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Pulmonology > Obstructive Lung Disease - Gupta > Flashcards

Obstructive Lung Disease - Gupta Flashcards

1
Q

Name the diseases involved in Obstructive Lung Disease?

A

Emphysema, chronic bronchitis, asthma, bronchiectasis

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2
Q

What is the role of Type II Pneumocytes following injury and destruction?

A

Following injury and destruction of the normally abundant Type I pneumocyte, Type II pneumocytes proliferative and are involved in repair.

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3
Q

Buzzword for Type II pneumocyte description

A

Hobnail - shaped

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4
Q

Another name for clara cells?

A

Club cells (fucking nazis)

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5
Q

Zebra body appearance. What type of cell is it?

A

Type II pneumocyte

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6
Q

Macrophage vesicles are more spread out or close together as compared to type II pneumocyte?

A

vesicles more spread out, look more branched

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7
Q

What is the definition of atelectasis?

A

Collapse of previously inflated lung resulting in relatively airless pulmonary parenchyma

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8
Q

What are the 3 types of atelectasis?

A

Resorption (obstruction), compression, contraction

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9
Q

Resorption (obstruction) atelectasis caused by?

A

mucous plugs, tumors

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10
Q

Compression atelectasis caused by?

A

filling of pleural cavity due to blood, air, tumor, pleural effusion

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11
Q

Contraction atelectasis caused by?

A

Fibrosis of lung or pleura

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12
Q

Trapped O2 in dependent alveoli involves what type of atelectasis?

A

Resorption. Dependent simply means alveoli that have an increased hemodynamic load (usually those at the bottom of the lung)

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13
Q

Which type of atelectasis prevents full expansion of the lung?

A

Contraction atelectasis

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14
Q

Mediastinum shift observed in resorption atelectasis?

A

Shifts TOWARD affected lung

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15
Q

Mediastinum shift observed in compression atelectasis?

A

Shifts AWAY from affected lung

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16
Q

Loss of elastic recoil seen in what type of obstructive lung disease?

A

Emphysema

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17
Q

COPD = ____ + _____

A

Emphysema + Chronic Bronchitis

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18
Q

Type of disorders (3) due to airway obstruction/narrowing?

A

Chronic bronchitis, asthma, bronchiectasis

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19
Q

Abnormal PERMANENT enlargement of airspaces accompanied by DESTRUCTION OF THEIR WALLS. What disorder?

A

Emphysema

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20
Q

What is NOT a significant feature in emphysema

A

Fibrosis = NOT SIGNIFICANT

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21
Q

How is emphysema classified?

A

according to the portion of acinus affected

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22
Q

What are the 3 types of emphysema?

A

Centriacinar, Panacinar, Paraseptal

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23
Q

Centriacinar emphysema facts. Associated with what? Predominantly affects what part of lung?

A

Associated with SMOKING Primarily affects UPPER LOBES - think, smoke hits upper lobes first. help you to remember both.

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24
Q

Panacinar emphysema facts. Due to what deficiency? Predominantly affects what part of lung

A

alpha 1 - antitrypsin deficiency. Primarily affects lower lung zones

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25
Q

Describe consequences of alpha 1 antitrypsin deficiency

A

alpha 1 antitrypsin produced in liver. It should neutralize proteases released by inflammatory cells. Excessive inflammation or absent/inactive A1AT leads to destruction of elastic tissue

26
Q

Paraseptal emphysema epidemiology?

A

Jacob, Tyler (tall, young..ish, very handsome adults)

27
Q

Describe pathophysiology of paraseptal emphysema?

A

Patients will develop bulla on edges of lungs. These can rupture, causing a pneumothorax in tall, young adults

28
Q

Alpha 1 antitrypsin deficiency causes?

A

Panacinar emphysema

29
Q

In addition to having panacinar emphysema, what other condition can a patient develop from having A1AT deficiency? Why?

A

Liver cirrhosis. due to misfolded protein (A1AT) accumulating in the ER of hepatocytes

30
Q

Key features of liver biopsy in panacinar emphysema

A

pink PAS positive hyaline globules

31
Q

Genetics of panacinar emphysema + liver cirrhosis. What is the normal allele? What are the mutated alleles? Which homozygotes are worst?

A

PiM = normal allele PiZ, PiS = mutated allele. PiZ much more common PiZZ homozygotes are at increased risk. PiMZ are usually not at risk unless they smoke

32
Q

Clinical definition of chronic bronchitis?

A

Persistent cough with sputum at least 3 months in at least 2 consecutive years

33
Q

Increased Reid Index associated with what disease?

