Pulmonary Diseases Flashcards

1
Q

What are the classifications of pulmonary diseases?

A

Pulmonary diseases can be classified into 2 broad categories:
1. Restrictive vs. Obstructive
2. Infectious vs. Non-infectious

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2
Q

What are restrictive disorders and obstructive disorders?

A
  1. Restrictive disorders refer to the inability of the person to breathe in adequate amounts of air. These individuals have low lung volumes on pulmonary function tests (PFTs). Examples include aspiration, pulmonary fibrosis, atelectasis, bronchiolitis, and pulmonary edema.
  2. Obstructive disorders refer to the inability of the person to completely exhale air which has been inhaled. On PFTs these individuals will have high lung volumes because they are retaining air in the lungs. Disease examples include asthma and COPD.
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3
Q

What are the 2 main types of acute respiratory failure?

A

Hypoxemia and hypercapnic respiratory failure

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4
Q

What is hypoxemic respiratory failure defined by? Why?

A

Defined as a PaO2 of < 50mmHg. This is typically due to inadequate diffusion of oxygen from the alveoli to the capillary. Disorders that can impair diffusion are pulmonary edema, pulmonary embolus, and pneumonia.

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5
Q

What is hypercapnic respiratory failure defined by? What are cause of this?

A

Defined as a PaCO2 > 50mmHg. This is typically due to inadequate alveolar ventilation. Causes of hypercapnia include depression of the respiratory center by medications, abnormalities of the spinal cord systems, disorders of the medulla, diseases of the neuromuscular junction, chest wall abnormalities, or COPD.

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6
Q

What is a pneumothorax? What are the two types?

A

Presence of air or gas in the pleural space. The air in the thoracic cavity may press on the lung and cause it to collapse completely, or it may be a small amount of air that does not cause any difficulties. They two main types are spontaneous and secondary pneumothorax.

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7
Q

Who and how does spontaneous pneumothorax occur?

A

Occurs in young, tall, thin, males. They may also occur as a result of bleb rupture in persons who have emphysema. Smoking increases risk for spontaneous pneumothorax. In some individuals there is a genetic component and a family history of this diagnosis.

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8
Q

What is a bleb rupture?

A

Bleb ruptures are usually in the apexes and may occur during exercise, while at rest, or while asleep. The rupture allows air into the pleural space.

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9
Q

What is a secondary pneumothorax?

A

This is caused by trauma. A tension pneumothorax occurs when air becomes trapped in the thoracic cavity and can’t escape. The site of injury on the pleural membrane acts as a one-way valve and only lets air into the thoracic cavity. The person may then experience a complete lung collapse. This can then lead to deviated trachea, SOB, and hypotension.

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10
Q

What are clinical manifestations of a pneumothorax?

A

Sudden pleural pain, decreased breath sounds, and hyperresonance to percussion.

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11
Q

What is pulmonary edema?

A

Accumulation of water in the pulmonary alveolar sacs. This prevents the proper exchange of gases and leads to dyspnea, chest pain, and hypoxia. These individuals will also have orthopnea or paroxysmal nocturnal dyspnea.

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12
Q

What is pulmonary edema the most common cause of?

A

Pulmonary edema is the most common cause of left sided heart failure.

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13
Q

What happens to the lungs in left sided heart failure?

A

The backup of blood to the lungs increases capillary hydrostatic pressure which pushes fluid out into the alveolar sacs. ARDS or inhalation of toxic gases can cause capillary injury which leads to the movement of fluid into the alveolar space.

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14
Q

What is post obstructive pulmonary edema?

A

This occurs after relieving airway obstruction. Inspiration against an occluded airway creates excessive intrathoracic negative pressure which leads to increased venous return to the right side of the heart and a decreased outflow of blood from the left side of the heart. This creates increased pulmonary blood volume and pressure which causes the pulmonary edema.

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15
Q

What are clinical manifestations of pulmonary edema?

A

Dyspnea, hypoxemia, pulmonary rales, dullness to percussion, S3 heart sound, and frothy sputum.

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16
Q

What is Acute lung injury?

A

Type of respiratory failure which results from massive lung inflammation and disseminated alveolar capillary damage. This damage significantly impairs gas exchange, and the patient will have huge issues with oxygenation.

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17
Q

What is ARDS?

