16 Upper and Lower Respiratory Disorders

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16 Upper and Lower Respiratory Disorders

Signs and Symptoms of Respiratory Disease

Table 16-1. Common Symptoms of Respiratory DiseaseSymptomCauses and Discussion

Dyspnea Difficulty with breathing

Due to stimulation of J receptors causing decrease in full inspiration

Causes of dyspnea

Decreased compliance (e.g., interstitial fibrosis)

Increased airway resistance (e.g., chronic bronchitis)

Chest bellows disease (e.g., obesity, kyphoscoliosis)

Interstitial inflammation/fluid accumulation (e.g., leftsided heart failure)

Cough Cough with a normal chest !ray

"ostnasal discharge is the most common cause

#octurnal cough

$%&D' due to acid reflu! in tracheobronchial tree at night

ronchial asthma' due to bronchoconstriction

"roductie cough

Chronic bronchitis' due to smoking cigarettes

*ypical bacterial pneumonia

ronchiectasis

Drugs causing cough

+C% inhibitors' inhibit degradation of bradykinin, causing mucosal swelling and irritation intracheobronchial tree

+spirin' causes an increase in * CD%- (bronchoconstrictors)

emoptysis Coughing up bloodtinged sputum

echanisms

"arenchymal necrosis

ronchial and/or pulmonary essel damage Causes

Chronic bronchitis (most common cause)

"neumonia, bronchogenic carcinoma

*, bronchiectasis, aspergilloma (fungus liing in a caitary lesion)

+C%, angiotensinconerting en0yme1 $%&D, gastroesophageal reflu! disease1 *, leukotriene1 *, tuberculosis.

Signs and Symptoms of Respiratory Disease

Table 16-1. Common Symptoms of Respiratory Disease

SymptomCauses and Discussion

Dyspnea Difficulty with breathing

Due to stimulation of J receptors causing decrease in full inspiration

Causes of dyspnea

Decreased compliance (e.g., interstitial fibrosis)



Increased airway resistance (e.g., chronic bronchitis)

Chest bellows disease (e.g., obesity, kyphoscoliosis)

Interstitial inflammation/fluid accumulation (e.g., leftsided heart failure)

Cough Cough with a normal chest !ray

"ostnasal discharge is the most common cause

#octurnal cough

$%&D' due to acid reflu! in tracheobronchial tree at night ronchial asthma' due to bronchoconstriction

"roductie cough

Chronic bronchitis' due to smoking cigarettes

*ypical bacterial pneumonia

ronchiectasis

Drugs causing cough

+C% inhibitors' inhibit degradation of bradykinin, causing mucosal swelling and irritation intracheobronchial tree

+spirin' causes an increase in * CD%- (bronchoconstrictors)

emoptysis Coughing up bloodtinged sputum

echanisms

"arenchymal necrosis

ronchial and/or pulmonary essel damage

Causes

Chronic bronchitis (most common cause)

"neumonia, bronchogenic carcinoma

*, bronchiectasis, aspergilloma (fungus liing in a caitary lesion)

+C%, angiotensinconerting en0yme1 $%&D, gastroesophageal reflu! disease1 *, leukotriene1 *, tuberculosis.

ulmonary !unction Tests

Calculation of the aleolararterial (+a) gradientpage 234

page 235

Calculate the +a gradient in a patient breathing 6.76 82 who has a "C82 of 36 mmg and "a82 of -6 mm g. "+82 9 6.76 (:;7) 36/6.3 9 ;;- mm g. +a gradient 9;;- -6 9 :- mm g, which is medically significant and indicates one or more of theaboementioned lung disorders or a righttoleft shunt in the heart.

page 235

page 23:

;. +a gradient is the difference between the aleolar "82 ("+82) and arterial "82 ("a82).

a. +a gradient is normally due to a mismatch between entilation and perfusion in thelungs. %!ample+n +a gradient e!ists when perfusion is greater than entilation in the

lower lobes.b. It is useful in differentiating causes of hypo!emia (decreased "a82).

ii ypo!emia due to pulmonary causes increases +a gradient.

iii ypo!emia due to e!trapulmonary causes has a normal +a gradient.

2. Calculation of the +a gradient



a. "+82 9 < 82 (:;7) arterial "C82/6.3

< 82 is the percentage of 82 the patient is breathing1 :;7 is the atmospheric

pressure (:56 mm g) minus the water apor pressure (-: mm g)1 and 6.3 isthe respiratory =uotient.

b. %!ample using normal alues

ii #ormal "+82 9 6.2; (:;7) -6/6.3 9 ;66 mm g

iii #ormal "a82 9 >4 mm g

iiii #ormal +a gradient 9 ;66 mm g >4 mm g 9 4 mm g

ivi edically significant +a gradient ≥ 76 mm g

2. Causes of hypo!emia with an increased +a gradienta. ?entilation defect

ii Impaired 82 deliery to the aleoli for gas e!change

iii %!ampleairway collapse due to the respiratory distress syndrome

b. "erfusion defectii Decreased or absent blood flow to the aleoli

iii %!amplepulmonary embolus

c. Diffusion defectii 82 cannot diffuse through the aleolarcapillary interface.

iii %!ampleinterstitial fibrosis, pulmonary edema

d. &ighttoleft cardiac shunt

%!ampletetralogy of @allot

ii Causes of hypo!emia with a normal +a gradient

a. Depression of the respiratory center in the medulla %!amplesbarbiturates, brain inAury

b. Bpper airway obstruction

ii Caf coronary (food blocking airway)

iii %piglottitis due to Hemophilus influenzae

iiii Croup due to parainfluen0a irus (narrows the trachea)

e. Chest bellows (muscles of respiration) dysfunctionii "araly0ed diaphragm

iii +myotrophic lateral sclerosis with degeneration of anterior horn cells

Calculate the +a gradient in a patient breathing room air who has a "C82 of 36 mmg and "a82 of -6 mm g. "+82 9 6.2; (:;7) 36/6.3 9 46 mm g. +a gradient 946 -6 9 ;6 mm g, which is not medically significant and indicates ane!trapulmonary cause of hypo!emia.

Calculation of the aleolararterial (+a) gradientpage 234

page 235

Calculate the +a gradient in a patient breathing 6.76 82 who has a "C82 of 36 mmg and "a82 of -6 mm g. "+82 9 6.76 (:;7) 36/6.3 9 ;;- mm g. +a gradient 9;;- -6 9 :- mm g, which is medically significant and indicates one or more of theaboementioned lung disorders or a righttoleft shunt in the heart.

page 235



page 23:

;. +a gradient is the difference between the aleolar "82 ("+82) and arterial "82 ("a82).a. +a gradient is normally due to a mismatch between entilation and perfusion in the

lungs. %!ample+n +a gradient e!ists when perfusion is greater than entilation in the

lower lobes.b. It is useful in differentiating causes of hypo!emia (decreased "a82).

ii ypo!emia due to pulmonary causes increases +a gradient.

iii ypo!emia due to e!trapulmonary causes has a normal +a gradient.

2. Calculation of the +a gradienta. "+82 9 < 82 (:;7) arterial "C82/6.3

< 82 is the percentage of 82 the patient is breathing1 :;7 is the atmospheric

pressure (:56 mm g) minus the water apor pressure (-: mm g)1 and 6.3 isthe respiratory =uotient.

b. %!ample using normal alues

ii #ormal "+82 9 6.2; (:;7) -6/6.3 9 ;66 mm giii #ormal "a82 9 >4 mm g

iiii #ormal +a gradient 9 ;66 mm g >4 mm g 9 4 mm g

ivi edically significant +a gradient ≥ 76 mm g

2. Causes of hypo!emia with an increased +a gradienta. ?entilation defect

ii Impaired 82 deliery to the aleoli for gas e!change

iii %!ampleairway collapse due to the respiratory distress syndrome

b. "erfusion defectii Decreased or absent blood flow to the aleoli

iii %!amplepulmonary embolus

c. Diffusion defectii 82 cannot diffuse through the aleolarcapillary interface.

iii %!ampleinterstitial fibrosis, pulmonary edema

d. &ighttoleft cardiac shunt

%!ampletetralogy of @allot

ii Causes of hypo!emia with a normal +a gradient

a. Depression of the respiratory center in the medulla %!amplesbarbiturates, brain inAury

b. Bpper airway obstruction

ii Caf coronary (food blocking airway)

iii %piglottitis due to Hemophilus influenzae

iiii Croup due to parainfluen0a irus (narrows the trachea)

e. Chest bellows (muscles of respiration) dysfunctionii "araly0ed diaphragm

iii +myotrophic lateral sclerosis with degeneration of anterior horn cells

Calculate the +a gradient in a patient breathing room air who has a "C82 of 36 mmg and "a82 of -6 mm g. "+82 9 6.2; (:;7) 36/6.3 9 46 mm g. +a gradient 946 -6 9 ;6 mm g, which is not medically significant and indicates ane!trapulmonary cause of hypo!emia.



pirometrypage 233

• Bseful in distinguishing restrictie from obstructie lung disease

;. ?olumes and capacities that are not directly measured by spirometrya. @unctional residual capacity (@&C)

*otal amount of air in the lungs at the end of a normal e!piration

b. *otal lung capacity (*C) *otal amount of air in a fully e!panded lung

c. &esidual olume (&?) ?olume of air left oer in the lung after ma!imal e!piration

2. *idal olume (*?)

o ?olume of air that enters or leaes the lungs during normal =uiet respiration2.

