Asthma, bronchitis, COPD, Pneumonia

Asthma main issue
airway reaction (inflammation) triggered by events it normally would not react to

asthma pathology
IgE antigen recognition
mast cell degranulation
bronchial smooth muscle constriction
increased mucous secretion and mucosal edema

classic asthma findings
bronchoconstriction, wheezing, coughing, dyspnea and chest tightness
exp. wheezing most common

1st line treatment of asthma
eliminate potential environmental irritants

Types of meds in asthma
corticosteriods and bronchodilators
leukotriene modifiers and mast cell stabilizers

Short acting bronchodilators
proventil, ventolin, alupent, terbutaline, albuterol

Long acting bronchodilators
salmeterol, formoterol, theophylline

Very important patient education in asthma
use of peak flow meter, written asthma plan, knowledge of process, when to take action, and environmental control.

inhaled preferred, (budesonide, fluticasone, mometasone, beclomethasone), short term oral use only when necessary

ihnhaled corticosteroid administration
use spacer, rinse mouth, good oral hygiene

cromolyn sodium
useful in exercise-induced asthma (not for acute symptoms)

leukotriene modifiers
decrease mucous, smooth muscle contractions, permeability
use with an inhaled corticosteroid.

theophylline “the dirty drug”
not commonly prescribed any longer due to narrow theraputic index and wide absorption range
has a massive side effect profile

inhaled anticholenergics
ipratropium bromide- relieves acute bronchospasm, decreases vagal tone, decreases mucous secretion

(xolair) prevents IgE from binding to mast cells. Very expensive, only for patients that have failed other treatment.

5 things to do in COPD
1. stop smoking
2. eliminate irritants
3. flu shot yearly
4. pneumonia vaccine as indicated
5. symptomatic therapy

Preferred meds in COPD
long acting beta agonists and anticholenergics

when to give ABX in COPD
purulent sputum (or change in sputum), use bactrim or tetracycline for 10-14 day course

guaifenesin, increases resp. tract fluids so mucous is thinner and less likely to adhere.

Cough in COPD
only suppress with anti-tussives if serious nonproductive (use benzonatate)

oral agents are systemically distributed, so a nasal agent is better, as they are locally absorbed and provide immediate relief

PaCO2 over 44mmHg (usu. from hypoventilation) (not blowing off enough CO2)

PaCO2 under 36mmHg (usu. from hyperventilation) (blowing off too much PaCO2)

chronic cough
cough more than 3 weeks

pleural pain
as a result of infection or inflammation of the parietal pleura

persistent, abnormal dilation of the bronchi: can be cylindrical (which is reversible and seen after pneumonia), or saccular, varicose. Hemoptysis occurs.
primary symptom is chronic productive cough (will have foul odor if not on ABX).
Clubbing of fingers common

inflammation of the small airways/bronchioles (common in children). Diffuse, can be from toxic gas inhalation.

s/s bronchiolitis
Increased rr, marked use of accessory muscles, low grade fever, dry NP cough, hyperinflated chest.
Can lead to pulmonary edema.

bronchiolitis obliterans
late-stage fibrotic process that occludes airways and causes perm. scarring of the lungs. Common after lung transplants.

Pulmonary fibrosis
excessive amount of connective tissue in the lungs which decreases compliance.

flail chest
cardinal sign deviated trachea. Pain, sob, and unequal chest expansion

transudative effusion
watery fluid from the capillaries as a result of increased intravascular hydrostatic pressure or decreased capillary hydrostatic pressure (CHF, liver/kidney disease)

exudative effusion
less watery, more WBC and plasma proteins, occurs d/t inflammation, infection or malignancy

pus in pleural space
can lead to perm. lung damage d/t compartmentalizing of the effected areas (cavatation)

changes in the lungs from inhaling inorganic particles
asbestos, talc, clay, cement, coal, silica

allergic alveolitis
ihalation of organic particles like grain, silage, bird droppings/feathers, wood dust, etc. triggers IgG immune response, granuloma formation is common. Can lead to pulmonary fibrosis.

ARDS pathology
acute lung inflammation and diffuse alveocapillary injury (to pulmonary endothelium). Inflammation and platelet activation, surfactant inactivation. Decreased compliance leads to rapid shallow breathing, resp. alkalosis, unresponsive hypoxemia.

ARDS phase 1
Exudative stage, excessive accumulation in alveoli

ARDS phase 2
Fibroproliferative stage, connective tissue proliferates in response

ARDS phase 3
Resolution, recovery stage. Pts might have cough, exercise intolerance, fatigue and anxiety.

Cardinal sign in ARDS
“batwing” consolidation on CXR

Treatment of ARDS
ICU, mech. vent, Oxygen, meds. Supportive

Obstructive pulmonary diseases
primarily worse with expiration (cannot expire enough air to move mucous plug, also d/t decreased elasticity of the alveolar walls)

Dx of chronic bronchitis
productive cough for 3months/yr for at least 2 years.
increased mucous production of thicker mucous
cilliary malfunction

pem. enlargement of the gas-exchanging airways (acini), along with the destruction of alveolar walls WITHOUT OBVIOUS FIBROSIS

centriacinar- destruction is in upper lobe of lung, associated with smoking.
panacinar- entire acinus destruction, more sporadic, older population and alpha1-antitrypsin deficiency.

pneumococcal pneumoniae
most common bacterial pneumonia. Alveoli fill (consolidation), RBC (red hepatization), fibrin deposition (grey hepatization), resolution.

acute bronchitis
often follows viral illness, no lung consolidation like in pneumonia

Lip cancer
exophytic- starts at the border (lower most comon)

Lung cancer
non-small cell most common. Squamous mets late, adenocarcinoma mets early. Large cell is undiffernetiated with rapid growth.
Small cell- excessive hormone secretion is indicated in 40% of cases. Mets early. Strongly associated with smoking.

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