pulmonary

patho

acute bronchitis

inflammation of the tracheobronchial tree

Attributed to an infection process

• manifests most often during respiratory infections

• Winter season

types of infectious organisms involved in acute bronchitis

Influenza

Parainfleunza 

Adenovirus 

Rhinovirus 

M pneumoniae and chlamydia pneumonia 

Streptococcus pneumoniae 

Bordetella pertussis

s/s of acute bronchitis

Purulent, productive cough 

Fever 

Malaise

Rhinorrhea, nasal congestion 

Sore short 

Wheezing 

Dyspnea

Chest discomfort 

Myalgia 

Arthralgias 

Rhonchi

pneumonia is classified based on

causative agent 

anatomical location of infection 

patho changes

epidemiological data 

causative agent in pneumonia

viral

bacteria

fungal

Anatomical location of infection in pneumonia

Throughout both lungs, or consolidation in one lobe

Pathophysiological changes in pneumonia 

Changes in interstitial tissue, alveolar septae, alveoli 

Epidemiological data in pneumonia

Nosocomial (hospital-acquired)

Community-aquired

Lobar pneumonia

Community-based, often in healthy young adults

Usually caused by streptococcus pneumoniae

Infection localized in one or more lobes

patho of lobar pneumonia 

Inflammation and vascular congestion 

Exudate forms in the alveoli

• Contains fibrin and forms a consolidated mass

• Produces rusty sputum  

Adjacent plerae frequently involved 

Infection may spread to pleural cavity

s/s of lobar pneumonia

Sudden onset 

Systemic signs 

• High fever with chills, fatigue, leukocytosis 

Dyspnea, tachypnea, tachycardia 

Pleural pain 

Rales

Productive cough 

• Typical rusty-colored sputum 

Confusion and disorientation

bronchopneumonia

Diffuse pattern of infection in both lungs 

Cause can be due to several species of microorganisms

patho bronchopneumonia

Inflammatory exudate forms in alveoli 

Onset tends to be insidious

s/s of bronchopneumonia

Moderate fever, cough, rales

Productive cough with purulent sputum-usually yellow or green

treatment of bronchopneumonia

antibacterial 

Legionnaires disease

Caused by legionella pneumophila 

• thrives in warm, moist environments 

• Often nosocomial infection

infections of Legionnaires disease if untreated

Causes severe congestion and consolidation 

Necrosis in the lung 

Possibly fatal

s/s of Legionnaires disease

Headache and muscle pain, chills, fever

Cough, chest pain, N/V/D, SOB

TB

Bacterial lung infection 

• Mycobacterium tuberculosis (ACID-FAST BACILLUS) 

• Characterized by pulmonary infiltrates and granulomas/tubercle

patho of TB

Spread by direct inhalation of infective droplet nuclei 

• Aerosol from infected individual produces 3000 infective droplets 

• Can only spread when in active form

development and s/s of TB

primary infection 

active infection 

reinfection (secondary) 

primary infection of TB

often asymptomatic

active infection of TB

Early symptoms vague 

Anorexia, malaise, fatigue, low grade fever, night sweats 

Pleuritic chest pain, cough (initially non productive), hemoptysis, purulence, weight lose, crackles and wheezes

reinfection (secondary) of TB

Reactivation of TB

Can occur years after primary infection 

Usually due to decrease in host resistance

As organism multiples large area of necrosis 

Can spread to other areas of the body 

s/s similar to active TB

mantoux skin test for TB

Skin injection

Positive reaction = at least a 10MM induration 

False positives = previous BCG vaccination

chest x-ray for TB

Required if mantoux is positive 

sputum culture for TB

most reliable for testing of TB

testing CXR results of TB

Pleural effusion (often associated with active TB) 

Calcification (shows past or resolved TB) 

Simon’s foci (nodules) 

Pleural effusion in tetsing CXR results of TB

Accumulation of fluid in the pleural space

In mid, upper lobes with locally lymph node inflammation

calcification in CXR results of TB

Indicates healing and dormancy 

Simon’s foci in CXR results of TB

Usually indicates reactivation of TB

Often seen in upper lobes

aspiration in obstructive disorder

Passage of food, fluid, emesis, other foreign material into trachea and lungs 

• Common problem in young children or individuals laying down when eating or drinking

s/s of aspiration

Coughing and choking with dyspnea 

Loss of voice if total obstruction 

Stridor and hoarseness

Wheezing 

Tachycardia and tachypnea 

Nasal flaring, chest retractions, hypoxia

complications of aspiration

aspiration pneumonia

respiratory distress syndrome

pulmonary abscess

systemic affects

aspiration pneumonia complication in aspiration

Inflammation-gas diffusion is impaired 

respiratory distress syndrome complication in aspiration 

May develop if inflammation is widespread 

pulmonary abscesses complication in aspiration

May develop if microbes are in aspirate 

systemic effect complication in aspiration

When aspirated materials are absorbed into blood 

COPD in obstructive disorder

Chronic and recurrent obstruction of airflow in the pulmonary airways

two types of COPD

emphysema 

chronic bronchitis 

predisposing factors of COPD

Smoking 

Occupational

Airway infection

Asthma

Airway hyper-responsivenes

Chronic bronchitis (shunting) in COPD

Compensation by increasing cardiac output and decreasing RR

Airway obstruction of the major and small airways 

• Long term inflammation of the tracheobronchial tree accompanied by 

  • Chronic productive cough 

  • Excessive mucus production

  • airway obstruction

+perfusion

-ventilation

most common irritants or infection in chronic bronchitis of COPD

smoke 

patho of chronic bronchitis in COPD

Chronic inflammatory response caused damage to the epithelial lining and smooth muscle 

