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Respiratory 2 – Pathology

Alyanna Villaluna Doctorials 2021/22

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Outline

Obstructive Lung Disease

COPD

Chronic Bronchitis
Emphysema
Asthma

Bronchiectasis

Restrictive Lung Disease

Idiopathic Pulmonary Fibrosis
Pneumoconioses

Coal Workers’ Pneumoconiosis
Silicosis
Berylliosis
Asbestosis

Hypersensitivity Pneumonitis – Sarcoidosis

Pulmonary Embolism vs Deep Vein Thrombosis (PE vs DVT)

Signs, Symptoms, Risk Factors
Well’s Score

Pneumonia

Lobar vs bronchopneumonia
Community acquired vs nosocomial

Lung Cancer

Small Cell Carcinoma (SCC)
Non-Small Cell Lung Carcinoma (NSCLC)

Adenocarcinoma
Squamous Cell Carcinoma
Large Cell Carcinoma
Carcinoid Tumour

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A

B

C

D

E

F

G

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Obstructive vs Restrictive Lung Disease

Obstructive

Lung does not empty; air is trapped
↓ FVC; especially during first second (↓↓ FEV1)
Results in a ↓ FEV1:FVC ratio (<70%)
TLC increased due to air trapping (↑ RV)
COPD, asthma, bronchiectasis

Restrictive

Air filling is restricted
↓ TLC, ↓ FEV1, ↓↓FVC 🡪 why?
FEV1:FVC usually normal to increased

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1. Obstructive Lung Disease

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COPD

Group of diseases characterized by airway obstruction
Lung does not empty and air is trapped 🡪 resulting in greater than normal lung volumes
Progressive and irreversible
Includes chronic bronchitis, emphysema, asthma, bronchiectasis

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Chronic Bronchitis

Defined clinically

Chronic cough lasting at least 3 months over a minimum of 3 years
Highly associated with smoking
Involves large airways like the bronchus
Characterized by hypertrophy of bronchial mucous glands
Reid Index >50%

Clinical Features

Productive cough
Cyanosis (blue bloater) 🡪 ↑ PaCO2 and ↓ PaO2

Alveolar hypoxia 🡪 pulm vasoconstriction 🡪 pulm HTN 🡪 right heart failure

Increased risk of infection and cor pulmonale
Secondary polycythemia

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So productive that patient will be coughing up “cups of mucus.”

Normally, the mucous glands take up about 40% or less of thickness of wall (epithelium, lamina propria (blood vessels), and submucosa (serous and mucous gland)

Smoking – brings in lots of pollutants – lung responds by increasing the amount of mucous (hyperplasia and hypertrophy of mucinous glands) 🡪 excess glands increase in thickness leading to >50% of wall.

This is called the Reid Index

Excess mucous causes ++ coughing, and also air trapping (obstruction)

Smoking: increased mucous production and secretion, decrease cilia activity, decrease alveolar macrophage function

Cyanosis - mucous plugs traps CO2

Secondary polycythemia 🡪 hypoxemia stimulates increased EPO production from kidneys 🡪 increased RBC production

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Emphysema

Destruction of alveolar air sacs

Causes of physiologic obstruction

Due to imbalance of proteases and antiproteases
Smoking is the most common cause
A1AT deficiency is a rare cause

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A) Destruction of alveolar air sacs

Loss of elastic recoil and collapse of airways during exhalation results in obstruction and air trapping
Normally: alveoli are like tiny balloons – fill up with air and then snap back which blows air out. If destroy walls, and lose elastic recoil then instead of many balloons, you are left with 1 big shopping bag where you can get air out.

Also, as air is squeezed out of the lung, it accelerates and drags a bit of the wall in
At the top (bronchus) you have cartilage that prevents collapse
At the level of alveoli and bronchioles (small airways) 🡪 you have the elastic recoil of the air sacs that prevent collapse

B) Due to imbalance of proteases and antiproteases

Inflammation causes release of proteases and elastases from neutrophils and macrophages
Normally: there is always a small amount of inflammation happening in the alveoli due to particles that make there way down there 🡪 macrophages ingest and cause inflammation 🡪 proteases are a by product of inflammation
A1AT neutralizes proteases

C) Smoking most common cause

Causes excessive inflammation and release of proteases
Centriacinar emphysema that is most severe in upper lobes – smoke rises

