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Pathology II > Pulmonary Path 1 > Flashcards

Pulmonary Path 1 Flashcards

1
Q

What are the classical classifications for pulmonary pathology?

A
  1. Degenerative
  2. Inflammatory
  3. Neoplastic
  4. Pleural (visceral, parietal, or both)
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2
Q

What factors are involved in maintaining adequate respiration?

A
  • Adequate intake of air
  • Rapid diffusion along alveolar ducts and through alveolar walls.
  • Adequate perfusion of pulmonary vasculature.
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3
Q

What is the functional unit of the lung?

A

Acinus: consists of the respiratory bronchiole and associated alveolar ducts and alveoli

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4
Q

What is the blood air interface?

A

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

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5
Q

What is Pulmonary Hypoplasia?

What can it be secondary to?

A

Defective development of one or both lungs results in
decreased lung weight and volume

May be secondary to:
• Space-occupying lesions in the uterus
• Congenital diaphragmatic hernia

• Found in 10% of neonate death autopsies

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6
Q

TE Fistulas

A

By far, the most common scenario is for the baby to eat, and it comes back up WITHOUT food getting into the lungs.

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7
Q

Which is the most common type of TE fistula?

A

C! Esophagus has fistulized with the distal trachea

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8
Q

What is the primary defect in Neonatal Respiratory Distress Syndrome (N.R.D.S.)?

What is the inverse relationship of NRDS?

Tx?

A
  • Primary defect: lack of surfactant –> Lungs won’t open and become fluid filled and membranes form as a result of loss of surfactant; this is a hyaline membrane disease of the newborn
  • Incidence of NRDS is inversely proportional to gestational age: Up to 60% of infants born at less then 28 weeks of gestation will develop NRDS

Tx: surfactant delivery or maternal treatment with corticosteroids to induces the formation of surfactant

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9
Q

What is Atalectasis?

A

an anatomic/physiologic/geometric CONCEPT, not a disease by itself, but seen in many disease states. In includes:
INCOMPLETE EXPANSION or COLLAPSE of a lung.

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10
Q

Reasons for atalectasis?

What is the most common cause?

A
  1. Reabsorption can be from a bronchial obstruction, such as a tumor.
  2. Compression can be from, say, a pleural effusion, or pneumothorax.
  3. Contraction can be from a diffuse lung fibrotic process

MOST COMMON CAUSE: Shallow breathing - not opening up alveoli in distal part of the lung —> bacteria and fluid can thrive in those areas. Tends to pull the lung towards it source.

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11
Q

What is Pulmonary Edema?

What is it generally a result of?

A

Accumulation of fluid in the lungs –> impaired gas exchange, possible respiratory failure

Generally due to either:
• Cardiogenic Pulmonary Edema: Failure of the heart to remove fluid from lung circulation
• Noncardiogenic Pulmonary Edema: direct injury to the lung parenchyma

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12
Q

Other causes of pulmonary edema?

A

Other Causes:
• Fluid overload (renal failure, iatrogenic)
• Hypoalbuminemia (liver disease, Nephrotic syndrome, severe malnutrition)
• Oncotic pressure is necessary to hold plasma in vascular space.
• Lymphatic obstruction (cancer)
• “Strange things”
• 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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13
Q

What are the 4 main pathologic mechanisms of pulmonary edema?

A

Increased venous pressure
Increased oncotic pressure
Lymphatic obstruction
Alveolar injury

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14
Q

Pathophysiology of Pulmonary 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.
  • May be acute or chronic
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15
Q

Differences between acute and chronic pulmonary edema.

A
  • Acute

* Rapid developing

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16
Q

S/sx of Acute Pulmonary Edema

A
  • Tachypnea
  • Extreme dyspnea (SOB)
  • Restlessness and anxiety (sense of suffocation)
  • May have marked bronchospasm and wheezing, known as cardiac asthma
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17
Q

Chronic Pulmonary Edema

A
  • Alveolar fluid may act as a culture medium for bacterial growth
  • Alveolar walls lose their elasticity and become fibrotic
  • Micro-hemorrhages occur
  • Macrophages phagocytize iron from micro hemorrhages = heart failure cells
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18
Q

ACUTE* RESPIRATORY DISTRESS SYNDROME (ARDS or D.A.D., i.e., Diffuse Alveolar Damage) (aka, “SHOCK” lung)

A

thought of as NON-cardiac pulmonary edema - much more leaks into the alveoli than just transudative fluid, i.e., fibrin, protein, cells, etc.. aka “shock lung”
It is NON-specific!!!

Severe acute lung injury (ALI)
• Low blood oxygen
• Increased permeability of pulmonary blood vessels
• Fluid accumulation in the lungs • Death of lung cells
• Epithelialcells
• Endothelial cells

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19
Q

ARDS is commonly due to what?

