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Pathology Term 4 SGU

Adult Respiratory Distress Syndrome (ARDS)

Rapid onset
Severe hypoxemia
Bilateral pulmonary infiltrates on CXR
Microscopy - Diffuse Alveolar Damage (DAD)

Alveolar-Capillary Membrane

extremely thin (2 um), gas exchange surface between alveoli air sacs and the blood, endothelial cells of the capillaries and epithelial cells of the alveoli, allows O2 in and CO2 out

Asteroid Body

seen in granulomatous disease such as Sarcoidosis
pink eosinophilic star shaped inclusion in giant cells

Asthma

Chronic inflammatory disease - REVERSIBLE
Hyperactive airways
Atopic, Non-atopic, Drug induced, Occupational

Atelectasis

Loss of lung volume due to alveolar collapse
Decreased oxygenation
V/Q mismatch
Resorption (obstruction), Compression (pleural effusion), Contraction (scarring)

Barrel Chest

Chronic Obstructive Lung Diseases such as Emphysema, air trapping in the lungs that cannot be exhaled, and increased intra-thoracic pressure allows chest wall to expand, hyperinflation results in barrel shaped torso.

Bleb

an irregular bulge in the plasma membrane

Blue Bloater

Description of a patient with Chronic Bronchitis
Blue due to cyanosis and bloated due to low respiratory drive, less respiration, less effort

Bronchial Cyst

a cyst within the airways
can have compression, infection, hemorrhage, rupture

Bulla

Focal regions of emphysema with no discernible septa/wall that measure greater than 1 cm

Brochiectasis

Permanent dilation of bronchioles secondary to destruction of the supporting tissue.
Obstruction (tumor or foreign body), Congenital (CF or Kartagener's), Necrotizing Pneumonia (S. aureus & Klebsiella)

Chronic Bronchitis

Clinical Diagnoses
Productive cough for 3 consecutive months or more in a 2 year period.
Hypertrophy or seromucous glands and goblet cells

Bronchiolitis Obliterans

Proliferation of fibroblasts in the airway tubes, not just the alveoli space. Inflammation and fibrosis.
Many causes, dry cough, FEV1 ~20% !!

Bronchiogenic Carcinoma

malignant neoplasm of the lung arising from the epithelium of the bronchus or bronchiole, may grow into the lumen and obstruct the airway, spreads to lymph nodes

Chronic Obstructive Pulmonary Disease (COPD)

4th leading cause of deaths in the US, 3rd world wide.
Obstruction to airflow, FEV1/FVC greatly reduced.
Asthma (reversible), chronic bronchitis, emphysema, bronchiectasis.

Coin Lesion

round, well circumscribed nodule, < 4 cm
usually an incidental finding on CXR
most commonly a benign tumor but 10-20 % of cases it is malignant (older adults and smokers)

Consolidation

region of lung tissue (normally spongy) that is filled with fluid, swelling or hardening of the normally aerated lung
opaque on CXR

Cor Pulmonale

enlargement of the right ventricle of the heart due to pulmonary disease/pulmonary hypertension
leads to right heart failure and death

Diffuse Alveolar Damage (DAD)

Histological Pattern
Usually seen in ARDS, TRALI, AIP
1) exudative - alveoli become flooded with transudate
2) hyaline membrane form (pink and lining air sacs)
3) organizing phase

Emphysema

abnormal permanent air space enlargement DISTAL to the terminal bronchioles
destruction of alveoli air sacs WITHOUT FIBROSIS

Empyema

collection of pus in the pleura around the lung

Extrinsic Allergic Aveolitis

Hypersensitivity Pneumonia, immunological response to extrinsic antigen, can be Type III or IV HSR, usually inhaled antigen (hot tubs, humidifiers, etc.)
Restrictive lung disease, ground glass opacity on CT
1) airway centered process
2) chronic inflammatory infiltrate
3) organizing pneumonia
4) giant cells
5) poorly formed non-necrotizing granuloma

Ghon Complex

parenchymal lesion + lymph node in TB infection
1-1.5 cm inflammatory consolidation (granuloma) with central caseous necrosis, associated lymphatics and lymph node (node can also show necrosis)

Goodpasture Syndrome

Primary Immune Disease affecting the lungs and the kidneys. Diffuse Alveolar Hemorrhage Syndrome. Antibodies targeted to the alpha 3 chain of type IV collagen deposit along the BM. Type II HSR. Shows a liner deposition pattern on immunofluorescence.

