RespPath Lect 2 - Respiratory Pathology and Pathophysiology Global Overview

Lecture 2
Prepared and presented by

Marc Imhotep Cray, M.D.
Photo: Colorized scanning electron micrograph of the lung, showing alveoli. Seeley’s Anatomy & Physiology. 10th ed. New York, NY: McGraw-Hill 2010
Respiratory Pathology
Lecture 2
Learning Objectives
1. To list and briefly discuss some of the most important diseases of the
respiratory (pulmonary) system
2. To describe the five major disease categories of the respiratory system
3. To understand the most common presenting symptoms & signs suggestive
of respiratory disease
4. To introduce the etiologic & pathologic factors, clinical features and
treatment approach for select respiratory diseases, including:
 Infections
 Obstructive Pulmonary Disease
 Restrictive Lung Disease
 Cystic Fibrosis
 Lung Cancer
Marc Imhotep Cray, M.D. 2

Lecture 2
Baron SJ and Lee CI. Lange Pathology Flash Cards. New York: McGraw-Hill, 2009
Lecture 2
Most important diseases of respiratory

(pulmonary) system:
 Collapse of alveoli (atelectasis) and pneumothorax
 Circulatory disturbances, such as pulmonary edema and chronic passive

congestion, and adult respiratory distress syndrome (ARDS)
 Infections such as rhinitis, laryngitis, bronchitis, and pneumonia
 Immunologically mediated diseases, such as asthma
 Environmentally induced diseases, such as pneumoconioses, asbestosis,

and silicosis
 Tumors
Lecture 2
Five Major Pulmonary Disease Categories:

1. Obstructive Pulmonary Diseases (OPDs)
2. Restrictive Lung Diseases (RLDs)
3. Vascular Lung Diseases
4. Pulmonary Infectious Diseases
5. Tumors of the Lung and Pleura

Lecture 2
Obstructive Pulmonary Diseases (OPDs)

 Chronic obstructive pulmonary disease (COPD) is characterized by a
reduction of pulmonary air flow as determined by spirometric function
tests with normal or increased total lung capacity (TLC), decrease forced
vital capacity (FVC) in combination with decreased forced expiratory
volume (FEV)
 COPD follows either increased resistance to airflow (e.g., by luminal

narrowing of air ducts) or loss of elastic recoil (by passive widening of air
spaces)

Lecture 2
OPDs (2)
 COPD can be caused by a number of different respiratory diseases,
including:
 Chronic bronchitis
 bronchiolitis
 Asthma
 cystic fibrosis (CF)
 bronchiectasis or
 α1-antitrypsin deficiency
 COPD may lead to progressive and destructive emphysema  cor

pulmonale
 characterized by reduced intrapulmonary blood flow pulmonary
hypertension right-sided heart failure
Lecture 2
Restrictive lung diseases (RLDs)

 In RLDs lungs have a limited potential to expand thus, compliance is
reduced
 Although extrapulmonary disorders such as chest abnormalities, intraabdominal
masses, and neuromuscular diseases also can limit lung expansion term RLD is
generally reserved for intrapulmonary parenchymatous diseases
 Spirometric tests show a reduced FVC with nml or proportionately

reduced FEV
 RLD occurs in acute and chronic forms

 Classic examples of acute RLD are the adult respiratory distress syndrome (ARDS) and acute
hypersensitivity pneumonitis
 Chronic forms include such pathogenetically different entities as idiopathic pulmonary

fibroses (fibrosing alveolitis), chronic interstitial pneumonitis in collagen-vascular diseases,
pneumoconioses, and sarcoidosis
Lecture 2
RLDs (2)
 Only patients in early stages of acute RLD may recover completely
 Later stages and especially chronic forms remit to scarring or progress

to extensive interstitial pulmonary fibrosis with honeycombing
pulmonary hypertension and development of cor pulmonale
 Recurrent superimposed infections further complicate course of RLD

Lecture 2
Vascular Lung Diseases

 Most common vascular lung diseases fall into 2 major categories:
1. clotting disorders with secondary vascular occlusion and
2. primary structural diseases of blood vessels
 Clotting disorders may cause occlusion of pulmonary vessels by

embolization (DVT to PE) or by in situ thrombosis (e.g., after
contraceptive medication with high estrogen content or after clotting
disorders in pancreatic carcinoma)
 In situ pulmonary thrombosis also may be a consequence of primary structural
diseases of lung vasculature

