Pathophysiology

1. Maximal voluntary Ventilation MVV (max. amount of air that can be breathed): ( Does not change with diseases ??)
2. Forced vital capacity FCV (full inspiration and forcefull expiration plottet against time): Obstruction lowers it
3. Forced expiratory volume FEV (Expiratory volume that can be achieved within a given time): (does not change ??)
4. FEV1.0 (Volue that can be expired in 1 sec): Percentage FEV1.0/FVC Obstructive is lower. Restrictrive not necessary lower but FVC is reduced
5. Forced inspiratory vital flow FIF (rapid maximal inspiration): used to determine respiratory dysfunction (inspiration needs more effort than expiration)

Inflammation of functional structures of lungs like alveoli and bronchioles

Etiology: smokin (damage to cilia), diabetes, viral infections, chronic bronchitis, or loss of cough reflex

Pathophysiology: Bacterial infection in alveoily that causes inflammation and fluid in alveoil. Lung not sterile anymore (usually gets filtered by cilia and moved to stomach).

Virus. Most important cause of upper respiratory tract infection. More contagious than bacterial respiratory tract infections. Transmission by inhalation of droplets (rather than touching) Incubation 1-4 days, contaigous 1 day before and up to 1-2 weeks of symptoms.

Three types of influenta can cause epidemics. Type A can infect multiple species -> more mutations and thus more contaigus in following years

Causes three types of infections: Uncomplicated upper respiratory infection, viral pneumonia, respiratory viral infection followed by bacterial infection.

Initially establishes upper airways. Virus kills mucus secreting, cilia and other endothelial cells (explains runny nose because extracellular fluids can escape)
If itsSpreads to lower respiratory tract it causes shedding of alveolar cells (due to bacterial adhesion on epithelial cells)

In early stages same as other viral infections. Fever, chills, muscle aching, headache, cough, sore throat and watery nasal discharge.

Treatment is designed to limit infection to upper respiratory tract. Rest, keep warm, manage fever and stay hidrated (antiviral drugs to treat influenza)

Most common risk factors: Smoking (increases with duration and intensity of smoking), industrial hazards, or familiar predisposition (genetic).

Most primary lung tumors arise from lung tissue. Classified into four major categories.

1. Small cell carcinoma and non small cell lung cancer: distinctive cell type, small round to oval shaped cells. grow in clusters, highly malignant and spread wide early. Brain metastase are common
2. Suamous cell lung cacinoma
3. Adenocarcinoma
4. Large cell carcinoma

Divided into those due to :
1. Involvement of lung and adjacent structures (irritations and obstruction of airways, cough, dyspnea, blood in spit)
2. Spread and metastasis
3. non-metastatic manifestatoins involving endocrine neurologic and connective tissue function.

Obstructive: Limits expiratory airflow, air can not get out

Restrictive: Decrease in total air volume lungs can hold, (air can not get in)

Vital capacity VC: Amount that can be in- and exhaled (VC =IRV +TV +ERV)

Inspiratory capacity IC: max. amount of air that can be inhaled (IC = IRV +VT)

Functional residual capacity FRC: Max amount of air that can be kept in lungs at normal expiration (FRC=ERV+RV)

Total lung capacity TLC: TLC= IRV + VT + ERV +RV

Type II alveolar cells synthesize pulmonary surfactant.

The substance decreases the surface tension in the alveoli and therefore allow easyer filling of the lungs (increase lung compliance). Has also a immune function in the lung and helps defending agains pathogens

Made out of phospholipids and proteins

Type II cells not available in premature babies (develop later), or insulin inhibits production of surfactant.
Without surfactant the large alveoli remain open, but the small ones collaps, making it hard to inhale. Airless portion of lungs becomes stiff and noncompliant. Barrier forms that prevents gas exchange -> hypoxemia (low concentration of O2 in blood)

Respiratory Distress Syndrom: common cause of respiratory disease in infants due to premature birth and immaturety in pulmonary development

A reversible airway disease caused by narowwing of the airways due to inflammation and increased secretion.

