Upper and lower respiratory disease

A-a gradient

A alveolar ( normal value pls?) a arterial ( normal value pls?) What is the normal value of A-a

gradient?

How to calculate normal pA02?0.21(760-47mmHg) – 40/0.8**

Physiology refreshment Which place have better ventilation? Which place have better perfusion? (Apex ? Lower lobe of lung? )

Hence, where is the most likely place for reactivation of TB?Where is the most likely place for lung infarction? ( Apex ? Lower lobe of lung?)

A-a gradient shouldn’t increase more than 30 mmHg hypoxemia

What is hypoxemia? ( decrease PaO2 ) What is the cause of hypoxemia? Which of the following increase A-a gap?

pulmonaryExtra-

pulmonary

Pulmonary cause1) Ventilation defect ( eg. Airways

collapse due to RDS )2) Perfusion defect ( eg. Pulmonary

emboli)3) Diffusion defect ( eg. Interstitial

fibrosis)4) RightLeft cardiac shunt ( tetralogy of

Fallot )

Extrapulmonary causes Normal A-a ratio1) Depression of respiratory center ( barbiturate overdose , brain injury )2) Obstruction of upper respiratory tract ( epiglossitis – heamophillus , croup – parainfluenza virus )3) Chest bellow dysfunction ( paralyze diaphragm , ALS )

Common symptom of respiratory disease DyspneaDue to stimulation of J-receptors ( hence cannot take full deep breathe )

Causes:Decrease compliance ( interstitial fibrosis)Increase airway resistance ( bronchitis)Chest bellow disease ( kyphosis, obesity )Inflammation/ fluid accumulation ( LS-HF)

Cough1) Nocturnal cough: GERD ( acid reflux to

bronchial tree )2) Bronchial asthma( bronchoconstriction)3) Productive cough: chronic bronchitis ,

bacterial pneumonia, bronchiectasis4) Drug-induced cough: ACE inhibitor

( bradykinin) Aspirin ( increase LTDE4)

Hemoptysis

Causes: Chronic bronchitis Pneumonia Bronchogenic carcinoma TB , bronchiectasis Aspergilioma

Sign of respiratory diease Tachypnea

More than 20 bpm Causes: restrictive lung disease,

pleuritic chest pain , pulmonary embolus with infarction.

Vocal fremitusE , 1,2,3 , 99 , 33 ( russian)Increase: lobar pneumonia ( increase consolidation ) Decreased: emphysema, asthma ( increase AP diameter & total lung volume )Absent: atelectasis , pleural effusion , pneumothorax

Percussion

Dull: atelectasis ( no air inside ), pleural effusion ( fluid ) Lung consolidation ( lobar pneumonia)

Hyper resonant: pneumothorax , asthma, emphysema

UPPER RESPIRATORY DISORDER Choanal atresia

90% bony ,10% membranous Baby turn BLUE ( cyanosis ) when breast

feeding Turn pink when start crying WHY?????

Nasal polyps

Develop as responses to chronic Inflammation. Allergic polyps ( adults ):Associated with IGE mediated allergies. Nasal polys ( child ):Associated with cystic fibrosis(sweat test )

OSA ( obstructive sleep apnea)Excessive snoring with intervals of breath cessation.MCC: obesity , nasal deviation etc..Respiratory acidosis hypoxemia. ( increase PaCO2)

Complication : Pulmonary HTN followed by RVH ( hypoxemia and acidosis stimulate smooth muscle cell in pulmonary to VASOCONSTRICT pul HTN RVH ( cor pulmonale )

Nasopharyngeal carcinoma Related to EBV Common in Chinese and Africans .

Squamous cell carcinoma, can metastasize to cervical lymph node.

Laryngeal carcinoma MCC : smoke + alcohol ( synergistic effect )Symptom: hoarseness of throat Squamous cell carcinoma

AtelectasisInadequate expansion of lung volume ( collapse )Symptom : fever and dyspnea

absent breathe soundabsent vocal fremitus

Causes: Resorption Compression loss of surfactant

Resorption atelectasis Air-way obstruction by thick secretion

( bronchioles, bronchi ,segmental bronchi)

Causes: mucus or mucopurulent plug aspiration of foreign materials centrally located bronchogenic carcinoma

Compression atelectasis Air or fluid in pleural cavity under

pressure compressed and collapse small airways beneath the pleura.

