Upper and Lower Respiratory Disorders

Chapter 16 Upper and Lower Respiratory Disorders



I. Symptoms and Signs of Respiratory Disease (Tables 16-1 and 16-2)

II. Pulmonary Function Tests

A. Calculation of the alveolar-arterial (A-a) gradient

1. A-a gradient is the difference in the partial pressure of oxygen (PO2) between the alveolar PO2 (PAO2) and arterial PO2 (PaO2).

a. A-a gradient is normally due to a mismatch between ventilation and perfusion in the lungs.

• Example—An A-a gradient exists when perfusion is greater than ventilation in the lower lobes.


b. It is useful in differentiating causes of hypoxemia (decreased PaO2; refer to Chapter 1).

(1) Hypoxemia due to pulmonary causes increases A-a gradient.


Table 16-1 Common Symptoms of Respiratory Disease

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Table 16-2 Signs of Respiratory Disease

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↑ A-a gradient: hypoxemia of pulmonary origin


(2) Hypoxemia due to extrapulmonary causes has a normal A-a gradient.


Normal A-a gradient: hypoxemia of extrapulmonary origin


2. Calculation of the A-a gradient

a. PAO2 = % O2 (713) − arterial PCO2/0.8


PAO2 = % O2 (713) − arterial PCO2/0.8


• % O2 is the percentage of O2 the patient is breathing; 713 is the atmospheric pressure (760 mm Hg) minus the water vapor pressure (47 mm Hg); and 0.8 is the respiratory quotient.

b. Example using normal values

(1) Normal PAO2 = 0.21 (713) − 40/0.8 = 100 mm Hg

(2) Normal PaO2 = 95 mm Hg

(3) Normal A-a gradient = 100 mm Hg − 95 mm Hg = 5 mm Hg

(4) Medically significant A-a gradient ≥ 30 mm Hg


Medically significant: A-a ³ 30 mm Hg


(a) A-a gradient normally increases with age.

(b) A-a ³ 30 mm Hg is set for highest specificity.

3. Causes of hypoxemia with an increased A-a gradient (refer to Chapter 1)


Hypoxemia + ↑ A-a: ventilation, perfusion, diffusion defects; right-to-left cardiac shunts


a. Ventilation defect

(1) Impaired O2 delivery to the alveoli for gas exchange

(2) Example—airway collapse due to the respiratory distress syndrome

b. Perfusion defect

(1) Decreased or absent blood flow to the alveoli

(2) Example—pulmonary embolus

c. Diffusion defect

(1) O2 cannot diffuse through the alveolar-capillary interface.

(2) Examples—interstitial fibrosis, pulmonary edema

d. Right-to-left cardiac shunt

• Example—tetralogy of Fallot


Calculation of the A-a gradient in a patient breathing 0.30 O2 who has a PCO2 of 80 mm Hg and PaO2 of 40 mm Hg: PAO2 = 0.30 (713) − 80/0.8 = 114 mm Hg. A-a gradient = 114 − 40 = 74 mm Hg, which is medically significant and indicates one or more of the above-mentioned lung disorders or a right-to-left shunt in the heart.


4. Causes of hypoxemia with a normal A-a gradient


Hypoxemia + normal A-a: depression of respiratory center, upper airway obstruction, chest bellows disease


a. Depression of the respiratory center in the medulla

• Examples—barbiturates, brain injury

b. Upper airway obstruction

(1) Epiglottitis due to Haemophilus influenzae

(2) Croup due to parainfluenza virus

• Mucosal edema narrows the trachea.

c. Chest bellows (muscles of respiration) dysfunction

(1) Paralyzed diaphragm

(2) Amyotrophic lateral sclerosis with degeneration of anterior horn cells


Calculation of the A-a gradient in a patient breathing room air who has a PCO2 of 80 mm Hg and PaO2 of 40 mm Hg: PAO2 = 0.21 (713) − 80/0.8 = 50 mm Hg. A-a gradient = 50 − 40 = 10 mm Hg, which excludes the lung as the cause of the hypoxemia and indicates an extrapulmonary cause of hypoxemia.


