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Pathology II Chamberlin Fall 2014 > Pulmonary Pathology Part I: Pulm Edema, Chronic Bronchitis, Emphysema, Asthma > Flashcards

Pulmonary Pathology Part I: Pulm Edema, Chronic Bronchitis, Emphysema, Asthma Flashcards

1
Q

What is the term for the functional unit of the lung consisting of the respiratory bronchiole and associated alveolar ducts and alveoli?

A

Acinus

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2
Q

Blood-air interface

A

The “space” between the endothelium and the type-1 pneumocyte/epithelium

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3
Q

Examples of congenital lung pathology?

A

Agenesis/hypoplasia
Tracheo-Esophageal (TE) fistula
Pulmonary vascular anomalies
Neonatal Respiratory Distress Syndrome (N.R.D.S.)

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4
Q

Embryonic Development of Lung: T or F?
A. Surfactant begins to be produced at 20 weeks
B. Alveoli begin to develop at 36 weeks
C. Alveolar ducts begin to develop at 30 weeks
D. Lung buds are an outgrowth of the foregut

A

A. False. about 25 weeks
B. True
C. False. 24 weeks
D. True

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5
Q

Pulmonary hypoplasia in the neonate may be secondary to:

A
  • Space-occupying lesions in the uterus
  • Congenital diaphragmatic hernia
  • Many others
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6
Q

The most common type of TE fistula?

What is the baby’s response to feeding?

A

Esophageal atresia with distal TE fistula

Food comes back up without going into the lungs

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7
Q

T or F? Neonatal Respiratory Distress Syndrome
A. Primary defect is lung had not yet developed alveoli
B. Etio: Oversedation of mom, head injury @ delivery, aspiration of blood/amnio fluid, Intra-uterine hypoxemia
C. Fibrous tissue forms from lack of surfactant
D. Tx = surfactant delivery or maternal Tx with steroids

A

A. False. lung will not open b/c no surfactant
B. True
C. False. Hyaline membranes form
D. True

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8
Q

Atelectasis: Reabsorption, Compression, or Contraction?
A. can be from a pleural effusion or pneumothorax.
B. can be from a diffuse lung fibrotic process.
C. can be from a bronchial obstruction, such as a tumor.
D. results from underperfused tissue

A

A. Compression
B. Contraction
C. Reabsorption
D. Contraction

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9
Q

Other than cardiogenic and non-cardiogenic, additional causes of Pulmonary Edema?

A
  • Fluid overload (renal failure, iatrogenic)
  • Hypoalbuminemia (liver disease, Nephrotic syndrome, severe malnutrition)
  • Lymphatic obstruction (cancer)
  • Injury to the capillaries of the alveolar septae
  • Infectious agents (i.e. Mycoplasma pneumonia)
  • Liquid aspiration (gastric contents, near-drowning)
  • Gas inhalation (too much oxygen, smoke)
  • Chemotherapeutic agents (Bleomycin)
  • High altitude sickness
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10
Q 
T or F: Pathologic mechanisms of pulmonary edema.
A. Decreased venous pressure
B. Decreased oncotic pressure
C. Venous obstruction
D. Alveolar injury
A

A. False. increased venous pressure
B. False. increased oncotic pressure
C. False. Lymphatic obstruction
D. True

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11
Q

Pathophysiology of Pumonary Edema

A
  • Capacity of the lymphatics to absorb and drain interstitial fluid is exceeded
  • Architecture of the alveolar epithelial cells breaks down.
  • Fluid entering the alveolar spaces reduces or halts gas exchange.
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12
Q

Pulmonary Edema: Cardiogenic or NON-cardiogenic?
A. Direct injury to the lung parenchyma
B. Failure of the heart to remove fluid from lung circulation
C. ARDS is this type of pulmonary edema

A

A. NON-cardiogenic
B. Cardiogenic
C. NON-cardiogenic

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13
Q

In addition to the typical pathophysiology of pulmonary edema, what additional feature is present in the pathophysiology of ARDS?
How easily are symptoms of ARDS resolved?

A

Decrease in surfactant production

exudates and diffuse tissue destruction of ARDS are not easily resolved

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14
Q

Etiology of ARDS?

A

Commonly due to
Sepsis, Widespread lung infections (pneumonia, TB), Gastric aspiration, Mechanical trauma (lung trauma, head trauma)
Also may be
Multi-organ failure, Burns, Inhaled gases and chemicals, ~ 20% no identified risk factor

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15
Q

Immune Response to ARDS?

A

If the immune system is intact, the damaging effects are balanced by:
•Antioxidants
•Anti-proteases
•Anti-inflammatory cytokines

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16
Q

Histopathology of ARDS?

A

Damage/death of
Type 1 Epith–lining the membrane of lungs and/or Endothel–lining blood vessel
**Increased permeability of pulmonary bv (capillary)
Type 2 Epith
**decreased surfactant production
Neuts produce oxidants, proteases, PAF, leukotrienes

17
Q

T or F? ARDS
A. Most deaths due to sepsis
B. 15% mortality rate, esp in young
C. Transudative fluid only leaks into alveoli
D. Often progresses to multi-system organ failure, death

A

A. True
B. False. 30 –70% mortality rate increases w age
C. False. Also fibrin, protein, cells, etc.
D. True

18
Q

Sn/Sx of ARDS?

