BSCI202 Exam 3

histology of bladder: smooth muscle structure and epithelium

-smooth muscle structure: mucosa: CT + transitional epithelium: walls are thick and folded in an empty bladder

-detrusor muscle: three layers of smooth muscle that are involuntary (PSNS active → detrusor muscle contracts to urinate)

trigone of urinary bladder

two openings from the ureters where urine enters, one opening to the urethra where urine exits

function of urethral sphincters

manage urine flow at the junction of the bladder and urethra. internal urethral sphincter is involuntary (when SyNS active → sphincter contract → close opening). external urethral sphincter is a voluntary muscle that relaxes to urinate.

urinary bladder

smooth, collapsible, muscular sac that temporarily stores urine; connects to ureters and urethra through trigone

ureter vs urethra vs urethral sphincter

-ureter: two tubes on either side of kidney that carry urine to bladder
-urethra: one tube that carries urine bladder out of the body
-urethral sphincters: muscles that surround the urethra to control urination

pathway of micturition

renal tubules → renal pelvis → ureters → bladder

renal tubules vs renal pelvis

-renal tubules (nephron): located primarily in the renal cortex and renal medulla to perform reabsorption and secretion
-renal pelvis: funnel-shaped in renal hilum connecting to ureter that collects urine from calyces and funnels to ureter

renal cortex vs renal medulla

-renal cortex: light-colored, outer region that contains cortical nephrons
-renal medulla: darker, inner region deep to the cortex that contains renal pyramids, renal columns, and papilla

renal pyramids vs renal columns vs papilla

-renal pyramids: triangular regions of tissue within the medulla that have a striped appearance
-renal columns: extensions of cortex-like tissue that separate the pyramids
-papilla: tip of pyramid that points towards inner part of kidney - where urine drips into collection system

calyces

-structure: cup-shaped structures that inclose the papilla of the pyramids
-function: collect urine continuously draining from pyramids and move it into renal pelvis

hilum

medial indentation
-critical entry and exit point for renal artery (bringing blood in), renal vein (taking blood out), ureter (taking urine to the bladder), and nerves

two main parts of nephrons (structural/functional units of kidney)

-renal corpuscle (glomerulus with capillary bed + Bowman’s capsule)
-renal tubule (PCT, loop of Henle, DCT)

histology of glomerulus: type of capillaries and characteristics

glomerulus is cluster of fenestrated capillaires
-large pores allow water and small solutes to pass through capillary walls while blocking blood cells and large proteins
-high pressure system that pushes plasma out of fenestrations
-fed and drained by arterioles (afferent and efferent respectively)

histology of glomerulus: filtration membrane

multi-layered barrier through which blood plasma must pass to enter capsular space as filtrate
-fenestrated endothelium of glomerular capillaries, basement membrane, filtration slits between podocytes

histology of glomerulus: Bowman’s capsule (visceral and parietal layer cells)

surrounds the glomerulus and has two distinct layers
-parietal (outer) layer: simple squamous epithelium: structural container
-visceral (inner) layer: clings directly do the glomerular capillaries: composed of podocytes that act as fine-mesh strainers

filtrate

the fluid that gets pushed through bowman’s capsule: contains water, salts, nutrients but no blood cells or large proteins

histology of proximal convoluted tubule (PCT)

-simple cuboidal epithelium
-dense microvilli to increase SA for reabsorption
-many mitochondria to provide ATP needed for active transport

histology of Loop of Henle (nephron loop)

-simple squamous epithelium
-thin descending limb: simple squamous epithelium: highly permeable to water but impermeable to ions
-thick ascending limb: simple cuboidal epithelium: impermeable to water but highly permeable to ions

histology of distal convoluted tubule (DCT)

-simple cuboidal epithelium
-no microvilli
-macula densa
-last part of tubule that can “sense” how much to absorb/secrete because it has the macula dense

histology of collecting duct

-principal cells: maintain water and salt balance
-ADH: cause these cells to express aquaporins and allow for massive water reabsorption
-aldosterone: increases Na+/K+ ATPase activity to reabsorb Na+ and excrete K+

