Restrictive Lung Diseases & Respiratory Function

Front 1

Clinical manifestations of asthma

Back 1

Elevated IgE levels
Allergic rhinitis
Eczema
Positive family history of allergy
Attacks associated with seasonal, environmental or occupational exposure

Front 2

What are the results of Asthma?

Back 2

Increased microvascular permeability
Mucosal edema
Inflammatory exudates
Bronchoconstriction
Leakage

Front 3

What causes inflammation of the airways?

Back 3

Acute bronchospasm (bronchoconstriction)
Mucosal edema
Mucous plug formation
Airway wall remodeling

Front 4

What are the chances of people with asthma developing permanent structural changes?

Back 4

1 in every 10

Front 5

Symptoms of severe Asthma attacks are:

Back 5

Use of accessory muscles of respiration
Intercostal retractions
Distant breath sounds with inspiratory wheezing
Orthopnea
Agitation
Tachypnea
Tachycardia

Front 6

What Are the Treatments of asthma?

Back 6

O2 therapy
Small-volume nebulizers
B2 agonists
Corticosteroids
Leukotriene modifiers
Mast cell inhibitors

Front 7

What are the sign and symptoms of Pneumonia?

Back 7

Crackles (rales) and bronchial breath sounds over affected lung tissue
Chills
Fever
Cough, purulent sputum
Viral
Fever, cough, hoarseness, coryza accompanied by wheezing/rales

Front 8

What is Acute Bronchits?

Back 8

Single occurrence or exacerbation of chronic preceded by URI

Front 9

What are the effects of bronchitis?

Back 9

Increased bronchial wall thickness
Resistance increases work of breathing
Increased O2 demands
Produce ventilation-perfusion mismatch with hypoxemia and hypercarbia
Increases pulmonary artery resistance
Pulmonary hypertension
Inflammation in bronchial walls with vasoconstriction of pulmonary blood vessels and pulmonary arteries
Affects airways not alveoli
Blue Bloaters

Front 10

What is Emphysema?

Back 10

Hyperinflation of alveoli and the destruction of alveolar walls as a result of inflammation

Front 11

What is the treatment for COPD?

Back 11

Bronchodilators – parental, oral, and inhalation -  a/w resistance
Antibiotics - Rx infection
Flu vaccines, pneumococcal vaccine
O2 Rx  low flow

Front 12

What is ARDS?

Back 12

Acute Respiratory Distress Syndrome

Front 13

What are the diagnostics criteria for ARDS

Back 13

Patient has an identifiable predisposing condition
The chest x-ray reveals diffuse, bilateral infiltrates – advances to white out as ARDS progresses
The patient doesn’t have CHF
The patient’s pO2/FiO2 ratio will be less than 200 (>300 is normal

Front 14

what are the stages of Edema Formation In ARDS

Back 14

A, Normal alveolus and pulmonary capillary
B, Interstitial edema occurs with increased flow of fluid into the interstitial space
C, Alveolar edema occurs when the fluid crosses the blood-gas barrier

Front 15

What are the medical Managemet for ARDS?

Back 15

Support respiration and ventilation
Mechanical ventilation with PEEP
Maintain hemodynamic stability
Monitor fluids and degree of pulmonary edema
Treat underlying condition
Monitor for complications

Front 16

What are the treatment of ARDS?

Back 16

Proning
Kinetic Therapy
Continuous Lateral Rotation Therapy

Front 17

What is pnuemonia?

Back 17

Acute inflammation of lung caused by microorganism

Front 18

The different types of pneumonia are:

Back 18

Community-acquired pneumonia
Hospital-acquired pneumonia

Front 19

What causes Oppotunistic Pneumonia?

Back 19

Pneumocystis carinii
CMV
Fungi
Patients with severe protein-calorie malnutrition, immune deficiencies, chemotherapy/radiation recipients, and transplant recipients are at risk

Front 20

What are the signs and symptoms of Pneumonia?

Back 20

Crackles (rales) and bronchial breath sounds over affected lung tissue
Chills
Fever
Cough, purulent sputum
Viral
Fever, cough, hoarseness, coryza accompanied by wheezing/rales

Front 21

What are the treatments of pneeumonia?

Back 21

Antibiotic/antiviral therapy
Oxygen for hypoxemia
Analgesics for chest pain
Antipyretics
Influenza vaccine
Pneumococcal vaccine
Fluid intake at least 3 L per day
Caloric intake at least 1500 per day

Front 22

What cause Tuberculosis?

Back 22

Transmitted by airborne droplets
Neutrophils and alveolar macrophages migrate to the lung site
These cells engulf the bacteria and seal off the bacilli colonies
Infected tissues with tubercle die and form caseation necrosis

Front 23

Those who are at risk for TB are

Back 23

Residents and employees of long-term care facilities and shelters
Prison inmates
Homeless
Alcoholics
IV drug users
Family members of infected persons
People born in a country where TB is common
HIV or other disease that suppresses the immune system
Medications that suppress the immune system

Front 24

what are the signs and symptoms of TB?