B. Spirometry (Fig. 16-1)

• Useful in distinguishing restrictive from obstructive lung disease

1. Volumes and capacities that are not directly measured by spirometry

a. Functional residual capacity (FRC)

• Total amount of air in the lungs at the end of a normal expiration

b. Total lung capacity (TLC)

• Total amount of air in a fully expanded lung

c. Residual volume (RV)

• Volume of air left over in the lung after maximal expiration

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16-1: Spirometry showing normal lung volumes and capacities and forced expiratory volume at 1 second (FEV1 sec) and forced vital capacity (FVC) findings in a normal person (A), a person with restrictive lung disease (B), and a person with obstructive lung disease (C). ERV, expiratory reserve volume; FRC, functional residual capacity; RV, residual volume; TLC, total lung capacity; TV, tidal volume; VC, vital capacity.


(From Goljan EF: Star Series: Pathology. Philadelphia, WB Saunders, 1998, p 229, Fig. 11-1.)



Volumes not directly measured by spirometry: TLC, FRC, RV


2. Tidal volume (TV)

• Volume of air that enters or leaves the lungs during normal quiet respiration

3. Forced vital capacity (FVC), forced expiratory volume in 1 second (FEV1 sec), and FEV1 sec/FVC

a. FVC is the total amount of air expelled after a maximal inspiration.

• Normal FVC is 5 L (see Fig. 16-1A).

b. Forced expiratory volume in 1 second (FEV1 sec)

(1) Amount of air expelled from the lungs in 1 second after a maximal inspiration

(2) Normal FEV1 sec is 4 L (see Fig. 16-1A).


Normal FEV1 sec/FVC: 4/5 L = 80%


c. Ratio of FEV1 sec/FVC is normally 4/5, or 80%.

4. Expiratory reserve volume (ERV)

a. ERV refers to the amount of air forcibly expelled at the end of a normal expiration.

b. ERV is commonly used to calculate residual volume (FRC − ERV = RV).


FRC – ERV = RV


5. Comparison of pulmonary function tests in restrictive and obstructive lung disease (Table 16-3)

C. Flow-volume loop

1. Plot of inspiratory and expiratory flow rate (liters/second) versus lung volume (liters)

• Patient takes a maximal inspiration followed by a maximal expiration.

2. Loop consists of an inspiration curve and an expiration curve (Fig. 16-2).

a. Maximal inspiration

• Begins at point A (RV) and extends to point B (TLC)


Table 16-3 Comparison of Pulmonary Function Tests in Restrictive and Obstructive Lung Disease

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16-2: Flow-volume loop. See text for discussion. PEF, peak expiratory flow; RV, residual volume; TLC, total lung capacity; VC, vital capacity.


(From Goljan EF, Sloka KI: Rapid Review Laboratory Testing in Clinical Medicine. St. Louis, Mosby Elsevier, 2008, p 71, Fig. 3-3.)



TLC and RV: TLC end of maximal inspiration; RV end of maximal expiration


b. Maximal expiration

(1) Extends from point B to point C (peak expiratory flow, PEF) and then trails off back to point A

(2) PEF occurs early in expiratory phase of the loop (point B to C).

• Due to elastic recoil of the lungs into airways with low resistance and large caliber

(3) Flow rate becomes linear from point C to A.

• Encounters increased resistance in the small airways

(4) Volume of air in liters between points A and B is the vital capacity (VC).

3. Flow-volume loop in obstructive lung disease (Fig. 16-3A)

a. TLC is increased (e.g., ∼︀8.5 L) and RV is increased (e.g., 4 L).

• Expiratory curve is shifted to the left of the normal curve.

b. Decreased PEF

c. Nonuniform emptying of the airways

• Concave configuration of the curve (arrow) is due to mucus plugs or collapsed small airways.

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16-3: Flow-volume loops in normal person, obstructive disorder (A), restrictive disorder (B). See text for discussion.


(From Goljan EF, Sloka KI: Rapid Review Laboratory Testing in Clinical Medicine. St. Louis, Mosby Elsevier, 2008, p 72, Fig. 3-4.)



Obstructive pattern: nonuniform emptying; expiratory curve shift to left of normal curve


4. Flow-volume loop findings in restrictive parenchymal disease (Fig. 16-3B)

a. TLC is decreased (e.g., ∼︀4 L).

b. RV is decreased (e.g., ∼︀0.3 L).

c. Expiratory curve is shifted to the right of the normal curve.

