INTRODUCTION TO PULMONARY MEDICINE

Anatomy
The structure of the lungs is adapted to the functions of:
_ Gas transport in airways
_gas mixing in acini
_gas transfer across the 80m sq surface area alveolocapillary membrane
_The airways
_the nose and the sinuses
_the pharynx
The conducting zone
-the tracheobronchial tree
_the trachea
_the main bronchi
_the bronchioles
The respiratory zone
- The acini
_the alveoli
_the alveoli cells :
Pneumocyte 1
pneumocyte 11
pneumocyte 111
brush cells
_the alveolar macrophages
Pulmonary defence mechanism
_the intersitium
Pulmonary circulation
Pulmonary arteries
Pulmonary veins
Lymphatics
The pleural:
Visceral
parietal
From the parenchyma, airways and pleural
Over the superficial pleural to the deep broncho vascular network avoiding septae
From the respiratory bronchi also follows lobular pathway and anastomose at hilar region
A major part of the left lung draws into the right tracheobronchi lymph nodes
-The chest wall:
Thoracic vertebrae
12pairs of ribs attached to the sternum
Inspiratory muscles
Diaphragm
Intercoastal muscles
Sternocleidomastoid muscle
The medisternum
Upper
Lower –anterior
-middle
-Posterior
_Control of respiration
Medullar oblongata
Defence mechanism
Classified into : _mechanical non specific
_immunologic
_anatomic

DIAGRAM

Tracheobronchial tract
Essential productive function consist of:
Filtration :particles more than 5um
Moistening of inspired air
Warming to body temperature
Reflexive closure of glottis e.g during swallowing
Lower airways
Mucociliary system disorder;
Ciliary dipkines
Ciliary fibrosis
Tissue clearance
Cough reflex _effernt _vagus nerve
_diaphragm
Sensory receptors;
Larynx
Tussigenic zone in ;-trachea
_Bronchial bifurcation
_Other zones;-ear canal,diaphragm
Cough centre
Medullar oblongata
Pons
_Cough is reflex explosive expiration aiming at expulsing foreign body and secretion from pharynx,
larynx and tracheobronchial tree
Loss of cough reflex;
Paralysis of muscles – polio
Retention of secretion with resultant infection
Mucosal proteins
Results from complex interaction between the mechanical and immunologic defence mechanism as
a result of microbacterial or viral invasion
They originate from;
Plasma by diffusion into the alveoli
Transferring
Alpha_1 protease inhibitor
Local production from alveolar macrophage
Complement
Lysosomes
_Selective transport
Secretion igA
_Some mucosal protein include;
 Complement I;
Cascade of about 20proteins
3 effective defence mechanisms:
_Chemotaxis and activation of immune cells
_Opsonization of bacteria
_Bactereolysis
NB: C3 defect _ recurrent airway infection: streptococci
Hemophillus
_Cytokines
Produced by metabolically acting immune cells
Activate other cells e.g interleukine
Interferon
TNF
Growth factor
Chemotactic factors
Protease inhibitors
Found in bronchial secretion
Diffuse from plasma
e.g alpha-1 protease inhibitors
alpha-2 macroglobulins
alpha-1 antichymotrypsin
Fibronectin
Found in epithelial and macrophages
Protects respiratory mucosa concomitantly with secretory IgA
_Immunoglobulins
Found in normal and pathogenic bronchial secretions
Include IgE, IgM ,IgG

