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Pathology > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What are the main risk factors for lung carcinoma and what are the symptoms

A
  • Smoking
  • Occupational exposure - arsenic, beryllium, silica, nicel
  • Radon gas
  • Pulmonary fibrosis
  • Pollution
  • Asbestos - adenocarcinoma most common tumour

Cough, haemoptysis, dyspnoea, chest pain, weight loss

-Paraneoplastic syndrome associated with small cell carcinoma

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2
Q

What are some of the local effects of a lung tumour

A
  • Hoarseness- invasion of recurrent laryngeal nerve
  • Diaphragm paralysis- Bovine cough and phrenic nerve invasion
  • Horner’s syndrome- Invasion of sympathetic ganglia
  • Superior Vena Cava syndrome - Tumour compresses SVC - swelling and flushing of face
  • Pancoast tumour- apical tumours that invade neural structures- Horner’s syndrome and nerve pain
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3
Q

List some of the examples of paraneoplastic syndromes

A
  • Neurological paraneoplastic syndromes - Eaton- lambert syndrome affects nerves
  • Cutaneous paraneoplastic syndromes- Acanthosis nigricans, hypertrochosis (excess hair)
  • Andrenocorticotrophic hormone production- Cushing’s
  • Musculoskeletal- Hypertrophic pulmonary osteoarthropathy
  • SIADH- small cell carcinoma
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4
Q

List the main types of primary lung carcinoma

A
  • Small cell carcinoma
  • Bronchogenic carcinoma
  • Non-small cell carcinoma (umbrella term) - Adenocarcinoma (50%), Squamous cell carcinoma and large cell carcinoma
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5
Q

Describe the features of an adenocarcinoma

A
  • Most common
  • More common in women
  • Less strong association with smoking than other lung carcinomas
  • Central or peripheral
  • Different patterns in one tumour
  • If well differentiated - will have glands

-Adenocarcinoma in situ- abnormal tumour spreads along alveolar walls and thickens them
Lepidic spread- abnormal cells use alveolar surfaces like a scaffold - If cells invade them it is a adenocarcinoma

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6
Q

How are non small cell carcinomas diagnosed

A

-Morphology and immunohistochemistyr checked to find it adencarcinoma , SCC, or large cell carcinoma

  • To find if primary or secondary- immunohistochemistry and thyroid transcription factor tested
    • IF TFF-1 POSITIVE IT IS PRIMARY *

-Molecular pathology tests for EGFR mutation and ALK mutation

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7
Q

Describe the features of squamous cell carcinoma

A
  • Central
  • Comes from squamous metaplasia through dysplasia
  • Highly associated with smoking
  • Necrosis may lead to cavitation - necrosis in centre while tumour is growing rapidly blood supply can’t keep up

Histology

  • Keratinisation - keratin produced by abnormal cells
  • Intercellular bridges
  • May have heterogeneity- mixed glandular and squamous carcinoma
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8
Q

Describe the features of large cell carcinoma

A
  • Usually central
  • No squamous or glandular features
  • Large cells, pleomorphic nuclei - different shapes and sites of nuclei
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9
Q

Describe the various neuroendocrine tumours of the lung

A
  • Carcinoid tumours - more order and cytoplasm
  • Atypical carcinoid
  • Small cell carcinoma- small and disordered cells
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10
Q

Describe the features of carcinoid tumours

A
  • Low grade tumours usually central obstructing a bronchus
  • malignant potential general good prognosis
  • Nested growth patter and granular chromatin

Atypical carcinoid
-Less well differentiated more likely to met

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11
Q

Describe the feature of small cell carcinoma

A

Poorly differentiated neuroendocrine carcinoma
poor prognosis
usually central part of lung has mets at presentation
-Hyperchormatic (dark staining) nuclei
-Indistinct nucleoli
-Smudged chromatin
-Nuclear moulding (very close together)

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12
Q

Describe the features of secondary metastatic carcinoma

A
  • Secondary lung tumours= more common than primary
  • Tend to present as multiple lung nodules

Carcinomas- breast kidney GI tract
-Sarcomas malignant melanoma and lymphoma

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13
Q

What are the various types of pleural tumours

A
  • Primary- Malignant melanoma

- Secondary- can be from anywhere , more common than primary eg. Primary lung carcinoma or breast carcinoma

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14
Q

Describe the features of malignant mesothelioma

A
  • Malignancy of mesothelial cells
  • Very aggressive
  • Associated with asbestos
  • Can be anywhere that has mesothelial lining- pleura, peritoneal, pericardial and scrotal sac
  • Long lag time between asbestos exposure and mesothelioma
  • Biphasic mesothelial cells differentiate along epithelioid (like glands) and sarcomatous (like spindle) routes
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15
Q

