Module 6

Question 1

1. Describe dyspnea, orthopnea and paroxysmal nocturnal dyspnea (PND).

Answer 1

dyspnea: shortness of breath, nostrils flare and accessory muscles of respiration are used. (sternocleiodomastoid, abs, internal intercostal muscles etc.)
orthopnea: dyspnea lying down (ab contents to put pressure on diagphragm)

PND: awakening of night w/dyspnea

Question 2

2. Describe 7 other symptoms/signs of respiratory disease.

Answer 2

dyspnea
cough
abnormal sputum
hemoptysis
abnormal breathing pattern
cyanosis
clubbing
pain

Question 3

3. Define hypercapnia (hypercarbia), its immediate cause, and three occurrences that can bring the immediate cause to happen

Answer 3

increase in CO2 in arterial blood, ventilation is difficult bc CO2 can diffuse faster.
Alveolar hypoventilation cab be from drugs, medullar disease, physiological dead space, emphysema.

Question 4

4. Define hypoxemia and explain the difference from hypoxia.

Answer 4

hypoxemia - decrease of oxygenation of the arterial blood

hypoxia - decrease of O2 in cells

Question 5

5. a. Explain the 3 mechanisms that can reduce oxygenation of the blood.

Answer 5

decrease alveolar O2 delivery
O2 diffusion from alveli to blood V/Q mismatch = hypoxemia + inadequarte Q makes dead space wasted = pulmonary embolism
Anatomical L to R shunt (not uncommon)

Question 6

b. By what two means can oxygen delivery to the alveoli be decreased? Be familiar with examples of conditions/diseases that can cause this.

Question 7

What does V/Q refer to?

Answer 7

V = alveolar ventilation
Q = Perfusion

Question 8

d. What is the most common cause of hypoxemia?

Answer 8

V/Q mismatch

Question 9

e. Describe the conditions of low and high V/Q and be familiar with examples of diseases that cause each.

Answer 9

High V/Q = inadequate perfusion - mostly emobli
Low V.Q = decreased diffusion across the alveolar capillary membrane, thickened membrane brought by edema or fibrosis, R-L shunt.

Question 10

What conditions can decrease diffusion across the alveolorcapillary membrane?

Answer 10

edema, fluid in blood and alvelous instersitial or space lining which O2 cannot diffuse through it because it is fibriotic or too thick.

Question 11

g. What is the difference between anatomical and physiological “right to left shunt”?

Answer 11

Moving blood through unventilated parts of the lungs “waste of energy”

Question 12

6. What causes, and is the result of, chest wall restriction?

Answer 12

decrease in tidal volume
chest is deformed, traumatized immobilized or heavy from fat accumulation.
eg. grose obese, neuromuscular diseases, polomyletitis and muscular atrophy

Question 13

7. Describe flail chest.

Answer 13

trauma of the chest wall, fracture of several consecutive ribs.
chest walls moves with inspiration and out with expiration = paradoxic movement with disruption it pulls outwards to the throacic cavity which prevents pulling from two sides.

Question 14

8. Define pneumothorax and its effect on the lung.

Answer 14

air presecnce in the pleural space, air pushes outside of the lung then collapse = the membrane space around the lungs.

Question 15

9. Define pleural effusion and how it usually occurs.

Answer 15

excess fluid in the pleural space and it occurs with the migration of fluid through capillary walls bordering the pleura.

Question 16

Define empyema and how it can occur.

Answer 16

infected pleural effusion - pus collection in pleural space.

complications of pneumonia, surgery etc.

Question 17

Describe atelectasis, its causes, and manifestations.

Answer 17

lung collapse/external compression.
eg, excess fluid in pleural space, tumour, abdominal distension, obstructed airway.
- develops after surgery
- dysnea, cough and terberculocytosis
- mostly from surgery, meds and not moving.

Question 18

What medical procedure often results in atelectasis and what measures can be taken to improve patients’ condition?

Answer 18

surgery - make the patients get up and walk to move around, breathe deeply and move positions when laying down.

Question 19

Describe bronchiectasis and identify some causes.

Answer 19

Permanent dilation of the
bronchi, secondary to other
diseases that cause chronic
inflammation of bronchial wall
(e.g., TB, cystic fibrosis).
• Chronic inflammation leads to
destruction of elastic and
muscular components of bronchi
walls and permanent dilation.
• Clinical manifestations include:
chronic cough, recurring lower
respiratory tract infection,
production of purulent sputum
(cupfuls), hemoptysis and
clubbing of the fingers (due to
chronic hypoxemia)

Question 20

Describe the pathophysiology behind cystic fibrosis and its treatment.

