[os 213] lec 13 lung defense mechanisms and approach to respiratory tract infections (b)

OS 213: Human Disease Treatment 3 (Circulation and Respiration)LEC 13: LUNG DEFENSE MECHANISMS AND APPROACH TO RESPIRATORY

TRACT INFECTIONSExam 2 | Dr. Joselito R. Chavez | August 16, 2012

OUTLINE I. Lung Defenses

A. ObjectivesB. Access to Lower Respiratory TractC. Mechanical Factors in Lung DefenseD. Defense in Distal AirwaysE. Inflammatory Response

II. Infections of the Upper Respiratory Tract

A. ObjectivesB. General CharacteristicsC. Upper Respiratory Tract Infections

II. Parapneumonic Effusion A. PneumoniaB. Lung AbscessC. Bronchiectasis

LUNG DEFENSESObjectives

To know the important lung defenses that protect the host against infection

To know the events related to the host lung inflammatory response when the defense barriers are overwhelmed

The lung serves as a filter – it is continuously exposed to various entities in the environment so it has to continuously protect itself

Access to Lower Respiratory TractAspiration Most common way of contracting a lower respiratory tract

infection (LRTI) Most common time access is during sleep when a small amount of

upper respiratory tract secretions (mucus and normal flora) is aspirated this is normal and you don’t get infected because of intact lung defenses, the volume of the aspirate is low and whatever the secretions you aspirate don’t have pathogenic bacteria

Other risk factors for aspiration: depressed sensorium, prolonged antibiotic therapy (normal flora is killed and replaced)

Manifestationo If the volume aspirated is small and the patient is not a carrier

of the pathogen, then he or she is unlikely to be colonized or be infected by the bacteria

o If the volume aspirated is large and the patient is a carrier, then there is a increased risk for contracting an infection via aspiration

Other factors to considero Patient lost consciousnesso Esophageal dysmotilityo Predisposing condition (i.e. tumor)

Inhalation Bacteria can be either inhaled due to its presence in the

community (i.e. at home, in the surroundings) or at the hospital (i.e. nosocomial infection)

You can inhale microorganisms in the hospital via o Unsanitized nebulizerso Patients in surgery that are exposed to unsanitized equipmento Respirators/ventilators (be wary of microbes in the tubes)o Ambulatory bago Anesthesia machine

Hematogenous Spread Pathogen spreads via blood Occurs when a wound becomes infected and the pathogen enters

the systemic circulation, reaching the pulmonary circulationo Diabetic foot infection goes to bloodstream and blood goes to the lungs

several times a minute and so organisms travelling via the bloodstream may infect the lungs

o Post-operative patient (GI surgery) bacteria gain access in the blood stream

o Ongoing condition that manifests close to the lungs Bilateral lobe infection (both lungs are infected) Usually, multiple areas of infection especially in the lower parts of

the lungs because it’s the most perfused

o Staphylococcus aureus

Contiguous Extension Non-pulmonary infection (usually in nearby organs) that extends

to the lungs Common conditions with contiguous extension to the lungso Liver abscess – the abscess will rupture and gain access to the

thoracic cavity, reaches the pleural space and pleura and eventually the lungs which causes infection

o Mediastinitis – infections from cardiovascular and endoscopic surgical procedures may spread to nearby areas such as the lungs and pleura

o Stab wound

Mechanical Factors in Lung Defense Turbinates and Nares Found in the nasopharynx and oropharynx Covered in respiratory epithelium (pseudostratified tall ciliated

columnar epithelium) and mucosa which will trap bacteria Coarse-to-fine hairs as tract goes down Angulations serve as deterrents to microorganisms Sinuses humidify the airway and thus preventing it from drying up

Tracheobronchial Tree Defense Mechanisms Dichotomous branching of the lungs (16+ divisions)o Creates more area for gas exchangeo Angulations are present to catch microorganisms and foreign

materials Mucociliary clearance helps in clearing the epithelium Local antibacterial factors (i.e. normal flora in the lungs) assist in

the elimination of foreign bodieso Prevent pathogens from binding to alveoli and mucosal cells

Gag Reflex and Cough Mechanisms Expulsive maneuvers that forcibly push out foreign material that

has irritated the respiratory tract receptors Includes sneezing reflex, bronchial spasm Impaired by intubation, stroke, surgical complications, presence

of malignancies, and some other anatomical and mechanical factors that affect these reflexes

