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316 terms

Lecture Exam 4

Conducting Pathway
Tubes that direct air down to the respiratory section where gas exchange actual happens
Nasal cavity -> terminal bronchioles
Tracheobronchiole tree
Ability to produce noise.
Force air through voice box, vibrating vocal ligaments which can change the frequency and pitch of the air passing through.
Sinuses resonate the sound.
Olfactory Epithelium
Roof of nasal cavity has this which has special receptors for sensing "scent".
On superior surface of superior concha
Bipolar neurons found here
Upper respiratory Track
-Nasal cavity
-Paranasal sinuses
-Pharynx (end)
Lower respiratory track
-Larynx (thyroid cartilage)
Respiratory bronchioles
Conducts air to the alveoli but also does gas exchange itself.
Inferior border of thoracic cavity
aka alveoli
Visceral pleural membrane takes on their shape
Conformation increases surface area to the size of a tennis court
Have elastic fibers around them which allow for inflation upon iinspiration
Have NO smooth muscle
Respiratory Track
Warms, filters and humidifies the air
Hair fibers in the nasal cavity which filter the air coming through it
Edey Currents
Currents formed in the nasal cavity increasing the time it stays in the nasal cavity, flowing around.
Increases filtration
Mucous membrane is highly vascularized, heat can easily be conducted into the air from them, warming it.
Mucous and serous glands also moisturize the air.
Connection between nasal cavity and pharynx
Area where stuffy nose can occur
Respiratory Epithelium
Pseudostratified ciliated columnar epithelium
Secretes a lot of mucous and serous fluid which is beat down toward the trachea
Cilia in the trachea beat back up toward the epiglottis
Elastic Cartilage
When you swallow, this gets pushed down, closing the epiglottis allowing the things to go down the esophagus
C-shaped cartilage rings
Surround the trachea
Tongue-like structure
Made up of elastic cartilage
Vocal Ligaments
Dense, regular collagenous tissue
Inferior to vestibular ligaments
There are two sets - 2 inferiors and 2 superiors
Air travels between all 4 producing sound
Vestibular Ligaments
Produce no sound
Found superior to true vocal ligaments
Vocal organ
Vocal folds covered by mucosa and the rima glottidis - opening between the folds
Rima glottidis
The space between the two true vocal folds
Part of the glottis
Ridge inside of the trachea where the trachea bifurcates into the right and left bronchi
Secondary Bronchi
Each feeds a lobe of the lung, meaning the right lung has 3 and the left lung has 2.
Primary Bronchi
Each feeds a lung
Left is longer than right
Tertiary Bronchi
Feeds a bronchopulmonary segment
Last segment to have cartilage
Bronchopulmonary Segment
Fed by tertiary bronchi
Everything else beneath tertiary bronchi
Extrapulmonary Bronchi
Primary Bronchi
On the outside
Intrapulmonary Bronchi
Second and Tertiary Bronchi
Within lung tissue
Root of the lung
aka Hilum
Region where vessels are coming and going from the lung (primary bronchus in, pulmonary artery in, pulmonary vein out)
Pleural Cavity
Space surrounding the lungs
Parietal pleural membrane
Covers the intercostal muscle
Part of the superior diaphragm and thoracic wall, allowing for expansion of the lungs upon muscle contraction
Where bronchoconstriction/dilation occurs
First section that has no cartilage
Contracting of the muscles to allow air into the lungs
To stop, and expire, just stop this, elastic recoil of alveoli will push air out
Creates vacuum
Neck muscles, scalenes etc help
Elastic fibers of alveoli are damaged.
Expiration doesn't happen easily even though inspiration still happens normally
Also damages walls of alveoli making lungs very easy to inflate, just hard to get stagnant air out.
Internal intercostal, abdominal muscle contractions help
Type 1 Neumocytes
Makes up the wall of the alveolus
Type 2 Neumocytes
aka Ceptil cells
Secrete pulmonary serfactant, which has a phospolipid component. When this mixes with water in alveoli, it decreases the surface tension.
Allow for your lungs to not collapse by decreasing surface tension of the water in the alveoli
Produced by the Type II alveolar cells
Contains phospholipids and apoproteins
Respiratory Distress Syndrome
Alveoli collapse in premature babies because they don't create pulmonary surfactant yet.
Dust Cells
Elevated in someone with a lung infection
Pressure Gradient
In order to allow air into the lungs, pressure within the lungs has to be lower than the air, only by a few mmHg
Contract intercostal muscles and contract diaphragm to be flat to expand the thoracic cavity because the pleural membrane attaches the lungs to these structures
Internal Respiration
Gas exchange between capillaries and tissues
External Respiration
Conduction of air
Gas exchange at respiratory membrane
Transport of gas in red blood cells of circulatory system
Interpulmonary Pressure
Pressure inside the alveoli
Has to be different than atmospheric to let air in
Negative in inspiration, positive in exhalation (+/-1)
Intrapleural Pressure
Always negative
During inspiration, it's more negative
Slightly below atmospheric pressure
~ -6 during inspiration, ~ -3 for exhalation
Expiatory Reserve Volume (ERV)
Pushes all of the air you possibly can out of the lungs past normal breathing
Inspiratory Reserve Volume (IRV)
Inspire all of the air you possibly can into your lungs past the normal
Vital Capacity
ERV + IRV showing the range of the lung
Obstructive Disease
Causes difficulty with expiration
Ex: emphysema
Restrictive Disease
Causes difficulty with inspiration
Ex: asthma
Diffuses into blood cells from plasma
23% binds to hemoglobin
70% made to carbonate by carbonic anhydrase which allows bicarbonate ion out and brings a Cl- into blood cell. In the lungs, it does this backward.
