Lecture Exam 4

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Conducting Pathway

Tubes that direct air down to the respiratory section where gas exchange actual happens
Nasal cavity -> terminal bronchioles
Tracheobronchiole tree

Phonation

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

-Nose
-Nasal cavity
-Paranasal sinuses
-Pharynx (end)

Lower respiratory track

-Larynx (thyroid cartilage)
-Trachea
-Bronchi
-Bronchioles
-Alveoli

Respiratory bronchioles

Conducts air to the alveoli but also does gas exchange itself.

Diaphragm

Inferior border of thoracic cavity

Acinus

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

Vibrissae

Hair fibers in the nasal cavity which filter the air coming through it

Naris

Nostril

Edey Currents

Currents formed in the nasal cavity increasing the time it stays in the nasal cavity, flowing around.
Increases filtration

Concha

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.

Choana

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

Epiglottis

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

Glottis

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

Carina

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

Bronchioles

Where bronchoconstriction/dilation occurs
First section that has no cartilage

Inspiration

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

Emphysema

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.

Serfactant

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

CO2

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

Liver
Gallbladder
Pancreas
Salivary glands

Bolus

Compacted, mucous-saturated mound of food from the mouth travelling toward the throat
Stretches the esophagus, causing the esophagus to respond with peristalsis

Stomach

Responsible for mechanical and chemical digestion
Food can be stored here
Not much absorption here, just aspirin and alcohol
Makes chyme

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

Gustation

Sense of taste

Deglutition

Conscious swallowing

Mucosa

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)

Submucosa

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

Serosa

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

Adventitia

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

Mesentery

Two layers of visceral peritoneum fused together
Blood vessels, nerve fibers and some loose CT
Holds your guts in place

Peristalsis

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.

Parasympathetic

Activates the GI tract
Rest and digest

Sympathetic

Deactivates the GI tract
Fight or flight

Tachycardia

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

Tongue

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)

Saliva

Mucins, buffers, water, enzymes (lysozymes etc), antibodies, lingual lipase in mouth

Lysozyme

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

Esophagus

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
Strong
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

GERD

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

Gastrin

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

Rugae

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

Ghrelin

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

HCl

Kills microbes
Protein denaturation (breaks hydrogen bonds to increase surface area of peptide exposed to enzymes)

Pepsinogen

Zymogen
Secreted from chief cells of gastric glands
Autocleaves itself into pepsin when activated by acid (HCl)
Begins protein digestion in the stomach

Zymogen

An inactive precursor of an enzyme, activated by various methods (acid hydrolysis, cleavage by another enzyme, etc.)

Pepsin

Active form of pepsinogen
Converts more pepsinogen
Active protease/prteolytic enzyme

Ulcers

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

Phospholipase

Excreted by H.pylori in stomach
Breaks down phospholipids in gastric-mucosal barrier allowing acid to get closer to stomach lining

Urease

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

Somatostatin

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

Secretin

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

Colipase

Secreted by the pancreas

Bile

Emulsifies fat in the stomach, allowing enzymes to access it

Ptylain

Salivary Amylase

Duodenum

Part of the small intestine that goes out of the peritoneal cavity
Has adventitia, not serosa

Cecum

First part of the large intestine

Villi

Folds of lamina propria and epithelium (mucosa)
Cells making up the simple squamous epithelium also have microvilli

Plica

Permanent folds to increase the surface area of the small intestine.
Has villi on top of it

Surface Area Increase

Microvilli
Villi
Plicae

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

Chemoreceptors

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

GLP-1

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

Byetta

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

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