Clinical Manifestations And Assessment Of Respiratory Diseases

Front 1

what are the major pathologic or structural changes associated with chronic bronchitis?

Back 1

Chronic inflammation and swelling of the peripheral airways
Excessive mucus plugging and accumulation
Partial or total mucus plugging
Hyperinflation of alveoli (air trapping)
Smooth muscle constriction of bronchial airways (bronchospasm)

Front 2

Anatomic Alterations of the Lungs with Chronic Bronchitis

Back 2

Bronchial walls are narrowed by vasodilation, congestion and mucosal edema
Submucosal bronchial glands enlarge and goblet cells to increase resulting in excessive mucus
The number and function of cilia lining in the tracheobronchial tree are diminished

Front 3

Definition of chronic bronchitis according to the American Thoracic Society

Back 3

characterized by a daily, productive cough for at least 3 consecutive months each year for 2 years in a row.

Front 4

Anatomic Alterations of the Lungs associated with Chronic Bronchitis

Back 4

Chronic inflammation and swelling of the peripheral airways
Excessive mucus production and accumulation
Partial or total mucus plugging
Hyperinflation of alveoli (air-trapping)
Smooth muscle constriction of bronchial airways (bronchospasm)

Front 5

Clinical data obtained at the bedside - chronic bronchitis

Back 5

Use of Accessory Muscles during inspiration

Front 6

Because polycythemia and cor pulmonale are associated with chronic bronchitis, what else might be seen?

Back 6

pitting edema
distended neck veins
enlarged and tender liver

Front 7

Main bronchodilators used in the treatment of COPD

Back 7

Short Acting:
Ipratropium bromide
Ipratropium bromide and alburterol sulfate (DuoNeb)
Long Acting:
Tiotropium bromide (Spiriva handihaler)

Front 8

What are the characteristics of Panacinar (Panlobular) emphysema

Back 8

An abnormal weakening and enlargement of all air spaces distal to the terminal bronchioles, the respiratory bronchioles, alveolar ducts, alveolar sacs and alveoli.

Hint 8

The alveolar-capillary surface area is decreased.
Found in the lower parts of the lungs and associated with a1-antitrypsin

Front 9

What does Centrilobular emphysema involve?

Back 9

The respiratory bronchioles in the proximal portion of the acinus. The respiratory bronchial walls enlarge, become confluent and then are destroyed

Hint 9

Centalobular emphysema is the most common form of emphysema and is often associated with chronic bronchitis.

Front 10

Radiologic Findings with Emphysema

Back 10

Translucent (dark) lung fields
Depressed or flattened diaphragms
Long and narrow heart
Enlarged Heart
Increased retrosternal air space (lateral radiograph)

Front 11

The immunologic Mechanism associated with Asthma

Back 11

1) Lyphoid tissue cells form specific IgE antibodies which attach to mast cells in the bronchial walls
2) the mast cell degranulates and releases chemical mediators such as histamine
3) Chemical mediators stimulate parasympathetic nerve endings in the bronchial airways

Front 12

Typical meds/agents used in the treatment asthma

Back 12

Sympathomimetics short and long acting
Parasympatholytics (anticholinergics)

Front 13

Aerosolized Medication Sympathomimetics - short to intermediate acting

Back 13

Metaproterenol (Alupent, Metaprel)
Terbutaline (Brethine, Brethaire)
Pirbuterol (Maxair)
Albuterol (Ventoline, Proventil)
Levalbuterol (Xopenex)

Front 14

Aerosolized Medication Sympathomimetics - long acting

Back 14

Salmeterol (Serevent)
Formoterol (Foradil)

Front 15

Aerosolized Medication Parasympatholytics (anticholinergics)

Back 15

Atropine sulfate (Dey-Dose Atropine Sulfate)
Ipratropium bromide (Atrovent)
Tiotroprium (Spirva)
Ipratropium bromide and Albuterol (Combivent)

Front 16

Three forms of bronchiectasis

Back 16

Varicose (fusiform)
Cylindrical (tubular)
Saccular (cystic)

Front 17

Cylindrical (tubular) bronchiectasis

Back 17

The bronchi are dilated and constricted in an irrecgular fashion similar to varicose veins, ultimately resulting in a distorted, bulbous shape

Front 18

Major pathologic or structural changes associated with bronchiectasis

Back 18

Chronic dilation and distortion of bronchial airways
Excessive production of often foul-smelling sputum
Smooth muscle constriction of bronchial airways
Hyperinflation of alveoli (air trapping)
Atelectasis, consolidation, and parenchymal fibrosis
Hemorrhage secondary to bronchial arterial erosion

Front 19

Bronchiectasis

Back 19

A) Varicose bronchiectasis
B) Cylindrical bronchiectasis
C) Saccular bronchiectasis

Front 20

What are the major structural changes associated with Pneumonia?