Describe the features of acute respiratory distress syndrome

A

-Any age can be affected
-Diffuse alveolar damage- non-specific acute alveolar injury due to range of noxious agents
There will be :
-Refractory hyperaemia- low partial pressure 02 in arterial blood despite increased ventilation

  • Radiography: Bilateral opacification progression to frank consolidation and formation of negative air bronchograms- lung may eventually white out
  • Multiorgan failure - multiple inflam pathways activated and hypoxia of organs
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16
Q

What are the 3 phases of diffuse alveolar damage

A
  1. Exudation - heavy dark - blood stained fluid exudate - congested pulmonary capillaries, fluid in the alveolar space
  2. Regeneration - 1/2 weeks after initial insult- proliferation of type 2 pneumocystis and differentiation into type 1 cells, regenerating epithelium grows under the hyaline membrane pushes membrane to the centre of alveoli
  3. Repair -
    * Diffuse alveolar damage on histology will always have a hyaline membrane
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17
Q

what are the 2 main consequences of diffuse alveolar damage

A

Consequences
1) Alveolar exudate chemically broken down and absorbed by lung - returns lung architecture to normal- healing by resolution

2) Healing by repair- scarring/ fibrosis and lung architecture is distorted
* Diffuse alveolar damage will cause rapid progressive interstitial fibrosis- if patients survive they will have chronic debilitating fibrotic lung disease*

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18
Q

What are the causes of ARDS and diffuse alveolar damage

A
  • Major trauma- increased ICP esp
  • Septicaemia
  • Gastric content aspiration
  • Toxic fumes or smoke inhalation
  • Major burns
  • Chemo- methotrexate, chlorambucil
  • Paraquat poisoning
  • Near drowning
  • Pneumonia needing ventilation
  • DIC
  • Massive Blood transfusion
  • Amniotic fluid embolism
  • Acute pancreatitis
  • Cardiac bypass surgery
  • Radiation injury
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19
Q

What are the antigens associated with these forms of Extrinsic allergic alveolitis

  • Farmers lung
  • Bird fanciers lung
  • Malt workers lung

What is the difference between acute exposure and repeated exposure

A

-Progression to fibrotic lung disease can be prevented by removing the antigen

Farmer’s lung - antigen is thermophillic bacteria source is mouldy hay grain or silage

Bird fanciers lung- antigen is budgie or pigeon proteins, source is avian droppings or feathers

Malt workers lung - antigen is Aspergillus cravats and source is mouldy barley

Acute exposure- Immune complex mediated type 3 hypersensitivity reaction- dyspnoea, never, cough 4-8 hrs post exposure - very unwell

Repeated exposure - Type IV cell mediated hypersensitivity, granulomas, interstitial fibrosis and progressive respiratory failure

20
Q

Describe the features of sacrcoidosis

A
  • Affects lungs and hilar lymph nodes
  • Immune disregulation to a certain antigen
  • Scandinavians and black people
  • Most common between 20-40
  • Decreased prevalence in smokers
  • Lymph nodes, liver, spleen, skin, heart and eye all involved - can progress to chronic fibrotic lung disease- cor pulmonate

Clinical features depend on the organ involved

  • Weight loss, fatigue, fever, erythema nodosum
  • Dry cough, dyspnoea, exercise intolerance
  • Hypercalcaemia and increased serum ACE coming from granulomas

Pathology will show:
Sharply circumscribed non-caveating granulomas distributed among lung lymphatics
Interstitial fibrosis

Diagnose with fibre optic lung biopsy

21
Q

Describe the features of COPD

A

Features - Emphysema (Destruction of alveolar wall- premature closure of airways due to descreaed pulmonary elasticity) and chronic bronchitis (airways limited by bronchial wall oedema and mucus plugging due to hypersecretion)

-Cigarette smoking = most important etiological factor

21
Q

Describe the features of COPD

A

Features - Emphysema (Destruction of alveolar wall- premature closure of airways due to descreaed pulmonary elasticity) and chronic bronchitis (airways limited by bronchial wall oedema and mucus plugging due to hypersecretion)

-Cigarette smoking = most important etiological factor

22
Q

Describe the clinical features of COPD

A

Chronic bronchitis

  • Cough with sputum for 3 months in 2 consecutive years
  • Mucus hyper secretion and mucus gland hyperplasia
  • Enlarged submucosal glands and change to pure mutinous type
  • Increased goblet cell and squamous metaplasia in overlying mucosa
  • Reid index- ratio of thickness of gland layer to thickness of bronchial wall is increased - Normal value is 0.3
23
Q