Defense in the Distal Airways Normal flora protects the airways by preventing pathogenic

bacteria from binding to mucosal cells Alveolar macrophages protect the alveoli Local proteinso Surfactant proteins A and D for opsonisationo Proteins are anti-bacterial and anti-viralo Engulfment of foreign materialso Recruitment of other cells

When the capacity of the alveolar macrophages to kill organisms is exceeded, then the macrophages initiate inflammatory response triggers syndrome of pneumonia

Inflammatory ResponseEvents in the Inflammatory Response Release of inflammatory mediators by macrophageso Interleukin (IL) 1, Tumor Necrosis Factor (TNF) leads to fever fever due to inflammatory reactions from the mediators not

from bacteria/viruses Chemokines – IL 8 and granulocyte colony-stimulating factorso Stimulate the release and attraction of neutrophils

(marginalized in nearby capillaries) to the lung thereby producing leukocytosis and purulent secretions

Released mediators, together with recruited neutrophils, create capillary leak in the alveoli

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Events that follow capillary leak: manifestation of pneumonia hemoptysis, cough (rusty sputum – characteristic of pneumococcal infection), radiographic infiltrates (increased densities), rales/crackles (local or diffused) upon PEo Correlate with pathology!

Pathophysiologic Events after Inflammatory Response Bacterial pathogens interfere + hypoxic vasoconstriction = hypoxia Increased respiratory drive (increased respiratory rate) decreases

CO2, which increases pH alkalosis Dyspnea is caused by the followingo Capillary leako Hypoxemia – most potent inductor of vasoconstrictiono Increased respiratory rate – compensatory response to

shunting or V/Q mismatch (i.e. breathing faster and deeper)o Increased secretiono Bronchospasm

Death may result from shunting, decreased compliance and changes in lung mechanism

Progression from respiratory alkalosis to acidosis due to slow breathing during the latter stage of the disease, increasing the levels of CO2

Inflammatory response is the direct cause of respiratory failure

INFECTIONS OF THE UPPER RESPIRATORY TRACTObjectives

To know the common upper respiratory tract infections (URTI) To characterize URTI as to clinical manifestations, etiology and

treatment

General Characteristics Typically mild, but has tremendous impact on public healtho High incidenceo High transmission rateso Causes loss of time from work and school

Viral or bacterial infection difficult to distinguisho Signs and symptoms are indistinguishable especially in early

stageso Rapid testing is generally unavailable, expensive and impractical

as most viral infections are non-fatal and self-limiting (complicated by bacterial infections)

Identifying URTIso No localizing featureso A group of disorders with a variety of descriptive names

Acute infective rhinitis Acute rhinopharyngitis Nasopharyngitis Acute coryza, acute nasal catarrh Common colds

Common viruses causing URTIo Rhinovirus, Influenza (e.g. A H1N1), Parainfluenza, Coronavirus,

Adenovirus Symptoms o Mild, acuteo Self limiting catarrhal syndromeo Median duration of ~1 week (5-7 days) if there is no bacterial

complication (0.5-2% of colds complicated by bacteria) Principal signs and symptoms o Rhinorrhea (whitish mucoid secretion) with or without

purulenceo Nasal congestiono Cough, sore throato Fever, malaise, sneezing, hoarseness – variableo Myalgia, fatigueo Between 0.5-2% of colds are complicated by bacterial infection

Individuals at risko Infants, elderly, chronically ill, immunocompromised (e.g. on

steroids, with malignancies, underwent transplant, AIDS)

Special attention to elderly because they have atypical presentations: loss of appetite, sleeping more frequently, falls due to electrolyte imbalance

o Such groups are at risk because acute manifestations can easily progress to pneumonia complications

Complicationso Rhinosinusitiso Otitis mediao Pneumonia (most important in clinical setting)

Treatment is symptom-basedo Decongestantso Non-steroidal Anti-inflammatory Drugs (NSAID)o Cough suppressant (Dextromethorphan)o Lozenges, topical anestheticso Fluids