• Expiratory curve is narrow because of decreased lung volumes.


Restrictive parenchymal: expiratory curve shifted to right of normal curve


III. Upper Airway Disorders

A. Choanal atresia

1. Unilateral or bilateral bony septum between the nose and the pharynx


Choanal atresia: newborn cannot breathe through the nose; cyanosis when breast-feeding


2. Newborn turns cyanotic when breast-feeding.

• Crying causes the child to “pink up” again.

B. Nasal polyps

1. Nasal polyps are non-neoplastic tumefactions (Fig. 16-4).

• Develop as a response to chronic inflammation

2. Allergic polyps

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16-4: Nasal polyp. Note the gray-white mass in the left nasal cavity.


(From Swartz MH: Textbook of Physical Diagnosis, 5th ed. Philadelphia, Saunders Elsevier, 2006, p 312, Fig. 11-24.)



Allergic polyp: most common polyp; adults


a. Most common polyp

b. Most often seen in adults with a history of IgE-mediated allergies

3. Nasal polyps are associated with aspirin and other nonsteroidal drugs.

a. Epidemiology


Triad asthma: aspirin, nasal polyp, asthma


• Most often occur in women with chronic pain syndromes

b. Pathogenesis

(1) Drugs block cyclooxygenase leaving the lipoxygenase pathway open.

(2) Leukotrienes (LT) C-D-E4 are increased, causing bronchoconstriction.

c. Clinical triad—nonsteroidal drugs, asthma, and nasal polyps

4. Nasal polyps are often associated with cystic fibrosis.


Nasal polyps in child: order a sweat test to rule out cystic fibrosis


C. Obstructive sleep apnea (OSA)

1. Epidemiology

a. Excessive snoring with intervals of breath cessation (apnea)


OSA: excessive snoring with periods of apnea


b. Causes

(1) Obesity (very common)

• Pharyngeal muscles collapse due to the weight of tissue in the neck.

(2) Tonsillar hypertrophy, nasal septum deviation

2. Pathogenesis

• Airway obstruction causes CO2 retention, leading to hypoxemia.

3. Clinical findings

a. Excessive snoring with episodes of apnea

b. Daytime somnolence often simulating narcolepsy

4. Laboratory findings

a. Decreased PO2 and O2 saturation during apneic episodes

b. Increase in arterial PCO2 (respiratory acidosis)


OSA: apnea causes respiratory acidosis and hypoxemia


5. Complications

a. Pulmonary hypertension (PH) leading to right ventricular hypertrophy

• Called cor pulmonale (see section VII)


OSA: risk for developing cor pulmonale


b. Secondary polycythemia

• Due to a hypoxemic stimulus for erythropoietin release

6. Polysomnography


Polysomnography: confirmatory test for OSA


• Confirmatory test that documents periods of apnea during sleep

7. Treatment

a. Nasal continuous positive airway pressure (CPAP)

b. Surgical correction of any obstructive lesions, weight loss

D. Sinusitis

1. Epidemiology


Sinus infections: maxillary in adults, ethmoid in children


a. Maxillary sinus is most often involved in adults.

b. Ethmoid sinus is most often involved in children.

c. Causes

(1) Upper respiratory infections (URIs); e.g., viral, bacterial

• Block drainage of sinuses into nasal cavity


Viral URI: most common cause of sinusitis


(2) Deviated nasal septum

(3) Allergic rhinitis

(4) Barotrauma

(5) Smoking cigarettes

d. Pathogens causing sinusitis

(1) Rhinoviruses

(2) Streptococcus pneumoniae (most common)


Streptococcus pneumoniae: most common bacterial pathogen causing sinusitis


(3) Anaerobes (chronic sinusitis)

(4) Systemic fungi (e.g., Mucor or Aspergillus species)

• Diabetics commonly have sinusitis due to Mucor species.

2. Pathogenesis

• Blockage of sinus drainage into the nasal cavity

3. Clinical findings

a. Fever

b. Nasal congestion

c. Pain over sinuses

d. Postnasal drip

4. Diagnosis

a. Gold standard for bacterial culture is sinus aspiration


Sinusitis: blockage of sinus drainage in nasal cavity


b. Sinus radiographs

c. CT scan is the most sensitive test.


