Everything You Need to Know (at least) for

ONN08/09

Name –

Year –

Matric no. –

Academic Session -

EDITORIAL“Permulaan perkara yang dihisab seseorang hamba pada hari kiamat ialah solat”

(Hadis Riwayat at-Tirmizi)

“Dengan nama ALLAH yang MAHA PEMURAH lagi MAHA PENYAYANG”

Most of the block involving one system in our body, like respiratory block, cardiovascular block and gastrointestinal block have one thing in common, which is, you’ll never understand the pathological condition of the disease involving unless you know the normal process first. Therefore, knowledge of normal thing is very important. So, take your time to open and revise 1st year medical syllabus in each of the system before entering the abnormal one. Good luck.

Onn Azli PuadeMedic 420011/2012

“A medical chest specialist is long winded about the short winded”

(Kenneth T Bird)

“Time is a great teacher, unfortunately, it kills all its pupils”

(Medden 2005/2006)

ONN08/09

FEVER (PYREXIA)

DefinitionIs a sensation of feeling cold despite the rising in body temperature above normal body temperature.

CausesBacterialBacterial endocarditisTuberculosisTyphoidLeptospirosis

ViralInfluenzaGlandular feverHIVCMV

FungalCandidiasisAspergillosisPneumocitis carinii

ProtozoalMalariaAmoebiasisToxoplasmosis

NeoplasiaHypernephromaLymphomaHepatomaLeukaemia

Connective tissue diseaseSLEPolyarteritis nodosaRheumatoid arthritisTemporal arthritis

Granulomatous diseaseSarcoidosisCrohn’s disease

Drug inducedPost immunization

OthersMyocardial infarctionPulmonary embolismMunchausen’s disease

Further history regarding Fever

1. Associated with chills and rigors?If yes – may indicates high grade fever in the case of Community Acquired PneumoniaIf no – may indicates low grade fever in the case of Influenza, TB or even malignancy

2. Associated with cough?Indicates Upper Respiratory infection, COPD, Community Acquired Pneumonia, tuberculosis, pulmonary embolism

3. History of diabetes mellitus or any contact with TB patient before?DM increase risk of getting myocardial infarction and pulmonary embolism. Contact with TB patient may increase risk of getting secondary tuberculosis

4. Any recent surgery?Any type of surgery especially abdominal surgery may prone to get nosocomial infection

5. Any history of family getting cancer?Malignancy can cause fever in which a condition we call as Paraneoplastic Syndrome

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Pathogenesis and Pathophysiology

Further investigaton regarding fever FBC and ESR

Low Hb – malignancy, anaemia of chronic diseaseHigh WCC – infection, leukaemiaHigh ESR – malignancy, connective tissue disease, tuberculosis

CXR – to look out for lung consolidation, lymphadenopathy, fibrosis etc Viral antibodies – hepatitis B, hepatitis C, HIV, CMV Sputum culture – for gram staining and acid fast bacilli

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Infectious agent enters body

Release of endogenous pyrogenes or leukocytes pyrogenes – IL-1

The interleukin enters blood circulation and reach hypothalamus

Bind to the endothelial cell wall and microglial cell

Stimulate the conversion of amino acid to prostaglandin E2 via arachidonic acid pathway

Reset the thermoregulatory setpoint of the body by increasing it to certain level

Releasing toxins called exogenous pyrogenes

Either bacteria or breakdown products of the bacteria engulfed by macrophage

Compensatory mechanism to reach the new setpoint

Stimulation of sympathetic nervous system

Vasoconstriction at skin

Repeated muscle contraction, excessive sweating

Muscle spasm

Body gets the sensation of feeling cold

Low grade fever

High grade fever

Chills

Rigors

Malignancy

COUGH (TUSSIS) AND SPUTUM

DefinitionIs a reflex explosive expiration that prevents aspiration as well as to remove foreign particles and secretion from the lung. Productive cough is cough with sputum and vise versa for non-productive cough

CausesAcute non-productive cough Chronic cough

Non-productive ProductiveInhalation of foreign material

Respiratory tract irritantRespiratory tract infection

AsthmaACE inhibitor

Gastro-oesophageal refluxPostnasal drip

Sarcoidosis

COPDBronchiectasis

Pulmonary oedemaLung ca

TuberculosisPulmonary embolisme

SmokingPneumonia

Further history regarding cough

1. How does it occurs and for how long?To differentiate between chronic cough and acute cough. Normally, chronic cough is a cough that has persisted for more than 3 weeks and it does indicates some disease as stated above. Sudden onset of an unrelenting bout of violent coughing may be due to inhaled foreign object or pulmonary embolisme