@orced ital capacity (@?C), forced e!piratory olume in ; second (@%?;sec), and @%?;sec/@?C

a. @?C is the total amount of air e!pelled after a ma!imal inspiration #ormal @?C is 4

b. @orced e!piratory olume in ; second (@%?;sec)

ii +mount of air e!pelled from the lungs in ; second after a ma!imal inspiration

iii #ormal @%?;sec is -

b. &atio of @%?;sec/@?C is normally 36<.

#ormal ratio is -/4, or 36<.

2. %!piratory resere olume (%&?)ii It refers to the amount of air forcibly e!pelled at the end of a normal e!piration.

ii It is commonly used to calculate residual olume (@&C %&? 9 &?).

7. Comparison of pulmonary function tests in restrictie and obstructie lung disease

Table 16-". Comparison of ulmonary !unction Tests in Restricti#e and $bstructi#eLung Disease

arameter Restricti#e Disease $bstructi#e Disease

*otal lung capacity Decreased Increased

&esidual olume Decreased Increased

@%?;sec Decreased Decreased

@?C Decreased Decreased

@%?;sec/@?C #ormal to increased Decreased

"a82 Decreased Decreased

+a gradient Increased Increased

+a, aleolararterial1 @%?, forced e!piratory olume1 @?C, forced ital capacity.



Upper %irway Disorders

Choanal atresia

;. Bnilateral or bilateral bony septum between the nose and the pharyn!2. #ewborn turns cyanotic when breastfeeding.

o Crying causes the child to Epink upE again.

Choanal atresia

;. Bnilateral or bilateral bony septum between the nose and the pharyn!2. #ewborn turns cyanotic when breastfeeding.

o Crying causes the child to Epink upE again.

#asal polyps

;. #asal polyps are nonneoplastic tumefactions.o Deelop as a response to chronic inflammation

2. +llergic polyps

a. ost common polyp

b. ost often seen in adults with a history of Ig%mediated allergies

2. #asal polyps associated with aspirin and other nonsteroidal drugsa. %pidemiology

ost often occur in women with chronic pain syndromesb. "athogenesis

ii Drugs block cycloo!ygenase leaing the lipo!ygenase pathway open.

iii eukotrienes (*) CD%- are increased, causing bronchoconstriction.

b. Clinical triadnonsteroidal drugs, asthma, and nasal polyps

2. #asal polyps are often associated with cystic fibrosis.

8bstructie sleep apnea (8+)

;. %pidemiologya. %!cessie snoring with interals of breath cessation (called apnea)b. Causes

i. 8besity (ery common) "haryngeal muscles collapse due to the weight of tissue in the neck.

ii. *onsillar hypertrophy, nasal septum deiation2. "athogenesis



o +irway obstruction causes C82 retention, leading to hypo!emia.2. Clinical findings

a. %!cessie snoring with episodes of apneab. Daytime somnolence often simulating narcolepsy

7. aboratory findings

c. Decreased "82 and 82 saturation during apneic episodesd. Increase in arterial "C82 (respiratory acidosis)

-. Complications

e. "ulmonary hypertension (") leading to right entricular hypertrophy

Called cor pulmonale (see section ?II)ii econdary polycythemia

Due to a hypo!emic stimulus for erythropoietin release

2. "olysomnography

o Confirmatory test that documents periods of apnea during sleep

2. *reatmento #asal continuous positie airway pressure (C"+")

o urgical correction of any obstructie lesions, weight loss

inusitis

;. %pidemiologya. a!illary sinus is most often inoled in adults.b. %thmoid sinus is most often inoled in children.c. Causes

i. Bpper respiratory infections (e.g., irus, bacteria)ii. Deiated nasal septum, allergic rhinitis, barotrauma, smoking cigarettes

d. "athogens causing sinusitisi. Streptococcus pneumoniae (most common)ii. &hinoiruses, anaerobes (chronic sinusitis)iii. ystemic fungi (e.g., Mucor or Aspergillus species)

Diabetics commonly hae sinusitis due to Mucor species.

2. "athogenesis

o lockage of drainage into the nasal caity2. Clinical findings

a. @eer, nasal congestion, pain oer sinuses

b. Computed tomography (C*) scan is the most sensitie test.



#asopharyngeal carcinomapage 23>

page 2>6

;. %pidemiologya. ost common malignant tumor of the nasopharyn!

b. ale dominantc. Increased incidence in the Chinese and +frican populations2. "athogenesis

o Causal relationship with %psteinarr irus (%?)2. "athologic findings

a. =uamous cell carcinoma or undifferentiated cancer

b. etastasi0es to cerical lymph nodes

aryngeal carcinoma;. %pidemiology and pathogenesis

a. ore common in men than in womenb. &isk factors

i. Cigarette smoking (most common cause)ii. +lcohol (synergistic effect with smoking)iii. =uamous papillomas and papillomatosis

uman papillomairus type 5 and ;; association

c. aAority are located on the true ocal cords2. aAority are keratini0ing s=uamous cell carcinomas.7. Clinical findings

o "ersistent hoarseness often associated with cerical lymphadenopathy

%telectasis

• oss of lung olume due to inade=uate e!pansion of the airspaces (collapse)

&esorption atelectasispage 2>6

page 2>;

;. "athogenesisa. +irway obstruction preents air from reaching the aleoli.

8bstruction occurs in bronchi, segmental bronchi, or terminal bronchioles.

b. Causes of obstruction

ii ucus or mucopurulent plug after surgery

iii +spiration of foreign material

iiii Centrally located bronchogenic carcinoma



b. Cause of aleolar collapse

ack of air and distal resorption of pree!isting air through the pores of Fohn in the

aleolar wallsb. Collapse may inole all or part of a lung.

ii Clinical findings

a. @eer and dyspnea oth usually occur within 2- to 75 hours of collapse.

b. +bsent breath sounds and ocal ibratory sensation (tactile fremitus)c. Ipsilateral eleation of the diaphragm and tracheal deiation

Collapsed lung gies up space, causing the preceding findings.

d. Collapsed lung does not e!pand on inspiration (inspiratory lag).

Compression atelectasis

;. +ir or fluid in the pleural caity under increased pressure collapses small airways beneath thepleura.

2. %!amplesa. *ension pneumothora! (air compresses lung)b. "leural effusion (fluid compresses lung)

7. *rachea deiates to the contralateral side.

+telectasis due to loss of surfactantGomen who hae to delier their babies prematurely receie glucocorticoids in order to increase fetalsurfactant synthesis thereby reducing the potential for deeloping &D. $ood maternal glycemic controldecreases the risk for &D.

page 2>7

;. urfactanta. ynthesi0ed by type II pneumocytes

i. tored in lamellar bodiesii. ynthesis begins in 23th week of gestation.

b. "hosphatidylcholine (lecithin) is the maAor component.c. ynthesis is increased by cortisol and thyro!ine.d. ynthesis is decreased by insulin.e. urfactant reduces surface tension in the small airways.

"reents collapse on e!piration, when collapsing pressure is greatestii &espiratory distress syndrome (&D) in newborns

a. "athogenesis

i. Decreased surfactant in the fetal lungs1 causes' "rematurity

aternal diabetes

@etal hyperglycemia increases insulin release.

Cesarean section

ack of stressinduced increase in cortisol from a aginal deliery



ii. Gidespread atelectasis results in massie intrapulmonary shunting. "erfusion without entilation

b. Collapsed aleoli are lined by hyaline membranes

Deried from proteins leaking out of damaged pulmonary esselsb. Clinical findings

i. &espiratory difficulty begins within a few hours after birth.ii. Infants deelop hypo!emia and respiratory acidosis.iii. Chest radiograph shows a Eground glassE appearance.

c. Complicationsi. upero!ide free radical damage from 82 therapy

ay result in blindness and permanent damage to small airways

(bronchopulmonary dysplasia)ii. Intraentricular hemorrhageiii. "atent ductus arteriosus (due to persistent hypo!emia)i. #ecroti0ing enterocolitis

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

. ypoglycemia in newborn

%!cess insulin decreases serum glucose producing sei0ures and damage

to neurons.