Back 24

Early: coughing, night sweats, coughing (dry at first), fever, chills, fatigue, weakness, dyspnea on exertion
Brown tinged sputum (hemoptysis, later), anorexia, wt. loss, pleuritic chest pain (sharp) esp. with coughing

Front 25

What are the medication for TB?

Back 25

Rifampin (RIF)= cause urine, tears, and sweat to be orange
Use of ETOH or INH increases risk of hepatotoxicity
Isoniazid (INH) = cause peripheral neuropathy vitamin B6 given to prevent
Other meds: pyrazinamide (PZA), ethambutol (EMB), streptomycin

Front 26

Restrictive Pulmonary diseases are:

Back 26

The result of decreased expansion of the lungs due to alterations in the lung parenchyma, pluera, chest wall, or neuromuscular function.

Front 27

Restrictive Pulmonary diseased can be classified as:

Back 27

Pulmonary or Extrapulmonary and represent acute or chronic patterns of lung dysfunction.

Front 28

Characteristics of the diseases:

Back 28

Decrease in total lung capacity, vital capacity, functional residual capacity, and residual volume.

Front 29

Interstitial Lung Diseases:

Back 29

A group of disorders that are characterized by acute, subacute, or chronic infiltration of alveolar walls by cells, fluid, and connective tissue.

Front 30

Diffuse Interstitial Lung Disease or
also known as Diffuse interstitial pulmonary fibrosis

Back 30

Restrictive lung disease characterized by thickening of the alveolar interstitium.

Front 31

Pathogenesis of diffuse interstitial lung disease:

Back 31

Not well understood but possibly related to an immune reaction that usually begins with injury to alveolar epithelial/capillary endothelial cells.

Front 32

Pathophysiologic changes for diffuse interstitial lung disease:

Back 32

Interstitial and alveolar wall thickening and increased collagen bundles in interstitium.

Front 33

Immune response in diffuse interstitial lung disease is characterized by:

Back 33

inflammation, fibrosis, and destruction

Front 34

Clinical Manifestations of diffuse interstitial lung disease:

Back 34

Most common- progressive dyspnea with nonproductive cough.

Others- rapid shallow breathing, clubbing of nail beds, bibasilar end-expiratory crackles, marked dyspnea with exercise

Front 35

Treatment for diffuse interstitial lung disease:

Back 35

Avoid tobacco smoke, administrations of anti-inflammatory and immunosuppresive agents

Front 36

Sarcoidosis

Back 36

Acute or chronic systemic disease of unknown cause although immunologic basis appears likely.

Front 37

Acute and chronic process of Sarcoidosis

Back 37

Acute occurs more likely in women in the second or third decade of life.

Chronic is seen more in third/fourth decades of life w/highest incidence in North America.

Front 38

Pathogenesis of Sarcoidosis

Back 38

Development of multiple, uniform, noncaseating epitheloid granulomas that affect multiple organ systems, most commonly lymph nodes and lung tissue.

Front 39

Clinical Manifestations of Sarcoidosis

Back 39

Malaise, fatigue, weight loss, fever, dyspnea, dry nonproductive cough.

Also, erythema nodosum, macules, papules, hyperpigmentation, subcutaneous nodules, hepatosplenomegaly, and lymphadenopathy

Front 40

Diagnosis of Sarcoidosis

Back 40

Leukopenia, anemia, increase eosinophil count, elevated sedimentation rate, and increased calcium levels

Also, 70% patients exhibit anergy (decreased sensitivity to specific antigens)

Front 41

Treatment for Sarcoidosis

Back 41

Administration of corticosteroids and management of symptoms.

For patients with progressive disease that doesn’t respond to corticosteroids the use of immunosuppresive agents maybe used.

Front 42

Hypersensitivity Pneumonitis

( Extrinsic allergic alveolitis )

Back 42

Both a restrictive and occupational disease.
Predominance in nonsmokers (80-90%)

Front 43

Pathogenesis of Hypersensitivity Pneumonitis

Back 43

The causative agent combines with serum antibody in the alveolar walls, leading to type III hypersensitivity reaction.

Genetic predisposition may be involved in exaggerated response to offending agent.

Front 44

Clinical Manifestations of Hypersensitivity Pneumonitis Acute:

Back 44

Acute- symptoms begins within 4-6 houts after exposure and resolve in 18-24 hours.

Symptoms: chills,sweating,shivering, myalgias, nausea, lethargy, headache, and malaise. May or may not have a fever.

Front 45

Clinical Manifestations of Hypersensitivity Pneumonitis Chronic:

Back 45

Progressive diffuse pulmonary fibrosis develops in upper lobes.

Acute febrile episodes and progressive pulmonary fibrosis with cough, dyspnea, fatigue, and pulmonale.

Front 46

Diagnosis of Hypersensitivity Pneumonitis

Back 46

Chest radiographs, skin testing, and laboratory findings could see an increased white blood cell count and decreased Pao2.