Causes: tension pneumothorax ( air ) pleural effusion ( fluid )

Loss of surfactant Surfactant function? Who synthesize surfactant ? Phosphatidylcholine is major component Synthesize is increased by cortisol

decrease by insulin.

RDS in newborn Causes: prematurity ( why/ manage?)

Diabetes mum (why/manage?) C-section (why/manage?)

Widespread atelectasis massive intrapulmonary shunting

Shunt? ( perfusion w/o ventilation) Symptoms: Respiratory difficulty few hours after birth Tachypnea Hypoxemia and respiratory acidosis Chest radiograph show “ground-glass”

appearance.

Complications: Superoxide free radical damage from o2 therapy (

may result in blindness and Broncho pulmonary dysplasia )

Intraventricular heamorrahge PDA ( hypoxemia after born, hence ductus remain

patent – machinery murmurs) Necrotizing enterocolitis ( intestinal ischemia

allow the entry of gut bacteria to intestinal) Hypoglycemia in newborn ( why baby had

macrosomia and hypoglycemia?)

Type 2 pneumocytes lamellar bodies Where surfactants is stored Why hyaline membrane? Degeneration of type 2 pneumocytes

and leakage of fibrinogen.

RDS adult What’s the difference btw infant RDS and

adult RDS? ( inflammation and neutroplil related injury )

Causes: Gram-ve sepsis ( MCC) Gastric aspiration Severe trauma with shock DIC, SARS , fat embolism etc etc.

Sign and symptom: Dyspnea/ tachypnea Late inspiratory crackles Severe hypoxemia not responsive to O2

treatment Pulmonary artery wedge pressure

<18mmHg ( in cardiogenic pul edema is >18mmHg)

Respiratory acidosis Increase A-a gradient.

Pathogenesis Acute dmg occur in alveolar wall cytokines

released attract neutrophils pulmonary capillaries destroyed become hyaline membrane( that’s why we have hyaline in ARDS, leaky capillaries syndrome ) neutrophils destroy type1 and 2 pneumocytes massive intrapulmonary shunts, no surfactant

Poor prognosis.

Pulmonary edema Edema due to alteration of starling forces Increase hydrostatic pressure:1. LHF,2. Volume overload3. Mitral stenosis Decrease oncotic pressure 1. Nephrotic syndrome2. Liver cirrhosis Infection Aspiration Drugs High altitude ARDS

PNEUMONIAPnuemon

ia

nosocomial

atypicaltypical

Community acquired

Typical pneumonia MCC: step pneumonia Sign and symptoms: 1. Sudden onset of high fever with

productive cough2. Chest pain3. Tachycardia4. Sign of consolidations ( increased vocal

fremitus, dullness to percussion, late inspiratory crackles, bronchial breath sound.)

Patchy infiltration and lobar consolidations on chest X-ray.

Consolidations ( collection of neutrophil in alveoli and bronchi )

Pathogenesis1. Micro aspiration of oropharyngeal

content when sleeping. ( MCC)2. Inhalation of aerosol drop.3. Bloodstream infection.

Bronchopneumonia

Acute bronchitis spread locally to lung Lower lobe and right middle lobe usually

involved. Patches of consolidations Micro abscess is present around area of

consolidations.

Lobar pneumonia

Complete or almost complete consolidations of whole lobe of lungs.

Complications

Lung abscess Empyema ( pus in pleural cavity ) Sepsis

Lab findings

Positive gram stain Neutrophilic leukocytosis Blood culture positive in 20% of cases.

Atypical community acquired pneumoniaMCC : mycoplasma pneumoniae

Sign and symptoms : Insidious onset , low grade fever Non-productive cough Chest pain Flu-like symptom NO SIGN of consolidations

What's the difference btw typical and non-typical pneumonia?

