Arteries: blood away from the heart
Veins: blood toward the heart
Capillaries: where blood interacts with tissues
between arteries and veins
Lumen: hollow space inside the artery
Tunica intima: innermost layer of the artery that actually touches blood (really thin)
Endothelium: simple squamous epithelium to prevent blood from clotting
Subendothelial layer: loose connective tissue that provides structural support to endothelium
Internal elastic lamina: elastic connective tissue that is able to stretch when the blood volume increases and shrink when the blood volume decreases
Tunica media: thick layer of smooth muscle that can constrict to reduce the size of the artery and increase pressure OR relax and cause vasodilation
Able to change the size of the lumen
Thicker in arteries than veins
External elastic lamina: elastic connective tissue that is able to stretch when the blood volume increases and shrink when the blood volume decreases
Tunica externa: loose connective tissue that is superficial, contains arteries, veins, and nerves needed
Provides hollow space so that each artery has its own blood supply and nerves
Nerves control contractions and provide energy for the smooth muscle of the tunica media to do its job
How to classify arteries:
The composition of their walls and how big they are
Thick walls, prevent them from collapsing when there is no blood (circular in histology)
Elastic arteries:
largest arteries
ex/ aorta
closest to the heart to carry large amounts of high pressure blood (highest pressure)
dampens pulsatile flow from the heart, makes the pressure more consistent for other blood vessels that can’t handle high amounts of pressure
There are rapid changes of blood pressure in arteries; if a capillary were to undergo a rapid change, it would pop
During systole (ventricles pumping), high pressure
During diastole (ventricles relaxing), lower pressure
Aortic dissection: over time, damage to the tunica intima → blood does dissection (forces its way through the walls and cuts through as it goes) → generating a large structure known as the ‘false lumen’
Caused by uncontrolled high blood pressure
Endothelium and connective tissue cannot manage high blood pressure → start to break down → blood sneaks in between tunica intima and tunica media → expands → creates space where blood and fluid collect
As blood continues to go into the false lumen, dissection grows into an aneurysm (a big bulge on the side of the artery)
If an aneurysm continues to get bigger, it can pinch the blood flow going through the actual lumen of the aorta and prevent blood flow to tissues → tissue death
If the false lumen gets really large, it can overstretch all of the walls of the aorta → aorta wall rupture → 100% chance of death
Symptoms: fatigue, abnormal pulse in chest
Difficult to detect
IF detected early, can be repaired
If survive → lots of complications
Aortic dissection repair:
Procedure:
Know there is a dissection, see a massive aneurysm
Go into the heart and find the area before and after the aneurysm and insert a large graft/stent (made of carbon or kevlar mesh) as a bypass to get past the location where the aneurysm has occurred
Problem:
lots of small branches
graft cuts off smaller arteries that are important → blood vessels that provide oxygen to the spinal cord get cut, damaged, or don’t receive blood → non-traumatic spinal cord injury
nerves don’t recover well from large anoxic injuries → doesn’t heal
ex/ can no longer walk
Usually patients with the risk of rupture are admitted to the hospital where their blood pressure is managed with meds (kept low to prevent rupture) so that the procedure can be done in the coming weeks and not as an emergency procedure
Risk of clotting forever because of stent → anticoagulants forever
Risk of leaks if high pressure → BP meds forever
Muscular arteries:
Slightly smaller than elastic arteries (midsize)
Contain blood flow to organs and limbs (like the stomach)
VERY thick tunica media → control how much blood flow enters each tissue
Vasoconstriction of unnecessary arteries to have more blood flow in other areas
Arterioles
Smallest arteries leading into capillary beds
Control blood flow into capillary beds through vasoconstriction and vasodilation
Same layers but smaller
Less smooth muscle in tunica media
Ex/ cold → skin turns blue to prevent heat loss (move blood flow to other organs)
prone to leak and burst
Function: get things in blood OUT, get things out of blood IN
Want: thin walls and potential for leakiness (but not overly leaky)
Can handle 1 RBC at a time, very fragile and small
Structure:
Endothelial cells on the inside (simple squamous epithelium)
Intercellular cleft: between endothelial cells, doors open/close to increase or prevent leakiness
Basement membrane (outside layer)
During inflammation →want capillaries to be more leaky
Infection in tissues → sinus, kidneys, skin, etc.