-intercalated cells: maintain acid-base balance
-type A (acidosis): active when blood is too acidic: excrete H+ into urine and reabsorb HCO3- and K+ back into blood
-type B (alkalosis): active when blood is too basic: reabsorb H+ and secrete HCO3- and K+ into tubule

impact of PSNS on urination

-dominant when you are relaxed and body is ready to eliminate waste
-causes detrusor muscle to contract and increase pressure inside the bladder to push urine towards the exit

impact of SyNS on urination

-active during stress or physical activity so you don’t urinate at bad time

-keeps internal urethral sphincter contracted (closed) to prevent urine from entering urethra from bladder
-must inactivate in order to open sphincter

List the 4 processes of the urinary system that allow to maintain homeostasis

glomerular filtration, tubular reabsorption, tubular secretion, excretion

Describe how glomerular filtration maintains homeostasis

-direction: from blood in glomerular capillaries to tubule (Bowman’s Capsule)
-mechanism: high blood pressure “pushes” about 20% of plasma through sieve-like membrane
-creates filtrate

Describe how tubular reabsorption maintains homeostasis

body takes back what it needs
-direction: proximal convoluted tubule → blood (peritubular capillaries)
-99% of the amount of fluid filtered daily has to be reabsorbed
-most is active transport
-100% of glucose and amino acids are reabsorbed

difference between thin descending limb and thick ascending limb of LoH for tubular reabsorption

purpose of loop of Henle is to establish a salt gradient to allow for water conservation
-thin descending limb: permeable to water, impermeable to ions
-thick ascending limb: permeable to ions, impermeable to water

what happens in the thin descending limb of the loop of Henle

As the filtrate moves down into the increasingly “salty” medulla of the kidney, water is draw out of the tubule via osmosis through aquaporin-1 channels. The fluid remaining inside the tubule becomes highly concentrated anad so by the time it reaches the bend of the loop, it is at its maximum osmolarity.

describe what happens in the thick ascending limb of the loop of Henle

It uses the Na+/K+/2Cl- active symporter to actively pump sodium, potassium, and chloride out of the filtrate and into the surrounding interstitial fluid. The filtrate becomes “diluted” as it ascends while the surrounding medulla becomes extremely salty. This saltiness is what pulls the water out of the descending limb in the first place.

Describe how tubular secretion maintains homeostasis

last minute disposal for substances that weren’t initially filtered out
-direction: blood in peritubular capillaries → tubule (filtrate)
-critical for pH balance (secreting extra H+ ions) and electrolyte balance (secreting extra K+)

Describe how excretion maintains homeostasis

final removal of finished waste product from body
-direction: tubules → exterior
-excretion = filtration - reabsorption + secretion

peritubular capillaries

tiny-low-pressure blood vessels that wrap around renal tubules (PCT+Henle+DCT+CD) to be the bridge between blood and urine

describe function and role in homeostasis of urinary system: blood volume and blood pressure homeostasis

When BP or BV is low, the kidneys reabsorb more water and sodium back into the blood to “fill the tank” and raise pressure. When BP is too high, excrete more sodium and water. This is controlled by the RAAS (renin-angiotensin-aldosterone system).

Describe the renin pathway of the RAAS (renin-angeiotensin-aldosterone system).

1. Juxtaglomerular apparatus (JGA) senses a drop in systemic BP/BV through either juxtaglomerular cells in the afferent arteriole sensing low blood pressure (reduced stretch) or macula densa cells in the DCT sensing a decrease in NaCl delivery.

2. Juxtaglomerular cells secrete renin into the blood.

3. Renin converts angiotensionogen into angiotensin I → enzyme converts to angiotensin II.

4. Angiotensin II causes blood vessels to constrict, which immediately increases BP.

5. Angiotensin II also triggers release of aldosterone from adrenal cortex which increases the activity of Na+/K+ pumps in the DCT/CD to reabsorb Na+ from urine back into the blood. Water follows and so increases blood volume.

Describe the intrinsic pathway of the RAAS system (tubuloglomerular feedback).