Hemothorax

blood accumulation on the pleural cavity

Heart Failure Cell

Hemosiderin containing macrophages in the alveoli.
Left heart failure -> pulmonary edema -> high pressure causes RBCs to pass through the vascular wall into the alveoli -> taken up by macrophages

Hemoptysis

coughing up blood
anytime vessels leak into the alveoli air sacs or into the airway tubes

Honeycomb Lung

pulmonary fibrosis, scarring of the lungs, gross appearance of lungs resemble a honeycomb
usually due to interstitial lung disease (viral, autoimmune) but can be idiopathic

Horner's Syndrome

cervical sympathetic plexus damage (usually due to compression from a tumor of the lung)
ptosis, meiosis, anhydrosis
ipsilateral enopthalmus (sinking in of the eye)

Hyaline Membrane

acellular proteinaceous material, glass like and pink on H&E or bright pink on PAS
characteristic of DAD (associated with ARDS)
diffuse inflammation of lung parenchyma
cytokines released by epithelium -> PMNs and T Cells
hyaline membrane formation in alveolar wall

Hydrothorax

serous fluid accumulation in the pleural cavity

Hypertrophic Pulmonary Osteoarthropathy

secondary to lung cancer (adenocarcinoma and all non-small cell lung cancer)
clubbing & increased bone deposition on long bones
painful swollen joints (ankles)
(also Bamberger-Marie Syndrome)

Idiopathic Interstitial Pneumonia

Restrictive Lung Diseases
Can include:
Desquamative Interstitial Pneumonia (DIP
DAD (in ARDS)
Non-specific Interstitial Pneumonia (NSIP)
Respiratory Bronchiolitis
Usual Interstitial Pneumonia (IPF, Collagen Vascular Disease CVD, drug toxicity, Pneumoconiosis)
Organizing Pneumonia (COP)
Lymphoid Interstitial Pneumonia (LIP)

Idiopathic Pulmonary Fibrosis (IPF)

chronic progressive lung disease (relentless)
bilateral interstitial fibrosis
mean survival, 3 years (transplant)

Non-small Cell Lung Cancer

70-75% of lung cancers
Adenocarcinoma
Squamous Cell Carcinoma
Large Cell Carcinoma
Can usually be surgically resected if caught early

Organizing Pneumonia

Bronchiolitis Obliterans Organizing Pneumonia (BOOP) when there is a known cause (CVD, pneumonia, transplant immune response)
Cryptogenic Organizing Pneumoia (COP) when unknown cause
Inflammation of bronchioles & surrounding lung tissue, persistent alveolar exudate undergoes organization & fibrosis, architecture in tact
Fibrosis in alveoli, alveolar ducts and bronchioles forms Masson Bodies

Pancoast Tumor

apical lung tumor, can spread to ribs and vertebrae
Horner's Synd.
Compression of blood vessels causing edema
Compress of recurrent laryngeal nerve, hoarseness
Compress esophagus, difficulty swallowing
Obstruct Thoracic Duct, chylothorax (lymph in pleural cavity)
Compress SVC, head and neck swelling

Paraneoplastic Syndrome

consequence of cancer in the body but not due to the local presence of cancer cells - mediated by hormones or immune response
caused by small cell lung cancer

Pink Puffer

patients with emphysema
They don't show hypoxic symptoms and cyanosis until late so they are pink
Thin & frail from increased effort of breathing
Pursed lips from creating back pressure to exhale

Plexiform Lesion

multiple lumen formed in a small artery at the branch point from a larger artery
proliferation of vasculature (looks re-canalized)
occur in pulmonary hypertension