WBCs in blood, need to get them out
Make capillaries more leaky to send WBCs to tissue
Problem: more fluid leakage → swelling
Do NOT want to see RBCs leaking out of capillaries (bleeding)
capillaries can be selective in what they leak out (fluid, plasma, H2O)
Pulmonary Edema:
Cause: heart failure → affects lungs
DCM- left ventricle struggles to pump and receive blood
Blood comes back to the heart faster than it can pump it out (congestion, backup)
Leads to increased pressure of blood in the lungs
Capillaries leakier than normal
Fluid leaks into the alveoli (where gas exchange occurs) → drowning, collection of fluid in the lungs (coming from overly leaky capillaries)
Treatment:
give a lot of diuretics
get more fluid out of blood (plasma) and pee it out →less volume → less pressure in capillaries → leak less →reduce pulmonary edema
Lumen: hollow space inside the vein
Valve: blood inside the veins has very little pressure (sometimes blood doesn’t flow because the pressure is less than gravity)
Prevent blood flow backwards by closing
Ex/ in legs
Tunica intima: innermost layer
Made up of endothelium (simple squamous epithelium) and the subendothelial layer (loose connective tissue)
Tunica media: don’t need a lot of smooth muscle because less pressure
Tunica externa: loose connective tissue → contains veins, arteries, and nerves needed to provide nutrients to tunica media
Walls significantly thinner than arteries
No need for stretchiness because slow blood flow and no massive pressure change → no need for internal and external elastic lamina
Histology - oddly shaped because of the thin tunica media and the lack of blood
Verricose veins:
caused by age, usually a cosmetic issue unless severe
Caused by: valves malfunction
Valves don’t properly close and blood moves backwards → blood pools in the veins & veins get stretched out and stay that way
Damage neighboring valves, gets bigger, twisted swollen vein (blood DOES flow out, but very slowly)
Close to the surface of the skin, so it shows
Treatment:
close the vein off
not problematic because some other veins can pick up the blood that used to go through that vein
burn the vein closed → no blood flow → shrinks within a few weeks
Veins
large vessels carrying large volumes (same rate it is pumped) of low pressure blood, bigger volume of blood
contain valves to prevent backflow, thin walls
run close to skeletal muscles to assist with blood flow back to the heart (contract muscle → squeeze vein → push blood back to the heart)
ex/ vena cava, brachian vein, femoral vein
Venule
function: receive blood from capillary beds
small vessels that exit capillary beds and merge to form veins
small vessels with thin walls
fragile, easily damaged, and blood flow restricted
bruise: trauma to a venule
they heal but they don’t respond well to surgery/transplant
lobes -
superior, middle, and inferior lobes on right side
superior, inferior lobes on left side
fissures separate the lobes
gas exchange occurs in the lungs
Alveolus: tiny sacs in the lungs where gas exchange occurs
alveolus surrounded by blood capillary
O2 in alveolus goes into the blood, CO2 from blood capillary goes out of the blood, into the alveolus → exhaled
Alveolar sac: collection of different alveoli stuck together
Capillary network: around each alveolus
trachea: air from the mouth, down the throat, to the lungs
lungs rub against ribs & heart → friction
layers:
visceral pleura: innermost
left pleural cavity/sac: space between visceral and parietal pleura
parietal pleura: outer layer
pleura - serous membrane with simple squamous epithelium adjacent to dense irregular connective tissue
makes serous fluid
1 continuous layer folded in on itself to form parietal and visceral pleura
Type II cells: secrete surfactant
Type I cells: structure of alveolar wall
simple squamous epithelium
O2 and CO2 diffuse → capillary
Macrophage: resident/alveolar WBC
If you breathe something bad in, resident macrophages kill/eat it
Fused basal lamina - shared basement membrane, easier for O2 and CO2 to diffuse into or out of blood
Epithelium is always next to a basement membrane (connective tissue)
Alveolar pores: to conserve space in the sac, holes instead of airways to bring more air in
Surfactant
surface tension: molecular attraction between water molecules
inside alveoli, there is water and vapor, should always be wet
allows cells to move (expand - breathe in, contract - breathe out)
water molecules in alveoli are attracted to each other
surface tension is strong → resists alveolar expansion
surfactant breaks apart surface tension
it is a detergent
reduces the attraction of water molecules
diseases of the lungs affect surfactant → loss of function
Blood flow and gas exchange
concentration gradients facilitate gas exchange
O2 in alveoli diffuse into O2-poor blood
CO2-rich blood diffuse into CO2-poor alveoli
Pneumonia: a symptom, not a disease
fluid in the alveoli increases to the point of standing water, alveoli full of water
can’t get air inside the alveoli → no gas exchange
can’t get to capillaries → can’t diffuse
have a LOT of alveoli, even with pneumonia, the majority of the alveoli are not full of fluid
Pulmonary edema/pneumonia
caused by infections
capillaries leak WBCs and fluid (leads to pneumonia)
necessary
normally, the body gets rid of fluid
if infection is very strong, send more WBCs (and more fluid) → pneumonia
ARDS: acute respiratory distress syndrome
very intense pneumonia
usually pneumonia is only in few spots of lungs
however, ARDS is when pneumonia is everywhere in the lungs and fast
lungs are completely underwater in 24-48 hrs
very fatal (death ~50% of the time)
triggers: infection, autoimmune, allergy, etc.
