Gas exchange by simple diffusion

External - at lungs

Internal - at tissues

• in the nasal cavities
• bony ridges
• increase surface area fir noisturizing and warming air
• Connects to paranasal sinuses

is one tonsil in the posterior nasal cavity (book)/nasopharynx (wiki), is the primary lymphatic tissue for breathing, has lymphocytes

Wiki calls it the pharyngeal tonsil

• from nasal cavity to larynx
• = throat
• has three parts:

1. nasopharynx
2. Oropharynx - uvula here; 2 palantine tonsils (can see); 2 lingual tonsils (cover base of tongue)
3. laryngopharynx

• Adam's apple here
• =voice box
• contains the vocal cords (ligaments) that sustends the glottis (opening)

• C shaped rings of cartilage hold it open
• contains cilia and goblet cells that secrete mucus (MUCOCILIARY ESCALATOR)

Primary - right and left, largest; cartilage rings continue

Secondary - one for each lobe (3 or right, 2 on left); cartilage rings continue

Tertiary - cartilage plates; very branched

• Pulmonary arteries (deoxygenated) travel along brochi
• Pulmonery arterioles around bronchioles
• Pulmonary capillaries surround alveoli, together form the respiratory membrane

holds lungs open

Created by tendancy of water molecules to cling to one another and form droplets.  Due to hydorgen bonding.

• lines the alveoli
• a lipoprotein that lowers surfact tension of fluid around each alveoli preventing their collapse
• Premature infants can lack this as in INFANT RESPIRATORY DISTRESS SYNDROME

from exercise, etc
uses accessroy mucles to increase size of thoracic cavity:

Erector spinae (back)

Pectoralis minor

Scalene (anterior neck)

Sternocleidomastoid (anterior neck)

= alveolar pressure

created by surface tension adhering peurae to thoracic wall.  When thoracic cavity is expanded, this decreases the pressure and draws in air until pressure equalizes with atmospheric pressure

• normally, expiration is totally passive and requires no muscles
• During exercise, singing, blowing, etc., uses internal intercostals and abdominals to create extra pressure forcing air out

• passive, no muscles
• Lungs simply recoil becasue of elastic nature
• diaphragm resumes it's normal dome shape
• lung space shrinks, increasing intrapulmonary pressure, pushing air out

• usually about 500 mL
• is the normal amount of air breathed in and out while relaxed

• is the maximum volume of air breated in and out
• = tidal volume + inspiratory reserve volume + expiratory reserve volume

• Is in the MEDULLA OBLONGATA; sends signals to the PHRENIC and INTERCOSTAL nerves
• Creates the basic respiratory pattern; without higher control, however, breathing is not totally normal, requires input from the Pons
• Responds directly from blood concentration of CO2 and H+ (not O2)

• Recieve O2 levels of blood and signal the primary respiratory center
• Located in carotid and aorta

• Breathing is irregular - sometimes, deep, sometimes shallow, sometimes apnea, etc.
• Due to respiratory contol occuring only from primary repirotory center which responds only to CO2,H+ (directly) and O2 concentrations (indirectly via carotid/aortic bodies)
• Breathing is continually adjusted
• "death rattle" from mucus build up.

3 ways:

1. ~10% as dissolved in plama and RBC cytoplasm
2. ~30% taken up by GLOBIN (protein portion of hemoglobin) forming CARBAMINOHEMOGLOBIN
3. ~60% combines with water and forms CARBONIC ACID (H₂CO₃) which dissociates in plasma into H+ and BICARBONATE (HCO₃^-); therefore, most CO2 is carried as bicarbonate.

Acidosis - pH is lowered from high H+ concentraions from insufficient respiration

Alkilosis - can be from hyperventilation; too many H+ ions are taken up, or too many CO2 is eliminated

Both conditions can be fatal

1. Acute Bronchitis - versus chronic from smoking, etc; usually is viral with secondary bacterial
2. Pneumonia - can be viral or bacterial and alveoli fill with thick fluid; often localized to lobule(s)
3. Pulmonary TB - creates capsules or tubercules

Decrease vital capacity and lung expansion, caused by Pulmonary Fibrosis, which can occur from a variety of reasons:

E.g. asbestos inhalation, Infant Respiratory Distress Syndrome (lack of surfactant and alveoli collapse), or idiopathic as in Sarcoidosis, etc.