Describe the features of emphysema

A

-Permanent dilation of any part of air spaces distal to the terminal bronchiole (respiratory acinus) without fibrosis - with associated destruction of alveolar walls

2 main forms
1. Centraiacinar (centrilobular)- respiratory bronchioles and destroys alveolar septa around them- most often found in cigarette smokers -upper lobes and lots of airspaces bigger than 1cm

  1. Paracinar (panlobular) - involves entire acinus (cotton candy lungs) - may be associated with alpha 1 antitypsin deficiency - large amounts of lung tissue destroyed
    - Paraseptal or irregular emphysema are the other forms
24
Q

Describe the features of asthma

A
  • Reversible airway obstruction- episodes of bronchospasm due to hyper- responsiveness
  • Immunologically mediated type 1 usually (hypersensitivity to antigens)
  • Incidence and prevalence in children and adults has increased substantially
  • Recurrent episodes of wheezing, SOB, chest tightness and cough
  • Over inflation of lungs - fail to collapse properly
  • Mucus plugs in bronchi and bronchioles infiltrated with eosinophils
25
Q

Describe the features of pulmonary oedema

A
  • Increased pulmonary capillary hydrostatic pressure and or increased pulmonary capillary permeability
  • Shift of water from intravascular compartment into interstitial lung spaces

Depends on 3 factors

  1. Capillary hydrostatic pressure
  2. Plasma oncotic pressure (due to plasma proteins)
  3. Permeability of vascular wall

Fluid in lung deposited in interstitial spaces- lung able to mop up excess fluid via lymphatics until a threshold- this is when fluid spills in alveoli

-Frothy fluid in airways, distended sub pleural lymphatics, enlarged hilar lymph nodes

  • SOB, Orthopnoea, Cough, hypoxia- interference with gas exchange due to fluid deposition
  • Paroxysmal nocturnal dyspnoea
  • X-ray- kersey B lines , upper lobe diversion, bat wing hilar regions

Microscopically
-Fluid in alveolar spaces pink staining, beads on a string congested appearance, heart failure iron macrophages( yellow staining)

26
Q

What are the causes of pulmonary oedema

A

Cardiogenic causes

  • LVF -Ventricular and supraventricular tachycardias -Mitral valve disease
  • Left atrial myxomas -Constrictive pericarditis, pleural effusion

Other
-IV fluid overload -Venous occulsive disease of the lung -Severe anaemia -Dilution of plasma proteins

-ARDS- cytotoxic/ irritant oedema due to capillary endothelial damage- loss of water, fibrin and fibrinogen in diffuse alveolar damage

  • Cerebral injury - Excessive adrenergic release from hypothalamus - neurogenic pul oedema
  • Renal failure - hypoproteinaemia, fluid overload, hypertensive HF
  • High altitude - Acute mountain sickness - prevented by inhaling nitric oxide and CCBs

-All increase lung capillary pressure

27
Q

Describe the features and effects of pulmonary embolism

A

Features
-Usually from a DVT - deep leg veins , deep pelvic veins, intracranial venous sinuses
-Thromboemolbism most common
Other types of embolism- Atheromatous, amniotic fluid (during labour), gas, fat, tumour, foregin material (IV drug user), Infected heart valves

Travel from legs in circulation to RSH then to lungs and occlude the pulmonary artery

Effects

  • Small emboli- can go unnoticed and lyse or if numerous can cause reduced liver function over time- pul HTN
  • Medium sized- resp and cardiac problems - due to ventilation perfusion mismatching - diagnostic tool
  • Large emboli- sudden death (saddle embolus)
28
Q

How do you prevent a PE

A
  • Prevent VTE in legs
  • Early mobilisation of surgical patients, TEDS and LMWHs
  • Risk factors- Virchows triad*
    - Immobilisation -Bed rest -Surgery -Obesity -Hyper-coagulable blood
    - Pregnancy

-Reduce and remove risk factors - give anticoags

29
Q

Describe the features of a pleural effusion

A

Accumulation of fluid within the pleural cavity
can be

  • Transudates- low protein concentration, few cells , CCF, cirrhosis and nephrotic syndrome- think organ failure states
  • Exudates- lung malignancy- rich in protein- uraemia, mesothelioma, TB, chylothorax, rheumatoid disease, SLE - due to irritation of lung lining or parenchyma usually due to acute infection
  • Empyema- Frank pus
  • If it is a blood stained pleural effusion always think malignancy*
30
Q