D) A1AT deficiency

Rare clinically but common on exams
Leaves lung vulnerable to protease damage
Causes panacinar emphysema
Liver cirrhosis may also be present
Deficiency is that protein is misfolded and cant be released from liver 🡪 piles up in cells (in the endoplasmic reticulum) and damages hepatocytes (globules are PAS positive)

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Emphysema

Clinical Features

Dyspnea and cough with minimal sputum

Unlike chronic bronchitis

Prolonged expiration with pursed lips
Weight loss 🡪 due to lots of work (exercise)
Increased anterior-posterior diameter of the chest (barrel-chest)
Hypoxemia and cor pulmonale are late complications

Pink Puffers 🡪 stay pink because are oxygenating because are able to overcome obstruction by pursing lips and breathing slowly

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- Dyspnea and cough with minimal sputum

Unlike chronic bronchitis

- Prolonged expiration with pursed lips 🡪 creates back pressure allowing air to move in and out without walls collapsing

- Weight loss

Increased anterior-posterior diameter of the chest (barrel-chest)

Normally: tendency of the alveoli is to collapse in and tendency of the chest wall is to expand out. Both forces are normally in balance 🡪 this setpoint is the FRC (functional residual capacity)
Without elastic recoil of the lungs, chest wall is able to expand out a little more, increasing the FRC and AP diameter of the chest
Classic finding in patients with emphysema
Fibrosis increases the elastic recoil of the lungs and therefore pulls in the chest wall which would decrease the FRC

Hypoxemia and cor pulmonale are late complications

Pink puffers – able to maintain oxygenation by pursed lip breathing and slow breathing
Eventually air sacs and capillaries surrounding air sacs are destroyed 🡪 loss of area for oxygen exchange 🡪 hypoxemia (↓ PaO2) 🡪 pulm HTN 🡪 cor pulmonale

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COPD

Hypoxic Drive

Patient’s have chronically elevated PaCO2
Tolerance of central and peripheral chemoreceptors to PaCO2
Body switches to hypoxic drive

Lower O2 levels now drives respiration

If COPD patient given too much oxygen, then you will take away they’re hypoxic drive 🡪 hypoventilation 🡪 increased PaCO2 🡪 respiratory acidosis

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Asthma

Reversible airway bronchoconstriction
Most often due to allergic stimuli (Type 1 Hypersensitivity) – atopic asthma
Often presents in childhood

Pathogenesis (Type I Hypersensitivity)

Allergens induce TH2 phenotype in CD4 T cells of genetically susceptible people; TH2 secrete:

IL-4 🡪 mediates class switch to IgE
IL-5 🡪 attracts eosinophils
Il-10 🡪 stimulates TH2 cells and inhibits TH1 cells (promotes this overall reaction)

Reexposure of allergen 🡪 IgE mediated activation of mast cells (acute early phase) 🡪 Release of histamine, leukotrienes, and platelet activating factor 🡪 Immediate Inflammation
Late Phase 🡪 bronchoconstriction and oedema (histamine and basophils) + inflammatory damage (neutrophils, basophils, monocytes, CD4) + epithelial damage and shedding

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Reversible airway bronchoconstriction

Most often due to allergic stimuli (type 1 hypersensitivity) – atopic asthma

Often presents in childhood

Pathogenesis

Allergens induce TH2 phenotype in CD4 T cells of genetically susceptible people

IL-4 🡪 mediates class switch to IgE

IL-5 🡪 attracts eosinophils

Il-10 🡪 stimulates TH2 cells and inhibits TH1 cells (promotes this overall reaction)

Early Phase

Reexposure of allergen 🡪 IgE mediated activation of mast cells: allergen causes IgE on mast cells to cross link 🡪 activates the mast cell

Release of histamine granules 🡪 vasodilation (arterioles) and vascular permeability (post capillary venule)

Release of leukotrienes C4, D4, E4 🡪 bronchoconstriction

Release of platelet activating factor 🡪 more histamine and serotonin release from platelets

Late Phase

Cytokines released during the early phase contribute to laste-phase effects

Histamine 🡪 further bronchoconstriction and oedema

Neutrophils, basophils, monocytes, CD4 T cells 🡪 inflammatory damage

Major basic protein (eosinophils) 🡪 epithelial damage and shedding

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Asthma

Clinical Features

Dyspnea and wheezing
Productive cough, Curschmann spirals admixed with Charcot-Leyden crystals
Severe, unrelenting attack can result in status asthmaticus and death

Non Allergic Causes

Exercise
Viral infection
Aspirin (aspirin intolerant asthma) – bronchospasm
Occupational exposure