1. Macula densa cells in DCT act as chemoreceptors that sense the concentration of salt in the filtrate.

2. If NaCl levels are too high, the macula dense cells use paracrine secretion (signaling molec that only act on nearby cells) of adenosine to cause immediate vasoconstriction of the afferent arteriole.

3. The local constriction reduces blood flow into the glomerulus.

4. Lowers hydrostatic pressure.

5. Brings glomrular filtration rate (GFR) back to normal levels.

*purpose is to protect individual nephron from being overwhelmed by high blood BP/BV. the scope of this is inside the JGA of that specific nephron

describe function and role in homeostasis of urinary system: osmolarity and electrolyte homeostasis

-osmolarity: how concentrated body fluids are
-kidneys selectively reabsorb/secrete ions like Na+, K+, and Cl- to keep electrolyte levels stable

describe function and role in homeostasis of urinary system: acid-base homeostasis

-regulate CO2/HCO3- buffer system
-if too acidic: type A cells secrete H+ ions into urine and reabsorb bicarbonate (HCO3-)
-if too basic: type B cells secrete bicarbonate into urine and reabsorb H+ ions

describe function and role in homeostasis of urinary system: production and secretion of calcitriol, renin, erythropoietin

-erythropoetin (EPO) stimulates bone marrow to produce RBCs when oxygen levels low
-renin released when BP drops to trigger RAAS system
-calcitriol

describe function and role in homeostasis of urinary system: calcium homeostasis

-calcitriol production helps kidneys absorb more calcium during hypocalcemia
-reabsorb calcium from filtrate/excrete in urine based on signals from parathyroid hormone

describe function and role in homeostasis of urinary system: excretion of waste products and obligatory urine production

-kidneys filter and excrete urea (from protein breakdown), uric acid (from nucleic acids), and creatinine (from muscle metabolism)
-obligatory urine of 500mL per day to flush out toxic wastes that would otherwise build up in blood

Compare and contrast blood plasma to filtrate and explain what structures allow for the differences and similarities.

Plasma still has large proteins and blood cells. Small solutes, water, and electrolytes are present in both.
-governed by three-layered glomerular filtration membrane in renal corpuscle: fenestrated capillary endothelium (fenestrations allow everything except blood cells to pass through), basement membrane (physical, negatively charged barrier against large proteins), podocytes and filtration slits are the final sieve.

role of DCT

adjust electrolyte balance and blood pressure based on hormonal signals
-aldosterone reabsorbs Na+ and water follows
-PTH reabsorbs Ca2+

Cortical vs juxtamedullary nephrons

-abundance: cortical make up about 85% of all nephrons in kidney, juxtameduallary are the other 15%
-primary role: cortical handles bulk of blood cleaning/reabsorption, juxtameduallary makes it possible to produce highly concentrated urine by saving water
-location: cortical in cortex, juxtamedullary in boundary of the cortex
-loop of Henle: cortical have very short loops that barely dip into outer medulla, juxtamedullary have very long loops that dive deeper into the inner medulla
-vascular supply: cortical surrounded by peritubular capillaries, juxtamedullary surrounded by the vasa recta

vasa recta

-specalized network of long, straight blood vessels that run parallel to the loops of Henle for juxtamedullary nephron
-preserves the saltiness (countercurrent exchanger). the goal is to provide oxygen to the kidney cells without “stealing” the salt the loop of Henle just put.
-As the blood vessel dives into the salty medulla, salt enters the blood and water leaves. By the time it reaches the bottom, the blood is very salty. As the vessel heads back towards the less salty cortex, the process reverses so salt leave and water re-enters to that the salt gradient is undisturbed.

Define mean arterial pressure (MAP) and glomerular filtration rate (GFR).

-MAP: the average pressure in arteries during a cardiac cycle - the “pushing” force that moves blood through body
-GFR: the total amount of fluid filtered by all your kidney’s glomeruli per minute

the problems with too high/low GFR

-too high: fluid moves so fast the kidney’s can’t grab back the good stuff (like glucose) before you pee it out. would also break capillaries of glomerulus.
-too low: blood is not being cleaned and waste products build up in blood because not being flushed out

How does the kidney keep GFR constant within the mean arterial pressure range of 80-180mmHg?

