All Flashcards
Which pneumocytes produce surfactant
T2
Max development of surfactant IuL
35th week
HMD treatment
Mild- CPAP
Severe- IMV+ surfactant replacement
Types and pathology of PAP
Impaired clearance of surfactant by macrophage
Primary- GMCSF Ab ( x macrophages)
Secondary- silicosis (x macrophages)
Investigations in PAP
BAL- Milky white/ PAS +
CXR- Diffuse fine reticulo-nodular infiltrates radiating from the hilum**
CT- CRAZY PAVING
MC bronchus for BXIS
Left main bronchus
(Horizontal, narrow—stasis of secretions-inflammation )
MC in babies
Mc lobe for aspiration overall/supine
RLL Superior»_space; RUL Posterior
Mc lobe for aspiration standing/sitting
RLL Posterior
Mcc if hemoptysis
TB
Mcc if massive hemoptysis
BXIS
Massive hempotysis criteria
> 150ml/ episode
> 400-600ml/day
Mccd hemoptysis
Aspiration of blood clot
Mx persistent hemoptysis
Brochial artery embolization
Resection of affected lobe
Pulmonary artery embolization (rare)
Pneumocytes having dividing capability
T2
Majority of pneumocytes
T2
Pneumocytes covering maximum area of lung
T1
Airway obstruction is prominent during?
Expiration (exp wheeze)
Inspiration is an active process- can overcome obstruction easily comparatively
Factors preventing collapse of alveoli
During expiration
Elastase—(a1 antitrypsin)
Surfactant
Emphysema features
Early- bulla, air trapped in alveoli/ inc RV FRC TLV
Late-Complete encircling of inflammation—decreased oxygen transport to blood
Ideal o2 flow rate and sat for COPD
1-2L/min
88-92%
Mechanisms of hypoxia
VP mismatch (emph/pte)
Shunt (cardiac/pulmonary)
(Pulm= pneum/ILD/Fibrosis/Atelectasis—damaged alveoli)
Diffusion defect (T1RF)
Hypoventilation(T2RF)
Rx for Intra pulmonary shunt/ damaged alveoli
IMV
Supplementary oxygen doesnt work
DLCO normal range and formula
Inhaled CO-Exhaled CO
70-90%
Alveolar conditions causing decreased DLCO
Emphysema
ILD
Fibrosis
Pneumonia
Blood conditions causing decreased DLCO
Anemia
PHTN
PTE
Increased DLCO?
PCV
Alveolar haemorrhage**
ASTHMA** (Eosiniphilic inflammation—increased NO production—inc vessel size)
Exercise
V/P ration is a measure of?
Max
Min
Alveolar oxygen tension
Max= apex
Min= base
(Max venti and max perfusion at BASE)
Tb 1° and 2° location
1= middle/lower zone (max ventilation)
2= apex (max v/q)
Volume at which outward recoil of chest equals inward recoil of lung?
FRC
FeV1 value
70-80%
FVC normal value
> 80%
PEFR significance
MEFR significance
P= flow in large airways (air first moves out of large airways) —-ASTHMA
M= average flow calculated during mid expiration (SMALL AIRWAY)—COPD/EMPHYSEMA
Measurement of RV
Helium dilution
N2 washout
Body plethysmograph ***
Obstructive LD spirometry
FeV1 decreases
FVC normal
RV = INCREASED***
Fev1/FVC = DECREASED
Restrictive LD spirometry
Fev1 DECREASED
FVC DECREASED
Fev1/FVC = normal/increased
Intrinsic RLD
Fibrosis
ILD
OLD
SARCOIDOSIS***
RV/TLC= normal****
(As alveoli gone)
Extrinsic RLD
Kyphoscoliosis
NM diseases (polio/GBS/MG/AL)
Diaphragm palsy
RV/TLC= INCREASES**
(RV normal/ TLC decreases)
Obstructive LD
Asthma
COPD
BXIS
Bronchiolitis
Breathing sounds in
Consolidation
Cavity
Large cavity
Tubular
Cavernous
Amphoric
Causes if rhonchi
Narrow lumen/free liquid/mucus
Asthma P. Edema COPD Foreign body Tumour
Increased vocal resonance is called
BRONCHOPHONY
Increased whispered sounds on steth?