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Bronchiectasis

Permanent dilation of the bronchioles and bronchi (large airways)
Loss of airway tone results in airway trapping

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Bronchiectasis

Causes

Due to necrotizing inflammation with damage to the airway wall – chronic airway inflammation and infection

Cystic fibrosis
Kartagener syndrome
Tumor of foreign body
Necrotizing infection
Allergic bronchopulmonary aspergillosis

Clinical Features

Cough, dyspnea, and foul-smelling sputum
Complications include hypoxemia (trapping of CO2), cor pulmonale, secondary amyloidosis

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Cystic Fibrosis (classic) – thick secretions that cause mucus plugging increasing the risk of infection 🡪 damage to airways 🡪 bronchiectasis

Kartagener syndrome – defect in dynein arm of cilia 🡪 defect in ciliary movement: sinusitis, infertility, situs inversus (heart on right), lung infection

Tumor or foreign body – obstruction causes increased risk of infection and airway damage

Necrotizing infection –

Allergic bronchopulmonary aspergillosis – HSR, large airways, aspergillosis

Classically seen in asthmatics and systic fibrosis – hypersensitive to aspergillosis 🡪 reaction damages airways 🡪 bronchiectasis

Amyloidosis – deposition of a misfolded protein

Can be localized or systemic
Systemic can be primary or secondary

Primary: deposition of amyloid light chain due to plasma cell problem – overproduction of light chain
Secondary: chronic inflammation produces an acute phase reactant (SAA) 🡪 AA 🡪 deposition

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2. Restrictive Lung Disease

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Restrictive Lung Disease

Important Principles

Problem with filling of the lung
↓ TLC
↓ ↓ FVC, ↓FEV1
FEV1:FVC ratio is increased (>80%)

Causes

Interstitial diseases of the lung

↓ diffusing capacity, ↑ A-a gradient, ↓ DLCO

Poor breathing mechanics

Poor effort – polio, myasthenia gravis, GBS
Structural – scoliosis, morbid obesity

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Idiopathic Pulmonary Fibrosis

Fibrosis of lung interstitium
Cyclical lung injury and healing
Must first exclude other causes

Clinical Features

Progressive dyspnea and cough
Fibrosis on lung CT
Finger clubbing
Treatment is transplant

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Pneumoconiosis

Interstitial fibrosis due to occupational exposure
Requires chronic exposure to small particles that are fibrogenic

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Coal Worker’s Pneumoconiosis

Macrophages engulf carbon particles 🡪 inflammation and fibrosis
Results in a shrunken lung
Also known as black lung disease – diffuse fibrosis
Association of rheumatoid arthritis and coal worker’s pneumoconiosis is Caplan Syndrome
Anthracosis:

Collection of carbon-laden macrophages
Not clinically significant
Happens from everyday exposure to pollution

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Silicosis

Seen in sandblasters
Macrophages respond to silica by releasing fibrogenic factors
Impairs formation of phagolysosome
Only pneumoconiosis that increases risk for TB
Commonly results in fibrotic nodules in upper lobes of the lung
“Eggshell calcifications of hilar lymph nodes on CXR”

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Berylliosis

Miners and workers in aerospace industry
Noncaseating granulomas in the lung, hilar lymph nodes, and systemic organs
Increased risk for lung cancer
Affects upper lobes

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Asbestosis

Construction workers, plumbers, shipyard workers
Fibrosis of lungs and pleura; causing cancer of lungs and pleura
Bronchogenic carcinoma is more common than mesothelioma in exposed individuals
Affects the lower lobes
Supradiaphragmatic (A) and pleural plaques (B) are pathognomonic
Asbestos (ferruginous) bodies (C) – pathological confirmation

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Pneumoconioses Summary

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Pathoma

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Hypersensitivity Pneumonitis

Granulomatous reaction to inhaled organic antigen (pigeon breeder’s lung)
Acute/Initial

Fever, cough, dyspnea, chest tightness, headache hours post exposure
Resolves with removal of antigen

Chronic

Chronic exposure leads to interstitial fibrosis

Classically see granulomas with eosinophils

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Sarcoidosis

Systemic disease of noncaseating granulomas in multiple organs

Classically seen in African American females

Etiology unknown
Granulomas usually in hilar lymph nodes and lungs
Asteroid body can be seen in giant cell

Clinical Features

Dyspnea and cough
Elevated serum ACE
Hypercalcemia
Can resolve spontaneously or with immunosuppression