Sinusitis: CT scan most sensitive


• Recommended if surgery is an option

5. Treatment


a. Decongestants

b. Antimicrobial therapy

(1) Recommendation is not to use antibiotics.

• Most cases are viral and resolve within 2 weeks

(2) If resolution does not occur, antibiotics often used include the following:

• Amoxicillin (most common drug), erythromycin, trimethoprim-sulfamethoxazole (TMP/SMX)

E. Nasopharyngeal carcinoma

1. Epidemiology

a. Most common malignant tumor of the nasopharynx

b. Male dominant

c. Increased incidence in the Chinese and African populations

2. Pathogenesis


Nasopharyngeal carcinoma: association with EBV


• Causal relationship with Epstein-Barr virus (EBV)

3. Pathologic findings

a. Squamous cell carcinoma or undifferentiated cancer

b. Metastasizes to cervical lymph nodes

F. Laryngeal carcinoma

1. Epidemiology and pathogenesis

a. More common in men than in women

b. Risk factors


Laryngeal carcinoma: cigarette smoking is the most common cause


(1) Cigarette smoking (most common cause)

(2) Alcohol (synergistic effect with smoking)

(3) Squamous papillomas and papillomatosis

• Human papillomavirus type 6 and 11 association

c. Majority are located on the true vocal cords (Fig. 16-5).

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16-5: Laryngeal squamous cell carcinoma involving the right vocal cord (arrow).


(From Damjanov I, Linder J: Pathology: A Color Atlas. St. Louis, Mosby, 2000, p 47, Fig. 3-16.)



Laryngeal carcinoma: most on true vocal cords; squamous cancer


2. Majority are keratinizing squamous cell carcinomas.

3. Clinical findings

• Persistent hoarseness is often associated with cervical lymphadenopathy.

4. Treatment is surgery.

IV. Atelectasis

• Loss of lung volume due to inadequate expansion of the airspaces (collapse)

A. Resorption atelectasis

1. Pathogenesis

a. Airway obstruction by thick secretions prevents air from reaching the alveoli.


Resorption atelectasis: most common cause of fever 24 to 36 hours after surgery


• Obstruction occurs in bronchi, segmental bronchi, or terminal bronchioles.

b. Causes of obstruction

(1) Mucus or mucopurulent plug after surgery

(2) Aspiration of foreign material

(3) Centrally located bronchogenic carcinoma

c. Cause of alveolar collapse

• Lack of air and distal resorption of preexisting air through the pores of Kohn in the alveolar walls

d. Collapse may involve all or part of a lung.

2. Clinical findings

a. Fever and dyspnea

• Both usually occur within 24 to 36 hours of collapse.

b. Absent breath sounds

c. Absent vocal vibratory sensation (tactile fremitus)


Resorption atelectasis: absent vibratory sensation, dullness to percussion, absent breath sounds


• Alveoli are collapsed.

d. Ipsilateral elevation of the diaphragm and tracheal deviation

• Only occurs if large areas of the lung are atelectatic

e. Collapsed lung does not expand on inspiration (inspiratory lag).

3. Treatment

a. Incentive spirometry after surgery

b. Positive-pressure breathing (CPAP) by face mask

c. Positive end-expiratory pressure (PEEP) on mechanical ventilation

B. Compression atelectasis

1. Air or fluid in the pleural cavity under increased pressure collapses small airways beneath the pleura.


Compression atelectasis: air under pressure or fluid in pleural cavity


2. Examples

a. Tension pneumothorax where air compresses the lung

b. Pleural effusion where fluid compresses the lung

C. Atelectasis due to loss of surfactant

1. Surfactant

a. Synthesized by type II pneumocytes


Surfactant: synthesized by type II pneumocytes


(1) Stored in lamellar bodies (Fig. 16-6)

(2) Synthesis begins in 28th week of gestation.

b. Phosphatidylcholine (lecithin) is the major component.

c. Synthesis is increased by cortisol and thyroxine.

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16-6: Electron micrograph of a type II pneumocyte showing a lamellar body (arrow) containing surfactant.