%cute Lung &n'ury

"ulmonary edema

;. %dema due to alterations in tarling pressure (transudate)a. Increased hydrostatic pressure in pulmonary capillaries

eftsided heart failure, olume oerload, mitral stenosis

b. Decreased oncotic pressure #ephrotic syndrome, cirrhosis

2. %dema due to microascular or aleolar inAury (e!udate)a. Infections (e.g., sepsis, pneumonia)b. +spiration (e.g., drowning, gastric contents)c. Drugs (e.g., heroin), shock, massie trauma

d. igh altitude

"ulmonary edema

;. %dema due to alterations in tarling pressure (transudate)a. Increased hydrostatic pressure in pulmonary capillaries

eftsided heart failure, olume oerload, mitral stenosis

b. Decreased oncotic pressure #ephrotic syndrome, cirrhosis

2. %dema due to microascular or aleolar inAury (e!udate)a. Infections (e.g., sepsis, pneumonia)b. +spiration (e.g., drowning, gastric contents)



c. Drugs (e.g., heroin), shock, massie trauma

d. igh altitude

+cute respiratory distress syndrome (+&D)page 2>7

page 2>-

• #oncardiogenic pulmonary edema resulting from acute aleolarcapillary damage.

;. %pidemiologya. Due to direct inAury to the lungs or systemic diseasesb. &isk factors for +&D

i. $ramnegatie sepsis (-6< of cases)ii. $astric aspiration (76< of cases)iii. eere trauma with shock (;6< of cases)i. Diffuse pulmonary infections, heroin, smoke inhalation

2. "athogenesis

a. +cute damage to aleolar capillary walls and epithelial cellsb. +leolar macrophages release cytokines.

i. Cytokines are chemotactic to neutrophils.ii. #eutrophils transmigrate into the aleoli through pulmonary capillaries.iii. Capillary damage causes leakage of a proteinrich e!udate producing hyaline

membranes.i. #eutrophils damage type I and II pneumocytes.

Decrease in surfactant causes atelectasis with intrapulmonary shunting.

c. ate findingsi. &epair by type II pneumocytesii. "rogressie interstitial fibrosis (restrictie lung disease)

7. Clinical findingsa. Dyspnea with seere hypo!emia not responsie to 82 therapy

b. +cute respiratory acidosis

4. "oor prognosis (∼56< mortality rate)

ulmonary &nfections

"neumonia

;. %pidemiologya. Classified as communityac=uired or nosocomial (hospitalac=uired)b. Communityac=uired pneumonia is further subdiided into typical or

atypical.2. *ypical communityac=uired pneumoniaa. %pidemiology

i. aAority are caused by bacterial pathogens.b. ost often due to Streptococcus pneumoniae

i. Inhalation of aerosol from an infected patientii. +spiration of nasopharyngeal flora while sleeping

c. ronchopneumoniai. egins as an acute bronchitis and spreads locally into the lungs



ii. Bsually inoles the lower lobes or right middle lobeiii. ung has patchy areas of consolidation

icroabscesses are present in the areas of consolidation.

d. obar pneumonia

Complete or almost complete consolidation of a lobe of lung

b. Complications

i. ung abscesses, empyema (pus in the pleural caity)ii. epsis

b. Clinical findingsi. udden onset of high feer with productie coughii. igns of consolidation (aleolar e!udate)

Dullness to percussion

Increased ocal tactile fremitus

ound is transmitted well through aleolar

consolidations. Inspiratory crackles (air moing through e!udate in the

aleoli)iii. Chest radiograph (gold standard screen)

"atchy infiltrates (bronchopneumonia) or lobar

consolidationi. aboratory findings

"ositie $ram stain

#eutrophilic leukocytosis

7. +typical communityac=uired pneumonia

c. %pidemiologyi. Bsually caused by Mycoplasma pneumoniae ii. 8ther pathogens

Chlamydia pneumoniae (*G+& agent) ?iruses (respiratory syncytial irus, influen0airus,

adenoirus) Chlamydia trachomatis (newborns)

d. "athogenesis

Contracted by inhalation (droplet infection)b. "atchy interstitial pneumonia

i. ononuclear infiltrateii. +leolar spaces usually free of e!udate

e. Clinical findingsi. Insidious onset, lowgrade feer, nonproductie cough

ii. @lulike symptoms "haryngitis, laryngitis, myalgias, headache

iii. No signs of consolidation

-. #osocomial pneumonia

f. %pidemiology1 risk factorsi. eere underlying disease



ii. +ntibiotic therapy, immunosuppressioniii. &espirators (most common source of infection)

g. "athogensi. $ramnegatie bacteria

Pseudomonas aeruginosa (respirators), Escherichia coli

ii. $rampositie bacteria (e.g., Staphylococcus aureus)

4. "neumonia in immunocompromised hosts

h. Complication of +ID and bone marrow transplantationi. Common opportunistic infections'

i. Cytomegaloirus (ii. Pneumocystis jiroveci

*rimethoprimsulfametho!a0ole is used for prophyla!is and

treatment.iii. Aspergillus fumigatus

5. *uberculosis (*)

A. %pidemiology and pathophysiologyi. Contracted by inhalation of Mycoacterium tuerculosis ii. Characteristics

trict aerobe, acidfast (due to mycolic acid in cell wall)

iii. creening "urified protein deriatie (""D) intradermal skin test

Does not distinguish actie from inactie disease

k. "rimary *i. ubpleural location

Bpper part of the lower lobes or lower part of the upper

lobesii. Bsually resoles

"roduces a calcified granuloma or area of scar tissue ay be a nidus for secondary *

l. econdary (reactiation) *i. Due to reactiation of a preious primary * siteii. Inoles one or both apices in upper lobes

?entilation (o!ygenation) is greatest in the upper lobes.

iii. Caitary lesion due to release of cytokines from memory * cellsm. Clinical findings

@eer, drenching night sweats, weight lossc. Complications

i. iliary spread in lungs due to inasion into the bronchus or

lymphaticsii. iliary spread to e!trapulmonary sites

Due to inasion of pulmonary ein tributaries

Fidney is the most common e!trapulmonary site.

iii. assie hemoptysis, bronchiectasis, scar carcinomai. $ranulomatous hepatitis, spread to ertebra ("ottHs disease)



:. Mycoacterium avium!intracellulare comple! (+C)

n. +typical mycobacteriumo. ost common * in +ID (often disseminates)

8ccurs when CD- * count falls below 46 cells/ii ystemic fungal infections

a. Contracted from inhalation of the pathogenb. "roduce a granulomatous inflammatory reaction with or without caseation

ii ummaries of respiratory microbial pathogens

Table 16-(. Summary of Respiratory )icrobial at*ogens

at*ogen Discussion

+iruses

&hinoirus ost common cause of the common cold

*ransmitted by hand to eyenose contact

&? ost common iral cause of atypical pneumonia and bronchiolitis (whee0ing) in children8ccurs in late fall and winter

"arainfluen0a ost common cause of croup (laryngotracheobronchitis) in infantsInspiratory stridor (upper airway obstruction) due to submucosal edema in trachea

+nterior !ray of neck shows Esteeple sign,E representing mucosal edema in the trachea (site ofobstruction)

C? Common pneumonia in immunocompromised hosts (e.g., bone marrow transplants, +ID)%nlarged aleolar macrophages/pneumocytes, contain basophilic intranuclear inclusionssurrounded by a halo

Influen0airus *ype + iruses are most often inoledemagglutinins bind irus to cell receptors in the nasal passages#euraminidase dissoles mucus and facilitates release of iral particlesInfluen0a + pneumonia may be complicated by a superimposed bacterial pneumonia (usuallyStaphylococcus aureus)

&ubeola @eer, cough, conAunctiitis, and e!cessie nasal mucus productionFoplik spots in the mouth precede onset of the rashGarthin@inkeldey multinucleated giant cells are a characteristic finding

+& Infects lower respiratory tract and then spreads systemically to produce seere respiratoryinfection@irst transmitted to humans through contact with masked palm ciets (China) and then fromhumantohuman contact through respiratory secretions (e.g., hospitals, families)Diagnose with iral detection by "C& or detection of antibodies

Chlamydia

C. pneumoniae econd most common cause of atypical pneumonia

C. trachomatis #ewborn pneumonia (passage through birth canal) +febrile, staccato cough (choppy cough), conAunctiitis, whee0ing

"ic#ettsia

Co$iella urnetii 8nly rickettsia transmitted %ithout a ector Contracted by dairy farmers, eterinarians

+ssociated with the birthing process of infected sheep, cattle, and goats, and handling of milk ore!crement

+typical pneumonia, myocarditis, granulomatous hepatitis

Mycoplasma

M. pneumoniae ost common cause of atypical pneumoniaCommon in adolescents and military recruits (closed spaces)Insidious onset with lowgrade feer Complications' bullous myringitis, cold autoimmune hemolytic anemia due to antiIIg antibodiesCold agglutinins in blood

,acteria



Streptococcus pneumoniae

$rampositie lancetshaped diplococcusost common cause of typical community ac=uired pneumonia&apid onset, productie cough, signs of consolidation

Staphylococcusaureus

$rampositie coccus in clumpsellow sputumCommonly superimposed on influen0a pneumonia and measles pneumoniaaAor lung pathogen in cystic fibrosis and intraenous drug abusersemorrhagic pulmonary edema, abscess formation, and tension pneumatocysts (intrapleural

blebs), which may rupture and produce a tension pneumothora!

