everything you need to know respiratory system
TRANSCRIPT
Everything You Need to Know (at least) for
ONN08/09
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Year –
Matric no. –
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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