Pneumothorax Pulmonary Edema

Injury to the lung that can cause pulmonary edema

Pulmonary Embolism

blockage of the main artery of the lung or one of its branches by a substance traveling in the blood stream
(usually thromboembolism, but also air, fat, amniotic fluid, septic, IV drugs, bone marrow)

Pulmonary Veno-occlusive Disease (PVOD)

Right upper lobe tumor of the lung can cause compression of the SVC
Noticeable swelling of the face in the morning with resolution upon being upright.
Congestion of the head, face, and neck results (can cause cerebral edema, rarely)

Rales

clicking, rattling, or cracking noises made by the lungs on inhalation

Reid Index

Ratio of the glands to the total wall thickness
Normally: glands/wall < 40%
In chronic bronchitis Reid Index reaches 50% or more

Restrictive Lung Disease

Heterogenous group of disorders characterized by a decreased FVC.
Interstitial, bilateral, patchy, fibrosis, decreased compliance, V/Q mismatch, pulmonary hypertension, cor pulmonale

Rhonchi

low pitched continuous sounds heard on auscultation usually due to bronchial secretions

Saddle Embolism

Large embolus lodged in both sides of the main pulmonary artery bifurcation.
Results in sudden death, acute right heart failure.

Schaumann Body

calcium and protein inclusions within Langhan's giant cells as part of a granuloma
Usually in sarcoidosis or hypersensitivity pneumonia

Severe Acute Respiratory Syndrome

Coronavirus
China, Hong Kong, Singapore, Canada
2003 Outbreak, 8,000 sick and 700 deaths
US not infected (only 8 people)

Small Airways Disease

in chronic obstructive lung diseases
Emphysema - respiratory bronchioles & alveoli destruction
Chronic Bronchitis - goblet cell metaplasia, mucous plugs, inflammation and fibrosis
Asthma

Status Asthmaticus

severe prolonged asthma attack, unresponsive to therapy, respiratory failure and death results
hyperinflation of lungs all the way around mediastinum on autopsy

Tension Pneumothorax

collection of air or gas in the pleural space
one-way-valve in area of damaged tissue allows air in but not out, compresses lung, tracheal deviation and mediastinal deviation

What mediates pain in pulmonary disease?

irritation of nerves in the pleura

What causes a productive cough?

anything that dumps material into the airways (infection, fluid, blood)

What causes a non-productive cough?

irritation of the airways without material inside
usually interstitial disease processes

What causes dyspnea?

any lung pathology!

What causes sputum production?

bacterial infection
hypertrophy of mucous glands and goblet cells
fluid extravasation into airways & alveoli

What are the telling signs of cyanosis?

blue coloration, usually in the extremities
clubbing of fingernails

What causes secondary polycythemia?

Overproduction of RBCs due to chronically low O2
High altitude or any cyanotic pulmonary disease (ex. COPD)

Orthopnea

Dyspnea when laying flat
Caused by pulmonary edema and left heart failure

Platypnea

Dyspnea that worsens upon standing
Hepatopulmonary syndrome causing dilation of the vessels of the lungs in patients with liver disease

What is normal serum hemoglobin?

13-18 g/dL in men
12-15 g/dL in women

What hemoglobin level defines cyanosis?

> 5 g/dL reduction

What is tactile fremitus?

palpable vibration on the wall of the thorax caused by friction rub between the parietal and visceral pleura

What is bronchophony?

abnormal sound in the lungs
increased resonance
patient repeats ninety-nine or Scooby Doo

What is ergophony?

increased resonance of voice sounds usually due to fibrosis or consolidation in the lungs
high-pitched quality to a person's voice

What radiographic studies are used in evaluating lung diseases?

CXR (AP or lateral)
CT scan (look for ground glass opacity)
PET scan (shows fluoro-deoxy glucose uptake in metabolically active tissue, cancers)
MRI
Bronchography and Arteriography

What are the factors evaluated in pulmonary function tests (spirometry)?

