PATHOLOGY - PATHOLO

LECTURE : LUNG PATHOLOGY

Teacher| 2nd TERM | A.Y. 2022-2023

OUTLINE

I. A IV. B
II.

LUNG PATHOLOGY
● Normal
○ 1000g
○ Right lung is heavier than the left because it has an
● Typical histology:
extra lobe ○ Bronchi → Bronchioles → Terminal bronchioles →
■ Right - 550g; Left - 450g Alveolar ducts → Alveoli
■ Right - upper, middle, lower lobe; Left - upper, ○ Alveoli - basic units of the lungs
lower lobe ■ Lined by Type 1 and Type 2 pneumocytes
■ Weight is important as anything that enters the ■ Type 1 - alveolar epithelium (simple squamous
lungs will affect its weight epithelium)
○ Capillaries are much numerous than the alveoli as ■ Type 2 - Macrophages of the lung
this is the site of gas exchange ○ Capillaries - for gas exchange
○ Pleura - covers the lung with the smooth visceral ○ There is a thin-lined interstitium in between the
surface, that is lined by mesothelial cells (simple capillaries and alveoli
squamous epithelium) ■ If there is an interstitial fibrosis, there will be
reduced gas exchange efficiency

CATEGORIES FOR DESCRIBING LUNG PATHOLOGY

● “Degenerative”
● Inflammatory
○ Most of the lecture will be comprised of this because
they are very varied in categories and types
● Neoplastic and Pleura ● Capillary is lined by the endothelium
● Lab: (Review, Cases, and/or Virtual Microscopy) ○ Endothelium should be thin-lined for gas exchange
(alveolar space to capillaries)
OVERVIEW ● Interstitial cells
● Normal Anatomy and Histology ○ Should be rare in number
● Pathology ■ Will increase due to a disease, which will thicken
○ Congenital the blood air interface (skin colored space in the
○ Atelectasis image) which will decrease gas exchange
○ Acute Pulmonary Injury efficiency
○ Obstructive vs Restrictive (infiltrative) concepts ● Right image - electronmicrograph
○ Obstructive Pulmonary Disease (COPD)
○ Restrictive (Infiltrative) Pulmonary Disease
○ Vascular Pulmonary Diseases
● Infections
● Neoplasms and Pleura (effusions, pneumothorax, tumors)

● Typical lung: ● Embryology:

○ The extra lobe in the right lung makes it heavier
■ Lobar pneumonia - specific to a lobe, depending
on its predisposition on which segment to attack
■ Atelectatic lung - collapse of a lobe due to lack of
airway/obstruction
○ The lungs developed from the laryngotracheal fold
and groove, which divides into the lungs buds
○ 5 weeks: The laryngotracheal fold and groove will
develop from the foregut
○ The laryngotracheal fold and groove will close to
disconnect the trachea and the esophagus
■ Some congenital diseases will cause it to still be
opened