body’s immune system thinks you will die, dilates all capillaries that go to the lungs (to save you (not)) → fluid rushes in, drown
ex/ COVID-19 triggered cytokine storm (signalling used to regulate capillary leakiness)
Body released storm of cytokines → very leaky capillaries → underwater lungs → death
capillaries are leaky to move WBCs into the lungs
break down bacteria and viruses in the fluid
pump out stuff that does targeted killing of bacteria and viruses but also makes the environment toxic → type I and II alveolar cells also die
walls become fragile → stop making surfactant →alveoli can’t expand even if air is pumped in
WBCs create fibrin inside alveolar walls and fluid → turn water-like fluid into jello-consistency
harder to cough out
TRY to prevent this
ex/ covid is longer if ARDS
should get antivirals ASAP to prevent ARDS
options after this point: mechanical ventilation
fluid in alveolus → alveolar collapse → need to reopen alveoli with high pressure from ventilator
ARDS doesn’t progress to all parts of the lungs at the same rate
repositioning in ‘prone’ can cause you to use other parts of the lungs where ARDS has not yet progressed and to reopen some alveoli
ventilation perfusion matching: controls how blood floes into lungs → goes into area with O2
prone position → encourages surfactant and pulls blood into regions with surfactant
lungs are permanently damaged and scarred
damage cannot be reversed
common for ARDS to require a lung transplant
the lungs are fragile → on a ventilator, physicians prescribe high amounts of pressure → alveoli pop and never recover (aka barotrauma)
BEST CASE: some lung damage, continue living as normal
COVID-19
hypoxemia caused by blood vessels, not lungs
vessels had receptors that COVID binded to
endothelium was damaged by infection, inflammation, etc. → blood clots made
microvascular capillary clotting: blood clots in capillary beds going to alveoli → no blood in the capillary for O2 to bind to → shortness of breath, hypoxemia, lungs still healthy
cytokine storm → ARDS
cytokine storm - possibly caused by genetics
antivirals given to people at risk to prevent ARDS (50/50 mortality)
At rest - not breathing/moving air in and out
Intrapleural pressure: pressure within pleural cavity (space filled with serous fluid that surrounds the lungs)
756 mmHg
Inspiration/inhalation - air in
758 mmHg (lower than atm - 760 mmHg, so air flows in)
diaphragm between thoracic and abdominal cavity contracts and pulls thoracic cavity down, makes more room in the thoracic cavity →less pressure on the lungs → air comes in
Expiration/exhalation - air out
763 mmHg (higher than atm - 760 mmHg, so air flows out)
diaphragm relax → put thoracic cavity back up, smaller → increased pressure → air pushed out of the lungs
Pressure gradients move air in and out
Breathing in - active, muscles contract
Breathing out - passive, muscles relax
Intrapleural pressure reduces friction when lungs open and close so that lungs aren’t rubbing against other structures
Intrapleural pressure must be less than the pressure of alveoli at ALL times
Why?
To keep alveoli open
If there is pressure exerted on alveoli by an external force, the alveoli will collapse
By surrounding the lungs with an area of lower pressure (intrapleural pressure), alveoli are encouraged to stay open
Experiment: Put balloon inside vacuum chamber
Pressure of air inside balloon constant
Vacuum chamber (pressure of outside chamber decreasing) → causes balloon to expand dramatically
Air inside alveolus is set pressure that changes when we breathe but pressure around it must be lower than the pressure inside the alveolus so that the alveolus can remain inflated
Do you want the pressure in the intrapleural space to stay lower than the alveoli at ALL times or just SOME of the times?
ALL times
Diaphragm: big, dome-shaped muscle at the bottom of the thoracic cavity but at the top of the abdominal cavity
At rest, this is the only muscle involved in breathing
Contract the diaphragm → air pushes in
Relax the diaphragm → air pushes out
Accessory muscles of respiration
Usually used when doing exercise (taking large, labored breaths)
Muscles of inspiration
Muscles of expiration
Letting the diaphragm relax is not going to push air out fast enough so must contract muscles to push out air faster
Majority of muscles relied on are the abs
Diaphragm
Under both volitional control (controlled) and autonomic control (sleep)
Lots of different mechanisms that help you determine when it is the right time to breathe
Problems can happen when you breathe too little and when you breathe too much
Sensors in brain, blood vessels, muscles, and the lungs tell you → breathe faster or slower
is there too little/much O2 in my blood? → increase or decrease respiratory rate
Is the pH of my blood too high/low?→ increase or decrease respiratory rate
ex/ too little O2 to tissues →tissues die →speed up breathing
Pathology
Pleural Effusion: Due to infection, immune issue, trauma, etc. → more fluid in pleural cavity (sometimes even blood)
Pressure in pleural cavity increases → squishes balloon of lungs → alveoli collapse →less available space for gas exchange
X-RAY: lung where pleural effusion was would be visibly smaller than a healthy lung
know something is squishing the lung
TREAT:
put in a chest tube→ drain the fluid in the cavity
What is causing this?
Infection
Treat the infection →this issue will go away on its own
If effusion is bad enough → more issues
can completely compress the lung to the point where one or both lungs can’t experience significant gas exchange
Pleural cavity is lined by epithelium which has a basement membrane around it (which contains blood vessels) → blood vessels provide nutrition and oxygen for epithelium that can produce serous fluid
Capillaries and lymphatic vessels have the job of reabsorbing excess fluid from tissue spaces
HOPEFULLY, over time, lymphatic vessels and blood vessels can absorb the excess fluid
Pneumothorax: something is causing a puncture either in the walls of the chest or in the alveoli themselves, which is allowing atmospheric air to enter the pleural cavity
NEED there to be certain times when intrapleural pressure is less than atmospheric pressure (inspiration); however, with pneumothorax, during inspiration and at rest, pressure inside pleural cavity due to atm air is higher than it should be → lung collapse
Atalectasis: alveolar collapse or lung collapse
pneumo - air
thorax - chest
TREAT:
short term, if severe:
set up chest tube in cavity, vacuum suction to draw air out of thoracic space (pleural cavity) and generate a lower pressure → allow lung to re-expand
Emergent chest tube placement
if not severe:
find leak, plug it
ex/chest wound→sew it up and make sure air doesn’t leak → reduce pressure →allow lung to expand
Hemothorax: blood within pleural cavity
Upper respiratory tract
Nasal cavity
Pharynx
Larynx
Lower respiratory tract
Trachea
Primary bronchi
Lungs
Most airways lined with the same kind of tissue - special kind of epithelial layer: respiratory mucosa
Respiratory Mucosa: pseudostratified columnar epithelium
2 kinds of cells
Ciliated cells
have cilia on top, works to move something around on the surface of a cell
cilia moves mucus around (mucus generated by goblet cells)
Goblet cells
unicellular, mucus-secreting glands (exocrine glands)
mucus produced lines the surface of the epithelium (lines nose, trachea, bronchi, all the way down except smaller branches because we don’t want mucus down there)
Why do we have this mucus?