TLC (total lung capacity, volume at max inhale)
RV (residual volume, volume after max exhale)
FVC (forced vital capacity, max exhale)
FEV (forced expiratory volume, exhale over time)
FEF 25-75% (forced expiratory flow, midway exhale)

What is a good measure of small airway disease?

FEF 25-75%

How is pulmonary function changed in obstructive lung disease?

FEV1:FVC ratio is REDUCED <70% of normal
TLC increased
FVC slightly reduced <80% of normal
FEV1 greatly reduced

How is pulmonary function changed in restrictive lung disease?

Reduced FVC
Reduced FEV1
NORMAL FEV1:FVC ratio

What are normal arterial blood gas measurements?

PaO2 75-100 mmHg
PaCO2 35-45 mmHg

What are the three types of Atelectasis?

Resorption, Compression, Contraction

Describe Resorption Atelectasis:

Obstruction of airway (mucous, etc.), no air flow to affected alveoli, all of the O2 within them is absorbed into the blood since there is no obstruction to perfusion, alveoli collapse

Where does the trachea shift in resorption atelectasis?

towards the affected side

Describe Compression Atelectasis:

pleural cavity compressed by fluid, exudate, tumor, blood or air causing the collapse of affected alveoli

Where does the trachea shift in compression atelectasis?

away from the affected side

Describe Contraction Atelectasis:

scarring in the lung causes fibrosis and pulling inward of the alveoli air sacs

Which atelectasis is not reversible?

Contraction

What is the histological name for ARDS?

Diffuse Alveolar Damage (DAD)

What are the direct causes of ARDS?

pneumonia, aspiration, emboli, inhalation injury, drowning, oxygen toxicity

What are the indirect causes of ARDS?

sepsis, trauma with shock, acute pancreatitis, severe burns, transfusion of blood products (TRALI), uremia, drugs

What does a CXR of ARDS look like?

bilateral pulmonary infiltrates
complete white out

Does ARDS respond to oxygen therapy?

no

What changes occur to the lung tissue in ARDS?

alveolar-capillary membrane compromise (alveolar epithelium and capillary endothelium)
blood gas barrier damage (loss of diffusion)
loss of surfactant (type II cell damage)
increased vascular permeability (fibrin and inflammatory mediators leak out of vessels)

What are the two phases in ARDS?

Acute (exudative) 0-7 days
Organizing (proliferative) 1-3 weeks

How do the lungs feel in the acute phase of ARDS?

like a rubber eraser
heavy and firm
not spongy

What characterizes the acute phase of ARDS?

HYALINE MEMBRANES
interstitial and intra-alveolar edema & hemorrhage
necrosis and sloughing off of epithelial cells

What characterizes the chronic phase of ARDS?

proliferation of type II pneumocytes (round up and protrude into the lumen) & surfactant production
organizing fibrin exudates, fibrosis, septal thickening

What is the mortality rate of ARDS?

40%

What therapy is given to ARDS patients?

supportive

What factors indicate a poorer ARDS prognosis?

increased age
bacteremia/sepsis
multisystem organ failure

What causes respiratory compromise after the cute phase in ARDS?

fibrosis

If normal function returns after ARDS, when does this occur?

6-12 months

What are the 4 obstructive lung diseases?

Emphysema
Chronic Bronchitis
Asthma
Bronchiectasis

What is significant about the epidemiology of COPD (stats)?

4th leading cause of death in the US
3rd leading cause of death in the world

Which of the obstructive diseases is reversible?

Asthma

What part of the airways is affected by Emphysema?

Alveoli air sacs and Respiratory Bronchioles
small airways distal to the terminal bronchioles

What is the main cause of the tissue destruction in Emphysema?

Protease: Anti-protease imbalance
and impaired tissue repair

What is the process of damage in Emphysema?

inhalation of toxic agents -> inflammatory response (PMNs, Macs, T cells) -> Elastase, Cytokines, Oxidant stress, Failure of Anti-oxidants and Anti-proteases, Epithelial cell injury and proteolysis of ECM, destruction of alveoli

What are the 4 types of Emphysema?

Centrilobular
Panlobular
Septal
Irregular

What does Emphysema look like on gross appearance?