-myogenic mechanism: mechanoreceptors: when high blood pressure stretches wall of kidney’s afferent arteriole (input), stretch receptors are activated and the muscle contracts. This narrows the pipe and increases resistance to lower the pressure getting into the filter so that the afferent arteriole blood flow and hydrostatic pressure of glomerular capsular goes back to normal. This means the GFR also returns to normal.
-tubuloglomerular feedback: chemoreceptors of macula densa at DCT that are in contact with the filtrate sense increase in NaCl. This is because PCT can’t reabsorb all of the salt because it is flowing too fast so salt at DCT increases. The macula densa stimulates JG cells to secrete renin. This leads to vasoconstriction and then a normal GFR because it allows the PCT to reabsorb enough of salt as filtrate flows through slower now.

net filtration pressure (NFP)

the total pressure that forces fluid out of the blood and into the kidney tubules - ALWAYS favors filtration
-glomerular hydrostatic pressure: pushes fluid out of the blood and into capsule
-glomerular oncotic pressure: the pulling force by proteins that stay trapped in blood that pulls fluid back into the capillaries (anti-filtration)
-Bowman’s hydrostatic pressure: pushes back against the capillary (anti-filtration) - think people in crowded room pushing against new people
-Bowman’s oncotic pressure: pulling force of proteins inside the capsule that pull fluid out of the blood

Why is homeostasis of GFR and net filtration pressure so important?

-GFR must stay at goldilocks speed so important nutrients can be reabsorbed while waste is removed
-NFP is the physical force that keeps the engine running. Stable NFP means blood cleaning never stops. Too high would tear the glomerular capillaries and filtration membrane.

Describe the extrinsic mechanisms involve din GFR.

-neural control: SyNS: vasoconstriction of afferent and efferent arterioles to drop GFR and divert blood away from kidneys and towards critical organs in extreme stress
-hormonal control: RAAS: if low BP/BV, kidneys release renin to create angiotensin II that vasoconstricts and systemically increases BP

what do DCT and CD depend on for reabsorption of NaCl, K+, and H2O

ANP (atrial natriuretic peptide), ADH (antidiuretic hormone)

role of PCT in reabsorption and secretion

reclaims vital substances from filtrate
-100% recovery of glucose and amino acids through sodium-dependent symporters
-reabsorbs sodium actively and water follows through aquaporins
-secretion moves substances (ex. H+) from systemic blood → peritubular capillaries→ tubule to be secreted. think of secretion as the second pass to clean blood because after the blood leaves the glomerulus, it doesn’t just go back to the heart, it wraps around the PCT in the peritubular capillaries. PCT cells grab them directly from these capillaries and pump into the lumen of the renal tubule.

role of loop of Henle in reabsorption and secretion

allows kidney to concentrate urine (save water in collecting duct later on)

-descending limb allows water to be reabsorbed via osmosis as loop goes into salty medulla
-ascending limb: actively pumps out ions to create a “salt gradient” in the kidney tissue

role of DCT in reabsorption and secretion

does the “surgical” adjustments after most of reabsorption is done and adjusts electrolyte levels based on immediate body needs
-Atrial natriuretic peptide (ANP) is released when high BP. It tells DCT to stop pumping Na+ back into blood so water stays in the tubule too. Urine becomes dilute and high in volume so blood volume drops and BP drops. Think of as anti-ADH.
-ADH also affects but more so CD
-Aldosterone expressed if decreased BV → reabsorbs Na+ and therefore water

role of CD in reabsorption and secretion

-where final volume and concentration of urine are decided
-ADH triggers opening of aquaporins in principal cells so that salt gradient in the medulla sucks water out of the duct and into the blood so urine becomes highly concentrated and low in volume
-ANP expressed in high BV/BP → secretes Na+ and inhibits H2O+Na+ reabsorption
-Aldosterone expressed if decreased BV → reabsorbs Na+ and therefore water

why is the loop of Henle a countercurrent multiplier

The more salt the ascending limb pumps out, the saltier the medulla becomes. The saltier the medulla becomes, the more water is puled out of the descending limb. This cycle multiplies the saltiness of the medulla.