2. Anything produce with the cough?Yellowish/greenish – indicates infection involving WCC like pneumonia and TBMucoid/purulent – COPD, bronchiectasisPink and frothy – pulmonary oedema due to alveolar granuleHaemoptysis – TB, lung ca, pulmonary embolismeClear – probably salivaBlack carbon specks – due to smoking

3. Associated symptoms?Fever – indicates infection Night sweats – indicates tuberculosisDyspnoea – sudden onset due to pulmonary embolisme, at night may due to asthmaOrthopnoea – may suggest pulmonary oedemaWheezing – due to asthmaChest pain – pleuritic chest pain, cardiac chest pain (see Chest Pain symptoms)

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Pathogenesis and pathophysiology

Further investigaton regarding cough and sputum Respiratory function test

Obstructive Lung disease- FEV1/FVC ratio is less than 80% Restrictive Lung disease- FEV1/FVC ratio is normal or higher

Sputum culture – for gram staining and acid fast bacilli CXR – to look out for lung consolidation, lymphadenopathy, fibrosis, collapse,

hyperinflated lung etc

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Irritant, bacteria or foreign object and secretion

Stimulate the receptor of the airway Bronchi and trachea for light touch1

Larynx and carina are the most sensitive Terminal bronchiole and alveoli for

corrosive chemical stimuli

Ascend via vagus nerve (CN X)

Reach the cough center located at the medulla of the brain

Processed and sent back to the

Glossopharyngeal nerve

Closure of glottis

Intercostals nerve

Contraction of intercostals muscle

Phrenic nerve

Contraction of diaphragm

Increase intrathoracic pressure

Opening of glottis

Explosive air going out

Expectoration of desquamated cells, dead neutrophils and

bacterial debris

Cough

Productive cough

CHEST PAIN

DefinitionThe uncomfortable (angina) or pain sensation of the chest area

Causes

Cardiovascular Myocardial infarctionAcute aortic dissectionPericarditis

Gastrointestinal Gastro-esophageal refluxPeptic ulcer diseaseGastritisOesophageal spasm

MusculoskeletalPersistent coughChest wall injuriesCostochondritisRib tumour, fractureHerpes Zoster

PulmonaryPneumoniaPulmonary embolismePneumothorax Central bronchial carcinomaInhaled foreign body

Further history about the chest pain

1. Character of the chest painSharp – chest wall injuries, pleuritic chest painTearing – acute aortic dissectionBurning – gastro-oesophageal reflux

2. Location of the painLocalize and anywhere – pleuritic chest painRetrosternally and radiates to jaw and left arm – cardiac chest pain and oesophageal refluxCentrally located and radiates to shoulder – pericarditisRadiates to back – aortic dissection

3. Precipitating factorInspiration (due to movement of thorax) – pleuritic chest painEffort, cold, food and emotion – cardiac chest pain Posture – gastro-oesophageal reflux

4. Relieving factorGTN – oesophageal spasm and cardiac chest painAntacid – gastro-esophageal refluxAspirin – pleuritic chest pain

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Pathogenesis and Pathophysiology (respiratory pathology)

Further investigation regarding chest pain FBC

Elevated white cell count will be expected with a pneumonia, and to a lessen extent in a myocardial infarction

Serum cardiac markersFollowing a myocardial infarction, cardiac troponin rises within 6 hours and remains elevated for up to 2 weeks

CXR Consolidation of lung can be seen in bronchopneumonia. Wedge-shaped shadow can be observed in pulmonary infarction. Rib fractures or secondary deposits in ribs can be seen in chest X-ray.

ECGNon-specific ECG changes in pulmonary embolisme such as tachycardia, right axis deviation, right ventricular strain and atrial fibrillation. Elevated ST segment in myocardial ischaemia, T wave inversion in myocardial injury and abnormal Q wave in myocardial infarction can be observed.

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Blood clot in the pulmonary vessels

Distal part of the clot does not received blood supply

Ischaemia at the distal part of the clot

Endothelial cell release chemical mediators like bradykinin, serotonin due to oxygen depressed

Chemical mediator enters blood circulation

Reaches pain receptor located at the pleural cavity

Send signal up to sensory cortex

Via lateral spinothalamic tract

Pain is appreciated

CHEST PAIN

HAEMOPTYSIS

DefinitionIs an expectoration of blood and bloodstained sputum.