(From Corrin B: Pathology of the Lungs. London, Churchill Livingstone, 1999, p 15, Fig. 1-26.)



Surfactant: cortisol increases synthesis, insulin inhibits synthesis


d. Synthesis is decreased by insulin.

e. Surfactant reduces surface tension in the small airways.

• Prevents collapse on expiration, when collapsing pressure is greatest

2. Respiratory distress syndrome (RDS) in newborns


Surfactant: ↓ surface tension


a. Pathogenesis

(1) Decreased surfactant in the fetal lungs; causes:

RDS: due to a decrease in surfactant


(a) Prematurity

(b) Maternal diabetes

• Fetal hyperglycemia increases insulin release.


RDS: prematurity, diabetes, C-section


(c) Cesarean section

• Lack of stress-induced increase in cortisol from a vaginal delivery


Women who have to deliver their babies prematurely receive glucocorticoids in order to increase fetal surfactant synthesis, thereby reducing the potential for developing RDS. Good maternal glycemic control decreases the risk for RDS.




Fetal surfactant: ↑ with maternal intake of glucocorticoids


(2) Widespread atelectasis results in massive intrapulmonary shunting.

• Perfusion without ventilation


RDS: intrapulmonary shunting


b. Collapsed alveoli are lined by hyaline membranes (Fig. 16-7).

• Derived from proteins leaking out of damaged pulmonary vessels

c. Clinical findings

(1) Respiratory difficulty begins within a few hours after birth.

(2) Grunting (see Table 16-2)

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16-7: Neonatal respiratory distress syndrome. Some of the dilated respiratory bronchioles and alveolar ducts are lined with a fibrin-rich membrane (hyaline membrane) (arrow). The subjacent alveoli are collapsed.


(From Damjanov I: Pathology for the Health-Related Professions, 2nd ed. Philadelphia, WB Saunders, 2000, p 128, Fig. 5-25.)



RDS: grunting, tachypnea, intercostal retractions


(3) Tachypnea

(4) Intercostal retractions

(5) Infants develop hypoxemia and respiratory acidosis.

d. Diagnosis

• Chest radiograph shows a “ground glass” appearance (Fig. 16-8).

e. Complications

(1) Superoxide free radical damage from O2 therapy

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16-8: Chest radiograph in respiratory distress syndrome. Note the fine, uniform granularity distributed throughout both lungs (“ground glass” appearance).


(From Katz D, Math K, Groskin S: Radiology Secrets. Philadelphia, Hanley & Belfus, 1998, p 380, Fig. 2.)



RDS O2 complications: blindness, bronchopulmonary dysplasia


• May result in blindness and permanent damage to small airways (bronchopulmonary dysplasia)

(2) Intraventricular hemorrhage

(3) Patent ductus arteriosus

• Due to persistent hypoxemia

(4) Necrotizing enterocolitis

• Intestinal ischemia allows entry of gut bacteria into the intestinal wall.

(5) Hypoglycemia in newborn


Hypoglycemia in newborn: due to excess insulin in response to fetal hyperglycemia


(a) Excess insulin decreases serum glucose, producing seizures and damage to neurons.

(b) Must give newborns glucose to prevent hypoglycemia

f. Treatment

• CPAP therapy with endotracheal tube with O2 and surfactant

V. Acute Lung Injury

A. Pulmonary edema (refer to Chapters 4 and 10)

1. Edema due to alterations in Starling pressure (transudate)

a. Increased hydrostatic pressure in pulmonary capillaries

• Left-sided heart failure, volume overload, mitral stenosis


Left-sided heart failure: most common cause of pulmonary edema


b. Decreased oncotic pressure

• Nephrotic syndrome, cirrhosis

2. Edema due to microvascular or alveolar injury (exudate)

a. Infections

• Examples—sepsis, pneumonia

b. Aspiration

• Examples—drowning (refer to Chapter 6), gastric contents

c. Drugs

• Example—heroin (refer to Chapter 6)

d. High altitude (refer to Chapter 6)

e. Acute respiratory distress syndrome (ARDS; see later)

