Obstructive Lung Disease - Gupta Flashcards

(62 cards)

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
Describe consequences of alpha 1 antitrypsin deficiency
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
Paraseptal emphysema epidemiology?
Jacob, Tyler (tall, young..ish, very handsome adults)
27
Describe pathophysiology of paraseptal emphysema?
Patients will develop bulla on edges of lungs. These can rupture, causing a pneumothorax in tall, young adults
28
Alpha 1 antitrypsin deficiency causes?
Panacinar emphysema
29
In addition to having panacinar emphysema, what other condition can a patient develop from having A1AT deficiency? Why?
Liver cirrhosis. due to misfolded protein (A1AT) accumulating in the ER of hepatocytes
30
Key features of liver biopsy in panacinar emphysema
pink PAS positive hyaline globules
31
Genetics of panacinar emphysema + liver cirrhosis. What is the normal allele? What are the mutated alleles? Which homozygotes are worst?
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
Clinical definition of chronic bronchitis?
Persistent cough with sputum at least 3 months in at least 2 consecutive years
33
Increased Reid Index associated with what disease?
Chronic bronchitis
34
4 key histologic features of chronic bronchitis
1. Submucosal gland hypertrophy of large airways 2. Increased # of goblet cells in smaller airways 3. Chronic (lymphocytic) airway inflammation 4. Peribronchial fibrosis
35
Reid Ratio is a ratio of gland:wall. Glands usually account for what % of submucosa. In Chronic bronchitis, what is this value? Describe why?
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
Chronic inflammatory disorder of the airways = ?
Asthma
37
2 types of asthma?
Extrinsic (hypersensitvity), intrinsic (non-immune mediated)
38
Extrinsic asthma due to what?
Type I hypersensitivity reaction to inhaled allergen
39
Intrinsic asthma due to what? List some factors that influence this
non-immunologic reaction (precipitated by respiratory infection, stress, exercise, cold, drugs,etc)
40
What drug is known to induce intrinsic asthma?
Aspirin
41
Describe mechanism of extrinsic asthma
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
4 key microscopic features of asthma
1) Thickened basement membrane 2) Submucosal gland hypertrophy 3) Bronchial wall smooth muscle hypertrophy 4) Eosinophil rich inflammatory infiltrate
43
Eosinophils are prevalent in what obstructive lung disease?
Asthma
44
Charcot Layden crystals. What are they and what disease are they associated with?
Associated with asthma. They are eosinophil derived crystals (breakdown products), seen with allergic rhinitis (as part of asthma)
45
Spiral shaped mucus plugs. What are they called? What disease?
Curschmann spirals, seen in asthma. Simply asthmatic mucus that coil up to form these spirals.
46
Pathophys of bronchiectasis?
- 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
What congenital/hereditary conditions cause bronchiectasis?
Cystic fibrosis, Immotile cilia syndrome (e.g. Kartegener)
48
Why does CF (cystic fibrosis) cause bronchiectasis?
Chloride transport defect results in thick, obstructive mucus secretions, increasing risk for infection
49
Why do immotile cilia syndromes causes bronchiectasis?
Immotile cilia interfere with bacteria clearance.
50
Kartagener is a defect in what?
dynein arm of cilia, affects your sperm too.
51
In addition to congenital/hereditary conditions, what are other causes of bronchiectasis?
- Nectrotizing pneumonia (mycobacteria, staph) - Bronchial obstruction (tumors, foreign bodies)
52
STEP 1. Most common type of TE fistula
85.8% of TE fistulas occur where esophagus is atretic (closed off) and lower esophagus connects just superior to carina (Type C).
53
STEP 1. Describe pathophys of TE fistula
Failure of fetal respiratory tract to separate from GI tract (ventral wall of foregut)
54
STEP 1. What stage of fetal lung development does surfactant start being produced?
During the sacculation stage (weeks 26-32). Transition to flat, type I alveolar cells and type 2 cells
55
STEP 1. Most common causes of acquired TE fistula
Esophageal cancer, chronic tracheostomy with NG tube.
56
STEP 1. Biggest question to ask patients with emphysema?
Family history to determine possible AIAT deficiency
57
STEP 1. Inflammation of the nasal mucosa = ?
Rhinitis
58
STEP 1. Rhinitis most commonly attributed to?
Rhinovirus
59
STEP 1. How does Rhinitis present?
as a common cold
60
STEP 1. 3 big causes of nasal polyps.
Repeated bouts of rhinitis, cystic fibrosis, and aspirin intolerant asthma
61
STEP 1. What is the triad of aspirin intolerant asthma? What % of asthmatic adults does this encompass
1) asthma 2) aspirin induced bronchospasm 3) Nasal polyps 10% of asthmatic adults
62
STEP 1. What is an angiofibroma? What key clinical manifestation is seen?
BENIGN tumor of the NASAL MUCOSA composed of large blood vessels and fibrous tissue. Presents with profuse epistaxis