Bicarbonate ion goes into lung, Cl- leaves. Bicarbonate then lets this out into the plasma and expires it.
Accessory Organs of GI tract
Salivary glands
Compacted, mucous-saturated mound of food from the mouth travelling toward the throat
Stretches the esophagus, causing the esophagus to respond with peristalsis
Responsible for mechanical and chemical digestion
Food can be stored here
Not much absorption here, just aspirin and alcohol
Makes chyme
Liquid product of food after stomach digestion
Small Intestine
Some mechanical digestion
Area of most nutrient absorption
Secretion and absorption happen all the way down
Large Intestines
Absorbs water and secretes mucous
Not much other absorption or secretion
Sense of taste
Conscious swallowing
First layer of the wall of the GI tract
Epithelial lining and loose connective tissue (lamina propria) just beneath
Simple columnar with goblet cells
Microvilli found here
Lamina Propria
A layer of loose connective tissue just deep to the basement membrane of GI tract
Where infection is fought off in the GI tract
Most GLANDS found here (exocrine and endocrine)
Dense connective tissue
Large blood vessels, lymphatic vessels and nerve fibers
Has some glands
Muscularis (Externa)
Has an inner circular layer and inner longitudinal
Nerve fibers between the layers and in submucosa
Inner circular layer
Runs the circumference of the GI tract
Constricts the tract when it contracts
Outer longitudinal layer
Runs the length of the GI tract
Flattens/widens the GI tract when in contracts
Oblique layer
Allows the stomach to do additional motions past those of the rest of the GI tract
Loose connective tissue with some blood vessels, nerve fibers and a simple squamous epithelium attached to it (where peritoneal cavity is)
Ex: Small and large intestines, stomach etc
Loose connective tissue with some blood vessels, nerve fibers etc
Ex: Esophagus, end of rectum, anus
Myenteric Plexus
Between inner circular and outer longitudinal muscles
Controls muscle function of GI tract
aka Auerbach's
Submucosal Plexus
Controls glandular secretions of GI tract
aka Meissner's
Two layers of visceral peritoneum fused together
Blood vessels, nerve fibers and some loose CT
Holds your guts in place
On mouth-side of the bolus, the inner circular layer is contracted and the outer longitudinal is relaxed
On anus-side of the bolus, the inner circular layer is relaxed and the outer longitudinal is contracted
These forces together cause this movement
Submucosa mucous secretion also helps
Esophageal mucous glands
Exception to the lamina propria having secretory glands
Found in the submucosa
Rhythmic Segmentation
Contract inner circular muscles on either side of the food particle, increasing the amount of time it's in the tract allowing for more efficient break down
Happens in intestines
Tonic Contraction
Contraction of the intestinal muscles for a prolonged period of time to store the bolus
Happens at sphincters and in proximal stomach
Long Reflex
Stretching or chemicals in the GI tract sends a signal to the CNS where it is told that there is food
Short Reflex
Chemicals from food/food digestion bind to receptors or stretching in the epthelium of the GI tract stimulates the submucosal and myenteric plexuses
Endocrine Hormones of GI tract
Hormones are secreted outside of the GI tract into the circulation but effect the organs of the GI tract.
Activates the GI tract
Rest and digest
Deactivates the GI tract
Fight or flight
Activating your gag relex or pooping will cause a massive parasympathetic response, increasing acetyl choline, and getting the heart out of this abnormal heart rate
Made of all skeletal muscle running in every direction to manipulate food in the oral cavity
Pushes food against hard palate and increase its surface area (Mechanical digestion)
Secretes mucous and lingual lipase
Senses food (taste)
Lingual lipase
Secreted from the tongue
Optimum pH of 5, activating it in the stomach to break up triglycerides (mouth pH ~7.2)
Mucins, buffers, water, enzymes (lysozymes etc), antibodies, lingual lipase in mouth
Degrades peptidoglycan in bacterial cell walls (Gram +)
Sublingual gland
Secretes mostly mucous
Parotid Gland
Secretes mostly protein (serous fluid)
Submandibular Gland
Secretes both serous fluid and mucous
Salivary Amylase
Breaks carbs into smaller fragments, but not into monosaccharides usually
Disaccharides and dextrins are made in general
Pharyngeal Constrictor muscles
Pushes the bolus toward the esophagus
Upper part is skeletal, lower is smooth
Uses peristalsis to transport bolus to stomach
Food is being digested as it's moving down, but this is not responsible for this
Upper Esophageal Sphincter
Skeletal muscle at the top of the esophagus
Keeps air from getting into the esophagus
Very weak
Lower Esophageal Sphincter
Esophagus opening up into the stomach
Atrophy of this can cause GERD
If pressure in the GI tract is greater than the pressure exerted by this, it can also cause GERD
Feels the same pressure as the peritoneal cavity
aka cardiac sphincter
Gastroesophageal reflux disease
Chyme is refluxing back into the esophagus
Can be due to:
Increased pressure in the gastric organs
Atrophied muscles in the cardiac sphincter
Cells that secrete acid are over-active in stomach
Gastric Intrinsic Factor (GIF)
Binds vitamin B12 and takes it to the small intestine
Pernicious anemia happens in its absence
Cardia of Stomach
Abundance of mucous glands
First section of stomach
Fundus of Stomach
Abundance of gastric glands (acids/enzymes)
Hump region, food storage
Body of Stomach
Abundance of gastric glands (acids/enzymes)
aka corpus
Pylorus of Stomach
Glands secrete mucous and gastrin (endocrine hormones) but not into the stomach
Gastric Pits
Invaginations of epithelium
Merge with gastric glands in the lamina propria
Endocrine hormone secreted from the pylorus of the stomach lining into the bloodstream
Up-regulates the stomach
Stimulates the secretion of fluid by gastric glands in the stomach
Stimulates both myenteric and submucosal plexus
3 layers of stomach
Inner oblique
Middle circular
Outer longitudinal
Allows the stomach to increase in size
Only visible when stomach is empty
Folds of mucosa and submucosa
Gastric Glands
Test tube-like projections of the epithelium in the stomach
Stops around the muscularis mucosae
Not located in the submucosa
Chief cells and parietal cells are found here
Primarily in fundus and body
Pump proton in and Cl- follows, making HCl
Gastroendocrine cells found at the base
Chief Cells
Found in the gastric glands of the stomach
Secrete enzymes, including pepsinogen and gastric lipase
Parietal Cells
Found in the gastric glands of the stomach
Secrete acid/produce proton
Pumps this proton in and Cl- follows, making HCl
ATPase pumps proton into stomach. Antacids work to stop this pump
Bicarbonate ion is shuttled out of the basal side into the blood, lowering its pH
Gastroendocrine Cells
Cells in the stomach which secrete gastrin, ghrelin and somatostatin (inhibitory in the stomach) into the lamina propria
Includes G cells, Gr cells, D Cells etc
Hormone manufactured primarily by the stomach that stimulates appetite and the secretion of growth hormone by the pituitary gland.
Makes you hungry
Secreted by Gr cells
Gastric-Mucosal Barrier
Insoluble mucous layer, different from epithelium mucous
Secreted from neck cells
Stuck on top of epithelium, doesn't mix with chyme
Bicarbonate ion stuck within it, pH ~7
H. pylori lives here
Phospholipids also sit on top to keep acid away
Kills microbes
Protein denaturation (breaks hydrogen bonds to increase surface area of peptide exposed to enzymes)
Secreted from chief cells of gastric glands
Autocleaves itself into pepsin when activated by acid (HCl)
Begins protein digestion in the stomach
An inactive precursor of an enzyme, activated by various methods (acid hydrolysis, cleavage by another enzyme, etc.)
Active form of pepsinogen
Converts more pepsinogen
Active protease/prteolytic enzyme
Too much acid or not enough mucous in stomach
Acid reaches lining of stomach
H. pylori responsible for ~80%
H. pylori
Associated with antral gastritis, duodenal ulcers, gastric ulcers when overgrown
When it metabolizes, it makes phospholipases and ureases, breaking down phospholipids in gastric-mucosal barrier and making NH4+ which binds to HCO3- lessening the amount for HCl neutralization.
Alkaline Tide
Blood becomes slightly basic every time we eat food because we run the bicarbonate buffer system in our stomach to produce acid then release the bicarbonate into our blood making it basic
Requires carbonic anhydrase
Excreted by H.pylori in stomach
Breaks down phospholipids in gastric-mucosal barrier allowing acid to get closer to stomach lining
Excreted by H. pylori in stomach
Breaks down urea forming NH4+ which competes with proton to bind to bicarbonate in the stomach lining, breaking down the gastric-mucosal barrier
Pyloric glands
Has gastroendocrine cells which secrete digestive enzymes
Cephalic Phase
Brain control of what's happening in the stomach
40% acid secretion
Prepares the stomach for food by sensory information
Short duration
Mucous, enzyme and acid production
Increased gastrin cells
Gastric Phase
Stomach controls of what's happening in the stomach
50% acid secretion
Homogenize and acidify chyme
Initiate protein digestion with pepsin (pepsinogen is up)
Long, 3-4 hours
Mechanoreceptors + chemoreceptors activated by food
Gastrin released by G cells to CNS
Vagus Nerve
Parasympathetically controls the myenteric and submucosal plexuses (churning and acid/enzyme release)
Cephalic control of stomach
Secreted by D cells in fasted state
Inhibits the G cells to decrease stomach activity
When food comes in, pH goes up (H+ level goes down) stopping D-cell stimulation and stopping this from being released allowing the G cells to release gastrin
Hypothalamus - Inhibits release of growth hormone in anterior pituitary
Pancreas - Islets of Langerhans
G cells
Secrete gastrin
Stimulates gastric secretions and activity
D cells
Secrete somatostatin
Inhibits gastrin release
Fasted State
Between meals
pH 5-6
Increased somatostatin release by D cells
G cells not active
Fed State
During meals
pH ~2
Decreased somatostatin release by D Cells
G cells secreting gastrin
Intestinal Phase