Lecture 2
Pulmonary Infectious Diseases

 Infections of lung present with different pathologic patterns and are
classified as:
 bacterial pneumonias
 atypical and viral pneumonias
 parasitic (e.g., Pneumocystis carinii pneumonia)
 fungal pneumonitis
 Most bacterial and viral pneumonias initially are acute inflammatory

diseases and, with adequate treatment, may resolve completely
 however, pneumonias caused by intracellular bacteria (e.g., Mycobacterium
tuberculosis), parasites, or fungi run a protracted and chronic course entailing an
immune response and incomplete resolution
o heal with focal or diffuse scarring and the risk of chronic restrictive pulmonary
disease
Lecture 2
Tumors of the Lung and Pleura

 As in other organs, tumors of lung are identified as carcinomas (e.g., of
bronchial epithelium, bronchial glands, or alveolar lining cells) or as
sarcomas (a cancer of connective tissue)
 They are classified according to their cell of origin (squamous cell

carcinoma [SCC], adenocarcinoma [AC], small-cell carcinoma [oat cell
carcinoma]) and to their degree of differentiation
 Their local extension and metastatic spread determine their prognosis

Lecture 2
Tumors of Lung and Pleura (2)

 Both tumor classification and documentation of its spread (grading and
staging) are important responsibilities of diagnostic pathology and form
basis for determining therapeutic intervention
 In addition, lungs are frequent sites of metastases from other locations

(e.g., breast, pancreas, testes, bone, malignant melanoma of the skin,
and others), which must be distinguished from primary lung tumors

Lecture 2
The Pleura
Pneumothorax
Pleural Effusion
Pleuritis
Tumors of the Pleura
 Solitary Fibrous Tumor of Pleura
 Malignant Mesothelioma

Lecture 2
Presenting Symptoms
Cough
 Acute: viral or bacterial bronchitis, URI, or pneumonia
 Chronic: asthma, postnasal drip, bronchitis, GERD
Hemoptysis
 Ask patient to estimate amount of blood
 Distinguish between epistaxis, hematemesis, and
hemoptysis

Lecture 2
Presenting Symptoms (2)

Dyspnea
 Timing, acuity of onset, exacerbating and alleviating
factors, degree of functional impairment
 Acute (pulmonary embolus) vs chronic (COPD)
 Exertional or resting, episodic or continuous
 Paroxysmal nocturnal dyspnea (PND)
 Orthopnea

Lecture 2

 What is dyspnea?
 Shortness of breath
 What is orthopnea?
 Dyspnea occurring when pt. is in supine position as a result of a
decrease in vital capacity caused by abdominal contents exerting
force against diaphragm
 What is paroxysmal nocturnal dyspnea (PND)?

 Dyspnea occurring several hours after lying down and is often
associated with congestive heart failure It is caused by an increase in
venous return to the heart resulting in mild pulmonary edema.

Lecture 2

Chest pain
 Many causes (cardiac, pulmonary, GI, musculoskeletal, etc.)
 Pulmonary causes: pleural disease, pulmonary vascular
disease, musculoskeletal
o lung parenchyma has no pain fibers
 Pleuritic chest pain: sharp or stabbing pain on inspiration
that can be positional

Lecture 2
Other important history

Cigarette smoking
 Quantified as # of packs smoked/d X # of cumulative years
(60pk year = 1 ppd X 60yrs or 2ppdX 30 yrs)
 Risk of lung disease is directly related to # of pack-years
exposure and inversely to age at onset of smoking
Other environmental exposures, travel
Family history (CF, alpha-1 antitrypsin deficiency)

Lecture 2
Physical Exam*
Watch the patient breath
RR, use of accessory muscles, paradoxical abdominal
breathing, ability to speak in full sentences
Shape of patient’s chest cavity
  AP diameter suggestive of COPD
Auscultation
 Rhonchi, rales, wheezing, rub
Clubbing
*See Pulmonary Physical Examination folder on thumb drive data.