Coryneacteriumdiphtheriae

$rampositie rod*o!in inhibits protein synthesis by +D"ribosylation of elongation factor 2 inoled in proteinsynthesis1 to!in also impairs Ko!idation of fatty acids in the heart*o!ininduced pseudomembranous inflammation produces shaggy gray membranes in theoropharyn! and trachea

Haemophilusinfluenzae

$ramnegatie rodCommon cause of sinusitis, otitis media, conAunctiitis (pink eye)Inspiratory stridor may be due to acute epiglottitis1 swelling of epiglottis produces Ethumbprint signEon lateral !ray of the neckost common bacterial cause of acute e!acerbation of C8"D

Mora$ellacatarrhalis

$ramnegatie diplococcusCommon cause of typical pneumonia, especially in the elderlyecond most common pathogen causing acute e!acerbation of C8"DCommon cause of chronic bronchitis, sinusitis, otitis media

Pseudomonasaeruginosa

$ramnegatie rod$reen sputum (pyocyanin)Gaterloing bacteria most often transmitted by respiratorsost common cause of nosocomial pneumonia and death due to pneumonia in cystic fibrosis1pneumonia often associated with infarction due to essel inasion

&lesiella pneumoniae

$ramnegatie fat rod surrounded by a mucoid capsuleost common gramnegatie organism causing lobar pneumonia and typical pneumonia in elderlypatients in nursing homesCommon cause of pneumonia in alcoholics1 howeer, S. pneumoniae is still the most commonpneumonia"neumonia associated with bloodtinged, thick, mucoid sputum1 lobar consolidation and abscessformation are common

'egionella pneumophila

$ramnegatie rod (re=uires I@ stain or Dieterle siler stain to identify in tissue)1 antigens can alsobe detected in urineGaterloing bacteria (water coolers1 mists in produce section of grocery stores1 outdoorrestaurants in summer1 rain forests in 0oos)

"neumonia associated with high feer, dry cough, flulike symptomsay produce tubulointerstitial disease with destruction of the Au!taglomerular apparatus leading tohyporeninemic hypoaldosteronism (type I? renal tubular acidosishyponatremia, hyperkalemia,metabolic acidosis)

Systemic !ungi

Cryptococcusneoformans

udding yeast with narrowbased buds1 surrounded by a thick capsule@ound in pigeon e!creta (around buildings, outside office windows, under bridges)ost common opportunistic fungal infection"rimary lung disease (-6<)' granulomatous inflammation with caseation

Aspergillusfumigatus

@ruiting body and narrowangled (L-4 degrees), branching septate hyphae +spergilloma' fungus ball (isible on !ray) that deelops in a pree!isting caity in the lung (e.g.,old * site)1 cause of massie hemoptysis

+llergic bronchopulmonary aspergillosis' type I and type III hypersensitiity reactions1 Ig% leelsincreased1 eosinophilia1 intense inflammation of airways and mucus plugs in terminal bronchioles1repeated attacks may lead to bronchiectasis and interstitial lung disease?essel inader with hemorrhagic infarctions and a necroti0ing bronchopneumonia

Mucor species Gideangled hyphae (M-4 degrees) without septaClinical settings' diabetes, immunosuppressed patients?essel inader and produces hemorrhagic infarcts in the lungInades the frontal lobes in patients with diabetic ketoacidosis (rhinocerebral mucormycosis)

Coccidioidesimmitis

pherules with endospores in tissues1 contracted by inhaling arthrospores in dust while liing orpassing through arid desert areas in the southwestern Bnited tates (Ealley feerE)1 increasedafter earth=uakes (increased dust)@lulike symptoms and erythema nodosum (painful nodules on lower legs1 inflammation ofsubcutaneous fat)$ranulomatous inflammation with caseous necrosis



Histoplasmacapsulatum

ost common systemic fungal infection1 endemic in 8hio and centralississippi &ier alleys1 inhalation of microconidia in dust contaminated with e!creta from bats(increased incidence in cae e!plorers, spelunkers), starlings, or chickens (common in chickenfarmers)$ranulomatous inflammation with caseous necrosiseast forms are present in macrophagesimulates * lung disease1 produces coin lesions, consolidations, miliary spread, and caitationarked dystrophic calcification of granulomas1 most common cause of multiple calcifications in the

spleen(lastomycesdermatitidis

easts hae broadbased buds and nuclei1 occurs in $reat akes region and central andsoutheastern Bnited tates1 maledominant disease"roduces skin and lung disease1 skin lesions simulate s=uamous cell carcinoma$ranulomatous inflammation with caseous necrosis

Pneumocystis jiroveci N

Cysts and tropho0oites present1 cysts attach to type I pneumocytes"rimarily an opportunistic infection1 occurs when CD- * count L266ost common initial +IDdefining infection"atients deelop feer, dyspnea, and seere hypo!emia1 diffuse intraaleolar foamy e!udateswith cupshaped cysts best isuali0ed with siler or $iemsa stains1 chest !ray shows diffusealeolar and interstitial infiltrates&!' *"/O gien prophylactically when CD- counts L266 cells/

N&ecent nomenclature change from P. carinii. +D", adenosine diphosphate1 C?, cytomegaloirus1 C8"D, chronic obstructie pulmonary disease1 I@, immunofluorescence1 "C&,

polymerase chain reaction1 &?, respiratory syncytial irus1 +&, seere acute respiratory syndrome1 *, tuberculosis1 *"/O,trimethoprimsulfametho!a0ole.

ung abscesspage 2>3

page 2>>page 2>>

page 766page 766

page 76;page 76;

page 762page 762

page 767

,$ 16-1 %S&R%T&$ S&T/S & T0/ LUS@oreign material locali0es to different portions of the lung, depending on theposition of the patient. In the standing or sitting position, material locali0es in theposterobasal segment of the right lower lobe1 in the supine position, the superiorsegment of the right lower lobe1 and in the rightsided position, the right middlelobe or the posterior segment of the right upper lobe. *he most commonaspiration site is the superior segment of the right lower lobe.

;. Causes of lung abscessesa. ost often due to aspiration of oropharyngeal material (e.g., tonsillar material)

i. +erobic and anaerobic streptococci and Staphylococci) Prevotella)*usoacterium

ii. 8ccurs in patients with depressed cough refle!es (e.g., after anesthesia)b. Complication of bacterial pneumonia (e.g., Staphylococcus aureus) &lesiella)



c. eptic embolism (e.g., infectie endocarditis)d. 8bstructie lung neoplasia

@rom ;6< to ;4< of abscesses are behind a bronchus obstructed by cancer.ii $ross findings

a. ?ary in si0e and locationb. *hose due to aspiration are primarily located on the right side


a. piking feer with productie cough (foulsmelling sputum)

b. Chest radiograph shows caitation with an airfluid leel.

+ascular Lung Lesions

"ulmonary thromboembolismpage 76-

In a patient with normal bronchial artery blood flow (originates from thoracic aortaand intercostal arteries) and entilation, a pulmonary embolus produces ahemorrhagic infarction in ∼;6< of cases. oweer, if the patient has decreasedbronchial artery blood flow (e.g., decreased cardiac output), or preiouslyunderentilated lung (e.g., obstructie lung disease), then occlusion of thepulmonary essel will likely result in a hemorrhagic infarction, which significantlyincreases risk of morbidity and death.

;. %pidemiology and pathogenesisa. ource

aAority (>4<) originate in the femoral einb. &isk factors for thromboembolism

tasis of blood flow (e.g., prolonged bed rest), hypercoagulable states

c. i0e of the embolus determines pulmonary essel that is occluded.

ii arge emboli occlude the maAor essels (saddle embolus)

iii mall emboli occlude mediumsi0ed and small pulmonary arteries.

b. "otential conse=uences of pulmonary artery occlusionii Increase in pulmonary artery pressure

iii Decrease blood flow to pulmonary parenchyma

ay cause hemorrhagic infarction.

