Within the document are discussions of chronic obstructive pulmonary disease (COPD) and pneumonia. It summarizes the pathogenesis of COPD as being caused by long-term smoke and irritant inhalation leading to airway and lung tissue damage, inflammation, and impaired lung function over time. Emphysema specifically involves destruction of alveoli walls, while chronic bronchitis involves inflammation of the airways. Complications discussed include respiratory infections, lung cancer, and cor pulmonale. Pneumonia is also briefly discussed through a clinical vignette of an alcoholic man presenting with fever, cough, and signs of consolidation on exam.

1. “Within the mind are all the
resources required for successful
living. Ideas are present in the
consciousness, which when released
and given scope to grow and take
shape, lead to successful events”
- Wings of Fire: An Autobiography of Dr. APJ Abdul Kalam.

2. “ Whether you think you can or
you can't, you are right…!”
– Henry Ford

3. CPC14: Mrs. PT. 64y Fem. SOB
 Mrs. P.T. 64 y female, to ED at TTH.
 Worsening SOB, years, worst today - At rest
• Previously SOB after exertion- COPD.
• Gradually worsening over the years, now O2 at night.
• Sputum chronic clear white, but light brown today.
• Cough - on and off for years, No wheeze, no hemoptysis,
• Chest pain worse with breathing today, fever, sweaty.
• Smoked 3 packs/day for 35 years; quit 7y ago.
 Foreign travel: Norfolk Island 3wks. No health problem.
 RX: Pneumonia, COPD, Emphysema, CCF

4. CPC: 2011 – 58M Chronic cough.
 Trevor is 58 year old Caucasian man,
 years of coughing. pneumonia 3 years ago; bronchitis
several times a year, Dyspnoea, Hoover’s & Campbell
sign positive, leans forward for breathing.
heavy smoker (30+/day); quit 3 years ago.
• Previous PFT: FEV1 = 1.3 FVC = 2.6 FEV1/FVC = 50%.
(too sick to perform PFT today.)
What is the significance of…
1. Leaning forward – “arms on knees”
2. Intercostal in-drawing
3. Hoover's sign ? Tracheal tug ?
4. Campbell's sign ?
1. Pathogenesis of symptoms ?
2. Further questions ?
3. Differential diagnosis ?
4. Learning issues? PFT

5. Clinical Feature - ? Pathogenesis
 SOB, Dyspnoea
 Cough
 Wheezing, Stridor.
 Rhonchi, Crackles/ Rales.
 Dullness
 Hyper-resonance
 Hyperventilation
 Tachypnoea
 Pleural rub
 Pleurisy (pleuritis)
 Sleep apnoea
central/obstructive.
• White sputum (frothy)
• Rusty, Yellow, green sputum
• Haemoptysis
• Night sweats
• Sleep apnoea
• Kussmaul’s breathing.
• Ataxic breathing
• Apneustic breathing.
• Cheyne-Stokes breathing.
• Paradoxical breathing
• Resp acidosis / alkalosis.

6. COPD: Questions
 What is Chronic Bronchitis & Emphysema ?
 Pathogenesis of COPD/CB/Emphysema ?
 Smoking – Disease, Pathogenesis ?
 Difference.. Obstructive / Restrictive disease ?
 What findings on PFT expected ?
 How is he maintaining normal pO2 & pCo2 ?
 why is he pink & puffing ?
 What Gross & Microscopic features in his lung ?
 What complications are expected ?
 Pneumoconiosis, TB, DPF,

7. COPD: Questions
 Bronchiectasis ?
 Atelectasis ?
 Lung abscess ?
 Honeycomb lung ?
 Pneumothorax ?
 Tension pneumothorax?
 Pleural effusion
 Emphysema types.
• Panacinar - α1AT def.
• Paraseptal
• Irregular
• Bullous
• compensatory
• Tuberculosis
• Primary, secondary, anergic,
milliary,
• caseous, fibrocaseous, fibrosing.
• Asthma – types.
• Atopic, non-atopic, drugs,
occupational etc.
• Pathogenesis, gross, micro
• Curschmann spirals, Charcot-
Leyden crystals.
• Pneumoconioses
• Silicosis, Anthracosis, Asbestosis
• IPF – Ideopathic pulm. fibrosis.
Text Book:
Robbins Basic Pathology, 8th or 9th edition

8. Core Learning Issues:
 Major:
• COPD Pathology – Restrictive / Obstructive.
• Emphysema & Bronchitis – types, pathology & clinical.
• Pathology of Tobacco related disorders.
• PFT - FEV1/FVC & its use and interpretation.
• Pneumonia – types & Pathology (Lobar, Broncho & Int.)
• Allergic bronchitis, Asthma, Tuberculosis * self study.
 Minor:
• Pneumoconiosis – Asbestosis, silicosis etc.
• Cor pulmonale, Pulmonary hypertension.
• Diffuse Pulmonary Fibrosis & honeycomb lung.
• Acute lung injury - ARDS, DAD, HMD of infants.
• Sarcoidosis ?