Upper Respiratory Tract InfectionsAcute Sinusitis Acute obstruction of sinus ostia Trapped secretions serve as a medium for growth leading to

impairment in ciliary clearance less than 4 weeks in duration – primarily as a consequence of

preceding viral URTI Viral etiology (most common): Rhinovirus, Parainfluenza,

Influenzao Symptoms of less than 7 days (mild to moderate symptoms)o Treatment

Facilitate sinus drainage Oral or topical decongestants – side effect (drying up) Nasal saline lavage

Bacterial etiology (S. pneumoniae and H. influenzae) emphasized by Dr. Chavez (clinical implication on the choice of antibiotics)o Severe symptoms >7 days (40-50% have bacterial etiology)o Treatment

Narrow spectrum agent against S. pneumoniae and H. Influenzae (covered by Amoxicillin)

Sinus aspiration, surgical intervention IV antibiotics in complicated cases

Clinical features o Nasal congestiono Facial pain or pressure headacheo Nasal dischargeo Cough, sneezing, fevero Toothache, halitosis are associated with bacterial infection

Complications (Emphasized by Dr. Chavez)o Meningitiso Epidural and cerebral abscesses

Fungal etiologyo Order mucorales

Rhizopus Rhizomucor mucor

o Immunocompromised patients Transplants Steroids Diabetes with ketoacidosis Hematologic malignancies

Non-infectious causeso Allergic rhinitiso Barotraumao Chemical irritationo Tumorso Granulomatous diseases

Pharyngitis Has the same symptoms and etiology with sinusitis, except

localized in the pharynx and has exudates o Adenovirus and streptoccocal pharyngitis – pharyngeal exudate

Constellation of coryzal symptoms (colds) Rhinovirus and coronavirus – mild


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Fever, myalgia, headache, cough Group A β-hemolytic streptococcus o Acute rheumatic fevero Acute glomerulonephritiso Peritonsillar abscesso Risk for above can be reduced by penicillin therapy

Symptoms of pharyngitis by Streptococcus Groups A, C, and Go Mild to severe spectrumo Pharyngeal pain, fever, chills, abdominal paino Hyperemic pharynx, tonsillar hypertrophy, exudate

Treatmento Streptococcal progenies

Penicillin given within 48 hours of onset of illness If allergic, erythromycin can be used instead

o Viral Pharyngitis (given within 36-48 hours of symptom onset) Amantadine Rimantadine Oseltamivir/ Tamiflu (Influenza A and B) Zanamivir (Influenza A and B)

Diagnosticso Standard has not been established (hard to differentiate viral

from bacterial)o Throat swab and culture

Does not differentiate colonization from infection (i.e. patient may harbor the bacteria but does not present with symptoms)

Rapid antigen detection has >90% specificity and 65-90% sensitivity very expensive and is usually done in research

Laryngitis Inflammatory process of the larynx Majority are acute Caused by same viruses as other URTI Differential: check for possible malignancies Etiologyo Virus

Rhinovirus, Influenza, Parainfluenza, Adenovirus, Coxsackie, Coronavirus, RSV

o Bacteria Group A streptococcus, C. diptheriae (common in ER), Moraxella

catarrhalis Causes of Chronic Laryngitiso M. tuberculosiso Fungal infections

Manifestationso Hoarseness (can also be caused by steroids)o Reduced vocal pitch or ophoniao URTI symptoms Cough Sore throat Nasal congestion

Diagnosis and Treatment Rhinorrhea Erythema, edema, nodules, ulcerations Treatment o Acute – humidification and voice rest o Chronic – depends on culture and biopsy (further testing)

If chronic, consider tumors and other granulomatous diseaseso Antibiotics (i.e. penicillin)

Group A Streptococcus coverage

COMPLICATIONS OF LOWER RESPIRATORY TRACT INFECTIONParapneumonic Effusion

Diseases associated with parapneumonic effusiono Bacterial pneumonia, lung abscess, bronchiectasis are probably

the most common causes of exudative pleural effusion in US

Pleural Fluid Confirmation Lateral Decubitus X-ray

o Range of fluid volume: 150cc-250cc which depends whether the patient is small or large (obliterate the sulcus) This is also equal to about 10mm fluid via X-ray.

o If >10mm, tap to rule out infection o Make sure that the patient was lying ipsilateral to the

suspected lesion for 30 minutes to allow formation of layers especially if fluid is viscous or if there are adhesions.