Alveolar space
Defence system classified as
Natural – non specific
Adaptive and specific supported by surfactant
Involves use of memory cells
Poorly diiferentiated
Well differentiated
This leads to the production of adaptive specific system
Short lived memory cells produce in a particular situation but reactivated incase of reinfection
The antigen specific reaction reoccurs in case of reoccurrence
Mechanism:
Phagocytosis
Surfactant system
Immune system
Phagocytosis
Key role in defence system
Direcr cytotoxicity
Activation of inflammatory process
Institution of reparatory process
These roles are accomplished by
 Alveolar macrophages
Opsonization of bacteria
Neutrophil granulocyte
Direct phagocytosis of bacteria
The intracellular destruction of bacteria follows through oxidase and proteases
The surfactant system
Produced by pneumocyte II
Function in the elasticity of the alveoli this prevents alveolar collapse
They also participate by:
Cytotoxic activity of alveolar macrophages on _tumor cell
_bacteria
Increases the migration speed of chemotactically stimulated alveolar macrophages
Cytotoxicity of ingested substances
Quartz
Dust particles

Immune system
The alveolar immune system(AIM) -central immunologic defence mechanisms of activity
Phagocytosis
Killer activities
Secretion of cytokines
Ag presentation
Coordinating repair mechanisms
Neutrophil granulocytes
Also found though in lesser amounts in airway and alveolar space but mostly in capillaries
adhering to capillary walls
Come into play chemotactically not directly, migrating directly from blood vessels through
interstitium into the alveolar space
Direct opsonization of micro organisms without prior opsonization
Lymphocytes
Found in lymphoid structure of the bronchial lamina propria and alveolar interstitium
Include B and T cells
B cells also participate in immune reactions type I, II,III
A T cell subpopulation function as cytotoxic effector cells with the capacity of destroying virus, tumor
and transplant cells with antibody mediation
T lymphocyte recognize Ag only when presented by a macrophage
Non specific functions of the lungs
_Alveolar stabilization –surfactant
_Fluid (water) regulation
_Hemostasis
Endothelial cells of the pulmonary capillary participate in complement cascade and formation or
dissolution of thrombi
Metabolic function
Carbon dioxide produced
Lipid metabolism resulting in the production of surfactant
Protein metabolisms _ production of hormones
The clinical presentation of chest diseases
Cough
 definition
defensive reflex designed to clear and protect the lower respiratory tract
Forced respiratory effort against a closed glottis which then opens allowing a sudden expulsion of air
from the lungs
Mechanism
Preceded by an initial deep inspiration
Cough reflex can be initiated by the stimulation of irritants receptors in the larynx, trachea and major
bronchi
Receptors respond to mechanical irritation by intra luminal materials such as
_dust
_Mucus
_Foreign particles or bodies
_Chemical irritants such as :fumes, toxic gases, sulphur dioxide
-Mechanical events within the thorax suddenly and largely
changes in air way caliber e.g. Lung collapse
The afferent pathways
Superior laryngeal and vagus nerve
Center
Medullar oblongata
Efferent
entire respiratory musculature
Clinically the Types of cough depend on the
Clinical description
Sound
Timing
Productivity
Cough may be:
Dry cough with irritative hacking quality
-Inflammatory condition
Pharynx
Tracheobronchi
Lower respiratory tract e g in early pneumonia
Whooping cough
Long Inspiratory sound
Tracheal and laryngeal
Abductor paralysis of vocal cords
Prolonged
Pressure on left recurrent nerve
Lesions in thorax
-bronchial carcinoma
-Oesophageal carcinoma
-Enlarged lymph node
-Neoplasia
4- Non productive cough
Swallowed sputum in children
Viscid secretion
5-Productive cough
Early morning phlegm _chronic bronchitis
 Post prandial cough, especially after lying down
Oesophageal
Pharyngeal
Neuromuscular
6- Dry persistent cough may signify neoplasia
Characteristics of the cough
Duration
few days - common cold
Several weeks- smoker
-Malignancy
-TB
Occurrence
-nocturnal -asthma
Aggravating factors
Dust
Cold air
Pollen
Associated symptoms
Fever
Weight loss
Vomiting
Productivity
-Sputum -color
-Purulent
- mucopurulent
-Amount produced
Abundant - bronchiectasis
-Blood stained hemoptysis
Bloody
-Breathlessness
Normal after exertion
Inappropriate to physical exertion or occurring at rest
-Variability of symptoms
Good days
Bad days
-Degree of exertion before onset
-Wheezes
Noises in the chest
May not be present at the time of examination but important
Chest pain
Usually musculoskeletal
May also be
Pleuritic _sharp and stabbing
Worse on breathing or coughing due to pneumonic focus
Pleural malignancies
Pneumothorax
Worse on breathing
Acting not stabbing
Intercostal neuralgia
Musculoskeletal
Epidermic myalgia
Coxsackie B infection
Associated symptoms
_fever
_Chest pain
_Pre eruptive nerpetic pain
Physical findings
Extra thoracic finding
1 Cyanosis -Blue colouration nail beds, lips, tongue by hypoxemic blood