"moth eaten"
Hyperinflated lungs
Bullae

What does Emphysema look like in histological appearance?

free floating alveolar septa
NO FIBROSIS
Destruction of elastin, collapse and trap air on exhalation

Describe Centrilobular Emphysema:

Smoking
Upper lung zones
Respiratory bronchioles are affected

Describe Panlobular Emphysema:

Alpha 1 AT Deficiency
Lower lung zones
Distal to respiratory bronchioles affected
Almost no normal alveoli

What is Alpha 1 Anti-trypsin Deficiency?

Chromosome 14 mutation
Pi gene: mutant PiZZ and normal PiMM
Misfolded Anti-trypsin protein can't leave hepatocyte
Protein accumulates in the liver, chronic liver disease
1% of all Emphysema
(can also be TGFB gene mutations or MMP gene mutations)

Describe Septal Emphysema:

Rare
Margins of the lung, sub pleura, upper lobes
May form bullae (large holes in alveoli)
can lead to pneumothorax - atelctasis

Describe Irregular Emphysema:

Paracicatricial
Surrounding a scar, the scar contracts and pulls alveoli air sacs open (only in extensive scarring)
asymptomatic

How does a patient with Emphysema present?

Pink Puffers
Barrel chest, weak and skinny, hunched forward, dyspnea, prolonged expiration, pursed lips
blood gases normal & not cyanotic until late
flat diaphragm on CXR

How is Chronic Bronchitis Diagnosed?

productive cough for > 3 consecutive months in 2 years

What is the major defining feature of Chronic Bronchitis?

Buckets of Sputum
Hypersecretion of Mucous
REALLY productive cough

Who gets Chronic Bronchitis?

SMOKERS
Urban Dwellers

What are typical inhaled irritants causing Chronic Bronchitis?

cigarette smoke, sulphur dioxide SO2, nitrogen dioxide NO2

Are there eosinophils present in Chronic Bronchitis?

no

Inhaled irritants induce what 3 things?

Hypertrophy of seromucous glands (Reid Index >50%)
Increased goblet cells (in bronchioles, metaplasia)
Infiltrate of PMNs, Macs, T Cells

What is the disease process of the small airways in Chronic Bronchitis?

goblet cell metaplasia in bronchioles
inflammation
smooth muscle hypertrophy (narrowing airway lumen)
peribronchiolar fibrosis

What two coexisting conditions complicate Chronic Bronchitis?

Emphysema
Infection

What causes the airway obstruction and collapse in exhalation in Chronic Bronchitis?

ongoing fibrosis and obstruction from inflammation
(not the mucous plugging)

What is the gross presentation of the lungs in Chronic Bronchitis?

Large Airways: Hyperemic, red, and swollen, mucinous and mucopurulent secretions causing mucous plugging, hypertrophy & hyperplasia of glands, increased Reid Index and inflammatory cells
Small Airways: goblet cell metaplasia, mucous plugging, inflammation and fibrosis

What does the fibrosis lead to?

lumen narrowing and obstruction of air flow

What does a patient with Chronic Bronchitis look like?

Blue Bloaters
Hypoxic, hypercapnic, and cyanotic
Can have many secondary infections (block a tube and get an infection behind it)
Decreased respiratory drive, overweight
Pulmonary Hypertension and Cor Pulmonale

Does COPD affect males or females more?

equal

What is responsible for respiratory drive in Chronic Bronchitis patients?

low O2 measured by peripheral chemoreceptors
(chronic hypercapnia has caused decreased sensitivity to low CO2 levels in central chemoreceptors)

What happens if you put a patient with Chronic Bronchitis on high oxygen therapy?

Depressed respiratory drive, no breathing, suffocation
The O2 sensors that are now responsible for respiratory drive will sense increased O2 and cause cessation of breathing but they are still hypercapnic

What defines Asthma?

REVERSIBLE bronchoconstriction
Anatomical airways narrowing
Chronic inflammatory disease
Hyperactive airways

What are the 4 types of Asthma?