Lecture 2
Signs of acute respiratory failure

Signs of acute respiratory failure include:
 tachypnea (respiratory rate >40/min)
 inability to speak because of dyspnea
 accessory muscle use with fatigue despite maximal
therapy
 confusion
 restlessness
 agitation
 lethargy
 a rising PCO2 level
 extreme hypoxemia
Lecture 2
Respiratory Infections
Upper respiratory infection
 Most are viral: common cold, pharyngitis, etc.
Lower respiratory infection
 Frequently viral
 Bronchitis: cough, wheezing, dyspnea
 Pneumonia: cough, fever, rapid respiration, dyspnea

Lecture 2
Pneumonias
Compare the diffuse, patchy bilateral infiltrates of “atypical” interstitial pneumonia

(A) with the localized, dense lesion of lobar pneumonia (B)
First Aid for the USMLE Step 1 2008, pg. 435

Lecture 2
Pneumonias (2): Classification

Lecture 2
Pneumonias (3)
Le T and Bhushan V. First Aid for the USMLE Step 1 2015 (McGraw-Hill 2015)

Lecture 2
Pneumonias (4): Gross and histopathology

•Lung, bronchopneumonia, gross [XRAY]
•Lung, bronchopneumonia, gross
•Lung, bronchopneumonia, gross
•Lung, lobar pneumonia, gross
•Lung, empyema, gross
•Lung, abscesses, gross
•Lung, abscesses, gross
•Lung, abscessing bronchopneumonia, gross
•Lung, bronchopneumonia, low power microscopic
•Lung, bronchopneumonia, high power microscopic
•Lung, bronchopneumonia, high power microscopic
•Lung, abscessing pneumonia, low power microscopic
•Lung, abscessing pneumonia, high power microscopic
•Lung, aspiration pneumonia, low power microscopic
•Lung, aspiration pneumonia, high power microscopic
•Lung, chronic abscess, gross

Lecture 2
Pulmonary Tuberculosis
Chandrasoma P, Taylor CR. Concise Pathology, 3rd ed. Stamford, CT: Appleton& Lange, 1998: 523

Lecture 2
Pulmonary Tuberculosis (2)
http://upload.wikimedia.org/wikipedia/commons/2/2f/Tuberculosis_symptoms.svg
Lecture 2
Pulmonary Tuberculosis (3)

 Caused by Mycobacterium tuberculosis
 Major global problem; Seen in pts with HIV,
other immunocompromised states,
developing countries, etc.
 Contracted by inhalation
Scanning electron micrograph of
Diagnosis suggested by: Mycobacterium tuberculosis
 chronic cough
 hemoptysis
 weight loss
 fevers
 night sweats
Marc Imhotep Cray, M.D. M. tuberculosis bacterial colonies 29

Lecture 2
Pulmonary TB (4)
Diagnosis: confirmed by CXR, PPD, sputum smears and culture
Mycobacterium tuberculosis Ziehl-Neelsen stain
 Treatment: 4 drug therapy
See Tuberculosis Treatment & Management Chest X-ray of a person with advanced tuberculosis
http://emedicine.medscape.com/article/230802-treatment http://upload.wikimedia.org/wikipedia/commons/9/9
c/Tuberculosis-x-ray-1.jpg
Lecture 2
Obstructive Lung Disease: General

Obstruction of air flow through airways
Major causes:
 asthma
 bronchiectasis,
 emphysema and bronchitis (COPD)
 Obstructive lung disease (COPD) Obstruction of air flow resulting in

air trapping in lungs Airways close prematurely at high lung
volumes, resulting in ↑ RV and ↓ FVC
 PFTs: ↓↓ FEV1, ↓ FVC→ ↓ FEV1/FVC ratio (hallmark), V/Q
mismatch
Lecture 2
Pathophysiology of Obstructive Lung

Disease
Air flow is decreased by: airway narrowing and/or loss of elastic
recoil of the lung
Airway Narrowing
 Airway inflammation
otobacco smoke, recurrent infection, immunologic
dysfunction
 Bronchoconstriction