A

Dyspnea, Tachypnea, Cyanosis, Respiratory fail/acidosis, Bilateral fluid on CXR

19
Q

T or F: Acute Interstitial Pneumonia
A. Same as ARDS except not 2ndary to something else
B. Describes localized acute lung injury
C: Etio: Gastric aspiration, lung infections

A

A. True
B. False. Widespread acute
C. False. No known etiology

20
Q 
Obstructive or Restrictive?
A. Less compliance/volume/gas exchange/cyanosis
B. Hyperexpansion on CXR
C. Ground glass on CXR
D. Air trapping/wheezing
A

A. Restriction
B. Obstruction
C. Restriction
D. Obstruction

21
Q 
Obstructive or Restrictive?
A. Has 2 categories (1) chest wall disorders (2) acute or chronic interstitial and infiltrative dz
B. Affects small airway expiration 
C. More lucency, less density on CXR 
D. More opacity, more density on CXR
A

A. Restrictive
B. Obstructive
C. Obstructive
D. Restrictive

22
Q

Emphysema, Chronic Bronchitis, or Asthma?
A. Chest tightness, dysp, wheeze, cough w/w/o sputum
B. Dyspnea, cough, wheeze, wt loss
C. Chronic small airway obstrxn –> repeated infections
D. Etio: Tobacco smk, smog, dust fr: grains, cotton, silica

A

A. Asthma
B. Emphysema
C. Asthma
D. Chronic Bronchitis

23
Q

Emphysema, Chronic Bronchitis, or Asthma?
A. Damages airway epithelium, inhibits macrophages
B. Xtra lg lungs/acini, loss of elastic recoil, apical blebs
C. Hyper-secretion of mucus in the large airways, inflamm
D. Bronchospasm and wheezing from the small airways

A

A. Chronic Bronchitis
B. Emphysema
C. Chronic Bronchitis
D. Asthma

24
Q

Emphysema, Chronic Bronchitis, or Asthma?
A. Pink puffer, pulse ox normal
B. Blue bloater, hypercapnia, hypoxemia
C. Often exists concomitant with emphysema
D. May develop corpulmonale, CHF

A

A. Emphysema
B. Chronic Bronchitis
C. Chronic Bronchitis
D. Emphysema and Chronic Bronchitis

25
Q

Emphysema: Centrilobular or Panacinar
A. Occurs in alpha 1 antitrypsin deficiency
B. Occurs predominantly in heavy smokers
C. More severe in lower lobes and anterior aspect of lungs
D. More severe in upper lobes
•

A

A. Panacinar
B. Centrilobular
C. Panacinar
D. Centrilobular

26
Q

What is the definition of COPD?

A
  • Irreversible enlargement of the airspaces distal to the terminal bronchiole
  • Destruction of alveolar walls loss of elasticity
  • No obvious fibrosis
27
Q

Pathophysiology of Emphysema

A

Damage to lung: Macrophages, T lymphocytes, Neutrophils, MMP, elastases

Oxidant-antioxidant balance: smoke free radical; depletion of SOD and glutathione

28
Q

What are the 4 classic histologic findings in bronchial asthma?

A

1) Inflammation
2) Bronchial (luminal) narrowing
3) Increased Mucous
4) Smooth muscle hyperplasia
What is the 5thfinding if the etiology is allergy? Ans: Increased eosinophils

29
Q

Asthma: Atopic, Non-atopic, Drug induced, Occupational?
A. Sampter’s triad (asthma, rhinitis/nasal polyps, hives)
B. Most common type; IgE mediated hypersensitivity
C. Etio: Fumes, organic/chem dusts, gases/other chem
D. Etio: Viral resp infx, air pollutants (SO2, ozone, NO2)

A

A. Non-atopic-Drug induced (aspirin)
B. Atopic
C. Non-atopic-Occupational
D. Non-atopic-Drug induced

30
Q

Causes of Asthma

A

Atopic (may be seasonal)
Allergy (assoc w hay fever and eczema)
Non-atopic
No allergy, Drug-induced (e.g, aspirin), Occupational asthma, Exercise-induced, Asthmatic bronchitis (smokers)
Other Causes
Respiratory infection (esp. viral), Environmental exposure to, Irritants, Cold air, Stress, Exercise

31
Q

Pathophysiology of Emphysema

A

Mild chronic inflammation throughout the airways, parenchyma and pulmonary vasculature
Increased numbers of Macrophages, T lymphocytes, Neuts
Activated inflammatory cells release LT, IL-8, TNF
These may damage lung or sustain the neutrophilic response

32
Q

What does alpha 1 antitrypsin do? What inhibits it?

A 
Inhibits proteases (esp. elastase)
Oxidants and free radicals in smoke inhibit alpha 1-antitrypsin
33
Q

Pathophysiology of Emphysema in a smoker

A

Nicotine and reactive oxygen species in smoke activate NF-kB
–>Turns on genes that encode TNF and IL-8
–>Attracts and activates neutrophils
–>Neuts release granules rich in elastases which damage lung tissue
Smoking also enhances elastase activity in MO

34
Q

What is the difference between reactive and restrictive airway conditions?

A

Reactive is hyper-responsive, such as asthma

Restrictive is reduced in volume, compliance, like fibrosis

35
Q

T or F? Atalectasis
A. Tends to expand to the affected side
B. Seen w bronchial obstruction, outside or pleural compression, and contraction as in a fibrotic process
C. A concept, not really a disease
D. Can be caused by shallow inspirations and prevented with incentive spirometry

A

A. False. unaffected side
B. True
C. True
D. True

36
Q

Pulmonary Pathology Classical classifications

A
  1. Degenerative
  2. Inflammatory
  3. Neoplastic
  4. Pleural
37
Q

T or F? Exercise-Induced Asthma
A. Possible Etio: With incr. resp rate, air not warmed and humidified enough b4 entering lung
B. Can be treated w mast cell stabilizer Intal b4 exercise
C. Inflammatory changes similar to other asthma types
D. Exercise-induced asthma is concomitant w other types

A

A. True
B. True
C. False. Lacks inflammatory changes
D. False. Occurs in ppl who do not have other types

Pathology II Chamberlin Fall 2014 (5 decks)

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