PECTORLIQUOY
E—->A change in sound pronunciation
AEGOPHONY
Wheeze types
Monophonic- Tumor
Polyphonic- COPD/ Asthma
Wheeze heard mainly during?
EXPIRATION
If during inspirtation—severe obstruction
Coarse crepts cause
BXIS
Airflow into secretions
Fine crepts cause
ILD
Fibrosis
Pneumonia
P Edema
(Popping of alveoli)
Velcro crepts due to?
Interstitial FIBROSIS
Aka cellophane crackles/ Bi-basilar
Stony dull note present in
Plef
No push pull lesion with positive breath sounds
Consolidation
AIRBRONCOGRAM++
Cf of HYDROPNEUMOTHORAX
Straight line (not meniscoid)
Shifting dullness
Succusion splash
T1RF PAO2 PaO2 PaCO2 A-a
Normal
Decreased
Normal»increased (Good diffusion)
A-a= INCREASED
T2RF PAO2 PaO2 PaCO2 A-a
Decreased
Decreased
Increased (RESP ACIDOSIS)
Normal
T1RF causes
ILD
Alveolar flooding (pneumonia/ards)
Fibrosis
PTE
T2RF causes- Hypoventilation / decreased respiratory effort
COPD
Central : brainstem injury/ narcotics
Obstructive: COPD (mc) / FB
Peripheral: NMJ Diseases
Diaphragmatic injury
Rx RF
IMV (in T1)
NIV (T2)
C/I NIV
UNCONCIOUS***
Altered sensorium/ unco-op Cardiac arrest Hemo unstable Nasal sx Active GIBleed
ARDS Cardinal features
SOB
Hypoxemia
Pulmonary infiltrates
Reduced lung compliance
(HALLMARK= DAD)
Other names of ARDS
Shock lung
Blast lung
Traumatic wet lung
Direct causes of ARDS
FANTTS
Fat embolism Toxin Transplant (reperfusion injury) Near drowning Aspiration Severe Pneumonia
Indirect causes of ARDS
CABG High altitude Pancreatitis Narcotic poisoning Head injury Sepsis (mc) BT
Normal PCWP
6-12
Pcwp in Cardiogenic PE
> 18
Interstitial edema 18-25
Alveolar edema >25
Which never occurs in T1 RF
HYPERCAPNEA
Berlin criteria for ARDS
Acute SOB
Pul. Infiltrates
Non cardiogenic PE
PaO2/Fio2 < 300. Or. PaO2<60’mmHg
Criteria for Resp failure
PaO2 < 60
PaCO2 > 45
Types of RF
1 Hypoxic
2 Hypercapneic
3 Peri-operative-Atelectasis-GA
4 Shock (Hypoperf of resp muscles)
Mild mod sever ards criteria
PaO2/FiO2
200-300 = mild 100-200 = mod <100 = sev
Rx ARDS
Low TV MV (4-6ml/kg/min)
Adequate PEEP
Steroids
Newer Rx ARDS
ECMO
PRONE VENTILATION (12-16 hrs)- decreased diap compression of alveoli
Misc causes of ARDS
HELD
Hanging
Eclampsia
LF
Renal failure
Presentation time of PTE
cin 2 weeks
Predisposing genetic factors for PTE
Protein C S def
F5L mutation
Hyper- Homocystinemia
R/F PTE
DVT (estrogen pills)
Varicose veins
Trauma
Prolonged immobilization
Pregnancy
Malignancy
Nephrotic syndrome (AT3 excretion)
Lung pathology PTE
HEMOPTYSIS
Platelet thrombus—serotonin—BRONCHOSPASM
LUNG ISCHEMIA
(Pleuritis/Plef/dyspnea/tachypnea)
Mc sign and symptom of PTE
Sign TACHYPNEA
Syp DYSPNEA
Cardio Pathology of PTE
RVH—pushed septum in LV—decreased BP—shock
Cor pulmonale types
RV dysfn due to 1° resp cause excluding causes of keft heart
Acute—-PTE
Chronic- COPD (mc)/ ILD / CF / OSA / BXIS
CXR Findings of COR PULMONALE
Kerley B lines
(LAP > 20 then KBL++)
Prominent ULobe veins
Cardiac shadow
B/L plef
Well’s scoring PTE
SAPHHaI-C
Signs and symptoms = 3 Alternative Diagnosis no? = 3 Prior PE/DVT = 1.5 Hemoptysis = 1 HR> 100 Immobilisation > 3 days or Sx cin 3wk =1.5 Cancer =1