9. The cigarette does the smoking,..!

10. Normal Lung
Tr.Air Sh
Br. Mar.
Colon air

12. Normal Lung Tissue

13. Lung
Histology
Type 1-Pneumocyte
Type 2
Bronchiole
Alveoli

14. There is only one secret to
staying young, being happy, and
achieving success - You've got to
“enjoy what you do”…!
Including studying pathology…..

15. Pathology of
COPD, Chronic lung
diseases & Pneumonia*
Dr. Shashidhar Venkatesh Murthy.
A/Prof. & Head of Pathology

16. Percent Change in Age-Adjusted Death Rates,
U.S., 1965-1998
4th leading cause of death, women more, smoking >80%
Proportion of 1965 Rate
3.0
3.0
2.5
2.5
2.0
2.0
1.5
1.5
1.0
1.0
0.5
0.5
0
0.0
Coronary
Heart
Disease
Stroke Other CVD COPD All Other
Causes
–59% –64% –35% +163% –7%
1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998

17. Pathology of Smoking
 Research evidence: smoking  disease
 >4000 chemicals, 43 carcinogens.
 >90% of COPD is due to smoking.
 15% of smokers develop COPD.
 Injury & inflammation central to damage.
 Smoking a single cigarette results in an acute
increase in neutrophils at 1 hour.
 Increased neutrophils in smokers, which
decrease following reduction/quitting.
 Patients with COPD have sputum neutrophilia
that persists even after cessation of smoking.

18. Smoking effects: FEV 1 & Age

19. Smoking related diseases:
 Non-neoplastic:
• Bronchitis, pneumonia, bronchiectasis.
• Chronic bronchitis, emphysema (COPD)
• Atherosclerosis  IHD, Stroke, MI.
• Gastritis, Peptic Ulcer, Oesophagitis.
• Arteriosclerosis – Berger’s disease.
 Neoplastic:
• Lung Cancer (many types)
• Oral, laryngeal & oesophageal cancer.
• Carcinoma of bladder, Pancreas, cervix, larynx.

20. Ask, Aspire, Achieve..!
…..Ask questions
J. Robin Warren
Australian 2005 Nobel price in Medicine - at RCPA conference 2006 Sydney.

21. Pathogenesis of
COPD
Dr. Shashidhar Venkatesh Murthy.
A/Prof. & Head of Pathology

22. Pathogenesis of COPD
1. Smoke, irritants, carcinogens.
2. Tissue irritation & destruction
3. Inflam  Mucous production.
4. Airway damage  Narrowing.
5. Alveolar damage  widening.
 Increase in
• Alveolar marcrophages
• CD8 Lymphocytes
• Neutrophils
• Proteases.
α1AT def..
Emphysema
 Airway inflam  Bronchitis
 Alveoli damage  Emphysema.
 Both  COPD.
Bronchitis Emphysema

23. The mind is everything.
What you think you become!
-- Buddha

24. Pathogenesis – Chronic Bronchitis
Irritation  COPD  Initiation  Promotion  Ca.
Chronic Bronchitis
3p
C-myc K-Ras
p53
Pathogenesis:
1. Smoking – carcinogens
2. 3p – tumor suppressor gene loss
3. Mutations (p53, KRAS, EGFR..)
4. Dysplasia
5. Infiltration
6. Spread
7. Metastases.

25. COPD Pathogenesis: Emphysema

26. COPD: Overlap of Clinical syndromes
COPD

27. Both affected  COPD (common)

28. Chronic Bronchitis - Emphysema:
Predominant
Bronchitis
Predominant
Emphysema
Age (yr) 40-45 50-75
Dyspnea Mild; late Severe; early
Cough Early; copious sputum Late; scanty sputum
Infections Common Occasional
Respiratory
Repeated Terminal
insufficiency
Cor pulmonale Common Rare; terminal
Airway
resistance
Increased Normal or slightly
increased
Elastic recoil Normal Low
Chest
Prominent vessels; large
radiograph
heart
Hyperinflation; small heart
Appearance Blue bloater Pink puffer

29. “Know more today about the
world than yesterday and
lessen the suffering of others.
You'd be surprised how far
that gets you.”
― Neil deGrasse Tyson

30. Lung Normal & in Smokers:

31. Smokers Lung: COPD - Emphysema
 Upper lobe – black
spots of anthracotic
(Co2) pigmentation
(centre of each lobule).
 Centrilobular alveolar
destruction with
carbon pigmentation.
 Other types: *
• Panacinar
• Paraseptal
• Bullous
• Interstitial
• Irregular.