Answer 20

Autosomal recessive disorder
• Mutation produces inability of cell membranes to transport
chloride ion. This causes a series of events, resulting in
increased absorbance of sodium and water from respiratory
secretions. This produces very thick mucous, which is
difficult for cilia to move. The mucous then accumulates,
increasing the risk of infections (especially with Pseudomona
aeruginosa).
• Recurring infections produce bronchitis, eventually
bronchiectasis.
• Treatment: includes antibiotics to control infection, possible
replacement of pancreatic enzymes (pancreas also affected).

Question 21

What is a pulmonary embolism and of what is the most common embolus comprised?

Answer 21

Occlusion of a portion of the pulmonary
vascular bed by an embolus.
• Most common embolus is a clot from deep
venous thrombosis involving the lower leg.
• Embolus could also be fat, air bubble, etc.

Question 22

What does obstruction of blood flow cause in the lung and what is the result if the clot is not dissolved soon enough?

Answer 22

Obstruction of blood flow causes pulmonary
vessels to constrict, resulting in impaired gas
exchange (V/Q mismatch). If clot is not
dissolved rapidly, the resulting hypertension
could possibly lead to right heart failure.

Question 23

What are the clinical manifestations of a pulmonary embolism?

Answer 23

Depends upon size and
location of obstruction
• Small emboli may go
unnoticed unless patient’s
health is otherwise
compromised.
• Moderate emboli: sudden
onset chest pain, dyspnea,
tachypnea, tachycardia
• Massive emboli: sudden
collapse, crushing chest
pain, shock – often fatal

Question 24

Define pulmonary hypertension, and explain how hypoxemia and certain heart conditions can lead to this condition

Answer 24

Elevated mean pulmonary artery pressure.
• Most cases develop as a serious complication of many acute
and chronic pulmonary disorders (e.g., COPD)
• A common cause is continued exposure of pulmonary vessels
to hypoxemia, which causes these vessels to constrict (unlike
systemic vessels, which dilate).
• Can also be caused by mitral valve disorders or left ventricular
diastolic dysfunction, which raise left atrial pressure.

Question 25

What is cor pulmonale, its primary cause, and its effects?

Answer 25

Right ventricular enlargement (hypertrophy, dilation, or both), caused by chronic pulmonary hypertension (higher than normal pulmonary artery pressure) • Results in increased systemic venous circulation = peripheral edema, etc. it can result because of low arterial circulation

Question 26

What is pulmonary edema? How is it commonly caused and how does it result in hypoxemia?

Answer 26

Excess “water” in the lungs – Most common cause is left-sided heart failure. Failure of left ventricle causes increased filling pressure, which causes back-up of blood in lungs, increasing pressure in lung capillaries. When this exceeds osmotic pressure of lung capillaries, fluid and RBCs leave capillaries and collect in the interstitial space – When there is too much interstitial fluid for lymph system to collect, edema occurs. Fluid eventually leaks into the alveoli: – fewer alveoli available to expand with air – means a reduction in surface area of respiratory membrane – thickening of available respiratory membrane (increased distance for oxygen molecules to diffuse)

Question 27

21. Describe clinical manifestations of pulmonary edema.

Answer 27

Clinical manifestations: dyspnea, cyanosis, increased physical effort in breathing, blood-tinged frothy sputum

Question 28

To what are obstructive lung diseases due?

Answer 28

Due to airway obstruction that is worse with expiration – emptying of the lungs is slowed

Question 29

What two diseases are grouped together under the title “chronic obstructive pulmonary disease”?

Answer 29

asthma, bronchitis and emphysema

Question 30

. What are the unifying symptom and sign of obstructive lung diseases?

Answer 30

unifying symptom is dyspnea and wheezing

Question 31

Define bronchial asthma.

Answer 31

chronic inflammation - to the bronchiole mucosa that causes hypersensitivity and obstruct airways. - genetic and environmental factors are at play

Question 32

Describe the early response stage of an asthma attack, including clinical manifestations.

Answer 32

Usual type I hypersensitivity response: allergen exposure to the bronchial mucosa activates B cells (plasma cells) to produce IgE which complexes with mast cells. – Further exposure cross-links the IgE, causing the mast cells to release a host of chemicals, which cause vasodilation, increased capillary permeability, mucosal edema, bronchial smooth muscle contraction and mucous secretion. (See diagram). Refer also to Module 2 – Type I hypersensitivity – Clinical manifestations at the beginning of an attack: chest constriction, expiratory wheezing, dyspnea, tachycardia, coughing.

Question 33

Describe the 4 steps in the late response stage of an asthma attack, including how respiratory alkalosis can arise in the late stage of an asthma attack, and how this can develop into respiratory acidosis.