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 ○ 6 weeks: When the laryngotracheal fold and groove
closes, it will form the trachea and the left and right
lobar bronchi
■ The number of lobes is the same as the adult
■ Pleura - the visceral mesoderm (mesothelial
cells) that lines the embryonic lungs
● Normal Chest X-ray
○ Use as reference point
○ Anterior view - apex of the heart is directed towards
the left side of the thorax
■ Apex - point of maximal impulse
■ Auscultation - listening to the sound of the lung,
heart, belly, and artery using a stethoscope
○ Clavicle is in the angle of the sternum
■ Auscultation of the lung is done from right to left
lung
● Alteration in the breath sound will allow you
to find which lobe has a problem
○ Costophrenic angle - angle of diaphragm and the ribs
■ It should be sharp (you can see in the lowest
edges of the lung on the image)
■ If the angle is curved, it indicates a presence of
fluid or air in the pleural space
○ Air should be black, and soft tissue and fluid should
be white
■ Any color changes signifies a disease
CONGENITAL
● Agenesis/Hypoplasia
○ The lungs did not grow, not compatible with life
■ Surfactant - induces lung maturity of the fetus
● Tracheal/bronchial anomalies, i.e., Tracheo-Esophageal
(TE) fistula
○ Most common congenital anomaly of the lung
● Vascular anomalies
○ Pulmonary hypertension
● Congenital Emphysema (Idiopathic usually)
● Foregut cysts
○ Failure of closure of the esophagus
■ Fluid accumulation
● Pulmonary Artery Malformations (CPAM)
○ Anomalous connections to the pulmonary artery by
certain vessels
● Sequestration (no connection to airways or pulmonary
arteries, but systemic)
■ 82% - distal esophagus connected
● Tracheo-Esophageal fistula without Esophageal atresia -
6%
○ Just a connection between esophagus and trachea
ATELECTASIS
● Technically not a disease
○ An anatomic physiologic geometric concept
● Definition
○ Anything that reduces lung volume
● Incomplete expansion
○ Resorption - obstruction to airway
○ Compression - fluid accumulation
■ If fluid accumulation - pleural effusion
■ If blood accumulation - hemothorax
■ If air accumulation - pneumothorax
● Collapse
○ Contraction - due to fibrosis (thickening of epithelium)
ACUTE PULMONARY INJURY
● Pulmonary Edema
● ARDS (Diffuse Alveolar Damage)
○ Acute Respiratory Distress Syndrome
○ Broken down alveolar wall
● Acute Interstitial Pneumonia
○ Typically a last resort diagnosis
PULMONARY EDEMA
● Alteration between protein in intravascular space and
extravascular space
● Increased venous pressure
○ Congestion of the lungs
○ Due to dilated alveolar spaces (top image)
● Decreased oncotic pressure
○ Oncotic pressure - presence of protein in the
intravascular space
○ Will happen with the release of albumin to the
kidneys/urine
○ Can also happen due to a kidney problem
○ With the decrease of oncotic pressure, there will be
an increase in the presence of fluid within the alveolar
space, with restricts the airways of the lungs (lower
image)
● Lymphatic obstruction
○ Decreased drainage of thoracic duct, which will cause
it to accumulate in the lungs
● Alveolar injury
○ Anything that damages the alveoli

● Failure in closing on the 6th week will cause anomalous

connection between the trachea and the esophagus
● Esophageal atresia - 9%
○ Trachea is intact but esophagus is atretic
■ Atresia - like agenesis, it did not grow
○ The middle section of the esophagus did not grow
● Esophageal atresia with Tracheo-Esophageal fistula
○ Segments of esophagus did not grow
○ A part of esophagus connects to the trachea
■ 1% - Proximal part of the esophagus connected
■ 2% - Both proximal and distal esophagus ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)
connected
● ARDS - clinical term