Chest CT Scan (if cannot demonstrate in lateral decubitus X-ray) o Shows other additional findings especially at the lymph nodes o Also used in cases where fluid does not form layers (adhesions

forming compartments) Chest Ultrasoundo For detection of fluid presence and measurement of volumeo Less expensive and more available than CT.

Procedures Thoracentesis o Done if there is 10 mm layering of fluid in lateral decubitus CXR

and if fever is persistent o Any less, then you have danger of puncturing the lungs and

causing pneumothorax (150 to 250 cc or more fluid) Factors to consider when doing more invasive procedures other

than thoracentesis (all point to empyema) Closed Tube Thoracostomy o Loculated fluido Pleural effusion pH <7.0o Pleural fluid glucose <3.3 mmol/L (<60mg/dl)o (+) gram stain or culture of pleural fluido Presence of gross pus in the pleural space

Management of complicated effusiono Instillation of fibrinolytic agents to lyse adhesions/loculationso Thoracoscopy – insertion of tube, done in general anesthesiao Decortication – open up patient then insert tube after

procedure to remove septations/loculations

Lung AbscessGeneral Characteristics Pulmonary parenchymal necrosis (2cm) and cavitation resulting

from infection Most often caused by aspiration Risk factorso Esophageal dysmotility – leads to aspirationo Seizure disorderso Bulbar dysfunction (myasthenia gravis, stroke history, tumors)o Predisposing conditions

Periodontal abscess Alcoholism (more chances for aspiration to occur)

Causative agents o Most common are anaerobic bacteria o Immunocompromised host: aerobic bacteria & opportunistic

pathogens Other bacteria: S. aureus, Klebsiella pneumoniae, Nocardia sp.,

Gram (-) bacteria, fungi, parasites Common symptoms of lung abscess (non-specific, same as TB and

malignancy) usually lasts 2-3 weeko Cougho Fevero Purulent sputum productiono Pleuritic chest paino Hemoptysis

PE findings o Rales on area of consolidation o Fetid breath not pathognomonic but take note of thiso Poor dentitiono Clubbing – also seen in cancer

Radiologic findingso Thick-walled cavitation in dependent portion of the lung (arrow

in Figure 1)


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o Air fluid level (circle in Figure 1)o Look for the dependent portions of the lung/common causes of

aspiration (see homework section at the end) Laboratory findings (results are non-specific and inconclusive)o Anemiao Leukocytosiso Erythrocyte Sedimentation Rate (ESR) elevated

Differential diagnoseso Malignancyo Pulmonary infarction (common in bed-ridden patients)o Pulmonary sequestrationo Infected bullae (need old films to compare as some individuals

may normally have this)

Figure 1. Radiologic Findings in Lung Abscess

Diagnostic procedures o Culture

Blood Sputum Pleural fluid

o Fiberoptic bronchoscopy – to rule out obstruction (because abscess can also be a result of obstructive pneumonia)

o Transthoracic or transtracheal aspiration – uncommon Treatment o Anaerobic coverage is important

Penicillin Clindamycin Carbapenems β-lactam/ β-lactamase inhibitor agents Metronidazole (if used alone, it is associated with high failure rate)

o Duration of medical treatment 4-6 weeks antibiotics Failure may suggest different antibiotic should be used or different

etiology like tumors, foreign bodies, bronchostenosis Utilize other procedures when patient is not responding

o Surgery Refractory hemoptysis (250 in one attack or 500cc/24hrs) Inadequate response to medical treatment Tissue diagnosis – if other disease entities are suspected

BronchiectasisGeneral Characteristics The most common cause is pus infection in third world countries

like the Philippines (common cause in the US is cystic fibrosis) Abnormal and permanent dilatation of bronchi Focal or diffuse Vascularity of the bronchial wall increases Bronchial arteries enlarged (may eventually rupture and cause

hemoptysis – can be fatal surgery to correct) Anastomosis between bronchial and pulmonary arterial

circulations also enlarge Pathological changes o Bronchial dilatation

o Associated with destruction and inflammatory changes in the walls of medium-sized airways often at segmental and sub-segmental bronchi

o Cartilage, muscle and elastic tissue of the walls are replaced by fibrous tissue

o Dilated airways contain pools of thick purulent materialo Peripheral airways are occluded by purulent secretion or

replaced or obliterated by fibrous tissueo Arises from bronchial and peribronchial inflammation

