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Pathology II > Pulmonary Path 1 > Flashcards

Pulmonary Path 1 Flashcards

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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:

Study These Flashcards
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

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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

Study These Flashcards
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

Study These Flashcards
A

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

25
ARDS prognosis
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
Resolution of the ARDS damage involves:
* 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
ACUTE INTERSTITIAL PNEUMONIA?
• 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
What constitutes the majority of pulmonary diseases that are not infections pneumonias?
OBSTRUCTION and RESTRICTION
29
What does obstruction mean?
Obstruction means small airway expiratory obstruction, air trapping, wheezing You should see more lucency and less density.
30
What does restriction mean?
Restriction means reduced compliance or less sponginess and less gas transfer You should see more opacity and more density.
31
Restrictive Airway Disease
• 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
Forced Expiration Curve
• 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
EMPHYSEMA
* 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
Which conditions does COPD include?
* Emphysema * Chronic bronchitis * (Asthma) * (Bronchiectasis, cystic fibrosis) * 4th most common cause of morbidity and mortality in the U.S.
35
Definition of COPD
• Irreversible enlargement of the airspaces distal to the terminal bronchiole • Destruction of alveolar walls
36
What are the forms of Emphysema?
Centrilobular and Panacinar
37
Centrilobular form of Emphysema
* 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
Panacinar form of Emphysema
* 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
Emphysema Pathophys
* 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
Protease-antiprotease mechanism of emphysema pathophysiology
• 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
More pathophys of Emphysema
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
Emphysema – Gross Morphology & Clinical Aspects
``` • 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
Dx of Emphysema
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
Death by Emphysema is often due to:
* Respiratory acidosis and coma * Right sided heart failure * Massive collapse of the lungs * Due to pneumothorax
45
Pink Puffer
Dyspnea Cough, wheeze Weight loss Cor pulmonale CHF
46
Definition and Etiology of Chronic Bronchitis:
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
Morphology of Chronic Bronchitis
• 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
Chronic Bronchitis - Histology
• 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
Is chronic bronchitis defined pathologically or clinically?
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
Chronic Bronchitis – Clinical Aspects
• 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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