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CPR 2 Pulm Section > Respiratory Pathology Pt. 2 > Flashcards

Respiratory Pathology Pt. 2 Flashcards

1
Q

What is the main problem in Restrictive Lung Disease?

A

-a volume restriction

almost always due to a fibrosing problem

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2
Q

What is the main problem in an Obstructive Lung Disease?

A

-decreased flow

due to air trapping

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3
Q

How is the FEV1/FVC ratio different b/w a Restrictive Lung Disease and an Obstructive Lung Disease?

A

Restrictive: FEV1/FVC is normal

Obstructive: FEV1/FVC is reduced

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4
Q

Is the FVC reduced in Restrictive Lung Disease or Obstructive Lung Disease?

A

Restrictive

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5
Q

Is total lung capacity increased in Restrictive Lung Disease or Obstructive Lung Disease?

A

Obstructive

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6
Q

Which way does the Flow-Volume Loop shift in Restrictive Lung Disease?

A

-to the right, and the shape remains the same

kind-of almond-shaped

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7
Q

Which way does the Flow-Volume Loop shift in Obstructive Lung Disease?

A

-to the left, and the shape looks like a “chair”

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8
Q

What are some of the major Obstructive Lung Diseases?

A
  • COPD/Chronic Bronchitis
  • Emphysema
  • Asthma
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9
Q

What is the most common cause of COPD/Chronic Bronchitis?

A

smoking

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10
Q

What is typically the first clinical manifestation of a lung injury due to smoking?

A

chronic bronchitis

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11
Q

What are the requirements for a clinical diagnosis of Chronic Bronchitis?

A

-persistent cough w/ sputum production for 3mos out of 2 consecutive years

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12
Q

What would you see on histology of Chronic Bronchitis?

A

-thickened submucosal layer due to mucous gland hyperplasia (which causes damage to the airway epithelium)

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13
Q

What are some complications of Chronic Bronchitis?

A

-squamous metaplasia, leading to dysplasia, and potentially carcinoma (resp. epithelium changes to squamous to better tolerate the irritation)

  • bronchiectasis
  • death from a respiratory infection
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14
Q

What is the physical feature that makes emphysema an Obstructive Lung Disease?

A

-the alveolar ducts are compressed

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15
Q

What would you see on a CXR of a patient w/ emphysema?

A
  • enlarged lungs that are abnormally dark d/t excess trapped air
  • flattened diaphragm
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16
Q

What would you see on a physical exam of a patient with emphysema?

A
  • barrel chest
  • diminished breath sounds
  • prolonged expiratory wheezing
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17
Q

Is Emphysema a clinical diagnosis or a pathologic diagnosis?

A

Pathologic: permanent enlargement and destruction of air spaces distal to the terminal bronchioles

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18
Q

What would you see in the typical “Blue Bloater” Chronic Bronchitis patient?

A
  • overweight
  • cyanotic
  • elevated Hb
  • peripheral edema
  • rhonchi (rough breath sounds) and wheezing
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19
Q

What would you see in the typical “Pink Puffer” Emphysema patient?

A
  • older
  • thin
  • severe dyspnea
  • quiet breath sounds
  • hyperinflated lungs and flattened diaphragm on CXR
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20
Q

What are the two types of Emphysema and what is dilated in each?

A

Centriacinar Emphysema: respiratory bronchioles (ex: as a result of COPD)

Panacinar Emphysema: Alveolar duct and alveolus (ex: as a result of alpha1-antitrypsin deficiency)

21
Q

What substance is able to damage the lung in alpha1-antitrypsin deficiency?

A

neutrophil elastase

22
Q

What area of the lung is most affected in alpha1-antitrypsin deficiency?

A

-the base of the lungs

basilar panacinar emphysema

23
Q

Explain why a basilar panacinar emphysema is seen in alpha1-antitrypsin deficiency.

A
  • damage is coming through the bloodstream, which surrounds the alveoli
  • blood volume is greater in the base of the lungs d/t gravity
24
Q

What type of clinical presentation might suggest alpha1-antitrypsin deficiency?

