wk 6 - respiratory pathology

Question 1

list the 4 main COPDs (chronic obstructive pulmonary diseases) and what COPD refers to

Answer 1

1. chronic bronchitis
2. emphysema
3. bronchiectasis
4. bronchial asthma

impaired airflow due to complete or partial obstruction at any level of the bronchial tree

Question 2

what is chronic bronchitis, what region is affected and what typically causes it?

Answer 2

irreversible, persistent, productive cough that lasts at least 3 months in 2 consecutive years
acute, doesn’t have irreversible changes in the bronchi walls
(conductive portion affected)

causes: smoking

Question 3

what happens the the structures for chronic bronchitis ? and what are symptoms

Answer 3

• loss of cilia
  -goblet cell hyperplasia (increase mucous)
  -proliferation of smooth muscle
  -thickening on bronchial walls
  -inflammation in the airways (narrowed airways)

symp: productive cough

Question 4

what is emphysema

Answer 4

irreversible and progressive destruction of alveolar walls without obvious fibrosis
(respiratory portion of the lungs affected)

causes: Chronic bronchitis, asthma, coal dust exposure,
smoking, genetics

Question 5

what happens to the structures in emphysema and symptoms?

Answer 5

-airspaces become over inflated
-inflammation and loss of elastic fibres and capillary beds
-pulmonary resistance/hypertension
-effects upper lobes

symp: dyspnea

Question 6

what is bronchiectasis

Answer 6

irreversible and progressive dilation of bronchi and bronchioles
(conductive portion affected)

causes: smoking, obstruction and infection, congential/heredity disease

Question 7

what happens to the structures for bronchiectasis?

Answer 7

-destruction of elastic tissue muscle
-chronic necrotising infection of the bronchi and bronchioles
-leading to scarring and permanently dilated

Question 8

what is bronchial asthma and causes and types?

Answer 8

hyper-reactive airways -> bronchospasm due to smooth muscle contraction

chronic inflammatory disorder (unknown cause)

can be intrinsic (non allergic) or extrinsic (type 1 hypersensitivity, atopic/allergy)

Question 9

what happens to the structures for bronchial asthma

Answer 9

-oedema in bronchial walls
-excessive mucous secretion
-smooth muscle hypertrophy
-innate defenses as symptoms

Question 10

what happens during acute asthmatic attacks

Answer 10

1. bronchoconstriction restricting ability to breathe
2. increase in mucous production
3. acute inflammation in the walls of airway

Question 11

what happens when multiple acute asthmatic attacks occur?

Answer 11

long term changes , irreversible

proliferation of goblet cells
increase in mucous secreting glands
hypertrophy of muscle- more reactive to contracting

Question 12

What is pneumoconiosis, which particles are commonly implicated in Australia & what can they cause a risk to/why?

Answer 12

chronic inflammation caused by inhalation of particles we cannot get rid of

-carbon
-coal
-silica
-asbestos

healing through scarring therefore it can cause an increased risk in
1. respiratory failure
2. right sided heart failure
3. hard to breathe so waste away
4. increased risk of cancer (mesothelial cancer)

Question 13

Describe the innate defences present in the conductive & respiratory portions of the lungs

Answer 13

innate defenses- anything thats not a lymphocyte is an innate defense
-sneezing
-coughing
-ciliated epithelium
-macrophages
-etc

Question 14

What is pneumonia & what are the major differences between lobar & bronchopneumonia

Answer 14

lobar- rare. caused by highly virulent micro organisms that affect healthy people.

broncho- common way to die. opportunistic microbes because they have low virulence, only causes disease because of the susceptibility of the host.

Question 15

Using a diagram, describe the pathogenesis of the 2 most common
primary lung cancers.

Answer 15

simple ciliated epithelial cell and goblet cells originate

adaptations, simple ciliated: metaplasia, goblet: hyperplasia

cancers, squamous cell carcinoma, adenocarcinoma

Question 16

Why are the lungs a common site for secondary cancers?

Answer 16

cancers break into lymph or blood and travel with it to the lungs. always travels back to the lungs to get reoxygenated.

Question 17

How are the lungs affected by left ventricular failure?

Answer 17

backward effects: pulmonary congestion and oedema

Question 18

How do lung diseases contribute to right ventricular failure?