Back 20

In flammation of the alveoli
Alveolar consolidation
Atelectasis (aspiration pneumonia)

Front 21

Radiographic findings associated with alveolar consolidation related to pneumonia

Back 21

Increased density (from consolidation atelectasis)
Air bronchograms
Pleural effusions

Front 22

Identify the organisms primarily responsible for causing pneumonia in the hospitalized patient.

Back 22

P. aeruginosa, S. aureus, K. pneumoniae, E. coli, Serratia species and oral anaerobes (aspiration)

Front 23

Treatment protocols for the management of postoperative atelectasis

Back 23

Oxygen therapy protocol
Hyperinflation therapy protocol
Mechanical Ventilation protocol

Front 24

This disorders that make up COPD

Back 24

Chronic bronchitis
Emphysema
Asthma

Front 25

Radiographic findings associated with chronic bronchitis

Back 25

Translucent (dark) lung fields
Depressed diaphragms and long and narrow heart

Front 26

Is pneumonia a restrictive or obstructive disease.

Back 26

Restrictive

Front 27

Definition of lung abscess:

Back 27

Necrosis of lung tissue that in severe cases, leads to a localized air and fluid-filled cavity

Front 28

First line drug to treat TB

Back 28

Isoniazid (INH) and rifampin (Rifadin) are first line agents prescribed for the entire 9 months.

Front 29

Wheal size in a positive TB test

Back 29

10 mm or greater is considered positive

Front 30

Identifiy the area of the lung where TB spores flourish

Back 30

Apex of the lung

Front 31

Most common fungal infection in the US

Back 31

Histoplasmosis

Front 32

Medication of choice to treate Histoplasmosis

Back 32

IV administration of amphotericin B

Front 33

Causes of non-cardiogenic pulmonary edema

Back 33

Increased capillary permeability
Lymphatic Insufficiency
Decreased intrapleural pressure
Decreased oncotic pressure

Front 34

Causes of cardiogenic pulmonary edema

Back 34

Arrhythmias producing low cardiac output
Congenital heart defects
Excessive fluid amin.
Left ventricular failure
Mitral or aortic valve disease
Myocardial infarction
Pulmonary embolus
Renal failure
Rheumatic heart disease
Systemic hypertension

Front 35

Major pathologic or structural changes of the lungs associated with pulmonary edema

Back 35

Interstitial edema
Alveolar flooding
Increased surface tension of pulmonary surfactant

Front 36

The use of mask CPAP to treat pulmonary edema

Back 36

Maski CPAP improves decreased lung compliance, decreases the work of breathing, enhances gas exchange, and decreases vascular congestion in patients with pulmonary edema

Front 37

Define pulmonary embolism

Back 37

pulmonary embolism occurs when a blood clot (thrombus) becomes disloged from veins elsewherein the body and moves (embolizes) into the pulmonary arterial circulation.

Front 38

Methods of testing that are useful in the diagnosis of pulmonary embolism

Back 38

XRay
Electrocardiogram (ECG)
Ventilation/perfusion scan (V/Q scan)
Fast computed tomography scan (CT)
Pulmonary Angiogram

Front 39

Define flail chest

Back 39

A flail chest is the result of double fractures of at least three or more adjacent ribs, which causes the thoracic cage to become unstable

Front 40

Different procedures, protocols and medications for managing the patient with flail chest

Back 40

Medication for pain and routine bronchial hygiene in mild cases.

Hint 40

In more severe cases stabilization of the chest is required to allow bone healing and prevent atelectasis.
O2 therapy protocol
Hyperinflation therapy protocol
Mechanical Ventilator protocol

Front 41

Define pneumothorax

Back 41

A pneumothrorx exists when gas (sometimes called free air) accumulates in the pleural space

Front 42

Major pathologic and structural
changes associated with a pneumothorax

Back 42

Lung collapse
Ateletasis
Chest wall expansion
Compression of the great veins and decreased cardiac venous return

Front 43

When to employ the use a chest tube to treat a
pneumothorax

Back 43

When the pneumothorax is larger than 20%, it should be evacuated. In more serious cases, a chest tube is inserted into the patients pleural cavity

Front 44

The most common cause of pleural effusion (2) The major causes of an exudative effusion

Back 44

Malignant pleural effusions
Malignant mesotheliomas
Pneumonias
Tuberculosis
Fungal diseases

Front 45

Describe the type fluid that makes up a
transudative pleural effusion

Back 45

thin watery containing a few blood cells and little protein

Front 46

Define the terms empyema and hemothorax

Back 46

Empyema is the accumulation of pus in the pleural cavity
Hemothorax is the presence of blood in in the pleural space

Front 47

Type of mediastinal shift associated with a pleural
effusion.