Additional changes seen in the Lung Parenchymao Fibrosiso Emphysema because of air trappingo Bronchopneumoniao Atelectasis o Can cause ventilation-perfusion imbalance and eventually,

hypoxemia Pathological patterns of bronchiectasis seen in chest CTo Cylindrical – bronchi uniformly dilated and end abruptlyo Varicose – bronchi irregular and beaded pattern of dilatationo Saccular – Cystic, ballooned bronchi at periphery ending in blind

sacs Development of bronchiectasiso The additive effects of pathogen plus the host inflammatory

response give rise to widespread epithelial injury characteristic of bronchiectasis

Figure 2. Natural History of Disease for Bronchiectasis

Infectious causes o Adenovirus and influenza viruso S. aureus, Klebsiella and anaerobeso Bordatella pertussis in childhoodo M. tuberculosis (most common worldwide)

Causes necrosis of parenchyma and airways, airway obstruction from bronchostenosis (from healing fibrosis) or extrinsic compression of lymph nodes

Non-Tb bacteria can be secondary infection or colonizer Mycobacterium avium can serve as primary pathogen

Non-infectious Causes o Toxic gas inhalation – e.g. Ammoniao Aspiration of gastric contentso Immune response

Allergic bronchopulmonary aspergillosis (ABPA) a condition characterized by an exaggerated response of the

immune system to the fungus Aspergillus fumigatus It causes airway inflammation, which can ultimately lead to

bronchiectasis 1-antitrypsin deficiency (antitrypsin acts by digesting elastase)

Host defense impairment that lead to bronchiectasiso Local

Endobronchial obstruction from stenosis Compression by lymphocytes, neoplasm, secretion

o Generalized Immunoglobulin deficiency Primary ciliary disorders (sinusitis, bronchiectasis, situs inversus)


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Cystic fibrosis (more common in Western countries)

Diagnosis and Treatment Clinical manifestationso Persistent, recurrent cough – rule out allergic reaction;

secretions pool on lying down position cough o Purulent sputum production o Repeated infection (yellow/greenish phlegm)o Hemoptysis o Fatigue, weight loss and myalgia because of infection

PE Findings (very non-specific)o Crackles, rhonchi, wheezeo Chronic hypoxemia signs: clubbing, pulmonary HPN right-

sided strain on the heart cor pulmonale symptomso Treated with oxygen

Radiographic findingso X-ray

Cystic bronchiectasis – cystic spaces with or without air fluid levels Honeycombing ‘Tram-tracks” dilated airways in parallel or “ring shadows”

o HRCT Scan Gold standard for detecting or confirming diagnosis

Figure 3. CT Scan Showing Normal Lung vs. with Bronchiectasis

Laboratory tests o Sputum AFB stain and culture (tuberculosis) o Fiberoptic Bronchoscopy – reveals location of obstructiono Pulmonary Function test/spirometry if with COPD– determine

changes in pulmonary volume/capacities or function and to assess if the patient can benefit from bronchodilators

Goals of treatment o Treatment of infection o Improved clearance of secretions o Reduction of inflammation o Treatment of underlying problem

Role of antibioticso Cornerstone of treatmento Given only during acute episodes of exacerbation (e.g. increase

in purulence, coughing frequency)o Quinolones, aminoglycosides, carbapenem, 3rd generation

cephalosporin for Pseudomonaso Amoxicillin, cotrimoxazole, levofloxacin as empiric therapyo Given 10-14 days

Other therapeutic approacheso Mechanical methodso Appropriate positioningo Mucolytic agentso Surgery (uncontrolled bleeding and pathology is localized)o Embolization (uncontrolled bleeding and pathology is diffused)

HOMEWORK AND OTHER STUFFEmpyema

Collection of pus in the space between the lung and the inner surface of the chest wall (between visceral and parietal pleura)

Caused by an infection that spreads from the lung

Risk factors: bacterial pneumonia, chest surgery, lung abscess, trauma/injury to the chest

Signs and symptomso Chest pain – worsens upon inspirationo Dry cougho Excessive sweatingo Fever and chillso General discomfort and uneasinesso Shortness of breatho Weight loss

Decreased breath sounds or abnormal sound (i.e. friction rub) Treatmento Remove the collection of pus – draining of the thoracic cavityo Antibiotics to control infection

