INTERNAL MEDICINE POSTING

THE RESPIRATORY SYSTEM

1.0 CHRONIC OBSRUCTIVE PULMONARY DISEASE
COPD is a disease state characterised by airflow limitation that is not fully reversible.

Aetiology
1. Cigarette: ↑ no of neutrophil granulocytes to release elactase and protease
: inactivate α1-AT
2. Infection: lead to exacerbation of disease
3. α 1-AT def: in normal, it act as protease inhibitor to inhibit proteolytic enzyme such as neutrophil elactase, which are
capable of destroying alveoli wall CT

Pathophysiology
There is ↑no of mucus secreting goblet cells in the bronchial mucosa, especially in the larger bronchi. In advance stage,
bronchi overly inflamed and there is presence of pus.
There is infiltration of the wall of bronchi with acute and chronic inflammatory cell, predominantly CD8+.
Squamous epithelium replace columnar sell, and scarring and thickening of the wall narrow the airway.
Initial inflammation of the smaller airway is reversible and will improve if smoking is stopped early. In later stage the
inflammation continue even if smoking is stopped.

Three mechanism has been suggested:

(a) Loss of elasticity and aveoli attachment of airway d/t emphysema
(b) Inflammation and scarring cause the small airway to narrow
(c) Mucus secretion block the airway

COPD consist of 2 disease:

Chronic bronchitis Emphysema
-persistent cough with sputum in at least 3 mth in at least 2 -Irreversible enlargement of the air spaces distal to terminal
consecutive yrrs bronchiole accompanied by destruction of their wall

Pathogenesis -4 types:
-initiating factor: tobacco smoke, air pollutant Centriacinar Proximal part of acini formed by respi
-lead to: bronchioles is affected with distal alveoli
(a) oxidative stress spared
(b)stimulate inflammatory cell and release of inflammatory Predominantly in heavy smoker
mediator Panacinar Acinar is uniformly enlarged
-airway lining fibrosis and ciliary dysfunctionprevent Assoc with α1-antitrypsin deficiency
mucus clearance and ↑ risk of infection Paraseptal/ Predominantly involve distal part
-mucous hypersecretion d/t hypertrophy of submucosal gland Dustal acinar Occur adjacent to fibrosis, pleura
-persistent inflammation Lead to spontaneous pneumothorax
Irregular Acinus is irregularly involved
Morphology Clinically insignificant
-chronic airway inflammation
-submucosal gland hypertrophy Pathogenesis
-goblet cell metaplasia -initiating factor: smoking, pollution, genetic predisposition
-narrowing of the bronchioles d/t mucous plugging, -lead to: oxidative stress, ↑ apoptosis and senescence
inflammation, fibrosis : inflammatory cell, release of inflammatory mediator
: protease- antiprotease imbalance (assoc with α1-AT
Clinical course Def)
-cough before dyspnoea with copious, purulent sputum
-blue bloater (bloated, plethoric, cyanosis): d/t renal hypoxia Morphology: voluminous lung overlapping the heart with
they retain fluid and ↑erythrocyte production lead to with large subpleural blebs
polycythemia
Histology: large, dilated alveoli separated by thin septa with
compressed respi bronchioles and vasculature

Clinical course: pink puffer (d/t overventilate and well

oxygenated), dyspnoea early then cough, weight loss

Clinical features
Symptom Sign
-productive cough with clear/ white sputum -mild- wheeze; severe-tachypnoeic with prolonged expiration
-wheeze/ breathlessness -responsive to CO2: breathlessness and rarely cyanosis
worsened by cold, foggy weather, atmospheric pollution Insensitive to CO2: no breathlessness but there is cyanosis
-systemic effect: HPT, osteoporosis, depression, weight loss, and oedema
reduced muscle mass
 Complication 1. Use of accessory muscle
1. Respiratory failure -eg. SCM, platysma, strap muscle of the neck
-occur when P02<60mmHg and PCO2>55mmHg -Cause elevation of the shoulders with inspiration & ↑
-chronic alveoli hypoxia and hypercapnia lead to constriction chest expansion
of pulmonary arterioles and hypertension
2. Contraction of abdominal muscle during expiration in
2. Cor pulmonale
pt with obstructed airway
-pulmonary HPT, RVH 3. In drawing of intercostals &supra clavicular spaces
-renal hypoxia lead to salt and water retention during inspiration
-central cyanosis and peripheral edema 4. pursed lip
-to provide continuous +ve airway pressure & to prevent
3. Pulmonary HPT airway collapse during expiration
5. leaning forward with arms on their knees
- to compress their abdomen & push diaphragm upward
6. Trachea tug (downward displacement of trachea
during inspiration)
-d/t ↑ diaphragmatic movement
7. Poor chest expansion

Diagnosis, Investigation and Management

Diagnosis Management
-clinical based 1. Lifestyle modification- smoking cessation
-breathlessness and sputum production 2. Bronchodilator
-look at family history for α1-AT -mild: SABA (salbutamol)
-severe: LABA (formoterol, salmeterol)
Investigation -anti- muscarinic: tiotropium, ipratropium
1. Lung function test 3. Bronchodilator
-normal TLC but d/t impaired expiration there is ↓VC and -prednisolone 30mg daily for 2 week, with measurement of
↑RV lung function before and after
shud be replaced by inhaled corticosteroid (beclometasone)
2. CXR, CT when there is improvement
-overinflation of the lung with large bullae 4. Antibiotic
-flattened diaphragm -give ASA sputum turn green and yellow
-help to eradicate infection and keep LRT free of bacteria
3. Hb level 5. Antimucolytic agent
-polycythemia -reduce putum viscosity
6. Diuretic therapy
4. Blood gases -for edematous pt for RVF 2nd to Cor pulmonale
-in advance cases, there is resting hypoxemia and hypercapnia 7. Oxygen therapy
-improved survival with continuous administration of oxygen
5. Sputum examination at 2L/ min via nasal prong t achieve O2 stauration of > 90%
-not useful as usual exacerbation usually cause by strep. Pneu 8. Pulmonary rehabilitation
and H. influenza -exercise training can diminish sense of breathlessness
9. Vaccine
6. ECG -pneumococcal polysaccharides and influenza
-Tall P wave (pul HPT), R>S in RVH 10. α 1-AT replacement
11. Air travel –advise to contact their airline for
7. Echo supplemental oxygen during flight
-assess cardiac function 12. Surgery
(a) Surgical bullectomy: enable adjacent collapsed lung
Nocturnal hypoxia to re- expand and start functioning again
-occur in pt with COPD when they r sleep d/t REM inhibit (b) Lung volume reduction surgery: increase elastic
intercostals and accessory muscle, shallow beathing ↓ recoil and enable diaphragm to work at better
ventilation and ↑ upper airway resistance mechanical condition
-lead to arousal of sleep (c) Single lung transplantation-for end- stage
-Management: X give sleeping tablets emphysema
: administer tight fitting nasal mask and bilevel 13. Management of Respiratory failure in COPD
+ve airway pressure (provide inspiratory and -oxygen therapy, removal of retained secretion
expiratory assistance) (physiotherapy, bronchoscopy, endotrachea tube), respiratory
support
2.0 BRONCHIECTASIS
Defintion Treatment
Abnormal and permanently dilated airways with inflamed, 1. Postural clearance: pt trained to tip themselves so that
thickened and irreversibly damaged bronchial wall affected lobes are uppermost at least 3 times daily for 10-
20 min
Aetiology 2. Antibiotic
1. Congenital: cystic fibrosis, primary ciliary dyskinesia, -cefaclor 500mg 3 times daily/ ciprofloxacin 500mg
Kartagener syndrome twice daily
2. Infection: necrotising pneumonia -if persistent despite regular
3. Bronchial obstruction: tumour, foreign body, mucous physiotherapyPseudomonas aeruginosaIV,
impact inhalation ceftazidime 2g
4. Others: RA, SLE, IBD, COPD, post- transplant 3. Bronchodilator
-for pt with airflow limitation
Pathogenesis 4. anti- inflammatory agent
Bronchial obstructionimpaired normal clearance 5. Surgery: rare, but if required resection and transplantation
mechanismpooling of secretion distal to obstruction2nd
infection and inflammationdestruction of supporting Complication
smooth muscle & elastic tissue and fibrosisdilation of -pneumonia
airways -pneumothorax
-empyema
Clinical feature -metastatic cerebral abscess
-mild: yellow, green sputum after infection -haemoptysis (d/t ↑pressure bronchial artery)
-moderate:halitosis (bad breath), febrile episode, pneumonia,
clubbing, coarse crackles Prognosis
-severe: foul- smelling, thick, khaki (brownish yellow) -greatly improved by antibiotic but pt may developed
coloured sputum respiratory failure/ cor pulmonale

Investigation
1. CXR, CT: dilated bronchi with thickened wall, multiple
cysts containing fluid
2. Sputum examination: staph. Aureus, pseudomonas
aeruginosa, H. influenza
3. Sinus X ray: to check for rhinosinusitis
4. Serum Ig: as 10% pt has Ab class/ subclass def
5. Sweat electrolytes: if cystic fibrosis is suspected
6. Mucociliary clearance
3.0 ASTHMA
Asthma is reversible chronic inflammatory disorder of the airway where is there episodic bronchoconstriction d/t airway
hyperresponsiveness to noxious stimuli.