A
  • Sepsis
  • Widespread lung infections (pneumonia, TB)
  • Gastric aspiration
  • Mechanical trauma (lung trauma, head trauma)
  • Multi-organ failure
  • Burns, Inhaled gases and chemicals ~ 20% no identified risk factor
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20
Q

Overview of Pathophysiology of ARDS

A

Increased permeability of capillary –> Flooding of fluid into the alveolus –> Loss of gas exchange function –> Decrease in surfactant production

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21
Q

Detailed pathophysiology of ARDS:

A
  • Damage to the capillary endothelium and type 1 epithelial cells
    • Increased permeability of capillary
    • Flooding of fluid into the alveolus
    • Loss of gas exchange function
  • Damage to type 2 epithelial cells: Decrease in surfactant production
  • Formation of microscopic clots (microthrombi): Decreased blood flow and oxygen levels
  • Hyaline membranes: The respiratory lining is covered with protein-rich fluid and dead alveolar epithelial cells
    Neutrophils are a major player in the damage of ARDS
    • They produce various pro- inflammatory products:
    • Oxidants, Proteases, Platelet activating factor • leukotrienes
22
Q

Symptoms and signs of ARDS

A
  • Dyspnea – labored breathing
  • Tachypnea – rapid shallow breath patterns
  • Cyanosis – bluish discoloration of tissues
  • Respiratory failure and possible acidosis
  • Bilateral fluid seen on chest x-rays
23
Q

Histopathology of ARDS

A

Damage to the endothelium: cells lining the blood vessel, OR
Damage to the epithelium: cells lining the membrane of the lungs, OR
Damage to both types of cells

24
Q

Protection from ARDS

A

If the immune system is intact, the damaging effects of the previous factors is balanced by: Antioxidants, Anti-proteases, Anti-inflammatory cytokines

25
Q

ARDS prognosis

A

The exudates and diffuse tissue destruction of ARDS are not easily resolved
• ARDS often progresses to multi- system organ failure and death; Most deaths are due to sepsis
• 30 – 70% mortality rate
• Mortality increases with age

26
Q

Resolution of the ARDS damage involves:

A
  • Resorption of the fluids and removal of debris (dead cells, etc) by alveolar macrophages
  • Replacement of epithelial cells with new functional cells performed by type II pneumocytes
  • Restoration of capillary endothelial cells: cells migrate from uninjured capillaries and bone marrow
27
Q

ACUTE INTERSTITIAL PNEUMONIA?

A

• Acute interstitial pneumonia is a clinicopathologic term that is used to describe widespread acute lung injury
• Think of it as ARDS with NO known etiology and a rapidly progressive clinical course!
ARDS is generally SECONDARY to something else, when it ISN’T, we can call it ACUTE INTERSTITIAL PNEUMONIA. Histologically, they cannot be differentiated!

28
Q

What constitutes the majority of pulmonary diseases that are not infections pneumonias?

A

OBSTRUCTION and RESTRICTION

29
Q

What does obstruction mean?

A

Obstruction means small airway expiratory obstruction, air trapping, wheezing You should see more lucency and less density.

30
Q

What does restriction mean?

A

Restriction means reduced compliance or less sponginess and less gas transfer You should see more opacity and more density.

31
Q

Restrictive Airway Disease

A

• Decreased capacity, flow rate normal.
• Two major classes of disease comprise the restrictive disorders:
• Chest wall disorders in the presence of normal lungs: poliomyelitis, severe obesity, pleural diseases and kyphoscoliosis
• Acute or chronic interstitial and infiltrative diseases of the lung
- ARDS = classic acute restrictive dz
- Chronic: dust inhalation, interstitial fibrosis, pneumoconiosis

32
Q

Forced Expiration Curve

A

• Restrictive – reduced expansion of the lung and decreased total lung capacity.
• ↓ total lung capacity –> decreased FVC
• Example: asbestos, ARDS, chest wall
disorder
• Obstructive – an increase in resistance to airflow due to partial or complete obstruction at any level. Air trapping.
• ↓ flow rate –> FEV1 usually decreased
• Example: emphysema, chronic bronchitis,
asthma

33
Q

EMPHYSEMA

A
  • COPD, or “END-STAGE” lung disease
  • Centri-acinar, Pan-acinar, Paraseptal, Irregular
  • (PROGRESSIVE) EXPIRATORY AIR TRAPPING, i.e., WHEEZING
  • Think of it like cirrhosis, but as END-STAGE of multiple chronic small airway obstructive etiologies
  • NON-specific
  • BULLAE (BLEBS)
  • Clinically likely to produce recurrent pneumonias, and progressive failure
34
Q

Which conditions does COPD include?

A
  • Emphysema
  • Chronic bronchitis
  • (Asthma)
  • (Bronchiectasis, cystic fibrosis)
  • 4th most common cause of morbidity and mortality in the U.S.
35
Q

Definition of COPD

A

• Irreversible enlargement of the airspaces
distal to the terminal bronchiole
• Destruction of alveolar walls

36
Q

What are the forms of Emphysema?