-May be i- peripheral-Poor circulation

Cold weather
ii-Central -blue tongue
-Warm extremities
-Previously defined as deoxyhaemoglobin of 5g/dl but may be be detected with
oxygen saturation of 87%
2 Finger clubbing
Loss of natural angle between nail and nail bed with enlargement of the end of the finger
Causes are both
Thoracic _suppurative lung disease
-Bronchiectasis
-Lung abcesses
-emphysema
-Fibrosing alvolitis
And other fibrotic diseases
Malignancies
-Bronchial
-Pleural
Extra thoracic - diverticulosis
May associate hypertrophic pulmonary osteoarthropathy (HPOA) in malignancy (95%)
Examination of the chest
Breathing pattern and chest configuration
Normal R.R – 10-14/min
More than 20/min –abnormal
Pneumonia
Interstitial lung disorder
Anxiety
Cheyne stokes respiration
Altered regular apnocic periods with periods of increasing and decrease ventilation
Chest expansion
Reduce on one side - underlying disorder
Indrawing of intercostals muscles
Air flow obstruction
Body configuration
Obesity
Weight loss
 Deformity _kyphosis
Pectus cannatus
Pectus excavation
Scoliosis
Chest palpitation
Identify trachea _supra sterna notch
_Apex beat
Detect transmitted vocal sounds
Vocal fremitus
Vocal resonance
Percussion of the chest
Dullness _solid tissue
_Fluid
Resonance hyperinflation
Auscultation of the chest
3 types of sounds
-Breath sounds
-Adventitious sounds
-Voice sounds
Normal breath sounds
-Vesicular
-Originate from air flow through bronchi
-Quete over areas of atelectasis
-Bronchial breathing heard over airless lung as in _consolidation
_Atelectasis
_Densfibrosis
Adventitious sounds
Confusing terminologies
Rales abandoned for crepitations
Interrupted non musical sounds
Crepitations may be coarse or moist due to movement of sputum in large airways
Coarse _respiratory tract infection
_COPD + respiratory tract
Fine inspiratory crepitations
-Pulmonary edema
-Fibrosing alvoelitis
Occasional mid to late inspiratory squawk and variety of pulmonary fibrosis
Rhonchi (wheezes) air way obstruction
When monomorphic single pitch at inspiration or expiration _localized air way obstruction
Several sounds of varying pitch i.e polyphonic heard randomly at inspiration or expiration are typical of
widespread airway obstruction of asthma and chronic bronchitis (sililarity )
Pleural rob superficial gralting noise over the pleura
Common presentation of respiratory diseases in conjunction with clinical and radiologic findings
1)syndrome of respiratory tract
Coryza
Acute pharyngitis
Quinsy
Acute epiglotitis
 Acute laryngitis

Lower respiratory tract infection

Acute tracheitis
-Acute bronchitis
-Pneumonitis
-Pneumonia
-Lung abcesses
-Pleurisy
-emphysema
2)syndrome of airway obstuction
3)Pleuropneumopathy
-Cough
-Breathlessness
-Chest pain
Possible _pneumothorax
_Pleurisy with pleural effusion
4)syndrome of solid lung, consolidation and atelectasis