CausesRespiratoryBronchial carcinomaPneumoniaTuberculosisChronic bronchitisPulmonary oedemaGoodpasture’s syndromeWegener’s granulomatosis

VascularPulmonary embolismPulmonary hypertensionHereditary haemorrhagic telangiectasia

SystemicCoagulation disorder

Further history regarding haemoptysis

1. Onset of the symptomsSudden or acute onset may be due to the pulmonary embolisme or acute respiratory infection. Long standing haemoptysis often associated with chronic bronchitis or bronchiectasis

2. Volume Volume of blood expectorated are needed to be ask to confirm that it is haemoptysis rather haematemesis

3. Associated symptomsDyspnoea –may associated with pulmonary embolisme or chronic lung disease or mitral stenosisOrthopnoea – may be due to pulmonary oedemaSputum – purulent sputum stained with blood may indicates chronic bronchitis or bronchiectasisWeight loss – suggestive tuberculosis and bronchial carcinomaNight sweats – tuberculosis

4. Other site of bleedingOther site of bleeding should be excluded as haematuria may be due to Goodpasture’s syndrome

5. Past medical and drug historyAnticoagulant drugsCongenital like haemophilia or acquired like usage DIC

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Pathogenesis and pathophysiology

Further investigation regarding haemoptysis

Sputum AnalysisSputum should be collected for microscopy, culture and cytology. When TB is suspected, serial culture should be taken from sputum, urine, bronchial washing or lung biopsy

FBCDecrease Hb with chronic haemoptysis resulting in normocytic normochromic anaemia. Increase WCC may be due to acute bleeding or respiratory tract infection. Monocytosis may be due to tuberculosis.

Clotting screenA clotting screen to identify any impairment that may prolong the PT and APTT

ECGNon-specific ECG changes in pulmonary embolisme such as tachycardia, right axis deviation, right ventricular strain and atrial fibrillation.

CXR Consolidation of lung can be seen in bronchopneumonia. Wedge-shaped shadow can be observed in pulmonary infarction.

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Blood vessel eroded

Blood escape from eroded blood vessel and enters the alveoli

Irritate receptor of the airway

Stimulate the cough reflex (see cough)

Expectoration of blood

HAEMOPTYSIS

Infection

Involving macrophage

Secretes α-TNF

Emboli stuck in the pulmonary circulation

Distal part of the endothelial does not receive blood supply

Bronchial carcinoma

Rapid growth of malignant neoplasm

Invasive growth

SHORTNESS OF BREATH (DYSPNOEA)

DefinitionIs an uncomfortable awareness of breathing or can be described as breathlessness

CausesSudden (second to minute) Acute (hours to days) Chronic (months to years)PneumothoraxPulmonary oedemaPulmonary embolismeAspirationAnaphylaxisAnxietyChest trauma

AsthmaRespiratory tract infectionLung tumoursPleural effusionMetabolic acidosis

COPDCardiac failureFibrosing alveolitisAnaemiaArrhythmiaValvular heart diseasePulmonary hypertension

Further history about dyspnoea

1. OnsetSudden, acute or chronic onset may indicates different type of disease the patient suffers from

2. Precipitating factorsPosition like recumbency may indicates pulmonary edema secondary to cardiac failure.Seasonal and in cold weather may be due to asthma and exercising also can worsen dyspnoea in heart failure

3. Relieving factorSitting upright – as in pulmonary edema and cardiac failureBeta agonist – as in asthma

4. Associated symptomsProductive cough – yellowish/greenish sputum indicates chest infectionHaemoptysis – may be due to pulmonary embolisme or bronchial caWheezing – due to asthma or inhaled foreign body

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Pathogenesis and pathophysiology

Further investigation regarding dyspnoea1. Arterial Blood Gas

To recognize the respiratory failure and the metabolic profile of the patient2. Peak expiratory flow rate

Reduce in peak flow may indicates asthma or chronic airflow limitation3. ECG

Eliminates probability of cardiac disease related to the symptoms4. FBC

To rule out any pulmonary infection as well as anemia

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Lung is ventilated but not perfuse

V/Q mismatch

Respiratory acidosis

Increase carbon dioxide (indirectly) and reduce oxygen (directly) level below 30

mmHg

Stimulate the chemoreceptor mainly the aortic and carotid body

Ascend via vagus and glossopharyngeal nerve

Terminates at the nucleus of the tractus sollitarius

Stimulate the medullary respiratory area

Increase the respiratory effort as a compensatory mechanism of respiratory

acidosis

DYSPNOEA

Alveoli surface covered with fluid/blood

Fibrosing alveoli/consolidated Destruction of lung parenchyma

SPECIAL SYMPTOMS

WHEEZING

DefinitionIs defined as continuous abnormal added sound either high pitch or low pitch (rhonchi) and have a musical quality. It can be heard in both expiration and inspiration which it tends to be louder on expiration because of the narrower airways during expiration

CausesHigh pitch – asthma, inhaled foreign bodyLow pitch – Chronic Obstructive Pulmonary Disease