If >4 = CTA with contrast(IxoC)»_space;V/Q Scan
Low score Mx of PTE
D-dimer (95% sensitive)
If positive. CTA
Otherwise r/o PTE
ECG PTE
Mc= Sinus tachycardia
Msp= S1Q3T3
2nd Mc = inv T wave in V1-4
CXR PTE
Mc = normal**
WESTERMARK SIGN
(Focal oligaemia)
HAMPTON HUMP
(Wedge opacity)
PALLAS SIGN
(Dil. R descending Pul. Artery)
Other Ix PTE
ECG
CXR
LL usg (r/o DVT)
D-dimer
CTA (Ixoc)
INVASIVE PUL ARTERIOGRAPHY (GST)
V/Q scan (prenancy/RenalF/Contrast intol
Rx Massive PE
Shock+RV dysfn
500ml NS
Vasopressors
Anticoagulants
Definitive: Thrombolysis»_space; sx embolectomy
Rx submassive(RV dysfunction) and Minimal PE (normal RV and BP)
S= > 70 years = Anticoagulant—Tlysis
< 70 years = Thrombolysis
Mcc of preventable hospital death/ Mccd in post sx patient
Acute PE
Anticoagulant? Thrombolysis? (Drugs)
Heparin bridge warfarin
Heparin f/b dabigatran (DTI)
Xa inhibitors
Thrombolysis : Alteplase»_space; streptokinase
Rx Pul Edema
Furosemide + NTG sublingual (HR>100)
F + NE/DP (HR<100/ Shock -)
F + DOBUTAMINE (HR<100 / Shock +)
New tx for PTE
Catheter directed thrombolysis (CDT)
PHTN diagnosis
MPAP > 25
Pul.Vascular Resistance > 3 WOOD UNIT
PHTN sex and age predisposition
F»M
Child bearing age
Mc symptom if PHTN
SOB
Initial Ix of PHTN
ECHO
Most accurate method of Ix
Pul. Artery Catheterization
WHO classification PHTN
1 DIRECT INVOLVEMENT
2 CARDIOGENIC
3 1° RESP D/O
4 Chronic Thromboembolic events
5 Miscellaneous
Group 1 causes PHTN
Genetic : BMPR2 gene (Inc BV smooth muscle)
AID : Ssc»_space; RA , SLE
Toxin : Rapseed oil/ Fenfluramine
High Altitude
GROUP 3 causes PHTN
COPD BXIS ILD OSA Hypoventilation
(Hypoxia—vasoconstriction)
Group 5 causes PHTN
Sickle cell Sarcoidosis Langerhans cell histiocytosis Lymphangio leiomyomatosis Morbid obesity
Rx PHTN
P3EG
PDE5= Sildenaf/Taladafil
ETRA= Ambrisentan/Bosentan
Prostacyclin = Iloprost (i.n)
Prostacyclin antagonist = Selexipag
Guanyl Cyclase + = Riociguat
Emergency PHTN RX
I.v EPOPROSTENOL
Regimen PHTN
ETRA + PDE5
Fail?
Add prostacyclin
Rx Airway remodelling in chronic untreated asthma
Bronchial thermoplasty
Main types of asthma
Atopic- Children/skin test+/ mild / IgE inc
(Mcc= dermatophagoides)
Idiosyncratic- Adults/ all normal/ severe
What structures does asthma involve
Large airway and small airway
NEVER ALVEOLI
Ix in Asthma
Spirometry (main)- Bronchodilator reversal
PEFR variability in a day (>20%)
Broncho-provocation by methacholine
(fev1 dec by >20%)
Bronchodilator reversal % diagnostic of asthma
Fev1 increase by 12% or 200’ml
C/f status asthmaticus
SOB at rest Single words Hr > 120 Rr>30 B/l wheeze Accessory muscles Resp acidosis Pulsus paradoxus
Diagnosis of status asthmaticus
PEFR <50% of expected
PaO2 < 60
SpO2< 90
Life threatening signs of SA
Altered sensorium Silent chest (collapsed bronchus) Dec resp effort (cyanosis) Bradycardia Pulsus paradoxus Hypotension
Rx status asthmaticus
O2 + SABA + SAMA (IpBro) + ICS
I.v steroid
Trial of MgsO4
Last resort- IMV : High flow (correct hypoxia)+ Prolonged expiratory time(dec hypercapnea)
Is inverse ratio ventilation useful in status asthmaticus?
