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Pathology dt2 > Chapter 13: Lecture lung part 1 > Flashcards

Chapter 13: Lecture lung part 1 Flashcards

1
Q

What topics of the lung will be discussed? (you obv don’t have to learn this, just to show you what you can expect)

A

• Normal anatomy/histology • Obstructive lung disease • Restrictive lung disease • Vascular diseases • Lung infections • Lung tumors

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2
Q

What is the main function of the lungs?

A

Gas exchange (O2 and CO2)

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3
Q

How much m2 is there in the lungs for gas exchange?

A

143 m2! (don’t learn by heart)

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4
Q

Through what infrastructure/logistics is the gas exchange in the lungs possible?

A
  • conducting airways - conducting vessels - innervation - defence (of hazards)
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5
Q

The air enters the lungs by a system. How is this system called?

A

Tracheobronchial system

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6
Q

Which muscles support the lungs?

A

Diafragm and intercostal muscles

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7
Q

What devices can be used for medical imaging (beeldvormend onderzoek) of the lungs?

A
  • X-thorax - CT - MRI - ultrasound - bronchioscopie (more invasive)
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8
Q

There are two types of examination for the lung in the pathology department. which two?

A

Cytology and histology

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9
Q

How/what is studied in cytology?

A

Cells (fluid is extracted): - sputum - broncho alveolair lagae (BAL) - Bronchial brush - Fine needle aspiration - pleural effusion

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10
Q

How/what is studied in histology?

A

Tissue (biopsy) - Lymph node biopsy - Bronchial biopsy - Core needle biopsy - Open lung biopsy - Surgical resection

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11
Q

Explain, from out- to inside the layers of cells in trachea (bronchi)

A

Cartilage - (seromucinous) glands - epithelium - lumen

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12
Q

What layers/structures can be distinguished in bronchioli?

A

No cartilage/glands! Alveoli, smooth muscle, epithelium, pulmonary arteries/veins

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13
Q

True/false: the cells change from ciliated simple columnar / cuboid epithelium to goblet cells the further you go into the lung

A

true

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14
Q

Are there microvilli or cilia in the lungs?

A

Cilia! (microvilli are in the intestine)

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15
Q

In which direction do cilia move?

A

Towards the mouth / upwards

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16
Q

Fill in: Because of smoking *mucous/squamous cells can change to *mucous/squamous* epithelium

A

mucous and squamous, respectively

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17
Q

During what circumstances/syndromes can the ciliary movement be disturbed?

A

Ciliary dyskinesia syndrome (without situs inversus), kartagener syndrom (with situs inversus) and smoking.

((In both syndromes -> the disturbed cilia affect the airways which result in dilation of the bronchi -> bronchiectasis))

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18
Q

At which part of the lung does gas exchange take place?

A

Alveoli

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19
Q

What type of cells line the alveoli?

A

Type 1 and 2 pneumocytes (you don’t need to know what they do etc)

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20
Q

What are A-E?

A

A = axial artery

B = interlobular septum

C = lymph vessel

D = bronchiole

E = vein

21
Q

There are different forms of atelectasis. When there’s fluid in the lungs, the form of atelectasis is…

A

compression atelectasis.

22
Q

What is atelectasis?

A

Atelectasis is the collapse or closure of a lung resulting in reduced or absent gas exchange

23
Q

What do DAD and ARDS stand for?

A

Diffuse Alveolar Damage and Adult Respiratory Distress Syndrom

24
Q

Is DAD and ARDS more or less the same?

A

Yeah, DAD is what you can see histology, which we then call ARDS

25
Q

Through what steps does DAD/ARDS develop (histology/clinically)?

A

1 Acute rapidly progressive respiratory insufficiency

2 Hypoxaemia → cyanosis

3 Pulmonary oedema

4 Progression to multi-organfailure (poor prognosis)

26
Q

How many causes of DAD are there, and what are some examples

A

100+ causes, due to infection, sepsis, shock, inhalation of toxic fumes

27
Q

We now continue to the next topic, vascular diseases related to the lung. What is the most common/important one?

A

Embolism (of legs)

28
Q

What happens when there is a truncus pulmonalis embolis?