Origin and role: ADH (aka vasopressin)

-origin: synthesized in hypothalamus and released by posterior pituitary
-trigger: high blood osmolarity (salty) or low BV
-target: collecting ducts of neprhon
-role: triggers insertion of aquaporins into cell membranes so that the salty medulla can “pull” water out of filtrate back into blood
-result: small volume of concentrated urine, increased blood pressure/volume

Origin and role: aldosterone

-origin: adrenal cortex
-trigger: angiotension II or high levels of K+
-target: DCT and upper collecting duct
-role: increases number of Na+/K+ pumps to reabsorb sodium and secrete potassium. Water is reabsorbed.
-result: increased BV/BP, decreased K+ levels in blood

Origin and role: RAAS

-renin is secreted by JG cells of kidney when low BP/Na+

Origin and role: atrial natriuretic peptide

-origin: atria of the heart
-trigger: high BP
-target: afferent arterioles and adrenal cortex
-role: dilates afferent arteriole and inhibits release of renin/aldosterone
-result: decreased BV/BP, increased urine output

Identify respiratory vs metabolic problem

-respiratory (lungs): by breathing slower/faster: if PCO2 is moving in the opposite direction of the pH
-metabolic (kidneys): by keeping in blood/peeing out bicarbonate: if the bicarbonate is moving in the same direction as the pH

How to kidneys maintain proper blood pH?

-secretion: moving excess H+ from blood into filtrate to be excreted
-reabsorption: bringing HCO3- back into the blood to act as a buffer

Role of intercalated cels in the CD

primary regulators of acid-base balance in blood
-type A intercalated cells work during acidosis by promoting H+ secretion and HCO3- reabsorption as well as create brand-new bicarbonate molecules to replenish body’s alkaline reserve
-type B intercalated cells work during alkalosis to promote HCOe- secretion and H+ reabsorption

Causes of respiratory vs metabolic acidosis

-respiratory acidosis: hypoventilation (buildup of CO2 → buildup of acid in blood → low pH)
-metabolic acidosis: cellular metabolism produces too many “fixed” acids or the body loses too much bicarbonate

Compensation of respiratory vs metabolic acidosis

-respiratory acidosis: kidneys secrete more H+ into the urine to get rid of the acid and reabsorb more HCO3- into the blood to act as a buffer
-metabolic acidosis: hyperventilation to “blow off” excess CO2 to reduce overall acid load in the blood + intercalated A cells decreases H+ reabsorption and increases HCO3- reabsorption to increase synthesis of new bicarbonate

Causes of respiratory vs metabolic alkalosis

-respiratory alkalosis: hyperventilation → decreased CO2 in blood → increase in blood pH
-metabolic alkalosis: loss of acid/accumulation of too much base by kidneys: ex. severe vomiting, consumption of alkaline products → too much HCO3- relative to H+ → increase in blood pH

Compensation of respiratory vs metabolic alkalosis

-respiratory: HCO3- secretion to be excreted inn urine, H+ reabsorption
-metabolic: hypoventilation to trap more CO2 in blood → forms acid when reacts with water

The three different acid-base buffering systems

1. chemical buffers

2. respiratory compensation

3. renal compensation

Explain chemical buffer system for acid-balance regulation

three major chemical buffer systems: bicarbonate, phosphate, protein buffer system
-in erythrocytes, hemoglobin binds to H+ ions generated during conversion of CO2 to bicarbonate to prevent internal environment from becoming too acidic

Explain respiratory compensation system for acid-balance regulation

CO2 reacts with water to form carbonic acid within MINUTES
-if pH drops, hyperventilation “blows off” CO2 to reduce acid load
-if pH rises, hypoventilation retains CO2 so more acid is added to blood