Pathogenesis and pathophysiology

NIGHT SWEATS

DefinitionIs a copious sweating during sleep. An etiology of fever may be an etiology of night sweats

CausesTuberculosis, AIDS, Hodgkin’s disease, brucellosis, lung abscess, bacterial endocariditis

Pathogenesis and pathophysiology

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Obstructed/narrowed airway

Airflow during respiration

Turbulent airflow when passes through

obstructed area

WHEEZING

Low grade fever

Increase temperature up to 8 folds during

sleep (3-5 am)

Increase sweating as a sympathetic nervous

system effectsNIGHT SWEATS

CYANOSIS

DefinitionIs an abnormal bluish discoloration of the skin and mucus membranes resulting from presence of 5 g/dl or more reduced haemoglobin in the blood. It can be classified to central and peripheral cyanosis.

CausesCentral cyanosis Peripheral cyanosis

Decrease O2 saturation Abnormal haemoglobinSevere respiratory diseasePulmonary oedemaPulmonary embolismeCyanotic congenital heart disease

MethaemoglobinaemiaSulphaemoglobinaemia

All causes of central cyanosisCold exposureAcrocyanosisArterial occlusionVenous occlusion

Further history and examination

1. OnsetBirth to few months of life – congenital cyanotic heart diseaseSudden onset – pulmonary embolisme, cardiac failure (precipitated by pneumonia/asthma)Slow progressive – chronic obstructive pulmonary disease

2. Associated symptomsChest pain (pleuritic) – as in pneumonia, pulmonary embolismChest pain (cardiac) – pulmonary edema secondary to myocardial infarctionDyspnoea – sudden onset in pulmonary oedema and pulmonary emboli, more gradual in asthmaFever – as in pneumonia and pulmonary emboli

3. Associated signsClubbing – cyanotic congenital heart diseaseElevated JVP – congestive cardiac failurePoor chest expansion – chronic bronchitis, asthmaUnilateral reduce chest expansion – lung consolidation secondary to pneumoniaCrepitation (localized) – lobar pneumoniaCrepitation (widespread) – bronchopneumonia, pulmonary oedema, chronic bronchitis

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Pathogenesis and pathophysiology

Further investigation regarding Cyanosis

Oxygen Saturation – usually below 85 %in the cyanosis patient Arterial Blood Gasses – decrease pO2 in severe lung dsease Full Blood Count – increase Hb in long standing cyanosis, increase WCC in Pulmonary embolisme ECG – elevated ST-segment in Myocardial Infarction, non specific St segment in pulmonary

embolisme CXR – abnormality in lung field

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V/Q mismatch

Increase carbon dioxide (indirectly) and reduce oxygen (directly) level below 30

mmHg

Poor oxygen saturation to bind with haemoglobin

Increase reduced haemoglobin more than 5 g/dl

Hypoxic state

Bluish discoloration of the mucus membrane

CENTRAL CYANOSIS

Hypoxaemic state

Poor blood supply especially to the extremities

Bluish discoloration of the skin

PERIPHERAL CYANOSIS

Occlusion of the blood vessel

Area distal to the blockage does not receive blood

supply

Altered lung parenchyma

Lung cannot function normally

CHEST EXAMINATION FOR RESPIRATORY AND ITS SIGNIFICANT(check Clinical Examination textbook for the method)

1. INSPECTION OF THE CHEST

Shape of the chestShape Pigeon chest Funnel chest Harrison’s sulcus

Character Outward bowing of the sternum

Localized depression of the lower end of the

sternum

Linear depression of the lower ribs just above the costal

margin at the site of attachment of the

diaphragmPathogenesis Repeated strong

contraction of the diaphragm while the thorax is still pliable

Developmental defects

Rapid and labored breathing during

childhood

Syndrome/disease Childhood respiratory illness, rickets

Developmental defect

Asthma in childhood, rickets

Movement of the chest during respirationNeither reduced, poor, bilateral or unilateral (see palpation of the chest)

2. PALPATION OF THE CHEST

Chest expansion Normal expansion – thumb move symmetrically at least 5 cm apart Reduced chest expansion in;a) One side – localized pulmonary fibrosis, consolidation, collapse, pleural effusion,

pneumothoraxb) Both sides – COPD, diffuse pulmonary fibrosis

Apex beatNormal apex beat – located at the 5th intercostals space at the left midclavicular line, 2 cm medially

Displaced apex beat due to Cardiomegally as in congestive cardiac failure secondary to systemic hypertension Mediastinal shift as in hyperinflated lung in COPD, lung collapse

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Lung collapse/lobar consolidation

Diminished movement during

inspiration

Lung is not ventilated at the

affected side

Asymmetrical chest expansion

Tactile fremitusNormal tactile fremitus – vibration on both sides of the chest at the comparable site is detected while the patient repeats ‘ninety-nine’

Increase in tactile fremitus Lobar consolidation as in pneumonia Compressed lung or tumour

Decrease in tactile fremitus Hyperinflated chest – emphysema Massive pulmonary oedema Bronchial obstruction

3. PERCUSSION OF THE CHEST

Normal percussion on the areas of lung is resonance. However, dullness can be percussed at the right midclavicular line in the 5th rib due to the organ liver and at the left side of the chest due to the organ heart.