Describe the features of a pneumothorax

A

Presence of gas or air within the pleural space
Spontaneous- young tall males due to developmental abnormality in upper lobes causing fibrosis and bull formation that may rupture
Primary- Without pre-existing lung disease
Secondary- With known lung disease

Traumatic- penetrating/ blunt trauma to chest
-Iatrogenic

-Air may enter through chest wall in trauma- fractured rib
OR
-Air enters through pleural space via defect in visceral pleura - due to underlying diseases or spontaneous

31
Q

Describe the features of pneumonia

A

-Infection affecting the distal airways especially alveoli

Classification

  • Aetiological- viral, bacterial, fugal
  • Anatomical- bronchopneumonia or lobal pneumonia- can be seen on Xray
  • Clinical- nosocomial, community acquired
  • Histological - KEY CELL IS THE NEUTROPHIL POLYMORPH - moves into alveolar space from alveolar capillaries

Treatment: Empirical therapy when acute or Isolate organism and determine sensitive for abx

Two main organisms: Haemophilus influenzae and staph pneumoniae

Pneumonitis= illness causing inflam of alveoli with no infection

32
Q

Describe the features of bronchopneumonia and what are its complications

A
  • Due to successive infection of conductive airways
  • Starts as widespread bronchitis and progresses to surrounding acini
  • Focal infam centered on airways
  • Bilateral and lower lobes affected
  • Acute inflammation in bronchioles and surrounding alveoli
  • Abx and physio, oxygen supplementation
  • Slow healing will scar

Risk factors

  • Old age/ infancy -Underlying debilitation - cancer, heart failure, chronic renal failure, CVA, malnutrition, alcoholism * Complication to anything that predisposes infection*
  • Acute bronchitis/ COAD/ CF
  • Post op period/ immobility - GA affects mucocillary clearance- limited resp movements due to absorption/ chest pain
  • Steroid therapy
  • Immune deficiency - HIV/AIDS

Complications
-Pleurisy, abscess, septicaemia

33
Q

Describe the features of lobar pneumonia

A
  • Entire love uniformly affected
  • Inflam extends to pleura or a major fissure - often associated with a pleural effusion- if bacteria access the effusion may cause an empyema
  • Seen as endogenous infection- weakened host immunity can cause a variant of strep throat to spread to lungs
  • Step pneumoniae - gram positiv - infection can also lead to septicaemia and meningitis

Ill quickly - features

  • Fever
  • Cough, rusty sputum
  • Acute pleuritic pain
34
Q

What are the various stages of pneumonia

A
  • Congestion- enlarged heavy fluid in alveolar spaces - infected lobe- vascular congestion PMNS and bacteria - not many neutrophil polymorphs
  • Red hepatisation- Fibrin in alveolar space as proteinaceous fluid clots - liver like consistency where alveolar spaces are packed with neutrophils, RBCs and fibrin- lung looses colour from hilum to pleura
  • Grey hepatisation- firm lung where RBCs lyse and fibrinous exudate persists in alveoli
  • Resolution after 8-10 days- chemical dissolution of exudate and absorption through pulmonary lymph nodes
35
Q

Discuss the different features in CAP and HAP atypical and pneumocystis pneumonia

A

CAP
-Gram positive, step pneumonia, Hinfluenzae, legionella , mycobacterium TB, staph aureus, Chlamydia pneumonia, mycoplasma pneumoniae, klebsiella pneumoniae (rare)

HAP

  • Noscomial- after 2 or more days of admission
  • Mostly gram negatives- Klebsiella, E . Coli, Pseudomonas, enterobacter

Atypical

  • Inflam in alveolar septa
  • Viruses, chalmydia, rickettsiae- will show chronic inflam in intersititum of lungs
  • Fever, dry cough, dyspnoea
  • Alveolar necrosis common in viral pneumonia

Pneumocystis carinii- immunocompromised

  • Opportunistic fungi
  • Immunocompromised patients esp AIDS
  • Pink frothy exudate in alveoli
  • Silver stain- round organisms

Legionella - contaminated air humidifiers and water cisterns

36
Q

What are the features of bronchiectasis

A

-Dilation of bronchi and suppruatiomn
-Can be due to childhood illness/ infection but has declined due to vaccines
-Abnormal dilation of bronchi
-Cough, foul smelling sputum, haemoptysis
Causes
-Obstruction of bronchus by tumour or foreign body
-Cystic fibrosis
-Immotile cilia syndrome
-Immunodeficiency
-Idiopathic
-Measles