32. Normal - Emphysema

33. Normal Emphysema

34. Normal - COPD
CB
Emphysema

35. Centrilobular
Emphysema:
Pink Puffer:
Lean/weight loss
No cyanosis
Forward stooping
Barrel chest
Flat diaphragm
Hyperlucent Lung

36. Whether you think that you
can or that you can't,
you are right…!
– Henry Ford

37. Chronic Bronchitis:
• Squamous
Metaplasia.
• mucous
gland.
Hyperplasia
Normal Chronic Bronchitis

38. Emphysema: Other types
 Panacinar
• Congenital, α1AT def.
 Paraseptal, Bullous
• Old scar.
 Irregular
• Past diffuse scaring.

39. Complications of COPD:
1. Pneumothorax, Infections,
Bronchectasis.
2. Polycythemia – hypoxia.
3. End-stage lung disease.
4. Acute Exacerbations.
5. Cor Pulmonale – Right heart failure.
• syncope, hypoxia, pedal edema, passive
hepatic congestion and death.
 Lung Cancer
RV
LV

40. Bronchiectasis:
 Permanent dilatation & Infection of
bronchi.
 Cough, copious purulent sputum, mixed
infections. Lower lobes common
 Secondary to COPD, Pneumonia or
localised obstructions.
 Complications:
• Pneumonia, empyema, septicemia,
meningitis.
 Types:
• Cylindrical, Saccular, Fusiform (no

41. Bronchiectasis:
• Permanent dilatation with secondary infection
• Pus* filled, *visible bronchi till *periphery.
• Abundant, greenish, sputum, mix culture +ve.

42. COPD Summary:
 Definition: Progressive Irreversible Chronic airflow
limitation due to inflammatory response to noxious
substances. Progressive decrease in PF.
 Diagnosis: FEV1<80%, FEV1/FVC <70%
 Etiology
• >90% smoking (15% of smokers COPD)
• Pollution, 1AT def. , genetic susceptibility, Asthma,
idiopathic.
 Clinical Syndromes: CB, Emphysema, COPD, Asthma, &
Bronchiectasis.
 Complications: Pulmonary failure, RS Cardiac failure,
Endstage disease, Cancer.

43.  Self Study
- Restrictive Lung Disorders.
- IPF, Diffuse fibrosis,
- Honeycomb lung.
- Pneumoconiosis
- Silicosis, Asbestosis, Coal.
- Tuberculosis.
- Asthma
- Good pasteur’s syndrome.
- DAD: ARDS/HMD

44. Pneumonia: Clinical vignette
 50y man, alcoholic, high fever, cough, copious foul
smelling brown sputum, pleuritic rt sided chest pain.
 HPC: wife reports that he was brought home in a semi-conscious
state a few days ago – drunk.
 Thin, distressed, pursed lip breathing, using accessory
muscles of respiration, cannot speak in full sentences,
leaning forwards…*
 39°C, RR-22/min, peripheral cyanosis.
 Chest-rib in-drawing, diminished air entry, soft expiratory
wheezes, bronchial breathing L lower post chest.
 PE: fever, consolidation right middle and lower lobes.
 sputum microscopy - abundant PMN and mixed oral
flora.
Pathogenesis, Differential diagnosis…..?

45. Pneumonia: Questions
 What is pneumonia? Types? pathogenesis?
 Lobar, Broncho & Interstial pneumonia?
 Community acquired / Nosocomial / hospital acquired
pneumonia ? What is the difference ?
 Acute, Chronic & recurrent pneumonia?
 Typical, Atypical pneumonia?
 Common organisms causing pneumonia?
 Microbiology – lab diagnosis, culture, tests.
 Gross and microscopy of pneumonia.
 Phases of pneumonia – Congestion, Red hepatization, Grey
hepatization, Resolution?
 Complications of pneumonia?
 Lipoid pneumonia, Carcinomatous & Aspiration pneumonia ?