Pathogenesis

Contracted by air droplets Mononuclear infiltrate Alveoli usually free of exudate. ( no sign

of consolidations )

Nosocomial pneumonia Sources : Respirators ( MCC ) Severe underlying diseases Antibiotics ImmunosuppressionMCC pathogen :1. Pseudomonas aureginosa2. E.coli3. Staph .auereus( staph in hospital , strep in self inhalation )

Tuberculosis Pathogen : mycobacterium TB Organisms resides in alveolar

macrophage. Produces a protein called cord factor to

prevent fusion of lysosomes and phagosomes. ( type 4 HSV )

Strict aerobes , acid fast ,cord factor is virulence factor.

Screening test : PPD ( purified protein derivatives

intradermal skin test ) Does not distinguish between active

infection from inactive diseases. Protein in cell wall is responsible for

PPD.

Primary TB Sub pleural location Upper part of the lower lobe and lower

part of the upper lobe Ghon focus in the periphery Ghon complex in the hilar lymph

nodes. What is Ghon focus/ complex? ( caseous necrosis )

Primary TB usually will reside itself. May produce calcified granuloma or

area of scar tissues. May be a nidus of secondary TB.

Secondary TB Due to reactivation of primary TB site.

( immunocompromised patients ) Involves 1 or both apices of upper lobe. ( why???? Can still recall??? ) ( Upper lobe highest ventilation , mycoplasma is

strict aerobes.) Cavitary lesion is due to release of cytokines from

memory T cells. NO GHON COMPLEX/FOCUS present in secondary

TB.

Clinical findings: Night sweat , fever , weight lost Complications : Miliary spread in lungs due to invasion of bronchus and

lymphatics. Miliary spread to extra pulmonary site.1. Spread through invasion of pul vein tributaries.2. Kidney most common affected.3. Adrenal involvement may produce Addison disease.

( primary hypocorticolism) Massive hemoptysis , bronchiectasis ,scar carcinoma Granulomatous hepatitis , spread to vetebrae ( Pott’s

disease )

Diagnosis: Broncho alveolar lavage Sputum culture Treatment: Isoniazid + rifampin + pyrazinamide Non-infections in 2 to 3 weeks Treat for additional 9-12 months. ( kills metabolic inactive persistors in

lesion)

Lung abscesses MCC : aspiration of oropharyngeal materials. Alcoholism Loss of consciousness Dental work Pathogens: Aerobic and anaerobic steptococci Staphylococcus Fusobacterium Anaerobes

Can be derived from bacterial pneumonia

Staphylococcus Klebsiella Septic embolism Obstructive lung neoplasia

Findings: Vary in size and places Located mainly in right side ( due to

aspiration of oropharynx ) Spiking fever Productive cough ( foul-smelling sputum

) Chest imaging show cavitation with an

air-fluid level.

Pulmonary thromboembolism 3rd MCC dead after AMI and stroke. Sources: 90% originate from lower extremities. Calf vein popliteal femoral vein lung.

Risk factors: Virchow triad ( hypercoagulability, stasis,

endothelial injury )

2 types of emboli ( small and huge ) Pulmonary artery occlusion may cause

hemorrhagic infarct when there is underlying lung diseases ( obstructive lung Dz/ decrease cardiac output )

Hemorrhagic infarct higher chance of morbidity and mortality.

Small emboli may produce raised, red-blue wedge shape infarction extend to pleural surface.

Pleural surface had fibrinous exudate ( produced pleural friction rub )

Majority located at lower lobe ( perfusion > ventilation )

Big emboli ( saddle embolus ) Sudden increase in pulmonary artery pressure Produce acute right ventricular strain and

sudden cardiac deathSymptom:1. Sudden onset of dyspnea and tachypnea 2. Fever3. Pleuritic chest pain ( pain on inspiration), friction

rub , effusion4. Expiratory wheezing ( release of thromboxane A2

from platelets – bronchoconstriction )

Lab findings: Respiratory alkalosis PaO2 < 80mmHg ( perfusion defect ) Increase A-a gradient Increase in D dimers

Pulmonary angiogram gold standard( defects in perfusion, normal in ventilation.)Chest x-rayD-dimer test.

