anatomy midterm 2 (not including thursday lecture)

arteries

blood vessels that send blood away from the heart

artery layers

1. tunica intima
2. tunica media
3. tunica externa

tunica intima of artery

endothelium: simple squamous epithelium
subendothelial layer: loose connective tissue
internal elastic lamina: extends because of new blood

tunica media of artery

has a bunch of smooth muscle for vasodilation and vasoconstriction
- thickest layer

tunica externa of artery

loose connective tissue that contains many more veins, arteries, and nerves
- has some smooth muscle because we want to control blood flow

elastic artery

arteries that can handle the pressure difference by stretching
- smooths out blood flow
- closest to the heart
- when the ventricles contract, pressure will increase (when ventricles relax, pressure decreases)
- pulse: the contraction/pressure of the blood in arteries
- blood pressure: systolic/diastolic \= 120mmHg/80mmHg

aortic dissection and repair

the aorta can handle only a certain amount of pressure; negative effects occur at the endothelium (tunica intima)
- tear \= aorta dissection
- blood enters the hole/tear of the endothelium and separates the walls of the artery (tunica intima and media) - this is the dissection
- this separation creates a false lumen
- the false lumen can become larger than the actual artery

problems with aortic dissection

- the false lumen puts too much pressure/restricts blood flow through the aorta leading to less blood delivery
- the aortic rupture that can lead to death

aortic dissection preventions

it is hard to find symptoms; maybe chest pain and fatigue or seeing a pulse in your stomach

aneurysm

a collection of blood within the walls of the artery
- swelling of the artery

aortic dissection repair

when walls are compromised, we need to bypass the aneurysm
- creates a false aorta to bypass the damaged one

muscular artery

big, but not as big as elastic artery (aorta)
- lot of smooth muscles within walls
- carry/restrict blood into organs/limbs
- more muscle \= more control of the flow of blood to an organ/limb
- think tunica media/muscular layer

arterioles

smallest arteries leading into capillary beds
- control blood flow into capillary beds through vasoconstriction and vasodilation
- way less smooth muscles

capillaries

smallest blood vessels that interact with tissues
- can handle 1 RBC at a time
- allow for exchange of material
- selectively leaky by controlling size of intercellular clefts
- increase vascular permeability during inflammation - the interstitial spaces are larger so more fluid, RBCs, and chemicals can move in and out of capillaries

capillary layers

1. endothelial cells
2. intercellular cleft
3. basement membrane

endothelial cells of capillary

simple squamous epithelium

intercellular cleft of capillary

holes/gaps to allow for leaking and absorbing
- tight junctions of the endothelium lead to intercellular clefts

basement membrane of capillary

supporting cells

pulmonary edema and treatment

fluid in the lungs
- more blood volume in pulmonary veins (left side of heart fails to pump blood and leads to blood congestion)
- increase blood pressure of capillaries which make them leaky and release materials (fluid) into lungs
- the flow of blood from lungs to the heart is typically easy
- use diuretics (make you pee) to reduce blood pressure by releasing fluid in the blood and getting it filtered out as urine
- makes capillaries less leaky
- less blood \= less blood flow to heart

veins

takes blood towards heart
- less pressure than arteries
- less smooth muscles because we are not worried about blood flow from heart

vein layers

1. tunica intima
2. tunica media
3. tunica externa

tunica intima of vein

- endothelium
- subendothelium
valves: prevents blood from moving backward; less pressure in veins means blood flow is susceptible to back flow which leads to blood clots

tunica media of vein

smooth muscle; much smaller than arteries
- no elastic lamina

tunica externa of vein

contains more blood vessels and nerves
- walls of veins are less thick: usually round with blood flows in a living organism but when there is no blood supply, veins sort of collapse and is no longer circular (less smooth muscles)

vericose veins and treatment

when veins do not work properly
- blood stays in veins, stretches out walls of vein, causes more damage to valves
- no consistent blood flow
treatment: prevention - move around more, engage leg muscles to squirt blood back to heart
- can also kill varicose vein: close off a place where blood gets clotted with laser burn
- affects blood flow in legs
- edema: blood filling, imagine inflammation
- normal legs rely on skeletal muscle contraction to put pressure on veins to push blood to heart
- mostly occur in legs because they experience gravity and pressure

