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Molecular Pathology > Respiratory Pathology > Flashcards

Respiratory Pathology Flashcards

1
Q

Disorders of the Bronchi & Lungs

A
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2
Q

What does Pleural space normally contain?

A

5-10 ml of clear fluid, which lubricates the opposing surfaces of the visceral and the parietal pleura during respiratory movements.

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3
Q

How is Pleural fluid formed

A

The formation of the fluid results from hydrostatic and osmotic pressures

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4
Q

What causes Fluid accumulation?

A

due to pathology present usually due to infection and/or cancer.

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5
Q

Effusions are either classified as …. ?

A

exudates or transudates.

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6
Q

Describe TRANSUDATE effusions.

A

Low protein

Low specific gravity

Low cellular content

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7
Q

What are they caused by?

A

an imbalance of hydrostatic and oncotic pressure

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8
Q

What are transudate effusions associated with?

A

kidney, heart or liver failure, or hypoalbuminaemia

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9
Q

Describe EXUDATE effusions

A

High protein content

High specific gravity

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10
Q

What are they caused by?

A

the increased permeability of capillaries, which can occur when the serous membranes are damaged by a disease process

Metastatic malignancy, infections, connective tissue diseases (e.g. SLE, rheumatoid disease), and inflammatory conditions (e.g. pancreatitis).

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11
Q

what are the consequences of Fluid or air that accumulates in the pleural space?

A

will reduce lung expansion and lead to respiratory compromise and hypoxia

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12
Q

Why is Thoracocentesis carried out?

A

is done to try and find the cause of a pleural effusion; it may also be done to help you to breathe easier.

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13
Q

What can Cytologic examination of the pleural fluid reveal?

A

cancer cells (poorly differentiated adenocarcinoma).

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14
Q

Why would an abdominal CT scan be done?

A

could reveal hepatomegaly and diffuse lymphadenopathy.

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15
Q

What is Hepatomegaly?

A

enlarged liver.

Non specific clinical finding

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16
Q

What can the Causes include?

A

infection, hepatic tumours, or metabolic disorder

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17
Q

What is the clinical significance of Lymphadenopathy?

A

Sometimes can mean serious illness, however it is usually a result of benign infectious causes

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18
Q

What is an Coroners autopsy (post mortem examination)?

A

Carried out because the cause of death is unknown, or following a sudden, violent or
unexpected death

To decide whether a legal investigation (inquest) is needed

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19
Q

What is Hospital post mortem?

A

to find out more about an illness or the cause of death, or to further medical research and understanding

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20
Q

Granulomatous Inflammation

what are FOREIGN BODY GRANULOMAS caused by?

A

Caused by relatively inert foreign bodies.

Foreign body granulomas form around materials such as talc, sutures, or other fibres that are large enough to not be phagocytosed.

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21
Q

What is there an Absence of?

A

inflammatory or immune response.

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22
Q

How can the foreign material can usually be identified?

A

in the centre of the granuloma, particularly if viewed with polarized light.

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23
Q

What are IMMUNE GRANULOMAS Caused by?

A

a variety of agents that are capable of inducing a persistent T cell mediated immune response.

Immune response produces granulomas usually when the inciting agent is difficult to eradicate, e.g. persistent microbe or a self antigen.

Macrophages activate T cells to produce cytokines, which activates other T cells, perpetuating the response.

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24
Q

Other diseases with granulomatous inflammation

A
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25
Q

What does acid fast stain (ZN) identify?

A

If see Reddish rods

are acid fast bacteria - Mycobacterium tuberculosis

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26
Q

What is A granuloma?

A

a circumscribed collection of epithelioid cells, usually surrounded by lymphocytes; it is a particular form of chronic inflammation

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27
Q

What’s the difference between granulation tissue and granulomatous inflammation?

A

Granulation tissue contains new small blood vessels, fibroblasts, and mononuclear cells in an oedematous extracellular matrix; it is part of the repair response.

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28
Q

Do granulomas in different organs look different?

A

Granulomas look similar regardless of the organ.

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29
Q

Which Granulomas do not have caseous necrosis?

A

Granulomas in sarcoidosis, early lesions in tuberculosis may also have noncaseating granulomas.

30
Q

What is essential to look for when establishing a cause of the granulomatous process.

A

specific organisms

31
Q

What is Urinalysis used?

A

Detection of: protein, red blood cells and white blood cells.

32
Q

What does a Urea and Electrolytes (U+Es) test dectect?

A

Detects levels of: Urea, Sodium, Potassium, Chloride, Bicarbonate and Creatinine.

33
Q

How is glomerular filtration rate (eGFR) estimated?

A

Derived using an equation and knowledge of amount of serum creatinine.

34
Q

Why carry out Full Blood Count (FBC)?

A

Erythropoietin controls red blood cell production and this may be affected by kidney damage.

35
Q

Why determine Parathyroid hormone (PTH) level?

A

Controls calcium levels, is often increased in kidney disease

36
Q

What are the Common indications for renal biopsy?

A
  • Nephrotic Syndrome
  • Acute kidney injury (AKI)
  • Chronic kidney disease (CKD)
  • Positive immunology tests with clinical indications of autoimmune renal disease
  • Abnormal mass detected
  • Renal transplant dysfunction
37
Q

Interpretation of the renal biopsy

How are sections examined?

A

Sections are examined by light microscopy, Immunofluorescence and electron microscopy.

Careful evaluation of glomeruli, tubules, the interstitium and the vessels is required

38
Q

What does the interpretation using light microscopy include?

A

the use of multiple sections stained with a variety of stains

39
Q

What are examined by immunofluorescence?