Approach to a patient with dyspnoea

Dyspnea _breathlessness inappropriate to level physical exertion occurring at rest
Variety of perceptions of difficulty or distress related to the breathing
Considered symptomatic when it occurs in inappropriate circumstances
Pathophysiologic condition related to dyspnea
Ventilatory requirement
Rate of ventilation needed to support the total body oxygen consumption and carbon dioxide
production
Dictated by metabolic factors
Level of exercise
Efficiency of ventilation
Ventilatory capacity
Ability to breath
Reduced by lung disease
Extra pulmonary process
Thoracic compression
NM disease
The ventilatory effort needed to meet these requirements may be increased by abnormal lung
mechanics on respiratory muscles fatique
Clinical condition presenting with dyspnoea
Onset may be dramatic, acute or chronic
Dramatically sudden _pneumothorax
_Pulmonary embolism
_Pulmonary edema
Acute over hours _pneumonia
_Acute pulmonary infiltration
_Allergic alveolitis
_Asthma
_Left ventricular
Subacute over days
-Pleural effusion
-Bronchogenic carcinoma
-Subacute pulmonary infiltration _sarcoidosis
Chronic over months or years
-Chronic airflow obstruction
-Diffuse fibrosing conditions
Chronic non pulmonary causes;-anemia
-HTN
Intermittent ;-episodic breathlessness
-Asthma
-Left ventricular failure
Classification of acute breathlessness by the grade of severity
I _able to do housework or job without difficulty
II a- confined to bed or chair but able to get up with moderate difficulty
B –confined to chair /bed but only get up with great difficulty
III -totally confined to chair or bed
IV- Moribund
Clinical condition presenting with dyspnoea
I)Obstructive air flow diseases
Characterized by decrease expiratory flow rates for a given lung volume
There may be end expiratory hyperinflation _alteration of the position of respiration
_Increase inspiratory work
_Muscle fatique
Total ventilatory capacity is decrease despite increase in lung volume
Consequent mechanism
Decrease capacity
Increase requirement and effort
Symptomatically
-Initially exertional dyspnoea
-Episodic worsening from intercurrent URT
-Environmental irritants causing bronchoconstriction
Variability of airflow obstruction is particularly characteristic of asthmatics whose lung mechanism may
be entirely normal at the time of evaluation
Episodic dyspnoea due to broncho spasms may follow exercise or exposure to allergens
Lesser common airflow obstruction
-Tumor
-Aspirated foreign body
In larynx and trachea obstruction lesion cause inspiratory stridor
II)Interstitial lung diseases
Progressive exertional dyspnoea may precede clinical and radiologic findings
Altering in lung mechanics sensed through vagal or respiratory muscles alterents are probably
responsible for such early dyspnoea
Compromise of the pulmonary capillary bed due to interstitial disease reduces the total alveolo-capillary
interface with resultant hypoxemia and ultimately pulmonary HTN thus further contribution to
dyspnoea
Total ventilatory capacity reduces with increasing severity of he disease
III)Cardiovascular diseases
Left ventricular disfunction
Pulmonary edema
Compromised gaseous exchange
Arterial hypoxemia
Decrease cardiac output
Decrease oxygen supply during exertion _lactic acidosis
Additional process include
- Bronchial hyper reactivity
-Respiratory muscle weakness
-Increase dead space ventilation
Incriminated cardiovascular diseases
-Cardiomyopathy
-Valvular disorders
-Pulmonary HTN
Others – acute pulmonary embolism
_Coronary ischemia
IV)Neuromuscular weakness
Neurologic or myopathic diseases
Phrenic nerve palsy
V)Hyperventilation syndrome
Chronic or episodic hyperventilation of no apparent cause _hysteria
Treatment _psychotherapy
_Anxiolytics
Metabolic and other conditions _anemia
_Metabolic acidosis
Anemia _decrease blood oxygen carrying capacity
Lactic acidosis
_Incurrent at a lower level of exertion thereby increasing ventilator requirements
Metabolic acidosis
_ Increase ventilatory requirements
Hyperthyroidism with increase BMR
Clinical evaluation
History and physical exam
Establish acuity of symptoms
Determine level of exertion
Note _onset
_Character
_Severity of dyspnoea
Also identify language and cultural factors in the description of
Identify possible exacerbating factors
 -Environment
-Temporal
-Postural factors
Establish _cardiovascular origin
_respiratory
Common diagnostic test used in evaluation of Dyspnoea
Acute dyspnoea
Indicated in nearly all patients
Chest radiograph
Arterial blood gas analysis
Commonly indicated
Measurement of peak flow or spirometry
ECG
Reserved for selected patients (based on clinical suspicion )
Ventilation /perfusion lung scanning
Respiratory secretion analysis nb
Chronic dyspnoea
Indicated in most patients
Pulmonary function test(especially spirometry but also measurement in lung volume , diffusing
capacity , and arterial blood gases in selected patients)
Chest radiograph
Blood chemistries and HB concentration
Consider if initial evaluation is non diagnostic
Exercise testing
Reserved for selected patients (based on clinical suspicion )
-Bronchoprovocation testing
-Chest CT scanning
-Esophageal pH monitoring
-Thyroid function testing
-Echocardiogram
-Other cardiac imaging procedures
-Bronchoscopy
-Biopsy of lung tissue
Treatment
Underlying condition
Pharmacologic approach
Pulmonary rehabilitation

