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Patho test 4

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Inflammation of pluera related to infection. Pain unilateral, lower lateral chest. Radiate to shoulder. Worse with chest movement.
Pleurisy
Fluid in pleural cavity. Transdate: CHF. Exudate: infection or infarction. Chlyothorax: lymph. Hemothorax: blood. Diminished breath sounds, dyspnea. Thoracentesis
Plueral effusion
Air in pleural cavity. Spontaneous: blister ruptures. c neg. pressure air leaks from alveoli to cavity. 2nd diseases, asthma, tb, pneumothorax, Cystfib, CA. Traumatic. Tension: air can enter but not leave, collapse lungs, affect vena cava and heart. Decr
Pneumothorax
Collapse of avleoli, shunting (blood flow gets not oxygen. Prim- Newborn 2nd, airway obstruction (muc plug) lung compression(tumor, pleural effusion), or loss of surfactant
Atelectasis
Limit expiratiory flow.
Narrowing broncial tree- inflammation histamine
Obstructive Airway Disease
Chronic inflammation Disorder. Pri- genetic. Airway obstruction- wheezing, breathlessness, cheast tightness, cough worse at night. Acute: Bronchoconstriction-chem med. mast cells. Late: Epithelial edema and injury, change musocilliary fuction and reduce
Asthma
Genetic, respiratory infection, excersize induced.
Treat: bronchodilator antiinflammatory agents, corticosteroid. Sever asthma (status asthmaticus) mechanical ventilation.
Asthma-causes
Obstruction of airflow not fully reversible. Hard to expirate. Heredity, asthma, smoking. Inflammation and fibrosis, hypertrophy submucosal, hypersecretion of mucus, loss of elastic lung fibers and alveolar tissue.
COPD Characteristics
Distruption of elastic fibers, loss of elastic recoil, enlargement of air space.
Destroy alveolar walls and capillary beds.
Causes: inherit, smoking
COPD Emphysema
Inflammation of airways. Enlarge, increase # mucous cells, hyperplasia of submucosal glands, increased mucous secretion
Causes: Smoking, irritant, and recurrent infection.
COPD Chronic Bronchitis
Permenant dilation of the bronci caused by destruction of muscle and elastic tissues. Usually bacterial infection.
Presentation: foul-smellign, purulent sputum or hemoptysis.
Causes: Infection and Inflammation.
COPD Bronchiectasis
Diagnosis: Decreased vital capacity and forced expiratory volume bec. hard to inspire hard to expire. Increased total lung capacity and residual volume because cant blow off co2.
Treatment: Bronchodilators
Low o2 flow, high o2 flow supress vent
COPD- Dignosis and treatment
Resp, disease in children. Causes: autosomal recessive multisystem disorder- defect in the regulation chloride ions. Dehydrated secretions-mucous accumulationm risk of infect and pneumonia.
Tx: mucolytic agents
Cystic Fibrosis
Inflam, fibrotic changes in interstitum or interavleolar septa- stiff/noncompliant lung.
Inspiration phase of longer.
Types: Occupational, druginduced, immunological(sarcodosis)
Interstitial Lung Diseases
PNEUMOCONIOSIS: inhalation of inorganic dusts
HYPERSENSITIVITY: organic dust
OCCUPATIONAL LUNG DISEASES
Mulitsystemic disease affects lungs and intrathoracic lymph nodes.
SARCOIDOSIS
A blood boren substance(blood clot,fat,air amnoitic fluid) lodges in a brabch of the pulmonary artery obstructs blood flow and increases dead space.
Cause: DVT
Cough with blood streaked sputum
PULMONARY EMBOLISM
elevation in left artial pressure( so pulmonary has to push hard to get through. Increased pulmonary blood flow, or increased pulmonary vascular resistance.
Patho: endothelial damage, coagulation abn. intimal fibrosis--obstruction of pulmonary arter
PULMONARY HYPERTENSION
Causes: aspiration of gastric content, trauma, sepsis, acute pancreatitis, hematologic disorders.