2. &edblue, raised, wedgeshaped area that e!tends to the pleural surfacea. "leural surface has a fibrinous e!udate (produces a pleural friction rub).

emorrhagic pleural effusion may also occur.

b. aAority are located in the lower lobes. "erfusion is greater than entilation in the lower lobes.


a. addle embolus

ii udden increase in pulmonary artery pressure



iii "roduces acute right entricular strain and sudden death

b. "ulmonary infarctionii udden onset of dyspnea and tachypnea

iii @eer

iiii "leuritic chest pain (pain on inspiration), friction rub, effusion

2. aboratory findings with a pulmonary infarction

a. &espiratory alkalosis (arterial "C82 L77 mm g)b. "a82 less than 36 mm g (>6< of cases)c. Increase in +a gradient (;66< of cases)d. +bnormal perfusion radionuclide scan

ii ?entilation scan is normal, but the perfusion scan is abnormal.

iii "ulmonary angiogram is gold standard confirmatory test.

e. "ositie Ddimers

"ulmonary hypertension (")page 76-

page 764

;. %pidemiology and pathogenesisa. "rimary "

i. "rimary type is more common in women.ii. ?ascular hyperreactiity with proliferation of smooth muscle

b. econdary "i. %ndothelial cell dysfunction

oss of asodilators (e.g., nitric o!ide), increase in asoconstrictors (e.g.,

endothelin)ii. ypo!emia and/or respiratory acidosis stimulate asoconstriction of pulmonary

arteries. Causes smooth muscle hyperplasia and hypertrophy

iii. Causes Chronic hypo!emia (e.g., chronic lung disease)

Chronic respiratory acidosis (e.g., chronic bronchitis)

oss of pulmonary asculature (e.g., emphysemal)

Increases workload for remaining essels

efttoright cardiac shunts

itral stenosis

ackup of blood into the pulmonary eins

2. "athologic findingsa. +therosclerosis of main elastic pulmonary arteries

Due to increased pressure on the endothelium leading to inAury

b. "roliferation of myointimal cells and smooth muscle cellsii Clinical findings

a. "rogressie dyspnea and chest pain with e!ertionb. Chest radiograph shows tapering of the pulmonary arteriesc. +ccentuated "2 (sign of ")d. eft parasternal heae (sign of right entricular hypertrophy, &?)

" imposes an increased afterload on the right entricle.e. &ightsided heart failure due to cor pulmonale



ii Cor pulmonale

o Combination of " and right &? leading to rightsided heart failure

$oodpasture syndrome

• "ulmonary hemorrhage with hemoptysis often precedes renal failure.

Restricti#e Lung Diseases

• *hese disorders are characteri0ed by reduced total lung capacity in the presence of a normal or

reduced e!piratory flow rate.

Causes of restrictie disease

;. Chest wall disorders in the presence of normal lungso %!ampleskyphoscoliosis, pleural disease (e.g., mesothelioma), obesity

2. +cute or chronic interstitial lung diseases

a. +cute interstitial disease (e.g., +&D, see section ?)

b. Chronic interstitial disease

i. @ibrosing disorders (e.g., pneumoconiosis)

ii. $ranulomatous disease (e.g., sarcoidosis)

"athogenesis of interstitial fibrosis

;. %arliest manifestation is an aleolitis.o eukocytes release cytokines, which stimulate f ibrosis.

2. %ffects of interstitial fibrosis

a. Decreases lung compliance

i. Decreased e!pansion of the lung parenchyma during inspirationii. Damage to type I/II aleolar cells and endothelial cells

@unctional loss of aleolar and capillary units

b. Increases lung elasticity

&ecoil of the lung on e!piration is increased.2. Clinical and laboratory findings in all restrictie lung diseases

ii Dry cough and e!ertional dyspnea

ii ate inspiratory crackles in lower lung fields

ii "otential for cor pulmonale

ii "ulmonary function test findings and arterial blood gases

i. +ll olumes and capacities are e=ually decreased.



ii. Decreased @%?;sec %!ample7 (normal -)

iii. Decreased @?C 8ften the same alue as @%?;sec (7) due to increased lung elasticity

i. Increased ratio of @%?;sec/@?C %!ample7/7 9 ;66< (normal is 36<)

. &espiratory alkalosis (arterial "C82 L 77 mm g)i. Decreased "a82

b. Chest radiograph findings

Diffuse bilateral reticulonodular infiltrates

"neumoconioses;. %pidemiology

a. Inhalation of mineral dust into the lungs leading to interstitial fibrosisi. ineral dust includes coal dust, silica, asbestos, and beryllium.ii. +ccounts for ∼24< of cases of chronic interstitial lung disease

b. "article si0e determines site of lung depositioni. ; to 4m particles

&each the bifurcation of the respiratory bronchioles and aleolar ductsii. maller than 6.4m particles

&each the aleoli and are phagocytosed by aleolar macrophages

c. Coal dust is the least fibrogenic particle.d. ilica, asbestos, and beryllium are ery fibrogenic.

2. Coal workerHs pneumoconiosis (CG")a. ources of coal dust (anthracotic pigment)

Coal mines, large urban centers, tobacco smokeb. "ulmonary anthracosis

i. Bsually asymptomaticii. +nthracotic pigment in interstitial tissue and hilar nodes

+leolar macrophages with anthracotic pigment are called Edust cells.E

b. imple CG"i. @ibrotic opacities are smaller than ;cm in upper lobes and upper portions of

lower lobes.ii. Coal deposits adAacent to respiratory bronchioles produce centrilobular

emphysema (see section IO).c. Complicated CG" (progressie massie fibrosis)

i. @ibrotic opacities larger than ; to 2cm with or without necrotic centersii. Crippling lung disease (Eblack lungE disease)iii. No increased incidence of * or primary lung canceri. Cor pulmonale may occur.. Caplan syndrome may occur.

CG" plus large caitating rheumatoid nodules in the lungs

7. ilicosis

d. %pidemiologyi. ost common occupational disease in the worldii. Puart0 (crystalline silicone dio!ide) is most often implicated

ources' foundries (casting metal), sandblasting, working in mines

e. "athogenesisi. Puart0 is highly fibrogenic and deposits in the upper lungs.



ii. Puart0 actiates and is cytolytic to aleolar macrophages. acrophages release cytokines that stimulate fibrogenesis.

f. Chronic e!posurei. #odular opacities in the lungs

Concentric layers of collagen with or without central caitation

Puart0 polari0es in the nodules.

ii. E%ggshellE calcification in hilar nodes &im of dystrophic calcification in the nodes

g. Complicationsi. Cor pulmonale, Caplan syndromeii. Increased risk for deeloping lung cancer and *

-. +sbestosrelated disease

h. $eometric forms of asbestosi. erpentine

Curly and fle!ible fibers (e.g., chrysotile)

"roduces interstitial fibrosis and lung cancer

ii. +mphibole

traight and rigid (e.g., crocidolite) "roduces interstitial fibrosis, lung cancer, mesothelioma

iii. Deposition sites &espiratory bronchioles, aleolar ducts, aleoli

i. ourcesi. Insulation around pipes in old naal shipsii. &oofing material used oer 26 years agoiii. Demolition of old buildings

A. +ppearance in tissuei. @ibers are coated by iron and protein (called ferruginous bodies)

acrophages phagocytose and coat the fibers with ferritin.

ii. $olden, beaded appearance in sputum or in distal, small airwaysk. +sbestosrelated disease

i. enign pleural pla=ues Calcified pla=ues on the pleura and dome of the diaphragm

*hey are not a precursor lesion for a mesothelioma.

ii. Diffuse interstitial fibrosis with or without pleural effusionsiii. "rimary bronchogenic carcinoma

&isk further increases if the patient smokes cigarettes.

8ccurs∼26 years after first e!posure.

i. alignant mesothelioma of pleura No etiologic relationship with smoking

+rises from the serosal cells lining the pleura

%ncases and locally inades the subpleural lung tissue

8ccurs∼24 to -6 years after first e!posure

. No increased risk for *l. Complications

Cor pulmonale, Caplan syndromeii erylliosis

a. %!posure in the nuclear and aerospace industryb. Diffuse interstitial fibrosis with noncaseating granulomasc. Increased risk for cor pulmonale and primary lung cancer



arcoidosispage 7;;

• ultisystem granulomatous disease of unknown etiology

;. %pidemiologya. +ccounts for ∼24< of cases of chronic interstitial lung diseaseb. Common in black +mericans and nonsmokers

2. "athogenesisa. Disorder in immune regulationb. CD- * cells interact with an unknown antigen.

&eleases cytokines causing formation of noncaseating granulomas

c. Diagnosis of e!clusion ust rule out other granulomatous diseases

7. ung diseasea. "rimary target organ

ii $ranulomas located in the interstitium and mediastinal and hilar nodes

iii $ranulomas contain multinucleated giant cells

Contain laminated calcium concretions (chaumann bodies) and stellate

inclusions (called asteroid bodies)b. Dyspnea is the most common symptom.

