems in ED:
PDE5 enzyme breaks down cGMP too quickly
Blood flow cannot be maintained
Solution:
PDE5 inhibitors (like Viagra) block the enzyme
cGMP stays high
Blood flow continues
Erection is sustained
Endometriosis:
Endometriosis occurs when endometrial tissue grows outside the uterus, such as: fallopian tubes, ovaries, bladder surface, vaginal tract, pelvic cavity, and/or intestines. This tissue:
Still thickens and breaks down each cycle, but has no exit path. It causes irritation, inflammation, and scar tissue.
Major Consequences → severe pelvic pain and increased risk of infertility
Menopause:
Menopause begins when only about 1,000 follicles remain. Key changes:
Ovaries become less responsive to FSH and LH
Estrogen and progesterone levels fall
Reproductive tissues regress: ovaries, uterus, vaginal tract
Blood vessels constrict and dilate unpredictably because of hormone shifts, causing hot flashes and temperature instability.
Grandmother Hypothesis:
This evolutionary theory suggests menopause exists so older females can stop investing energy in reproduction and help ensure survival of grandchildren.
Lecture 8: Reproductive System – Chapter 8
Fertilization (How the Sperm Enters the Egg):
When a sperm reaches the egg, it undergoes the acrosomal reaction, which is a type of exocytosis. Key enzymes released:
Hyaluronidase breaks down the cells surrounding the egg (granulosa cells)
Acrosin digests the zona pellucida (outer protective layer of the egg)
Only the head and midpiece of the sperm enter the egg
The paternal mitochondria are destroyed, so all mitochondria in the embryo come from the mother.
The “first to win the race” idea is misleading, only sperm that can perform the acrosomal reaction successfully can fertilize the egg.
Polyspermy Blocks (Preventing Multiple Sperm Entry):
The egg prevents more than one sperm from entering using two blocks:
Fast Block:
Sperm binding opens sodium channels
The egg membrane depolarizes
This prevents any additional sperm from attaching
Slow Block:
Sperm penetration triggers calcium influx
Cortical granules release their contents
Sperm receptors are destroyed
The membrane swells and pushes other sperm away
A fertilization membrane forms and becomes impenetrable
These two systems ensure only one sperm fertilizes the egg.
Stages of Prenatal Development:
Developmental stages:
Blastocyst: First 2 weeks
Embryo: Day 16 to week 8
Fetus: Week 9 until birth
This timeline is based on structural development, not size.
hCG (Human Chorionic Gonadotropin):
hCG is:
Secreted by the blastocyst, then the placenta
Peaks at 10-12 weeks
Stimulates the corpus luteum to keep growing
Causes the corpus luteum to double in size
Without hCG:
The uterus would expel the blastocyst and placenta
Pregnancy would terminate early
This is also the hormone detected in pregnancy tests.
Estrogens in Pregnancy:
Estrogens:
Stimulate growth of the fetus and mother
Enlarge the uterus and mammary glands
Increase elasticity of the pubic symphysis
Types:
Estriol is the most abundant estrogen in pregnancy
Estradiol is the most potent
Sources:
First 12 weeks: mainly from the corpus luteum
After 12 weeks: from the placenta
The adrenal glands secrete androgens which the placenta converts into estrogens
Progesterone:
Progesterone initially comes from the corpus luteum, later comes from the placenta. Functions:
Suppresses FSH and LH
Suppresses uterine contractions
Stimulates growth of decidual cells in the endometrium
Helps nourish the blastocyst
Stimulates growth of secretory cells in mammary gland
Progesterone is the “pregnancy-maintenance hormone”
hCS (Human Chorionic Somatomammotropin)
hCS:
Secreted by the placenta
Begins around the 5th week
Increases throughout pregnancy
Proportional to uterus size
Actions:
Reduces insulin sensitivity
Has effects opposite of insulin
Does not reach the fetus
Reduces mother’s glucose use
Forces more glucose to be available for the fetus
Stimulates release of fatty acids from fat cells
Result: The mother shifts to fat metabolism so the fetus gets the glucose.
Hormone Levels:
hCG peaks early, estrogen and progesterone rise steadily, and hCS increases with fetal growth
Hormonal Control of Childbirth:
Childbirth is triggered by changes in the progesterone-estrogen balance:
Progesterone keeps the uterus relaxed
Estrogen promotes contractions
At labor onset:
The posterior pituitary releases more oxytocin (OT)
The uterus increases oxytocin receptors
Oxytocin stimulates uterine contractions and the fetus to release prostaglandins
Prostaglandins work with oxytocin to intensify contractions
Labor Contractions:
Labor contractions:
Start about 30 minutes apart
Progress to every 1-3 minutes
The body of the uterus contracts more than the cervix
This pushes the fetus downward
Stretching of the cervix increases oxytocin release
This is a positive feedback loop
During contractions:
Uterine arteries are compressed
Blood flow temporarily decreases
Between contractions, the uterus must relax to restore blood flow
Stages of Labor:
Stage 1 – Dilaton → cervix widens, amniotic sac ruptures, amniotic fluid is discharged
Stage 2 – Expulsion → begins when the baby’s head enters the vaginal canal, ends when the baby exits, suction may be used to clear mucus from airways
Stage 3 – Placental Stage → uterus contracts again, placenta detaches and is expelled, umbilical cord is checked for 2 arteries and 1 vein
Digestive System Changes in Pregnancy:
Common Changes → morning sickness, constipation and heartburn, increased basal metabolic rate (BMR), and increased appetite
Nutrient Demands → the fetus eventually needs more nutrients than the intestine can absorb; the mother must mobilize body stores
Required Nutrients Increase → protein, calcium and phosphates, iron (for red blood cell formation), and vitamins (especially folic acid)
Circulatory System Changes:
During pregnancy:
Blood volume increases by about 30%
Cardiac output increases
The growing uterus compresses lower veins, causing hemorrhoids, varicose veins, and/or edema
Respiratory System Changes:
Respiratory changes include:
Increased tidal volume
Increased oxygen demand
Progesterone increases sensitivity of CO2 receptors
Breathing rate and depth adjust to keep CO2 lower
This promotes CO2 removal from the fetus
Late pregnancy:
The uterus pushes on the diaphragm
Causes air hunger, a feeling of inadequate breathing
Postpartum Period:
The postpartum period lasts about 6 weeks. During this time:
Anatomy and physiology gradually return to normal
Reproductive organs move back toward their pre-pregnancy state
This is the recovery phase after delivery.