No
Normal I:E = 1:3
IRV= 2:1
Rescue Rx asthma
LDICS + LABA
Type of drugs in asthma
Controllers : SABA LABA SAMA (bronchodilators)
Relievers : ICS LT (dec inflammation)
Step1-step 5 asthma mx
1 - 2 LDICS + Anti LT 3 LDICS + LABA + Anti LT 4 MDICS+ LABA + Anti LT + Tiotropium 5 HDICS + LABA + Oral steroids + Tio
Fail?
Anti IgE
Anti IL5– MEPOLIZUMAB
/RESLIZUMAB
DOC Exercise induced asthma
Short term : SABA
Long Term : ICS
RECOVERY TIME= 30 min
Samters triad
Asthma+ nasal polyp + aspirin sensitivity
AERD quatrad
Samters triad + Rhinosinusitis
Aspirin Exacerbated Respiratory Disease
Brittle asthma types
1- freq fluctuations/ HDICS+ oral steroids+ continuous B agonists
2- severe sudden anaphylaxis / inj ADR
Chronic bronchitis definition
Cough > 3 months for 2 consecutive years
C/f of chronic bronchitis
COUGH** : purulent/blood
Cyanosis (BLUE BLOATERS)
Pulmonary Edema (cor pulmonale-RVF)
Crackles and wheeze
OBESE
Chronic bronchitis index?
Reid Index
Thickness of mucus/Thickness of bronchial wall
Type of failure in CB
T2RF (bronchioles get damaged, not enough PAO2)
T2= Hypercapneic—-> RESP ACIDOSIS
DLCO in CB
NORMAL
Etiology Emphysema
Smoking (xElastase)
A1 antitrypsin deficiency
Pollution
Coal exposure
A1AT Deficiency features
Chr 14
A/w Liver disease
Young AOE
Family H/o
Cf Emphysema
DYSPNEA**
Pursed lip breathing (accessory muscles) Pink skin (PINK PUFFER) Lean build (cachexia dt inc WOB) HOOVER SIGN (Paradox CW movement) Inc AP Diameter
Type of RF in emphysema
T1RF—-> normal paCo2—RESPIRATORY ALKALOSIS
Organisms responsible for acute exacerbation of COPD
Moraxella
S. Pneumoniae
H. Influenzae
Types of emphysema***
Centrilobular
Panlobular
Paraseptal
Distal Acinar
Pan lobular v/s Centrilobular (mc)
All resp tree. Central bronchioles
Lower Lobe. Upper Lobe + Up LL
A1AT. Smoking
GOLD Staging COPD (Fev1)
Mild >80%
Mod 50-80
Sev 30-50
Vsev <30
Prognostic index COPD
BODE
BMI
Obstruction
Dyspnoea
Exercise Capacity (6MWT)
Rx COPD
STOP-BASS M
Smoking cessation
Tx (ILD» COPD)
O2
PDE5 (ROFUMILAST- dec inflammation)
Bronchodilator(LAMA>LABA)
Abx (Azithro—against H.infl—mc in exacerbations)
Sx (bullectomy—c/I in diffuse emph)
Steroids (systemic+ ics)
Mucolytics (N Acetyl Cysteine)
Bronchodilators in COPD Drugs
LABA- Indacetrol, Olodetrol
LAMA- Tio Umclinidium Glycopyrronium
Best modality to reduce mortality in COPD
Low flow O2
14-15 hr/day
COPD ABCD Rx
A- SABA/SAMA B-LABA/LAMA C-LAMA D-LAMA——fail—-LAMA+ LABA —-asthma?—-LABA+ ICS
+ ROFULMILAST + AZITHROMYCIN
BXIS vicious cycle
Initiating event—Abn clearance of airway secretions—stasis and obst—Infection and inflammation (PSEUDOMONAS)—destruction and dilatation of airway—abn clearance—
Three layered sputum in BXIS
Serous—Mucus—-Pus
C/f BXIS
Mc- PRODUCTIVE COUGH
Coarse crepts
Dilated airway
Mccd BXIS
RHF
Cor pulmonale
Etiology of BXIS
GOBII
OBSTRUCTION
BRONCHIAL INJURY
TRACTION BXIS
GENETIC
IDIOPATHIC
Obstructive causes of BXIS