Intestinal control of what's happening in the stomach
10% acid secretion
Controls the entry of chyme into the duodenum
Long, many hours
Distention of duodenum sends negative signals to CNS
Releases inhibitory endocrine hormones (CCK, GIP, Secretin)
Release of gastrin to complete digestion, inhibits stomach
Cholecystokinin (CCK)
Hormone released from small intestine in response to presence of fats, causes contraction of gall bladder and release of bile to small intestine (to aid digestion of fats)
Decreases motility of stomach
Stimulates EXOcrine cells in the pancreas to secrete digestive enzymes
Proton stimulates its release from I Cells
Released by the duodenal endocrine cells when the pH in the duodenum falls as acidic chyme enters
Increases the secretion of bile and buffers (bicarbonate) by the liver and pancreas to decrease acidity
Any nutrient and protons will stimulate it to be released from S Cells
Gastric Inhibitory Peptide (GIP)
aka Glucose Insulinotropic Hormone
Secreted by endocrine cells in duodenal mucosa
Inhibits gastric emptying
Inhibits gastric secretion
Stimulates insulin secretion by endocrine beta cells in pancreas to prepare for the absorption of glucose
Glucose stimulates this to be released from K Cells
Gastric Lipase
pH optimum 2-5 (stomach conditions)
Made by chief cells
Minimal breakdown of fat
Secreted by the pancreas
Emulsifies fat in the stomach, allowing enzymes to access it
Salivary Amylase
Part of the small intestine that goes out of the peritoneal cavity
Has adventitia, not serosa
First part of the large intestine
Folds of lamina propria and epithelium (mucosa)
Cells making up the simple squamous epithelium also have microvilli
Permanent folds to increase the surface area of the small intestine.
Has villi on top of it
Surface Area Increase
Crypts of Lieberkuhn
aka Enteric/Intestinal glands
Located between villi
Tube-like structure
Only contain endocrine-secreting cells (no enzymes, not a lot of mucous) which release into general circulation
Enteroendocrine cells found here: CCK, GIP, secretin, GLP-1
Stimulates an afferent nerve of the enteric nervous system upon reception of nutrients which comes back to stimulate the release of CCK, GIP etc from crypts of lieberkuhn
Glucose in the small intestine stimulates this to be released from L Cells in small intestines
Glucagon-like peptide
GLP-1 has a longer half-life than glucagon but it's not effective as a diabetes therapy because it gets digested quickly because it's short
Stimulates beta cells to release insulin
I Cells
Make CCK
K Cells
Make GIP
S Cells
Make Secretin
L Cells
Make GLP-1
Incretin effect
The response of insulin is stronger and faster if glucose is ingested rather than injected due to the effect of GLP-1 and GIP
In saliva of gila monsters
GLP-1 analog, causing insulin to be released in the prey
It has a longer half-life than human GLP-1
Shown to stimulate a generation of new insulin-secreting cells in the pancreas
Decreases output of glucose from the liver
(Impairs gluconeogenesis)
Treatment for diabetes
Lymphatic Vessels
Begin at the periphery of the body, ex: in the villi of the small intestine
Merge to common ducts that dump into subclavian veins
Drains excess fluid into circulation
Highly specialized lymphatic capillaries
Found in the villi of intestinal mucosa
Absorb digested FAT (especially large, complex ones) and fat-soluble end products of digestion such as fatty acids, vitamins a, d, e, k and deliver it to the blood
Duodenal papilla
Where digestive enzymes and bicarbonate from the pancreas and bile are dumped into the small intestine
Pancreatic duct and common bile duct both open here
Lipases, proteases, etc all come from pancreas to here
Islets of Langerhans
Endocrine portion of pancreas
Proteases of Pancreas
Procarboxypeptidase (a and b)
All are zymogens, active in small intestine
Cut after different amino acids
Becomes trypsin
Becomes chymotrypsin
Procarboxypeptidase (a and b)
Becomes carboxypeptidase a and b
Enzymes of Pancreas
Pancreatic amylase (same as salivary amylase)
Pancreatic lipase
Breaks down RNA
Brush Border
Enzymes in the membrane of the small intestine
Ex: enterokinase, peptidases, dipeptidases, tripeptidases
Enzyme of the brush border that converts trypsinogen into trypsin
Activates chymotrypsinogen and procarboxypeptidase a and b and trypsinogen into their active counterparts
Cilia draw bile here and it removes water from the bile
CCK comes and binds to muscle here to push bile into the duodenum
The cells of this and the biliary system release bicarbonate when secretin tells it to
If removed, doesn't cause much problem, can take lipase pill or reduce fat ingestion
Bruner's gland
Glands in the submucosa of the gallbladder that secrete bicarbonate to neutralize the chyme in the duodenum
Pouch-like structures of the large intestine
Periods of tonic contractions allowing for segmentation, storage of feces and movement of feces
Also creates potentially weak areas
Muscularis Externa of Colon
Longitudinal muscle only seen in three areas due to structure of the haustra
Small, pouch-like herniations through the muscular wall of a tubular organ such as the colon.