Pulmonary hypertension Mean pulmonary arterial pressure > 25mmHg

at rest ( normal 15 mmHg ) > 30mmHg when exercise ( normal 20 mmHg)

Primary pulmonary hypertension Women > men Genetic predisposition Vascular hyperactivity with proliferation of

smooth muscle

Secondary pulmonary hypertension Endothelial cells dysfunction ( decrease NO , increase endothelin ) Hypoxemia , respiratory acidosis ( smooth muscle hyperplasia and

hypertrophy )Causes :1. Chronic lung disease2. Living in high altitude3. OSA4. Emphysema5. Recurrent pulmonary emboli6. Left to right cardiac shunt7. Mitral stenosis8. drugs

Findings: Atherosclerosis of pulmonary artery Exertional dyspnea ( mc presenting

sign) Chest pain Accentuated P2 Left parasternal heave ( RVH ) Right sided failure ( cor pulmonale)

Diagnosis ECG ( right ven hypertrophy , right atrial

enlarge , right axis deviation) Chest X ray Doppler echocardiogram

Restrictive lung diseases Reduced total lung capacity in presence of

normal or reduced expiratory flow rate. Decrease FEV1 Decrease TLC Decrease FVC Increase ratio FEV1/FVC Respiratory alkalosis ( PaCo2 < 33mmHg) Decrease PaO2Normal physiological value pls?

Sign and symptoms: Dry cough and exertional dyspnea Late inspiratory crackles in lower lung

field Potential for cor pulmonale Decrease lung compliance Increase lung elasticity ( contribute

less air in the lung )

Causes:Chest wall disorders: Kyphoscoliosis Obesity Pleural disease

Acute or chronic interstitial lung diseases: Acute interstitial lung disease ( ARDS ) Chronic interstitial lung disease ( idiopathic pulmonary

fibrosis , pneumoconiosis ) Granulomatous disease ( sarcoidosis )

Pneumoconiosis Inhalation of mineral dust leading to interstitial lung diseases Silica , asbestos, beryllium are very fibrogenic.

Coal worker pneumoconiosis Sources of coal dust ( anthracotic agent ) Coal mine , large urban area, tobacco smoke Crippling lung disease ( black lung disease ) No increase TB or primary lung cancer Cor pulmonale may occur Caplan syndrome may occur ( rheumatoid arthritis +

pneumoconiosis )

Silicosis Most common occupational disease in the world Quartz, sand blasting , mines etc. Quartz highly fibrogenic and attract

macrophages. Macrophages release cytokines and stimulate

fibrogenesis. Nodular opacities found on chest x ray on

chronic exposure. egg-shell calcification in hilar nodes.

Can get cor pulmonale Can get caplan syndrome. Increase risk of cancer and TB.

AsbestosisSources: Insulation around pipe in old naval ships Roofing materials, ceiling tiles, floor tiles

> 20 yrs ago Demolition of old building Automobile shop

Macrophages coated the asbestos fibers with ferritin and protein ( ferruginous bodies )

Golden beaded appearance in sputum or distal air ways.

Asbestos related diseases: b9 pleural plaque Most common asbestos lesion. Not a precursor lesion for mesothelioma.

Primary bronchogenic carcinoma Synergism with smoking Takes 20 years to developed.

Malignant mesothelioma of pleura Non-association with smoking Arises from serosal cells lining the pleura Locally invades subpleural lung tissue 25-40 years to developed.

No increase risk for TB Cor pulmonale , caplan syndrome.

Sarcoidosis Multisystem non-infectious granulomatous

disease that produce chronic interstitial lung disease.

25% cases of interstitial lung disease Unknown origin CD4TH cells react with unknown antigens, release

cytokines causing formation of non-caseating granuloma.

It’s a diagnosis of exclusion ( must rule out every possibility of granulomas diseases )

Targets a lot of organs Lung as primary organ dyspneaGranulomas located in interstistium and mediastinal and hilar lymph nodes.Granulomas contain giant multinucleated cells .( Schaumann bodies –laminated calcium concretions)( Asteroid bodies – stellate inclusions.)