Lecture 2
Pathophysiology (2)
Loss of elastic recoil
 COPD: loss of airway tone and decreased tethering by
surrounding lung
 Asthma: bronchoconstriction and mucus plugging allowing
airways to collapse at higher lung volumes and trap excessive
air
 Increased ventilation: increased airflow resistance may not
allow lungs to completely empty during expiration

Lecture 2
COPD Gross and histopathology

•Lung, bronchiectasis, gross
•Lung, bronchiectasis, gross
•Lung, bronchiectasis and fibrous pleural adhesions, gross
•Lung, bronchiectasis, low power microscopic
•Lung, chronic bronchitis, medium power microscopic
•Lungs, bullous emphysema, gross
•Lung, centrilobular emphysema, gross
•Lung, centrilobular emphysema, gross
•Lung, emphysema, microscopic

Lecture 2
Chronic Obstructive Lung Disease

COPD
Slowly progressive, irreversible airway obstruction
 Again, it is closely linked to smoking
Exacerbations of disease by bacterial/viral infections, heart
failure, medication non-compliance, etc.
Characterized by dyspnea, sputum production (with chronic

bronchitis)

Lecture 2
COPD: types
Chronic bronchitis (defined clinically)
 persistent cough with sputum production for at least 3
months in 2 consecutive years
Emphysema (defined based on pathologic findings)

 abnormal enlargement of air spaces
 permanently dilated airways distal to terminal bronchioles
with alveolar destruction and bullae formation
 degree of obstruction in patients with COPD correlates
more closely with severity of emphysema

Lecture 2
Bronchitis vs Emphysema

Lecture 2
COPD
Physical Exam
  AP diameter,  RR
Laboratory data;
 Pulmonary function test is sensitive way to make
diagnosis in early stages
 ABG: hypoxia, hypercarbia (advanced)
 CXR: hyperinflation, flattened diaphragms, increased AP
diameter, widened retrosternal air space (with
emphysema)

Lecture 2
COPD: Hyperinflation

Lecture 2
COPD: flattened diaphragms, lucency

Lecture 2
COPD
Treatment
 STOP smoking (if this is cause)
 Treat exacerbations of bronchitis with antibiotics
 Most meds have not been found to be helpful
 Ipratropium bromide MDI (atrovent MDI) is helpful
(anti-cholinergic)
 Steroids not usually helpful unless inflammatory
component

Lecture 2
Asthma
 Obstruction of lumen of
bronchiole by mucoid exudate,
goblet cell metaplasia, epithelial
basement membrane thickening
and severe inflammation of
bronchiole in a patient with
asthma
Klatt EC. Robbins and Cotran Atlas of Pathology, 3rd Ed. 2015

Lecture 2
Asthma (2)
Gross and histopathology
 Chronic, inflammatory disorder of the •Lungs, hyperinflation with
airways status asthmaticus, gross
 3-5% of the population is affected •Lung, cross section,
 Imbalance between proinflammatory hyperinflation with status
asthmaticus, gross
and inhibitory cytokines
•Bronchial mucus plug with
 Episodic airway narrowing, increased asthma, gross
airway reactivity, and reversibility •Bronchial asthma, low
power microscopic
•Bronchial asthma, high
power microscopic

Lecture 2
Asthma (3)
Trigger: extrinsic allergens, intrinsic factors, or no identifiable
cause
Types: extrinsic, intrinsic, exercise induced, ASA(acetyl salicylic
acid) sensitive, occupational, allergic bronchopulmonary
aspergillosis (ABPA)
Precipitants of asthma: postnasal drip, GERD, cold exposure,
gases/fumes, emotional stress, hormones, resp. infections

Lecture 2
Asthma (4)
Diagnosis (one or combination):
 wheeze, chronic episodic dyspnea, and chronic cough
 Sputum production, chest pain or tightness
Testing:
 History, CXR (to rule out other causes), pulmonary function
testing (with or without challenge)

Lecture 2
Asthma (5)
Treatment
 Education (removal of offending agents)
 Peak flow meters
 Inhaled corticosteroids (ex. fluticasone)
 Long and short acting bronchodilators
oEx. salmeterol, albuterol
 Leukotriene inhibitors (ex. montelukast)
 Theophylline (limited use today due to potential toxicity)