Mucosa forms an outpouching, where feces can get trapped and the bacteria produce gasses etc which cause them to burst into the sterile peritoneum
Disease called diverticulitis which can lead to peritonitis
Secreted from the chief cells of the stomach but only as an infant
Coagulates milk protein making it travel more slowly through the digestive system for more efficient digestion
Renal Hilum
Includes 3 Vessels
Renal Artery in
Renal Vein out
Ureter out
Kidney Functions
Blood Filtration
Blood volume/pressure regulation
Removal of organic wastes (urea, uric acid, creatinin)
pH balance of plasma (absorption and secretion of bicarbonate and H+)
Byproduct of protein digestion (converted amino group)
Uric Acid
Byproduct of nucleic acid metabolism
Byproduct of creatin metabolism
EPO (Erythropoietin)
JG Cells of kidney spit this out if oxygen tension is too low in the blood
This then stimulates the creation of more blood cells which increases the ability to bind oxygen and therefore increases the oxygen tension of blood
Filtering unit of kidney
~1 million per kidney
Merge into the ureter
Dump everything that is small enough to dissolve into our plasma into here
Selectively reabsorbs things after dumping everything, allowing only wastes to ureter
Transport Maximum
You can only move so much glucose back into your bloodstream because there are only so many receptors so if too much is eaten, you can get spill-over
Active Vitamin D
Released by the kidneys
Regulates calcium levels
Stimulates osteoclast activity
Stimulates osteoblast activity to a lesser degree
Reduces calcium loss in the urine
Promotes calcium absorption in the intestine (by stimulating calcitriol production)
Produced by the C-cells of the thyroid gland
Decreases serum calcium levels
Stimulates osteoblasts
Reduces calcium reabsorption
Decreases calcium absorption
Retroperitoneal organ responsible for filtration, pH regulation, blood volume regulation etc
Has a lot of fat supporting it
Retroperitoneal Organs
Inferior Vena Cava
Renal Capsule
Dense, irregular collagenous tissue covering the renal cortex
Renal Medulla
Made up of renal pyramids, ~6-7 per kidney
Loops of Henle (simple squamous) and collecting ducts (cuboidal cells) found here
Cortical Columns
Cortical extensions into the renal medulla between the renal pyramids
Renal pelvis
Where the major calyx empties into the ureter
Contains pacemaker cells which stimulate smooth muscle of the ureter to pass urine down
Renal Cortex
Contains connective tissue, vessels and nephrons (bowman's capsules, proximal convoluted tubules and distal convoluted tubules)
Proximal Convoluted Tubule (PCT)
Contains microvilli, does absorption
Hydrostatic pressure sends plasma into here
Reabsorbs water (90%) and solutes (~100%)
Regulates bicarbonate levels
Capillary network within the bowman capsule
You filter blood into here
Distal Convoluted Tubule (DCT)
Does not contain microvilli, doesn't absorb
Things that we don't want but still have after filtration end up here for excretion (drugs, toxins)
Transport proteins, NKCC2s, are found here in the macula densa. It is a Na, K, 2Cl symporter into the cell.
Na/Cl symporters also found here, inhibited by thiazides
Hormone-regulated re-absorption of water happens here
Collecting duct
Opens into the minor calyx through the renal papilla
Many collecting tubules open into here
Regulates bicarbonate and proton levels along with PCT
ADH stimulates aquaporins here to lessen water loss
Renal Corpuscle
Bowman's capsule and glomerulus
Where primary filtration happens
Renal Bloodflow
Renal Artery
Segmental Artery
Interlobar Artery
Arcuate Artery
Interlobar Artery
Afferent Arteriole
Efferent Arteriole
Peritubular capillaries or Vasa Recta
Interlobar Vein
Arcuate Vein
Interlobar Vein
Renal Vein
Fenestrated Capillaries
Have "windows" in plasma membranes of endothelial cells allowing for filtration and diffusion
Sinusoidal Capillaries
Liver, bone marrow
Big gaps between endothelial cells
Cortical Nephron
80% of nephrons
Located in cortex except for short loop of Henle in renal pyramid
Peritubular capillaries
Most responsible for filtering blood
Juxtamedullary Nephron
20% of nephrons
Long loop of Henle which transverses medulla
Key to ability to produce concentrated urine by regulating blood pressure, blood volume etc
Vasa Recta
Peritubular capillaries
Made by the efferent arteriole
Wraps around your PCT, DCT and loop of Henle
This allows for the re-absorption and excretion of things missed in the initial entrance of stuff
Glomerular Filtrate
Plasma that has been pushed through the fenestrated capillaries of the peritubular capillaries into Bowman's capsule
As this flows through the nephron, things can be filtered in or out by size
Peritubular Fluid
Interstitial fluid around the peritubular capillaries of the nephron
Taking something from the tubular fluid and putting it into the peritubular fluid
Take something from the peritubular fluid and putting it into the tubular fluid
Back up to filtration
Urinary Pole
Opening to the PCT from the Bowman's capsule
Vascular Pole
Where the afferent and efferent arterioles enter/exit the Bowman's capsule
Opening faces the DCT
Pedicels of these cells interdigitate to create a visceral layer on the glomerulus
Slit Diaphragm
Prevents large things from getting into the nephron
They are small slits between pedicels that regulate what can get in and out of the Bowman's capsule
Juxtaglomerular Apparatus
Cells of DCT and afferent arteriole and cells between them interacting
Cells communicate with one another to regulate blood pressure, blood volume and GFR
GFR (glomerular filtration rate)
How fast something is filtering through your nephron
If we dilate afferent arteriole or constrict the efferent arteriole, it goes up
If we constrict afferent arteriole or dilate efferent arteriole, it goes down
If too fast or too slow you can absorb too much or little
Kidney can sense this rate and adjust blood pressure
Stays constant over a wide range of blood pressures
125 mL/min
Juxtaglomerular Cells (JG Cells)
Very close to the glomerulus of the afferent arteriole, smooth muscle cells become modified
Secrete endocrine hormones, no longer contractile
Mechanoreceptor - Senses stretch on afferent arteriole Chemoreceptor - Senses the partial pressure of oxygen
Secretes renin in response to low blood pressure
Affected by norepinephrine
Macula Densa Cells
Cells of the distal convoluted tubule in close proximity to the JG cells of the afferent arteriole
Transport proteins, NKCC2s, are found here. It is a Na, K, 2Cl symporter.