Skin lesionsViolaceous rash on nose and cheeks ( lupus pernio ) Eye lesionsUveitis , blurry visions Liver lesionsGranulomatous hepatitis ( MC non-infection granulomatous hepatitis .. Other is TB infection )

Lab findings: Increase ACE ( granulomas in kidneys) Hypercalcemia ( increase synthesis of 1-

a-hydroxylase in macrophage in granulomas hypervitaminosis D )

X-ray findings: Enlarge hilar and mediastinal lymph

nodes ( potato nodes )Rx: steroids if necessary.

Idiopathic pulmonary fibrosis 30% cases of RLD Repeated alveolitis release of cytokines

produce interstitial fibrosis alveolar fibrosis leads to proximal dilatation of small airways.

Fever ,dyspnea with exertion Non-productive cough Late inspiratory crackles. Honey comb appearance lung

Hypersensitivity pneumonitis Extrinsic allergic alveolitis due to exposure of known allergensFarmer lungInhalation of thermophilic actinomyces in moldy hay.IgG type 3 HSV type 4 HSV ( chronic exposure )

Silo filler diseaseInhalation of gases ( nitric dioxide ) from plant materialsImmediate HSV reaction with dyspnea

Byssinosis Workers in textile factoriesExposure to endotoxin from bacteria growing on the cottonDyspnea upon exposureMondays morning blue/fever diseases.

Drugs associated with interstitial pulmonary fibrosis

Amiodarone Bleomycin and busulfan Cyclophosphamide Methothrexate & methysergide Nitrosourea & nitrofurantoin

COPD Progressive, largely irreversible obstruction to airflow out

of the lung. Cigarette smoking Majority of patients have emphysema and chronic

bronchitis. Elastic tissues is destroyed ( easy to come in, hard to get

out ) TLC increase RV increase A-P diameter increase Tidal volume everything else decrease Decrease FEV1/FEC ratio.

Emphysema Increase compliance , decrease elasticity Permanent enlargement of all parts of

respiratory units Respiratory bronchioles , alveolar ducts ,

alveolar Smoking main cause Alpha 1 antitrypsin deficiency 2 types : centriacinar , panacinar

Centrilobular emphysema Most common type of emphysema among

smokers Apical segments of upper lobe Distal terminals bronchioles and respiratory

bronchioles affected ( site of elastic tissue destruction )

Air trapped behind distal bronchioles and distends the respiratory bronchioles

Increase RV , TLC etc.

Panacinar emphysema Usually genetic or acquired ( smoking ) Associated with alpha-1-antityrpsin deficiency Emphysema developed at early age. Location at lower lobes All parts of respiratory units elastic tissues are

destroyed Air trapped distal to terminal bronchioles

distend to entire respiratory units.

Clinical findings: Dyspnea severe and early in the disease Hypoxemia is late in disease ( why?) Patients call pink-puffer. ( respiratory alkalosis,

hyperventilation ) Barrel chest Breathe sound is diminished. ( hyperinflation ) Hyperlucent lung fields Increase A-P diameters Vertically orientated heart Depressed diaphragm ( hyper inflated lung)

Chronic bronchitis Productive cough for at least 3 months , 2

consecutive years Causes : smoking , cystic fibrosis Hypersecretion of mucus occurs in bronchus

and its subdivision. Obstruction to airflow occurs from mucus plugs

located in segmental bronchi and bronchioles. Irreversible fibrosis might occur in chronically

inflammed bronchi and bronchioles.

Changes in bronchus Hypersecretion of submucosal mucus secreting

glands in trachea and bronchi. ( sputum overproduction )

Loss of ciliated epithelium and squamous metaplasia.

Changes in bronchioles Mucus plug in lumen ( block exodus of CO2 ) Goblet cells metaplasia Chronic inflammation and fibrosis narrowing

lumen.