Hyperresonance Hyperinflated chest such as emphysemaPneumothoraxBronchial asthma

DullnessAtelectasisPleural effusionPneumothorax

Absence of liver dullnessHyperinflated chest

Absence of cardiac dullnessEmphysema or asthma

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Lung consolidation/pleural

effusion

High pitched sounds travel to the chest

area upon saying the words ninety-nine

Sound travel faster in fluid and fastest in

solid compared to the travelling via the air

Increase tactile fremitus

4. AUSCULTATION OF THE CHEST

Abnormal breath sound i) Continuous breath sound

Wheeze is defined as continuous abnormal added sound either high pitch or low pitch (rhonchi) and have a musical quality. The causes of rhonchi and wheeze is just the same except for that high pitched wheeze is produced in the smaller bronchi and can be heard without the aid of the stethoscope, vise versa for the rhonchi (see wheezing)

Stridor 1 is a rasping or croaking noise loudest on inspiration which indicates obstruction of the larynx, trachea or large airways. These causes include;

Sudden onset (minutes) Gradual onset (days, weeks)Anaphylaxis

Toxic gas inhalationAcute epiglottitis

Inhaled foreign body

Laryngeal or pharyngeal tumourCriciarytenoid rheumatoid arthritis

Bilateral vocal cord palsyTracheal carcinoma

Paratracheal compression by lymph nodesPost tracheostomy

ii) Discontinuous breath soundPleural friction rub can be defined as when thickened, roughened pleural surfaces rub together as the lung expands or contracts. It can be distinguished from pericardial rub base on its existing during respiratory cycle.Causes – pleurisy secondary to pneumonia or pulmonary infarction, malignant involvement of the pleura, spontaneous pneumothorax or pleurodynia

1 An intense continuous monophonic wheeze loudest over the extrathoracic airways and can be heard without the aid of stethoscope

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Crackles are discontinuous, explosive popping sound originated from the airways. In order to help with the clinical diagnoses, the timing and pitching of the crackles is important as stated below;

Vocal resonance (see tactile fremitus)

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CRACKLES

Early-inspiratory crackles(Cease before the middle

of inspiration)

Pan-inspiratory crackles

Medium coarseness

COPD, disease of the small airways

Fine/Rales(high pitched, discrete and can be cleared by

cough)

Medium crackles(presence of alveolar

fluids disrupt the function of the

normally secreted surfactant)

Coarse/crepitation(loud bubbly noise, unpleasant gurgling

quality and not cleared by cough)

Pulmonary fibrosis Left ventricular failure with pulmonary

oedema

Bronchiectasis

SPECIAL signs

NICOTINE STAINING

DefinitionStaining of the finger due to tar content of the cigarettes, not the nicotine as nicotine is colorless

Causes – cigarettes smoking

MUSCLE WASTING

DefinitionWasting of the small muscles of the hand especially thenar and hypothenar muscle.

Causes – tumour compressing the brachial plexus

FLAPPING TREMOR (ASTERIXIS)

DefinitionThe excessive shivering or vibrating of the hand

Causes – hypercapnia in COPD

DISPLACEMENT OF THE TRACHEANormal trachea is located centrally and slightly to the right

Abnormal displacement is due to theTowards the lesion Away from the lesionUpper lobe collapseUpper lobe fibrosisPneumonectomy

Massive pleural effusionTension pneumothorax

Hyperinflated lung

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Tumour compressed the brachial plexus

Cut off innervations of the hypothenar

muscle

Muscular atrophy MUSCLE WASTING

PNEUMONIA

DefinitionInflammation of the lung causes by bacteria or virus which the alveoli becomes fills with inflammatory cells and solid

Causes Pathogen

Streptococcus pneumoniaeHaemophilus influenza, Mycoplasma pneumoniaStaphylococcus aureus, Legionella sp., Moraxella catarrhalis, Klebsiella pneumoniaCorxiella bunetii, anaerobes, viruses