Lecture 2
Cystic Fibrosis
 An Obstructive Lung Disease
Autosomal recessive genetic

disorder
Affects Pulm, GI and GU systems
Most common lethal genetic

disorder A breathing treatment for cystic fibrosis, using a mask
 1/25 carrier frequency nebulizer and a ThAIRapy Vest
 1/3200 live births affected http://en.wikipedia.org/wiki/File:CFtreatmentvest2.JPG

Lecture 2
Cystic Fibrosis (2)

Abnormal chloride channel leads to thick and viscous
secretions in resp, hepatobiliary, GI, and reproductive
tracts
Resp tract: persistent inflammation and infection
causes bronchial wall destruction; mucus plugging of
small airways causing parenchymal destruction
• colonization by S. aureus, H. influenza, P. aeruginosa
Marc Imhotep Cray, M.D. http://en.wikipedia.org/wiki/File:Cystic_Fibrosis_Respiratory_Infections_by_Age.svg 48

Lecture 2
Cystic Fibrosis (3)

Testing:
 Chloride sweat test
 Genetic testing
Median survival
 14 years in 1969 to  30 yrs. since 1995

Lecture 2
Cystic Fibrosis (4)

Pathology:
 Pulmonary: cough, sputum production, clubbing
 Upper Resp tract: nasal polyps, sinusitis
 GI: exocrine pancreatic dysfunction, diabetes, cirrhosis,

salivary gland inflammation
 GU: azoospermia, decreased fertility rate in women,

nephrolithiasis

Lecture 2
Cystic Fibrosis Summary

 Mutation: Cystic fibrosis transmembrane conductance regulator
(CFTR) gene on chromosome 7
 Epidemiology: 1 in 3500 live births; whites predominantly;

uncommon in Asians and African Americans
 Mechanism: Impaired resorption of chloride from lumen of

sweat ducts resultant impaired absorption of sodium
impaired secretion of chloride into airways, pancreatic
ducts, and gastrointestinal tract resulting in less secretion
of sodium and water and, therefore, viscid secretions

Lecture 2
Cystic Fibrosis Summary (2)

 Manifestations of cystic fibrosis
 Fibrosis of pancreas
 Recurrent pulmonary infections with Pseudomonas aeruginosa,
Staphylococcus aureus, and Burkholderia cepacia
 Chronic bronchitis, bronchiectasis
 Meconium ileus
 Biliary cirrhosis leading to impaired absorption of the fat
soluble vitamins A, D, E, and K
 Infertility in males secondary to absence of vas deferens
 Laboratory studies: Increased concentration of chloride in

sweat (i.e., positive sweat chloride test)

Lecture 2
Marc Imhotep Cray, M.D. http://en.wikipedia.org/wiki/Cystic_fibrosis 53

Lecture 2
CF Treatment
 Aggressive airway hygiene
 Nutritional support including pancreatic enzyme
replacement
 Antibiotics
 Bronchodilators

Lecture 2
Restrictive lung disease (Interstitial

lung disease [ILD])
 Many pulmonary disorders are characterized by interstitial
inflammatory infiltrates and have similar clinical and radiologic
presentations
 grouped as interstitial, infiltrative or restrictive diseases
 may (1) be acute or chronic, (2) be of known or unknown etiology and
(3) vary from minimally symptomatic to severely incapacitating and
lethal interstitial fibrosis
 Restrictive lung diseases are characterized by decreased lung volume

and decreased oxygen diffusing capacity on pulmonary function studies

Lecture 2
Restrictive lung disease (2)

 Restricted lung expansion causes ↓ lung volumes (↓ FVC and
TLC) PFTs FEV1/FVC ratio > 80%.
 Types:
1. Poor breathing mechanics (extrapulmonary, peripheral
hypoventilation):
a. Poor muscular effort polio, myasthenia gravis
b. Poor structural apparatus scoliosis, morbid obesity

Lecture 2
Restrictive lung disease (3)