Clinical findings: Productive cough Dyspnea occur in late stage Hypoxemia and respiratory acidosis

early in disease . Blue bloaters ( cyanosis ) Stocky or obese Expiratory wheezing and rhonci

Lab findings: Large , horizontally oriented heart Increase bronchial markings TLC RV increase ( less than

emphysema ) Chronic respiratory acidosis ( PaCo2 >

45mmHg ) Hypoxemia early

Comparison emphysema vs chronic bronchitis Parameters Emphysema Chronic

bronchitis

PaO2 Decreased decreased

PaCO2 Normal to decreased

Increased

pH Normal to increased

Decreased

Cyanosis Absent ( pink puffers )

Present ( blue bloaters )

Habitus Thin Obese / stocky

Cor pulmonale Rare Common

Onset of hypoxia Late Early

Onset of dyspnea Early Late

Bronchial asthma Targets bronchi and non-respiratory

bronchioles Children > adults ( 50-80% develop

before age 5) Intrinsic and extrinsic factor

Extrinsic asthma Type I HSV due to extrinsic allergens Related to CD4 TH2 release IL4 and IL 5 Inhaled antigens cross-link IgE antibodies

on mast cells on mucosal surface. Released histamine and other pre-formed

mediators ( bronchoconstriction , mucus production, influx of leukocytes )

LTC, D, E4 promote bronchoconstriction

Clinical findings: Bronchi : thickening of basement membrane ,

edema , inflammatory infiltration, hypertrophy of submucosal glands, hypertrophy of smooth muscle cells

Bronchioles : Curschmann spirals ( shed epithelial cells ) , Charcot-Leyden-crystals( crystalline granules in eosinophils )

Goblet cells metaplasia Thick basement membrane Smooth muscle cells hypertrophy and hyperplasia.

Expiratory wheezing Nocturnal cough Increase A-P diameter Initially respiratory alkalosis

respiratory acidosis ( bronchospasm not relieved )

Eosinophilia, positive skin test allergens Check FEV1

Intrinsic asthma non-immune Causes: virus induced respiratory

infection Air-pollutans Aspirin NSAIDs induced Stress , exercise cigarette smoke

Bronchiectasis Permanent dilation of bronchi and

bronchioles causing repeated episodes of airway infection and inflammation.

Due to chronic destruction of cartilage and elastic tissues by chronic necrotizing infections.

Causes: Cystic fibrosis TB Bronchogenic obstruction ( bronchogenic

carcinoma) Primary ciliary dyskinia ( absent dynein arm

in cilia – Kartagener syndrome ) Kartagener syndrome – sinusitis , male

infertile ,female infertile ( why?) dextocardia (why?)

Findings: Mostly in lower lobes Dilated bronchi and bronchioles fill with pus Dilated airways ( tube-like/saccular ) extend

to lung periphery. productive cough ( cupful sputum ) Sometimes massive hemoptysis Digital clubbing Cor pulmonale

Cystic fibrosis Autosomal recessive Whites ( 98%) Defect in CFTR gene ( loss of CI- reabsorption in

sweat glands ) ( diagnosis sweat test ) In epithelial cells ( decreased CI- excretion out of

epithelial cells , increase water and NA+ reabsorption into epithelial cells )

Hence , the secretion is extremely dehydrated. Bronchioles, pancreatic ducts ,bile ducts,

meconium, cervix and seminal fluids.

Clinical findings: Nasal polyps Heat exhaustion Respiratory failure/ infections ( pseudomonas aueruginosa

MC ) Pneumothorax ( rupture of blebs ) Malabsorption ( 80%) ( pancreatic exocrine deficiency,

atrophy glands , chronic pancreatitis ) Type I DM Infertility in males ( 95%) ( atresia of vas deferens ) Meconium ileus Gallstone ( stasis of thickened bile ) Secondary biliary cirrhosis ( obstruction of bile )

Increase serum immunoreactive trypsin level

Sweat chloride > 60mmoL/L ( adults children)

Pancreatic enzyme replacement Vitamins ( fat-soluble ) replacement

Lung tumor Associated with > 30% death in men Associated with > 25% death in women Causes: Smoke ( MC ) Radon gas Asbestos Second hand smoke Genetic factors

Divide into small cells and non-small cells carcinoma

Primary lung cancer in decreasing incidence:

Adenocarcinoma Squamous cell carcinoma Small cell carcinoma Large cell carcinoma Bronchial carcinoid.