2. kin lesionsa. #odular lesions containing granulomasb. ?iolaceous rash occurs on the nose and cheeks (called lupus pernio).c. %rythema nodosum

ii "ainful nodules on lower e!tremities

iii Inflammation of subcutaneous fat

7. %ye lesions1 produces ueitis'

o lurry ision, glaucoma, and corneal opacities2. ier lesions

o $ranulomatous hepatitis3. 8ther multisystem findings

a. %nlarged saliary and lacrimal glandsb. Diabetes insipidus (hypothalamic and/or posterior pituitary disease)c. $ranulomas in the bone marrow and spleen

2. aboratory findings

a. Increased angiotensinconerting en0yme (+C%)ii $ood marker of disease actiity and response to corticosteroid therapy

b. ypercalcemia (4< of cases)ii Increased synthesis of ;Qhydro!ylase in granulomas (hyperitaminosis D)

c. 8ther findingsii "olyclonal gammopathy

iii Cutaneous anergy to common skin antigens (e.g., Candida)

Due to consumption of CD- * cells in granulomas and loss of cells in

aleolar secretions



2. Chest radiograph

a. %nlarged hilar and mediastinal lymph nodes (called Epotato nodesE)b. &eticulonodular densities throughout the lung parenchyma

2. "rognosis

a. "rogressie disease or intermittent disease with periods of actiity and remissions

b. etween ;6< and ;4< deelop seere interstitial fibrosis, leading to cor pulmonale and death.

Idiopathic pulmonary fibrosis

;. %pidemiologya. +ccounts for ∼;4< of cases of chronic interstitial lung diseaseb. ore common in males than in femalesc. Bsually occurs in indiiduals oer -6 to :6 years old

2. "athogenesisa. &epeated cycles of aleolitis triggered by an unknown agent

b. &elease of cytokines produces interstitial fibrosis7. +leolar fibrosis leads to pro!imal dilation of the small airways.

o ung has a honeycomb appearance.

Collagen ascular diseases +ny une!plained pleural effusion in a young woman is % until proed otherwise."leural fluid contains an inflammatory infiltrate (e!udate), and % cells (neutrophilswith phagocytosed D#+) are sometimes present. 8ne of the key criteria fordiagnosing % is the presence of serositis, pleuritis with a pleural effusion being ane!ample of this type of inflammation.

;. +ccount for ∼;6< of cases of chronic interstitial lung disease2. ystemic sclerosis

o ost common cause of death is lung disease.

7. ystemic lupus erythematosus (%)

a. Interstitial lung disease occurs in 46< of patients.

b. "leuritis with pleural effusions

2. &heumatoid arthritis (&+)a. &heumatoid nodules in lungs plus a pneumoconiosis is called Caplan syndrome.

b. "ulmonary findings in &+

i. Interstitial fibrosis with or without intrapulmonary rheumatoid nodules

ii. "leuritis with pleural effusions

ypersensitiity pneumonitispage 7;;

page 7;2



;. %!trinsic allergic aleolitis associated with e!posure to a #no%n inhaled antigeno Does not inole Ig% antibodies (type I hypersensitiity) or hae eosinophilia

2. @armerHs lung

a. %!posure to Saccharopolyspora rectivirgula (thermophilic actinomycetes bacteria) in

moldy hayb. @irst e!posure

"atient deelops precipitating Ig$ antibodies (present in serum)

c. econd e!posure

ii +ntibodies combine with inhaled allergens to form immune comple!es.

*ype III hypersensitiity reaction

iii Immunocomple!es produce an inflammatory reaction in lung tissue.

b. Chronic e!posure

+dditional component of granulomatous inflammation (type I? hypersensitiity)

2. ilo fillerHs diseaseii Inhalation of wheat weeil protein

ii Causes an immediate hypersensitiity reaction associated with dyspnea7. yssinosis

ii %pidemiology

ii 8ccurs in workers in te!tile factories

iii Contact with cotton, linen, hemp products

b. Clinical findings

ii Deelop dyspnea on e!posure to cotton, linen, or hemp products

iii Gorkers feel better oer the weekend (no e!posure to antigens)

Depression occurs when returning to work on onday (Eonday morning

bluesE)

Drugs associated with interstitial fibrosis

;. +miodarone2. leomycin and busulfan7. Cyclophosphamide-. ethotre!ate and methysergide

4. #itrosourea and nitrofurantoin

&adiationinduced lung disease

;. +cute pneumonitis may occur ; to 5 months after therapy.2. Clinical findings

o @eer, dyspnea, pleural effusions, and radiologic infiltrates

7. ome patients deelop chronic radiation pneumonitis.



$bstructi#e Lung Disease

• 8bstruction to airflow out of the lungs

page 7;-

page 7;4

;. "ermanent enlargement of all or part of the respiratory unito &espiratory bronchioles, aleolar ducts, aleoli

2. %pidemiology

a. Causes

i. Cigarette smoking is the most common cause.ii. Q;+ntitrypsin (++*) deficiency

b. *ypes of emphysema associated with smoking or loss of ++*

i. Centriacinar (centrilobular) emphysemaii. "anacinar emphysema

2. "athogenesisa. Increased compliance and decreased elasticity

i. Imbalance between elastase and antielastases (e.g., Q;antitrypsin, ++*)ii. Imbalance between o!idants (free radicals) and antio!idants (e.g., glutathione)iii. %lastase and o!idants derie from neutrophils and macrophages.i. #et effect of the preceding is destruction of elastic tissue.

b. Cigarette smoke is chemotactic to neutrophils and macrophages.

*hey accumulate in the respiratory unit and release free radicals and elastases.ii @ree radicals in cigarette smoke inactiate ++* and antio!idants.

"roduces a functional ++* deficiencyii #ormal function of elastic tissue

i. @ibers attach to the outside wall of the small airwaysii. @ibers apply radial traction to keep the airway lumens open.

b. Destruction of elastic tissue causes loss of radial traction.

mall airways collapse, particularly on e!piration.ii ites of elastic tissue destruction in emphysema

i. Distal terminal bronchiole at its Aunction with the respiratory bronchiole (&)ii. +ll or part of the respiratory unit

c. ite of obstruction and air trapping in emphysema

i. During e!piration, the distal terminal bronchioles collapse preenting egress of air out of the respiratory unit.

ii. *rapped air distends parts of the respiratory unit that hae lost their elastic tissuesupport.

2. Centriacinar (centrilobular) emphysema (seea. %pidemiology

ost common type of emphysema in smokersii "athogenesis



i. "rimarily inoles the apical segments of the upper lobesii. Distal terminal bronchioles and the &s are the sites of elastic tissue destruction.iii. +ir trapped behind the collapsed distal terminal bronchioles distends the &s.

*he trapped air increases &? and *C.

7. "anacinar emphysemaa. %pidemiology

i. +ssociated with ++* deficiency $enetic or ac=uired causes (cigarette smoke inactiates ++*)

ii. $enetic type of ++* deficiency +utosomal recessie disorder

phenotype is normal.

#ormal amounts of ++* are synthesi0ed in the lier.

RR phenotype has decreased synthesis of ++* by the lier.

iii. %mphysema deelops at an early age in the genetic type.b. "athogenesis

i. "rimarily affects the lower lobesii. Distal terminal bronchioles and all parts of the respiratory units are the sites of

elastic tissue destruction.iii. +ir trapped behind the collapsed terminal bronchioles distends the entire

respiratory unit.c. aboratory finding

+bsent Q;globulin peak in a serum protein electrophoresis2. Clinical findings in centriacinar and panacinar emphysema

ii "rogressie dyspnea and hyperentilation

i. Dyspnea is seere and occurs early in the disease.ii. ometimes patients are called Epink puffers.E

d. Centriacinar type fre=uently coe!ists with chronic bronchitis.

e. reath sounds are diminished due to hyperinflation.

f. Cor pulmonale is uncommon.

-. Chest radiographa. yperlucent lung fields

b. Increased anteroposterior diameter

c. ?ertically oriented heart

d. Depressed diaphragms due to hyperinflated lungs

4. "ulmonary function tests and arterial blood gasesa. Increased *C due to an increase in &?

b. Decreased @%?;sec (e.g., ; ersus -1 see

c. Decreased @?C (e.g., 7 ersus 41 see

Decreased @%?;sec/@?C ratio (e.g., ;/7 9 77<)ii Decreased "a82 deelops late in the disease.

Destruction of the capillary bed matches destruction of the respiratory unitii #ormal to decreased arterial "C82 (respiratory alkalosis)

7. 8ther types of emphysema unrelated to smoking or ++* deficiencyii "araseptal emphysema

i. ocali0ed disease in a subpleural location "rimarily targets the aleolar ducts and aleoli

ii. Does not produce obstructie airway diseaseiii. Increased incidence of spontaneous pneumothora!