Patho: Increased alveolar-capillary membreane permeability, permits fluid, plasma proteins and blood cells into interstitium---decreased surfactant--hy
ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)
Lungs fail to oxygenate the blood adequately. Causes: impared resp.center, airway obstruction, paralysis.
Characteristics: Hypoventilation: depression of resp. center. due to drug effects, ect.
Impaired diffusion:o2 unable to diffuse from avleo
RESPIRATORY FAILURE
Virus infection of the upper respiratory tract.self Limited and last about 7 days.Presentation: excessive production of nasal secretion and tearing of the eyes,
headache, malaise, chills, fever, and exhaustion Spreading of the disease:contact.The mo
Common Cold
inflammation of the nasal mucosa and sinusitis by virus or bacteria. Acute: <4 weeks – facial pain, headache (sinusitis head usually exaggerated by
bending, coughing, and sneezing), purulent nasal drainage, decreased sense of
smell and fev
Rhinosinusitis
acute viral infection of the upper respiratory tract. Type A is able to infect multiple species and frequently mutate and develop new subtype. Complications: uncomplicated rhinotracheitis, viral pneumonia, bacteria infection
after viral infection. P
Influenza
inflammation of the parenchymal structures of the lung. It is classified into typical (bacterial) or atypical (viral or mycoplasmal. Another classification is community-acquired pneumonia and hospital-acquired
pneumonia
Pneumonia
Pneumococcal Pneumonia: it is caused by S. pneumoniae, which is a grampositive
diplococcus. It is the most common cause of community-acquired
pneumonia.Treatment: antibiotic
Community-Acquired Pneumonia
caused by Legionella pneumonphila, a gram-negative rod. dry cough, disturbance of central
nervous system, diarrhea
Legionnaire
mycoplasmas are small free-living agents
having characteristics of virus and bacteria. Dry, hacking and nonproductive
cough.
Mycoplasma and viral pneumonia:
lower respiratory tract infection. Risk factors: persons requiring mechanical ventilation such as endotracheal tube
intubation, tracheostomy, immunosuppressive, or chronic lung disease. bacteria: Pseudomonas aeruginosa, enterobacter species,
Es
Hospital-Acquired Pneumonia
mycobacterium tuberculosis. It retain red dye in
acid fast staining and is also called acid fast bacilli. air borne disease spread crowed. bacilli are aerobic, infect the upper lob or upper part of lower
lobe of the lung
Tuberculosis
Person with first contact. bacilli entered the lung, it engulfed by macrophage. The bacilli drain along the lymphatic system and formed the
caseous granulomas. The Ghon’s focus and the caseous granulomas is called
Ghon’s complex. erode a bl
Primary Tuberculosis
reinfection or reactivation of a previously healed primary lesion. productive with purulent and
blood tinged sputum.
Secondary Tuberculosis
The organism is usually in the soil. antifungal therapy such as Amphotericin B
Fungal Infection
fever, cough, night sweats, weight loss. May spread to mini
Histoplasmosis:
fever, cough, pleuritis pain, arthritis without effusion, erythema
nodosum. May spread to other organs such as liver and spleen, skin and mininges
Coccidioidomycosis:
May spread to
skin, bone, or prostate
Blastomycosis
Most lung cancer arise from the bronchial epithelium. Bronchogenic carcinoma:aggressive, locally invasive, and widely metastatic tumor.
Lung cancer
small round to oval cells grow in clusters. It has strongest
association with smoking. It is highly malignant, tends to infiltrate early in the
course, and rarely resectable. One half of person die with 12 to 15 weeks.
Small cell lung cancer:
it is most common in men and is closely related to
smoking. It originate in the central bronchi and spread into major bronchi and hilar
lymph nodes
Squamous cell carcinoma:
It is most common in non-smoking women. It originate in more
peripheral lung tissue such as bronchiolar or alveolar tissues
Adenocarcinoma:
it is highly anaplastic and occurs in more peripheral areas of the
lung. It has a poor prognosis
Large cell cancer:

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