A

Chronic bronchitis

34
Q

4 key histologic features of chronic bronchitis

A
  1. Submucosal gland hypertrophy of large airways
  2. Increased # of goblet cells in smaller airways
  3. Chronic (lymphocytic) airway inflammation
  4. Peribronchial fibrosis
35
Q

Reid Ratio is a ratio of gland:wall. Glands usually account for what % of submucosa. In Chronic bronchitis, what is this value? Describe why?

A

Reid Ratio = Gland:Wall Normally, glands are 40% of wall (wall = basement membrane to perichondrium). Look at picture in notes In chronic bronchitis, glands > 50% of wall, due to hypertrophy of submucosal glands

36
Q

Chronic inflammatory disorder of the airways = ?

A

Asthma

37
Q

2 types of asthma?

A

Extrinsic (hypersensitvity), intrinsic (non-immune mediated)

38
Q

Extrinsic asthma due to what?

A

Type I hypersensitivity reaction to inhaled allergen

39
Q

Intrinsic asthma due to what? List some factors that influence this

A

non-immunologic reaction (precipitated by respiratory infection, stress, exercise, cold, drugs,etc)

40
Q

What drug is known to induce intrinsic asthma?

A

Aspirin

41
Q

Describe mechanism of extrinsic asthma

A

Type 1 hypersensitivity - Allergen comes in and binds to IgE on mast cells - Mast cells degranulate releasing histamine, leukotrienes, eosinophil chemotactic factors (IL-5) - These cause inflammation, mucus hyper secretion, bronchoconstriction = Ty Tantisook

42
Q

4 key microscopic features of asthma

A

1) Thickened basement membrane
2) Submucosal gland hypertrophy
3) Bronchial wall smooth muscle hypertrophy
4) Eosinophil rich inflammatory infiltrate

43
Q

Eosinophils are prevalent in what obstructive lung disease?

A

Asthma

44
Q

Charcot Layden crystals. What are they and what disease are they associated with?

A

Associated with asthma. They are eosinophil derived crystals (breakdown products), seen with allergic rhinitis (as part of asthma)

45
Q

Spiral shaped mucus plugs. What are they called? What disease?

A

Curschmann spirals, seen in asthma. Simply asthmatic mucus that coil up to form these spirals.

46
Q

Pathophys of bronchiectasis?

A
  • PERMANENT airway DILATION associated with smooth muscle and elastic tissue destruction - Repeated cycles of airway obstruction and inflammation leads to FIBROSIS of airway walls
47
Q

What congenital/hereditary conditions cause bronchiectasis?

A

Cystic fibrosis, Immotile cilia syndrome (e.g. Kartegener)

48
Q

Why does CF (cystic fibrosis) cause bronchiectasis?

A

Chloride transport defect results in thick, obstructive mucus secretions, increasing risk for infection

49
Q

Why do immotile cilia syndromes causes bronchiectasis?

A

Immotile cilia interfere with bacteria clearance.

50
Q

Kartagener is a defect in what?

A

dynein arm of cilia, affects your sperm too.

51
Q

In addition to congenital/hereditary conditions, what are other causes of bronchiectasis?

A
  • Nectrotizing pneumonia (mycobacteria, staph) - Bronchial obstruction (tumors, foreign bodies)
52
Q

STEP 1. Most common type of TE fistula

A

85.8% of TE fistulas occur where esophagus is atretic (closed off) and lower esophagus connects just superior to carina (Type C).

53
Q

STEP 1. Describe pathophys of TE fistula

A

Failure of fetal respiratory tract to separate from GI tract (ventral wall of foregut)

54
Q

STEP 1. What stage of fetal lung development does surfactant start being produced?

A

During the sacculation stage (weeks 26-32). Transition to flat, type I alveolar cells and type 2 cells

55
Q

STEP 1. Most common causes of acquired TE fistula

A

Esophageal cancer, chronic tracheostomy with NG tube.

56
Q

STEP 1. Biggest question to ask patients with emphysema?

A

Family history to determine possible AIAT deficiency

57
Q

STEP 1. Inflammation of the nasal mucosa = ?

A

Rhinitis

58
Q

STEP 1. Rhinitis most commonly attributed to?

A

Rhinovirus

59
Q

STEP 1. How does Rhinitis present?

A

as a common cold

60
Q

STEP 1. 3 big causes of nasal polyps.

A

Repeated bouts of rhinitis, cystic fibrosis, and aspirin intolerant asthma

61
Q

STEP 1. What is the triad of aspirin intolerant asthma? What % of asthmatic adults does this encompass

A

1) asthma 2) aspirin induced bronchospasm 3) Nasal polyps 10% of asthmatic adults

62
Q

STEP 1. What is an angiofibroma? What key clinical manifestation is seen?

A

BENIGN tumor of the NASAL MUCOSA composed of large blood vessels and fibrous tissue. Presents with profuse epistaxis

Pulmonology (31 decks)

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