Due to rupture of subpleural blebs

d. Irregular emphysema

i. ocali0ed disease is associated with scar tissue.

ii. Does not produce obstructie airway disease

Chronic bronchitispage 7;4

page 7;5

*urbulent airflow in the bronchi is conerted to laminar airflow in the terminal(nonrespiratory) bronchioles. *he terminal bronchioles undergo parallel branching,which reduces airflow resistance and spreads air out oer a large crosssectionalarea. mall airway disease associated with e!piratory whee0ing is due to narrowingof the terminal bronchioles by mucus plugs, inflammation, and fibrosis. ucus plugslocated in a pro!imal terminal bronchiole preent the e!odus of a large amount ofC82 arising from the distally located airways producing respiratory acidosis.

page 7;5

page 7;:

;. %pidemiologya. "roductie cough for at least 7 months for 2 consecutie yearsb. Causes

i. moking cigarettesii. Cystic fibrosis

2. "athogenesisa. ypersecretion of mucus in bronchib. 8bstruction to airflow in the terminal bronchioles

+irflow obstruction is pro!imal to the obstruction in emphysema.b. Irreersible fibrosis of terminal bronchiolesc. Changes in the bronchi

i. ypersecretion of submucosal mucussecreting glands in trachea and bronchi "rimarily responsible for sputum oerproduction

ii. +cute inflammation (neutrophils) often superimposed on chronic inflammationiii. oss of ciliated epithelium and presence of s=uamous metaplasia

b. Changes in the terminal bronchiolesi. ucus plugs in lumens (block the e!odus of C82)ii. $oblet cell metaplasiaiii. ypertrophy of mucoussecreting glandsi. Chronic inflammation and fibrosis narrowing the lumen

7. Clinical findings

c. "roductie coughd. Dyspnea occurs late in the disease.e. Cyanosis of skin and mucous membranes

i. Decreased 82 saturation from hypo!emiaii. "atients are called Eblue bloaters.E

f. *end to be stocky or obese



g. %!piratory whee0ing and sibilant rhonchih. Cor pulmonale is commonly present.

-. Chest radiograph

i. arge, hori0ontally oriented heart A. Increased bronchial markings

4. "ulmonary function tests and arterial blood gases

k. ess increase in *C and &? than emphysemal. Chronic respiratory acidosis

i. +rterial "C82 greater than -4 mm gii. icarbonate greater than 76 m%=/

m. oderate to seere hypo!emia early in the disease

5. ummary of findings in chronic bronchitis and emphysema

Table 16-2. Comparison of /mp*ysema and C*ronic ,ronc*itis

arameter /mp*ysema C*ronic ,ronc*itis

"a82 Decreased Decreased

"aC82 #ormal to decreased Increased

p #ormal to increased Decreased

Cyanosis +bsent "resent

abitus *hin tocky

Cor pulmonale &are Common

8nset of hypo!emia ate %arly

8nset of dyspnea %arly ate

+sthmapage 7;:

page 7;3

80one (87) is an air pollutant that deries from interactions of 82 with o!ides ofnitrogen and sulfur, and hydrocarbons. It forms highly reactie free radicals in theairways that cause inflammation and irritation, often precipitating asthma.

;. %pidemiologya. %pisodic and reersible airway diseaseb. "rimarily targets the bronchi and terminal bronchiolesc. ost common chronic respiratory disease in childrend. %!trinsic and intrinsic types

2. %!trinsic asthmaa. "athogenesis

i. *ype I hypersensitiity reaction with e!posure to e!trinsic allergens *ypically deelops in children with an atopic family history to allergies

ii. Initial sensiti0ation to an inhaled allergen



timulate induction of subset 2 helper * cells (CD- *2) that release

interleukin (I) - and I4 I- stimulates isotype switching to Ig% production.

I4 stimulates production and actiation of eosinophils.

iii. Inhaled antigens crosslink Ig% antibodies on mast cells on mucosal surfaces. &elease of histamine and other preformed mediators

@unctions of mediators timulate bronchoconstriction, mucus production, influ! of

leukocytesi. ate phase reaction (-3 hours later)

%ota!in is produced.

Chemotactic for eosinophils and actiates eosinophils

%osinophils release maAor basic protein and cationic protein.

Damage epithelial cells and produce airway constriction

b. 8ther mediators inoledi. *CD%- cause prolonged bronchoconstriction.ii. +cetylcholine causes airway muscle contraction.

c. istologic changes in bronchii. *hickening of the basement membraneii. %dema and a mi!ed inflammatory infiltrateiii. ypertrophy of submucosal glandsi. ypertrophy/hyperplasia of smooth muscle cells

d. istologic changes in the terminal bronchiolesi. @ormation of spiralshaped mucus plugs

Contain shed epithelial cells called Curschmann spirals

"athologic effect of maAor basic protein and cationic protein

ii. Crystalline granules in eosinophils coalesce to form Charcoteyden crystals.iii. "atchy loss of epithelial cells, goblet cell metaplasiai. *hick basement membrane. mooth muscle cell hypertrophy and hyperplasia

e. Clinical findingsi. %pisodic e!piratory whee0ing (inspiratory as well when seere)ii. #octurnal coughiii. Increased anteroposterior diameter

Due to air trapping and increase in residual olume

f. aboratory findingsi. Initially deelop respiratory alkalosis

"atients work hard at e!pelling air through inflamed airways.

ay progress into respiratory acidosis if bronchospasm is not relieed

&espiratory acidosis is an indication for intubation and

mechanical entilation.ii. %osinophilia, positie skin tests for allergens

g. *reatment of mild disease

etereddose inhaler with a K2agonist (e.g., albuterol)b. *reatment of more adanced disease

i. etered lowdose inhaler with corticosteroidsii. Bse of leukotriene inhibitors

7. Intrinsic asthma

b. #onimmune



c. Causesi. ?irusinduced respiratory infection

%!amplesrhinoirus, parainfluen0a irus, respiratory syncytial irus

ii. +ir pollutantsiii. +spirin or nonsteroidal drug sensitiity (see section III)

i. tress, e!ercise, cigarette smoke

ronchiectasispage 7;>

page 726

;. %pidemiology and pathogenesisa. "ermanent dilation of the bronchi and bronchioles

Due to destruction of cartilage and elastic tissue by chronic necroti0ing infections

b. Causes

ii Cystic fibrosis

ost common cause in the Bnited tates

iii Infections

* is the most common cause worldwide.

+denoirus, Staphylococcus aureus) Hemophilus influenzae

iiii ronchial obstruction

%!amplepro!imally located bronchogenic carcinoma occludes the

lumen.ivi "rimary ciliary dyskinesia

+bsent dynein arm in cilia

Dynein arm contains +*"ase (adenosine triphosphatase) for moement

of the cilia.vi +llergic bronchopulmonary aspergillosis

2. $ross findingsa. ost commonly occurs in the lower lobesb. Dilated bronchi and bronchioles are filled with pus

ii Dilated airways e!tend to the lung periphery.

iii Dilations are tubelike and/or saccular.

7. Clinical findingsa. Cough productie of copious sputum (often cupfuls)b. emoptysis that is sometimes massiec. Digital clubbing, cor pulmonale

-. Chest radiograph findings

o Crowded bronchial markings e!tend to the lung periphery.2. Cystic fibrosis (C@)

a. %pidemiologyii +utosomal recessie disease

iii "rimarily affects whites

Bncommon in +sians and black +mericans

b. "athogenesisii *hree nucleotide deletion on chromosome :



#ucleotides normally code for phenylalanine.

iii "roduction of a defectie C@ transmembrane conductance regulator (C@*&) for

chloride ionsiiii C@*& Cl is degraded in the $olgi apparatus.

Due to defectie protein folding

ivi oss of C@*& Cl causes decreased #aS and Cl reabsorption in sweat glands.

asis of the sweat test

vi %ffect of loss of C@*& Cl in other secretions

Increased #aS and water reabsorption from luminal secretions

Decreased Cl secretion out of epithelial cells into luminal secretions

#et effect is dehydration of body secretions due to lack of #aCl

ecretions are dehydrated in bronchioles, pancreatic ducts, bile

ducts, meconium, and seminal fluid.c. Clinical findings

ii #asal polyps (24< of cases)

iii &espiratory infections/failure

Pseudomonas aeruginosa is the most common respiratory pathogen.

8ther common pathogensS. aureus) H. influenzae

Cor pulmonale commonly occurs.iiii alabsorption

"ancreatic e!ocrine deficiency

+trophy of glands from dehydrated secretions blocking the lumens

ivi *ype ; diabetes mellitus

Due to chronic pancreatitis

vi Infertility in males

+tresia of as deferens

vii econium ileus

mall bowel obstruction in newborn

viii econdary biliary cirrhosis

Due to obstruction of bile ductules by thick secretions

Lung Tumors

• "rimary lung cancer is the most common cancer killer in both men and women.