Other Tissues

Skin – cutaneous nodules or erythema nodosum
Uvea –uveitis
Salivary and lacrimal glands – can mimic Sjogren; how have non caseating granuloma

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Sarcoidosis

“A Grueling Disease”

ACE enzyme ↑

Granulomas → non-caseating

Rheumatoid arthritis

Uveitis

Erythema nodosum

Lymphadenopathy

Interstitial fibrosis

Negative TB

Gammaglobulinemia

D → vitamin D ↑ due to ↑ 1α-hydroxylase activation, leads to hypercalcemia

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3. Deep Vein Thrombosis (DVT) vs Pulmonary Embolism (PE)

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DVT

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Signs and Symptoms

Calf warmth
Tenderness
Swelling
Erythema
Mild fever
Pitting edema

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DVT – Wells Score

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Pulmonary Embolism

Usually due to thromboembolism with DVT being most common cause – femoral, iliac, or popliteal veins
Most often clinically silent because the lung has dual blood supply and embolus is usually small
Pulmonary Infarction in about 10% of PEs

Clinical Presentation

Asymptomatic
Classic presentation
Catastrophic hemodynamic collapse
Sudden death

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Signs

Tachypnea (96%)
Wheeze (58%)
Tachycardia (44%)
Fever > 37.8
Diaphoresis
Calf/thigh swelling
Cyanosis
Hypotension
Raised JVP
Pleural rub

Blood supply of lungs – pulmonary and bronchial arteries

Infarction if large/medium PE in patients with cardiopulmonary dysfunction 🡪 susceptible to damage

1. Asymptomatic-can present as CTEPH (chronic thromboembolic pulmonary hypertension). Presents as persistent or progressive dyspnoea. (Proximal DVT more likely than distal DVT)

2. Classic presentation is Acute SOB, Pleuritic Chest Pain, Cough → palpitations, new onset AFib, syncope, fever, haemoptysis, delirium in the elderly

3.Catastrophic haemodynamic collapse–acute right ventricular dysfunction, which can lead to arrhythmia, haemodynamic collapse and shock. Most massive PE will die with hours of the event. A patient may survive a herald embolism and left untreated then 1/3 will die within hours of the event after a bigger embolism

4. Suddendeath-80% of unexpected deaths in hospital are due to PE. In 40% of deaths, patients had seen their doctor in the weeks prior to their death. 10% die within 1 hour. 30% die from recurrent pulmonary embolism

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PE –Wells Score

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4. Pneumonia

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Pneumonia

Infection of the lung parenchyma
Occurs when normal defences are impaired or organism is highly virulent

Clinical Features

Fever and chills
Cough (productive or dry)
Tachypnea
Pleuritic chest pain
Decreased breath sounds
Crackles
Dullness to percussion
Elevated WBC
CXR - consolidation

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Lobar Pneumonia

Consolidation of entire lobe of lung
Usually bacterial
Most common causes are Strep. Pneumoniae (95%) and Klebsiella

Right Middle Lobe air sacs filled with neutrophils and exudate

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Lobar Pneumonia

Congestion

Dilation of blood vessels and edema

Red hepatization

Exudate with neutrophils and blood

Grey hepatization

Breakdown of RBCs

Resolution

Healing

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Bronchopneumonia

Consolidation that runs along the small airways distributed in a patchy manner
Caused by a variety of bacteria

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Bronchopneumonia

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Interstitial (atypical) Pneumonia

Inflammation within interstitium (connective tissue of alveolar air sac)
Diffuse infiltrates within the lung
Increase in lung markings
Usually viral
Signs and symptoms are relatively atypical

Mild upper respiratory symptoms
Minimal sputum, cough, low fever

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Interstitial (atypical) pneumonia

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Aspiration Pneumonia

Patients at risk for aspiration
Due to anaerobic bacteria in oropharynx

Bacteroides
Fusobacterium
Peptococcus

Classically causes a right lower lobe abscess

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Community Vs Hospital Acquired

Community

Develops in the outpatient setting or within 48 hours of admission to hospital
Streptococcus pneumoniae
Haemophilus Influenzae
Mycoplasma pneumoniae

S. Aureus, legionella, Moraxella, Chlamydia

Nosocomial (hospital)

Develops > 48hrs after admission to the hospital
Most commonly gram negative enterobacteria or S. Aureus most common

Bacteroides, clostridia

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5. Lung Cancer

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Lung Cancer

Symptoms are non specific

Cough, weight lose, hemoptysis, post obstructive pneumonia

CXR will reveal a “coin lesion” or solitary nodule

Next step?