2. Interstitial lung diseases (pulmonary, lowered diffusing capacity):
a. Adult respiratory distress syndrome (ARDS)
b. Neonatal respiratory distress syndrome (hyaline membrane
disease)
c. Pneumoconioses (coal miner’s silicosis, asbestosis)
d. Sarcoidosis
e. Idiopathic pulmonary fibrosis (repeated cycles of lung injury
and wound healing with ↑ collagen)
f. Goodpasture’s syndrome
g. Wegener’s granulomatosis
h. Eosinophilic granuloma (histiocytosis X)
i. Drug toxicity (bleomycin, busulfan, amiodarone)
Lecture 2
Lung Cancer
 Lung cancer is a leading
cause of cancer death
 Presentation: cough,
hemoptysis, bronchial
obstruction, wheezing,
pneumonic “coin” lesion on
x-ray film
Squamous cell carcinoma in the right lower lobe First Aid for the
USMLE Step 1 2008, pg. 434

Lecture 2
Lung Cancer (2)

Risk Factors
 Leading cause of death
 Cigarette smoking is responsible for >90% of lung cancers
 Risk increases with dose and length of exposure to cigarette
smoking
 Heavy occupational exposure to asbestos is second most
important cause

Lecture 2
Lung Cancer: Types

 Bronchial carcinoid tumors
 Small cell cancer (oat cell carcinoma, assoc. with smoking)
 Non-small cell cancer
oSquamous cell cancer (assoc. with smoking)
oAdenocarcinoma
oLarge cell
oAnaplastic carcinoma
Note:
 Metastasis: breast, liver, renal, colon  Oat cell is a neoplasm of
neuroendocrine Kulchitsky cells
 Pleural Ca  Non small cell carcinomas (NSCC) are
any epithelial derived lung cancers
oMesothelioma that are not small cell carcinoma (SCC)
• associated with asbestosis o They are relatively insensitive to
chemotherapy
Lecture 2
Lung Cancer: Types (2)

Lung Cancer Lecture 2
Gross and histopathology

•Lung, squamous cell carcinoma, gross [CT]
•Lung, squamous cell carcinoma, gross [XRAY]
•Lung, squamous cell carcinoma, medium power microscopic
•Lung, squamous cell carcinoma, high power microscopic
•Lung, peripheral adenocarcinoma, gross
•Lung, bronchioloalveolar carcinoma, gross
•Lung, bronchioloalveolar carcinoma, microscopic
•Lung, oat cell carcinoma, gross
•Lung, oat cell carcinoma, high power microscopic
•Lung, hamartoma, gross
•Lung, hamartoma, microscopic
•Lung, metastatic carcinoma, gross [XRAY]
•Lung, metastatic carcinoma, microscopic
•Pleura, metastatic carcinoma, microscopic
•Lung, mesothelioma, gross
•Lung, mesothelioma, high power microscopic
Lecture 2
Lung Cancer: Clinical Presentation

Symptoms can be quite non-specific
Symptoms may relate to location and size of tumor
 Cough, hemoptysis, post-obstructive pneumonia, chest pain,
wheezing, hoarseness
 bone metastases: swelling, pain
 hepatic metastases: jaundice, hepatomegaly
 weight loss, anorexia

Lecture 2
Lung Cancer: Evaluation

 History and physical examination
 CXR/CT scan
 No lab is helpful
 Bronchoscopy
 VATS (video-assisted thoracic surgery)

Lecture 2
Lung Cancer: Treatment

 Options depend on tumor type, size, stage of disease,
and performance status of the pt.
 Surgical removal with Stage I, II, IIIA non-small cell cancer
(if operable)
 Chemotherapy with radiation for limited stage disease in
small cell cancer
ofrequent metastases to the brain

Lecture 2
Lung Cancer: Survival

 15-25% survival 5 years after the diagnosis
 Considerable debate about screening for lung cancer
orecent discussion on chest C.T. as screening tool
oCXR is not a sensitive way to screen for cancer

Lecture 2

Lecture 2
Sources and further study:

eLearning:
IVMS General and Systems Pathology Cloud Folder
IVMS Respiratory Module Cloud Folder
Internet Pathology Laboratory for Medical Education