Intraluminal: Cancers / Carcinoid / FB
Extraluminal: TB lymph node—RML collapse = BROCKS SYNDROME (BXIS + RML Collapse)
Bronchial injury causes BXIS
Infection : TB Adenovirus Bacterial
CTD: SLE RA Ssc
Genetic causss BXIS
Yellow nail syndrome (cong lymphedema+ plef + yellow nails)
BXIS Sicca (KARTAGENER)— Situs+polyp+BXIS
CF
WILLIAM CAMPBELL SYN (Airway cartilage defect)
Lobes of BXIS preference
LL»RML»Lingula
Diseases and lobes
PACTS CM ICI
UL) Post Radiation / AnkSpond / ABPA / CF / TB / Sarcoidosis
ML) Ciliary Dyskinesia / Myco Avium
LL) IPF (busalfan, bleomycin) /Chronic Aspiration/ Idio BXIS/ SLE/ RA
Ix BXIS
Volumetric multidetector CT»_space; HRCT
HRCT App of BXIS
Tram track/Tree bud/ Bronchial wall thickening
Rx BXIS
Airway clearance- mucolytics + physio
Abx (during exacerbations)
O2 (if hypoxia)
Resection (If localized)
Tx (if diffuse)
Prophylactic abx in BXIS
Inhaled : Colistin/ Genta/ Tobra
Oral : FQ/ Azithro
Eosinophilic lung diseases pathology wise classification
UNKNOWN: AEP/ CEP / Hyper Eosinophilic syndrome / Churg -Strauss
KNOWN: Loffler syndrome (parasite infection) / ABPA / Drugs (NSIP) / TPE
NSIP= Nitrofurantoin Sulfonamide INH Penicillamine
TPE cause
Lymphatic filariasis +++
D/t immune reaction to filariae
TPE c/f
Paroxysmal wheeze/cough
Eosinophilia > 3000
CXR- Diffuse miliary lesions
MOTTLED OPACITIES
Restrictive LD spirometry
Microfilaria ABSENT on PBS
(Cleared in lungs only)
Triad of Idiopathic Pulmonary Hemosiderosis
IDA + HeMoptysis + Alveolar infiltrates
RECURRENT EPISODES OF. DAH (Alveolar capillary tortuosity)
AEP v/s CEP
Smokers. - - Asthma + - Peripheral Eo+ >25%. > 40% eosi on BAL RespF+ -
Radiological features of CEP
REVERSE BAT WING APP
PHOTOGRAPHIC NEGATIVE OF P. EDEMA
ABPA HSr
1 3 4
Ix ABPA
(H/o asthma OR CF)
Peripheral Eosinophilia (1000ng/ml)
SKIN TEST + for aspergillus fumigatus
Aspergillus sensitive IgE and IgG
CXR= UPPER ZONE INFILTRATES
CT= Para hilar BXIS (central)
Cf ABPA
Hemoptysis
Bronchispasm
BXIS
Rx ABPA
Steroids
Itraconazole
INVASIVE PULMONARY ASPERGILLOSIS
CT findings
(Trans bronchial angio-invasion)
Active phase : Halo sign (centre fungus- peripheral blood)
Recovery phase : Air crescent sign( immunity clearing the central fungus)
Rx VORICONAZOLE
Aspergilloma other name and CT finding + rx
Saprophytic Pulmonary Aspergillosis
CT- 1) Monads sign ( crescent)
2) shifting ball on decubitus
Rx- resection
Which conditions can aspergilloma be present in
TB
Sarcoidosis
Histoplasmosis
Hypersensitivity Pneumonitis features
D/D ABPA or Asthma
Aka Extrinsic Allergic Alveolitis
HSR 3,4
NO PERIPHERAL EOSINOPHILIA
Skin test +ve for aspergillus Ag
Biopsy of HS Pneumonitis
Non caeseating GRANULOMAS
Cellular bronchiolitis
Inflammation of INTERSTITIUM
Diagnostic criteria for HSPneumonitis
Serum precipitins against known Ag
Inspiratory creeps
Weight loss
Infection + on re-exposure
Occurrence of symptoms in 4-8 hours
Exposure to known Ag
Farmers lung?