46. Goodpasture Synrome:
? Etiology
? Clinical
?Pathogenesis
? Diagnosis.

47. Diffuse Alveolar Damage (DAD):
? Etiology
? Clinical
?Pathogenesis
? Diagnosis.
Diffuse bilateral consolidation
with honeycombing in both lower
lobes, focal in upper lobes.
Microscopy: Hyaline membrane
in ARDS.

48. Saddle Thomboemobulus:
? Etiology
? Clinical
?Pathogenesis
? Diagnosis.

49. The cigarette does the smoking,..!

50. Clinical Problem Solving - Course
Free online course from UCSF
https://class.coursera.org/clinprobsolv-001/class/index

51. Restrictive lung disorders:
Definition: Reduced expansion of lung.
A. Intrinsic Lung Disorders:
• Sarcoidosis, diffuse fibrosis, pneumoconiosis.
• Tuberculosis, Interstitial Pneumonia
B. Extrinsic Disorders (chest wall):
• Scoliosis, Kyphosis, Gross Obesity,
• Pleurisy, rib fracture etc.
C. Neuromuscular Disorders:
• Paralysis of the diaphragm, Myasthenia Gravis,
Poliomyelitis,
• Generalized Weakness – malnutrition.

52. Restrictive Disorders: Pathogenesis
 Interstitial inflammation
& fibrosis.
 Lymph+Macrophages.

53. Idio. Pulm. Fibr.(IPF)
 >50y, ?viral, ?Imm ?Env
 "dry Velcro like inspiratory
crackles.
 UIP (usual Int. Pneum) /
Cryptogenic fibrosing alveolitis.
 Bilateral, lower and peripheral
coarse reticulonodular
shadowing and small lungs.
CT – Peripheral honeycomb &
scarring.
Poor prognosis. (~3years)

54. Idiopathic Pulmonary Fibrosis:
UIP/IFA

55. Pneumoconioses:
 Disease due to inhaled dusts
 inorganic (mineral) or organic
 Reaction may be inert, fibrous,
allergic or neoplastic.
 Morphologic Types:
 Inert - coal-worker's pneum.
 Fibrous - asbestosis, silicosis
 Allergic - extrinsic allergic
alveolitis (Bird
 Neoplastic - mesothelioma, lung
carcinoma.

56. Silicosis:
 Inorganic – sand &
stone dust.
 Toxic to macrophages –
destruction fibrosis.
 Scattered multiple
small,fibrotic Nodules
 Surrounding Irregular
emphysema.
 Restrictive pattern of
PFT.


57. Asbestosis:
 Asbestos bodies in sputum.
• (Protein & Hemosiderin)
 “Inconsumable”, Beaded 5-
100mm x 0.25mm.
 Within alveoli at lung bases.
 Dyspnoea, dry cough
 Clubbing is common.
 Diffuse fibrosis: Honey comb
lung:
 Massive fibrosis: Coal-miners.

58. Coal Miner’s Lung:
 Athraco-Silicosis:
 Dense cardon
pigmentation –
Anthracosis and
nodules of silicosis.
 Commonly seen in
coal miners.

59. Sarcoidosis:
 Granulomatous, immune,
multisystem,
 ??? Etiology.
 Multiple fine nodules.
 Like TB (no caseation).
 Smokers – Uncommon
 SOB, Erythema nodosum,
lymphadenopathy, hypercalcemia,
nephrocalcinosis, occular, skin &
nerve damage.. Etc.
 Stage I asymptomatic to Stage IV –
Pulm fibrosis.

60. Honeycomb lung: click for online link

61. Tuberculosis:
 Mycobacterium tuberculosis (typical)
 Atypical mycobacteria – HIV
 Primary & Secondary, Pulm/non-pulm
 Chronic, Hypersensitivity, debilitating,
weight loss.
 Upperlobe, nodular/cavity/fibrosing.
 Pleural effusion
 Caseating Granuloma
• lymph, marcrophages fibrosis
Macrophages - LH giant cells.
 Systemic spread, miliary spread.
 Tuberculin Test – hypersensitivity.