we breathe in air, dirt, viruses, etc.
body wants to prevent bad stuff from reaching alveoli
mucus is there to coat all of the airways so that the particles we breathe in get trapped in the mucus, then the cilia move the mucus away from alveoli so that you don’t suffocate or drown→move mucus out of lungs
mucus also wet, we need alveoli to be wet and the air we breathe in isn’t always moist
as air is breathed in, picks up some moisture from mucus →when it gets to the alveoli, there is not a large difference between how moist the air is and how moist alveoli walls are, so alveoli do not dry out
when air is breathed out, want to keep moisture, so mucus does a good job of trapping some of the moisture → moisture not lost from body with each breath
When respiratory epithelium is inflamed: Rhinitis
usually in the upper airways and in the nose and sinuses (sinusitis)
Why?
Infection or response to something inhaled (ex/ allergy) →mucosal epithelium inflamed →body starts pumping more blood, oxygen, nutrition to these cells →cells do their jobs faster
ex/ goblet cell does job faster→secretes more mucus
ex/ciliated cell does job faster →cilia move faster→move more mucus out of lungs and out of body→ mucus leaves body faster than it can dry → runny nose
defense mechanism
if body is encountering something bad (infection) & wants to prevent spread, starts secreting more mucus and moving it out →move infection out of body more quickly
TREAT:
drugs - pseudoephedrine (Sudafed) (stimulant)
vasoconstrictor
inflammation → blood vessels dilate to provide more oxygen and nutrition at the level of the inflamed tissue
vasoconstriction drug →less energy delivered to inflamed cells→ less inflammation because can’t produce as much mucus → no runny nose
PROBLEM: vasoconstrictor works everywhere, not just nose
if you already have hypertension→ increases blood pressure more
Anterior nares/external nares: nose holes, openings that air goes in/out of
Vestibule: area inside nose but outside skull
Enter skull → covered in respiratory mucosa
Add moisture to air breathed in, makes sure it is homeostatic temp and moisture before going to lungs
Catches particles in mucus
Adaptation: Increase surface area of respiratory mucosa to add moisture and catch particles by - turbinates/conchae (large bony projections/folds that stick out into nasal cavity covered with respiratory epithelium)
air comes in and bounces off surfaces →gets hotter and more moist
Adaptation to increase surface area: sinuses (enclosed cavities of respiratory epithelium trapped within bones of skull) →air flows in and gets hot and moist → lungs
Frontals
Ethmoids
Sphenoids
Maxillary
Problem: sinuses are large but passageways of air through the sinuses is small
tiny little passageway opening into a large sinus
inflammation of respiratory epithelium →secreting more mucus & tissue/individual cells swell up → block passageways that come in and out of sinuses
if air can’t get out of sinus, mucus produced also can’t get out
over time, as inflammation progresses & still pumping out a lot of mucus but passageways blocked, mucus gets stuck →increase in pressure until pain (sinus headache, clogging of sinuses, pressure buildup from mucus)
TREAT:
Sudafed - cause inflammation to go down → vasoconstriction reduces inflammation of epithelium →epithelium relaxes & shrinks → open up passageways again →mucus falls out and leaves
prevent addiction
Sinus plasty or sinoplasty: find narrow passageways that lead into sinuses and expand them by removing bone & epithelium → hoping epithelium scars and more doesn’t grow in its place
Balloon sinoplasty: take balloon and insert it into part with narrow passageway & expand it and hope it crushes neighboring bone and opens up the passageway
Olfactory mucosa: makes it so that you can smell stuff
Pseudostratified columnar epithelium
Goblet cells
Nerve endings - olfactory receptor cells (neurons that project down through the layer of epithelium and have olfactory hairs on the end
Olfactory hairs hang out in the mucus & bind to chemical particles in the air you breathe in → trigger neurologic response where once these hairs bind to what you are breathing → signal gets transferred up to the nerve → signal goes through olfactory tract where it is perceived → brain knows what you are smelling and can tell if it smells good (interprets signal)
Epithelium between olfactory receptor cells: supporting cells (sustentocytes)
Supporting cells: provide nutritional support to these neurons to help make sure that they are well regulated, that they have enough O2 to do their jobs, and to keep them protected in a relatively harsh environment of the inside of your nose
COVID loss of smell caused by die off of supporting cells → no nutrition for neurons
new research shows covid also infiltrated nervous system → probably infected the actual neuron itself
back of the mouth: pharynx
point where you have connection between your nose, mouth, and throat
nasopharanx behind nose
oropharanx behind mouth
hypopharynx/laryngopharanx behind larynx
Olfactory nerve: comes down right above nasal cavity and ends at olfactory bulb
Branches of olfactory nerve penetrate down through the skull and into the olfactory mucosa (on the roof of the nasal cavity)
in the pharynx
palatine tonsil - the ones we usually focus on
lingual tonsil, palatine tonsil, pharyngeal tonsil
now: using antihistamines, antivirals, antibiotics rather than doing a tonsilectomy
because tonsils have immune function
larynx: voicebox and gateway to the trachea, surrounded by cartilage