HostMucociliary tract impairment as in smokingLoss or suppression of cough reflex – coma, sedatives, drugsDisturbed pulmonary circulationInterfered immune response – immunodeficiency patient, alcohol, anoxia

Classification

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PNEUMONIA

Clinical classification Morphology classification

Community Acquired Hospital acquired/nosocomial

Bronchopneumonia Lobar pneumonia

Typical Atypical

Common

Rare

Acquired in the places other than hospital

Acquired more than 48 hours after admission to the hospital

Common pathogens is as stated above

1. S pneumonia2. H influenzaEtc.

Common pathogens are;1. Staphylococcus

aureus2. Pseudominas sp.3. Klebsiella sp.4. Bacteroides5. Clostridia

Consolidation of a large portion or the entire

lobe

Patchy consolidation involving one lobe or multi

lobe and frequently affecting bilateral and

basal.

Pathogenesis (applied to the lobar pneumonia)

1. Congestion- Occurs in the first few days (1-2 days)- Lung become heavy, red and boggy due to the vascular engorgement as an acute

inflammatory response (see acute inflammation in the foundation block)- Presents of few neutrophils and numerous bacteria

2. Red hepatization- Occurs at the 2-4 days- Lung become firm, airless and liver like consistency due to the exudation of erythrocytes,

neutrophils and fibrin in the alveoli space3. Gray hepatization

- Occurs at the 4-6 days- Lung become dry and grayish brown due to the disintegration of the erythrocytes- More neutrophils and consistent exudation of the fibrinosuppurative element

4. Resolution- Occurs at the 7-9 days- Exudated material becomes consolidated and it is enzymatically digested to produce

granular, semi-fluid debris- The digested material is either reabsorbed, coughed up, ingested by macrophage or

organized

Signs and symptoms

Symptoms Signs- fever with chills and rigors- productive cough- pleuritic chest pain- dyspnoea

- reduce chest expansion- increase tactile fremitus- dullness on percussion- bronchial breath sound- crackles, increase vocal resonance- pleural rub

Prognosis- Lung abscess- Empyema,- Seeding through other part of the body- Fibrosis

PULMONARY TUBERCULOSIS

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DefinitionIs an inflammation of the lung caused by the bacillus Mycobacterium sp. and characterized by the formation of the nodular lesions (tubercles) in the tissue

CausesPathogens

1. Mycobacterium tuberculosis2. Mycobacterium bovis3. Mycobacterium avium4. Mycobacterium intracellulare

ClassificationPrimary tuberculosis Secondary tuberculosis

Presence of Ghon focus with hilar lymphadenopathy usually in children

reactivating or regenerating of primary lesion usually occurs in children

Signs and symptoms

Symptoms Signs- Low-grade fever- Cachexia- Anemia of chronic disease- Dyspnoea - Night sweats- Haemoptysis- Productive cough

- Lymphadenopathy- Tachypnoea

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Pathogenesis

Prognosis

- Apical fibrocalcific arrested- Miliary tuberculosis via lymphatic channel- Systemic military tuberculosis via hematogenous spread- Pleural effusion, empyema- Lymphadenitis- Systemic amyloidosis- Scar cancer

BRONCHIECTASIS

Definition

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Mycobacterium enters body via;1. Inhalation2. Ingestion of sputum/contaminated milk3. Direct penetration through abraded skin

Enters of the alveolar macrophage via receptor mediated endocytosis (mannose receptor)

Mycobacterium replicates within phagosome by inhibiting the fusion of the lysosome and phagosome

Infected macrophage presents the bacteria with MHC class II

Production of IL-12

Maturation of TH1 cell

Produce IFN-γ

Activates macrophage by stimulation of the production of the phagolysosome of the infected macrophage

Production of α-TNF by activated macrophage

Formation of granuloma and caseous necrosis

Permanent dilation of bronchi and bronchioles caused by destruction of the muscle and elastic tissue resulting from or associated with chronic necrotizing infection

Causes1. Congenital – primary ciliary dyskinesia, cystic fibrosis, congenital hypogammaglobunaemia2. Acquired – infection during childhood, pneumonia, allergic bronchopulmonary aspergillosis3. Others - obstruction and severe infection, smoking

Pathogenesis

Signs and symptoms

Symptoms Signs Fever CachexiaHaemoptysisCough with voluminous, purulent, foul smelling sputum

ClubbingCyanosisWidespread CracklesSign of respiratory failureSign of cor pulmonale

COR PULMONALE

Definition

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Anatomical defects of the ciliary tract/impaired respiratory tract

clearance/obstruction and infection

Pooling of secretion distal to the obstruction

Inflammation of the airways

Inflammatory reaction which induce the secretion of protease and TNF

Destruction of smooth muscle and elastic tissue

BRONCHIECTASIS

Is an enlargement of the right ventricle resulting from the diseases affecting the lungs and pulmonary vessels.