Back 47

Mediastinal shift to the unaffected side

Front 48

Structural / pathologic changes associated with
pleural effusion

Back 48

Lung compression
Atelectasis
Compression of the great veins and decreased cardiac venous return

Front 49

Radiographic technique used for identifying a
pleural effusion

Back 49

Chest X-Ray

Front 50

Type of breath sounds, fremitus, and percussion
note associated with kyphoscoliosis

Back 50

Bronchial breath sounds
Increased tactile and vocal fremitus
Dull percussion note

Front 51

Define “pneumoconiosis”

Back 51

general term used to describe diseases of the lungs that are caused by the chonic inhalation of inorganic dusts and particulate matter usually of occupational or environmental origin

Front 52

Structural / pathologic changes associated with
pneumoconiosis

Back 52

Destruction of the alveoli and adjacent pulmonary capillaries
Fibrotic thickening of the respiratory bronchioles, alveolar ducts, and alveoli
Cystlike structures (honeycomb appearance)
fibrocalcific pleural plaques
Airway obstruction caused by inflammation and excessive bronchial secretions
Bronchospasm
Bronchogenic carinoma
Mesothelioma

Front 53

Describe the chest radiograph for the patient
suffering from asbestosis

Back 53

Small round opacities scattered throughout the lung
Irregularly shaped opacities
Irregular cardiac and diaphragmatic borders
Pleural plaques
Honeycomb appearance

Front 54

Identify the type of hypoxemia associated with
capillary shunting in “pneumoconiosis”

Back 54

The hypoxemia that develops in pneumoconiosis is most commonly caused by alveolar thickening, fibrosis, and capillary shunting. Hypoxemia caused by capillary shunting is often refractory to oxygen therapy.

Front 55

Define cancer

Back 55

Cancer is a general term that refers to abnormal new tissue growth characterized by the progressive, uncontrolled multiplication of cells.

Front 56

Identify those types of cancers that are considered
non-small cell lung cancer.

Back 56

Squamous (Epidermoid) Cell Carcinoma
Adenocarcinoma (Including bronchioalveolar cell carcinoma)

Front 57

Type of lung cancer most associated with smoking

Back 57

Small-cell lung cancer

Front 58

Describe the origin of squamous cell carcinoma

Back 58

The tumor originates from the basal cells of the bronchial epithelium and grows through the epithelium before invading the surrounding tissues.

Front 59

Lettering and numeric elements of the TNM
classification system for staging lung cancer

Back 59

Stage 0: the cancer is limited to the lining of the bronchial airways (TisNOMO)
Stage I: the tumor is less than 3 cm and located in lobar or distal airways (T1NOMO)
Stage II: The cancer has invaded neighboring lymph nodes (T1N1MO)
Stage III A: the tumor is any size - local invasion involves chest wall, diaphragm, mediastinal, pleural or parietal pericardium (T3N1MO)
Stage III B: the cancer has spread locally to areas such as mediastinum, heart, blood vessels, trachea, esophagus, vertebral body (T4 and N, MO)

Front 60

Best treatment option for the patient with small cell
carcinoma of the lung

Back 60

Chemotherapy - either alone or in combination with radiation therapy

Front 61

Is ARDS an obstructive or restrictive disease?

Back 61

Restrictive

Front 62

Major structural / pathologic changes associated
with ARDS

Back 62

Interstitial and intra-alveolar edema and hemorrhage
Alveolar consolidation
Intra-alveolar hyaline membrane
Pulmonary surfactant deficiency or abnormality
Atelectasis

Front 63

Ventilation strategy for managing the patient with
ARDS in terms of setting the tidal volume and
respiratory rate

Back 63

low tidal volumes and high respiratory rate
initial tidal volume set at 4 to 8 ml/kg and ventilatory rate as high as 35 breaths/min

Front 64

Refractory hypoxemia associated with ARDS

Back 64

the hypoxemia that develops in ARDS most commonly is caused by widespread alveolar consolidation, atelectasis, and capillary shunting. Hypoxemia caused by capillary shunting often is refractory to oxygen therapy.

Front 65

Commonly prescribed medications used in the
treatment of ARDS

Back 65

Antibiotics
Diuretic Agents
Corticosteroids

Front 66

Define “extrinsic allergic alveolitis”

Back 66

also called hypersensitivity pneumonitis - is an immunologically medicated inflammation of the lungs caused by the inhalation of a variety of offending agents such as pollen, animal dander, organic dusts and spores.