big, hollow tube with hyaline cartilage (rigid, strong, keeps things the same shape, resists forces)
epiglottis: to get past laryngopharanx
food goes posterior → esophagus
air goes anterior → trachea
Epiglottis: door
swallow → epiglottis closes and shuts off access to voice box, larynx, trachea to prevent food from going to lungs
Arytenoid cartilage: attached to muscles and vocal fold/chord (tone, pitch, sound, volume)
moves, unlike other cartilages
glottis: space between vocal chords
air goes through the glottis
glottis changes in size
breathing → more open
talking → muscles pull chords together so that they vibrate → glottis gets smaller
when arytenoid cartilage moves, vocal chords follow
Cricoid cartilage: forms complete ring around the lower portion of the larynx
strong
Thyroid cartilage: Adam’s Apple
anterior surface of larynx
moves up/down when you swallow
Trachea: macroscopic tube (1” diameter)
Annular ligaments: pink rings, allow trachea to move
Tracheal cartilage: cartilage rings with ligaments in between
prevent things from collapsing (rigid hyaline cartilage)
only cover from the front, spine protects it from the back
Trachealis muscle: constrict and relax airway
ex/ asthma, can spasm → get tighter
Carina: area of split of trachea
Primary/main bronchi →lobar/secondary bronchi → segmental/tertiary bronchi
Lobar bronchi → smaller branches (30-40 divisions)
each time the bronchus splits, it gives off 2 branches that are much smaller than it was
Terminal bronchioles → Respiratory bronchioles → Alveolar sacs & alveoli
terminal bronchioles: smallest airway in the body that doesn’t directly have alveoli attached to it
respiratory bronchioles: alveoli are attached to it
alveolar sacs & alveoli: smallest part of airways
Asthma: rapid onset inflammation in the respiratory mucosa
Respiratory mucosa is in all airways except the smallest 3
Inflamed respiratory mucosa → muscle contraction & cells get bigger → airways get smaller
People with chronic asthma have an enlarged epithelium and increased mucus production
Untreated asthma → scar tissue
Asthma is more complex than bronchospasm
can’t treat all symptoms of asthma with an inhaler
Inhaler treats bronchospasm component of asthma
anti-inflammatory drugs, drugs that help to break up excess mucus, or reduce mucus secretion (steroidal anti-inflammatories)
2 inhalers: 1 rescue inhaler (albuterol or ventolin) + 1 maintenance inhaler (inhaled corticosteroid → reduce chronic inflammation in patient’s airways with asthma, ex/ Q-var)
Respiratory bronchioles
terminal bronchi (no alveoli) → respiratory bronchi (alveoli)
external G-force (centrifugal force) because of inertia and gravity →affects flow of blood
sharp turn → blood in the brain goes to the rest of the body
no blood in the brain → sleep
no blood in the brain for a long time → die
Valsalva Maneuver: close glottis so air can’t get in or out, tighten abs
increase pressure in thoracic cavity
push on lungs, heart, abdominal cavity
squishing vein, not arteries, in thoracic cavity (superior and inferior vena cava that return blood to the heart)
keeps blood in the brain for a longer time (usually bad, but good for pilots) and maintain pressure → stay conscious
Oral cavity: mouth
Gingivae: stratified squamous epithelium
Vestibule
Oral Mucosa:
~40 layers of stratified squamous epithelium: to handle the stress of the mouth
large basement membrane of connective tissue
Teeth
Enamel: prevents microorganisms in mouth from entering teeth
Crown: part of the tooth exposed in the mouth
Dentin: works like compact bone, has osteons, canals, etc.
Pulp cavity: hollow space at the center of the tooth, contains blood vessels and nerves
the nutrition that keeps the tooth alive comes from here
Neck: region covered by the gums but outside the bone
Root: where bones comes together
Root canal: hollow tube that allows blood vessels and nerves to enter tooth from the jaw
the way that nutrition gets to tooth
Teeth Organization (Medial to Lateral; ~32 teeth)
Central Incisor & Lateral Incisor
4 on top, 4 on bottom
big, flat teeth with single surface (chopping surface) to cut pieces off of food and to bite
Cuspid (canine)
2 on top, 2 on bottom
1 sharp point
hold onto prey (large) → evolution to smaller because not grabbing onto animals with our teeth
First premolar (bicuspid) & Second premolar (bicuspid)
4 on top, 4 on bottom
2 sharp points, flat surface between them
grate and grind food
First molar & Second Molar & Third Molar
6 on top, 6 on bottom
break food into smaller bits
Third Molar
Wisdom teeth
usually removed because of crowding → causing pain
Why? Theories:
dentistry is relatively new; 150 years ago, people didn’t brush their teeth → common for ancestors to lose teeth, especially when young → extra set that come in when teen (3rd molar is backup if tooth lost in childhood)
aesthetic → attractive evolutionarily (smaller jaws)
3rd molar doesn’t fit anymore
Muscles of Mastication
Temporalis: closer of jaw
Masseter: closer of jaw
Lateral pterygoid: protrude jaw, move jaw side to side
Medial pterygoid: protrude jaw, move jaw side to side
Salivary glands
Saliva: wettend mouth, makes food stick together, easier to chew
plays a role in mechanical and chemical digestion
Amylase: digestive enzyme in saliva that breaks down complex carbs and starches into simple sugars that are easier to absorb
Parotid gland: by the ear
Submandibular gland
Sublingual gland: below tongue, when speaking and spit
Chewing - mechanical digeston prepares food for the stomach
Tongue and taste buds
Papillae: bumps on the tongue; surface structures that protect the taste buds