• Poorly ventilated lung with normal perfusion 

• So the mucus and ciliary response impaired 

• Obstruction from inflammation and secretions 

  • Unable to clear bacteria and mucus normally

Ventilation perfusion (V:Q) mis-match in chronic bronchitis in COPD results in 

Cardiac output increases 

Ventilation decreases 

Results in rapid circulation of poorly ventilated lung causing 

• Hypoxia

• Polycemia 

• CO2 retention

s/s of chronic bronchitis in COPD

Productive cough 

Progression to intermittent dyspnea over time 

Accessory muscle use 

Clubbing 

Reddish blue skin: “blue bloater”

Over time: progressive heart failure (cor pulmonale) and respiratory failure 

• Weight gain 

• Edema

emphysema (dead space) in COPD

Compensation by increasing RR and decreasing cardiac output  

Abnormal, permanent enlargement of air spaces or alveoli

• Recurrent inflammation release enzymes that damage the lung cells causing the enlargement

+ventilation

-perfusion

causes of emphysema

Smoking 

Alpha 1 antitrypsin deficiency

Distinguishing characteristics in emphysema COPD

Airflow limitation caused by lack of elastic recoil in the lungs 

patho of emphysema in COPD

Destruction of the alveolar airspaces leads to 

• Decreased elastic recoil 

• Impaired and decreased surface area for gas exchange 

Decreased recoil leads to 

• Air trapping 

• Increased intrathoracic pressure

Ventilation-perfusion (V:Q) Mis-Match in emphysema of COPD results in 

Hyperventilation 

Cardiac output decreases

Results in limited blood flow through an oxygenated lung 

tissue hypoxia 

• suffering from low oxygen levels 

pulmonary cachexia 

• muscle wasting and weight loss

respiratory failure 

• eventually failure 

s/s of emphysema of COPD

Emaciated 

Barrel chest

Pursed lip breathing 

Accessory muscle use 

Tachypnea

Neck muscle enlarged 

Tripod sitting position 

Wheezing 

Distant heart tones 

Decreased breath sounds 

Grunting 

“Pink puffers”

Cystic fibrosis (CF)

Inherited (genetic) disorder 

• Gene located on chromosome 7

• Mean survival age 37 

• Produces tenacious mucus from exocrine glands

patho fo CF

lungs

sweat glands

digestive tract 

reproductive tract 

patho of the lungs in CF

Mucus obstructs airflow in bronchioles and small bronchi

Causes permanent damage to bronchial walls

patho of sweat glands in CF

Sweat has high sodium chloride content 

Dehydration can increase viscosity of mucus

patho of digestive tract in CF

Meconium ileus in newborns (obstruction) 

Blockage on pancreatic ducts 

• Decrease in pancreatic enzymes into digestive tract 

Obstruction of bile ducts 

Salivary glands often mildly affected

patho of reproductive tract in CF

Obstruction of vas deferens (male)

Obstruction of cervix (female)

s/s of CF

Meconium ileus 

Salty skin 

Fatty stools 

Signs of malabsorption 

• Steatorrhea, abdominal distention 

Chronic cough and frequent respiratory infections

Failure to meet normal growth milestones 

Issues with chronic Dehydration

diagnosis of CF

Genetic testing

Sweat test (1st thing they do)

Pulmonary function test

asthma

Periodical reactive airway disorder 

• Present as an acute attack 

• Hypersensitivity and hyper-response

• Genetically or environmentally induced 

• Reaction classified as mild, intermittent, or severe

classifications of asthma

Acute 

Chronic 

Extrinsic 

• Most common in children, grow out of it, has a trigger 

Intrinsic 

• Starts in adulthood, hyper-response triggered by URI, cold, stress, smoke

asthma is characterized by 

Sudden, spasmodic narrowing of bronchial airway due to 

• Inflammation and increased mucus secretion 

• Contraction of smooth muscle

• Increased secretion of thick mucus into passages

s/s of asthma

Sudden dyspnea

Weezing

Chest tightness

Diminished breath sounds (especially to lower lobes)