Answer 18

disease change the resistance within the lung so the right side has to work harder

Question 19

explain the adaptations that smoking causes in the conductive region of the airways

Answer 19

Smoking irritates the ciliated epithelium of the conductive airways, which stimulates increased secretion of mucous (hyperplasia of goblet cells) and metaplasia (simple ciliated cells that are stable become labile stratified squamous cells). This results in loss of the mucociliary escalator thus predisposing individuals towards obstruction from mucous, respiratory infections and injury from inhaled particulates

Question 20

what is the significance of saying a cancer in the lung is undifferentiated

Answer 20

indicates the cells of the cancer can no longer resemble the cell type that the cancer arose in. undifferentiated tumours are usually malignant, aggressive and resistant to treatment also.

Question 21

what is the most common malignancy diagnosed in the lungs

Answer 21

secondary or metastatic cancer

Question 22

why do the lungs frequently become involved in metastatic cancers?

Answer 22

Cancers that enter the blood usually do so from lymph, capillaries or venules and since all venous blood
returns to the lungs for re-oxygenation, they are commonly affected by secondaries.

Question 23

There are a number of mechanisms that protect the respiratory portions (alveoli) of the lungs, what factors may compromise or overcome these

Answer 23

Anything that damages, paralyses or removes the cilia on the epithelium will compromise our defense against particulate inhalation e.g. metaplasia from smoking, excess mucous secretion (smoking, asthma, CF, inflammation) damage from heat/acute smoke from fire, very cold air, etc. A loss of the cough reflex and prolonged bed rest/inactivity will promote ‘wet lungs’

Question 24

possible outcomes of pneumonia (infection/impairing the lungs defense)

Answer 24

The outcomes of acute are resolution (healing without scarring), organization (healing with scarring) and chronic inflammation. Resolution usually occurs in this case but organization may occur following necrosis

Question 25

Apart from the host’s defenses, what other factors determine whether inhalation of the particulate causes disease

Answer 25

Factors inherent to the particulate: Amount breathed in, solubility, toxicity and size/shape of the particles

Question 26

What aetiological agent is common to all 4 COPD’s

Answer 26

Smoking, smoking is a risk factor for all and when you have one you are at greater risk of developing the other three

Question 27

What type of reaction occurs in atopic asthma, explain what occurs during the attack?

Answer 27

Type 1 hypersensitivity TH2 cells cause IgE secretion of B cells following maturation to plasma cells. During the attack, the IgE which has become bound to mast cells awaiting re-exposure to the antigen is bound causing degranulation of mast cells and eosinophils which results in the release of histamine, serotonin and leukotrienes. The inflammatory mediators cause increased mucous secretion from goblet cells and deeper mucous-producing glands so that the lumen of the airways is full of mucous. At the same time, hyperaemia and oedema occurs in the walls of the airways (the walls are now thicker and oedematous). Under the influence of the PNS, we get contraction of the smooth muscle within the walls of the airways leading to bronchoconstriction. Therefore, the bronchoconstriction narrows the lumen of the airways which are full of mucous, and the walls are thick and oedematous.

Question 28

What impact does emphysema have on the rest of the body?

Answer 28

pulmonary hypertension- increased resistance due to loss of capillaries from alveolar wall destruction right ventricular hypertrophy due to resistance which can lead to heart failure (Cor pulmonale). hypertrophy of chest muscles and energy causing weight loss to expel air from overinflation. Respiratory acidosis from accumulating carbon dioxide

Question 29

Where do most lethal pulmonary emboli derive from?

Answer 29

Most large pulmonary emboli are derived from the deep veins of the lower limbs (iliac & femoral veins)

Question 30

What factors predispose an individual towards pulmonary embolism? (DVT)

Answer 30

Stasis and hyper coagulative states

Question 31

Will pulmonary emboli always lead to infarction, what factors should be considered

Answer 31

no, depends on: 1. size of emboli 2. age/ health The lung receives two blood supplies (pulmonary and bronchial) and there is usually residual oxygen in the alveoli. In young people with good vasculature, there is often sufficient collateral circulation to maintain the tissue when a vessel becomes blocked, provided of course that the clot is not too large. As we age the cardiovascular system is less efficient and capillary beds regress meaning the same size clot is more likely to result in infarction when occurring in an older person

Question 32

In pneumoconiosis does the lung heal through organisation or resolution?

Answer 32

Organisation- chronic inflammation as stimulus remains

Question 33

what is typically seen in the airways of sufferers with atopic asthma?

Answer 33

1. Inflammatory mediators (including histamine) release. 2. Bronchoconstriction (caused by PNS) to relieve symptoms. 3. Oedema in the bronchial walls. vasodilation causes hyperaemia & increased vascular permeability results in exudate building up in the wall of the airways. 4. Increased mucous production.

Question 34

define pneumonia

Answer 34

any infection of the lung or conditions that impair clearing mechanisms (eg cough reflex, injury to cilia)