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● In Pathologic terms: DAD (Diffuse Alveolar Damage)
○ Aka “Shock” lung
■ Usually predisposition to death
■ Alveolar edema
■ Forms after 48 hrs from initial trauma
■ Syndrome of the acute respiratory failure with the
characteristic of non-cardiogenic pulmonary
edema
■ Anything that is terminal or a full blown
manifestation will produce a shock lung
● Non-specific pattern of lung injury
● Infection
● Physical injury
● Toxic
● Chemical
● DIC (Disseminated Intravascular Coagulation)
○ Happens because of widespread bacterial infection,
i.e., septic infection
■ Elaboration of cytokines and coagulation
process; can’t be controlled locally anymore
○ Widespread blood clot formation
● ETC
● Decrease in available airway
● There are more exudative fluid than transudative fluid
○ Presence of fibrin, proteins, inflammatory cells in the
alveoli
● Alveolar walls are unrecognizable
ACUTE INTERSTITIAL PNEUMONIA
● Think of it as ARDS with no known etiology
● Wastebasket diagnosis
○ When it can’t be associated with the other causes of
ARDS
● Idiopathic inflammation of the lung that is caused by
ARDS
● Histologically similar to ARDS
OBSTRUCTION VS RESTRICTION
● Obstruction
○ Anything that obstructs the airways
○ Can be air or blood
○ Large or small airways involved
○ Can affect inspiration or expiration
○ Obstruction is mostly small airway expiration
■ If it starts from the large airways, the patient will
immediately die as it affects a larger part
■ Manifestation: wheezing (like in asthma)
● Wheezing - produces a high pitched sound
due to a small airway obstruction
○ Hyperexpansion of lung volume on CXR(Chest
X-Ray)
■ Airway traffic in the alveolar spaces; air gets
trapped
■ More loosely, less density
● Restriction
○ Less compliance
■ Doesn’t expand as normal
○ Infiltrative
○ Reduced lung volume, dyspnea, cyanosis
■ Due to reduced gas transfer
○ Reduced gas transfer
■ Problem in interstitial fibrosis
■ Causes less spongy lung appearance
● Term for restrictive pulmonary diseases
■ Lung float test - to see whether the lungs of an
autopsy patient will float or sink when placed in a
bucket of water. It is used to find out if there is a
presence of air, or water, inside the lungs. Helpful
in determining the presence of restrictive lung
disease or pulmonary edema
○ “Ground glass” appearance on CXR
■ Hyaline membrane disease
OBSTRUCTIVE PULMONARY DISEASES (COPD)
● Umbrella term: Chronic Obstructive Pulmonary Disease
(COPD)
● Emphysema (almost always chronic)
● Chronic Bronchitis → Emphysema
○ Inflammation of Bronchi
● Asthma
● Bronchiectasis
● All 4 conditions are generally interconnected
EMPHYSEMA
● COPD, or “end-stage” lung disease
● Centri-acinar, pan-acinar, paraseptal, irregular → types
○ Differ in the segments they affect
○ Centro-acinar → usually in hilum, affecting mostly the
central portions of the lungs, only a specific region
○ Pan-acinar → diffuse involvement of the lung
parenchyma, involves the whole lung/acinus
○ Paraseptal → mostly affecting the septal portion
○ Irregular → varying in affected areas
● Progressive airway trapping (i.e. wheezing) because of
damage to alveolar walls
○ Airway space expansion (histologic) → damage to
alveolar walls
○ Air is retained in alveolar spaces
○ There is wheezing but the usual cause is smoking
■ Different from wheezing in asthma → in asthma
there is usually an allergic cause or
hypersensitivity reaction, with emphysema it’s
basically due to smoking or anything that
damages the alveolar walls or produce alveolar
injury
● Like cirrhosis, thought of as end-stage of multiple chronic
small airway obstructive etiologies
○ Usually in elder population
● Non-specific but can occur with chronic bronchitis because
it is also caused by smoking
● Increased crepitance, bullae (blebs)
○ More air present in alveolar spaces
○ In comparison with restrictive lung disease: restrictive
lung disease has decreased crepitance because of
the reduced gas transfer or lung volume
○ Bullae is a collection of air due to hyperinflation of
lung
○ “Bubbly” appearance
○ Bullae is the hallmark of chronic obstructive lung
disease
○ Because of air trapping, there would be accumulation
of air in peripheral spaces
○ Complication: if bullae ruptures, there would be
leakage of air towards your pleural space
(pneumothorax)
■ Treatment for pneumothorax: injection of syringe
in the spaces between pleura and lung to relieve
the patient of air in the pleural space
■ Removal of air in the pleural space to restore
lung expansion → ability to take in more air
■ You cannot inject it directly into the bleb because