Answer 33

Begins 4-8 hours after the early response; can be more severe than initial attack 1. Release of inflammatory chemicals – Chemokines released by cells in early response call other inflammatory cells: neutrophils, eosinophils and lymphocytes, to the area. – Inflammatory chemicals released by these cells cause further bronchospasm, edema and mucous secretion. 2. Cell damage + mucous accumulation – Damage from these chemicals occurs to ciliated epithelial cells. Mucous accumulates and cellular debris forms plugs in the airways impeding alveolar ventilation. (See diagram) – Untreated inflammation can lead to long-term airway damage that is irreversible. Air trapping → hypoxemia → respiratory alkalosis – The obstructed airway makes it more difficult to expire, causing air to be trapped in alveoli, increasing alveolar gas pressures. This causes decreased perfusion of blood over the alveoli (capillaries collapse), leading to hypoxemia – The hypoxemia stimulates the respiratory centre → hyperventilation – CO2 diffuses out of blood causing hypocapnia and respiratory alkalosis. Impairment of respiratory muscles → respiratory acidosis – The continued obstruction of airways increases air trapping (incomplete expirations), which hyperexpands the lungs and thorax, decreasing the tidal volume and increasing hypoxemia. – At this point, CO2 levels will rise, leading to hypercapnia and respiratory acidosis; the situation is life-threatening if treatment does not reverse the process quickly (mechanical ventilation may be required).

Question 34

What are the mainstays of treatment for asthmatics?

Answer 34

Mainstays of treatment are avoidance of allergens, and inhalation of anti-inflammatories, bronchodilators and adrenaline in acute attack

Question 35

What is chronic obstructive pulmonary disease characterized by?

Answer 35

airway obstruction that causes difficulty exhaling = both emphysema and bronchitis

Question 36

Define chronic bronchitis. What is it very commonly caused by?

Answer 36

– Very commonly caused by smoking – Definition: Hypersecretion of mucous and chronic productive cough for at least 3 months of the year, for at least 2 consecutive years.

Question 37

Describe the development of chronic bronchitis.

Answer 37

The airway becomes inflamed with inspiration of irritants. Edema occurs, along with the production of thick, tenacious mucous. 2. Continual inflammation leads to increases in size and number of mucous glands and goblet cells in the airway epithelium.

Question 38

Why is the term “blue bloaters” used?

Answer 38

“blue bloaters” (hypoxemia and edema, | caused by eventual right heart failure) - no o2

Question 39

Describe the treatment of chronic bronchitis.

Answer 39

bronchodilators and expectorants as needed to control cough and reduce dyspnea. – Stop smoking – Chest physical therapy – Eventually antibiotics (infection), steroids (last resort), home oxygen therapy

Question 40

What is emphysema characterized by?

Answer 40

Characterized by a loss of lung elasticity and abnormal enlargement of the airspaces distal to the terminal bronchioles, with destruction of the alveolar walls and capillaries.

Question 41

What is the difference between the physiological/anatomical causes of the obstruction of emphysema and chronic bronchitis?

Question 42

What are two causes of emphysema?

Answer 42

“Obstruction” results from changes in the lung tissue (primarily loss of elastic recoil), rather than from mucous production and inflammation, which is the case with chronic bronchitis. – Can be an inherited condition (minority – due to insufficiency of alpha1-antitrypsin that combats proteases released by normal amounts of inflammatory cells)), or through the inhalation of cigarette smoke, air pollution, etc. that increases number of inflammatory cells.

Question 43

Describe the development of emphysema.

Answer 43

1. Inflammation occurs, and inflammatory cells (neutrophils, macrophages) release proteases that cause destruction of alveolar septae. This eliminates part of capillary bed and increases volume of acini (alveoli cluster distal to terminal bronchioles). 2. This produces large air spaces within the lungs (bullae), and on the surface of the lungs, next to the pleura (blebs). These air spaces can not function in gas exchange, which increases hypoxemia. 3. Damage from inflammation includes a loss in the elastic lung tissue, which helps to keep air passages open. This results in expiration becoming difficult, thus trapping air in the lungs. 4. This hyperexpands the thorax (barrel chest), making it difficult to breathe, causing hypoventilation and hypercapnia

Question 44

Define blebs and bullae.

Answer 44

air bubbles in next to pleura (blebs) | air bubbles in lungs (bullae)

Question 45

Why is the term “pink puffer” used?

Answer 45

“pink puffers” (there is initially little hypoxemia (increased breathing can keep up with oxygen demand until late stages of the disease) but classic tripod breathing position, with lips pursed to increase lung pressure during exhalation, in an attempt to keep breathing passages open)

Question 46

Describe the treatment of emphysema.

Answer 46

must include cessation of smoking (if the patient smokes), and inhalation of corticosteroids and bronchodilating drugs. – Oxygen therapy, if required – Possible lung reduction surgery or transplant