surrounded by deep groove where taste buds exist
Taste buds: nerve endings close to tongue
Gustatory epithelial cells & gustatory hairs: bind to food and stimulate the neuron to brain where the taste is perceived
Tastebuds and hairs under the surface for their protection
Taste pore: the only way for dood to access the taste bud and bind to gustatory hairs
Stratified squamous epithelium of tongue: heals fastest, lots of layers, hard to damage reproductive/dividing cells
it is TRUE that there are parts of the tongue are more sensitive to certain tastes BUT they are not exclusive
all taste buds can taste each taste, but it is just more sensitive in certain areas
Palate, Uvula, Pharynx
Palate: roof of the mouth, separates oral and nasal cavity
2 parts: hard, soft
Uvula: exhibits characteristics of both the oral mucosa on the bottom and the respiratory mucosa on the top; dangles in the back of the throat
bottom - stratified squamous epithelium
top - pseudostratified columnar epithelium with cilia
Pharynx: tube that connects nose, mouth, and throat
Esophagus
relies on muscle contractions (peristalsis) to move food down
down through the throat, past the thorax, down into the abdomen
sphincter: collection of smooth muscles that completely close off the tube
Upper esophageal sphincter: back of the throat
Lower esophageal sphincter/cardiac sphincter: where the stomach and the esophagus meet
esophagus and the heart are touching→ when people have reflux, they think it is a heart attack
Histology
mucosa epithelium - stratified squamous epithelium
lamina propria - connective tissue
muscularis mucosa - smooth muscle layer that wraps around lamina propria
submucosa - blood vessels, nerves
muscularis externa - where peristalsis happens → closes off esophagus → thicker at the sphincter
adventitia/cirrosa: outer edge
Stomach
inlet - esophagus
fundus: part of hollow organ farthest from the outlet
cardia: where food enters, adjacent to the esophagus
body: largest hollow portion of the stomach
antrum: narrowing portion of the stomach
pylorus: outlet
pyloric sphincter: valve that limits food flow from the stomach to the duodenum of the small intestine
walls thicker because threy move smooth muscle
Stomach layers
Muscularis externa - move food around while digesting → mechanical digestion
Rugae of mucosa: wrinkles on inner surface of the stomach
designed to allow stretch
extra tissue is smushed together →eat a lot → flattens out and expands the stomach
Layers of stomach wall (inner to outer)
Superficial
Surface epithelium: lining of the stomach (simple columnar epithelium), a lot of secretions of acids & enzymes that break down proteins but also break down the stomach because the stomach is made of protein
a lot of mucus-secreting cells and goblet cells
Muscularis Externa
Deeper
Gastric pits (wavy, not smooth surface)
Gasric glands
most of secretion cells exist here
Mucous neck cells: goblet cells that move out mucus through the pit to line the stomach
Parietal cells: secrete HCl
Chief cells: secrete pepsinogen (inactive form of pepsin)
Deeper
pepsinogen interacts with HCl to become pepsin
pepsin: aggressive, active enzyme that breaks down proteins and makes it easier to digest and absorb
pepsinogen until acidic environment (safer so that the stomach is not digested)
entero-endocrine cell: regulates activity of other cells
send signals to neighboring cells to turn them on or off
Gastroesophageal Reflux Disease (GERD)
something in the stomach moves backwards into the esophagus (acids, enzumes, food)
chronic, on a regular basis, hard to manage
esophagus can’t protect its epithelial cells from acid
at the risk of damage, scarring, and perforation because of acid
2 parts
leaky sphincter
too much acid in the stomach (oversecretion)
treated by medications (proton pump inhibitors) to reduce the production of acid
Procedure:
Fundoplication: procedure where fundus is stretched and wrapped around the esophagus
tight, more pressure, reinforce sphincter (less leakiness)
too tight → hard to swallow and move food down → reduced vomiting even when needed
permanent procedure
where absorption happens
Small intestines
small diameter (same as the thumb) but long (>20 ft)
Organization
Duodenum
pyloric sphincter to duodenum
Jejunum
Ileum
enters large intestine
Function: absorption, increase surface area to get the most nutrition
Lacteal: lymphatic vessel that absorbs large fats from food through lymphatic system, processed, go back to blood
Circular folds: macroscopic folds in epithelial layer of walls of small intestine, increase surface area across same length
Blood capillary network: in each villus, carry nutrition absorbed to the rest of the body
Villi: velvet appearance (look like small fingers), increase surface area
Crypt lumen: on the surface of small intestine, deeper into the walls to increase surface area, intestinal crypt
Simple columnar epithelium also has microvilli on the surface to maximize absorption by increasing the surface area
Enterocyte: individual cells with microvilli that line the intestine
Goblet cells: secrete mucus
Celiac Disease: immune response/allergy to gluten (protein in wheat)
disease of the small intestine
How to fix: don’t eat gluten
Diagnosis: only with biopsy
gluten allergy → inflammation
gluten sensitivity →mild reaction
Generates chronic inflammation if eat gluten with allergy (diarrhea, upset stomach, permanent damage to villi)
Villi knocked down and replaced with fibrin (less absorption of nutrition)
Large Intestine - colon, large diameter (6-8 ft long)
dirtier environment than the small intestine
bacteria, etc.