Extra-glomerular Mesangial Cells
Triangular patch of cells between the macula densa and the JG Cells
Stimulated by adenosen or high Na to stimulate the afferent arterioles to contract
aka Lacis cells
Cells of the JG Apparatus
JG Cells
Macula Densa Cells
Extra-glomerular Mesangial Cells
Released when the afferent arteriole is understretched
Stimulates the conversion of angiotensiogen to angiotensin 1
ACE (angiotensin converting enzyme)
Converts angiotensin 1 to angiotensin 2 primarily in the lungs
Angiotensin 2
Stimulates vasoconstriction in the vascularture to increase blood pressure which stops the mechanical stimulation of the afferent arteriole, stopping renin release
Vitamin D is converted to this in the liver and gets converted to calcitriol in the kidney
1-alpha−hydroxylase enzyme
Converts calcidiol to calcitriol in the kidney
Transporter protein
Found in the macula densa
Na, K, 2Cl symporter into the cell
Cell changes in conformation when these come in
Creates a stepwise gradient
ADO (adenosine)
Signalling molecule
Binds to extra-glomerular mesangial cells and then they stimulate the smooth muscle cells of the afferent arteriole to contract, decreasing blood flow into the glomerulus
Tubulo-glomerular Feedback
If GFR is too fast (too much Na comes in from the NKCC2), it will stimulate adenosen to bind to extraglomerular mesangial cells to stimlate smooth muscle of afferent arteriole to contract and tell JG Cells to stop renin secretion, slowing the GFR
Glomerulus communicating with the nephron (DCT)
Decrease GFR
Constrict afferent arteriole
Dilate efferent arteriole
Less sodium through NKCC2
Less renin secretion by JG Cells
Increase GFR
Dilate afferent arteriole
Constrict efferent arteriole
More sodium through NKCC2
More renin secretion by JG Cells
True Portal System
Capillary bed feeds into vein that feeds into another capillary bed
Renal system doesn't count because an arteriole connects the peritubular capillaries to the glomerulus
Hydrostatic Pressure
Water pressure
Term often used to describe blood pressure.
Effective Filtration Pressure (EFP)
(Glomerular Hydrostatic Pressure + Capsular Osmotic Pressure) - (Glomerular Osmotic Pressure + Capsular Hydrostatic Pressure)
Starling Forces of the Kidney
Glomerular Hydrostatic Pressure
Capsular Osmotic Pressure
Glomerular Osmotic Pressure
Capsular Hydrostatic Pressure
Glomerular Hydrostatic Pressure
Favor filtration
Blood coming into the glomerulus
Capsular Osmotic Pressure
Favor filtration
Small, almost negligible (~0mmHg)
Have solutes in capsular space that draw fluid from the glomerulus into the space
Glomerular Osmotic Pressure
Favor reabsorption
Glomerulus has a lot of solutes and this causes fluid to come back into the glomerulus from the capsule
Capsular Hydrostatic Pressure
Favor reabsorption
Fluid coming into the capsule causes increase in pressure, making some fluid go back in
Causes and increase in blood volume due to re-absorption of water in the kidneys
Smaller volume of urine
Binds to V1 or V2 receptors
Upregulates aquaporins on collecting duct
Descending Limb
Permeable to water but not to solutes
Leads to ascending limb
Ascending Limb
Permeable to solutes but not to water (NKCC2s)
Empties into collecting duct
Loop diuretics
Diuretics that work at the Loop of Henle
Block the movement of salt into your medullary tissue (NKCC2s in the ascending limb of loop of Henle)
Inhibits urea track
Can regulate blood pressure by decreasing blood volume
Urea Track
Urea is sucked back into the tissue, goes into the descending limb, goes up the ascending limb and gets reabsorbed to be stored in the medullary tissue
This with the NKCC2 causes the medullary to be concentrated with urea and salts allowing osmosis to bring water into the kidney from the nephron
Angiotensin 2 Effects
Constriction of efferent arterioles
Increased thirst
Increased ADH production
Increased fluid consumption and retention
Increased Na retention
Increased vasoconstriction
Therefore, increased blood pressure and volume
Supraoptic nuclei
Angiotensin 2 binds here and causes release of ADH from the herring bodies of the posterior pituitary
blood pressure forces water and solutes across the wall of the glomerular capillaries and into the capsular space
Secondary Active Transport
Sodium gradient is used to drag glucose or amino acids into the cell
Happens in the small intestines to get glucose into the body and in the PCT of the kidney
So effective that none escapes into urine
Countercurrent Multiplication
Stepwise increase in gradient of solutes along the loop of Henle/down the medulla
Concentration highest at the hairpin of the loop
NKCC2 responsible for this
Vasa Recta
Capillaries surrounding juxtamedullary nephrons
Follows the structure of the loop of Henle to soak up the salt as it goes down
Prevents our blood from washing out our salt gradient in the medulla
Stimulates the production of Na/K pump and increases their activity, making more Na and Cl to come into the cell and the DCT
Yellow steroid hormone produced by the zona glomerulosa of the adrenal gland
Diuretic, less effective than loop diuretics because it is not as effective for blood volume control
