Class Notes

Location of Neurons in the CNS:

(1) Inspiratory Neurons: Medulla
(2) Expiratory Neurons: Medulla
(3) Phrenic Nerve Motor Neurons (A nerve that originates in the neck (C3-C5) and passes
down between the lung and heart to reach the diaphragm, it is important for breathing
because it passes motor information to the diaphragm and also receives sensory
information from it) : Cervical Spinal Cord
(4) Pneumotaxic Center (PRG, regulates the amount of air a person can take into the body in
each breath, inhibits inspiration, if destroyed the respiratory frequency may be unchanged
BUT the depth will increase because of prolonged inspiration): Pons
(5) Dorsal Respiratory Group (synapses to the motor neuron that innervate the inspiratory
muscle ALWAYS THE TIME) : Medulla
(6) Ventral Expiratory Group (synapses to the motor neuron that innervate the expiratory
muscle and also the inspiratory muscle during exercise NOT ACTIVE DURING REST) :
Medulla
(7) Vagus Nerve, functions to inhibit inspiration, usually slows down breathing.
(8) pre-Botzinger complex, important in the generation of respiratory rhythms in mammals.

CO2 undergoes upon entering a systemic capillary

Distinguish between CENTRAL and PERIPHERAL chemo-receptors

Location
Respond to
Sense the change in___?

Central
Medulla
An Increase in PCO2

Peripheral
Carotid bodies
An Increase in PCO2
Also respond to O2
Decrease in pH

Decrease in pH
Ventilation Increases
(Freq and Tidal volume)
The physiological role of the peripheral chemoreceptors is most important for regulation of
arterial oxygen and blood pH.
Periodic Ventilation at High Altitude
Periodic Ventilation involves alternating periods of deep breathing and shallow breathing (short
and quick breaths). This is important because at high altitude, the body senses low oxygen levels
and this becomes the main drive to breathe. Breathing faster and deeper at high altitude leads to
a profound reduction in the carbon dioxide level in the blood.

When O2 decreases, it defuses into Glomus Cell. The golmus cells have potassium channels
which close when the PO2 decreases. When K Channels close, the cell depolarizes and this
causes Voltage-gated Calcium channels to open, Ca2+ enters the cell and causes the exocytosis of
neurotransmitters. The neurotransmitter binds onto receptors on sensory neurons and signals the
medulla centers to increase ventilation.
Decrease in PCO2 removes the stimulation
for ventilation, whereas, the decrease in
oxygen stimulates ventilation (much less)

Normal pH (7.35-7.45), the arteriole pH is maintained very tightly between 7.35-7.45.

Two organs responsible for maintaining pH
(1) Kidney
(2) Lungs
Buffers:
(1) HCO3
(2) Proteins, hemoglobin, phosphates in cells
(3) Phosphates, ammonia in urine
Proximal Tubule Cell

Secretes 3 Bicarbonate (HCO3-) out and one Na+ in.

Process:
(1) Na+/H+ antiport secretes H+
(2) H+ in filtrate combines with filtered HCO3- to form CO2
(3) CO2 diffuses into cell and combines with water to form H+ and HCO3(4) H+ is secreted again and excreted
(5) HCO3- is reabsorbed
(6) Glutamine is metabolized to ammonium ion and HCO3
(7) NH4 is secreted and excreted
(8) HCO3- is reabsorbed

Type A Function in Acidosis (Too much acid in fluid)

(1) Brings K+ in and H+ (Proton Pump) out in the lumen of collecting ducts.
(2) CO2 diffuses into the cell to form carbonic acid and the left over H+ is pumped out of the
cell into the lumen
(3) Carbonic acid acts as a buffer to lower the concentration of H+
(4) K+ is then pumped out of the cell into the interstitial space where it is reabsorbed

Type B Function in alkalosis (Too much base in fluid)

HendersonHasselbalch equation

KNOW THESE NUMBERS:

(1) pKa of the bicarbonate carbonic acid couple is 6.1
(2) The normal bicarbonate concentration is 24 mmol
(3) PCO2 is 40 mmHg (40*0.03=1.2)
(4) (24/1.2)=20
(5) Log10(20)=1.3
(6) 6.1+1.3=7.4
(7) pH=7.4, if the ratio of bicarbonate over PCO2 is greater than 20 the blood will be more
basic (alkalosis), if it is less than 20 then the blood will be more acidic (acidosis).