CausesPrimary causesIdiopathicSecondary causesPulmonary vascular disorder – pulmonary embolismePulmonary obstructive disorder – COPD, obstructive sleep apnoeaPulmonary restrictive disorder – interstitial lung disease

Pathogenesis

BRONCHIAL ASTHMA

Definition

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Pulmonary structures or pulmonary vascular disorder

Normal flow in the pulmonary circulation obstructed

Increase pulmonary vascular resistant

Pulmonary hypertension (>50 mmHg)

Flow of the blood obstructed especially at the right ventricle

Right ventricular pressure increase

Increase workload of the heart

Hypertrophy of the heart as a compensatory mechanism

Right ventricular hypertrophy

COR PULMONALE

Is a condition of subjects with widespread narrowing of the bronchial airways, which changes in severity over short periods of time either spontaneously or under treatment. It is characterized by several episodes of dyspnoea, cough and wheeze caused by reversible airways obstruction

Causes Bronchial muscle swelling – triggered by variety of stimuli Mucosal swelling/inflammation – mast cell and basophil degranulation Increase mucus secretion – inflammatory mediators

Precipitating factorsCold airExerciseEmotionAllergens (house dust mite, pollen and animal fur)InfectionDrugs (aspirin, NSAIDs, β-blockers)

Further history regarding asthma

1. History of acid reflux, eczema, allergy?This has a known association with asthma

2. Exercise and disturbed sleepQuantify the exercise tolerance and quantify as nights per week as they can be a sign of serious asthma

3. Occupational historyIf symptoms remit at weekend or holidays, something at work may be a trigger. Certain substance such as dust, pollens can cause asthma

Drugs of asthma Sympathomimetics (ß2 receptor agonists) Methylxanthines Antimuscarinics Corticosteroids Mast cell stabilizers Leukotriene pathway inhibitors Others – anti-IgE monoclonal antibodies

Pathogenesis

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Inhalation of the allergens and causative factors

Immunoglobulin E (IgE) simulates

Abnormal antibodies (IgE) stimulates mast cells in the lung interstitium

Release histamine and SRS-A (slow reacting substance of anaphylaxis),

Signs and symptoms

Symptoms SignsIntermittent dyspnoea

WheezeNon-productive cough

TachypnoeaProlonged expiration

TachycardiaUsage of accessory muscle of respiration

Audible wheeze (rhonchi)Hyperinflated chest

Hyperresonance percussionPolyphonic wheeze

Tachycardia

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Definition

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Inhalation of the allergens and causative factors

Immunoglobulin E (IgE) simulates

Abnormal antibodies (IgE) stimulates mast cells in the lung interstitium

Release histamine and SRS-A (slow reacting substance of anaphylaxis),

Emphysema – is a permanent dilation of the alveoli distal to the terminal bronchioles accompanied by destruction of their wall without fibrosisChronic bronchitis – persistent productive cough for at least 3 consecutive months in at least 2 consecutive years

CausesEmphysema – smoking and rarely α1-antitrypsin deficiency (functional or congenital)Chronic bronchitis – smoking

Pathogenesis

Signs and symptoms

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Tobacco smoking

Nicotine

Act as chemoattractant for neutrophil

Reactive oxygen species (free radical)

Activates inflammatory cell

Release IL-8, leukoterine B4 and

TNF

Increase the level of oxidant

Depletes the antioxidant level at the lung

Inactivation of antiprotease

(functional α1-antitrypsin deficiency)

More neutrophil

Increase neutrophil elastase

Tissue damage

EMPHYSEMACongenital α1-antitrypsin deficiency

protease-antiprotease imbalance

Oxidant-antioxidant imbalance

Symptoms Are not specific to distinguish between chronic bronchitis and emphysema. However, symptoms of COPD include;

Productive cough Dyspnoea Weight loss Fever

SignsEmphysema Chronic bronchitis

Pink puffer appearance – pursed lip breathing & well oxygenated

Barrel shaped chest (increase AP diameter) Tachypnoea Reduced expansion Hyperinflated chest Hyperresonance and absence liver dullness Decrease breath sound Early inspiratory crackles Sign of right heart failure

Blue bloaters – cyanosis Hyperinflated chest Reduced expansion Hyperresonance on percussion Reduced breath sound Low pitched wheezes Early inspiratory crackles Sign of right heart failure

Drugs for COPD Β2-agonist (salbutamol, procaterol, fenoterol) Antibiotics (co-trimoxazole, cefprozil, cefuroxime) Anticholinergics Corticosteroids (prednisolone, prednisone) Methylxantines (doxofylline, aminophylline)