Biopsy is necessary for diagnosis

Benign Lesions

Granuloma
Bronchial hamartoma: often calcified on imaging

Remember, young patients are much more likely to have a benign lesion than to have cancer

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Lung Carcinoma

Small cell carcinoma (15%)

Usually treated with chemo
Surgery not possible

Non-small cell carcinoma (85%)

Surgery
Does not respond well to chemotherapy and radiation

Metastasis from lung go to: Liver, adrenal, bone, brain
Metastasis to lung from: breast, colon, prostate, bladder 🡪 more common than primary lung cancer

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Small Cell Carcinoma

Treated up front with chemotherapy
Poorly differentiated small cells
Arises from neuroendocrine cells
Male Smokers
Central location
Rapid growth and early metastasis

Paraneoplastic Syndromes

ADH
ACTH
Eaton-Lambert syndrome
Antibodies against neurons (myelitis, encephalitis, subacute combined degeneration)

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Paraneoplastic syndromes are rare disorders that are triggered by an altered immune system response to a neoplasm. They are defined as clinical syndromes involving nonmetastatic systemic effects that accompany malignant disease. In a broad sense, these syndromes are collections of symptoms that result from substances produced by the tumor, and they occur remotely from the tumor itself.

When a tumor arises, the body may produce antibodies to fight it by binding to and destroying tumor cells. Unfortunately, in some cases these antibodies cross-react with normal tissues and destroy them, which may result in a paraneoplastic disorder.

In other cases, paraneoplastic syndromes result from the production and release of physiologically active substances by the tumor. Tumors may produce hormones, hormone precursors, a variety of enzymes, or cytokines.

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Non-Small Cell Carcinoma

Adenocarcinoma (40%)

Glands or mucous production

Squamous cell carcinoma (30%)

Keratin pearls or intercellular bridges

Large cell carcinoma (10%)

Don’t see any of previous features

Carcinoid tumor (5%)

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Adenocarcinoma

Glands or mucin production
Most common in non smokers
Most common in female smokers
Peripheral location

Adenocarcinoma in situ

Bronchioloalveolar carcinoma
Columnar cells that grow along pre-existing bronchioles and alveoli
Peripheral
Excellent prognosis

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Squamous Cell Carcinoma

Keratin pearls or intercellular bridges
Most common tumor in male Smokers
Central location
Paraneoplastic Syndrome

PTHrP

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Large Cell Carcinoma

Poorly differentiated large cells
No keratin pearls, no intercellular bridges, no glands, no mucin production
Associated with smoking
Central or peripheral
Poor prognosis

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Carcinoid Tumor

Well differentiated neuroendocrine cells
Chromogranin positive
Not related to smoking
Central or peripheral
Classically forms a polyp like tumor in bronchus
Low grade malignancy
Carcinoid syndrome

Flushing
Diarrhea
Wheezes

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Lung Cancer

Small cell carcinoma
Squamous cell carcinoma
Adenocarcinoma
Large cell carcinoma
Carcinoid tumor

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SPHERE of Complications

S: SVC syndrome
P: pancoast tumor
H: Horner Syndrome
E: endocrine (paraneoplastic)
R: Recurrent laryngeal nerve compression
E: Effusions (pleural or pericardial)

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Pancoast Tumor

Tumor located in the apex of the lung
Pancoast syndrome 🡪 invasion/compression of local structures

Recurrent laryngeal nerve
Sympathetic chain 🡪 Horner syndrome
SVC syndrome 🡪 facial plethora, ↑JVP, edema

Can raise ICP 🡪 headaches, dizziness, ↑ risk of aneurysm rupture

Brachiocephalic vein 🡪 unilateral symptoms
Brachial plexus 🡪 sensorimotor symptoms

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Learning Objectives

Review the difference between restrictive and obstructive lung disease
Review COPD, asthma, bronchiectasis, and pulmonary fibrosis
Explain the signs, symptoms, and risk factors of PE and DVT
Emphasize the difference between the Well’s score for DVT and the Well’s score for PE
Discuss pneumonia, differentiate between lobar and bronchopneumonia, and between community-acquired and nosocomial pneumonias
Discuss lung cancer, including pancoast tumor and its relation to Horner’s syndrome, and the paraneoplastic syndromes
Differentiate between pneumoconiosis and hypersensitivity pneumonitis

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References

Pathoma 2019
First Aid 2019
Past Doctorial Presentations

Emily 2017
Michael 2018
Omar 2019
Adrian 2020