The graph shows that the pH decreases as the PCO2 decreases.

Digestive System has FOUR functions:
(1) Digestion: Chemical and mechanical breakdown of food into absorbable units
(2) Motility: Movement of material from GI lumen to ECF
(3) Secretion: Movement of material through the GI tract as a result of muscle contraction
(4) Absorption (Not Regulated): Movement of material from cells into lumen or ECF
First Step of Digestion
Secretion of saliva by three pairs of salivary glands:
(1) sublingual glands under the tongue
(2) submandibular glands under the mandible (jawbone)
(3) parotid glands lying near the hinge of the jaw
Secretory epithelium, the liver, and the pancreas, creates a soupy mixture known as chyme.

Gastrin is important for gastric acid (HCl) secretion in the parietal cells of the stomach
(1) Gastrin is released by G cells in the pyloric antrum of the stomach
(2) Gastrin binds to cholecystokinin B receptors to stimulate the release of histamines.
(3) The histamines come from paracrine cells, the histamines bind to H-2 receptors.
(enterochromaffin-like cells) ECL secretes histamine.
(4) This causes the insertion of H+/K+ ATPase pumps into the apical (lumen) membrane of
parietal cells.
Three ways to stimulate HCl secretion:
(1) Gastrin causes H+/K+ ATPase pumps to be inserted into the apical membrane of the
parietal cell. Acetylcholine and proteins (peptides) in stomach via receptors that detect
peptides in the food and then stimulate gastrin secretion.
Gastric chief cell (Exocrine cells)

(1) Secretes pepsinogen (proteases), which is converted into pepsin, which is crucial in the
digestive process in the stomach. Attacks proteins in the center and breaks it up into
smaller peptides. Digests proteins in the stomach.
(2) Secretes gastric lipase, which hydrolyzes triglycerides into fatty acids and
monoglycerides
Four enzymes in the stomach:
(1) Salivary amylase
(2) Lingual Lipase
(3) Gastric Lipase
(4) Pepsin
(5) Food enters the esophageal sphincter and then enters the stomach, which breaks the food
up into chyme.
D Cells (Inhibitory cell):
(1) Secreted from the somatostatin, stimulated by acid in the stomach and this inhibits gastric
acid secretion.

Gastric Phase:
(1) Food (amino acids or peptides) is going to stimulate chemoreceptors which will secrete
gastrin. The vagus nerve also stimulates secretion of gastrin.
(2) Gastrin stimulates the parietal cells to secrete HCl or also causes the ECL cells to secrete
histamine, which also stimulates HCl secretion.
(3) Acid stimulates the release of pepsinogenpepsin.

(4) A decrease in pH (lower than 3), the D cells senses this and secretes somatostatin, which
inhibits the G cell, ECL cell, chief cell and parietal cell.
Gastric juice contains urea. Helicobacter pylori (H. pylori), a gram-negative bacterium found in
the stomach have an enzyme called urease that catalyzes the hydrolysis of urea into ammonium
and CO2.
Chyme is created in the stomach, it is squirted into the duodenum. The duodenum secretes
secretin in response to the hydrochloric acid in chyme. The secretin will stimulate the secretion
of bicarbonate from the pancreas, it will also inhibit gastric secretion.
CCK causes the contraction of gallbladder to squeeze out bile (increases gallbladder secretion =
increase bile secretion/digestive enzymes). CCK is responsible for stimulating the digestion of
fat and protein. Acinar cells secrete pre-cursors of a digestive enzyme. CCK also decreases
appetite.
Carbohydrates secrete 2 hormones that is stimulated by the duodenum
(1) GIP (Gastric inhibitory polypeptide), stimulates the islets of the Langerhans to secrete
insulin.
(2) GLP-1 also increases insulin secretion by the pancreases.
Ulcers:
(1) Zollinger-Ellison syndrome is caused by excessive acid secretion, can be cured by H+
pump inhibitors. This causes the H+ pump in the parietal cells to not be able to be
pumped out into the lumen of the stomach and form HCl.
(2) H. pylori is the most common cause of ulcers, they secrete urease, which breaks down
urea present in the stomach into CO2 and ammonia, the ammonia neutralizes the stomach
acid. H. pylori attacks the lining of the stomach, which protects the body from acid.
Cure is antibodies and H+ pump inhibitors (decrease acid secretion).
(3) Chronic aspirin or NSAID can also cause ulcers. The body has three ways to proect the
stomach from digestive juices (1) mucus which is the physical barrier between the lumen
and the epithelium (2) bicarbonate to neutralize the acid and (3) blood circulation to the
stomach lining that aids in repair. However, chronic aspirin and NSAID prevents these
mechanisms. Cure: H+ pump inhibitors, stop taking the drug, atropine, cimetidine or
ranitidine.