A

Acute respiratory distress syndrome is the most severe form of acute lung injury and is characterized by bilateral lung infiltrates seen on chest x-ray which are not explained by cardiac failure or fluid overload and a low ratio of partial pressure of oxygen to the fraction of inhaled oxygen.

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18
Q

What is the pathogenesis of ARDS?

A
  1. Inflammatory Phase: Occurs within the first 72 hours. The inflammatory cascade is triggered by an injury to the capillary membranes, which then increases the capillary permeability. Fluid, proteins, and blood cells then leak into the pulmonary interstitium and alveoli and impair gas exchange. Surfactant is inactivated and its production is impaired. The lungs lose compliance, work of breathing increases, alveolar ventilation decreases, and hypercapnia develops.
  2. Proliferative Phase: Pulmonary edema resolves, and surfactant is being produced again. This phase lasts 1-3 weeks. Intra alveolar exudate turns into a cellular granulation tissue and worsens the hypoxemia.
  3. Fibrotic Phase: Occurs between 14-21 days. There can be overlap between this phase and the proliferative phase. Here, the alveoli undergo fibrosis and ultimately this causes a decrease in pulmonary function which may be permanent. This leads to a decrease in functional residual capacity and a continuing V/Q mismatch with right to left shunting. The fibrosis causes pulmonary HTN.
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19
Q

What are clinical manifestations of ARDS?

A

hyperventilation, respiratory alkalosis, organ dysfunction, metabolic acidosis, decreased tidal volume, hypercapnia, decreased cardiac output, and hypotension.

A PF ratio of 201-300 is mild disease, 101-200 is moderate disease and <100 is severe disease.

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20
Q

What is asthma?

A

Reactive airway disease triggered by an allergic reaction.

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21
Q

What is the pathogenesis of asthma?

A

Asthma is an IgE mediated reaction. The airway narrows, and the disease is marked by dyspnea and expiratory wheezing. Cellular level changes include bronchial smooth muscle hypertrophy, goblet cell hyperplasia, thickening of the basement membranes, proliferation of eosinophils, and bronchial mucous plugs. These changes lead to air trapping which causes decreased alveolar perfusion, increased alveolar gas pressure, decreased ventilation and a creased V/Q ratio. Hyperventilation also occurs secondary to increased lung volumes which can cause CO2 retention and respiratory acidosis. The presence of respiratory acidosis is a precursor to respiratory failure.

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22
Q

What are symptoms during an asthma attack?

A

Chest constriction, expiratory wheezing, prolonged expiration, tachycardia, and tachypnea. Severe attacks are accompanied by the use of accessory muscles and inspiratory/expiratory wheezing. A silent chest and PaO2 <70 mmHg are signs of impending death.

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23
Q

How is asthma triggered in children?

A

Exacerbations in children are usually triggered by viral infections. In children, the most common of these is RSV.

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24
Q

What are clinical manifestations of RSV?

A

Expiratory wheezing, faint breath sounds, and sometimes a barrel chest. In severe cases they may have retractions, nasal flaring and accessory muscle use.

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25
Q

What is COPD?

A

Results in obstruction of airflow and is typically not reversible and is progressive.

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26
Q

What are risk factors to COPD?

A

Smoking, occupational dusts and chemicals, and indoor air pollutants.

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27
Q

What are the two main types of COPD?

A

Emphysema and chronic bronchitis

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28
Q

What is the genetic component of COPD?

A

An inherited mutation in the alpha 1 antitrypsin gene causes emphysema to develop at an early age, even in persons who do not use tobacco products.

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29
Q

What is the pathogenesis of emphysema?

A

Dilation of the airways and the destruction of the alveolar walls. Both of these defects cause a decrease in the elastic recoil. As a result, air is trapped in the lungs and cannot be completely exhaled. As the amount of air trapped increases, the thoracic cavity changes shape to accommodate for the increase lung volumes and becomes the shape of a barrel. Alveolar destruction results in the formation of bullae in the lung tissue, which are pockets of air and do not assist with gas exchange.

30
Q

What are clinical manifestations of emphysema?

A

They tend to have pursed lip breathing and use the tripod position to help improve their breathing. They have a high metabolic rate because they have shallow rapid breaths and burn a lot of calories. As a result, they tend to be thin. They will have hyper resonant sound with percussion.

31
Q

What is chronic bronchitis?

A

Condition marked by the presence of a productive cough which occurs over the course of a minimum of three consecutive months for 2 sequential years.