A

Centrilobular and Panacinar

37
Q

Centrilobular form of Emphysema

A
  • Central parts of the acini formed by respiratory bronchioles are affected while distal alveoli are spared
  • More severe in upper lobes
  • Occurs predominantly in heavy smokers
38
Q

Panacinar form of Emphysema

A
  • Acini are uniformly enlarged from the respiratory bronchiole to the terminal blind alveoli
  • More severe in lower lobes and anterior aspect of lungs
  • Occurs in alpha 1 antitrypsin deficiency
39
Q

Emphysema Pathophys

A
  • Mild chronic inflammation throughout the airways, parenchyma and pulmonary vasculature
  • Increased numbers of Macrophages, T lymphocytes, and Neutrophils
  • The activated inflammatory cells release Leukotriene, IL-8, TNF
  • These may damage lung or sustain the neutrophilic response
40
Q

Protease-antiprotease mechanism of emphysema pathophysiology

A

• Alpha 1-antitrypsin normally present in serum, tissue fluids and macrophages –> Inhibits proteases (esp. elastase)
• Oxidants and free radicals in smoke
inhibit alpha 1-antitrypsin
• Neutrophils are the major source of cellular proteases
• α1-AT deficiency: patients may develop severe emphysema in their teens or twenties

41
Q

More pathophys of Emphysema

A

In smokers, neutrophils and macrophages accumulate in alveoli
• Nicotine and reactive oxygen species in smoke activate NF-kB
• Turns on genes that encode TNF and IL-8
• This attracts and activates neutrophils
• The neutrophils release granules rich in elastases which damage lung tissue
• Smoking also enhances elastase activity in macrophages
• In addition matrix metalloproteinase (MMP) from macrophages and neutrophils also destroy lung tissue
Oxidant-antioxidant imbalance
• Normally the lung contains healthy amounts of antioxidants
• Superoxidedismutase • Glutathione
• These keep oxidative damage to a minimum
The free radicals in tobacco smoke deplete these, adding to the tissue damage

42
Q

Emphysema – Gross Morphology & Clinical Aspects

A 
• Voluminous lungs
• Apical blebs or bullae
• Enlarged acini due to destruction of intervening walls of alveoli
• Loss of elastic recoil
• Manifests after at least 1/3 of
functioning lung has been lost
• Dyspnea is progressive
• Some pts. complain of cough or wheezing
43
Q

Dx of Emphysema

A

Expectoration depends on chronic bronchitis
• In patients without much chronic bronchitis:
• Weight loss is common
• Pt is barrel-chested, sits hunched over
• Pursed-lip breathing
• Expiratory airflow limitation - Best measured by spirometry
• Peak flow meter is an alternative measure
• Pulse oximetry is often normal
• Pts. over ventilate –> PINKPUFFER
• Over time - develop cor pulmonale and CHF

44
Q

Death by Emphysema is often due to:

A
  • Respiratory acidosis and coma
  • Right sided heart failure
    • Massive collapse of the lungs
    • Due to pneumothorax
45
Q

Pink Puffer

A

Dyspnea
Cough, wheeze
Weight loss
Cor pulmonale CHF

46
Q

Definition and Etiology of Chronic Bronchitis:

A

Definition
• Persistent cough with sputum production for at least three months in at least two consecutive years, in the absence of any other identifiable cause.
• Related to cigarette smoking and breathing smog

Etiology
• Tobacco smoke
• Dust from grains, cotton, silica

47
Q

Morphology of Chronic Bronchitis

A

• Hyper-secretion of mucus in the large airways
• Similar to emphysema (often concomitant)
• Cigarette smoke predisposes to infection
- Loss of cilliary function of epithelium
- Damages airway epithelium: increased mucus production
- Inhibits function of bronchial and alveolar macrophages

48
Q

Chronic Bronchitis - Histology

A

• Increased thickness of the mucous gland layer
• Increased numbers of goblet
cells within the bronchi
- Proteases released from neutrophils (elastase and MMP) stimulate mucus hypersecretion
• Reduced number of ciliated cells.
• Infiltrates of lymphocytes within the bronchial epithelium.

49
Q

Is chronic bronchitis defined pathologically or clinically?

A

Chronic Bronchitis Does Not Have Characteristic Pathologic Findings - It’s Defined Clinically
Bronchus with increased numbers of chronic inflammatory cells in the submucosa in a patient with chronic bronchitis.

50
Q

Chronic Bronchitis – Clinical Aspects

A

• Persistent cough with sputum production
• Over time, dyspnea on exertion develops
• May develop
- Hypercapnia
- Hypoxemia
- Mild cyanosis –> BLUEBLOATER
• Course may include
- Cor pulmonale
- CHF
• Death may be due to superimposed acute infections

Pathology II (2 decks)

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