Processes:
(1) Carbohydrates stimulates GLP-1 and GIP to secrete insulin
(2) Acid stimulates secretin which secretes pancreatic bicarbonate to neutralize the acid.
(3) Fats and Lipids stimulates CCK, which stimulates pancreatic enzyme secretions
(bile/digestive enzymes)
Pancreas secretes zymogens and trypsinogen which gets converted into trypsin from
enteropeptidase in the brush border. The trypsin activates other enzymes.

Digestion of Carbohydrates:

(1) Glucose polymers digest to disaccharides with the help of pancreatic amylase.
(2) Carbohydrates are also digested in the mouth by salivary amylase, secreted by the
salivary glands.
(3) THREE types of disaccharides:
(a) Maltase : Maltose 2 glucose
(b) Sucrase: Sucrose Fructose + Glucose
(c) Lactase : Lactose Galactose + Glucose
Absorption of Carbohydrates (glucose is absorbed in the proximal tubule)

(1) Glucose enters the cell via the SGLT (Sodium glucose transporter) symporter (Brush
border side) (low affinity, can only transport glucose at very high concentration)
(2) Fructose enters the cell via the GLUT-5 transporter (apical, brush border side)
(3) Both Glucose and fructose leaves the cell (basolateral side) via the GLUT-2 transporter
(4) GLUT-1 is present in most cell (normal affinity), GLUT-3 (high affinity), GLUT-4
transporters (insulin dependent), synthesized and inserted into intracellular vesicles, and
ONLY when the target cell receives insulin will there be exocytosis of these vesicles
which will allow the cell to transport glucose.

Protein Digestion:

(1) Endopeptidase cleaves peptide bonds in the middle (digests internal peptide bonds)
Produces smaller peptide bonds.
(2) Exopeptidase digests terminal peptide bonds to release amino acids (the outside ends)
releases single amino acids.
Protein Absorption:
(1) Proteins Peptides
(2) Di and tripeptides co-transport with H+ (hydrolyzes by peptidases within the cell)
(3) Amino acids co-transport with Na+
(4) Small poeptides are carried (IN TACT) across the cell by transcytosis
Lipid Digestion:
(1) Triglyceride gets hydrolyzed by lipase and colipase into monoglycerides and free fatty
acids.
Lipid Absorption:
(1) Bile salts (recycled about 10 times) from the liver coats the fat droplets.
(2) Pancreatic lipase and colipase break down fats into monoglycerides and fatty acids stored
in micelles.
(3) Monoglycerides and fatty acids enter the cells by diffusion.
(4) Cholesterol is transported into the cells by a membrane transporter.
(5) Absorbed fats (triglycerides) combine with cholesterol and proteins in the intestinal cells
to form chylomicrons.
(6) Chylomicrons are released into the lymphatic system.
(7) Note: Removal of the terminal ileum (located in the small intestine) will prevent the
absorption of the bile salts, which can be recycle (~10 times). Only IRON II is absorbed
in the duodenum (portion of the small intestine).
Importance of Colon:
(1) The importance of the colon is the absorption of irons and water.
(2) About 9 L of fluid enters the body (into the lumen), 7 L is secretion fluid. Absorption
mainly happens in the small intestine (7.5 L) and about 1.4 L from the large intestine and
only 0.1 L in feces.
Anatomy of the Large Intestine:
(1) Lleum empties into the cecum.