Respiratory Pathology Flashcards

1
Q

Explain the adaptations that smoking evokes (causes) in the conductive region of the airways.

A

Smoking irritates the ciliated epithelium of the conductive airways, which stimulates increased secretion of mucous and metaplasia to stratified squamous epithelium. This results in loss of the mucociliary escalator thus predisposing individuals towards obstruction from mucous, respiratory infections and injury from inhaled particulate

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2
Q

Are the changes from smoking reversible?

A

Yes, the metaplasia is reversible if smoking ceases however, if there has been scarring due to infection and necrosis the scar tissue will remain

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3
Q

What is the significance of saying that a cancer found in the lung is “undifferentiated”?

A

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

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4
Q

What is the most common malignancy diagnosed/found in the lungs?

A

secondary or metastatic cancer.

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5
Q

Why do the lungs frequently become involved in metastatic cancers?

A

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.

All venous blood goes back to the lungs and the lymphatic system joins the venous system. Most cancers will spread in the lymph first or in the venous blood because they will enter through a capillary bed.

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6
Q

Bronchopeumonia

A

is common, affecting immune-compromised individuals and involving an opportunistic infection. bacteria breathed in travels down the airways lodging in the terminal bronchioles and stimulating an inflammatory response in the surrounding alveoli

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7
Q

Lobarpneumonia

A

is rare, involves bacteria of high virulence, which are either breathed in or travel to the lungs during septicaemia. It may affect anyone who comes into contact with the pathogen and results in an inflammatory response that affects the entire lung or lobe of a lung.

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8
Q

Possible outcomes of Pneumonia

A

The outcomes of acute are resolution (healing without scarring), organization (healing with scarring) and chronic inflammation.

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9
Q

What are the possible complication of pneumonia?

A
  • Pleurisy/pleuritis, when the inflammatory response has been very strong the fluid and plasma proteins (oedema) including fibrin leaks into the pleural lining leading to pain and the risk of scarring.
  • If the bacteria cause a lot of necrosis it can lead to the formation of an abscess(s)
  • If the bacteria get into the blood they can cause septicaemia and infections in other organs
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10
Q

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

A

Anything that damages, paralyses or removes the cilia on the epithelium will compromise our defence 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’

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11
Q

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

A

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

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12
Q

What aetiological agent is common to all 4 COPD’s?

A

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

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13
Q

What changes occur in the airways of chronic asthma sufferers?

A

Hyperplasia of goblet cells and the deeper mucous secreting glands and hypertrophy of the smooth muscle within the walls of the airway. The excess mucous section can result in metaplasia of the ciliated columnar cells so that they become stratified squamous cells.

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14
Q

What is the definition of chronic bronchitis?

A

Chronic productive cough persisting for at least 3 months and in 2 consecutive years

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15
Q

Define Bronchiectasis and explain how it develops

A

Bronchiectasis is the irreversible, progressive dilatation of the bronchi and bronchioles caused by obstruction with mucous plugs followed by chronic necrotising infections. The infections destroy the elastic tissue and lead to scarring which leads to permanently dilated airways

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16
Q

What is emphysema?

A

Progressive irreversible destruction of alveolar walls typically without fibrosis. Note the alveolar walls are thin but contain elastic fibers and capillary beds which when lost cause increased pulmonary resistance/pulmonary hypertension.

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17
Q

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

A

The loss of alveolar walls means the loss of capillaries, less pulmonary capillaries increase resistance resulting in pulmonary hypertension. The resulting right ventricular hypertrophy can eventually lead to heart failure. The lungs are overinflated in emphysema and the individual must recruit muscles and expend energy to expel air. This results in hypertrophy of some chest muscles causing the thoracic cavity to adopt a barrel-like shape. The caloric demands typically result in loss of fat and muscle. While oxygen levels are sufficient, accumulating carbon dioxide causes respiratory acidosis and gives the patient a pinkish hue

18
Q

What is pulmonary congestion?

A

Pulmonary congestion is the passive accumulation of blood within the vessels of the lung that may be caused by obstruction of blood flow through the lungs or through the left side of the heart due to valve disease or failure of the left ventricle.

19
Q

What causes pulmonary congestion?

A

Hyperaemia, the active version will occur when there is infection or necrosis of lung tissue and, like congestion, will lead to oedema

20
Q

What pathology is more likely in an individual suffering from pulmonary congestion?

A

Within the lungs there is an increased chance of haemorrhagic infarction and greater susceptibility towards pulmonary infections.
The congestion will increase pressure in the right side of the heart and therefore lead to right ventricular hypertrophy and potentially failure. In severe, prolonged cases, congestion may be evident in the vena cava and liver

21
Q

Where do most lethal pulmonary emboli derive from?

A

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

22
Q

What factors predispose an individual towards pulmonary embolism?

A

Coagulative Sates

23
Q

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

A

Pulmonary emboli do not always cause infarction; it depends upon the size of the emboli as well as the age and health of the individual. 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.

24
Q

What is the most common cancer found in the lungs

A

Secondary or metastatic cancer

25
Q

Which two cellular adaptations precede the development of the majority of (primary) lung cancers?

A

Hyperplasia & metaplasia

26
Q

If mutations occur to proliferating goblet cells, what cancer could it form?

A

Adenocarcinoma, as it is a glandular epithelial cell

27
Q

List two innate defenses of the respiratory system:

A

Ciliated epithelium & mucous, cough/sneeze reflex, macrophages

28
Q

List two conditions that can reduce the innate defences of the respiratory system.

A

Smoking, asthma & cystic fibrosis as these patients will often have impaired muco-ciliary clearance; coma, immobility & congestion predisposes to “wet lungs” or oedema & immune-suppressing treatments impair macrophages as well as many other immune and inflammatory cells.

29
Q

In pneumoconiosis does the lung heal through organization or resolution?

A

Organization -> increases risk of cancer

30
Q

What type of inflammation if observed in pneumoconiosis?

A

Chronic as the stimulus remains

31
Q

List two possible causes for pulmonary congestion?

A

left ventricular failure, pulmonary emboli, obstruction of vessels within the lungs by mucous plugs, primary or secondary tumours or contracting scar tissue

32
Q

Pulmonary congestion leads to hypertrophy of which ventricle?

A

Pulmonary congestion leads to pulmonary hypertension (there is increased resistance to blood entering the lungs) & therefore the right ventricle will work harder & thus hypertrophy.
Pulmonary congestion is a consequence of left ventricular failure.

33
Q

What is pneumoconiosis

A

interstitial lung disease caused by breathing in certain kinds of dust particles that damage your lungs

34
Q

What is Pneumonia?

A

inflammation in our respiratory system

35
Q

How are lungs affected by left ventricular failure?

A

In left sided heart failure the backwards affects are pulmonary congestion which will lead to an increase in hydrostatic pressure leading to pulmonary oedema.

36
Q

How do lung diseases contribute to right ventricular failure?

A

Lung disease leads to pulmonary hypertension, resistance of blood flow entering what should be a low-pressure circuit and the right side of the heart will have to hypertrophy to overcome that resistance. Then we will start to see failure.

37
Q

Asthma

A

a condition in which your airways narrow and swell and may produce extra mucus

38
Q

Chronic Bronchitis

A

long-term inflammation of the bronchi

39
Q

Bronchiectasis

A

chronic condition where the walls of the bronchi are thickened from inflammation and infection

40
Q

Emphysema

A

over-inflation of the alveoli