Front 47

Treatment of Hypersensitivity Pneumonitis:

Back 47

Identify offending agent and prevent further exposure. May require change in environment or occupation.

Front 48

Occupational Lung Diseases

Back 48

Result from inhalation of toxic gases or foreign particles.

Front 49

Pneumoconiosis

Back 49

Parenchymal lung disease caused by inhalation of inorganic dust particles.

Front 50

Atmospheric pollutants:

Back 50

Sulfur oxides, nitrogen oxides, and tobacco smoke

Front 51

Clinical Manifestations of Occupational Lung disease

Back 51

Pneumoconioses generally produce no symptoms in early stages but as it progesses: productive cough and dyspnea.

Front 52

Treatment of Occupational Lung disease:

Back 52

Preventative measures are key to limiting onset and severity.

Prevent further parenchymal damage and relieve signs/symptoms

Front 53

Acute Respiratory Distress Syndrome

(ARDS)

Back 53

Damage to alveolar-capillary membrane.

Front 54

Mortality rate of ARDS

Back 54

30-63%

Front 55

Major disorders associated with ARDS

Back 55

Shock, Trauma, Embolism, Head Injury, Aspiration, Drug Overdose, Inhaled toxins, Radiation, Hematologic disorders, metabolic disorders, Burns, Cancer, anaphylaxis, eclampsia, radiation pneumonitis, high-altitude exposure

Front 56

Four characteristics of ARDS:

Back 56

Injury to alveoli from wide variety of disorders
Changes in alveolar diameter
Injury to pulmonary circulation
Disruption in 02 transport/utilization

Front 57

Common findings of ARDS:

Back 57

Sever hypoxemia
Decrease in lung compliance
Decrease in FRC
Diffuse, fluffly alveolar infiltrates on chest radiograph
non-cardiogenic pulmonary edema

Front 58

ARDS leads to three major pathophysiologic processes:

Back 58

Noncardiogenic pulmonary edema, with “leaky” pulmonary capillaries
Atelectasis w/ lack of surfactant
Fibrosis associated with inflammatory deposition of proteins.

Front 59

ARDS Symptoms

Back 59

Respiratory rate increased and symptoms of tissue hypoxia may be present.
Crackles, wheezing, dyspnea, pulmonary edema.

Front 60

ARDS Treatment

Back 60

Therapy to enhance tissue oxygenation until inflammatory process resolves. Mechanical ventilation with PEEP and supplemental oxygen is mainstay treatment.

Front 61

What is flail chest?

Back 61

Flail chest results from multiple rib fractures as a result of trauma to the chest wall.

Front 62

What is severe acute respiratory syndrome?

Back 62

Caused by a coronavirus. Caused by person to person contact, mostly through droplets. Can spread through contaminated surfaces.

Front 63

Clinical Manifestations of SARS

Back 63

Fever, myalgias, headache, nonproductive cough, and dyspnea

Front 64

What is Pulmonary Tuberculosis?

Back 64

Caused by mycobacterium tuberculosis, an acid fast aerobic bacillus. Most common sites are the lung and the lymph nodes.

Front 65

What is pulmonary tuberculosis subdivided into?

Back 65

Primary and reactivating

Front 66

What is the difference between primary and reactivating tuberculosis?

Back 66

Primary is the initial infection while the reactivating occurs many years after initial infection

Front 67

What are the clinical manifestations of tuberculosis?

Back 67

History of contact with an infected person, low grade fever, cough, night sweats, fatigue, weight loss, malaise and anorexia. Chronic cough is the most common symptom.

Front 68

How do you get a diagnosis of tuberculosis?

Back 68

Sputum culture and characteristic nodules on chest radiographs

Front 69

What is a restrictive lung disease?

Back 69

Restrictive pulmonary disorders are those that restrict lung expansion.

Front 70

Charcterized by the accumulation of air pleural space

Back 70

Pneumothorax

Front 71

Pleural Effusion

Back 71

A pathologic collection of fluid or pus in the pleural cavity as a result of another disease process.

Front 72

A viral dsisease in which the poliiovirus attacks the motor nerve cells of the spinal chord and brianstem

Back 72

Poliomyelitis

Front 73

A degenarative disease of the nervous system that involces both upper and lower motor neurons

Back 73

Amytrophic Lateral Sclerosis

Front 74

Muscular Dystrophies

Back 74

A hereditary disease( X-linked recessive), passed from mother to sons.

Front 75

A disorder that is pressumed to have a immunologic basis

Back 75

Guillain-Barre Syndrome

Front 76

A bony deformity of the chest wall occurs as a result of of kyphosis.

Back 76

Kyphoscoliosis

Front 77

Ankylosing Spondylitis

Back 77

A progressive inflammotory disease leading to immobilty of the vertebral joints and fixation if the ribs.

Front 78

Flail Chest

Back 78

Chest wall instability due to fracture at two distant sites on the same rib.