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CPR 2 Exam 2 > Singh Pathology of Respiratory System #2 > Flashcards

Singh Pathology of Respiratory System #2 Flashcards

1
Q

In restrictive lung disease what will the FEV1/FVC ratio be, what will TLC be, and what will the FVC be in comparison to normal?

A
  • FEV1/FVC will be normal
    • everything is reduced so ratio stays normal
  • TLC decreased
  • FVC will be reduced
  • Volume restriction
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2
Q

How will the FEV1/FVC ratio, TLC and FEV1 present with an Obstructive lung disease?

A
  • Low FEV1
  • Low ratio
  • Increased TLC
  • Decreased flow and trapped air
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3
Q

How do you diagnose chronic bronchitis?

A

Persistent cough with sputum production for 3 months out of 2 consecutive years

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4
Q

What is the pathophysiologic mechanism behind chronic bronchitis?

A

Mucous gland hyperplasia causing damage to airway epithelium

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5
Q

What are the five complications of chronic bronchitis?

A
  • Bronchiectasis
  • Hypoxia
  • Squamous metaplasia leading to dysplasia leading to carcinoma
  • Pulmonary hypertension and cor pulmonale
  • Death from infection
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6
Q

What is emphysema?

A
  • irreversible airspace enlargement occurring distal to terminal bronchial
  • Obstructive Lung Disease
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7
Q

____emphysema due to smoking is an advanced obstructive lung disease in continuity with chronic bronchitis

A

Centrilobular emphysema due to smoking is an advanced obstructive lung disease in continuity with chronic bronchitis

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8
Q

Why is emphysema due to smoking centrilobular?

A
  • Obstruction from chronic bronchitis constricts the terminal bronchiole so dilation starts at the respiratory bronchiole and moves distally from there as the disease advances
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9
Q

How will emphysema present on CXR?

A
  • Enlarged lungs with flattened diaphragm
  • Barrel chest with increased AP diameter
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10
Q

Clinically how will emphysema present?

A
  • Diminished breath sounds with prolonged expiratory wheezes
  • Barrel Chest
  • PFT’s show restrictive pattern
    • Decreased TLC
    • Decreased FVC
    • FEV1/FVC
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11
Q

How will Chronic bronchitis present in a patient? (“blue bloaters”)

A
  • Overweight and cyanotic
  • Elevated hemoglobin
  • Peripheral edema
  • Rhonchi and wheezing
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12
Q

How will emphysema present? (“pink puffers”)

A
  • Older and thin
  • Severe dyspnea
  • Quiet chest
  • XR with hyperinflation and flattened diaphragm
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13
Q

Why does Hgb increase in chronic bronchitis?

A
  • Smoking related exposure to CO creates carboxy hemoglobin shifting the oxygen dissociation curve to the left
  • This reduces oxygen carrying capacity and compensation is to make more hemoglobin
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14
Q

What is the function of alpha 1 antitrypsin & where is it made?

A
  • coats lungs and protects them from neutrophil elastase
  • synthesized in liver and secreted into blood to inhibit neutrophil elastase
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15
Q

Genetics behind alpha 1 antitrypsin deficiency? How do you diagnose?

A
  • encoded by Pi gene on chromosome 14
  • Z allele is associated with decreased alpha 1 AT
  • Homozygous PiZZ individuals have this deficiency
  • Serum testing is primary means of diagnosis
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16
Q

Complications of Emphysema?

A
  • Pneumothorax with lung collapse
  • Pulmonary htn and cor pulmonale
  • CAD
  • Resp failure
17
Q

3 components that make up Asthma?

A
  • Recurrent airway obstruction with reversible component
  • Airway hyper responsiveness
  • Airway inflammation
18
Q

Atopic extrinsic asthma characteristics?

A
  • ⅔ of all patients
  • Any age but typically childhood
  • Fhx of asthma
  • Elevated IgE
  • Allergens can trigger
19
Q

Non atopic intrinsic asthma characteristics?

A
  • ⅓ of all patients
  • Often older patients
  • Normal IgE
  • Triggers are cold exercise and infection
20
Q

What are the bronchoconstriction mediators to asthma?

A
  • Leukotrienes C4, D4, E4
  • Histamine
  • Prostaglandin D2
  • Ach
21
Q

What kind of damage occurs with a1 AT deficiency?

A

Pan acinar emphysema due to the alveoli being bathed in blood carrying neutrophil elastase

22
Q

What are the bronchoconstriction mediators to asthma?

A
  • Leukotrienes C4, D4, E3
  • Histamine
  • Prostaglandin D2
  • Ach
23
Q

What causes mucus secretion in asthma?

A

Leukotrienes C4, D4, E4

24
Q

What causes increased vascular permeability in asthma?

A

C4, D4, E4

25
Q

What recruits inflammatory cells in asthma?

A

Interleukins

26
Q

What are the long term effects of uncontrolled asthma?

A
  • Progressive structural changes to airways with fibrosis, smooth muscle hyperplasia and increased goblet cells and submucosal glands
27
Q

What is Status Asthmaticus?

A
  • Unremitting potentially fatal asthma attack
  • Bronchial occlusion by thick mucus
    • Curschmann spirals coiled mucus plugs
  • Eosinophils and their breakdown products called charcot leyden crystals
28
Q

What is Aspirin Sensitive asthma associated with?

A
  • Asthma, Nasal polyps, & recurrent rhinitis ( samter’s triad)
29
Q

How does Aspirin sensitive asthma occur?

A

by blocking Cyclooxygenase you activate the 5-lipoxygenase pathway which increases Leukotrienes C4-E4

30
Q

What is Bronchiectasis?

A
  • Permanent dilation of airways due to inflammatory destruction
    • dilated bronchi extend to pleural surface
31
Q

What is Kartagener’s syndrome (primary ciliary dyskinesia)?

What results?

A
  • Dysfunction of dynein arm of microtubules
  • Microtubules are needed for movement of cilia and flagella
  • Triad of
    • Sinusitis
    • Bronchiectasis
    • Situs Inversus
      • relies on motile cells to rotate
    • also see male infertility due to lack of flagella on sperm
32
Q

What happens in Allergic Bronchopulmonary Aspergillosis?

A
  • Aspergillosis sits in the airways and doesn’t invade, but IgE is increased leading to thick dark mucus in the bronchi
  • Associated with bronchiectasis in advanced disease
  • Positive skin test and background of asthma or CF

CPR 2 Exam 2 (17 decks)

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