veins classification

largest vessels carrying volumes of low-pressure blood
- bigger volume of blood
- contain valves to prevent back flow
- thin walls
- run close to skeletal muscles to assist with blood flow to heart
- come out of organs, limbs, vena cava

venules classification

small vessels that exit capillary beds and merge to form veins
- small vessels with thin walls
- fragile, easily damaged and blood flow restricted
- baby veins, collect blood that leaves the capillary beds

location of lungs

in thoracic cavity, heart sits between two lungs

right lung

1. superior lobe
2. middle lobe
3. inferior lobe

left lung

1. superior lobe
2. inferior lobe
lobes are separated by fissures

lung layers

1. lungs
2. visceral pleura: deeper
3. pleural cavity: fluid-filled
4. parietal pleura: more superficial
5. thoracic wall
6. pleura \= serous membrane

alveolus

super small, hollow sacs that are close to capillaries to allow gases such as oxygen and carbon dioxide to diffuse (because simple squamous epithelium)

gas exchange

- movement of O2 into and CO2 out of blood is facilitated by passive diffusion (concentration gradients)
- blood entering lungs from body is O2 rich and CO2 deficient

cells that surround alveoli

1. Type I cell of alveolar wall
2. Type II (surfactant secreting) cell
3. macrophage
4. alveolar pores
5. capillary endothelium

Type I cell of alveolar wall

made of simple squamous epithelium
- external wall of alveolus

Type II (surfactant secreting) cell

create surfactant- a chemical that breaks up IMF of H2O to reduce surface tension
- a "detergent"
- cuboidal cells
- surfactant and surface tension
- surfactant: decreases surface tension and allow the alveoli to expand

macrophage

WBC that eat up the debris that makes it to the lungs

alveolar pores

how individual alveolus connects to their neighbor sacs

capillary endothelium

an alternating system of different cells to maintain a single layer of cells

blood flow and gas exchange

we live simple diffusion
- think of concentration gradients

pneumonia

infection of lungs; fluid collection in lungs
- can be caused by many things, but body will send WBC to alveoli
- increase capillary "leak" quality
- air cannot fill in the lungs so less gas exchange
- too much fluid in the lungs (jello-like consistency) \= scar tissue due to surface tension \= alveoli collapse
- potential complications: barotrauma (lung exploding)

ARDS (acute respiratory distress syndrome)

- acute \= fast, instantaneous
- causes low blood oxygen levels
- normal lung develops pneumonia-like symptoms in a matter of hours - days
- capillaries will be leakier to kill off whatever is in lungs
- send fluid to lungs but overcompensate
- fluid has WBC, TNF, IL, that is traveling in a thick, jelly substance
- thick substance makes alveoli to collapse because there are stronger IMFS bringing the walls of the alveoli together
- proteins are sent to inactivate type II cells and not enough surfactant can be produced
- WBC after working on the pathogen leads to scar tissue in the lungs because alveoli are "closed" shut and cannot expand

ARDS treatment

by external means
- collapsed alveoli \= collapsed lungs
- sometimes you can add extra O2, but not a lot of improvement
- recruitment: muscle help force air into our lungs
- put the patient on a ventilator
- barotrauma
- a patient can use a rotoprone bed

barotrauma

what is left behind after ARDS, alveoli rupture

rotoprone bed

a device that will alter the patient's positions so the surfactant can be repositioned in a way that it sits on a region of the lungs that are still healthy