Appendix: on the surface of the cecum
Cecum: large sac-like region that collects food
Ileum: where small intestine empties into the large intestine
Iliocecal valve: prevents bad environment from going to the small intestine (which could absorb bacteria or viruses) and prevent poop from going back
Ascending colon: goes up
Right colic (hepatic) flexure
Transverse colon
Left colic (splenic) flexure
Haustra: balloon, bubbly structures; folds to help with absorption by increasing surface area
farther apart than folds in small intestine
Descending colon: goes down
Sigmoid flexure
Sigmoid colon: looks like sigma
Rectum: last stop before poop leaves
Anus: where poop leaves the body
Structure of Large Intestine
consistency of food moving through the intestine changes
paste in the small intestine → dry in the large intestine because the large intestine absorbs water and electrolytes (thicker, harder, more solid)
has the potential to damage walls (villi can’t handle it)
Colonocyte
like an enterocyte but the colon
take water, electrolytes and move into the bloodstream
Colonic crypt: protects goblet cells (more in the colon because mucus provides lubrication for dry poop and protects walls)
Smooth surface, nothing sticking up into the lumen
Appendicitis
Appendix: likes to get inflamed
hollow pouch, can burst if inflamed
if burst, bad stuff in colon → abdominal cavity → blood →bloodstream →death
Appendix has a lot of immune cells
immune/lymphatic function
Sometimes, things get trapped in appendix, not moving for a long time → inflammation to try to move it out
when inflamed → appendix walls swell & appendix shuts off → whatever is trapped stays trapped → body sends WBCs → get bigger → swollen till it pops because no exit for excess fluid
Some success with antiinflammatories
Appendectomy done laparascopically (20-30 min procedure without anesthesia time)
Pooping
Rectum - continence
Rectal valves; poop is going fast, so it is slowed down with turns to passively keep poop from escaping too quickly
Sphincters: very strong external and internal anal sphincters
External anal sphincter: skeletal musle, control poop (continence)
Internal anal sphincter: smooth muscle, autonomic control
Pressure builds up, sphincter releases, feel sense of urgency
Spinal Cord Injury
Muscles and control of them are damaged → incontinence
Taught to trick body into going bathroom when they want to - bowel and bladder training program
Liver
largest organ by mass
dense with a lot of unique and homogenous cells
on the right side of the body
right lobe and left lobe on anterior side
caudate lobe (superior) and quadrate lobe (inferior) on posterior side
gallbladder posterior and inferior to liver, near quadrate lobe
lobes separated by ligaments and fissures
Hepatic Portal System
Liver: the first place absorbed food is procesed
Hepatic Vein: carries blood from the liver to the heart (not nutrient rich)
Hepatic Portal Vein: carries nutrient-rich blood from intestines to liver to drop off nutrients
Structure of liver
Hepatic lobule: octagon structures made up of hepatocytes
Hepatocytes: liver cells that function in digestion, processing of blood from intestines
Bile canaliculi: bile capillaries
Portal triad
bile duct
portal venule
come into each lobule at point of portal triad
portal arteriole
Blood from portal venule and portal arteriole → sinusoids carry blood through the walls of the lobule & dump blood into the central vein → hepatic vein → heart
Sinusoids: let blood come into close contact with hepatocytes → mix of arteriole blood (with O2) and venule blood (O2 poor blood, but nutrient rich) good for hepatocytes
mix →hepatocytes do enzymatic activity → reduce toxicity in blood
ex/ alcohol
neurotoxin
hepatocytes secrete alcohol dehydrogenase into blood in the presence of high BAC, deactivate it (will not damage nervous system badly)
ex/ tylenol
body views tylenol as bad, liver works hard to deactivate it →inflammation of liver → hepatitis → liver failure
Store sugar in liver
Blood with sugar → sinusoids → absorbed into hepatocytes → stored for later use
Proteins stored and taken in by the liver → turned into more useful protein through protein synthesis and remodelling (done inside sinusoids and hepatocytes)
Hepatocytes:
mess with proteins
store sugar
work to detoxify blood
secrete bile
Bile: digestive enzyme that helps break down fats (needs to go from liver to intestines- goes through bile ducts)
Bile cannaliculi (bile capillaries) carry fluid bile into larger bile duct → leave liver → go down into intestines
Extrahepatic bile duct anatomy
right hepatic duct & low hepatic duct carry bile as it leaves the liver → common hepatic duct (merge L +R)
gallbladder: storage space for excess bile (if not used)
high fat diet → fat stored in liver (hepatocytes) → get bigger (swell) →liver gets bigger → harder for blood to flow through, regulation, filtration → liver function decreases
Cirrhosis: scarring of the liver
chronic inflammation
ex/ alcohol, hepatitis A, B, C
leads to inflammation →scarring
cirrhosis not reversible
Ascites: massive accumulation of fluid inside abdominal cavity, secondary to cirrhosis
coming from blood that cannot flow through the liver anymore
weekly drain procedure
BP low, dehydrated, electrolyte balance bad, blood volume low
TREAT:
liver transplant
can survive outside the body for a while BUT prone to rejection
can do a part of the liver because it grows (can use a living donor)
If really severe, use whole liver from deceased patient
hardened pieces of bile
break down → send immune cells → inflammation → gallbladder must be removed
Why?