Classification
Extrinsic asthma Intrinsic asthma
-most common -no evidence of allergen sensitization
-occur in atopic individual -less common +ve family history
-immune mediated type 1 hypersensitivity -serum IgE normal
-usually begin in the childhood, triggered by environmental -eg.
allergen (a) Drug induced asthma
-assoc with allergic rhinitis, eczema- atopy -aspirin sensitive asthma where aspirin inhibit
cyclooxygenase pathway of arachidonic metabolism that
produce prostaglandin and switch the entire pathway to
produce leukotreine
(b) occupational asthma: triggered by fumes, organic and
chemical dust, toluene, formaldehyde

Aetiology
1. Atopy 2. Occupational sensitizer
-characteristic: run in families, have wealing skin reaction to -LMW: eg. reactive chemical (bond chemically to epithelial
common allergen in the environment, have IgE cell to activate them as well as provide hapten recognized by
-genetic: T cell
(a) gene controlling production of cytokine -HMW: eg. flour, organic dusts involving IgE entibodies
(b) novel asthma gene (SETDB2, RCBTB1) implicated in IgE
synthesis 3. Cold air and exercise
(c) ADAM33 assoc with airway hyperresponsiveness and -exercise induced wheeze triggered by histamine, Pg, Lt
tissue remodelling
-environment 4. Atmospheric pollution and irritant dusts
hygiene hypothesis: growing up in relatively clean -experience worsening of symptom
environment may predispose towards an IgE while growing
up in dirtier environment can allow the immune system to 5. Diet
avoid developing allergic reaction (as component of bac, -↑ intakes of fresh fruit and vege have been shown to be
virus, fungi will stimulate toll like receptor will direct protective, d/t ↑ intake of antioxidant and flavonoids
immune response from allergic to protective)
6. Drugs
-NSAIDS: COX inhibitor which lead to ↑ synthesis of lt by
eosinophils, mast cell, macrophages
-B blocker: direct PNS that tend to produce
bronchoconstriction

Pathogenesis
-Type I (IgE mediated) hypersensitivity reaction
-exaggerated Th 2 response to normally harmless environmental antigen in genetically predisposed individual which release
several cytokine to stimulate B cell to produce IgE
(a) IL-4: stimulate production of IgE
(b) IL-5: activate eosinophils
-IgE bind to Fc receptor on submucosal mast cell
-Repeated exposure trigger mast cell to release granules content to produce cytokine and other mediator
(a)Leukotriene C4, D4, E4: bronchoconstriction and vascular permeability
(b) Histamine: bronchoconstriction
(c) prostaglandinD2: bronchoconstiction
(d)PAF: plt aggregation, release serotonin
-lead to:
(a) Immediate reaction: bronchoconstriction, vasodilation, ↑ vascular permeability, ↑ mucous production
(b) late reaction: recruitment of leukocytes (eosinophil, neutrophil, Tcell )

Investigation
1. Lung function test 4. Trial of corticosteroids
(a) Peak expiratory flow rate: on walking, prior to taking -prednisolone 30mg orally daily for 2 weeks with measure
a bronchodilator, before bed after a bronchodilator before and immediately after the course
for long term assessment of pt’s disease substantial improvement in FEV1 indicate there is
(b) Spirometry: asthma can bediagnosed by demonstrate reversible and inhaled steroid is beneficial
 >15% improvement in FEV1 following
bronchodilator 5. Blood and sputum tets
2. Exercise test: useful for children (run for 6min at -eosinophilia
workload sufficient to ↑ hr> 160bpm)
 Indirect test that induce release of endogenous 6. CXR
mediator which then cause bronchoconstriction -overinflation
3. Bronchial provocation test
-test for bronchial hyperresponsiveness 7. Skin test
-ask pt to inhale gradually increasing concentration of -identify allergic trigger factor
histamine to induce transient airflow limitation insusceptible
individual

Treatment
Type Example MOA S/E
Bronchodilator
1. B agonist -bind to B adrenoreceptor to activate CVS: tachycardia, tremor, palpitation
SABA Salbutamol, adenyl cyclase which convert ATP to MSK: tremor
terbutaline CAMP
-↑CAMP: ↑ bronchodilation,
LABA Salmeterol, microciliary function, block release
formoterol of mediator

2. Methylxanthine Theophylline -block phosphodiesterase that convert >20mg: GIT: anorexia, nausea, vomiting
(oral) CAMP to 5-AMP : CNS: headache, anxiety
Aminophylline - ↑CAMP: ↑ bronchodilator, >40mg: CNS: convulsion
(IV) microciliary function, block release : CVS: serious arrhhthmia
of mediator -low therapeutic index
3.Muscarinic Ach + muscarinic -administration route only by inhalation,
antagonist receptorbronchoconstriction and ↑ hence less systemic side effect
SAMA Ipratropium mucus
bromide Muscarinic antagonist competitively
LAMA Tiotropium inhibit MR bronchodilation and ↓
bromide mucus
Anti- inflammatory agents
1. Corticosteroid Beclomethasone 1. Effect on inflammatory Inhalation-local effect (sorethroat, voice
Budesonide mediators hoarseness, oral candidiasis)
Fluticasone -inhibit phospholipase enzyme lead
to ↓ PG, LT Oral/ parenteral-systemic (cataract,
adrenal suppression, Cushing like
2. Effect on inflammatory cell syndrome)
-inhibit neutrophil and eosiniphil
migration
-release macrophages proteolytic
enzyme

3. ↑ effect on B agonist agent

-does not relax airway SMC (as this
job is done by bronchodilator)
-but can ↓ bronchial reactivity and
cause contraction of engorged vessel
in bronchial mucosa to reduce
swelling
2. Mast cell Cromolyn Block Ca influx↓ mast cell PK: inhalation
stabilizer Necrodomil degranulation Hence s/e is local
sodium -cough, throat irritation, dry mouth,
paradoxical bronchospasm

recommend in children and pregnancy

3. Lt Receptor Montelukast, Block LT cysteine type receptor -cough
Antagonist Zafirlukast ↓ bronchus inflammation, ↓ mucus -headache
PK: oral secretion, bronchodilation -dyspepsia
-M>Z as M is -sleep disorder, neuropsychiatric
taken without symptom
regards to meal -hepatotoxicity (rare)
 and also once-a-
day tx
4. Lt synthesis Zileuton -inhibit 5-lipooxygenase enzyme to -cough
inhibitor prevent leukotriene synthesis -headache
PK: oral -dyspepsia
-sleep disorder, neuropsychiatric
symptom
-hepatotoxicity!!!-least prescribe
5. Omalizumab -humanized monoclonal Ab which Viral infection, URTI, injection site
PK: SC every 2-4 bind to free IgE to interrupt the signal reaction
weeks that may trigger the allergic
inflammatory cascade

Status asthmaticus
Severe attack of asthma d/t poorly responsive to adrenergic
agents

Management
-oxygen
-bronchodilator ( salbutamol, ipratropium bromide)
-magnesium sulphate (relax SMC)
-IV theophylline
-steroid
4.0 PNEUMONIA
Pneumonia is defined as inflammation of the substance of the lungs.