Kartagener’s Syndrome It is an inherited disorder of the cilia wherein there is primary

ciliary dyskinesia. As a result, mucus and bacteria cannot be expelled and frequent

lung infections will develop Occurs in 1/32,000 live births Distinguishing symptom: situs inversus – internal organs are on

the “wrong side” (i.e. heart is found in the right side) 3 main symptoms are chronic sinusitis, bronchiectasis and situs

inversus Treatment focuses on the prevention of respiratory infections

with use of antibiotics and respiratory therapy

Embolization Therapy Embolization – non-surgical, minimally invasive procedure that

occludes or blocks one or more blood vessels that contain abnormalities

Embolitic agents are placed through a catheter into a blood vessel to prevent flow into that area

Catheter embolization is used too Control or prevent abnormal diffused bleeding, i.e. bleeding

from injury, tumor, or GI tract lesionso Close off vessels that supply blood to a tumor; the end result

should be that the tumor will shrink or the growth rate will lessen

o Treat aneurysms

Locations of Aspiration Generally, the right middle and lower lung lobes are the most

common sites of infiltrate formation due to the larger caliber and more vertical orientation of the right mainstem bronchus

Patients who aspirate while standing can have bilateral lower lung lobe infiltrates

The right upper lobe is a common area of consolidation in alcoholics who aspirate in the prone position


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The superior segments of RLL, LLL and axillary subsegments of anterior and posterior segments of RUL are common sites for aspiration and will account for 85% of all lung abscesses.

Gravitational forces determine the site of aspiration. Position of the patient at the time of aspiration determines the segment the aspiration is most likely to occur.

Basal segments of RLL used to be the most common site for aspiration during 1940 to 1960. During this period ENT surgery and dental work was done in sitting position with ether as the anaesthetic. The right main bronchus is in straight line with trachea while left main takes off at an angle. In this position gravity facilitates lodging of the aspirate to basal segments of RLL.

In supine position and with the patient on back superior segment of RLL is the most dependent segment.

In right lateral decubitus position the axillary subsegments of anterior and posterior segments of RUL is the dependant site for aspiration. Abscess is located in the middle of lateral CXR corresponding to RUL bronchus take off.

When the patient is on abdomen, aspiration does not occur, thus it is extremely unlikely for any anterior segments, middle lobe and lingula to be the site for aspiration lung abscess. When lung abscess is encountered in these sites one should suspect partial airway obstruction or trouble with deglutition as the predisposing factor for lung abscess.

Source: http://www.meddean.luc.edu/lumen/MedEd/medicine/pulmonar/cxr/lasegs.htm

http://www.meddean.luc.edu/lumen/MedEd/medicine/pulmonar/cxr/lasegs.htm



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Jereel: Hello Block B! Pasensya na medyo humaba ‘yung trans dahil sinama namin lahat ng mga sinabi ng guro at mga nakalagay sa mga nakaraang transes na makatutulong sa mas malalim nating pag-unawa sa asignaturang ito. Nais ko lang na batiin ang mga kaibigan ko. Bestie Allison, salamat sa paglagay ng plastic cover sa librong binigay ni Dr. Roa. Oo nga pala, malandi ka. :)) Tato, tulog ka nang tulog. Sa susunod sasapakin na kita. Magdala ka nga ng Cheetos. Terence, bigyan mo ko ng pasalubong galing Malaysia bukod pa sa kape. Kay Ginnie at sa mag-aaral na miyembro ng Block-B ngunit nagiging Block A tuwing sasapit ang tanghalian na si Alexeis, hello! Mag-aral ulit tayo sa coffee shop o kaya naman mag-kape tayo ulit sa 14A04 habang nag-aaral para sa OSCE. Jim, hinay-hinay lang. Baka mahulog na talaga ang loob niya sa’yo. :> Sa Ikapitong pangkat ng Pharma, magaling, magaling at isa pang magaling ang ginawa natin! Hindi tayo gaanong ginisa kanina. Sa Filipino block noong mga taon ng Intarmed na itago natin sa pangalang Block 13, mabuhay kayo at ang ating wikang pambansa! Nasaan na ang ating damit na pantaas? hahaha. Ako’y nasasabik na sa Derma dahil marami daw magaganda. Bow.


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[os 213] lec 13 lung defense mechanisms and approach to respiratory tract infections (b)

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