62. Restrictive vs Obstructive
Interstitial - (stiff lung)
Increased tissue
Relatively normal
FEV1:FVC ratio
Normal PEFR.
Types:
Acute – ARDS,Viral.
Chronic -
pneumoconioses &
sarcoidosis, Int. fibrosis.
Obstructive (soft lung)
Destruction of tissue.
Low FEV1:VC ratio
Low PEFR.
Types:
•Localised & Diffuse
•Reversible & progressive.
•COPD
•Asthma
•Bronchiectasis,

63. Pulmonary Function Testing:
 FVC - Forced Vital Capacity – Liters - diagnosis of obstructive and
restrictive diseases.
 FEV1 - Forced Expiratory Volume in One Second –
obstructive/restrictive diseases.
 FEV1/FVC - FEV1 Percent (FEV1%) - it indicates what percentage
of the total FVC was expelled from the lungs during the first second
of forced exhalation. critically important in differentiating obstructive
from restrictive diseases.
 FEV3 - Forced Expiratory Volume in Three Seconds – equal to FVC
in normal.
 FEV3/FVC - FEV3% - normal is 1 or 100%
 PEFR - Peak Expiratory Flow Rate - this is maximum flow rate
achieved by the patient. For monitoring response to treatment.
 FEF - Forced Expiratory Flow - is a measure of how much air can be
expired from the lungs (liters/second or liters/minute). The FVC
expiratory curve is divided into quartiles and therefore there is a FEF
that exists for each quartile. The quartiles are expressed as
FEF25%, FEF50%, and FEF75% of FVC.

64. PFT: interpretation:
 Check FVC & FEV1 – normal  normal PFT
 If FVC and/or FEV1 are low - Pathology.
 Check FEV1/FVC ratio:
 FEV1/FVC% (<70%) - Obstructive.
 FEV1 /FEVC% (>80%)- Restrictive.
 An improvement in FEV1 of 200ml or more after
bronchodilator suggests versibility  Asthma.

65. “A person with belief never grovels
before anyone, whining and whimpering
that it’s all too much, that he lacks
support, that he is being treated unfairly.
Instead, such a person tackles problems
head on and then affirms, I am greater
than anything that can happen to me.”
- Wings of Fire: An Autobiography of Dr. APJ Abdul Kalam.

66. Asthma: Reversible & intermittent COPD
 Increased irritability of bronchi causes
bronchospasm
 Paroxysmal attacks
 Hyper inflated lungs
 Mucus plugs in bronchi
 Enlarged bronchial mucous glands

67. Asthma Types:
 Atopic – Immune, hypersensitivity, IgE.
 Non-atopic – Non immune - infections
 Aspirin-induced – Genetic, excess cyclo-oxygenase
inhibition.
 Occupational – Immune, hypersensitivity.
 Allergic bronchopulmonary aspergillosis:
Hypersensitivity to inhalation of spores.

68. Asthma Pathogenetic Types:
 Extrinsic (Immune)
• Atopic - IgE
• Occupational - IgG
• A. Bronchopulomonary Aspergillosis - IgE
 Intrinsic (Non immune)
• Aspirin induced
• Infections induced
• Excercise

69. Asthma: Reversible & intermittent
obstruction
 Hyperresponsive airways
• Increased irritability of bronchi causes
bronchospasm
 Episodic attacks
 Inflammation
 Excessive and thick mucus plugs
 Hyperplasia of mucous glands and smooth
muscle, minimal fibrosis

70. Asthma Types:
 Atopic – Immune, hypersensitivity.
 Non-atopic – Non immune - infections
 Aspirin-induced – Genetic hypersensitivity.
 Exercise induced
 Occupational – Immune, hypersensitivity.
 Allergic bronchopulmonary aspergillosis:
Hypersensitivity to inhaled aspergillus Ag

71. Asthma Pathogenetic Types:
 Extrinsic (Immune)
• Atopic - IgE
• Occupational - IgG
• A. Bronchopulomonary Aspergillosis - IgE
 Intrinsic (Non immune)
• Aspirin induced
• Infections induced
• Excercise

72. Asthma Pathogenesis:
INFLAMMATION
Hygiene hypothesis?
Airflow Limitation
SYMPTOMS
Cough Wheeze
Dyspnoea
Airway
Hyper-responsiveness
Genetic*
TRIGGERS
Allergens, Exercise,
Cold Air, SO2 Particulates
INDUCERS
Allergens,Chemical sensitisers,
Air pollutants, Virus infections

73. Asthma : Pathogenesis
Early phase (immediate) and late phase reactions

74. Asthma Pathology:
Barnes PJ
Allergen
Mucus
hypersecretion
Hyperplasia
Leukotrienes
C4, D4 & E4
Th2 cell Neutrophil
Vasodilatation
New vessels
Plasma leak
Oedema
Subepithelial
fibrosis
Sensory nerve
activation
Cholinergic
reflex
Mast cell
Bronchoconstriction
Hypertrophy/hyperplasia
Eosinophil
Macrophage/
dendritic cell
Mucus plug
Epithelial shedding
Nerve activation
Leukotrienes
Ach
Histamine
Prostaglandin D
Platelet
activating factor
Interleukins