Front 67

Clinical findings associated with chronic interstitial
lung disease (ABGs, PFTs, Shunting and DO2)

Back 67

pH increased, PaCO2 decreased, HCO3- (slightly) decreased PaO2 decreased

Front 68

Goal of plasmapheresis in treating chronic
interstitial lung disease

Back 68

Reduces the circulating anti-GBM antibodies that attack the patient's flomerular basement membrane.

Front 69

Define Guillain- Barre Syndrome (GBS)

Back 69

Relatively rare disorder of the peripheral nervous system in which flaccid paralysis of the the skeletal muscle and loss of reflexes develop in a previously healthy patient

Front 70

What is the usual onset of GBS?

Back 70

The onset of Guillain-Barre syndrome frequently occurs 1 to 4 weeks after a febrile episode such as an upper respiratory or gastrointestinal illness.

Front 71

Etiology of GBS

Back 71

The precise cause of Guillain-Barre syndrome is not known.It is probably an immune disorder that causes inflammation and deterioration of the patient's peripheral nervous system.

Front 72

Structural / pathologic changes associated with
GBS

Back 72

Mucus accumulation
Airway obstruction
Alveolar consolidation
Atelectasis

Front 73

The goal of plasmapheresis in GBS

Back 73

Remove the antibodies from the plasma that contribute to the immune system attack on the peripheral nerves.

Front 74

Identify treatment modalities beneficial in the
management of the GBS patient

Back 74

Plasmapheresis
Infustion of immunoglobulin
Corticosteroids

Front 75

Identify non-cardiopulmonary manifestations
associated with myasthenia gravis.

Back 75

Weakness of striated muscles:
Eye muscles - drooping of the upper eyelids
Extraocular muscles - double vision
Muscles of the lower protion of the face - speech impairment
Chewing and swallowing muscles
Skeletal muscles of the arms and legs

Front 76

Useful techniques used in diagnosing myasthenia
gravis

Back 76

Clinical history
Neurologic examination
Electromyography
Blood analysis
Edrophonium test
CT or MRI

Front 77

Beneficial treatment modalities in managing the
severely ill patient with myasthenia gravis.

Back 77

Adrenocorticotropic hormone (ACTH)

Front 78

Identify the probable cause of myasthenia gravis

Back 78

The cause appears to be related to circulating antibodies of the autoimmune sytem (anti-ACh receptor antibodies)

Front 79

Clinical findings associated with myasthenia gravis
(PFTs, ABGs, DO2, and Shunting)

Back 79

FVC, FEVt, FEF 20%-75%, FEF 200-1200, PEFR, MVV, FEF 50%, FEV1% all decreased

Hint 79

ABG's
pH decreased
PaCO2 increased
HCO3- increased (slightly)
PaO2 decreased

DO2 -decreased
Shunting - increased

Front 80

Describe the role of the thymus gland in
myasthenia gravis

Back 80

The thymus gland in the myasthenic patient frequently appears to be the source of anti-ACh receptor antibodies

Front 81

Recognize the treatment options for managing the
patient with myasthenia gravis

Back 81

Cholinesterase inhibitors
Immunosuppressants
Adrenocorticotropic hormone therapy
Thymectomy
Plasmapheresis

Hint 81

O2 therapy protocol
Bronchopulmonary hygiene therapy protocol
Hyperinflation therapy protocol
Mechanical ventilation protocol

Front 82

Cite the most common sleep disorder seen in the
clinical setting

Back 82

Obstructive sleep apnea

Front 83

Recognize the general clinical manifestations
associated with obstructive sleep apnea (OSA)

Back 83

Chronic loud snoring
Hypertension
Morning headaches
Systemic hypertension
Congestive heart failure
Nausea
Dry mouth upon awakening
Intellectual and personality changes

Hint 83

Memory loss
Depression
Sexual impotence
Nocturnal enuresis
Excessive daytime sleepiness
Auto accidents
Pulmonary hypertension and/or cor pulmonale

Front 84

Recognize that polysomnography as a means of diagnosing OSA

Back 84

Include an EEG and electro-oculogram (EOG) to identify sleep stages. Use a monitoring device for airflow, and ECG to identify cardiac arrhythmias, impedance pneumography, intercostal elctromyography

Hint 84

Esophageal manometry to monitor the patient's ventilatory rate and effort, ear oximetry or transcutaneous O2 monitoring

Front 85

Pneumothorax

Back 85

Right-side pneumothorax. GA, Gas accumulation; DD, depressed diaphragm; CL, collapsed lung. Inset, Atelectasis, a common secondary anatomic alteration of the lungs