Classification:
Type Example
Site of spread 1. Community acquired pneumonia
-infection of lung parenchymal in pt who have acquired the infection in the community/
<48hrs of admission to hospital
-common etiological agent:
(a) Typical: Strep pneumoniae, Staph. aureus, H. influenza, Klebsiella pneumoniae,
Moraxella catarrhalis
(b) Atypical: mycoplasma pneumoniae, chlamydophila pneumonia, chlamydophila
psittaci, legionella pneumophila, coxiella burnetti
-Risk factor:
(a) Age: <16 or >65 y/o
(b) Co-morbidities: HIV, DM,CKD, recent viral respiratory infection
(c) Other respi condition: cystic fibrosis, bronchiectasis, COPD, obstructing lesion
(d) Lifestyle: cigarette, alcohol,IVDU
(e) Iatrogenic: immunosuppressant therapy

2. Hospital acquired pneumonia

-new episode pneumonia develop 48hrs/ > after admission to hospital and did not appear
to be incubating at the time of admission
-common etiological agent: gram –ve bac (pseudomonas, E.coli, klebsiella), anaerobic
(enterobacter), staph. Aureus including MRSA, acinetobacter
-predisposing factor: ↓immune system, ↓cough reflex, disordered mucociliaray clearance,
bulbar and vocal cord palsy, immobility and ↓conscious level, vomiting, dysphagia,
achalasia, reflex, nasogastric tube, endotracheal tube, dental and sinus infection,
abdominal sepsis, IVC, infected emboli

3. Ventilator associated pneumonia

-HAP that develop 48-72 hrs after intubation
Morpholgy 1. Bronchopneumonia: patchy consolidation of lung d/t extension of infection frm
bronchioles to the lung (most common org: strep. Pneu, H. influenza; affect extreme
ages and debilitated)
2. Lobar pneumonia: fibrinosupurative consolidation of a large portion of the lobe/
entire lobe of the lung (involve more virulent bacterium; affect fit as well as extreme
age and debilitated)
Etiological type 1. Infective: viral, bacterial, fungal, TB
2. Non- infective: toxins, chemical, aspiration
Clinical Typical Atypical
-sudden onset -gradual onset
-high fever -low- grade fever
-productive cough -non- productive cough
-dyspnoea -dyspnoea
-sweat, rigor, pleuritic chest pain, -constitutional symptom
hemoptysis, tachypnoea, tachycardia, -CXR: diffuse bilateral pulmonary
rhonchi, toxic appearance infiltrate
-CXR: lobar/ lobular opacity
-↑WBC
Duration Acute and chronic

Pathophysiology
Interference of local defense mechanism Interference of systemic resistance
1. Loss/suppression of cough reflex 1. Defect in innate immunity: assoc with pyogenic bacterial
-in coma, anaesthesia, NMJ disorder, drug infection
-lead to aspiration of gastric content 2. Defect in CMI: assoc with intracellular microbes,
2. injury to mucociliary apparatus microorganism of low virulence
-cause: cigarette smoke, inhalation of hot or corrosive gas
- impaired ciliary function/ destruction of ciliary apparatus
3. Accumulation of secretion
 -cystic fibrosis, bronchial obstruction
4. Interference of bactericidal action of alveolar macrophages
-in alcohol, tobacco smoke, anoxia and oxygen intoxication
5. Pulmonary congection and edema
Sign and symptom
Symptom (HT) Sign (PE)
1. Cough 1. Inspection
-initially dry, short and painful -reduced movement of chest wall on side of consolidation
-later productive with mucopurulent sputum -intercostal recession and use of accessory muscle
-color of sputum: usually yellowish/ greenish
-sometimes hemoptysis 2. Palpation
-rusty color (reddish brown): seen in pneumococcal -normally centrally located; if shift to same side indicate
pneumonia collapse consolidation
2. Fever -↑tactile fremitus
-high grade: bac
-low grade with evening ↑ temperature: TB 3. Percussion: dull
3. Pleuritic chest pain 4. Ascultation
-dull aching chest pain on breathing -bronchial breath sound @ area of consolidation
4. SOB -coarse crepitation
-indicate extent of consolidation and underlying aetiology -↑ vocal resonance
5. Non specific symptom -rhonchi (indicate endobronchial narrowing/ obstruction),
-headache, vomiting, loss of apetite pleural rub
6. Generalised fatigue: common in acute bacterial infection -pleural rub (consolidation extend to lund periphery)
7. Aspiration: ask for any foreign body aspiration/ vomiting
that cause pneumonia

Investigation and assessment

Investigation Assessment (CURB-65 score)
1. FBC C: confusion present
-neutrophilic leukocytosis (bacterial pneumonia) U: plasma urea level>7mmol/L
-very high/ low (severe case) R: RR>30/ min
2. Renal profile B: systolic BP <90mmHg, diastolic BP <60mmHg
-severity 65: age>65
3. LFT
4. ABG 1 point for each
-early stage: hypoxia and hypocapnia (↑RR)
-late stage: hypoxia and CO2 retention 0-1 Outpatient
5. CRP: ↑ 2 Admit to hospital
6. Sputum culture and antibiotic sensitivity 3+ ICU
-strep. Pneumonia: gram +ve diplococcic ↑score, ↑mortality
-staph. Aureus: gram +ve cocci in chain
-Ziehl Neelsen stain
7. Blood culture: +ve in pneumococcal
8. CXR
-consolidation (lobar/ broncho)
-complication: parapneumonic effusion, intrapulmonary
abscess formation for empyema
9. CT
-detect presence and exact location of consolidation
-look for endobronchial obstruction d/t foreign body/ tumor

Management
1. Oxygenation
-maintain saturation btw 94%-98% provided the pt X CO2 retention

2. IV fluid
-required in hypotensive pt
-consider in those with severe illness, older, vomiting otherwise adequate oral intake should be encouraged

3. Antibiotics
-administered within 4hrs of presentation in hospital
-treatment should not be delayed while investigation are awaited
-parenteral antibiotic should be switched to oral once temperature settle for 24 hrs
-if pt fail to response, alternate diagnosis is considered (eg. MRSA), resistant organism, resistant infection, TB,
immunocompromised, development of complication, pre- existing lung disease
-antibiotic must be adjusted specifically once culture and sensitivity result are advailable
-Regime use

(a) HAP: Tazocin (Piperacillin+Tazobactam)

(b) HCAP: Cetriazone (3rd generation cephalosporin) and azithromycin (macrolides)
(c) CAP: Augmentin (Amoxycillin+Clavulanate) and azithromycin(macrolides)

4. Chest physiotherapy
-assist expectorant in pt who suppress cough because of pleural pain or when mucus plug lead to bronchial collapse

5. Inotropic agent and mechanical ventilation may required

6. Isolation
-in this emerging and challenging new disease eg. SARS, H1N1, it is important to consider isolation if airborne or droplet
infectious cases are diagnosed

Prognosis
Most pt respond promptly to antibiotic therapy (fever may last for several days and CXR take several weeks/ mth to resolve
especially in old age). Delayed recovery suggest either that a complication has occurred or diagnosis is incorrect
1. Para- pneumotic effusion
-develop if consolidation is up to the lung periphery (reactive pleural effusion)/ if pneumonia is cause by highly virulent
organism.
-usually small in qty and resolve following appropriate Ab treatment, rarely the fluid may increase in qty and may get
secondarily infected

2. Empyema
-Presence of pus in pleural cavity
-Clinical feature: very ill, high fever, neutrophil leucocytosis

3. Sepsis
4. Atelectasis d/t secretion cause bronchial passage resulting in collapse- consolidation
5. Lung abscess
-result from localized suppuration of the lung assoc with cavity formation
-usually following staph/ gram –ve bacterial infection
-clinical feature: persisting, worsening pneumonia, copious foul semlling sputum
6. Respiratory failure
7. DVT, PE
8. Pneumothorax
9. ARDS, RF, multi organ failure
10. Ectopic abscess formation
11. Hepatits, pericarditis, myocarditis, meningoencephalitis
12. Recurrent pneumonia
13. Non- resolving pneumonia

4.1 ASPIRATION PNEUMONIA

-d/t aspiration of gastric content into the lung can produce extremely severe and fatal illness owing to intense destructiveness
of gastric acid.
-usual site at right middle lobes and apical/ posterior segment of the right lower lobes
???
5.0 TUBERCULOSIS
TB is caused by 4 main mycobacterial sp. Termed MTb. (M. tuberculosis, M. bovis, M. africanum, M. microti). Which is acid
fast bacilli