B. Acute respiratory distress syndrome (ARDS)

• Noncardiogenic pulmonary edema resulting from acute alveolar-capillary damage


ARDS: noncardiogenic pulmonary edema


1. Epidemiology

a. Due to direct injury to the lungs or systemic diseases

b. Risk factors for ARDS


ARDS risk: sepsis, gastric aspiration, severe trauma


(1) Gram-negative sepsis (>40% of cases)

(2) Gastric aspiration (>30% of cases)

(3) Severe trauma with shock (>20% of cases)

(4) Diffuse pulmonary infections

• Severe acute respiratory syndrome (SARS), hantavirus

(5) Heroin

(6) Smoke inhalation

(7) Acute pancreatitis

(8) Cardiopulmonary bypass

(9) Disseminated intravascular coagulation

(10) Amniotic fluid embolism, fat embolism

2. Pathogenesis


ARDS: acute alveolar-capillary damage; sepsis most common cause


a. Acute damage to alveolar capillary walls and epithelial cells

b. Alveolar macrophages and other cells release cytokines.

(1) Cytokines are chemotactic to neutrophils.

(2) Neutrophils transmigrate into the alveoli through pulmonary capillaries.


Alveolar macrophages: cytokines chemotactic to neutrophils


(3) Capillary damage causes leakage of a protein-rich exudate producing hyaline membranes.

(4) Neutrophils damage type I and II pneumocytes.

• Decrease in surfactant causes atelectasis with intrapulmonary shunting.


ARDS: neutrophil damage to type I and II pneumocytes


c. Late findings

(1) Repair by type II pneumocytes

(2) Progressive interstitial fibrosis (restrictive lung disease)

3. Clinical findings

a. Dyspnea/tachypnea

b. Late inspiratory crackles

4. Laboratory findings

a. Severe hypoxemia not responsive to O2 therapy

• PaO2 < 50 mm Hg


ARDS: severe hypoxemia, PA wedge pressure < 18 mm Hg, ↑ A-a gradient


b. Pulmonary artery wedge pressure < 18 mm Hg

• Important in distinguishing ARDS from cardiogenic pulmonary edema

c. Respiratory alkalosis or normal PaCO2

d. Increased A-a gradient, due to:

(1) Intrapulmonary shunting

• Related to atelectasis

(2) Diffusion abnormalities

• Related to hyaline membranes, alveolar infiltrate

e. Chest x-ray

(1) Bilateral interstitial infiltrates initially

(2) Progresses to widespread alveolar consolidation with air bronchograms (80%)

5. Treatment

a. Treat underlying disease

b. Hemodynamic monitoring

c. Mechanical ventilation

d. Nitric oxide inhalation

e. Corticosteroids

6. Poor prognosis (40–50% mortality rate)

VI. Pulmonary Infections

A. Pneumonia

1. Epidemiology

a. Classified as community-acquired or nosocomial (hospital-acquired)

b. Community-acquired pneumonia is further subdivided into typical and atypical.

2. Typical community-acquired pneumonia

a. Epidemiology

(1) Majority are caused by bacterial pathogens.

(2) Most often due to Streptococcus pneumoniae (50–75%; Fig. 16-9A)

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16-9: A, Gram stain of Streptococcus pneumoniae. The sputum stain shows numerous lancet-shaped diplococci with the tapered ends pointing to each other. A few neutrophils contain phagocytosed bacteria. B, Bronchopneumonia showing patchy areas of consolidation (arrows) representing collections of neutrophils in the alveoli and bronchi. C, Lobar pneumonia. The lower lobe is uniformally consolidated. D, Posteroanterior radiograph of a right lower lobe pneumococcal pneumonia. Note the alveolar consolidation and the visible border of the right ventricle indicating that the middle lobe is not involved.


(A from Henry JB: Clinical Diagnosis and Management by Laboratory Methods, 20th ed. Philadelphia, WB Saunders, 2001, Plate 50-1; B from Kumar V, Fausto N, Abbas A: Robbins and Cotran’s Pathologic Basis of Disease, 7th ed. Philadelphia, WB Saunders, 2004, p 749, Fig. 15-33; C from Corrin B: Pathology of the Lungs. London, Churchill Livingstone, 2000, p 162, Fig. 5.2.5; D from Kliegman RM, Jenson HB, Behrman RE, Stanton BF: Nelson Textbook of Pediatrics, 18th ed. Philadelphia, Saunders Elsevier, 2007, p 1798, Fig. 397-2A.)