A

A number of antigens

40
Q

Kidney biopsy Specimens processed for Light microscopy.

What is the Tissue fixed in ?

A

10% neural buffered formalin.

41
Q

How is specimen loss during processing avoided?

A

the specimen is gently wrapped in biowrap paper.

42
Q

What thickness are sections are cut at? Why?

A

around 2µm (thinner than a standard histology section 4µm).

Thinner sections allows for better assessment of the glomerulus for the diagnosis of renal diseases.

43
Q

Roles of histological stains

A
44
Q

How is Amyloid formed?

A

Formed by normally soluble proteins, which assemble to form insoluble fibers that are resistant to degradation.

45
Q

Where can Amyloid can be deposited?

A

in any tissue or organ.

46
Q

What is Amyloidosis>

A

rare disease that occurs when amyloid builds up organs and can lead to life threatening organ failure.

47
Q

What is the gold standard test used to identify amyloid in tissues?

A

Congo Red

48
Q

What must Congo Red stained tissue sections be examined using?

A

polarised light microscopy, allowing the. characteristic ‘apple green’ birefringence to be seen.

49
Q

What is Direct Immunofluorescence best performed on?

A

unfixed, frozen tissue

Sections are cut using a cryostat.

50
Q

The antigens that are examined include?

A
  • Immunoglobulins (IgG, IgA and IgM)
  • Complement components (C3, and C1q)
  • Fibrin
  • Kappa and lambda

Accurate localisation of deposits is possible

51
Q

Which tissue is Electron Microscopy (EM) used for?

A

Tissue fixed with glutaraldehyde.

52
Q

EM cannot be performed on tissues exposed to which fixatives?

A

mercury based fixatives.

tissue can be recovered from the paraffin block, or from frozen tissue if no glomeruli are available in the EM sample.

53
Q

Are all modalities necessary?

WHICH DIAGNOSES ARE OVERLOOKED WITHOUT FLUORESCENCE?

A 
Light chain associated diseases
IgA nephropathy/Henoch Shonlein purpura
IgM nephropathy
C1q nephropathy
Anti glomerular basement membrane disease
Humoral (C4d) transplant rejection
Fibronectin glomerulopathy
54
Q

WHICH DIAGNOSES ARE OVERLOOKED WITHOUT ELECTRON MICROSCOPY?

A

Fibrillary glomerulopathy/ immunotactoid glomerulopathy
Nail patella syndrome
Lipoprotein glomerulopathy
Dense deposit disease
Alport’s syndrome
Thin glomerular basement membrane nephropathy
Collagenofibrotic glomerulopathy

55
Q

Anti Neutrophil Cytoplasmic Antibody

WHAT IS MYELOPEROXIDASE (MPO)?

A

Commonly recognised p ANCA (indirect immunofluorescence)

It is a 140kDa cationic protein found predominantly in azurophilic granules of neutrophils and monocytes.

56
Q

WHEN IS MYELOPEROXIDASE (MPO) FOUND?

A

Found in 90% of patients with microscopic polyarteritis and other vasculitides

Found in 30-40% of patients with Goodpastures syndrome.

57
Q

WHAT IS PROTEINASE 3 (PR3)?

A

Known as c ANCA

A 28kDa protein.

58
Q

What is The primary function?

A

is thought to be the degradation of extracellular proteins at sites of inflammation.

59
Q

When is it found?

A

found in >90% patients with Granulomatosis with polyangiitis (Wegener’s

The levels of PR3 correlate with disease activity and usually disappear on effective treatment reappearing on re emergence of the disease.

60
Q

How is Goodpasture’s disease caused?

A

GBM autoantibodies bind to their reactive sites in the glomerular/alveolar basement
membranes and activate the complement cascade, resulting in tissue injury.

61
Q

What is considered as a genetic marker for susceptibility to anti GBM disease?

A

The specific human leukocyte antigen type (HLA DRB1*1501)

62
Q

How do Anti GBM disease is responsible for up to 20% of acute renal failure?

A

due to crescentic glomerulonephritis.

63
Q

What does Typical presentation consists of?

A

the combination of renal and pulmonary insufficiency.

60-80% of patients have pulmonary and renal disease,

20-40% have renal disease alone,

and less than 10% have disease that is limited to the lungs.

64
Q

How is Goodpasture’s disease diagnosed?

A

Detection of anti GBM antibodies.

65
Q

How is anti GBM antibodies detected?

A

ELISAs for anti GBM antibodies are highly sensitive (> 95%) and specific (> 97%).

Anti GBM antibodies, in one third of the patients, are detected simultaneously with ANCA, most frequently MPO.

66
Q

How is disease with renal involvement, diagnostically confirmed?

A

A renal biopsy is essential in diagnosing suspected anti GBM disease

Immunofluorescence studies are essential, EM studies required to rule out glomerular basement membrane nephropathy.

67
Q

Untreated anti GBM disease has an almost universally poor outcome,

What is death caused by?

A

renal failure or lung haemorrhage.

68
Q

Main Treatment?

A

Plasmapheresis in conjunction with cyclophosphamide and prednisone.

Treatment with plasmapheresis, corticosteroids, and immunosuppressive agents has dramatically improved prognosis, and the 5 year survival rate exceeds 80%.

69
Q

Purpose of Plasmapheresis?

A

removes circulating anti GBM antibodies and other mediators of inflammation (such as complement), while the immunosuppressive agents minimize new antibody formation.

70
Q

What could prevent the use of cyclophosphamide?

A

Concern for latent TB

Molecular Pathology (10 decks)

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