Pathogenesis
1. Route of entry: airborne infection
2. Primary TB:
-once inhaled, bacterium ingested by alveolar macrophages and proliferate in it, causing the release of neutrophil
chemoattractant and cytokines, resulting in inflammatory cell reaching the lung
-macrophages present the Ag to T lymphocytes
-Delayed hypersensitivity reaction (Type IV) occur where TH1 response produces IFN-gamma that activae macrophages to be
bactericidal as well as to differentiate into epithelioid cell, which will fuse forming Langerhand giant cell
-Formation of granuloma which consist of caseous necrosis surrounded by epitheloid cell and Langerhand giant cell with
multipl nuclei, both derived frm macrophages.
-Subsequently, the caseated area heal completely and many become calcified. Some of these nodule contain bacteria which are
contained by immune system and dormant for many yrsGhon focus (CXR: small calcified nodule often within the upper
parts of the lower lobes or lower part of the upper lobes.
3. Latent TB
-within 2-8 weeks, special immune cells called macrophages ingest and surround the tubercle bacilli. The cells form a barrier
shell, called a granuloma, that keeps the bacilli contained and under controlled
4. Reactivation TB
-if the immune system cannot keep the tubercle under control, the bacilli begin to multiply rapidly (TB disease). This process
can occur in different areas in the body, eg. lungs, kidney, brain, bone

Type of TB
1. Pulmonary TB
-productive cough, haemoptysis, weight loss, fever, night sweat, hoarseness voice (if laryngeal nerve is involved), pleuritic
pain
-CXR: consolidation with/ without cavitation
(a) Primary TB: in previously unexposed person (at lower part of upper lobes and upper part of lower lobes)
(b) Secondary TB: in previously sensitized host, may arise yrs after primary infection ( when host’s immune system is
weakened (at apex of upper lobes of 1 or both the lungs)

2. LN TB
-extrathoracic nodes are more common
-usually present as firm non- tender enlargement of cervical/ supraclavicular node which necrotic centrally and can liquefy
-the overlying skin is frequently indurated and thee can be sinus tract formation but characteristically there is no erythema

3. Miliary TB
-when org drain through lymphatics entering the venous blood and circulating back into the lung
-feature: microscopic and small foci of yellow- white consolidation through the lung parenchyma
-lead to pleural effusion, empyema, fibrous pleuritis

4. Others
-endobronchial, endotracheal, laryngeal TB
-lymphadenitis
-isolated TB (eg. TB meningitis, Renal TB, Addison disease, osteomyelitis, Pott disease, Salpingitis)

Risk factor
1. Contact with high- risk groups 3. Lifestyle factor
-originated/ frequent travel to high incidence areas -drug/ alcohol misuse
-homelessness/ hostel/ overcrowding
2. Immune deficiency -prison inmates
-HIV infection
-corticosteroid/ immunosuppressant therapy 4. Genetic
-chemotherapeutic drugs
-nutritional deficiency
-DM
-CKD
-Malnutrition/ body weight too low
HT and Lab investigation
HT (c) PCR with nucleic acid amplification: differentiating btw
1. Cough-duration > 2 weeks, dryproductive MTb and non-TB bacterial and identify TB in smear –ve
2. Fewer-low grade sputum specimen (but culture and stain is still necessary as
3. Night sweat-usually drenching PCR only useful at initial state because it will remain +ve
4. Haemoptysis in advanced cases d/t bronchiectasis despite after treatment)and identiry drug resistance
5. Pleuritic chest pain
6. Dyspnoea 3 CXR
7. Constitutional syndrome: LOW, LOA (a) Primary dz
8. Symptom of extrapulmonary TB -Parenchymal dz: dense homogenous consolidation at lower
-Renal TB: hematuria part of upper lobe and upper part of lower lobes, lobar/
-TB Meningitis: headache and confusion segmental atelectasis (segmental collapse)
-TB spine: back pain -lymphadenopathy-mediastinal hallmark of priTB, typically
-TB larynx: hoarseness unilateral and rt side
-pleural effusion: unilateral
Lab investigation -military disease: involve both lung with slight lower lobes
1. Mantoux test (Tuberculin Skin Test) predominance
-indicated in delayed hypersensitivity reaction after injection (b) Post-primary disease
of purified protein derivative (PPD) -Parenchymal disease:
-look at induration (raised formation) patchy heterogenous consolidation usually at apex
-+ve result: poorly defined linear and nodular opacities
(a) >6mm: in non vaccinated adult involved > 1 pulmonary segment
(b) >15 mm in BCG vaccinated adult cavitation is hallmark of reactivation within consolidation
with air- fluid level
2. Microbiological diagnosis tuberculoma (0.5-4cm well defined density)
-sputum AFB, Mycobacterium culture with drug -Lymphadenopathy: uncommon
susceptibility -Pleural effusion: less frequently, unilateral and septated
-pleural tapif pleural effusion -airway involvement: bronchial stenosis lead to lobar collapse
(a) stains: Auramine rhodamine stain, Ziehl Neelsen stain and hyperinflated lung field, traction bronchiectasis in upper
(b) culture: Lowenstein Jensen agar, Middlebrook agar (as lobes
liquid/ broth culture take shorter time than solid culture)

Management
2HRZE/ 4HR or 6HE: 2 month of HRZE (daily or three times a week) for initiation phase and 4 mth of HR or 6 mth of HE
(daily or three times a week)

2HRZS/ 4HR or 6HE: 2 month of HRZS (daily or three times a week) for initiation phase and 4 mth of HR or 6 mth of HE
(daily or three times a week)

-combination: avoid resistance & shortened period of treatment

Type and class MOA and clinical indication S/E
Isoniazide -inhibit mycolic acid synthesis (essential part of -hepatitis
-bactericidal mycobacterium cell wall) -peripheral neuropathy (d/t ↑ excretion
-inta/ extrac -used in: of pyridoxine)
-structurally similar to (a) active TB: combination -allergic: fever, skin rash, SLE
pyridoxine (b) latent TB: single
Rifampin -bind to DNA dependent RNA polymerase to inhibit -orange coloration
-bactericidal RNA synthesis -hepatitis
-intra/ extra -used in: -P450 induction
(a) Active TB: combination
(b)Leprosy: +dapsone
(c) prophylaxis for TB
Pyrazinamide -converted by pyrazinamidase to pyrzinoid acid to -arthralgia
-Bactericidal produce intracellular acidic environment (disrupt -gout (compete with uric acid for
-inta cell membrane metabolism and transport) excretion lead to hyperuricemia)
-hepatotoxicity
Etambutol -inhibit arabinosyl transferase that catalyse Optic neuritis
-bacteriostatic polymerization of arabinoglycan C/I: children (too young for assessment
of visual acuity) and diabetic
 retinopathy
Streptomycin -inhibit protein synthesis by binding to 30s -nephrotoxicity
-extracellular ribosomal subunit -ototoxicity
-vertigo, Hearing loss
C/I: pregnant
6.0 PLEURAL EFFUSION
Pleural effusion is fluid in the pleural space
(a) Haemothorax: blood
(b) Empyema: pus
(c) Chylothorax: chyle
(d) Haemopneumothorax: blood and air

Cause
Transudate Exudate
-protein <30g/l -protein>30g/l
-LDH< 200IU/l -LDH >200IU/l

Cause: Cause
-↑ venous pressure ( cardiac failure, constrictive pericarditis, d/t ↑leakiness of pleural capillaries 2nd to malignancy,
fluid overload) infection and inflammation
-hypoproteinemia (cirrhosis, nephritic syndrome, -pneumonia, TB
malabsorption) -pulmonary infarction
-hypothyroidism -RA, SLE
-Meigs’ syndrome (rt PE + ovarian fibroma) -CA( bronchogenic carcinoma, malignant metastasis,
lymphoma, mesothelioma, lymphangitis carcinomatosis

HT Lab investigation
-asymptomatic OR CXR
-dyspnoea -small effusion: blunting of costophrenic angle
-pleuritic chest pain (sharp and made worse by deep -large effusion: water dense shadow with concave upper
inspiration) border
: +concurrent pneumothorax completely
PE horizontal upper border
-Palpation: ↓ chest expansion Ultrasound: useful in identify pleural effusion and guide
: tracheal deviation (away from site of lesion) diagnostic or therapeutic aspiration
-Percussion: stony dull
-Ascultation: diminish breath sound Diagnostic aspiration
: bronchial breathing (d/t compression of lung) -percuss the upper border of pleural effusion and choose a site
-look for aspiration mark and sign of assoc disease 1-2 intercostal space below it (don’t go beyond abdomen)
-infiltration down pleura with LA-lidocaine
-attach a 21G needle to a syringe and insert it at just upper
border of appropriate ribs
-draw 10-30ml of pleural fluid and send it to lab for clinical
chemistry, bacteriology, cytology, immunology