Coughing

Thick, clear, yellow sputum

Rapid pulse and respiration 

Accessory muscle use 

Severity depends on 

• Cynosis 

• Ability to lie flat 

• Ability to speak

• Accessory muscle use

status asthmaticus

Life-threatening complication of asthma 

• Not responding to treatment 

• See more swelling and thicker secretions 

• Caused by prolonged bronchospasm and severe hypoxia 

• Diagnosed when a severe asthma attack is resistant to bronchodilator therapy 

• Hypersensitivity to ASA may precipitate

additional symptoms of asthmaticus 

Bronchial edema 

Tenacious, thick secretions 

Mucus plugging 

Atelectasis

pulmonary embolism (PE) is vascular disorder

Occlusion of a portion of the pulmonary blood vessels by an embolus or thrombus 

Most common site of organization 

• DVT: deep vein thrombosis 

If massive, can cause death 

Emboli → matter that enters the systemic venous circulation 

Thrombus → blood clot that causes obstruction

risk factors of PE

Current DVT

Prior history of DVT or PE

Recent surgery or pregnancy 

Prolonged immobilization 

Malignancy - especially lungs or prostate

Obesity 

Advancing age

Hypercoagulability 

Smoking 

Estrogen therapy 

CHF

Major trauma

patho of PE

Emboli travels via vena cava to the side of the heart and then to the pulmonary artery → RA to RV to PA

Pulmonary vasoconstriction causes HTN 

• Absent blood flow

  • Ventilation available 

  • Perfusion limited 

• Decrease surfactant

  • Leads to atelectasis 

  • More hypoxemia 

Infarction or dissolution 

• Infarct: rare, invasive 

• Dissolution: reabsorption

s/s of PE

Dyspnea

Pleuric chest pain 

Apprehension restlessness, feeling of impending doom

Cough, hemoptysis, crackles

Decrease SAO2, tachypnea, tachycardia 

Pleural friction rub 

ST changes (ECG)

Diaphoresis , fever

Petchiae (chest, axillae)

atelectasis in vascular disorder 

Collapse of lung tissue 

atelectasis results from

Compression 

• Outside the airway, enlarged heart or lymph nodes 

Absorption (2 types) 

• Obstruction – something keeps air from entering airways 

• Hypoinflation – incomplete expansion

pleural effusion in vascular disorder

Presence of excessive fluid in the pleural cavity 

causes of pleural effusion 

Increased pressure in the pleural cavity 

Separation of pleural membranes

patho of plural effusion

Increased amount of fluid enters the pleural space

• Increased pressure in the pleural cavity causes separation of the pleural membranes 

This separation prevents expansion of the lungs during inspiration

exudative effusions in pleural effusion

Response to inflammation

Fluid leaked contains proteins and WBCs

transudate effusions in pleural effusion

Water effusions (hydrothorax)

Result in increased hydrostatic pressure or decreased osmotic pressure in blood vessels 

• Fluid shift occurs 

Commonly associated with liver and kidney disease

s/s of pleural effusion

Dyspnea 

Cyclic chest pain 

Increased respiratory and heart rates

treatment of pleural effusion

Remove underlying causes 

Analyze fluid 

Chest drainage: thoracentesis

Pneumothorax in vascular disorder 

Accumulation of gas in the pleural space causing lung collapse on affected side

closed pneumothorax

Cause increased pleural pressure which does not allow the lungs to expand normally

Types 

• Spantaneous 

  • Primary: healthy individuals 

  • Secondary: associated with underlying condition

open pneumothorax

Air enters the pleural space and causes pressures to turn positive

Types 

• Traumatic 

  • Blunt or penetrating trauma 

  • Chest injuries, surgical complications 

  • Fractured ribs 

• Tension   

  • Associated with open chest injuries 

  • Life-threatening, displaced structure

  • Air enters the pleural space but cannot leave

s/s of pneumothorax

Sudden, sharp pleuritic pain 

Asymmetrical chest wall movement 

Shortness of breathe 

Cynosis 

Respiratory distress

additional s/s of tension pneumothorax

Mediastinal shift **

Decreased cardiac output 

Hypotension 

Tachypnea and tachycardia

flail chest in vascular disorder

Results from fractures of ribs, which allows ribs to move independently during respiration

during inspiration patho of flail chest

• Flail or broken section moves inward rather than outward 

  • Inward movement of ribs prevents expansion of affected lung 

• Large flail section con compress adjacent lung tissue  

  • Pushing air out of that section and u the bronchus 

  • Air (stale) from damaged lung crosses into the other lung with newly inspired air

during expiration patho of flail chest 

Unstable section pushes outward by increasing intrathoracic pressure 

Large flail section 

• Paradoxical movement of ribs alters airflow during expiration 

Air from unaffected lung moves across into affected lung 

Hypoxia results from limited expansion and decreased inspiratory volume

ARDS (acute respiratory distress syndrome) in vascular disorder

Disruption to pulmonary capillary membranes

causes of ARDS

Shock

Sepsis

Trauma

ARDS is characterized by 

Severe dyspnea, rapid onset 

Hypoxiemia 

Pulmonary infiltrates and edema 

Restlessness, apprehensions, retractions

patho of ARDS

Injury to alveolar wall and capillary membrane 

This causes 

• Release of chemical mediators 

• Increases permeability of alveolar capillary membranes 

• Increased fluid and protein in interstitial area and alveoli 

• Damage to surfactant-producing cells

complications of ARDS

pneumonia

CHF