Approach to a patient with cough

Cough –important clinical symptom hence consultation
Most common respiratory symptoms hence most common morbidity related reason for an office visit
Plays important role in the life of a patient either beneficial or detrimental
Beneficial _defence mechanism preventing foreign body from entering the lower R.T
Indicator of and underlying pathological process that may be trivial to life threatening
Detrimental _mechanism of disease spread that is process builds up intra thoracic, pressure up to
300mmHgand expiration velocity up to 800km/h both high then necessary leading to complication that
may be _musculoskeletal
 _Torn chest muscle
_Rib fracture

Pulmonary _pneumothorax
_Pneumomediasternum
Cardiovascular and neurologic
-Dysrythmia
-Syncope
Protocol for the evaluation and treatment of chronic cough
Basic anatomy and physiology related to the symptom
Determine the intrinsic and extrinsic influences causing the symptoms
Identify the most common disease that cause the symptom
Clinically evaluate a patient with cough _history
_ _Physical findings
_Ancillary investigation
Developing an effective and cost effective strategy for treatment
Anatomy and pathophysiology
1)Cough reflex
Receptors _pulmonary location _nasal
_Glottis
_Tracheobronchial
_Cardiac
Extra pulmonary _nasopharyngeal
_Umbilical
_ Diaphragmatic
Respond to chemical and mechanical stimuli
Afferent pathways _vagus
_Trigerminal
_Glossopharyngael
_Phrenic nerve
Cough centre _medulla oblongata
Efferent pathways _phrenic nerve and diaphragm
_Spinal motor nerves
_Respiratory muscles
Vagus nerve _smooth muscle of bronchial tree
2)phases of cough
i)inspiratory phase
deep inspiration resulting in a high lung volume
glottis opens widely to enable rapid entry of large amounts of air into the lungs
ii)Compressive phase
closure of glottis
contraction of expiratory muscles
sudden opening of the glottis
iii)expiratory phase
clearance function of cough
removal of undesirable material from respiratory tract
coordinated movements of the glottis
respiratory muscles
tracheobronchial tree
the high pleural and intrathoraic produced during the inspiratory phase by contraction of
the expiratory muscles dynamically compress the tracheobronchial tree thus decrease the
cross-sectional area of air way maintains a high linear velocity for an effective cough
Various clinical situations that impair cough reflex include
NM disease _spinal cord transection
_Guillain-barre syndrome
_Amyotrophic lateral sclerosis
_Muscular dystrophy
_Poliomyelitis
_Myasthenia gravis
By impeding dynamic compression of the airways
Others_costochondritis
_Multiple rib fractures
_Acute surgical abdomen
CNS depression
-Drug over dose
-General anaesthesia
-CNS diseases
Air way obstructive disorders
-COPD
-Cystic fibrosis
-Bronchiectasis
-Central obstructing mass lesions
Differential diagnosis
Acute cough _last <3weeks with minor consequences
May be transient or indicative of a life threatening disorder
Most commonly _URT -viral or bacterial
-Common cold
May also reveal life threatening disorder
-Pneumonia
-Aspiration pneumonia
-Congestive cardiac failure
-Pulmonary embolism
Diagnostic protocol for evaluation of acute cough
1.when accompanied with rhinorrhea ,pharyngitis ,and nasal congestion, assume the cause to
be an URT infection