Pleural biopsy
-using Abram’s needle guided by thorascopic and CT guided

Management
-chest drainage using diagnostic tic tap or intercostals drain
-pleurodesis (obliteration of pleural cavity)for recurrent
effusion
-surgery: persistent collection and increasing pleural thickness
7.0 EMPYEMA
-presence of pus in the pleural space
-should be suspected if a pt with resolving pneumonia develop recurrent fever
-on diagnostic aspiration: pleural fluid typically yellow and turbid with pH <7.2, ↓glucose and ↑LDH
-treatment: drained using chest tube under radiological guidance

8.0 PNEUMOTHORAX
Pneumothorax is the presence of air in the pleural space

Aetiology Clinical feature

-spontaneous d/t rupture of subpleural bulla (especially in Symptom
young men) -asymptomatic (especially if fit, young, small pneumothorax)
-other cause: asthma, COPD, TB, pneumonia, lung abscess, -sudden onset of dyspnoea and pleuritic chest pain
carcinoma, cystic fibrosis, lung fibrosis, sarcoidosis, CT -sudden deterioration of asthma and COPD
disorder (Marfan’s, Ehlers-Danlos), trauma, iatrogenic -mechanically ventilated patient may present in hypoxia
(subclavian CVP line insertion, pleural insertion or biopsy,
transbronchial biopsy, percutaneous liver biopsy, +ve Sign
pressure ventilation -Palpation: ↓ lung expansion
: tracheal deviation (away from)
-Percussion: hyper- resonance
-Ascultation: diminish breath sound

Clinical approach
1. Chest tube insertion and drain
(a) Indication
1. Pneumothorax-ventilated, tension, persistent,recurrent or large 2nd spontaneous pneumothorax (if>50y/o)
2. Malignant pleural effusion
3. Empyema or complicated parapneumonic effusion
4. Traumatic haemopneumothorax
5. Air transfer
6. Post- operatively (thoracotomy, oesophagectomy, cardiothoracic surgery)
(c) Complication
-thoraco and abdominal organ injury
-lymphathic damage, eg. chylothorax
-damage to long thoracic nerveBell wing scapula
-arrhythmia

(d) Watch out for

-retrograde flow back into the chest
-persistent bubblingthere may be a continual leak from the lung
-blockage of the tube from clots or kinking- non swinging or bubbling
-malposition (check using CXR)

(e) Removal
-considered when the drain is no longer bubbling and CXR shows re- inflation
-give analgesia beforehand
-smart withdrawn during expiration or Valsava (forceful attempt expiration through a closed airway)
-close the hole immediately with the pre- placed suture

2. Aspiration
-identify 2nd intercostals space mid- clavicular line/ 4-6th intercostals space in the midaxillary line
-infiltrate with 1% lidocaine down to pleura overlying the pneumothorax
-insert IV cannula into the pleural space. Remove the needle and connect the cannula to a 3- way tap and 50ml syringe.
Aspirate up to 2.5L of air. Stop when resistance is felt/ if pt cough excessively
-Request CXR to confirm resolution of pneumothorax. If successiveful, consider discharging the pt and repeat CXR after 24hrs
to exclude recurrence and again after 7- 10 days
-Avoid air travel for 6 weeks and diving for permanently

Tension pneumothorax
occur when vulvular mechanism is developed which air can be sucked into the pleural space during inspiration but not expelled
during expiration. Hence, intrapleural space remain +ve throughout breathing and lund deflates more. The mediastinum shift,
VR to heart ↓ and cardiac embarrassment.

Symptom: acute respiratory distress, chest pain, respiratory arrest

Sign: hypotension, distended neck veins, asymmetrical lung expansion, tracheal and apex deviated away from the site,
hyperresonance to percussion

Clinical approach
1. 100% oxygen
2. Insert a large bore IV cannula usually through 2nd intercostals space in the mid- clavicular line or safety triangle for chest
drain insertion. Then remove the stylet which allow thetrapped air to escape, usually with audible hiss. Tap securely
3. Proceed to formal chest drain insertion

9.0 MEDIASTINAL LESION

-Lesion in region btw pleural sac

(a) Retrosternal goitre: enlargement of the thyroid of colloid goitre, malignant dz, thyrotoxicosis can cause displacement of
trachea to the opposite side. Pt complaint of dyspnoea, dysphagia, hoarseness and vocal cord paralysis (d/t stretching of
recurrent laryngeal nerve)
(b) Thymic tumor (thymomas): enlarged by cysts (rarely symptomatic) or by tumor (myasthenia gravis)
(c) Pleuropericardial cysts: 70% situated anteriorly in the cardiophrenic angle on the rt side. Diagnosis by needle aspiration.
No treatment is required unless ↑ size then surgical excision.

10.0 COR PULMONALE

Rt heart failure d/t chronic pulmonary arterial hypertension.

Cause of cor pulmonale

1. Lung disease 4. Neuromuscular disease
-chronic asthma, COPD, bronchiectasis, pulmonary fibrosis, -myasthenia gravis, poliomyelitis, motor neuron disease
lung resection
5. Hypoventilation
2. Pulmonary vascular disease -sleep apnoea, enlarged adenoids in children
-pulmonary emboli, pulmonary vasculitis, primary pulmonary
HPT, ARDS, sickle cell disease, parasite infection 6. Cerebrovascular disease

3. Thoracic cage abnormalities

-kyphosis, scoliosis, thoracoplasty

Clinical feature Management

Symptom: dyspnoea, fatigue, syncope -treat underlying causes
Sign: cyanosis, tachycardia, raised JVP, peripheral edema, -treat respiratory failure
hepatomegaly, RV heave, pan systolic murmue acute: 24% O2 and monitor ABG and gradually ↑ O2 if
(tricuspid regurgitation) PCO2 stable
COPD: long term O2 therapy for 15h/d
Investigation -treat cardiac failure (with diuretics eg furosemide)
1. FBC: ↑Hb and haematocrit (2nd PCV) -consider venesection for PCV if haematocrit >55%
2. ABG: hypoxia and hypercapnia -consider heart- lung transplantation in young pt
3. CXR: enlarged RA & RV, prominent pulmonary artery
4. ECG: rt axis deviation (RVH)
11.0 PULMONARY EMBOLISM
After PE, lung tissue is ventilated but not perfused, producing intrapulmonary dead space which result in impaired gas
exchange. After some hrs the non- perfused lung no longer produced surfacteant. Alveolar collapse occur and exacerbates
hypoxaemia. Another haemodynamic consequence is ↓ cross sectional area result in elevation in pulmonary arterial pressure
and ↓ CO. Infarction is rare because oxygen continue to be supplied by bronchial circulation and airway
Clinical feature Investigation
-sudden onset of unexplained dyspnoea 1. Small and medium size emboli
-if infarction is present: pleuritic chest pain, haemoptyis -CXR: often normal, sometimes can see linear atelectasis and
blunting of costophrenic angle
1. Small/ medium size emboli -ECG: normal, sometimes can see sinus tachycardia, AF,
-PE impacted in terminal pulmonary vessel tachyarrhythmia
-symptom: pleuritic chest pain, breathlessness, hemoptysis -Blood test: ↑ ESR ( d/t polymorphomuclear leucocytosis in
-sign: pleural rub, crackles, exudative peural effusion pulmonary infarct)
-D dimer: diagnosis of pulmonary embolism
2. Massive PE -V/ Q scanning: demonstrate underperfusion
-acute obstruction of Rt ventricular outflow tract -ultrasound scanning: detection of clot in pelvic/ iliofemoral
-lack of coronary blood supplycentral chest pain vein
-↓ CO syncope -CT/ MRI
-sign: tachycardia, tachypnoea, hypotension, raised JVP, Rt
ventricular heave 2. Massive PE
-CXR: show pulmonary oligoaemia, dilatation of pulmonary
3. Recuurent PE artery
-pulmonary HPT -ECG: Rt atrial dilatation(peaked P wave), Rt axis deviation,
RBBB
-Blood gas: arterial hypoxaemia and hypocarbia
-Echo: LV vigorously contracting, RV dilated