it will rupture → more complications
● Clinically likely to produce recurrent pneumonia and
progressive lung failure
○ If not corrected
○ Progressive damage to alveoli → inability to expire air
→ retained in lungs
● Acinus vs. alveolus
○ Acinus is much bigger and involves alveolar ducts
and terminal bronchioles
○ Alveolus is the basic unit of lung, smallest portion
***bullae is posteriorly located, air spaces at the back of the
lungs. (back because the vertebrae and heart are visible)
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***4 factors to determine in chest x-rays for emphysema:
1. Hyperexpansion → larger lung volume than normal,
engorged pulmonary vessels
2. “Flattened” diaphragms → blunted costophrenic angle
3. Presence of bullae (seen in superior lobes)
4. Increased lucency (grayish compared to normal) →
because of the presence of air in lower lobes
(mid-inferior)
○ There is air trapping in emphysema, so this is an
indication of more air present in lower lobes
CHRONIC BRONCHITIS
● Inhalants, pollution, cigarettes, chronic cough
○ Usual causes
● Can often progress to emphysema
○ The usual causes (particularly smoking) damages
alveolar walls as well
● Infection or inflammation of the bronchi
● Pathology: mucus hypersecretion, early, i.e. goblet cell
increase (hyperplasia on the lining)
○ In response to these toxic substances (usual causes),
the the airway will thicken to protect itself to avoid
exposure of the deeper layers of the respiratory tract
○ Obstruction → reduces luminal diameter
● Chronic bronchial inflammatory infiltrate → could also
decrease the diameter of respiratory airways as well
ASTHMA
● Similar to chronic bronchitis but:
○ Wheezing is hallmark (bronchospasm, i.e.
“wheezing”)
■ Bronchospasm → there is a hyperreactive airway
in the bronchi
■ Anything hyperreactive to the airway reduces the
luminal diameter of the lower respiratory tract
■ Wheezing → high pitched sounds due to a
turbulent flow or obstruction to the flow of air in
the lungs
● High pitched sounds because during laminar
flow, there are no sounds produced.
Anything that is restricting the outflow of air
or blood, air or blood may hit the walls of
airway or blood vessel, producing turbulent
sounds like wheezing and Korotkoff sounds
○ Strong allergic role, i.e., eosinophils, IgE, allergens
■ Most common: dust, pollen, pet hair
○ Often starting in childhood, usually seen in young
adults
○ Atopic (allergic) or non-atopic (infection
■ Predispositions
■ Atopic → hypersensitivity reaction
● In pediatrics, there is a thing called atopic
march → you had an allergy before, it will
manifest into a different hypersensitivity
condition when you encounter the same
allergen (for example, you experienced
asthma the first time, during the next
exposure, you may experience compact
dermatitis then urticaria)
● Different hypersensitivity conditions or
manifestations upon multiple exposures to
allergens as you age
○ Chronic small airway obstruction and infection
1. Mucus hypersecretion with plugging → plugging
due to mucus hardening
2. Lymphocytes/eosinophils → particularly eosinophils
for an allergic cause
3. Lumen narrowing → because of hypersecretion
and inflammation
4. Smooth muscle hypertrophy → because of a
hyperreactive airway (due to exposure to allergen),
unique to asthma
● Inflammation with allergic etiology
● Hypersensitivity reaction with predispositions in the airway
● Typical pathology: hyperreactive airway
***note the presence of inflammatory infiltrates (bronchioles
and bronchi. There is also a thick mucus production.
Supposedly the lumen should be more expanded than what is
seen above but due to mucosal hypersecretion, there is a
presence of thick mucus and inflammatory infiltrates. A
germinal center can also be seen due to intense inflammation.
***the cartilage determined the identity of the airway
(bronchus vs. bronchiole). The one above is a bronchus (the
cartilage is present).
***there is also the presence of overexpanded alveoli in
relation with air trapping/emphysema because of reduced
outflow of air (results in accumulation of air in the alveoli,
rendering the breakdown of alveolar walls, producing air
trapping/emphysema).
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 ● “Nonspecific” interstitial fibrosis
● “Cryptogenic” organizing pneumonia
● “Collagen” vascular diseases
● Pneumoconioses
● Drug reactions
● Radiation changes
● Anything fibrotic in the lung would reduce gas exchange
● Biggest category of restrictive lung diseases
● Follows inflammation → reparative process
● Reduced incidence for an infectious cause (not bacterial
nor viral)
● Autoimmune etiologies