COVID-19

- SARS-CoV2 binds to ACE-2 receptor in humans
- receptors are primarily found in the walls of the capillaries near alveoli
- cells die \= inflammatory response \= slow blood flow/stopped blood flow \= increase leakiness of capillaries \= shortness of breath/ARDS/pulmonary edema

mechanics of respiration

acute/muscular control
- pressure of the pleural cavity is lower than the lungs at all times (healthy conditions)
1. lungs at rest
2. inhalation (inspiration)
3. exhalation

lungs at rest

at atmospheric pressure (760 mmHg)
- intrapulmonic pressure is the same as atmospheric pressure
- intrapleural cavity is around 755 mmHg (cavity pressure is always lower than the pressure inside the lungs so the lungs are able to expand during inhalation)
- prevents alveoli from collapsing

inhalation (inspiration)

increase volume, decrease pressure
- "negative pressure breathing"
- lungs: about 758 mmHg
- cavity: 754 mmHg
- lungs increase in size and air passes in through a gradient difference (high to low, from the environment to internal)
- diaphragm contracts to move down (increases the thoracic cavity space)

exhalation (expiration)

decrease volume, increase pressure
- lungs: around 763 mmHg
- cavity: around 756 mmHg
- diaphragm is relaxed and decreases the thoracic cavity space

inhalation muscles

sternocleidomastoid muscle, external intercostal muscles, parasternal intercostals, diaphragm

exhalation muscles

internal intercostals, external abdominal oblique, internal abdominal oblique, transversus abdominis, rectus abdominis

quiet respiration

diaphragm is the primary muscle working
- accessory muscle of respiration: help increase the thoracic cavity to take in more air
- diaphragm is skeletal muscle and we have the ability to conscioiusly control its contractions

when diaphragm contracts

downward pulling \= increase in thoracic cavity and decrease in pressure

when diaphragm relaxes

thoracic cavity decreases, pressure comes back to about atmospheric

neurological control of lungs

- breathing is a passive process and comes from hypothalamus (subconscious action but can be controlled if really tried)
- autonomic: involuntary actions, like smooth muscles, have a mind of their own
- diaphragm is skeletal muscle and can be categorized as part of the autonomic and somatic nervous system
- "When do I breathe?" O2 in blood and muscles are low

pleural effusion

blood vessel leaks into pleural cavity
- fluid will increase the cavity and makes it hard for alveoli to stay open (will collapse) less air to the lungs

pneumothorax

want pressure of cavity to be lower than pressure of lung (too much air in pleural cavity)
- chest wound, poke a hole in pleural cavity will increase pressure of pleural cavity and make alveoli collapse
- on x-ray, lungs look black but with pneumothorax there is little grey

emergent chest tube replacement

draining out fluid in pleural cavity
- need to insert tubes to help with air delivery and drain the fluid out of cavity

upper respiratory tract

1. nose
2. mouth
3. throat

lower respiratory tract

1. trachea
2. bronchi
3. lungs

respiratory mucosa

good for adding moisture to airway
- line a majority of respiratory tract
- pseudostratified columnar epithelium
- have goblet cells to secrete mucus
- cilia is good at moving material trapped in mucus out of respiratory tract so it doesn't make it to alveoli

mucociliary action

- want to get rid of particles away from getting to the lungs
- push mucus out of body with movement by cilia

rhinitis

runny nose/inflamed respiratory mucosa in nasal cavity
- inflammation in mucus membrane of our nose
- will produce more mucus because more blood flow to the tissue, cilia will be moving faster
- body's response to pathogen in the airway-thus inflammatory response

rhinitis treatment

take decongestion meds: sudafed
- increase blood pressure
- reduces production of mucus
- vasoconstriction: to restrict blood flow so no more inflammation \= less leakiness of capillaries \= decrease in swelling
- watch out for too high blood pressure

nasal cavity

nose is primary structure for breathing

nares

single nose holes leads to vestibule
- external and internal

nasal cavity details

have turbinates
- warm, moist, and clean
- superior turbinate
- middle turbinate
- inferior turbinate

sinus

used to increase surface area, warm air, add moisture, similar purpose as turbinates

sinuses

1. frontal: forehead
2. sphenoid: bridge of nose
3. ethmoid: on top of sphenoid sinuses
4. maxillary sinus: cheeks, near nose

sinusitis

inflammation in the sinus (mucosal epithelium) \= goes hand in hand with rhinitis
- sinuses have small entry points: hard to get air in/out
- more mucus production \= more pressure on wall of sinus
- responsive for decongestion meds to open holes and release fluid

chronic sinusitis

always inflamed sinuses (vs. acute)
- leads to degrading sinus walls because of the biome that is made
- not responsive to meds
- treatment: surgically remove bone + tissue to get to the sinus and insert a balloon to open the sinus again