3. Massive PE
-CXR: show pulmonary oligoaemia, dilatation of pulmonary
artery
-ECG: pul HPT
-Leg imaging: thrombi
-Multidetectot CT: small emboli
Dignosis Treatment
-PE consider when pt have unexplained cough, chest pain, 1. High flow O2 (60-100%)
haemoptysis, new onset AF, pul HPT 2. Anticoagulation-LMWH
3. Massive pulmonary embolism- IV fluid and inotropic
-↑risk pt: CT angiography+ve confirm diagnosis agent to ↑ pumping of rt heart
-ve but ↑ D dimerVenous 4. Fibrinolytic, eg. streptokinase
Ultrasonography
-↓ risk pt: D dimer assay-ve rule out Prevention
+veCTA 1. Anticoagulation with Vitamin K antagonist for a period
of 3-6 mth with INR: 2.0 -3.0
2. Cancer or pregnant: LMWH

12.0 LUNG ABSCESS

Severe localised suppuration within the lung associated with cavity formation on CXR and CT, often with fluid level
Cause Clinical feature
-aspiration pneumonia -persistent and worsening pneumonia asso with production of
-TB large amount of sputum, often foul smelling d/t growth of
-Pneumonia from certain sp. (eg Staph Aureus, Kleb. sputum
Pneumonia) -clubbing
-septic embolism containing staphylococci -normocytic anaemia
-spread from amoebic liver abscess (@rt lower lobe following -↑ESR and CRP
transdiaphragmatic spread)
-bronchial onstruction by endoluminal cancer
-foreign body inhalation

13.0 PULMONARY COMPLICATION OF AIDS

The upper airway and lungs serve as a physical barrier to air- borne pathogens and any damage will decrease the efficiency of
protection, leading to an increase in upper and lower respiratory tract infection. The sinus mucosa may also function
abnormally in HIV infection and is frequently the site of chronic inflammation. Response to antibacterial therapy and topical
steroids is usual but some pt require surgical intervention.
Lymphoid interstitial pneumonitis is well described in paed HIV but is uncommon in adult. There is infiltration of
lymphocytes, plasma cells and lymphoblast in alveolar tissue. EBV may be present. The pt present with dyspnoea and dry
cough, which may be confused with pneumocystis infection. CXR show reticular nodular shadowing. Therapy with steroid
may produce clinical and histological benefit in some pt.

15.0 SARCOIDOSIS
A multisystem granulomatous disorder, commonly affecting young adult and presenting with bilateral hilar lymphadenopathy,
pulmonary infiltration and skin or eye lesion

Granuloma: a mass or nodule composed of chronically inflamed tissue formed by the response of mononuclear phagocyte
system to an insoluble or slowly soluble antigen/ irritant

Aetiology Immunopathology
-Berylium poisoning Typical sarcoid granuloma consist of focal accumulation of
-Epstein- Barr virus epitheloid cells, macrophages and lymphocytes, mainly T cell
-occupational depressed CMI
-genetic sequestration of lymphocytes within the lung
-social -lymphopenia
-environmental -bronchoalveolar lavage: great ↑ in no of lymphocytes
-transbronchial biopsies: infiltration of the alveolar walls and
interstitial spaces with leucocytes
-delayed hypersensitivity response

Clinical feature Investigation

-there are 4 stages which is important in determining 1. Imaging- CXR, CT
prognosis 2. FBC- normochromic normocytic anaemia with raised
Stage 1 Bilateral hilar lymphadenopathy ESR
Stage 2 BHL + Pulmonary infiltrates 3. Serum biochemistry- ↑ serum calcium and
Stage 3 Pulmonary infiltrates hypergammaglobulinemia
Stage 4 Fibrosis 4. Transbronchial biopsy- most useful
5. Serum ACE level- test is useful in assessing disease
1. Bilateral hilar lymphadenopathy activity and response to treatment
-usually symptomless (occasionally dull ache in chest, 6. Lung Function Test- show restrictive lung disease (↓
malaise, mild fever) and usually detected in chest X ray, CT, TLC, FEV1, FVC)
transbronchial biopsies, bronchoalveolar lavage. Treatment
1. Hilar lymphadenopathy- no need treatment
2. Pulmonary infiltration 2. Persistent infiltration with normal lung function test-
-usually asymptomatic (with normal lung function) but monitoring
occasionally there is symptom eg. dyspnoea, cor pulmonale, 3. Abnormal lung function- corticosteroid (prednisolone
death 30mg for 6 days, reducing to alternate day 15mg for 6-
-CXR: mottling to generalized fine nodular shadows 12 mth)

3. Extrapulmonary infiltration Prognosis

Skin lesion: erythema nodosum -5% death in UK as a result of respiratory failure and cor
: lupus pernio (chilblain- like lesion) pulmonale or rarely myocardial sarcoidosis and renal damage.
Eye lesion: anterior uveitis (misting of vision, pain and red
eye), posterior uveitis (progressive loss of
vision)
: conjunctivitis
: uveoparotid fever- bilateral uveitis+parotid
Gland enlargement+facial nerve palsy
Keratoconjuctivitis
Metabolic manifestation-↑ 1α- hydroxylation
hypercalcemia and hypercalciuria
renal calculi and nephrocalcinosis
CNS
Bone and Join involvement: bone cysts found in digits with
assoc swelling
Hepatosplenomegaly
Cardiac involvement (ventricular dysrhythmias,conduction
defect, congestive cardiac failure)
16.0 LUNG CANCER
Incidence in Msia
-3rd most common cancer in general population
-commonest cancer in male and 5th commonest cancer in female

Risk factor
Tobacco smoking -contain potential carcinogens including initiators (benzypyrenes) & promoter (phenol)
-Number of pack-years = (packs smoked per day) × (years as a smoker)
Number of pack-years = (number of cigarettes smoked per day/20) × number of years
smoked.
-risk of active smoker: 60 x greater than non smoker
-risk of passive smoker: 2 x greater than non smoker

Industrial hazards -abestos, arsenic, chromium, uranium, nickel, vinvyl chloride, mustard gas, high dose
ionising radiation
Air pollution -chronic exposure to air particulates in smoglung irritation, inflammation, repair
-radon gas (radioactive gas from natural breakdown of uranium
Molecular genetic -depend on histologic subtypes
Squamous Cell Carcinoma TP53 mutation, loss of expression of RB &
p16, CDKN2A inactivation
Small Cell Carcinoma TP53 mutation, MYC amplification, RB,
3p deletion
Adenocarcinoma Oncogenic gain-of-function mutation
involving growth factor receptor signalling
pathway

Classification
Type Features
Small Cell CA -most aggressive, highly malignant, metastasize early
-strong relationship to smoking
-commonest associated with ectopic hormone production (paraneoplastic syndrome)
-arise from neuroendocrine cells and often secrete polypeptide hormones
-gross: most often hilar/ centrally
-histologic feature: small round blue cell (small cell with scanty cytoplasm, ill- defined
cell borders, finely granular nuclear chromatin, absent & inconspicuous nucleoli, salt and
pepper appearance, nuclear molding,) and Azzopardi effect (basophilic staining of
vascular walls d/t encrustation by DNA from necrotic tumor cells)
Squamous Cell CA -most common in men and strongly associated with smoking
-arise centrally (cause obstructing lesion of bronchus with post- obstructive lesion)
-relatively late metastasize
-gross: occasionally cavitates with central necrosis
-histologic: presence of keratinisation (keratin pearls, individual keratinisation,
intracellular bridge)
Adenocarcinoma -commonest in women (non- smoker, associated with EGFR)
-metastasize widely and earlier
-Gross: peripherally located, smaller lesion
-Histology: glandular differentiation or mucin production by tumour cell
-Immunohistochemistry:+ve for TTF-1
Large Cell Carcinoma -poorly differentiated malignant epithelial tumor lack of squamous & glandular
differentiation
-Histologic differentiation: pleomorphic, large nuclei, prominent nucleoli, moderate
amount of cytoplasm