Streptococcus pneumoniae: most common cause of typical community-acquired pneumonia


b. Pathogenesis

(1) Inhalation of aerosol from an infected patient

(2) Aspiration of nasopharyngeal flora while sleeping

c. Bronchopneumonia

(1) Begins as an acute bronchitis and spreads locally into the lungs

(2) Usually involves the lower lobes or right middle lobe

(3) Lung has patchy areas of consolidation (Fig. 16-9B).


Bronchopneumonia: acute bronchitis with local extension into parenchyma


• Microabscesses are present in the areas of consolidation.

d. Lobar pneumonia

• Complete or almost complete consolidation of a lobe of lung (Fig. 16-9C)

e. Complications

(1) Lung abscesses, empyema (pus in the pleural cavity)

(2) Sepsis

f. Clinical findings

(1) Sudden onset of high fever with productive cough

(2) Chest pain

(3) Tachycardia

(4) Signs of consolidation (alveolar exudate)


Typical pneumonia: signs of consolidation (alveolar exudate)


(a) Dullness to percussion

(b) Increased vocal tactile fremitus

• Sound is transmitted well through alveolar consolidations.

(c) Late inspiratory crackles

(d) Bronchial breath sounds

(e) Bronchophony and egophony

(5) Chest radiograph (gold standard screen)


Chest radiograph: gold standard for diagnosing pneumonia


(a) Patchy infiltrates (bronchopneumonia) or lobar consolidation (Fig. 16-9D)

(b) Sensitivity 50% to 85%

(6) Laboratory findings

(a) Positive Gram stain


Positive Gram stain: more useful than culture


1. More useful than culture

• Cultures are still obtained.

2. Sensitivity 80%

(b) Neutrophilic leukocytosis

(c) Blood cultures positive in 20% of cases.

3. Table 16-4 (Fig.16-10A to I) summarizes important respiratory microbial pathogens.

4. Atypical community-acquired pneumonia

a. Epidemiology

(1) Usually caused by Mycoplasma pneumoniae

Table 16-4 Summary of Respiratory Microbial Pathogens

image image image image image image image

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16-10: A, Parainfluenza virus producing laryngotracheobronchitis. Frontal radiograph showing narrowing of the trachea (arrows) producing the classic steeple sign. B, Cytomegalovirus. The enlarged nuclei of many of the type I pneumocytes contain large inclusions (basophilic staining with hematoxylin and eosin stain) surrounded by a clear halo. C, Tonsillitis due to Corynebacterium diphtheriae. Note the gray, pseudomembrane covering the tonsils. D, Cryptococcus neoformans. The yeast form produces a clear capsule around a central faint nucleus. E, Aspergillus fumigatus. Lung biopsy stained with Gomori methenamine-silver shows septated hyphae and fruiting body (inset). F, Coccidioides immitis. Note the spherules containing endospores (arrow). G, Histoplasma capsulatum. Laminated granuloma at the lung periphery produces puckering of the pleural surface. H, Histoplasma capsulatum. Alveolar macrophage contains intracellular yeast forms. I, Blastomyces dermatidis. Note the yeast forms with broad-based buds (arrow).


(A from Pretorius ES, Solomon JA: Radiology Secrets, 2nd ed. St. Louis, Mosby, 2006, p 464, Fig. 57-4; B from Damjanov I, Linder J: Pathology: A Color Atlas. St. Louis, Mosby, 2000, p 56, Fig. 4-24; C courtesy of Franklin H. Top, Department of Hygiene and Preventive Medicine, State University of Iowa College of Medicine, Iowa City, Iowa, and Parke, Davis & Company’s Therapeutic Notes; D and F from Klatt E: Robbins and Cotran’s Atlas of Pathology. Philadelphia, WB Saunders, 2006, pp 127, 126, Figs. 5-92, 5-91 on right, respectively; E, G, I from Kumar V, Fausto N, Abbas A: Robbins and Cotran’s Pathologic Basis of Disease, 7th ed. Philadelphia, WB Saunders, 2004, pp 400, 754, 755, Figs. 8-49B, 15-37, 15-39A, respectively; H from Murray PR, Shea YR: Medical Microbiology, 2nd ed. St. Louis, Mosby, 2002, p 773, Fig. 74-10.)