Source and organism
Mouldy hay- Micropolyspora faeni
Hot tub lung?
HSPneumonitis d/t mycobacterium avium
Source- contaminated h2o
Bagassosis lung?
Sugarcane dust— Thermoactinomyces sacchari
Malt worker lung?
Mouldy barley—— Aspergillus clavatus
Bird fancier’s lung?
Pigeon excreta—- Avian protein
Etiology ILD
INHALATIONAL
(Organic-HSPneumonitis ; Inorganic-Silica ,Asbestos)
DRUGS (NABB)
(Nitrofurantoin/ Amiodarone / Bleomycin /Busalfan)
AID
(SLE/RA/Ssc)
SYSTEMIC DISEASES (Sarcoidosis/IBD)
IDIOPATHIC (mc)
Clf ILD
Progressive dyspnea
End expiratory Bi-basilar fine crepts**
Types of ILD
CAR LUND
UIP (aka IPF)
NSIP ( Non specific)
AIP (Acute)
COP (Cryptogenic Organising)
Respiratory Bronchiolitis ILD
LIP (Lymphocytic)
DIP (Desquamative)
ILD IxOC
HRCT
GGO(early)—-> Consolidation(late)—-> Interstitial Fibrosis——> Traction BXIS——-> ADVANCED ILD
Features of ADVANCED ILD
Honeycombing
Sub-pleural involvement
Worst prognosis ( inc chance of PNTx)
C/f UIP Vs NSIP
M. F. Smoker. Non smoker Chronic. Sub-acute Clubbing+. Clubbing+ Fine crepts. Fine crepts.
Biopsy UIP vs NSIP
Fibroblastic foci. Rare
Heterogeneous. Lymphocytic
CT UIP vs NSIP
Honeycombing+. Rare
Low zone GGO
Taction BXIS (both)
Rx UIP
PIRFENIDONE**
Ninentanib
Rx NSIP
STEROIDS
HAMAN RICH SYNDROME??
AIP
SOB+ Hypoxemia+ diffuse infiltrates
High mortality
Massons’s bodies seen in?
COP
Accumulation of granulation tissue
B/L consolidation
Rx STEROIDS
ILD s a/w smoking
UIP RBILD DIP LCH Pulm Hemorrhage syndrome
ILD rare in smokers
Sarcoidosis
HSPneumonitis
Sarcoidosis main feature?
Multi system disorder with non caeseating granulomas
Etiology sarcoidosis?
TB
AID
Propioniibacterium**
MC site of involvement of Sarcoidosis
Lungs
Scadding staging of Lung (Sarcoidosis)
1 Hilar LN B/L
2 Lung infiltrates + Hilar LN
3 Lung infiltrates only
4 Fibrosis
CAVITATION IS NEVER SEEN IN SARCOIDOSIS
Sarcoidosis syndromes
LUPUS PERINIO
(Rash under eyes and cheek)
LOFGREN SYNDROME—good px
(ENL+ Uveitis+ Arthritis + Hilar LN)
HEERFORDT SYNDROME
(Uveitis+Parotiditis+CN7 palsy+ Fever)
(
Ix Sarcoidosis
CBC- Lymphopenia (sequestration of lymphocytes in lung)
S.ACE- Increased***
Vit D- Increased—Hypercalcemia
CT- Uniform hilar lymphadenopathy
(TB= central necrosis)
BAL***- CD4/CD8 ratio increase
(NOT BLOOD)
Ixoc= BIOPSY- NC GRANULOMAS
GALLIUM SCAN- 1) Panda sign (parotid&lacrimal gland)
2) Lambda sign (Mediastinal LN)
KVIEM SLITZBACH TEST
(Skin test-anergy test)
Rx sarcoidosis
Self resolution (asymptomatic)
HCQ/Steroids/Mtx (symptomatic)
Mc OLD
Silicosis
Malignancy OLD order
Asbestosis > silicosis > cwp
1st symptom in byssinosis
Chest tightness
Asbestosis occupation
Ship building
Construction
Silicosis occupation
Sand blasting
Stone crushers
Asbestosis radiology
Lower zone Fibrosis
HOLLY LEAF APPEARANCE**
Pleural plaques (msp but asymptomatic)
Benign plef*
Asbestosis Cx