Inhibits Na/Cl symporters in DCT
Inhibits the movement of salt in medullary tissue, osmosis is reduced and less fluid moves into the medullary
V1 Receptors
ADH binds here, causing vasoconstriction on vascular smooth muscle
V2 Receptors
ADH binds here, causing upregulation of aquaporins on the collecting ducts of the kidneys
Generates cAMP which activates protein kinase A and aqaporins traverse to the membrane
Retroperitoneal organ
Pear-shaped muscular organ located in the midline of the pelvis
3 regions: body, fundus and cervix
Uterine Tubes
Open into the side walls of the uterus and come into contact with the ovaries on their other end
Simple colmunar epithelium
Has cilia to beat sperm around and move ovum or fertilized ovum around
Convoluted mucosa
Muscular, can contract to facilitate movement
4 regions: infundibulum, ampulla, isthmus, intramural
Ovarian Ligament
Connects the ovary to the side wall of the uterus
Mucosal folds of the Fallopian tube
Contain smooth muscle
They move to gather the egg and bring it into the tube
Ectopic Pregnancy
Egg gets fertilized outside of the uterus
Layers of Uterus
Endometrium - Vasculature, endothelium, CT
Myometrium - mass of smooth muscle
Perimetrium - CT/adventitia
Female gonad within pelvic cavity
Cortex is a lot of cells (80% of cancer is here)
Medulla is a lot of vasculature and some CT
Surrounded by germinal epithelium
Germinal Epithelium
The outer layer of the ovary
Modified visceral peritoneal membrane
Gives rise to follicular cells
Tunica Albuginea
Dense, irregular Ct capsule visceral to the germinal epithelium
Oogonia and all supporting cells around it
aka ova
Egg without supporting cells
Functional/parenchymal cells found here
Born from the yolk sac
Mitotically divide while migrating to the ovarian cortices ~7 million made, ~ 1 million survive
Yolk sac
Eggs originate here and migrate through the mesentery into the embryo and into ovarian cortexes
While they travel, they mitotically divide
Primordial Follicle
Contains primary oocyte covered in a squamous layer of follicular cells
Follicles we have at birth, ~1 million per ovary
Stimulated by leutinizing hormone to continue cell cycle where they get stuck in meiosis 2
Make up the reserve at the surface of the ovary
FSH not responsible for this developing from oogonia
Primary oocyte
Eggs we have at birth, ~1 million per ovary
Stuck in prophase 1
Stimulated by leutinizing hormone to continue cell cycle where they get stuck in meiosis 2
FSH not reponsible for this developing from primordial
Releases paracrine factors telling follicular cells to become cuboidal and then stratify
Granulosa Cells
When follicular cells surrounding the oocyte become cuboidal rather than squamous
Degeneration of follicles that are unused
Happens between birth and menarche, dropping number of follicles from ~1 million to ~300,000
The first occurrence of menstruation in a woman
By this time, number of primary oocytes has dropped from ~1 million to ~300,000 per ovary
Secondary Follicle
Follicle stuck in meiosis 2 after release
Fertilization has to occur to get it "unstuck" (have to have FSH to continue)
A lot larger than primary
Antrums build up between the cells
aka Antral follicle
5 Stages of Development
Primordial Follicle
Primary Follicle
Multilaminar primary follicle
Secondary Follicle
Mature Follicle
Fluid-filled spaces between granulosa cells of secondary follicles
Contains hormones like estrogen and progesterone
Graafian (Mature) Follicle
All antrums coalesce into one
Granulosa cells become mural granulosa cells
Liquor folliculi forms
Build up of fluid causes cumulus oophorus to detach from mural granulosa allowing the oocyte to float freely in the liquor folliculi
Mural Granulosa cells
Follicular cells around a mature oocyte
Stratified cuboidal
Converts androstenedione into estradiol (potent estrogen) with aromatase
Corona Radiata
A capsule of several layers of granulosa cells that surrounds the developing secondary oocyte
Remains intact for when the secondary oocyte enters the uterine tubes
Cumulate Cells
Connects the secondary oocyte to the follicle
Eventually they build up fluid around them and break apart, making the follicle part of the outer wall of the ovary and releasing the oocyte
Zona Pellucida
In the outer wall of the oocyte
Proteins in membrane of sperm interact with proteins here when fertilization occurs
Follicular cells
Derived from mesothelial lining of the ovary (germinal epithelium)
Single layer at first
Analgous to oogonia
Theca Interna
Cellular layer of stromal cells of multilaminar primary oocytes
Produce androstenedione in response to LH surge
Analogous to Leydig cells (produce testosterone in men)
Theca Externa
Vascular/CT layer of stromal cells of multilaminar primary oocytes
Loosely arranged
Converts androstenedione into estradiol
Most potent form of estrogen
Inhibits FSH - dominance - one follicle "wins" and the other can no longer develop because it secretes the most
Leydig cells
Make testosterone in presence of LH
Liquor folliculi
Fluid inside antrum of secondary follicle