possibly dietary component (not eating enough fats)
If small stones leave and get trapped in bile duct, BAD THINGS (life-threatening)
Organization
tucked under liver and stomach
Hepatopancreatic duct/ampulla (short duct)
Acinar cells: secrete enzymes to break down proteins to digest
Pancreatic islets: endocrine (release insulin and glucagon)
Most people have 1 pancreatic duct
some people have accessory pancreatic duct
If gall stone stuck in duct, BAD (block flow and cause inflammation, block enzymes →pancreatitis)
posterior to lower ribs to protect kidneys
Retroperitoneal space:
retro: posterior
peritoneum: connective tissue that lines abdominal cavity
surrounded by fat and connective tissue
Structure of kidneys
Renal cortex: outer edge
Renal medulla: inner edge
Major calyx: tubes collecting urine
Papilla of pyramid: pointy part of pyramid
Renal pelvis: mini bladder, storage for urine within kidney until flowing into ureter
Minor calyx
Ureter
Renal Pyramid in renal medulla
Renal column
Renal hilum (dent)
Renal artery
Renal vein
Ureter
Nephron
majority of nephrons in cortex (outer edge)
cortical nephron: majority exists in cortext
juxtamedullary nephron: 50% medulla, 50% cortex, larger loop of Henle
vasa recta: specialized peritubular capillaries that follow the loop
Glomerular filtration:
afferent arteriole
glomerular capsule: tissue structure that surrounds capillaries
glomerulus: site of filtration (passive process where blood flows into glomerulus → glomerular capillaries (squiggles) → very leaky, selective filtration → only in glomerulus (passive)
efferent arteriole
proximal convoluted tubule
peritubular capillaries
loop of Henle
nephron loop
distal convoluted tubule
collecting tubule
bladder → out of body
Reabsorption - from tubule back to blood capillaries
Secretion - from blood capillaries to tubules
3 parts of tubules:
proximal tubule, distal tubule, loop of henle
reabsorption and secretion → controlled processes done between blood vessels and tubules
JOB of the kidneys: make sure that there isn’t too much waste to help make sure that the volume of blood is balanced and that there is the right amount of electrolytes hanging out in your blood at any given time
ability of kindeys to filter blood (remove things you don’t need and keep stuff you do)
Juxtaglomerular Apparatus
Afferent Arteriole → glomerular capillaries → efferent arteriole
distal convoluted tubule runs right next to afferent and efferent arterioles just before emptying into collecting duct
fluid going through is urine
Macula densa: detects quality of urine, senses how concentrated urine is (salts, water, etc.) & makes changes to future urine based on what it detects
Extraglomerular mesangial cells: like smooth muscle, pinch down on afferent arteriole and make it harder for blood to get into the glomerular capillaries →less blood → less filtration → less pee → good thing during dehydration
Granular cells: secrete renin hormone
in renin-angiotensin pathway
renin released → converted eventually to angiotensin → vasoconstricts → increase BP
renin released when BP is low (blood volume low)
Podocytes: work to restrict how much filtration occurs
capillaries leaky
podocytes wrap themselves around capillaries in glomerulus and can increase/decrease how leaky it is
areas of capillary covered by podocyte don’t leak, except in areas with filtration slits (which open/close for more/less filtration to occur)
Urine is primarily composed of water and electrolytes
Has other substances that the body doesn’t like
kidneys take waste products and move them out of blood (ex/ urea is a neurotoxin, causes loss of control over muscles, hallucinations, etc.)
Diabetes and kidneys
Early symptom →peeing a lot →why?
diabetes → abnormally elevated sugar in blood → inflammation of blood vessel walls → scarring, swelling, plaques forming, bad blood flow →high pressure in capillaries, leakier capillaries (glomerular capillaries) → pee a lot
Increased pressure in capillaries becomes chronic
pressure in kidneys → more fluid and large things leaking out of capillaries (RBCs, large proteins → damage to glomerulus)
makes capillaries damaged faster → scarred → closed off → blood can’t flow in anymore → glomerulus can’t balance blood, filter blood, regulate BP → die fast because of kidney failure
How to fix:
keep blood sugar levels lower
reduce inflammation, reduce leakiness, prevent irreversible damage
If not fixed asap,
transplant (easy because people have 2 kidneys)
dialysis (usually indefinite OR bridge transplant)
put blood through kidney → filter blood, adjust blood volume, etc., machine is like a big kidney, keep them alive, 4-6 hrs a day 3x a week (difficult)
continuous renal replacement therapy: 0 function kidneys, will die without a transplant
22 hr/day dialysis
only off of dialysis when changing filtration
Kidney stones: accumulation of waste products and electrolytes
ex/ urea sits → crystals → solid stones, ex/ calcium
usually stuck in ureters and urethra, can be made up of several things
when stone blocks ureter, becomes an issue
kidney swelling → high pressure → can’t function → blood can’t flow in → kidney could be inflamed, damaged, or die → blood can’t be filtered
Procedure:
Lithotrypsy: use electromagnetic radiation to shock stones to explode inside of you, pee it out (painfully)
Ureters: connect kidneys to bladder
lumen, transitional epithelium (tissues that can stretch with large volumes of urine) makes up mucosa
Bladder: holds urine
2 ureteric orifices: holes where the uror empty into the bladder
opening to the urethra
triangle between ureteric origices and urethra: trigone
walls of bladder: really thick and have a lot of muscle in them (smooth muscle - detrusor muscle)
generating urination reflex is relaxation of sphincter and contraction of detrusor muscles
Internal urethral sphincter: smooth muscle (autonomic)
relaxation of this when bladder stretched → urgency to pee
External urethral sphincter: skeletal muscle (direct control)
Urogenital diaphragm/pelvic floor: skeletal muscle (direct control)
Continence: after spinal cord muscles spasm and stay there chronically → become tight → patients can’t pee → must use catheter and push up past spasmed muscles into the bladder to help drain the bladder on their own
transitional epithelium
Urethra: connect bladder to outside world
transitional epithelium
not peeing → want muscularis (muscles in wall of urethra) to contract to prevent UTI
UTI: bacterial/fungal/viral infection in urinary tract
why females higher rate of utis?
male penis is where urethra empties into the world
urethra in its own space → less UTIs
female urethra empties into shared space (vestibule) where the external urethral orifice is shared and closed off from the rest of the world by the labia (next to the vaginal orifice)
labia cover up both in vestibule
creates potential for cross-contamination → higher chance of UTIs