Squamous cell and small cell carcinoma Greatest smoking association Centrally located ( main stem bronchus ) High frequency of p53 mutation May ectopic secret PTH-related peptide In small cells carcinoma , may ectopic secret ADH or

ACTH. Keratin red pearl under pap smear ( squamous cell

carcinoma ) Small cells carcinoma looks like lymphocytes Auput tumors with neurosecretory granules and S-100

antigen positive.

Adenocarcinomas Weakest smoking related Women > men Peripherally located Filters in cigarettes remove large

carcinogens leaving small one to move peripherally.

Common site of metastasis: Hilar lymph node most common site Adrenal gland Liver Brain Bone

Solitary pulmonary nodules Coin lesion, peripheral lung nodule <

5cm Causes in decreasing order : Granulomas ( TB, histoplasmosis ) Malignancy ( primary cancer ) Bronchial hamartoma

Metastatic cancer Most common lung cancer Cancers most often responsible for metastasis: Breast cancers Colon cancer and renal cell carcinoma Sites for lung metastasis: Parenchyma Pleura and plueral space ( malignant effusion) Lymphatics ( cause severe dyspnea )

Symptoms: Dyspnea Cough Weight lost Chest pain Hemoptysis

Pancoast tumor Related to small cell carcinoma at

extreme apex of lung Destruction of superior cervical

sympathetic ganglion produce Horner syndrome ( ipsilateral lid lag, ipsilateral anhydrosis, ipsilateral miosis )

Superior vena cava syndrome

Paraneoplastic syndrome Digital clubbing ( due to reactive

periosteal changes in underlying bone ) Muscle weakness ( Eaton-lambert

syndrome )– antibody directed againts calcium channel.

Ectopic hormone secretion Related to small cells carcinoma

Diagnosis X ray ( central mass – squamous and

small cells ) ( peripheral mass – adenocarcinoma scar carcinoma )

Sputum cytology Fine needle aspiration Bronchoscopy with lavage

Mediastinum and pleural disorders Mediastinal mass Usually metastatic primary lung cancer in old patients Usually primary disease in young adults Anterior mediastinum is most common site Most common primary mediastinal masses in

descending orders:1. Neurogenic tumor ( posterior mediastinum)2. Thymomas3. Pericardial cysts4. Malignant lymphomas5. Teratoma

Pleural effusion Fluids move from parietal pluera to pleural space

to lungPathogenesis: Increase hydrostatic pressure in visceral pleura

( congestive heart failure ) Decreased oncotic pressure( nephrotic syndrome) Increased vessel permeability of visceral pleura

capillaries ( pulmonary infarction, pneumonia ) Metastasis to pleura ( metastatic breast cancer )

Types of pleural effusion Transudates ( CHF , nephrotic syndrome ) Exudates ( pneumonia , TB ,infarction, metastasis ) pH > 7.4 = transudate pH < 7.4 = exudate Dullness of percussion Absent breath sound Absent vocal fremitus Contralateral shift of mediastinum ( large effusions)

Blunting of costophrenic angle Obscuration of diaphragm

Spontaneous pneumothorax Men > women 20-40 yrs Tall, thin habitusCauses:1. Idiopathic ( rupture of apical sub plural blebs )2. COPD3. Marfan syndrome4. Scuba diving5. Insertion of subclavian catheter

Pathogenesis Rupture of subpleural or intrapleural bleb produces

a hole in the pleural. Hence, loss of negative intrathoracic pressure

causes a portion or entire lung to collapse Sudden onset of dyspnea with pleuritic type chest

pain Tympanitic percussion note Absent breathe sound Trachea deviated to the side of collapse and

diaphragm is up.

Tension pneumothorax Penetrating trauma to the lung ( knife ) Rupture of tension pneumocyst ( S aureus

pneumonias ) Pathogenesis: Flap-like pleural tear allow air into pleural

cavity but prevent its exit. Increased pleural cavity pressure Produced compression atelectasis

Findings: Sudden onset of dyspnea and pleuritic chest

pain Tympanitic percussion note and absent

breath sound Trachea and mediastinal structure deviated

to the contralateral side if tension pneumothorax is large.

Compromised venous return to heart ,if pneumothorax is located on left side.

Relieved pressure first by inserting a needle into second intercostal space on midclavicular line.

Insert chest tube.

Thank you