IFP (UIP)
● Usual interstitial pneumonia
● Idiopathic, i.e., not from any usual caused, like lupus,
scleroderma
○ Sometimes the cause is unknown but it is usually
related to lupus and scleroderma
***the following are the histologic findings in asthma:
● Fibrosis in the lungs → restricts relation of alveoli to
1. Inflammation
capillaries
2. Bronchial narrowing
○ Interstitial fibroblast proliferation → reduced
3. Increased mucus secretion
opportunity for diffusion or gas exchange
4. Smooth muscle hypertrophy
○ Fibrosis can be seen using trichrome staining
***all of these would produce an obstructive pulmonary disease
● Unknown cause + increased fibrosis → autoimmune
BRONCHIECTASIS
● Dilatation of the bronchus, associated with, often,
necrotizing inflammation
○ Congenital
○ TB, other bacteria, many viruses → most common
cause is TB
○ Bronchial obstruction (i.e., large airway, not small
airway)
■ By large airway, it describes the bronchi
○ Seen also in rheumatoid arthritis, SLE, IBD
(Inflammatory Bowel Disease)
● Not a specific disease, it is a condition where your large
bronchi are damaged and dilated due to a variety of
causes
***op = organizing pneumonia

NON-SPECIFIC INTERSTITIAL PNEUMONIA

● Wastebasket diagnosis, of any pneumonia (pneumonitis)
of any known or unknown etiology
○ Fibrosis
○ Cellular infiltrate (lymphs and plasma cells)
○ As long as you have fibrosis and inflammation of any
known or unknown etiology
● Pneumonia → infection of lower respiratory tract
○ Upper respiratory tract infection involves
nasopharynx, oropharynx, larynx, and tonsils
■ Pharyngitis
RESTRICTIVE (INFILTRATIVE) PULMONARY DISEASES ● Infectious pathogen is usually unknown
● Reduced lung volume, reduction of contraction of lungs
● Reduced compliance, reduced gas exchange
○ Reduction in being spongy
○ Typically will not comply when squeezed or moved by
respiratory motion
● Are also diffuse, increased density, decreased crepitance
○ Opposite to this is obstructive lung
disease/emphysema
● Heterogeneous etiologies
○ Fibrosing
○ Granulomatous
○ Eosinophilic
○ Smoking related CRYPTOGENIC ORGANIZING PNEUMONIA (COP)
○ PAP (Pulmonary Alveolar Proteinosis) ● Idiopathic → unknown cause but is usual in transplanted
● Presence of anatomical and functional barrier to your gas lungs
exchange causing it to reduce between endothelial cell ● “Bronchiolitis obliterans”
and type I pneumocyte ● Also produces onion skinning
● Affects pulmonary circulation because of hypersensitivity
reaction or graft-versus-host disease
○ Attacks vessels, producing diffuse inflammation all
throughout the lung

FIBROSING
● Idiopathic Pulmonary Fibrosis (IPF)

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 SARCOIDOSIS
● Affects the whole body → mainly lung, but can manifest in
eye, skin or anywhere
● Unknown etiology
● autoimmune, genetic factors
● Females >> Males
● Blacks >> Whites
● Young adult black women

COLLAGEN VASCULAR DISEASE

● Rheumatoid arthritis
○ Systemic condition
○ Affects joints, heart, lungs, and vessels
○ Reduction of collagen in the lungs → affects vessels
in the lungs
● SLE (“Lupus”)
● Progressive Systemic Sclerosis (Scleroderma)
● Inflammation of the vessels in the lungs (caused by the
conditions above) ● Non-caseating granulomas are the rule
● Mucosal hypersecretion ● “Asteroid” bodies within these granulomas are virtually
diagnostic but hard to find
○ Star-shaped body found in sarcoidosis

PNEUMOCONIOSES
● Occupational in cause
● “Coal miners lung”
○ Lungs are exposed to carbon/coal
● Dust or chemicals or organic materials
○ Coal (anthracosis) → accumulation of carbon
○ Silica (silicosis)
○ Asbestos (asbestosis)
○ Be, FeO, BaSO4, Chemotherapy may also cause
pneumoconiosis
○ HAY, FLAX, BAGASSE, Insecticides, etc.
■ Fertilizers, antiparasitic sprays
● Anything that irritates the lung due to an occupational
hazard or substance would also produce bronchiotic (?)
component as well
○ May also produce chronic obstructive component as
well as restrictive
***caseating granuloma vs. noncaseating granuloma
● Both have giant cell formation but caseating granuloma
has presence of caseating necrosis
● Tuberculosis cause (left), sarcoidosis (right)
● In granulomas
○ Anything that acts as a barrier for spread of infection,
production of inflammation, or foreign bodies forms
granuloma which is composed of your fibrosis,
histiocytes, giant cells, lymphocytes
SMOKING RELATED
● DIP (Desquamative Interstitial Pneumonia)
○ M>>F
○ Cigarettes
○ 100% survival
○ Desquamative because the alveolar wall epithelium is
thinning out into the alveolus
○ Alveolar spaces are exfoliated, restricting gas
exchange → reduced blood-air interphase because of
dysformation (malformation) or exfoliation of alveolar
macrophages