A

-a young smoker presenting w/ chronic bronchitis and emphysema at a very early age (30-40)

25
Q

What gene encodes for alpha1-antitrypsin?

A

Pi gene on chromosome 14

  • Z allele is associated w/ decreased alpha1-antitrypsin
  • majority of homozygotes develop emphysema
26
Q

How is alpha1-antitrypsin tested for?

A

-serum testing

27
Q

What some complications of emphysema?

A
  • respiratory failure
  • coronary artery disease
  • R heart failure
  • pneumothorax w/ lung collapse
28
Q

What are the three major components of asthma?

A

-recurrent airway obstruction w/ a REVERSIBLE component

  • airway hyperresponsiveness
  • airway inflammation
29
Q

What is the “definition” of asthma?

A

bronchial hyperresponsiveness triggered by allergens, infection, etc.

30
Q

What factors are responsible for the narrowed lumen in asthma?

A
  • muscle constriction
  • mucus
  • inflammation
31
Q

What are the two types of asthma and which is more common?

A

Atopic (extrinsic)
–more common

Non-atopic (intrinsic)

32
Q

What are the characteristics of atopic asthma?

A
  • Dx in childhood
  • family Hx
  • elevated IgE (Type I hypersensitivity)
  • eosinophils, mast cells, lymphocytes
  • triggered by allergens
33
Q

What are the charactertistics of non-atopic asthma?

A
  • older patients
  • normal IgE
  • T lymphocytes and neutrophils
  • triggered by cold, exercise, and infection
34
Q

What are the main leukotrienes active in asthma?

A

C4
D4
E4

35
Q

Why is it important to properly manage asthma?

A
  • repetitive attacks lead to airway remodeling/fibrosis, smooth muscle hyperplasia, and increased goblet cells
  • changes may be irreversible because they no longer respond to therapeutic agents such as bronchodilators and corticosteroids
36
Q

What is status asthmaticus?

A

unremitting, potentially fatal asthma attack

37
Q

What are the characteristics of status asthmaticus?

A
  • bronchial occlusion by thick mucus
  • coiled mucus plugs (“Curschmann spirals”)
  • eosinophils
  • breakdown product (“Charcot Leyden crystals)
38
Q

What two other conditions are highly associated with atopic asthma?

A
  • seasonal allergies

- eczema

39
Q

What is Samter’s Triad?

A
  • nasal polyps
  • recurrent rhinitis
  • unique sensitivity to aspirin

–seen in Aspirin-Sensitive Asthma

40
Q

How does aspirin cause asthma?

A
  • inhibits the cyclooxygenase path of arachidonic acid, so it must go down the lipoxygenase path
  • lipoxygenase path creates leukotrienes C4, D4, E4
41
Q

What is Bronchiectasis?

A
  • necrotizing inflammatory response

- end stage process of infection, obstruction, ABPA, CF, TB, and primary ciliary dyskinesia

42
Q

What is seen physically on the lungs with Bronchiectasis?

A

-dilated bronchi extending to the pleural surface

43
Q

What is the pathogenesis of Primary Ciliary Dyskinesia?

A

-dysfxn of the dynein arm of microtubules

44
Q

What are the cilia (w/ the help of dynein) responsible for during embryonic development?

A

–rotating our organs

45
Q

What is the triad of Primary Ciliary Dyskinesia?

A
  • sinusitis
  • bronchiectasis
  • situs inversus
  • –> you’ll see dextrocardia and a R gastric bubble on imaging
46
Q

How is male fertility affected in Primary Ciliary Dyskinesia?

A
  • male infertility d/t dysfxnal microtubules in the flagella

- sperm can’t swim

47
Q

What is Allergic Bronchopulmonary Aspergillosis?

A

-exaggerated hypersensitivity response to Aspergillus infection overlying chronic lung disease (ex: CF or asthma)

48
Q

What are the clinical characteristics of Allergic Bronchopulmonary Aspergillosis?

A
  • increased serum IgE
  • positive skin test
  • thick, dark mucus in bronchi
  • –>w/ fungal septated hyphae

CPR 2 Pulm Section (9 decks)

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