Exam 4- Pulmonary

Question 1

TB

Answer 1

Highly contagious and is transmitted from person-to-person in airborne droplets. TB is diagnosed by a positive tuberculin skin test (TST; purified protein derivative [PPD]), sputum culture, immunoassays, and chest radiographs.

Question 2

Normal aging changes

Answer 2

• Normal alterations include: (1) loss of elastic recoil, (2) stiffening of the chest wall, (3) changes in gas exchange, and (4) increases in flow resistance.
• These changes are gradual and usually without adverse consequences in healthy individuals.
• They are influenced by environmental and sociocultural factors, nutritional status, respiratory disease, body size, gender, and race.

Question 3

Asthma

Answer 3

Acute Asthmatic Responses. Inflammatory mediators are produced in asthma including histamine, prostaglandins and leukotrienes.

Question 4

Chronic bronchitis

Answer 4

Chronic Bronchitis is defined as hypersecretion of mucus and chronic productive cough that continues for at least 3 months of the year (usually the winter months) for at least 2 consecutive years.

Continual bronchial inflammation causes bronchial edema and increases the size and number of mucous glands and goblet cells in the airway epithelium. Thick, tenacious mucus is produced and cannot be cleared because of impaired ciliary function

Question 5

Emphysema

Answer 5

Destruction of alveoli through the breakdown of elastin within the septa. Expiration becomes difficult because loss of elastic recoil reduces the volume of air that can be expired passively and air is trapped in the lungs. Air trapping causes hyperexpansion of the chest (barrel chest), which puts the muscles of respiration at a mechanical disadvantage

Question 6

Early asthmatic response

Answer 6

antigen exposure to the bronchial mucosa activates the above mediators causing vasodilation, increased capillary permeability, mucosal edema, bronchial smooth muscle contraction (bronchospasm), and tenacious mucus secretion from mucosal goblet cells with narrowing of and obstruction to airway.

Question 7

Late asthmatic response

Answer 7

begins 4 to 8 hours after the early response. Hypoxemia further increases hyperventilation, causing Paco2 to decrease and pH to increase (respiratory alkalosis). With progressive obstruction of expiratory airflow, puts the respiratory muscles at a mechanical disadvantage. This leads to a fall in tidal volume with increasing CO2 retention and respiratory acidosis. Respiratory acidosis signals respiratory failure.

Question 8

Pnemoconiosis

Answer 8

Any change in the lung caused by inhalation of inorganic dust particles, usually occurs in the workplace.
The dusts of silica (silicosis), asbestos (asbestosis), and coal (black lung) most common causes.
NOT reversible and Treatment is usually palliative and focuses on preventing further exposure.

Question 9

Non small cell lung cancer

Answer 9

Nonproductive cough or hemoptysis is common. Chest pain is a late symptom associated with large tumors. These tumors can remain fairly well localized and tend not to metastasize until late in the course of the disease

Question 10

Small cell lung cancer

Answer 10

most common type of neuroendocrine lung tumors. This cell type has the strongest correlation with tobacco smoking. Because these tumors show a rapid rate of growth and tend to metastasize early and widely, this type of carcinoma has the worst prognosis of all lung cancers

Question 11

Pneumonia

Answer 11

Aspiration of oropharyngeal secretions is the most common route of lower respiratory tract infection; thus the nasopharynx and oropharynx constitute the first line of defense for most infectious agents. Another route of infection is through the inhalation of microorganisms that have been released into the air when an infected individual coughs, sneezes, or talks, or from aerosolized water, such as that from contaminated respiratory therapy equipment.

Clinical Manifestations: cough, dyspnea, fever, chills, malaise, and pleuritic chest pain. Physical examination may reveal signs of pulmonary consolidation, such as inspiratory crackles, increased tactile fremitus, egophony, and whispered pectoriloquy. Individuals also may demonstrate symptoms and signs of underlying systemic disease or sepsis

Question 12

PE

Answer 12

Aveolar dead space causing hypoxemia due to absent blood flow to a lung segment causes a ventilation-perfusion mismatch (increased dead space with decreased production of surfactant). Wide spread vasoconstriction impeding blood flow. Pulmonary embolus is the end result of a deep vein thrombosis or blood clot elsewhere in the body.

Chest x-ray findings are nonspecific in PE and often can be normal for the first 24 hours until atelectasis occurs in the lung.
serum d-dimer level measures a product of thrombus degradation by the fibrinolytic system and, if normal, makes the presence of a PE highly unlikely.
single or multidetector spiral CT arteriography. This highly sensitive and specific test has replaced the radionucleotide ventilation-perfusion scan in most hospitals.

Question 13

ARDS

Answer 13

Disorders that result in ARDS cause acute injury to the alveolocapillary membrane producing massive pulmonary inflammation, increased capillary permeability, severe pulmonary edema as a result of bronchioles filling with fluid, shunting, mismatch, and hypoxemia. The clinical manifestations of ARDS are progressive as follows:
Dyspnea and hypoxemia with poor response to oxygen supplementation
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Hyperventilation and respiratory alkalosis
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Decreased tissue perfusion, metabolic acidosis, and organ dysfunction
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Increased work of breathing, decreased tidal volume, and hypoventilation
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Hypercapnia, respiratory acidosis, and worsening hypoxemia
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Decreased cardiac output, hypotension, and death