75. Asthma Morphology:
 Bronchial obstruction with overinflation
• Small areas of atelectasis (collapse) may be seen
 Inflammation & thickening of mucosa.
 Bronchial wall smooth muscle hypertrophy
 Thickening of bronchial basement membrane.
 Mucus plugging of bronchi
 Curschmann spirals: whorls of shed epithelium
within mucus plugs
 Charcot-Leyden crystals: Within aggregates of
eosinophils – crystalloids of galectin-10

76. Asthma
Morphology:
Asthma Microscopy
1.Mucous Plugs +eosinophils
2.Goblet cell hyperplasia
3.Inflammation + Eosinophils
4.Smooth muscle hyperplasia
5.Mucous gl. Hyperplasia.

77. Asthma – Lung Gross features:
 Inflamed thick bronchi obstructed by mucous plugs.

78. Asthma : Microscopy
 Inflammed
bronchi
Obstruction by
mucous plug
 Alveoli (normal)

79. Asthma : Microscopy
 Dilated BV
 Inflammatory cells
Cartilage
Mucous plug over
the surface.

80. Asthma : Microscopy

81. Hyperinflation Status Asthmaticus:

82. Status Asthmaticus : Mucous plug

83. Status Asthmaticus : Mucous plug

84. Curschmann spirals:

85. Charcot-Leyden Crystals:

86. “ Whether you think you can
or you can't, you are right…!”
– Henry Ford

87. Lung volumes

88.  Total Lung Capacity (TLC) - the total volume of the lung, the volume of
air contained in the lung at the end of maximal inspiration
 Inspiratory Reserve Volume (IRV) - volume, which can be inspired
beyond a restful inspiration
 Tidal Volume (TV) – volume of a single breath, usually at rest
 Functional Residual Capacity (FRC) - The amount of air left in the lungs
after a tidal breath out, the amount of air that stays in the lungs during
normal breathing
 Vital Capacity (VC) – maximum volume which can be ventilated in a
single breath
 Inspiratory Capacity (IC) - the maximal volume that can be inspired
following a normal expiration
 Expiratory Reserve Volume (ERV) – volume, which can be expired
beyond a restful expiration
 Residual Volume (RV) – volume remaining in the lungs after a maximum
expiration

89. Volumes
 Forced Vital Capacity (FVC) - the volume of air
that can forcibly be blown out after full
inspiration, measured in litres
 Forced Expiratory Volume in 1 Second (FEV1) -
the maximum volume of air that can forcibly
blow out in the first second during the FVC
manoeuvre, measured in liters
 FEV1/FVC (FEV1%) - in healthy adults this
should be approximately 75–80%.
• Obstructive diseases (asthma, COPD) FEV1 is ↓ & FVC n/↑ so FEV1/FVC is
decreased (<80%, often ~45%).
• In restrictive diseases (Lung fibrosis/silicosis) FEV1 and FVC are both reduced
proportionally and the FEV1/FVC value may be normal or even increased as a
result of decreased lung compliance

90. Obstructive lung diseases
 airway obstruction
 restricted expiration
  FEV1,  FEV1/FVC
  compliance,
elasticity
 Chronic bronchitis
• Bronchiolitis
 Asthma
 Emphysema
 Bronchiectasia
 Cystic fibrosis
Normal
Asthma
COPD

91. Flow volume curves

92. Condition Major changes Causes Symptoms
Chronic Hyperplasia Tobacco smoking Productive
bronchitis and hypersecretion and air pollutants cough
of mucus glands
Bronchiectasis Dilation and scarring Persistent severe Cough, purulent
of airways infections sputum and fever
Asthma Smooth muscle Immunologic Episodic wheezing
hyperplasia or idiopathic cough and dyspnea
Excessive mucus
Inflammation
Emphysema Airspace enlargement Tobacco smoking Dyspnea
Genetic and wall destruction

93. Bronchogenic Carcinoma:

94. Asthma pathogenesis:

95. Pathophysiology of Cor-Pulmonale:

96. 2013 feedback
 Did not go well - reorganize talk.
 No Asthma, restrictive disorders &
pneumonia – next week.
 Check quiz – remove unwanted.
 Next year combine pneumonia + COPD.