Chronic disease, that causes episodes of obstructions in airways

Smoking (or exposure to), family history (genetic), allergies age and environemental triggers are risk factors.
Cause is airway narrowing due to inflammation, broncospasm and increased secretion

Hyperresponsiveness to a variety of stimuly

T2-helper cells respond to allergenes and stimulate (via different other cells) chronic inflammatory response. A inflammatory cytokine form mast cells play a cruical role in initiation and amplification.

Activated mast cells release histamins -> allergic reaction -> contraction and swelling of airways -> Swollen mucosa glands secrete more mucus -> chronic inflammation can lead to airway remodeling
 

Often worse at nigh (assumably due to hormone levels that change at night)
Episodic Wheezing (whistling while breathing due to inflammation and narrowing of airways)
Feelings of chest tighntess
Asthmatic attack, airways becomes narrowed (bronchospasm, inflammation, mucus secretion)
Expiration becomes prolonged due to progressive airway obstruction (FEV1 and PEF are decreased)
Hyperinflation of lungs due to trapped air (Increased residual volume and decreased Forced Vital Capacity) -> Increased wotk of breathing that can cause dyspnea and fatigue
With progression hypoxia (too little O2) and hypercapnia (too much CO2)
Vascular resistance may increase as a result of hypoxemia (too little O2 in tissue)

Physical examination and family history but most prominent a spirometer.
 

FEV1/FVC decreases due to obstruction (FEV1 becomes smaller, FEV stays the same)

Relaxation techniques and controlled breathing can help

Drugs antiinflammatory or smooth muscle relaxer offer quick reliefe 

Chronic obstructive pulmonary disease.
Diseases that limit the expiratory airflow, characterized by recurrent obstruction of airways

Smokin is the most common cause. Less common is heredetary and other factors as asthma.

Inflammation and fibrosis (loss of elasticity) of the bronchal wall along with excess mucosal secretion -> obstruction in airflow and ventilation/perfusion mismatch -> loss of elasticity causes trapped in air and can lead to lung collaps

Emphysema: Enlargement of airspaces (hyperinflation of lungs) and destruction of lung tissue
Chronic obstructive bronchitis: increased mucus production, obstructon in airways

Increased work of breathing and decreased effectiveness, dyspnea, Expiratory phase is prolonged and wheezes can be heard.
Too low O2 and too high CO2 can develop (imbalance of ventilation and perfusion). Severe hypoxemia leads to vasoconstriction which further impairs gas exchange in lungs -> Hypotension which can lead to heart failure (right sided)

Spirometery and physical examination. FVC is increased, FEV1 is decreased -> FEV1/FVC is dicreased. RV and TLC are increased

To treat, stop smoking, and oxygen therapy. Bronchodilator  drugs

chronic respiratory disease in childern. It involces exocrine glands in the lining of the respiraitory (also GI and reproductive) tract. It causes a exvessive thick mucus that obstructs

It is cused by mutations in a single gene 

The CFTR gene (cystic fibrosis transmembrane conductance regulator), affects Cl- channels and makes them impermeable.  No reabsorption of NaCl in sweat. The impaired absorption of Na affects water content (less water) of mucous and makes it more sticky

Caused by accumulation of viscous mucous. Bacterias stick and lung infections occure, Chronic bronchitis

Lungs are stiff and hard to expand, despite normal functioning airways

Caused by inhalation of dust and particles that inure alveoli.

Stiff and non compliant lungs, thus makes it hard to inflate (decrease in all lung volumes), due to inflammation that leads to replacement of lung tissue with fibrous scar tissues. Some affect the distal alveoli others the proximal (causes an obstruction and does not really impact lung volumes)

FEV1/FVC is not affected (no problem with expiration) but the TLC is. 

Dyspnea (due to stiff lungs), decreased oxygenation, tachypnea (rapid breathing, compensates decreased tidal volume)

Develops when a blood borne substance blocks pulmonary artery and obsturcts bloodflow.

Age, obesity and physical incativity or high blood pressure, smoking increase chances. History of blood clothing.
Occur from deep vein thrombosis