wk 6 - respiratory pathology Flashcards
list the 4 main COPDs (chronic obstructive pulmonary diseases) and what COPD refers to
- chronic bronchitis
- emphysema
- bronchiectasis
- bronchial asthma
impaired airflow due to complete or partial obstruction at any level of the bronchial tree
what is chronic bronchitis, what region is affected and what typically causes it?
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
what happens the the structures for chronic bronchitis ? and what are symptoms
- 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
what is emphysema
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
what happens to the structures in emphysema and symptoms?
-airspaces become over inflated
-inflammation and loss of elastic fibres and capillary beds
-pulmonary resistance/hypertension
-effects upper lobes
symp: dyspnea
what is bronchiectasis
irreversible and progressive dilation of bronchi and bronchioles
(conductive portion affected)
causes: smoking, obstruction and infection, congential/heredity disease
what happens to the structures for bronchiectasis?
-destruction of elastic tissue muscle
-chronic necrotising infection of the bronchi and bronchioles
-leading to scarring and permanently dilated
what is bronchial asthma and causes and types?
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)
what happens to the structures for bronchial asthma
-oedema in bronchial walls
-excessive mucous secretion
-smooth muscle hypertrophy
-innate defenses as symptoms
what happens during acute asthmatic attacks
- bronchoconstriction restricting ability to breathe
- increase in mucous production
- acute inflammation in the walls of airway
what happens when multiple acute asthmatic attacks occur?
long term changes , irreversible
proliferation of goblet cells
increase in mucous secreting glands
hypertrophy of muscle- more reactive to contracting
What is pneumoconiosis, which particles are commonly implicated in Australia & what can they cause a risk to/why?
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)
Describe the innate defences present in the conductive & respiratory portions of the lungs
innate defenses- anything thats not a lymphocyte is an innate defense
-sneezing
-coughing
-ciliated epithelium
-macrophages
-etc
What is pneumonia & what are the major differences between lobar & bronchopneumonia
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.
Using a diagram, describe the pathogenesis of the 2 most common
primary lung cancers.
simple ciliated epithelial cell and goblet cells originate
adaptations, simple ciliated: metaplasia, goblet: hyperplasia
cancers, squamous cell carcinoma, adenocarcinoma
Why are the lungs a common site for secondary cancers?
cancers break into lymph or blood and travel with it to the lungs. always travels back to the lungs to get reoxygenated.
How are the lungs affected by left ventricular failure?
backward effects: pulmonary congestion and oedema
How do lung diseases contribute to right ventricular failure?
disease change the resistance within the lung so the right side has to work harder
explain the adaptations that smoking causes in the conductive region of the airways
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
what is the significance of saying a cancer in the lung is undifferentiated
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.
what is the most common malignancy diagnosed in the lungs
secondary or metastatic cancer
why do the lungs frequently become involved in metastatic cancers?
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.
There are a number of mechanisms that protect the respiratory portions (alveoli) of the lungs, what factors may compromise or overcome these
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’
possible outcomes of pneumonia (infection/impairing the lungs defense)
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
Apart from the host’s defenses, what other factors determine whether inhalation of the particulate causes disease
Factors inherent to the particulate:
Amount breathed in,
solubility,
toxicity and
size/shape of the particles
What aetiological agent is common to all 4 COPD’s
Smoking, smoking is a risk factor for all and when you have one you are at greater risk of developing the
other three
What type of reaction occurs in atopic asthma, explain what occurs during the attack?
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.
What impact does emphysema have on the rest of the body?
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
Where do most lethal pulmonary emboli derive from?
Most large pulmonary emboli are derived from the deep veins of the lower limbs (iliac & femoral veins)
What factors predispose an individual towards pulmonary embolism? (DVT)
Stasis and hyper coagulative states
Will pulmonary emboli always lead to infarction, what factors should be considered
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
In pneumoconiosis does the lung heal through
organisation or resolution?
Organisation- chronic inflammation as stimulus remains
what is typically seen in the airways of sufferers with atopic asthma?
- Inflammatory mediators (including histamine) release.
- Bronchoconstriction (caused by PNS) to
relieve symptoms. - Oedema in the bronchial walls. vasodilation causes hyperaemia & increased vascular permeability results in exudate building up in the wall of the airways.
- Increased mucous production.
define pneumonia
any infection of the lung or conditions that impair clearing mechanisms (eg cough reflex, injury to cilia)