History Taking
Local Effect Paraneoplastic syndrome
1. Cough -complex of disorder in cancer pt not explained by tumor/
-d/t involvement of central airway secretion of hormones indigenous to the tissue
-pt may complaint of 3 week cough with loud, brassy, bloody SIADH ADH
2. Breathlessness Cushing Syndrome ACTH
-central tumor occlude large airways result in lung collapse Hypercalcemia PTH-rp
and breathlessness on exertion Hypocalcemia Calcitonin
3. Haemoptysis Gynaechomastia Gonadotrophin
-tumor bleeding into airway Carcinoid syndrome Serotonin, bradykinin
 4. Chest pain Other non- metastatic extrapulmonary manifestation
-peipheral tumor invade chest wall/ pleura, resulting in sharp
pleuritic pain
-large volume mediastinal nodal disease: dull central chest
ache
5. wheeze
-monophonic d/t partial obstruction of airway by tumor
6. Hoarseness
-mediastinal nodal/ direct tumor invasion of the mediastinum
results in compression of the lt laryngeal nerve
7. Nerve compression
-pancoast tumor (commonly frm small cell CA)
invade brachial plexus causing C8/ T1 palsy with small
muscle wasting in the hand
compression of the sympathetic chain lead to Horner’s
syndrome (miosis, ptosis, anhidrosis)
8. Recurrent infection
-obstruction of the airway results in post- obstructive
pneumonia
9. Paralysis of ipsilateral hemidiaphragm
-invasion of phrenic diaphragm
10. Dysphagia
-d/t esophageal invasion
11. SVC obstruction
-venous congestion (prominent vein on chest) and edema of
head and arm

Metastatic Spread
1. Liver: rt upper quadrant pain, anorexia, nausea, weigt
loss
2. Bone: bony pain and pathological fracture, risk of spinal
cord compression
3. Brain: SOL↑ICP
Lambert Eaton myasthenc syndrome
-d/t autoantibodies directed against to neuronal calcium
channel

Acanthosis nigricans
-hyperpigmentation of the skin

CT abnormalities
-hypertrophic pulmonary osteoarthropathyclubbing
-except small cell CA

Investigation
1. Radiological
(a) Chest X ray Peripheral nodule, hilar enlargement, consolidation, lung
collapse, pleural effusion, bony secondaries

(b) CT scan Indicate extent of disease, staging based on TMN

Look for other sites, eg. liver and adrenal gland for metastasis

(c) PET (Positron emmison tomography) To look for extent of mediastinal nodal involvement and
highlighting distant metastases

(d) Radionucleic bone scan If suspected bone metastasis

2. Scanning
(a) Fibreoptic bronchoscopy Define the bronchial anatomy and to obtain biopsy and
cytological specimens
**loss of sharp angle of carinapresence of enlarge
subcarinal LN

(b)Endobronchial untrasound For staging and visualize the majority of mediastinal nodes
and then to allow for needle aspration
 3. Cytological examination Sputum and pleural fluid
4. Fine needle aspiration and biopsy For peripheral lesion & superficial L
5. Histologic examination Of lung & pleural biopsy/ surgical resection
6. FBC Anaemia, biochemistry (for liver involvement,
hypercalcemia, hyponatremia)
7. Lung Function Test For assessment of fitness for treatment/ lobectomy

TMN Staging

Treatment
NSCLC Excision is treatment of choice for peripheral tumour, with no metastatic spread
Curative radiotherapy: if respiratory reserve is poor
Chemotherapy+ radiotherapy for more advanced disease
SCLC May respond to chemotherapy but chemotherapy but invariably response
**nearly always disseminated at presentation

1. Surgery
-performed in early stage NSCLC (stage I,II, IIIA)
-if pt with stage III will be treated with chemotherapy to downstaging disease to make it amenable to surgical resection

2. Radiation
-in pt with adequate lung function and early stage NSCLC
-S/E: radiation pneumonitis

3. Chemotherapy
-improve response rate and extends median survival in NSCLC

4. Palliative care
-to make pt’s remaining life symptom free and as active as possible
-exp:
(a) Radiotherapy: for bronchial pbstruction, SVC obstruction, hemoptysis, bone pain, cerebral metastasis
(b)SVC stent, radiotherapy, dexamethasone: SVC obstruction
(c) Endobronchial therapy: tracheal stenting, cryotherapy, laser, brachytherapy
(d) Pleural drainage/ pleurodesis: for symptomatic pleural effusion
(e) Drugs: analgesia, steroids, anti- emetics, codeine, bronchodilator, anti- depressant
(f) psychological and emotional support
17.0 OCCUPATIONAL LUNG DISEASE
Exposure to dusts, gases, vapours and fumes at work can cause several different types of lungs disease
-acute bronchitis and pulmonary edema frm irritant such as sulphur dioxide, chlorine, ammonia, oxides of nitrogen
-pulmonary fibrosis d/t mineral of dusts
-occupational asthma
-hypersensitivity pneumonitis
-bronchial asthma d/t industrial agent (eg. asbestos, radon, polycyclic hydrocarbon)

TYPE FEATURE
Coal worker pneumoconiosis -d/t inhalation of coal particles & other admixed form of dust
Anthracosis Most innocuous
Inhaled carbon pigment engulfed by alveolar/ interstitial
macrophages, which then accumulate in the CT along lymphatics
Simple CWP Coal macule/ larger coal nodules heavily at upper lobes or upper
part of lower lobes
1. Small opacities definitely present but few in no.
2. Small round opacities numerous but normal lung markings still
visible
3. Small round opacities very numerous and normally lung
marking obscured
-benign with little decrement in lung function
Complicated CWP Round fibrotic masses several cm, usually at upper lobes and have
(progressive necrotic central cavities with apical destruction of the lung result in
massive fibrosis) emphysema and airway damage

Pathogenesis: presence of fibrogenic promotic factor leading to

formation of immune complex, analogous to development of large
fibrotic nodule

Clinical feature: dyspnoea, cough with black sputum

Silicosis Usually in stonemasons, sand- blaster, pottery and ceramic worker

Inhalation of pro- inflammatory crystalline silicon dioxide

Pathogenesis: after inhalation, the particles are phagocytosed by the macrophages then
activate inflammasome lead to release of inflammatory mediators, especially IL-1 and IL-18

Morphology:
-early: tiny, discrete pale to blackened nodules in the hilar LN and upper zones of the lung
-when disease progress: eggshell calcification
-proggressive massive fibrosis

Clinical feature: pulmonary function are either normal or moderately effected early in the
course, and most patient do not develop SOB until progressive massive fibrosis exposed

Asbestosis Pathogenesis:
-depend on size, shape and solubility of diff asbestos (straight and stiff amphibole is
>fibrogenic than flexible serpentine
-once phagocytosed, asbestos activate the inflammasome and stimulate the release of
proinflammatory factors and fibrogenc mediator

Morphology: diffuse pulmonary iinterstitial fibrosis with presence of asbestos bodies (golden
brown, fusiform, beaded rods with translucent centrcoated with iron- containing
proteinaceous material

Clinical feature:
1. Asbestosis
-parenchymal interstitial fibrosis +/- fibrosis of pleura
-symptom: breathlessness, finger clubbing, bilateral basal end inspiratory crackles
2. Localised pleural fibrous plaques or rarely diffuse pleural fibrosis
3. Recurrent pleural effusion
 4. Lung CA
5. Mesothelioma
6. Laryneal cancer
Byssinosis -developed in ppl worked in cotton mills
-Pathogenesis: endotoxin from bacteria present in raw cotton causing constriction of the
airway of the lung
-Clinical feature: tightness in the chest, cough and breathlessness with monday sickness
(symptom start at first day of work and improves as the weeks progresses)

Berylliosis d/t inhalation of beryllium lead to progressive dypnoea with pulmonary fibrosis
18.0 RESPIRATORY FAILURE
Pulmonary gas exchange is sufficiently impaired to cause hypoxaemia +/- hypercarbia
Type I / acute hypoxaemic respiratory failure Type II or ventilatory failure
-occur in disease that damage lung tissue -occur when alveolar ventilation is insufficiency to excrete
Eg. pulmonary edema, pneumonia, acute lung injury, lung volume of CO2 being produced by tissue metabolism
fibrosis d/t ↓ ventilator effort, inability to overcome an ↑ resistance to
-d/t rt- to- lt shunt and V/Q mismatch ventilation, failure to compensate for ↑ deadspace and CO2
production