Mesothelioma—pleural+ peritoneal (msp)
Lung Ca- Adenocarcinoma / SCC
Smoking is a synergist
Silicosis radiology
Upper zone nodules—-merge—PMF
Egg shell calcifications with B/L Hilar lymphadenopathy
Silicosis cx
Silico-TB
Lung Ca
SLE, Ssc
CWP Radiology
Upper zone lesions—merge —-PMF
CWP cx
COPD
CAPLAN syndrome
(RA + silica/coal)
Never CANCER*****
Silicosis D/D
PAP
Apnea vs hypopnea
> 10s no breathing
> 30% reduction in airflow a/w >3% fall in SpO2
Types of Sleep Apnoea Syndromes
Central Sleep Apnoea (CSA)
(No effort/ CHF, Narcotic use)
Obst Sleep Apnoea (OSA)
(Obesity/ inc effort/ upper airway close/ SNORING**)
Pathophysiology OSA
Apnea—hypoxia—p. Vasoconstriction—PHTN
Apnea—Arousal—catecholamines—CAD/MI/Stroke/ Uncontrolled glycemic status/ arrythmias/ SCD
Apnea—arousal—decreased sleep— behaviour changes/RTA/Depression
R/f OSA
Obesity
Acromegaly ( large tongue)
Males
Cranio-facial abnormalities
IxOC OSA
POLYSOMNOGRAPHY (sleep study)
Rx OSA
Depends upon episodes
< 5 = normal
5-14 = LSM
15-30 = CPAP (mxoc)
> 30 = CPAP/ Sx
Sx= UVULO-PALATO-PHARYNGO-plasty
Pickwickian syndrome?
OBESITY HYPOVENTILATION SYNDROME
Lung Adenocarcinoma features
Peripheral location
Females and young Males
Non smokers
Asbestos+
Clubbing ++ (Last stage- Hypertrophic Osteoarthropathy)
Hematological Paraneoplastic syndromes
Trosseau syndrome (migratory thrombophlebitis)
Mets to opposite lung ++
Mutation in EFGR
Lung SCC features
C5PAA
Central
Cigarette smoking a/w
Clubbing +++
hyperCalcemia (Life threatening)
Cavity formation (also + in LCC Lung)
Polyuria (Ca++ effect on tubules)
Abdominal pain (PTH related peptide)
Altered Sensorium
Features of Small CC Lung
Central
Strongest a/w smoking
Chemo and radiosensitive***
Rapid recurrence
SVC obstruction +++
Poorest prognosis
Paraneoplastic syndromes
Horner syndrome?
SAMPLE
+ve in lung ca.
Sympathetic ganglion Anhidrosis Miosis Ptosis Loss of CilioSpinal rfx Enopthalmos
Mets of Lung Ca
Mc BRAIN
Msp ADRENALS
Rx NSCLC
Resectable (1 to 3A) —- SX
Non resectable (3b-4) —- Chemo
SCC= Gemcitabine + Cisplatin/Paclitaxel
Adeno= Cisplatin + Pemetrexed/Bevacizumab
Rx SCLC
Chemo
CISPLATIN + ETOPSIDE
Targeted Rx Adenocarcinoma Drugs
EGFR x = Erlotinib/Gefitinib
ALK x = CRIZOTINIB
New immunotherapy drugs in Lung Cancer
Anti PD4 antibodies
NIVOLUMAB
PEMBROLIZUMAB
PD4 is a brake protein of T cells, cancer cells attach to this protein and disable T cells.
Pancoast tumor histology
SCC» Adenocarcinoma
Pancoast Syndrome?
Horner + 1&2 rib destruction + C8T1T2 (pain and weakness @ ulnar distribution)
Pancoast tumor Ixoc
MRI
Lung Ca GST
Biopsy
Paraneoplastic syndrome Small cell
SIADH (decreased Na)
ACTH (decreased K)
Calcitonin (decreased Ca)
Lamberton Eaton (Ab against cancer cell similar to P/Q Presynaptic Ca++ channels)
Gonadotropins (Gynecomastia)
Vasopressin
AnF
GRp (Gastrin releasing peptide)