Blockage of airflow requires extra time to ventilate

Asthma

COPD

• is an obstructive pulmonary disorder
• sensitivity to irritants
• causes smooth muscle of bronchioles to spasm
• Immune cells release chemicals causing spasm
• bronchial inflammation also

• A class of obstructive pulmonary disorders that are chronic
• Includes chronic bronchitis and emphysema

is a COPD

Are degenerative changes to bronchi from irritants (usually smoke); including loss of cilia and function; infections are more likely

 Emphysema IS 1 of 2 types of COPD (the other is chronic bronchitis).  Emphysema symptoms are below:

• Is a COPD
• often preceeded by chronic bronchitis
• alveoli are distended and damaged, reducing surface area for gas exchange
• Air is trapped in thoracic cavity, with typical chest ballooning and diaphragm flattening
• Elastic tissue breaks down
• Ability to exhale therfore compromised
• Residual volume increases
• CO2 increases from increased residual volume and reduced O2 exchange
• Because of reduced O2, the heart works extra hard and can be overworked
• O2 to brain reduced as well
• Treatments are drugs that dilate bronchi/ioles by relaxing smooth muscles of bronchioles; inhaled O2; surgery to remove the diseased portion so good tissue can regenerate

• Overall respiratory fitness decreases
• Are decreases in max breathing capacities; increases fatigue
• Ventilation in not as effective
• Intercostal muscles weaked and inelasticity of ribs causes refuced inspiratory volume
• less recoil from loss of elasticity reduced expiratory reserve volume
• Increases residual air from less effective exhalation
• Less efficient gas exchange b/c respitory membrane thickens
• Are less cilia and they are less effetive
• more diseases are prevalent
• Pneumonia and other pulmonary diseases are leading causes of death in elderly
• Rib cage calcifies so can;t expand as well and lung tissue becomes thicker and gas exchange diminishes

1. Fluid Balance - excess fluid is returned to circulation
2. Fat absorption - from the GI tract; delivered to blood by LACTEALS which are specialized lymph capillaries in interstitial villi
3. Defense - WBCs in lymph vessels/organs and blood and interstitial areas; fight foreign cells, dead/dying cells and precancerous or cancerous cells

• Largest lymphatic vessel that collects from below the thorax, left arm, left head and neck
• Emties in to LEFT SUBCLAVIAN VEIN

• Red bone marrow and thymus
• Where lymphocytes originate (marrow) and mature (marrow and thymus)

•  location of all blood stem cells
• Adults: sternum, vertebrae, ribs, skull, parts of pelvic girdle and proximal heads of humerus and femer
• Is where B lympocytes mature

• Where t-cells mature
• between trachea and sternum
• Is largest in children
• Produces hormone THYMOSIN which aids in t-cell maturity, etc.
• Without the thymus the body will not reject foreign antigens
• Necessary for recognition of self verses non self

• Locations where lymphocytes encounter and bind with antigens and proliferate to fight infection
• Spleen, lymph nodes, tonsils, peyer patches, appendix

• upper L abdominal cavity behind stomach
• compartamentalized with red and white pulp that surround venous sinuses and contains lymphocytes, macrophages to remove old and dead RBCs
• Red Pulp - filters blood
• White Pulp - concentrated lymphocytes that filter out bacteria
• largest lymph organ
• holds a reserve of blood in case of hemorrhagic shock while also recycling iron.^[3] 
• Recently, it has been found to contain in its reserve half of the body's monocytes within the red pulp.

• connective tissue encapsulates and compartamentalizes
• Each has B-cells and a sinus with macrophages
• Also have t-cells
• Tend to cluster in axilla, groin and neck

Have the same function as lymph nodes, but are not encapsulated.  Are the first to encounter pathogens through nose and mouth

1. Pharyngeal tonsil = adenoids; in the nasopharynx
2. Lingual tonsils - cover base of tongue
3. Palantine tonsils - back of oral cavity (can see)

1. BARRIERS TO ENTRY - physical and chemical; FIRST LINE OF DEFENSE; include skin, mucus membranes, cilitaed cells, sebaceous glands have chemicals to kill certain skin bacteria; sweat evaporates and leaves salts; sweat, tears and saliva have LYSOZYMES; saliva and urine flush; normal FLORA prevent other pathogenic bacteria from growing
2. INFLAMMATORY REACTION - caused by tissue damgae, produces redness, swelling, heat and pain; are 5 steps.
3. NATURAL KILLER CELLS - kills virus infected and tumopr cells by cell to cell contact.  Are large granular lymphocyes similar to lyphocytes, but have no specificity or memory
4. PROTECTIVE PROTEINS - COMPLEMENT SYSTEM - are proteings made by liver casuing cascade of chemical events, activating other proteings.  This is activated by pathogens.  E.g. INTERFERON is a protein produced by virus infected cells that interferes with virus relication.  Other compements can punch holes in walls of bacteria.
5. NON-SPECIFIC PHAGOCYTIC WBCs - neutrophils, eosonophils, basophils, monocyes and mast cells.

1. Chemicals like histamin from basophils cause capillary dilation and increases permeability of capillaries; Mast cells (similar to basophils) releases chemicals also; increased blood flow bringing WBCs
2. Increases capillary permeability allows fluids, proteings, clotting facts into tissues, causing swelling and pain (also from inflammatory chemicals)
3. Edema and clotting walls of area
4. Phagocytes, mostly neutrophils and monocytes, migrate.  They are amoeboid and can change shpae to squeexe through capillary walls.
5. Monocytes differentiate into macrophages (even larger) and can eat a lot of pathogens ~1:100; releases colony stimulateing factors that go through blood to red bone marrow stimulating production of WBCs, mainly neutrophils.  Pus are the dead macrophages, bacteria, tissue and WBCs.

