9.1 Disorders of the Respiratory Function pt. 1

Question 1

What is Pleuritis or pleurisy?

Answer 1

inflammation of the parietal pleura

Caused by viral infections, cancer, lung infections, and surgery.

Question 2

What is a pleural effusion? How does fluid normally enter and exit the pleural cavity?

Answer 2

abnormal collection of fluid in the pleural cavity. Normally fluid enters via capillaries in parietal pleural and exits via lymphatics.

Question 3

What does pleural effusion cause

Answer 3

compromises ones ability to expand their lungs-> shortness of breath

Question 4

Describe transudate (hydrothorax) and recall what can cause this

Answer 4

changes forces involved in capillary exchange. Moves fluid out of capillary and into interstitial space. Caused by heart failure, malignancy, kidney failure or liver failure.

Question 5

Describe exudate and what can cause this. How do we test for exudate?

Answer 5

found most often with pathological process that has caused inflammation. Unhealthy tissue dies and releases contents (LDH) (intracellular). A thoracentesis tests the pleural effusion for LDH and other proteins.

Question 6

Describe a hemothorax and what can cause it

Answer 6

collection of blood in the pleural space

Causes: cancer, blood clotting disorders, and trauma near lungs

Question 7

Describe a pyothorax (empyema) and what can cause it.

Answer 7

infection in tissues that are near the pleural cavity. infections can causes abscesses and those can pop. The pus that goes into pleural space is called empyema.
Causes: invasion by bacteria by the lungs

Question 8

Describe a chylothorax and what can cause it

Answer 8

contains a milky fluid consisting of lymph. Lymph will contain fat
droplets (chylomicrons).
Causes: trauma and cancer

Question 9

Describe a urinothorax and what can cause it

Answer 9

movement of actual urine into the pleural space. If urine cannot get out, then it can sometimes seep into pleural cavity.
Causes: obstruction or trauma that involves ureters

Question 10

What is the most common cause of a primary spontaneous pneumothorax?

Answer 10

Blister on the surface of the lung. If it pops, air from the lung alveoli will flow to the pleural space causing the lung to collapse.

More common in smokers and tall, slender men.

Question 11

Secondary pneumothorax is more common in those with lung diseases such as COPD. What are causes that
may lead to this in children?

Answer 11

effects of measles, foreign body aspiration and certain congenital malformations of the lung (such as Marfan syndrome, Ehlers-Danlos syndrome, and alpha 1-antitrypsin deficiency)

Question 12

What is the difference between an open and a tension pneumothorax?

Answer 12

Open: opening in pleural space that’s unsealed. Expiration=volume decreased equals positive pressure. Inspiration=volume increased equals negative pressure.
Tension: injury that allows air to enter the pleural space but not with exhalation

Question 13

Tension pneumothorax

Answer 13

Pressure increased in the chest. Shifts mediastinum to the opposite side of chest and compresses vena cava. This leads to decreased cardiac output and venous return.
Tx: needle or chest tube into affected area to release drainage

Question 14

What is atelectasis?

Answer 14

incomplete expansion of the lung. Alveoli is deflated

Question 15

What is the difference between primary and secondary (acquired) atelectasis?

Answer 15

• Primary: lungs of newborn do not fully expand due to lack of surfactant.
• Secondary: partial or complete collapse of lungs that have once been fully expanded. Sometimes due to lack of surfactant or airway obstruction
• anesthesia could cause this-

Question 16

Asthma

Answer 16

Obstructive airway disorder caused by an immunological reaction.
-Causes: bronchoconstriction, inflammation of bronchioles, and increased mucus

Question 17

Asthma symptoms

Answer 17

wheezing, shortness of breath, chest tightness, and a cough

Question 18

Extrinsic (allergic or atopic) Asthma

Answer 18

Type 1 hypersensitivity that begins in childhood.

Causes: Family history, airborne allergens, overproduction of IgE

Question 19

Explain the pathophysiology of atopic asthma

Answer 19

• Antigen presenting cell (APC) presents allergen to naïve helper T-cells. Helper T-cells secretes IL-4 which triggers more naïve cells to differentiate into T helper 2 cell (TH2).
• TH2 interacts with B cells and release IL-4 to cause B cells to produce IgE antibodies.
• IgE binds to mast cells.
• TH2 cells also release IL-5 which activates eosinophils and IL-13 which causes mucus secretion.
• Allergen binds to IgE on mast cells. This causes cytokines and histamine to be released.

Question 20

What does histamine, IL-13, cytokines, and leukotrienes do?

Answer 20

• Histamine: vasodilator and increase vascular permeability
• IL-13: increased mucus production by goblet cells
• Cytokines: trigger intrapulmonary parasympathetic nerves to release ACH = increase in bronchoconstriction and mucus secretion
• Leukotrienes: contribute to bronchoconstriction and vascular permeability

Question 21

Late response in extrinsic Asthma

Answer 21

Due to damage done by recruited leukocytes (eosinophils, neutrophils, basophils)
-Eosinophils release toxic substances that cause further damage and inflammation

Question 22

What happens with airway remodeling?

Answer 22

Repeated asthmatic episodes brings lasting changes to the airway. Immune cells like mast cells, macrophages, eosinophils, and neutrophils accumulate underneath a thickened basement membrane.
Underlying smooth muscle cells undergo hypertrophy and hyperplasia.
This causes excess mucus

Question 23

Risks for atopic asthma

Answer 23

• polymorphisms in genes that code for cytokines and cytokines receptor.
• exposure to second hand smoke in fetuses and young children
• growing up in industrialized areas

Question 24

Intrinsic (Non-Atopic Asthma) triggers

Answer 24

Not caused by allergies
Triggers: respiratory viral infections, air pollutants (smog), occupational exposure, and harmless actions (exercise, the cold)

Question 25

Explain how NSAIDs can be a trigger of intrinsic asthma

Answer 25

Symptoms: chronic rhino sinusitis, nasal polyps, and bronchial asthma

• NSAIDS decrease the production of a prostaglandin called PGE-2
• PGE-2 inhibits enzymes that produce leukotrienes (bronchoconstrictors)

Question 26

What are the cardinal symptoms of asthma?

Answer 26

chest tightness, dyspnea or shortness of breath, coughing that may or may not produce sputum, and wheezing

Question 27

How can skin and blood tests help with a diagnosis of asthma?

Answer 27

can reveal allergic responses to particular antigens and blood tests can reveal specific IgE antibodies as well as eosinophilia counts

Question 28

For someone having an asthmatic attack, how would you expect FEV1/FVC ratio and PEF values to change?

Answer 28

• low FEV1/FVC RATIO

- PEF: decrease before an asthma attack

Question 29

Drugs that help Asthma

Answer 29

o Short-acting beta-2 agonist (SABA): bronchodilators (increase cAMP)
o Long acting beta-2 agonist (LABA): bronchodilators (increase cAMP)
o Phosphodiesterase inhibitors: Theophylline (increases cAMP)
o Anticholinergics: block effects of parasympathetic nervous system and causes bronchodilation
o Inhaled corticosteroids: anti-inflammatory effects
o Leukotriene receptor antagonists (LTRAs): block effects of bronchoconstricting leukotrienes
o 5-lipoxygenase inhibitors: block effects of bronchoconstricting leukotrienes
o Anti-IgE monoclonal antibodies: Omalizumab binds up IgE to decrease effect on mast cells.