PULMONARY HYPERTENSION

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DefinitionA condition in which there is raised blood pressure (>50 mmHg) within the blood vessels supplying the lungs

CausesPulmonary embolismeArterial septal defectHeart failureDisease of the mitral valveChronic lung disease

Pathogenesis

Pulmonary structures or pulmonary vascular disorder

Normal flow in the pulmonary circulation obstructed

Increase pulmonary vascular resistant

Pulmonary hypertension (>50 mmHg)

Signs and symptoms

Symptoms SignsDyspnoea

Cold extremitiesHoarseness (pulmonary artery compression of left

recurrent laryngeal nerve)Paroxysmal Nocturnal Dyspnoea

OrthopnoeaSigns of pulmonary oedema

TacypnoeaPeripheral cyanosis

Small volume due to low cardiac outputIncrease JVP

Right ventricular heaveSign of right ventricular failure

PLEURAL EFFUSION

ONN08/09

DefinitionIs a collection of fluid in the pleural space

TypesCollection consisting of

1. Blood – haemothorax2. Chyle – chylothorax3. Pus – empyema

Causes Transudate – cardiac failure, hypoalbunaemia, hypothyroidism, Meigs syndrome Exudate – pneumonia, neoplasm, tuberculosis, pulmonary infarction, trauma Haemothorax – severe trauma, rupture of pleural adhesion containing a blood vessel Chylothorax – trauma, surgery, carcinoma or lymphoma Empyema – pneumonia, lung abscess, bronchiectasis, tuberculosis

Pathogenesis

Signs and symptomsSymptoms Signs

No signs Trachea and apex beatReduce expansion on the affected site

Stony dullness on percussionReduce/absent breath sound

Reduce vocal resonance

ONN08/09

Infection

Exudation of inflammatory cells

Exudation to the pleural surface

Accumulation of fluid inside the pleural cavity

Pleural effusion

NORMAL VALUES OF THE INVESTIGATION

HaematologyRBC Male (4.6 - 6.5 x 1012 /L)

Female (3.9 – 5.6 x 1012 /L)White cell countAdult 4 – 11 x 109 /LInfant (full term at birth) 10 – 25 x 109 /LInfant (1 year) 4 – 18 x 109 / LBasophil 0 – 0.1 x 109 /L (0 – 1%)Eosinophil 0.01 – 0.44 x 109 /L (1 – 6%)Neutrophil 2 – 7.5 x 109 /L (40 – 75%)Monocyte 0.2 – 0.8 x 109 /L (2 – 10%)Lymphocyte 1.3 – 3.5 x 109 /L (20 – 45%)

ESR male (3 -5 mm/hr)Female (4 – 7 mm/hr)

Arterial Blood GasesPaO2 75 – 100 mmHgPaCO2 35 – 45 mmHgpH 7.35 – 7.45HCO3 22 – 36 mmol/L

Chest X-rayLung field anterior ribs (6 – 7)

Posterior ribs (9 – 10)Cardiothoracic ratio 50 – 55%

Peak flow meter male (600 L/min)Female (400 L/min)

Spirometry FEV1/FVC ratio is 80%

ONN08/09

THANK YOU FOR ALL THE LECTURES OF PPSP USMKK FOR ESPECIALLY AS STATED BELOW FOR CHECKING, CORRECTING ALL THE FACTS WHICH WERE PUBLISHED AND FOR TEACHING MEDICAL STUDENT BATCH 2008/2009 2ND YEAR WITH HARDWORKING AND GREAT DEDICATION

1. ASSOCIATES PROF OTHMAN MANSOR2. DR THIN THIN WIN @ SAFIYA3. DR SAMARENDA S MUTUM4. DR ISKANDAR ZULKARNAIN ALIAS5. DR MOHD ASNIZAM ASARI

REFERENCE 1. PPSP lectures Lecture notes 2nd year 2008/20092. Oxford Concise Medical Dictionary, 6th edition – definition3. Clinical Examination, 5th edition, Nicholas J Talley and Simmon O’Connor – clinical signs4. Differential diagnosis, 2nd edition, Andrew T Raftery and Eric Lim – clinical signs and symptoms5. Pathology Basis f Disease, 7th Edition, Robbins and Cotran – pathogenesis of diseases6. MIMS respiratory guide, Malaysia Edition 2004/2005

ONN08/09Al-fatihah kepada arwah bapa saya, Puade bin Mahbar yang telah meninggal dunia pada 20 Ogos 2008 di Muar pada umur 66 tahun, semoga roh arwah dicucuri rahmat dan ditempatkan di kalangan orang-orang yang