Mycoplasma pneumoniae: most common cause of atypical pneumonia


(2) Other pathogens

(a) Chlamydophilia pneumoniae

(b) Viruses

• Respiratory syncytial virus, influenzavirus, adenovirus

(c) Chlamydia trachomatis in newborns

b. Pathogenesis

• Contracted by inhalation (droplet infection)

c. Patchy interstitial pneumonia


Atypical pneumonia: interstitial pneumonia; no signs of consolidation


(1) Mononuclear infiltrate

(2) Alveolar spaces usually free of exudate

d. Clinical findings

(1) Insidious onset, low-grade fever

(2) Nonproductive cough

(3) Chest pain

(4) Flu-like symptoms

• Pharyngitis, laryngitis, myalgias, headache

(5) No signs of consolidation

5. Nosocomial pneumonia

a. Epidemiology; risk factors:

(1) Severe underlying disease

(2) Antibiotic therapy

(3) Immunosuppression


Water loving bacteria: Pseudomonas aeruginosa, Legionella pneumophila


(4) Respirators

• Most common source of infection

b. Pathogens

(1) Gram-negative bacteria

• Pseudomonas aeruginosa (respirators), Escherichia coli

Pseudomonas aeruginosa: nosocomial pneumonia; contracted from respirators


(2) Gram-positive bacteria (e.g., Staphylococcus aureus)

6. Pneumonia in immunocompromised hosts

a. Complication of AIDS and bone marrow transplantation

b. Common opportunistic infections:

(1) Cytomegalovirus (Fig. 16-10B)

(2) Pneumocystis jiroveci (see Fig. 3-3)


Pneumocystis jiroveci: most common pathogen causing pneumonia in AIDS


• Trimethoprim-sulfamethoxazole is used for prophylaxis and treatment.

(3) Aspergillus fumigatus (Fig. 16-10E)

7. Tuberculosis (TB)

a. Epidemiology and pathogenesis

(1) Contracted by inhalation of Mycobacterium tuberculosis

(2) Organism resides in phagosomes of alveolar macrophages

• Produces a protein that prevents fusion of lysosomes with phagosome

(3) Characteristics

(a) Strict aerobe, acid-fast (due to mycolic acid in cell wall)

(b) Cord factor is virulence factor


TB: acid-fastness due to mycolic acid


(4) Screening

(a) Purified protein derivative (PPD) intradermal skin test


TB: cord factor is virulence factor


(b) Does not distinguish active from inactive disease

(5) Protein in cell wall

• Responsible for positive PPD

(6) Drug resistance

(a) Chromosome mutations involving mycolic acid

(b) Chromosome mutations involving catalase peroxidase

• Enzyme is required to activate isoniazid


PPD: does not distinguish active from inactive TB


b. Primary TB

(1) Subpleural location (Fig. 16-11)

(a) Upper part of the lower lobes or lower part of the upper lobes

image

16-11: Primary tuberculosis. Note the tan-yellow subpleural granuloma with caseation necrosis and the tan-yellow area of caseation necrosis in the hilar lymph node in the mid-lung field. The two of these together is called a Ghon complex. The inset shows an acid-fast stain with numerous Mycobacterium tuberculosis organisms.


(The gross picture of primary tuberculosis is from Klatt, E: Robbins and Cotran’s Atlas of Pathology. Philadelphia, WB Saunders, 2006, p 197, Fig. 8-4; inset from Hoffbrand AV: Color Atlas: Clinical Hematology, 3rd ed. St. Louis, Mosby, 2000, p 136, Fig. 7-85B.)



Primary TB: upper part lower lobes; lower part upper lobes; Ghon complex


(b) Ghon focus (caseous necrosis) in periphery

(c) Ghon complex (caseous necrosis) in hilar lymph nodes

(2) Usually resolves

(a) Produces a calcified granuloma or area of scar tissue

Related posts:

  1. Skin Disorders
  2. Lymphoid Tissue Disorders
  3. Vascular Disorders
  4. Hepatobiliary and Pancreatic Disorders

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Jun 25, 2017 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on Upper and Lower Respiratory Disorders

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