Pulmonary Pathology
Each section consists of a series of images demonstrating gross and microscopic pathologic
findings for a variety of disease processes. A short description accompanies each image.
http://library.med.utah.edu/WebPath/webpath.html#MENU
Textbooks:
Kumar V and Abbas AK. Robbins and Cotran Pathologic Basis of Disease 8th ed. Philadelphia:
Saunders, 2014
Rubin R and Strayer DS Eds. Rubin’s Pathology: Clinicopathologic Foundations of Medicine,
6th Ed. Baltimore: Lippincott Williams & Wilkins, 2012

Lecture 2
e-Medicine (Medscape) Articles

Obstructive Airway Diseases
 Alpha1-Antitrypsin Deficiency
 Asthma
 Bronchiectasis
 Bronchiolitis
 Bronchitis
 Chronic Bronchitis
 Chronic Obstructive Pulmonary Disease
 Emphysema
 Status Asthmaticus

RespPath Lect 2 - Respiratory Pathology and Pathophysiology Global Overview

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RespPath Lect 2 - Respiratory Pathology and Pathophysiology Global Overview

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Lecture 2

Prepared and presented by

Marc Imhotep Cray, M.D. 2

Most important diseases of respiratory

 Circulatory disturbances, such as pulmonary edema and chronic passive

 Infections such as rhinitis, laryngitis, bronchitis, and pneumonia

 Immunologically mediated diseases, such as asthma

 Environmentally induced diseases, such as pneumoconioses, asbestosis,

Five Major Pulmonary Disease Categories:

2. Restrictive Lung Diseases (RLDs)

3. Vascular Lung Diseases

4. Pulmonary Infectious Diseases

5. Tumors of the Lung and Pleura

Marc Imhotep Cray, M.D. 5

Obstructive Pulmonary Diseases (OPDs)

 COPD follows either increased resistance to airflow (e.g., by luminal

Marc Imhotep Cray, M.D. 6

 COPD may lead to progressive and destructive emphysema  cor

Restrictive lung diseases (RLDs)

 Spirometric tests show a reduced FVC with nml or proportionately

 RLD occurs in acute and chronic forms

 Chronic forms include such pathogenetically different entities as idiopathic pulmonary

 Later stages and especially chronic forms remit to scarring or progress

 Recurrent superimposed infections further complicate course of RLD

Marc Imhotep Cray, M.D. 9

Vascular Lung Diseases

 Clotting disorders may cause occlusion of pulmonary vessels by

Marc Imhotep Cray, M.D. 10

Pulmonary Infectious Diseases

 Most bacterial and viral pneumonias initially are acute inflammatory

Tumors of the Lung and Pleura

 They are classified according to their cell of origin (squamous cell

 Their local extension and metastatic spread determine their prognosis

Marc Imhotep Cray, M.D. 12

Tumors of Lung and Pleura (2)

 In addition, lungs are frequent sites of metastases from other locations

Marc Imhotep Cray, M.D. 13

Marc Imhotep Cray, M.D. 14

Marc Imhotep Cray, M.D. 15

Presenting Symptoms (2)

Marc Imhotep Cray, M.D. 16

Presenting Symptoms (3)

 What is paroxysmal nocturnal dyspnea (PND)?

Marc Imhotep Cray, M.D. 17

Presenting Symptoms (4)

Marc Imhotep Cray, M.D. 18

Other important history

Marc Imhotep Cray, M.D. 19

*See Pulmonary Physical Examination folder on thumb drive data.

Marc Imhotep Cray, M.D. 20

Signs of acute respiratory failure

Marc Imhotep Cray, M.D. 22

Compare the diffuse, patchy bilateral infiltrates of “atypical” interstitial pneumonia

Marc Imhotep Cray, M.D. 23

Pneumonias (2): Classification

First Aid for the USMLE Step 1 2008, pg. 468

Marc Imhotep Cray, M.D. 25

Pneumonias (4): Gross and histopathology

Marc Imhotep Cray, M.D. 26

Marc Imhotep Cray, M.D. 27

Pulmonary Tuberculosis (2)

Pulmonary Tuberculosis (3)

Diagnosis suggested by: Mycobacterium tuberculosis

Marc Imhotep Cray, M.D. M. tuberculosis bacterial colonies 29

Mycobacterium tuberculosis Ziehl-Neelsen stain

 Treatment: 4 drug therapy