A

Circulation/perfusion stops -> acute death

29
Q

What happens when there is a large embolus?

A

Lung infarction

30
Q

What happens if there is a smaller embolus in the smaller pulmonary arteries?

A

There is no immediate death, but you can see there is fibrosis, and there will be short of breath (anticoagulative therapy will be started)

31
Q

What are the different types of obstructive lung diseases?

A

Emphysema, chronic bronchitis and astma

32
Q

From the different obstructive lung diseases (emphysema, chronic bronchitis and astma) which are a smaller, and which are a bigger airway disease?

A

Small: emphysema, chronic bronchitis Big: asthma

33
Q

What are the characteristics of emphysema?

A

alveolar wall destruction, overinflation (not reversible)

34
Q

What are the characteristics of chronic bronchitis?

A

Productive cough, airway inflammation (often by smoking)

35
Q

What is a characteristic of astma?

A

Reversible obstruction, caused by bronchial hyperresponsiveness (triggered by allergens/infection/etc)

36
Q

What is seen in emphysema on cellular level?

A

The alveoli are damaged (of pressure), resulting in a large lumen/pockets of air, so there is a smaller surface area

37
Q

Does emphysema develop slowly?

A

Yes, many patients are asymptomatic until very sever

38
Q

What will be formed in emphysema to try compensate for the lost surface area?

A

Bulla/bullous

39
Q

How can an infection for a patient with emphysema be fatal?

A

There is already a short surface area for gas exchange, and theinflammation will result in the further damage, and since there is so little left, the patient dies (an infection is normally not a problem in healthy individuals)

40
Q

What are differences between obstructive and restrictive lung disease?

A

Obstructive lung disease: characterized by an increase in resistance to air flow caused by partial or complete obstruction at any level (emphysema, chronic bronchitis, bronchiectasis, and asthma). At the end of a full exhalation, an abnormally high amount of air may still linger in the lungs.

Restrictive lung disease: characterized by reduced expansion of lung parenchyma and decreased total lung capacity mainly due to pulmonary fibrosis affecting the walls of the alveoli. People with restrictive lung disease cannot fully fill their lungs with air. Their lungs are restricted from fully expanding.

41
Q

What are the major categories of restrictive lung disease?

A

Fibrosing, granulomatous, eosinophilic and smoking-related

42
Q

What mineral dust-induced restrictive lung diseases are there?

A

Coal dust, silica (silicosis), asbestosis (many diseases) (you don’t actually need to know these, just remember that this can be a cause)

43
Q

Infectious diseases can also result in lung diseases. Name some. (don’t learn this, just for illustration)

A

Community-acquired bacterial pneumonia, community-acquired viral pneumonia, nosocomial pneumonia, aspiration pneumonia, chronic pneumonia, necrotizing pneumonia and lung abscess, pneumonia in the immunocompromised host (there are of course many examples for each category)

44
Q

What happens more often/commonly, bacterial or viral pneumonia?

A

viral

45
Q

How does bronchopneumonia look different from lobular pneumonia?

A

Bronchopneumonia: patchy consolidation (solidifaction of the lung due to replacement of the air by exudate in the alveoli)

Lobar pneumonia: Consolidation of a large portion of a lobe or of an entire lobe.

46
Q

What inflammatory cells are seen in acute pneumonia?

A

Neutrophils (disturbing gas exchange)

47
Q

What happens after the first/acute phase of acute pneumonia, which cells enter?

A

After neutrophils, fibroblasts enter the alveoli (might lead to fibrosis)

48
Q

Explain the 4 steps of bacterial infection (Leannec) (which cells are involved)

A
  1. Congestion of hemorrhagic exudate (large component of red blood cells released from ruptured blood vessels) (24h).
  2. Red hepatinisation, granulocytes and erythrocytes present -> production of fibrin and fluid (pleural effusion) (>24h).
  3. Grey hepatinisation, breakdown of eryhtrocytes and hemoglobine (3-8 days).
  4. Resolution, sometimes fibrosis and bronchiectasies (>8-9 days).

Pathology dt2 (39 decks)

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