Complications
-Lung abscess, brain abscess , empysema, amyloidosis

37
Q

What are the features of a lung abscess

A
  • Local area of suppuration walled off by granulation and fibrous tissue
  • Primary abscess- not preceded by other inflam process in lung - aspiration of infected oropharyngeal contents, risk factors loss of consciousness, loss of gag reflex, dysphasia, right side most common
  • Secondary abscess- Underlying condition causes it
    • Bronchial carcinoma -Foreign body in airway -Bronchiectasis -Staphyloccoal or klebsiella

Outcomes: Spontaneous rupture into bronchus and pus spread throughout lung cyst and pneumatocele formation

38
Q

What are the expected lung function tests in restrictive lung disease

A
  • Reduced FEV1
  • Normal FEV1:FVC ratio

Ratio is the same but volume of air inhaled is lower

39
Q

What are the various causes of restrictive lung disease and what are the clinical features

A
  • Neuromuscular problems- difficult expanding thorax - amyotrophic lateral sclerosis
  • Chest wall- obesity - is a major cause
  • Pleural disease- stiffness and fibrosis of pleura
  • Stiff lungs- parenchymal lung disease - interstitial oedema- fluid in lung interstitum, cellular infiltration- chronic inflam cell infiltration, fibrosis- scarring of lungs

Features

  • Restrictive lung function tests - normal ratio but low FEV1
  • Breathless and hypoxic
  • Bilateral shadowing on lung radiology
40
Q

What is the pathology behind parenchymal lung restrictive disease

A
  • Area affected is the alveolar capillary wall +/- the intra-alveolar space
  • Chronic inflam leads to fibrosis and thus thickening of space between the capillary and alveolar walls- impaired gas exchange
  • Fibrosis leads to destruction of alveoli and decreased expansibility of the lung
41
Q

Describe the 3 features that lead to honeycomb lung

A
  1. Intra-alveolar fibrosis- caused by cryptogenic organising pneumonia, granulation tissue in alveolar lumen, eventually incorporated into alveoli walls to give interstitial fibrosis, cough, SOB, malaise, steroid responsive
  2. Obliterative fibrosis- Destruction of multiple alveoli due to extensive fibrosis - usually end stage, end stage progressive diffuse alveolar damage (DAD) that leads to adult respiratory distress syndrome - think about the causes of this
  3. Interstitial fibrosis- Classified into 2 groups
    a) Exudates- Damage to lining cells of alveoli cells and capillaries causing exudate formation - Affects lung base, asbestos, interstitial fibrosis (RA, SLE), interstitial oedema, ARDS, idiopathic pul fibrosis
    b) Granulomas- Collections of macrophages with/ without giant cells- inflam process leading to fibrosis - group 2 is called granulomatous inflammatory process - sarcoidosis, extrinsic allergic alveolitis, silicosis
42
Q

What is pneumoconiosis

A
  • A type of interstitial fibrosis
  • Permanent alteration of lung structure due to inhalation of mineral dust
  • Due to exudates of transudates or granulomatous inflammation
  • Disease- asbestosis, silicosis, coal workers pneumoconiosis
43
Q

How does asbestos affect the lungs

A
  • Inhaled asbestos fibres can induce chronic inflam and fibrosis
  • Asbestos bodies- dumbbell shaped by deposition of protein and iron on asbestos fibres
  • Diagnosis: Fibrosis and asbestos bodies
  • Lung biopsy needed for diagnosis to show fibrosis and asbestos bodies
44
Q

Discuss the features of Tuberculosis

A
  • Chronic recurrent infection of the lung caused by mycobacterium tuberculosis - via resp route
  • Interstitial TB caused by mycobacterium bovid from infected milk
  • At risk groups: Homeless, prisoners, elderly, poor, malnourished, Immunosuppressed, alcoholism, chronic renal failure

Mycobacterium tuberculosis- Ziehl nelson stain used to detect in tissue- PCR used for confirmation of diagnosis - important and culture may be slow 3-6 weeks

Caseating granuloma- rimmed with palisading epitheliod histiocytes (macrophages that have changed to epithelial cell secreting interleukins), langhan’s giant cells and inflammatory cells

Primary TB- parenchymal nodule usually in upper lobe- Ghon focus

  • Involved hilar lymph nodes + ghon focus= primary complex/ ghon complex
  • Will have sub pleural distribution in primary- can occur in any lobe

Secondary TB- reactivation - dormant viable mycobacteria or previously infected patient- caveatting lesions in upper lobe apices, caseous necrosis discharged into bronchi and cavities left formation of upper cavity in upper lung lobe

Pathology (12 decks)

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