32
Q

What is the pathogenesis of chronic bronchitis?

A

The mucus secreting cells in the airways undergo a hyperplasia and secrete excessive amounts of mucus. This mucus can be hard to clear due to its viscosity and impaired ciliary function. it may plug the airway and impair oxygenation. The hyperplasia of these cells is typically triggered by a chronic irritant such as smoking. The airways become narrow, causing obstruction and air retention.

33
Q

What are clinical manifestations of chronic broncitis?

A

Poor exercise tolerance, wheezing, and dyspnea. They will have signs of obstruction on PFTs. The main sign is a decreased FEV1. The hypoxemia causes polycythemia and cyanosis, which can lead to pulmonary HTN and cor pulmonale.

34
Q

What is pneumonia?

A

Inflammatory/infectious process which results int he accumulation of inflammatory exudate in its alveolar sacs.

35
Q

What is community acquired pneumonia?

A

Occurs outside of the healthcare system in common bacteria which include:

  1. Streptococcus Pneumoniae, Staphylococcus Aureus, Streptococcus Pyogenes, and Klebsiella Pneumoniae are common in the elderly and come from viral infections.
  2. Hemophilus Influenza is commonly seen in infants and children. It occurs commonly in those adults with COPD.
36
Q

What is hospital acquired pneumonia?

A

Diagnosed 80 hours after being admitted to the hospital. Common causes include Klebsiella, Pseudomonas aeruginosa, and E coli.

37
Q

What is the pathogenesis of pneumonia?

A

Develops from aspiration of oral secretions into the lower respiratory tract or through the inhalation of a microorganism in the air which is present from a sneeze, cough, or a person talking. Endotracheal tubes become colonized with bacteria. Once bacteria reach the alveoli, macrophages trigger the immune and inflammatory cascades.

38
Q

What is the difference between CAP and PCP?

A

CAP has an acute onset where they suddenly feel bad. PCP presents insidiously.

39
Q

What are clinical manifestations of pneumonia?

A

Cough, chills, malaise, pleuritic chest pain, pulmonary rales, tactile fremitus, egophony, and whispered pectoriloquy.

40
Q

What is tuberculosis?

A

Pulmonary infection which occurs worldwide and most commonly in disadvantaged populations. It is caused by the mycobacterium TB and is spread via air droplets containing the organism.

41
Q

What is multidrug resistant TB?

A

Defined as tuberculosis that is resistant to both isoniazid and rifampin.

42
Q

What is extensive drug resistant TB?

A

This term is used when the mycobacterium is resistant to fluoroquinolones and at least one of three injectable second line drugs: amikacin, kanamycin, or capreomycin.

43
Q

What occurs in a primary TB infection?

A

Macrophages engulf the mycobacterium and form a granuloma called a tubercule. This triggers the inflammatory cascade, which causes the center of the lesion to necrose and eventually calcify. This infection is usually asymptomatic and usually does not cause active disease.

44
Q

What occurs in a secondary TB infection?

A

The tubercule has activated, and the infection has spread to additional sites within the lung. Individuals will experience fever, hemoptysis, pleural effusion, wasting and weight loss. Lesions often occur in the apices of the lungs. These individuals are infectious and spread the disease.

45
Q

What is a pulmonary embolus?

A

PE is a partial or completely occlusion of blood flow int he pulmonary artery. Most commonly results from a DVT in the lower extremities. It may arise from tissue fragments, a foreign body, an air bubble, fat embolus from a fracture, or amniotic fluid.

46
Q

What is the pathogenesis of pulmonary embolus?

A

When the embolus lodges in the pulmonary circulation it triggers the release of serotonin, histamine, catecholamines, angiotensin II inflammatory mediators, and toxic oxygen free radicals. This causes vasoconstriction which further impedes blood flow. This causes an increase in the pulmonary artery pressure and can lead to right ventricular dilation and increased afterload. The decrease of absent blood flow to a portion of the lung leads to a V/Q mismatch and a decrease in surfactant production. This causes atelectasis and hypoxemia.

47
Q

What is a saddle embolus?

A

A PE that sits on the bifurcation of the pulmonary artery. It can occlude all blood flow to the lungs and is a very serious situation.

48
Q

What are clinical manifestations of a pulmonary embolus?

A

Chest pain, syncope, unexplained anxiety, and hemoptysis.