Further evaluation is usually unrevealing and not cost-effective
2.if facial pressure, headache, ear ache, or persistent nasal stuffiness is present, obtain sinus
roentgenograms (or CT) to detect sinusitis
3.if systemic symptoms are present with cough, obtain a chest roentgenogram .(pneumonia
aspiration, tumors, and pleural effusion , among others, can be diagnosed or strongly
suspected)
4.if there are: a)clinical findings suggestive of deep venous thrombosis(DVT);b) a dyspnea
hemoptysis, or pleuritic pain with a non diagnostic chest roentgenogram;c)coexisting risk
factors for DVT; or d)oxygenation abnormality unexplained by the chest roentgenogram ,
obtain a V/Q lung scan followed by non invasive studies of the legs for DVT.
5.when aspiration is strongly suspected, obtain a cineradiographic barium swallow
Chronic cough
-Post nasal drip
-Asthma
-GERD
-Chronic bronchitis
-Bronchiectasis
-Cough due to ACE
Miscellaneous condition
-TB
-Bronchogenic carcinoma
-Metastatic carcinoma
-Interstitial lung abcesses including sarcodiosis
Left ventricular failure
Pertussis
Cardiac pace making
Cerebral air embolism
Aspiration of the nasal septum broken off due secondary to cocaine use
Capsicum (hot pepper)exposure
Hodgkins disease
Anatomic diagnostic protocol for evaluation of chronic cough
1.perform a history and physical exam(PEX) for all patients
2.order a chest roentgenogram(CXR) for all patients
3.for patients who are active cigarette smokers, are exposed to environmental irritants , or are
taking an ACE inhibitor , no further studies should be ordered until the patient hs been
removed from the source of irritation or medication for at least 4weeks
4.subsequent studies depend on the results of the initial evaluation
a.if the history and PEX suggest postnasal drip syndrome , obtain a sinus roentgenogram and
allergy evaluation .
b.if the history, PEX, and CXR donot suggest an etiology , obtain a non specific pharmacological
bronchoprovocation challenge with methacholine or histamine (PFT)
c.if the history , PEx, CXR and PFT donot suggest an etiology, order test for gastroesophageal
reflux disease. If cineradiographic barium swallow is non diagnostic, perform 24-hour
esophageal pH probe monitoring
d.if the CXR is abnormal and consistent with infection or malignancy, perform expectorated
sputum studies, fiberoptic bronchoscopy or both
e.if the cause of cough has not been determined after the above studies, perform fiberoptic
bronchoscopy and cardiac studies as a last resort
5.the cause of cough is determined by observing the specific therapy eliminates cough as a
complaint. If the evaluation suggest >one possible cause, therapies are initiated in the same
sequence that the abnormalities are discovered. If the therapy helps but does not totally
eliminates cough, it is continued while additional specific therapies are given.
Therapy
Underlying disease should be categorized into
Antitussive therapy _control
_Prevent
_elimination
Protussive therapy _makes cough more effective
Antupitussive therapy – indicated when cough is _annoying
_irritative
Complication represents a real hazard
Specific therapy
Aetiology orientation
-e.g anti TB drug for TB
-anti allergic in allergic condition
-anti asthmatic
Non specific therapy
-Decrease cough frequency and severity
-Act on cough reflex