olfactory mucosa

smell, respiratory mucosa with nerve endings involved in smell
- looks similar to the respiratory mucosa
- olfactory receptor cells \= sensory neurons
- hair (cilia) sits at the lumen side to send signals to the brain
- hairs have different receptors \= different responses
- COVID does not affect receptor cells, rather the supporting (sustentacular cells): damage/die and affects receptor cells from functioning

pharynx

connecting tubes that connect food and air passage (connects nasal cavity to the larynx)
- nasopharynx
- oropharynx
- hypopharynx/laryngopharynx

tonsils

functions in immune response
- tonsils contain WBC to attack
- located in pharynx
- leaving behind tonsillectomy (remove our tonsils)

pharyngeal (adenoid) tonsil

back of the nose

palatine tonsil

either side of the uvula

lingual tonsil

back of the tongue

larynx

voice box
- connects pharynx of trachea

epligottis

elastic cartilage, a flap that covers the glottis (opening where larynx sits)
- covers trachea when we swallow food
- chamber that makes sounds

laryngitis

swelling of vocal fold together

glottis

only passageway for air
- closed: vibrations between the vocal folds/vocal ligament/vocal cord when talking
- opened: allow for more air to come through
- covered with cartilage (hyaline)
- cartilaginous shield/rings for larynx to keep airway open

arytenoid cartilage

what makes up our voice
- connect thyroid cartilage
- posterior
- hyoid bone: provide points of connections when swallowing food

thyroid cartilage

anterior
- laryngeal prominence (adam's apple): anterior
- anchor for vocal ligaments

cricoid cartilage

all around the trachea
- wraps all the way around the larynx

trachea

tube for air to go to lungs (carries air from larynx to bronchi)
- cartilage rings to keep the airway open - C shaped rings
- (hyaline) cartilage \= support
- annular ligament \= allows for movement
- the trachea + esophagus are super close to each other

bronchi

past the trachea (around the manubrium of the sternum) and it splits into the bronchi

subsequent branch of trachea

1. trachea
2. carina (intersection before branching)
3. main/primary bronchus
4. lobar/secondary bronchi: goes to each lung
5. segmental/tertiary bronchi
- a bunch of unnamed divisions later
- after the trachea, primary, secondary, and tertiary bronchi
6. terminal bronchiole: smallest airway WITHOUT alveoli directly attached to them
- still has respiratory mucosa
7. respiratory bronchioles: have alveoli on surfaces
- lack respiratory mucosa because now they want to be dry (not have surface tension)
8. alveolar sac: the grapes
- respiratory mucosa is all there except for these last 3 division (we want this to be dry)

bronchitis

inflamed bronchi
- fat epithelium, contraction of smooth muscle, more mucus, and a smaller lumen
- take some meds: bronchodilators (inhalers) or mucinex (for chest congestion, coughing)

respiratory bronchioles

terminal bronchiole branches to the respiratory bronchiole with alveoli

centripetal force

think about turning on curves on freeway,
G force is about 1 at rest

airway and blood flow consideration

adults have stronger hearts than children

valsalva maneuver

take air in and close your glottis to keep the air in
- trap air in lungs, tighten abs, increase pressure of thoracic cavity
- veins will be squeezed, blood in brain stays there and can't get back to heart
- train pilots to keep blood in brain and not be affected by G force

valsalva maneuver problem

a technique that starves the heart of blood - no blood to pump \= decrease blood pressure all over
- high blood pressure in brain but low pressure in whole body
- use for short term, too long \= pass out
- makes you poop, high thoracic pressure traps blood in brain and squeezes ab muscles

mouth

we can breathe through this but is mostly adapted to food
- oral mucosa moisture is provided to the food we eat
- cells reproduce constantly \= new cells push old cells out \= good healing

stratified squamous epithelium of mouth

layers for protection against abrasion with the basal membrane

basal membrane of mouth

connective tissue
- oral mucosa does not secrete mucus

major region of teeth

1. crown
2. neck
3. root

crown

fully exposed in the mouth

neck

a tooth that is covered by gingiva (gums)