Explain renal compensation system for acid-balance regulation

most powerful but SLOWEST

-if pH low, secrete excess H+ into urine + reabsorb HCO3- + intercalacted cells in CD synthesize new bicarbonate

ovaries

female gonads that produce female gametes (ova) and secrete estrogen/progesterone

duct system: fallopian (uterine) tubes and vagina

-vagina: located between bladder and rectum, extends from cervix to body’s exterior. acts as birth canal + receives penis.
-fallopian tubes: site of fertilization because it receives the ovulated oocyte. attached to uterus. fimbriae are finger-like projections that surround the ovary and draw oocyte into the tube. mucosa consists of ciliated epithelium and smooth muscle to move the oocyte toward the uterus.

uterus: function and structure

-function: receives, retains, and nourishes a fertilized egg
-three regions: fundus (rounded dome above fallopian tube entrance), body, cervix (protrudes into vagina)
-uterine wall has three layers: endometrium (mucosal lining where implantation occurs), myometrium (middle layer that’s a thick layer of smooth muscle responsible for labor contractions), perimetrium (outermost serous layer)

vulva: structure and function

-function: accessory glands to provide lubrication during sexual excitement
-structure: contains bartholin’s glands (equivalent of bulbourethral glands in males), parayrethral glands (female equivalent of prostate), clitoris (area of abundant nerves for sexual sensation - contains erectile tissue), labia majora and minora

cells that promote the development of ova

theca cells for the external layer, granulosa cells for the internal layer

theca cells of the ovaries

external layer
Promote development of ova by surrounding the follicle and expressing luteinizing hormone receptors. When stimulated by LH, theca cells produce androgens (male sex hormones)

granulosa cells of the follicles

internal layer
-directly surround the oocyte and express Follicle Stimulating Hormone receptors
-when stimulated by FSH, hyperplasia and hypertrophy of granulosa cells to protect and sustain oocyte. They also produce the aromatase enzyme, which converts the androgens from theca cells into estrogens.

development of follicles (primary, secondary, tertiary)

follicle development = process of immature egg (oocyte) maturing within a protective housing

-primordial follicle: the most immature stage (birth) - primary oocyte surrounded by single layer of follicle cells
-primary follicle: starting at puberty, follicles begin to grow → cuboidal
-secondary follicle: granulosa cells hyperplasia into multiple layers + theca cells begin to form around outside
-tertiary follicle: mature stage: antrum (fluid-filled cavity) forms → eventually ruptures during ovulation to release secondary oocyte

development + role of corpus luteum

-role: acts as hormone factory to secrete progesterone to 1) maintain endometrium for potential implantation and 2) provide negative feedback to the hypothalamus to lower FSH/LH and prevent another ovulation
-development: after ovulation, the ruptured follicle collapses. the remaining granulosa and theca cells differentiate into lutein cells to form the corpus luteum. will degenerate into a scar if no pregnancy occurs → start of menstruation. if pregnancy → keeps producing hormones until placenta takes over

early follicular phase of the hypothalamic-pituitary-gonadal axis (cyclical development of ova)

previous corpus luteum has degenerated so low estrogen and progesterone → hypothalamus releases GnRH (gonadotropin-releasing hormone) → GnRH stimulates anterior pituitary to secrete follicle-stimulating hormone (FSH) and luteinizing hormone (LH)

leading up to ovulation phase of hypothalamic-pituitary-gonadal axis (cyclical development of ova)

dominant follicle matures → estrogen levels rise → massive release of luteinizing hormone from pituitary → triggers mature tertiary follicle to rupture and release secondary oocyte

luteal phase of hypothalamic-pituitary-gonadal axis (cyclical development of ova)

ovulation ends → remains of follicle transforms into corpus luteum → corpus luteum secretes high levels of progesterone and some estrogen → negative feedback on hypothalamus and pituitary to inhibit release of GnRH/FSH/LH to prevent development of more follicles

What happens in utero (before birth)? (Ovarian cycle)

-female fetus develops lifetime supply of eggs
-oogonia (stem cells) undergo rapid mitosis to create immature oocytes
-primary oocytes: most of those cells die by time of birth and leave the primary oocytes

What happens in infancy and childhood? (Ovarian cycle)