IF ANTIGENS GET INTO BLOOD CAN THEN CAUSE A SPECIFIC IMMUNITY REACTION.

are for specific immunity and cancer cell destructiuon, are three types:

1. B - form antibodies against and neutralizes antigens (cell surface proteins) of foreign cells; "humoral immunity"
2. T - destroy's any foreign cell via cell-mediated immunity
3. Natural Killer Cells also cell-mediated immunity

=WBCs

are less amount than RBCs; unlike RBCs, can leave circulation into tissues, are two types: Granular and agranular.

are the most abundanct WBC, are the first to respond to infection, engulf pathogens by phagocytosis

Per Heberlein, they change the function of the offending cell.

• Type of leukemia where immature WBCs (lymphoblasts) are over produced.
• Is most common in childhood (another peak in old age)
• Cure rate is about 80%

• mature in the bone marrow (but is not why are "b" cells; is from "bursa" of the fabricius, an organ in chickens where these cells were first indentified)
• Give rise to PLASMA CELLS which produce antibodies
• There are millions of groups, or clones, of immature b-cells; each clone is preprogrammed to produce particular antibody to a specific antigen

• are the immunoglobulins
• Produced by plasma cells, which are differentiated b-cells
• Combine with and neutralize foreign antigens
• Antibody receptor forms lock-and-key with antigen
• Are secreted into blood, lynph, and other fluids

= Antibodies

= Most significant of the gamma globulin proteins of plasma

• identify and neutralize foreign objects, such as bacteria and viruses
• Antibodies are produced by a kind of white blood cell called a plasma cell, which is a differentiated B-cell (differentiation usually occurs in the lymph nodes).  B-Cells are a type of lymphocyte (T, B and NK cells).

• A class of proteins secreted by various types of cells, including helper t-cells
• Assists in immune response in numerous ways
• The INTERLEUKINS are a group of cytokine
• Also used as therapy for cancer or other immune defeciencies

• Allows t-cells to conduct cell mediated immunity by "presenting" the antigen to the t-cell.
• They are specialized macrophages that present antigen by linking the antigen to the protein MHC on it's membrane

• are proteins on membrane of APCs (present antigen to t-cell).
• In humans the MHC is HLA.

• the protein complex found on human APCs (present antigen to t-cell) responsible for binding pathogenic antigens and presenting to t-cells
• These are on all human cells, and there are over 50 types.  Each human has a unique combination, marking "self cells" so as not to be attacked.
• Are reponsbible for tissue rejections (histo=tissue)
• When the HLA protein binds with foreign antigen, the t-cell can "analyze" their differences and know whether there is a difference.

1. CYTOTOXIC T-CELLS = Tc = CD8 Leukocytes -- store PERFORIN which punches holes in membranes of foreign cells
2. HELPER T-CELLS = Th = CD4 Leukocytes -- secrete CYTOKINES which enhance response of other immune cells.  These are the targets of HIV

Production of antibodies either:

1. Naturally by formation of memory b/t-cells from past infection or
2. Artificially - by vaccination

1. IgE Mediated = "immediate allergic response" -- antibodies (IgEs) are attached to MAST CELLS and BASOPHILS.  Whenthe IgE attached to an allergen, the mast cells and basophils secrete histamine, etc.  Includes ANAPHYLACTIC SHOCK.
2. T-Cell Mediated = delayed response - from memory t-cells; happens at site of entry, e.g. TB skin test.  Also includes contact dermatitis, poison ivy, etc.

• Is an IgE mediated (fast) allergic reaction
• When allergen enters blood stream (bee stings, penacillin, etc)
• Sudden drop in BP from increased vessel dilation and capillary permeability (histamine)
• Epinephrine is given to delay reaction

• increased infections and disorders
• Thymus degenerates, decreased t-cells
• B-cells may not clone
• Increased autoimmunities because of decreased self differentiation
• Decresed vaccine response
• Increased cancer from decreased t-cells

K A D E

Can overdoese on these, unlike water soluble B and C

is a hematological disorder characterized by an abnormally low number of neutrophils, the most important type of white blood cell, in the blood. Neutrophils usually make up 50-70% of circulating white blood cells and serve as the primary defense against infections by destroying bacteria in the blood. Hence, patients with neutropenia are more susceptible to bacterial infections and, without prompt medical attention, the condition may become life-threatening (neutropenic sepsis).

Neutropenia can be acute or chronic depending on the duration of the illness. A patient has chronic neutropenia if the condition lasts for longer than 3 months. It is sometimes used interchangeably with the term leukopenia ("deficit in the number of white blood cells"), as neutrophils are the most abundant leukocytes, but neutropenia is more properly considered a subset of leukopenia as a whole.

Deeper breathing than usual, from panic attack, acidosis or purposefully.  Effects of numbness/tingling, lightheadhedness, dizineess, etc caused NOT by lack of O2, but by extra expulsion of CO2 which raising blood pH (more alkinline), therby causing reflexive arteriole constriction.