Atopic
Non-atopic
Drug Induced (aspirin)
Occupational

What is the defining cell type in Asthma?

eosinophils

Describe Atopic Asthma:

Allergic sensitization, Type I HSR, IgE mediated
Antigen exposure -> IgE crosslinked on Mast cells -> degranulation

What 2 other conditions can patients with Asthma have?

allergic rhinitis
eczema

What type of T Cell is involved and what cytokines?

Th2 Cells
IL4 - stimulates IgE production (more cross linking)
IL5 - activates eosinophils
IL10 - increase Th2, stop Th1 proliferation
IL13 - mucous production & IgE production by B cells

What characterizes the Early Phase of Atopic Asthma?

Vagal stimulation -> bronchoconstriction
Increased mucous
Vasodilation
(immediate, vascular mediated)

What characterizes the Late Phase of Atopic Asthma?

Activation of eosinophils, PMNs, and T Cells
Epithelial cells activate and recruit more Th2 cells
(4-24 hours, immune response mediated)

What are some triggers of Asthma?

dust, pollen, animals, foods

What skin test is used to test for allergic reactions to possible antigenic asthma triggers?

Wheal and Flare skin test

Describe Non-atopic Asthma:

serum IgE is NORMAL, no previous sensitization
Inhaled NO2, SO2, or O3
Viral induced mucosal damage lowers vagal threshold

Describe Drug-Induced Asthma:

Caused by Aspirin
Inhibits arachidonic acid COX pathway
Shifts towards Lipoxygenase pathway, produces more Leukotrienes C4, D4, E4 (bronchoconstriction)

What other signs and symptoms present in Drug-Induced Asthma?

recurrent rhinitis, nasal polyps, urticaria (hives), bronchospasm

Describe Occupational Asthma:

REPEATED exposure to fumes, organic dusts, chemical dusts, gases
(epoxy resins, plastics, toluene, cotton, platinum)
Chronic daily exposure causes sensitization
Patient will be better on weekends and vacations

What are 2 defining histological features found in the mucous of asthma patients?

Curschmann Spirals (thin pink curly spirals on H&E)
Leyden Crystals (from MBP produced by eosinophils)

What is the gross appearance of Asthma in the lung?

Occlusion of airways by think mucous
Hyperinflation of the lungs
Edema, patchy epithelial necrosis

How does the lung tissue appear on histology in Asthma?

Mucous plugs with Curschmann spirals and Leyden crystals
Bronchial smooth muscle hypertrophy
basement Membrane thickening
Inflammation with EOSINOPHILS

How dos Asthma present on Spirometry?

FEV1 < 30%
Hyperventilation
Intervals of normal values between attacks
Chronic condition will show residual respiratory defects even in symptom free intervals

How does Asthma present?

Recurrent sudden attacks of respiratory distress
Hypoxia, hypercapnia, respiratory acidosis
Tightness of chest
Wheezing and Rhonchi
Thick sputum
Progressive hyperinflation with air trapping distal to mucous packed bronchi
Attacks last hours and subside (therapy or on own)

What are the three defining signs of any chronic obstructive lung disease?

Hypoxia
Hypercapnia
Respiratory Acidosis

What is Churg Strauss Disease?

Cutaneous, GI, Renal, and Lung Disease
Allergic Granulomatosis and Angiitis
ANCA-MPO in 50% of cases
Eosinophilia (eosinophils chewing on blood vessels)
Infiltration of vessels and perivascular tissue by eosinophils, small vessel necrotizing vasculitis
Extravascular necrotizing granulomas
Death due to cardiac involvement

What is Brochiectasis?

Permanent dilation of bronchi and bronchioles from destruction of supporting tissue

What 3 things cause Brochiectasis?

Bronchial Obstruction (tumor, foreign body)
Congenital Conditions (CF, Imm. Def., Kartagener's)
Necrotizing Pneumonia (Staph aureus & Klebsiella)

Describe Brochiectasis due to bronchial obstruction:

Obstruction hampers clearance -> Iinfection -> damaged and weakened bronchial walls -> Bronchectasis

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