-ovaries functionally inactive
-oocytes continue to die off

What happens in puberty to menopause? (Ovarian cycle)

-HPG (hypothalamus-pituitary-gonadal) activates
-each month, a small group of follicles is recruited to resume development but only one reaches full maturity

What happens during follicle maturation? (Ovarian cycle)

-in response to FSH, follicles grow primary→secondary→tertiary
-dominant follicle emerges and starts producing lots of estrogen
-LH surge triggers the primary oocyte to finally complete Meiosis I
-secondary oocyte is produced and immediately begins Meiosis II but is arrested again in metaphase II

What happens durinv ovulation? (Ovarian cycle)

tertiary follicle ruptures and releases arrested secondary oocyte into fallopian tube

What happens in the luteal phase? (Ovarian cycle)

-empty follicle transforms into corpus luteum, which secretes progesterone to support a potential pregnancy
-if no fertilization, corpus luteum degenerates and secondary oocyte dies
-if fertilization, sperm penetrating oocyte triggers completion of meiosis II, creating mature ovum and a second polar body

What happens in menopause? (Ovarian cycle)

-remaining supply of follicles is gone/no longer responsive
-ovaries stop functioning as endocrine organs

Uterine vs ovarian cycle

-ovarian: maturing and releasing an egg
-uterine: preparing uterus for implantation

What happens in the menstrual phrase? (uterine cycle)

beginning of cycle and happens if no fertilization happened
-hormonal trigger: estrogen and progesterone levels fall to lowest points because corpus luteum from previous cycle degenerated
-physical change: functional layer of endometrium sloughs off
-result: bleeding (menses)

What happens in the proliferative phrase? (uterine cycle)

uterus prepares for arrival of fertilized egg
-hormonal trigger: developing follicles in ovaries begin to secrete increasing amounts of estrogen
-physical changes: regeneration of functional layer of endometrium so the lining thickens, becomes more vascularized, and develops glands
-culminates in massive estrogen spike → LH surge from pituitary → ovulation

What happens in the secretory phrase? (uterine cycle)

synchronized with ovarian luteal phase and maintains environment for implantation
-hormonal trigger: post-ovulation corpus luteum secretes high levels of progesterone
-physical changes: progesterone causes endometrium to increase blood supply, secrete nutrients, reach max thickness
-if fertilization happens, embryo produces human chorionic gonadotropin (hCG) to maintain corpus luteum. if not, degenerates and triggers next menstrual phase.

Describe the mechanism of action of the “pill”. 

inhibits ovulation (release of egg from ovary)
-synthetic hormones mimic state of constant, low-level hormone elevation that creates negative feedback at the hypothalamus and pituitary gland → no LH surge so ovulation is never trigger
-causes mucus at cervix to become thick and sticky
-endometrial lining remains thin because there is no natural build-up of secretory phase

testes: function, location, internal structure

-function: primary reproductive organs that produce both gametes (sperm) and sex hormones
-location: paired organs housed within scrotum (sac of skin hanging outside abdominopelvic cavity)
-structure: each testis surrounded by two layers (outer tunica vaginalis and inner fibrous tunica albuginiea). extensions of tunica albuginea divide testis into lobules. seminiferous tubules are “sperm-forming” factories where spermatogenesis happens

spermatogonia vs sertoli cells vs leydig cells

-spermatogonia: stem cells that mitosis to become future sperm
-sertoli cells: nourish developing sperm and form blood-testis protective barrier around them
-leydig: produce testosterone when stimulated by LH

seminal vesicles: function, locatioon

-function: 60% of semen
-locaton: base of bladder

prostate: function, location

-location: encircles upper part of urethra + is 25% of semen
-function: secretes milky fluid that helps activate sperm

bulbourethral glands: function, location

-location: pea-sized glands inferior to prostate
-function: produces pre-ejaculate to cleanse urethra of acidic urine and serve as lube during intercours

pathway sperm takes to leave the body

testes (production in seminiferous tubes)→ epididymis (maturation + storage) → ductus (vas) deferences (transport via peristalsis) → ejaculatory duct (vas deferens and seminal vesicle secretions meet) → urethra