***left: ferruginous bodies of asbestosis, right: silica nodules

of silicosis
● Alveolar macrophages
GRANULOMATOUS
● Sarcoidosis, i.e., non-caseating granulomas (Idiopathic) PAP (PULMONARY ALVEOLAR PROTEINOSIS)
● Hypersensitivity (dusts, bacteria, fungi, Farmer’s lung, ● Very rare, usually acquired
Pigeon breeder’s lung) ● Accumulation of proteinaceous material in alveoli
○ Cryptococcosis → pigeon breeder’s lung from feces ○ More voluminous than pulmonary edema
of pigeon ○ Less fluid, more protein
● Minimal cellular infiltrate
● Like pulmonary edema, but much protein

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● Restricts gas exchange
● Laboratory finding: anti GM-CSF autoantibody

***left: pulmonary edema (fluid accumulation), right:

proteinosis

VASCULAR PULMONARY DISEASES ***narrowing causes HTN, and HTN causes narrowing
● Pulmonary embolism (with or usually without infarction)
● Pulmonary hypertension, leading to cor pulmonale HEMORRHAGIC SYNDROMES
● Hemorrhagic syndromes
● Goodpasture syndrome: Ab’s to the alpha-3 chains of
○ Goodpasture syndrome
collagen IV, GBM deposits too
○ Hemosiderosis, idiopathic
○ GBM deposits because collagen type IV is for
○ Wegener granulomatosis → multiple granulomas +
basement membrane
chronic renal failure
● Idiopathic Pulmonary Hemosiderosis, to be differentiated
from chronic CHF
PULMONARY EMBOLISM ○ Accumulation of iron
● Usually secondary to debilitated states with ● Wegener granulomatosis
immobilization, or following surgery ○ Vasculitis affecting lungs, kidneys, and other organs
○ Bedridden, icu, immobilized
● Usually deep leg and deep pelvic veins, not superficial
veins
○ Produces deep vein thrombosis (DVT)
● Follows virchow’s triad
○ 1. Flow problems
○ 2. Endothelial disruption (vascular injury)
○ 3. Hypercoagulability
○ Anything that is procoagulant would produce PE
● Usually do not infarct, usually ventilate
● When they do infarct, the infarct is hemorrhagic because it
comes from an airway problem → leads to damage in
blood vessels
● Decreased PO2, acute chest pain, V/Q mismatch
○ V/Q (ventilation-perfusion) assesses if ventilation and
perfusion occur simultaneously or if you have intact ***CHF produces hemosiderin-laden macrophages in the lung
ventilation with intact perfusion (heart failure cells are located in the lungs, particularly alveoli).
● DX: Chest CT, V/Q scan, angiogram to assess or monitor When you have pulmonary HTN or CHF, there would be
pulmonary vessels extravasation of your macrophages or iron deposits. In
● RX: short term heparin, then long term coumadin/warfarin idiopathic pulmonary hemosiderosis, the hemosiderins are
○ Coumadin or warfarin is an anticoagulant drug → more numerous and voluminous in alveoli in comparison to
reduces internal hemmorhage CHF.

***saddle embolism → looks like a saddle of a horse

PULMONARY HYPERTENSION
● COPD, CIPD (vicious cycle)
● CHD (Congenital HD, increases left atrial pressure)
● Recurrent PEs
● Autoimmune, e.g., PSS (Scleroderma), i.e., fibrotic
pulmonary vasculature → inability to contract or expand
the vessels (very rigid), turbulent flow