Clinical manisfestation
-use of accessory muscle of respiration
-intercostal recession
-tachypnoea
-tachycardia
-sweating
-pulsus paradoxus (abnormal large ↓ in systolic BP during inspiration)
-inability to speak, unwillingness to lie flat
-agitation, restlessness, diminished conscious level
-asynchronous respiration (a discrepancy in the timing of movement of abdominal and thoracic compartment)
-paradoxical respiration (abdominal and thoracic compartment move in opposite directions)
-respiratory alternans (breath- to- breath alteration in the relative contribution of intercostals, accessory muscle and diaphragm

Lab investigation
Pulse oximetry -can be applied on ear lobes or finger
-measure the changing amount of light transmitted through the pulsating arterial blood and
provide a continuous, non- invasive assessment of arterial oxygen saturation (SPO2)
-reliable, easy to use and don’t require calibration but not a sensitive guide to changes in
oxygenation
SPO2 within normal limit in pt receive supplemental oxygen does not exclude the
possibility or hypoventilation with CO2 retention
Arterial Blood Gas analysis Indication
-any unexpected deterioration in an ill pt
-anyone with acute exacerbation of chronic chest condition
-anyone with impaired consciousness and respiratory effort
-sign of CO2 retention, eg. bounding pulse, drowsy, tremor (flapping), headache
-cyanosis, confusion, visual hallucination
-to validate measurement from transcutaneous pulse oximetry

Site: radial artery (most common), femoral artery (less uncomfortable d/t less sensitive and
pt cannot see the needle), brachial artery (be careful as median nerve lie closely medial to it
and it is an end artery)
**don’t use site with AV fistula d/t hamodialysis

Procedure
-get kit ready, including portable sharp bin, pre-heaprinized syringe, 23G needle, glove,
alcohol swab, gauze swab, tape
-feel thoroughly for the best site. Look at both site
- wipe with alcohol swab. Let the area dry. Get urself comfortable
-ask an assistant to hold the hand and arm with the wrist slightly extended
-before sampling, expel any excess heparin in the syringe
-hold the syringe like a pen, with the needle bevel up between 2 fingers of your another
hand (the ones used to palpate the pulse) and insert the needle when the pulse is at highest
volume. Let the pt know you are about to take the sample.
-The plunger will move up on its own in pulsative manner if you are in the artery. The
blood collected should be bright red if it show arterial blood.
-remove the needle when enough blood has been taken and apply little pressure (abt 5min)
until any leakage is stemmend to avoid large lump followed by massive bruise
-expel any air from the syringe as this will alter the oxygenation of the blood. Cap and label
the sample. Send it by express delivery to the lab. If there is delay of time, put the sample in
a bag of ice

Interpretation
1. Acid- base balance
pH
-normal pH is 7.35-7.45
 -pH <7.35 is acidosis and pH >7.45 is alkalosis
CO2
-normal=4.7-6.0kPa
-d/t respiratory problem
-↑ in acidosis and ↓ in alkalosis
 HCO3-
-normal: 22-28mmol/L
-d/t metabolic problem
-↑ in alkalosis and ↓ in acidosis

2. Oxygenation
-Normal PO2=10.5- 13.5kPa
-Hypoxia: PO2<8kPa d/t VQ mismatch, hypoventilation, abnormal diffusion, rt- to- lt
shunt

3. Ventilatory Deficiency
-Normal PCO2=4.5-6kPa
-PCO2 <4.5kPa indicates hyperventilation and >6.0kPa indicates hypoventilation

Type I respiratory failure: PO2<8kPa and PCO2<6.0kPa

Type II respiratory failure: PO2<8kPa and PCO2>6.0kPa

Capnography -Continuous breath-by-breath analysis of expired CO2 concentration

-used to:
(a) confirm tracheal intubation
(b) continuous monitor tidal PCO2 to detect acute airway problems
(c) detect apparatus malfunction
(d) detect acute alterations in cardiorespiratory function

Management
Depend on the cause
Type I Respiratory Failure Type II Respiratory failure (the respiratory centre is relatively
-treat underlying cause insensitive to CO2 abd respiration could be driven by
-give 02 (35-60%) by facemask to correct hypoxia hypoxia)
-assisted ventilation if P02<8kPa despite 60% O2 -treat underlying cause
-oxygen therapy (24%) must be given with care.
Nevertheless, should not leave hypoxia untreated
-recheck ABG after 20min. If PCO2 is steady, increase O2
concentration to 28%. If PCO2 is risen >15kPa and pt still
hypoxic, consider assisted ventilation
-if fail, consider intubation and ventilation.

1. Oxygen therapy
Type Feature
Adult Nasal Canula -to give low flow rate of O2
-advantage: comfortable (allow pt to eat & drink), ideal for pt requiring low dose O2 and
home use
-disadvantage: oxygen dose cannot be controlled, not appropriate for pt in respiratory
distress

Adult face mask with nebulizer -to deliver nebulised solution

jet mask -advantage: able to combine O2 and nebulised solution delivery simultaneously
-disadvantage: oxygen dose cannot be controlled, noisy, nebulised solution may irritate
eyes
 Adult venturi mask -provide precise % of O2 at high flow rate
-colour coded adaptor: signify diff O2 concetration that is delivered and flow rate of O2
needed

Simple face mask -used when ↓ dose of O2 is required

-advantage: quick and easy too set up
-disadvantage: non- specific inspiratory flow of O2, flow rate set < 5/lpm may cause CO2
rebreathing

Adult partial rebreather mask -used @ situation where pt require high concentration of oxygen to pt
-it has a reservoir bag that supplies high concentration of oxygen to patient
-the reservoir contain some exhaled gas
-10- 15l/min O2

Oxygen toxicity: routine administration of supplemental O2 will lead to associated vasoconstriction

2. Mechanical ventilation
Type Feature
1. Controlled mechanical -used in pt whom respi effort is absent
ventilation
(a) Volume controlled -the airway pressure varies according to ventilator setting and pt lung mechanic
ventilation
(b) Pressure controlled - the airway pressure varies according to pt lung mechanic
ventilation
2. Positive end- expiratory -+ve airway pressure can be maintained at a chosen level throughout expiration by
ventilation attaching a threshold resistor valve to the expiratory limb of the circuit
-help to reexpand the underventilated lung and redistribute the lung water from alveoli to
perivascular interstitial space hence ↓ shunting and ↑PO2.\
-disadvantage: impede venous return, ↑ pulmonary vascular resistance, ↓ CO

3. Continuous positive airway -oxygen and air are delivered under pressure via endotracheal tube, tracheostomy, tight
pressure fitting facemask or a hood
- improve oxygenation, more complaint lung, and reduce work of breathing

4. Positive support ventilation -spontaneous breath are augmented by the preset level of positive pressure triggered by
pt’s spontaneous respiratory effort
5. Intermittent mandatory -allow the pt to beathe spontaneously btw mandatory tidal volume delivered by ventilator
ventilation which is timed to coincide with pt’s own inspiratory effort
6. Lung protective ventilation -to avoid exacerbating lung injury by avoiding overdistension of alveoli
-alveolar volume is maintained by PEEP while tidal volume is limited to 6-8ml/g ideal
body weight
7. High frequency oscillation -gas oscillates at a rate of 60- 300 cycle/min with tidal volume 103ml/kg
-both inspiration and expiration is actively controlled by sine wave pump

Indication
1. Acute respiratory failure, with sign of respiratory distress (eg. RR>40l/min, inability to speak, pt exhausted)
2. Acute ventilator failure d/t myasthenia gravis or Gullain- Barre syndrome
Benefit
1. Relieve the exhaustion (relief the work of breathing, rest the respiratory muscle)
2. Effect of oxygenation (application of +ve pressure can prevent or prevent atelectasis—lung collapse)

Complication
1. Airway complication- d/t tracheal intubation and tracheostomy
2. Disconnection, failure of gas and power supply, mechanical fault
3. Cardiovascular complication
-+ve airway pressure to the lung can impede venous return and distend alveoli, thus strectching the pulmonary capillaries and
cause a rise in pulmonary vascular resistance, thus produce fall in cardiac output
4. Respiratory complication
-↑ microvascular permeability and release of inflammatory mediator leading to ventilator associated lung injury.
-overdistension of the lung can rupture alveoli and air to dissect centrally along perivascular sheath
5. Ventilator associated pneumonia
-d/t leaking of infected oropharyngeal secretion past tracheal tube cuff
-reduced by pt semi-recumbent rather than supine and by oropharyngeal decontamination