Contains plasma components, glycoproteins, and hormones (progesterone, estradiol, activin, inhibin) which regulate LH and FSH
antagonist to inhibin
Enhances FSH biosynthesis and secretion
Participates in the regulation of the menstrual cycle
Secreted by oocyte to induce hypertrophy in primordial follicular cells
Inhibits the production and release of LH and FSH
Steroid hormone produced by thecal cells
Intermediate in the synthesis of estrogens/androgens
Absorbed by granulosa cells and converted to estrogens
Cumulus Oophorus
Mound of granulosa cells on the side of the antrum that covers the oocyte and secures it to the follicle wall
Release of the secondary oocyte from the graafian follicle due to FSH stimulating theca interna cells to produce androstenedione by stimulating upregulation of LH receptors
Granulosa cells convert androgens to estrogen with aromatase
Relies on GNRH and estrogen release, which causes FSH/LH release
Meiosis Inducing Substance (MIS)
Patch of cumulus cells holding the secondary oocyte to the graafian follicle secrete this
Released upon LH stimulation
Stimulates the oocyte to go from primary to secondary
Cells are now stuck in meisois 2 (metaphase)
Stigma of the Ovarian Cortex
Area of the ovarian surface where the Graafian follicle will burst through during ovulation and release the ovum
It will then heal and the residual follicle made into a corpus luteum
LH Surge
Caused by surge of estrogen
Release of MIS, primary oocyte becomes secondary oocyte suspended in metaphase 2
Mural granulosa cells loosen up because of fluid building up between cells
Ovarian surface loses blood (becomes stigma)
CT degenerates (antrum and peritoneal cavity become continuous)
14th day before the beginning of menstruation
Corpus luteum
Yellow endocrine tissue which produces hormones, estrogen(low) and progesterone (high) which prepares the uterine lining for receiving an embryo
Forms in a ruptured Graafian follicle following the release of an ovum
Induced by LH surge
Inhibits LH/FSH
hCG protects this from breaking down in pregnancy
"Picks up" secondary oocyte
Oocyte travels from here to the ampulla for fertilization
The outer two-thirds of the fallopian tube
Fertilization of the ovum by a spermatozoon usually occurs here after 24 hours
Makes sperm capable of fertilization
Granulosa-Lutein Cells
Derived from mural granulosa cells
Produce progesterone and convert androgens to estrogens
High estrogen
Low progesterone
Low estrogen
High progesterone
Due to corpus luteum presence
Theca-Lutein Cells
Derived from theca interna cells
Produce progesterone and androgens
Inhibits LH
Induces degeneration of corpus luteum
Released by corpus luteum (kills itself)
hCG (Human chorionic gonadotropin)
Maintains corpus luteum
Only comes from placenta (after fertilization and implantation)
Keeps progesterone high and estrogen low to maintain endometrium
In the hypothalamus
Regulates the release of GNRH and therefore LH/FSH
Long loop - gonadic secretions (steroids) go up to stimulate GNRH
Low gonadal steroids
Feedback is sensitive, keeping LH/FSH low
Gonadotrophins are low
Low gonadal steroids, slight increase
Decreasing sensitivity to feedback
Rising gonadotrophins
Pulse rate of GNRH increases
Adult level of gonadal steroids
Low level of feedback sensitivity to keep LH and FSH elevated
High level of gonadotrophins
Hormones (FSH and LH) that stimulate the development of ovaries and testes
Positive coorelative cue to beginning puberty and to high adipose tissue
High levels stimulate kisspeptin neurons in the hypothalamus, which affects GNRH levels
Kisspeptin Neurons
Influence GNRH secretion
Found in the pituitary
Stimulated by leptin
Stimulates theca cells to produce LH receptors
High levels stimulate a follicle to mature
Estrogen inhibits this, causing the release of LH, causing ovulation
LH receptors
Found on theca cells
When LH binds to these, they produce androstenedione which is converted to estrogen in the granulosa cells which inhibits more FSH and LH release
Corpus Albicans
Menstrual flow consists of these
Degenerated corpus luteum (gone through atresia)
Muscle of uterus
Stimulated by oxytocin to contract
Estrogen stimulates the proliferation/hyperplasia of this
Inner longitudinal, middle circular and outer longitudinal layers of smooth muscle
Top surface is serosa, the rest adventitia, because the peritoneal cavity sits on top
Becomes engorged with blood during arousal
Sinusoidal tissue
Analgous to penis
Labia majora
Analgous to scrotum
Labia minora
Analgous to urethral surface of penis
Fibromuscular tubular structure
Nonkeratinized stratified squamous epithelium
Terminal end of uterus extending into the vagina
Simple columnar to a nonkeratinized stratified squamous
simple columnar; ciliated and nonciliated secretory cells
lamina propria: simple branched tubular glands (uterine)
Peg Cells
In oviducts
Nutrient secretions
Inducers of capacitation (required to render sperm competent to fertilize an oocyte)
An increase in the fragility of the membranes of sperm cells when exposed to the female reproductive tract. Required so that the acrosomal enzymes can be relased to faciliate fertilization.