%pidemiology;. Incidence of lung cancer is declining in men but increasing in women.2. "eak incidence is at 44 to 54 years of age.7. Causes

a. Cigarette smoking

b. &adon gas (uranium mining)c. +sbestos, chromium, nickel, beryllium, arsenic, inyl chloride

-. "rimary lung cancer in decreasing incidencea. +denocarcinomab. =uamous cell carcinomac. mall cell lung carcinomad. arge cell carcinomae. ronchial carcinoid

4. =uamous and small cell lung carcinomasa. $reatest smoking association



b. *end to be centrally located (i.e., main stem bronchus)5. +denocarcinomas

a. Geakest smoking associationb. *end to be more peripherally located

*umor and tumorlike disorders

Table 16-3. Tumors and Tumor-li4e Disorders of t*e Lung

Type of Tumor orDisorder

Location inLung Comments

+denocarcinoma "eripheral ore common in women +ssociated with cigarette smoking*umors may deelop in scars or spread along aleolar walls and mimiclobar pneumonia (bronchioloaleolar)

=uamous cell carcinoma Central ore common in mentrong association with cigarette smoking

*end to caitateay ectopically secrete "*related protein

mall cell carcinomaN Central ore common in mentrong association with cigarette smoking

+rise from neuroendocrine cells (Fulchitsky cells)&apidly growing cancer that metastasi0es earlyay ectopically secrete +D or +C*

arge cell carcinoma "eripheral Bndifferentiated cancer that metastasi0es early

ronchial carcinoid Central No association with cigarette smokingowgrade cancer of neuroendocrine originCarcinoid syndrome is rare (does not re=uire lier metastasis)

Carcinoma metastatic tothe lung

ultifocal ore common than primary cancer Bsually presents with dyspnea

ronchial hamartoma Central #onneoplastic proliferation of cartilage and adipose tissue +ppears as solitary EcoinE lesion on chest radiograph

Nee +C*, adrenocorticotropic hormone1 +D, antidiuretic hormone1 "*, parathyroid hormone.

+ solitary pulmonary nodule or coin lesion is the term applied to a peripheral lungnodule smaller than 4cm. Causes of a solitary pulmonary nodule in descendingorder include granulomas (e.g., *, histoplasmosis), malignancy (usually primarycancer), and a bronchial (chondroid) hamartoma. "atients younger than 74 yearsold hae a ;< risk of a solitary coin lesion representing a malignancy, but patients46 years old and up hae a 46< to 56< risk of malignancy, usually a primarycancer. In ealuating solitary coin lesions, comparing preious chest !rays forchanges in si0e of the nodule is the most important initial step.

etastatic cancer ;. %pidemiology

a. ost common lung cancerb. Cancers most often responsible for metastasis

i. "rimary breast cancer most common causeii. Colon cancer, renal cell carcinoma

2. ites of lung metastasisa. "arenchyma



b. "leura and pleural space (malignant effusions)c. ymphatics (causes seere dyspnea)

7. Dyspnea is the most common symptom.

Clinical findings in primary lung cancerpage 72;

page 722page 722

page 727page 727

page 72-

;. Cough is the most common symptom (:4< of cases).;. Dyspnea, hemoptysis, weight loss, chest pain2. "ancoast tumor (superior sulcus tumor)

a. Bsually a primary s=uamous cancer located at the e!treme ape! of lungb. Destruction of superior cerical sympathetic ganglion produces ornerHs

syndromei. Ipsilateral lid lagii. iosis (pinpoint pupil)iii. Ipsilateral anhydrosis (lack of sweating)

7. uperior ena caa syndrome-. "araneoplastic syndromes

a. Digital clubbing

Due to reactie periosteal changes in the underlying boneii uscle weakness (%atonambert syndrome)

ii%ctopic hormone secretion (see aboe)

Common sites for metastasis

;. ilar lymph nodes most common site2. +drenal gland (46< of cases)

7. ier (76< of cases), brain (26< of cases), bone (usually osteolytic)

"rognosis

;. #onsmall cell cancers fare better than small cell carcinoma.

2. 8erall combined 4year surial rate is ∼;4<.

)ediastinum Disorders

ediastinal massespage 72-



page 724

;. %pidemiologya. Bsually metastatic primary lung cancer in older patientsb. Bsually primary disease in younger patientsc. +nterior compartment is the most common site.d. ost common primary mediastinal masses, in descending order'

i. #eurogenic tumors Bsually malignant in children and benign in adults

ii. *hymomas (see below)iii. "rimary cysts

Bsually a pericardial cyst

i. alignant lymphomas Bsually nodular sclerosing odgkinHs lymphoma in a woman

. *eratoma2. *hymoma

a. %pidemiologyi. ocated in the anterior mediastinumii. enign (:6<), malignant (76<)

b. %pithelium, not lymphoid tissue, is the neoplastic component.

c. aAority e!press systemic symptoms of myasthenia graisi. ess than ;6< to ;4< of myasthenia patients hae a thymoma.ii. aAority (54:4<) hae follicular cell hyperplasia in the thymus.

ite for synthesis of antiacetylcholine receptor antibodies

d. 8ther thymoma associationsi. ypogammaglobulinemia, pure &C aplasia

ii. Increased incidence of autoimmune disease (e.g. $raesH disease

ediastinal massespage 72-

page 724

;. %pidemiologya. Bsually metastatic primary lung cancer in older patientsb. Bsually primary disease in younger patientsc. +nterior compartment is the most common site.d. ost common primary mediastinal masses, in descending order'

i. #eurogenic tumors Bsually malignant in children and benign in adults

ii. *hymomas (see below)iii. "rimary cysts

Bsually a pericardial cyst

i. alignant lymphomas

Bsually nodular sclerosing odgkinHs lymphoma in a woman. *eratoma

2. *hymomaa. %pidemiology

i. ocated in the anterior mediastinumii. enign (:6<), malignant (76<)

b. %pithelium, not lymphoid tissue, is the neoplastic component.c. aAority e!press systemic symptoms of myasthenia grais (

i. ess than ;6< to ;4< of myasthenia patients hae a thymoma.



ii. aAority (54:4<) hae follicular cell hyperplasia in the thymus. ite for synthesis of antiacetylcholine receptor antibodies

d. 8ther thymoma associationsi. ypogammaglobulinemia, pure &C aplasia

ii. Increased incidence of autoimmune disease (e.g. $raesH disease)

leural Disorders

oement of pleural fluid

• #ormally moes from parietal pleura into the pleural space and into the lungs

oementof pleuralfluid

• #ormally moes from parietal pleura into the pleural space and into the lungs

Causesofpleuraleffusion

;. Increased hydrostatic pressure in the isceral pleura (e.g., congestie heart failure)2. Decreased oncotic pressure (e.g., nephrotic syndrome)7. 8bstruction of lymphatic drainage from the isceral pleura (e.g., lung cancer)

-. Increased essel permeability of isceral pleural capillaries (e.g., infarction)

4. etastasis to the pleura (e.g., metastatic breast cancer)

*ypes of pleural effusions

;. *ransudatesa. Bltrafiltrate of plasma inoling disturbances in tarling pressuresb. %!ampleincreased hydrostatic pressure or decreased oncotic pressure

2. %!udatesa. "roteinrich and cellrich fluid

Due to an increase in essel permeability in acute inflammationb. %!amplespneumonia, infarction, metastasis

7. aboratory findings distinguishing e!udates from transudatesa. "leural fluid protein/serum protein ratio aboe 6.4

ii Indicates an e!udate

iii *ransudates hae alues below 6.4.

b. "leural fluid lactate dehydrogenases/serum lactate dehydrogenase ratio aboe 6.5



ii Indicates an e!udate

iii *ransudates hae alues below 6.5.

pontaneous pneumothora!

;. Causesa. Idiopathic (most common)b. "araseptal emphysema, arfan syndrome

2. "athogenesisa. &upture of a subpleural or intrapleural bleb produces a hole in the pleura.b. "leural caity pressure is the same as the atmospheric pressure.

i. oss of the negatie intrathoracic pressureii. Causes a portion of lung or the entire lung to collapse

7. Clinical findings

a. udden onset of dyspnea with pleuritic type of chest pain

b. "hysical e!aminationi. *ympanitic percussion noteii. +bsent breath sounds

iii. *rachea deiated to the side of the collapse

*ension pneumothora!

;. Causesa. "enetrating trauma to the lungs (e.g., knife wound)b. &upture of tension pneumatocysts (see section ?I)

2. "athogenesisa. @laplike pleural tear allows air into the pleural caity but preents its e!it.

imilar in concept to filling a tire up with air

b. Increased pleural caity pressurec. "roduces compression atelectasis (see section I?)

7. Clinical findingsa. udden onset of seere dyspneab. "hysical e!amination

ii *ympanitic percussion note and absent breath sounds

iii *rachea and mediastinal structures deiate to contralateral side.

Compromised enous return to the heart, if the pneumothora! is located

on the left side

b. *reatment

Insert a needle into the pleural caity to reliee the pressure

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16 Upper and Lower Respiratory Disorders

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