Protussive therapy
Makes cough more effective without increasing cough frequency
e.g hypertonic saline aerosol _bronchitis
amiloride _ cystic fibrosis
terbutaline in bronchiectasis
Approach to a patient with hemoptysis
Expectoration of blood usually signifies a condition that requires recognition and treatment
even if the condition may be self limiting
Also the severe pulmonary hemorrhage is a medical and surgical emergency
The clinical challenge range from the reassurance of an ambulatory patient with an alarming
but innocuous problem to the resuscitation of a drowning person
Some major clinical distinctions include _mild hemoptysis
_Pulmonary TB
_Lung cancer
_Bronchitis
_Idiopathic
Severe life threatening hemoptysis i.e bleeding 400- 600ml/24h
-Pulmonary TB
_ Bronchiectasis
-Lung cancer
 -Mycetoma
-Bronchitis
-Idiopathic
Because the lung is in effect a sheet of blood numerous injuries on either side of the alveolo-
capillary membrane can cause varying degrees of hemorrhage –hemoptysis
Capillary hemorrhage associated with pulmonary venous HTN commonly results in bloody
pulmonary edema in patients with congestive cardiac failure
Microvascular oozing reflects immunological mediated injury_ vasculitis
_Pulmonary renal syndrome
- Inhalation of irritants and fumes
-Drugs –penicillamine
Pulmonary capillaritis cause potentially treatable systemic diseases e.g
-Frequent _wegners granulomatosis
-Microscopic polyangitis
-SLE
Infrequent
-Primary capillaritis without systemic diseases
-Capillaritis associated with idiopathic pulmonary fibrosis
-Rheumatoid arthritis
-Scleroderma
-Mixed connective tissue diseases
-Henoch-schönlein purpura
-Behçet`s syndrome
-Autologous bone marrow transplantation
Diagnostic approach
History and physical exam establishing the setting in which the bleeding occurred
Subglottic origin is obvious hence airway upper airway bleeding
-Sinuses
-Nasal polyps
-Nasopharyngeal and laryngeal neoplasm
-GIT aspiration
Should also be considered (associated nausea and vomiting )
Radiologic studies
-Chest X-ray
-Apical cavitory lesions of TB
-Central mass lesions of carcinoma
-Focal consolidation _pneumonia
diffuse radiographic infiltration should suggest widespread aspiration of blood on microvascular
bleeding
other imaging procedures have complementary applications e.g bronchography _
bronchiectasis
CT scans
MRI _bronchogenic cyst
_Vascular etiologies of bleeding
 _Arterial aneurysms
Arteriography _ precise vascular source of bleeding for eventual surgery
Laboratory test
Complete blood count
Exam for expectorated sputum _gram
_Acid fast stain for mycobacteria
sputum cytopathology for neoplasm especially with suggestive radiologic abnormalities
-evaluate immune state of the patient
-search for associated systemic diseases
-Collagen vascular profiles
-Anti glomerular basement membrane
Spirometry and arterial blood measurements provide useful estimates of pulmonary reserve
and the physiologic impact of bleeding
Pulmonary – ventilation-perfusion scan to assess pulmonary embolism
Cardiac ultrasound to evaluate mitral stenosis
Routine otolaryngologic evaluate hemoptysis
Bronchoscopy with a fiberoptic bronchoscope is indicated in clinically significant hemoptysisand
enables diagnosis of _bronchial adenoma
_Bronchogenic carcinoma

Clinical condition
diaphragm