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9 Respiratory Pathology > 9.4 COPD > Flashcards

9.4 COPD Flashcards

1
Q

What do they do in asthma:

IL4

IL5

IL10

A

all secreted by Th2 T cells (humoral immunity)

IL4: induce IgE

IL5: attract eosinophils

IL10: increase Th2, decrease Th1

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1
Q

Kartagener syndrome

  • mech
  • complications (4)
A
  • defect of cilia (dynein arm), necessary for cilia movement
    1. sinusitis (cilia cannot move out infection)
    2. infertility (sperm)
    3. situs inversus
    4. bronchiectasis (infection in lung leads to inflammation)
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3
Q

allergic bronchopulmonary aspergillosus (ABPA)

  • what is it
  • classic populations
A
  • allergic HSR to Aspergillus, leads to chronic inflammation and bronchiectasis
    1. cystic fibrosis
    2. asthmatics
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4
Q

chronic bronchitis

  • mech at cell level
  • histology finding
A
  • hypertrophy of mucinous glands in the submucosa that produce mucus
  • “Reed index”: normal ratio is
  • chronic bronchitis: >50% of bronchial wall is mucinous glands
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4
Q

chronic bronchitis

-clinical presentation, complications (4)

A
  1. productive cough, tons of mucus
  2. “blue bloaters”–cyanosis (mucus traps CO2, so higher PACO2 and lower PAO2)
  3. increased risk of infection
  4. cor pulmonale
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4
Q

nonallergic causes of asthma (4)

A
  1. exercise
  2. viral infection
  3. aspirin-intolerant asthma (remember bronchospasm and nasal polyps)
  4. occupational exposures (eg dust)
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5
Q

A1AT deficiency:

-what are the genetics involved

A

disease severity based on alleles:

  1. PiMM–PiM/PiM normal. A1AT is produced
  2. PiMZ–PiM/PiZ: half of A1AT produced, so asymptomatic but high risk of emphysema with smoking
  3. PiZZ–PiZ/PiZ: high risk of panacinar emphysema and liver cirrhosis
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8
Q

emphysema

-cellular mech

A
  • imbalance of proteases and antiproteases
  • proteases released by neutrophils and macrophages constantly (constant inflammation)
  • antiproteases (eg alpha-1 antitrypsin) neutralizes proteases to prevent damage
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8
Q

What do you see in mucus of asthma pts?

A
  1. MBP crystals (Charcot Leyden crystals)
  2. desquamated epithelium (Curschman spirals)
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9
Q

emphysema

  • 2 categories
  • how do their presentation differ?
A
  1. smoking–centriacinar (closer to smoke), upper lobes more severe (smoke rises)
  2. A1AT deficiency–panacinar, lower lobes more severe
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10
Q

chronic bronchitis

  • diagnosis definition
  • cause
A
  • chronic productive cough lasting at least 3 months, over min of 2 years
  • highly assoc with smoking
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11
Q

Emphysema caused by A1AT deficiency:

  • what non-lung complication occurs?
  • histology
A
  • Liver cirrhosis may occur
  • A1AT is misfolded and accumulates in hepatocytes
  • pink, PAS-positive globules in ER of hepatocytes
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12
Q

structural difference between bronchus and bronchioles

A

bronchi have cartilage

bronchioles don’t

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13
Q

what can cause complication of secondary amyloidosis?

A

Bronchiectasis

-chronic inflammation leads to SAA production, SAA converts to AA, AA deposits.

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13
Q

Causes of bronchiectasis (5)

A
  1. cystic fibrosis (mucus leads to infection)
  2. Kartaganer syndrome (cannot move mucus out, infection)
  3. tumor/foreign body (blockage)
  4. Infection, necrotizing
  5. ABPA (Allergic bronchopulmonary aspergillus)
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14
Q

bronchiectasis

  • clinical presentation
  • complications
A
  • cough, dyspnea, foul smelling sputum
  • hypoxemia, cor pulmonale, secondary amyloidosis
16
Q

Early vs late phase of asthma

A

early: histamine, leukotrienes
late: MBP from eosinophils (Charcot-Leyden crystals in mucus)

17
Q

bronchiectasis

-mech of disorder

A
  • chronic inflammation damages bronchi and bronchioles, leads to enlarged airways
  • dilated airways lose their tone, causes air trapping.
19
Q

pink, PAS-positive globules in hepatocytes

-what’s this

A
  • A1AT accumulation inside hepatocytes b/c of misfolding.
  • A1AT cannot enter blood, so results in panacinar emphysema
20
Q

emphysema

-2 causes

A

imbalance of proteases and antiproteases

  1. smoking (inflammation leads to increased proteases)
  2. A1AT deficiency (buildup of proteases)
21
Q

emphysema

-clinical presentation

A
  1. dyspnea and cough with minimal sputum
  2. “pink puffer” with pursed lips
  3. weight loss, very thin (b/c extra work of pursed lips)
  4. barrel chest
22
Q

Asthma:

describe cellular mech, from initial exposure to allergen

A

In genetically susceptible individuals:

  1. first exposure to allergens induce Th2 T-cells
  2. Th2 cells secrete IL4, 5, 10.

IL4–IgE

IL5–attract eosinophils

IL10–increase Th2, decrease Th1

  1. Next allergen exposure leads to IgE-mediated release of histamine from mast cells. Also, mast cells produce leukotrienes. (bronchoconstriction, inflammation, edema)
  2. late phase: eosinophils make major basic protein, which damages cells
23
Q

Histamine:

  1. where does vasodilation occur?
  2. where does fluid leakage occur?
A
  1. arterioles
  2. post-capillary venules

9 Respiratory Pathology (7 decks)

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