49
Q

What are the two main types of lung cancers?

A

Non-small cell lung cancer and neuroendocrine tumors

50
Q

What are the three subtypes of non-small cell lung cancers?

A
  1. squamous cell carcinoma
  2. adenocarcinoma
  3. large cell undifferentiated
51
Q

What are squamous cell carcinomas associated with?

A

Smoking and COPD. They are typically located in the hila and project into the bronchi. These individuals will have a nonproductive cough or hemoptysis. Pneumonia and atelectasis are common as they can obstruct airflow.

52
Q

What are adenocarcinomas associated with?

A

More commonly found in women, Asians, and nonsmokers. They usually are found in the lung parenchyma. These tumors tend to be asymptomatic and are discovered on routine chest x-rays.

53
Q

What are large cell carcinomas associated with?

A

They arise centrally and can distort the trachea

54
Q

What are neuroendocrine tumors?

A

They arise from bronchial mucosa and the most common of these tumors are the small cell carcinomas.

55
Q

What are small cell lung carcinomas?

A

They tend to arise from the central part of the lung. This cancer has the strongest correlation with smoking. These tumors are aggressive and metastasize early. It has the worst prognosis of all lung cancers.

56
Q

What are complications of lung cancers?

A

Superior vena cava syndrome, hoarseness, pleural effusions, and malnutrition/weight loss.

57
Q

What are risk factors of PAH?

A

Drugs, left ventricular heart failure or left sided valvular heart disease, COPD, and pulmonary embolus can call cause PAH.

58
Q

What is the diagnostic criteria to have PAH?

A

If they have a mean pulmonary arterial pressure of greater than 25 mmHg at rest. (Normal PA pressure is between 15-18 mmHg.

59
Q

What genetic defect can cause PAH?

A

The gene which codes bone morphogenetic protein receptor type II (BMPR2).

60
Q

What is the pathogenesis of PAH?

A

Too much vasoconstriction and not enough vasodilation occurs. This imbalance causes a constriction of the pulmonary artery. There are increased calcium and serotonin levels which cause vasoconstriction. The higher pressure in the pulmonary artery causes the right ventricle to work harder. The right ventricle will compensate for the increased workload by enlarging and will eventually fail, causing cor pulmonale.

61
Q

What will you see on a chest x-ray with those who have PAH?

A

Enlarged right ventricle and pulmonary artery. They will have signs of right sided heart failure as well.

62
Q

What is cor pulmonale?

A

Secondary to pulmonary artery hypertension. The right ventricle is usually not made to push against high pressures. In the setting of PAH, it must push against the higher pulmonary artery pressure and eventually fails. This will lead to symptoms of right sided heart failure.

63
Q

What is croup?

A

Upper respiratory infection which may be caused by a virus or bacteria that leads to inflammation and obstruction. Viral coup causes subglottic edema that leads to obstruction. Most cases resolve spontaneously.

64
Q

What are clinical manifestations of croup?

A

Rhinorrhea, sore throat, seal like barking cough, hoard voice and inspiratory stridor.

65
Q

What is cystic fibrosis?

A

Autosomal recessive disorder which results from a defective gene or chromosome 7. Average life span is 30 years old.

66
Q

What is pathogenesis of CF?

A

It affects the airways, GI tract, and reproductive tract. The CF transmembrane conductance regulator gene mutation results in the production of an abnormal protein called the cystic fibrosis transmembrane conductance regulator protein. This protein makes the chloride channel on the surface of epithelial cells, especially those which line the airways, bile ducts, pancreas, sweat ducts and paranal sinuses. Chloride intracellular balance is maintained in these cells by chloride channels. When these channels fail, they are unable to secrete chloride out of the cell and the cell increases absorption of sodium.

67
Q

What is the effect of CF on the lungs?

A

Occlussion of airways, decrease in elastic recoil (difficulty with exhalation) and increased susceptibility to infections

68
Q

What is the effect of CF on the pancreas?

A

Vicious secretions disable the pancreas’ ability to release pancreatic enzymes into the gut to assist with digestion.

69
Q

What is the effect of CF on the sweat glands?

A

The process is opposite here, and the Cl and Na are secreted extracellularly and into the sweat, so these people have high concentration of Na in their sweat.

70
Q

What are clinical manifestations of CF?

A

Excessive sputum production, recurrent PNA, clubbing, development of barrel chest, and pulmonary rales.