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PP > 3 - Chronic Inflammation + Histological Interpretation > Flashcards

3 - Chronic Inflammation + Histological Interpretation Flashcards

1
Q

What happens after acute inflammation

A
  • complete resolution
  • repair with connective tissue (fibrosis) if there has been substantial tissue destruction
  • chronic inflammation where there is prolonged inflammation with repair
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2
Q

What is chronic inflammation

A

prolonged inflammation with associated repair
- Delayed onset
- Variable duration
- Variable appearances
- Limits damage + initiates repair
- Can cause debilitating symptoms

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3
Q

How does chronic inflammation arise

A
  • takes over from acute inflammation if resolution is not possible with acute inflmmation
  • Develops alongside acute inflammation (severe/persistent irritation)
  • arises ‘de novo’ eg autoimmune conditions, eg RA or IBD
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4
Q

How does chronic inflammation arise

A
  • takes over from acute inflammation if resolution is not possible with acute inflmmation
  • Develops alongside acute inflammation (severe/persistent irritation)
  • arises ‘de novo’ eg autoimmune conditions, eg RA or IBD
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5
Q

Histological features of chronic inflammation

A
  • Cells such as neutrophils, eosinophils, plasma cells and macrophages present
  • Giant cells (several phagocytes) may be present
  • Fibroblasts + myofibroblasts (responsible for regeneration + repair) laying down collagen → fibrosis
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6
Q

Monocyte vs macrophage

A

monocyte when in circulation
macrophage aka histiocyte once it enters tissue spaces

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7
Q

Macrophage appearance

A
  • Large cells (due to lots of cytoplasm)
  • Abundant, bubbly / foamy cytoplasm (many phagosomes + phagolysosomes) → allows it to fuse with pathogen to form phagosome
  • ‘slipper shaped’ nucleus
  • Can sometimes see debris/pigment (dark purple) that has just been broken down
  • Variable appearances depending on what they’re destroying (so difficult to identify)
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8
Q

Macrophage function (3)

A

removal of pathogen and the debris
antigen presentation where it presents the antigen on cell surface to the immune system → stimulates immune response
synthesis+ release of inflammatory mediators which control + regulate the inflammatory response

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9
Q

Lymphocyte appearance

A
  • Much smaller (comparable in size to RBC)
  • Mainly nucleus
  • Thin rim of cytoplasm (often lost in histology)
  • Therefore stain mainly dark purple
  • Two types: B and T cell, but can’t differentiate these on histology
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10
Q

T cell vs B cell

A

T cell
Variety of types eg
- Helper (assist other inflammatory cells)
- Cytotoxic (destroy pathogens)

B cell
- Mature into plasma cells
- Produces antibodies
- Neutralises pathogens

☞ can’t differentiate between the two on histology

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11
Q

Plasma cell appearance (histology)

A
  • Eccentric nucleus (looks like a clock, ish)
  • Peri-nuclear clearing (ie clearing round nucleus) due to Golgi
  • lots of Golgi (as produces lots of antibodies)
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12
Q

Plasma cell function

A

These are fully differentiated B lymphocytes
produces antibodies

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13
Q

Eosinophil appearance (histology) ‘a-o-sin-o-phil’

A
  • bi lobed nucleus
  • granular cytoplasm (stains red) – represents packets of chemical mediators
  • ‘looks like tomato with sunglasses’
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14
Q

Eosinophil function

A

release a variety of mediators
- Hypersensitivity reactions (eg asthma)
- Parasitic infections (eg helmlinths)

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15
Q

What are giant cell

A
  • Huge cells
  • Share the same cytoplasm
  • Contain multiple nuclei (multinucleate)
  • Due to fusion of multiple macrophages due to process of ‘frustrated phagocytosis’
  • There are three types (next card)
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16
Q

What are the 3 types of giant cells + their histological features

A
  • foreign body nuclei are randomly arranged
  • Langerhans have rim of nuclei around outside (either partial or complete circle) ☞ can be seen in tuberculosis
  • touton have ring of nuclei in the middle ☞ can be seen in fat necrosis
17
Q

What type of cell is specifically seen in tuberculosis

A

Langerhans giant cell
These have a rim of nuclei around the outside (either partial or complete ring)

18
Q

Cell types in chronic inflammation

A

generally non-specific
☞ Proportion of cell types can indicate a diagnosis eg:
- RA = mainly plasma cells
- Chronic gastritis = mainly lymphocytes
- Whipple’s disease (rare bacterial infection) = mainly macrophages

19
Q

Effects of chronic inflammation

A
  • Fibrosis deposition of collagen eg chronic colecystitis, liver cirrhosis
  • impaired function eg IBD + altered bowel function
  • Rarely, increased function eg thyrotoxicosis in Grave’s disease
  • atrophy eg atrophic gastritis (chronic inflammation of stomach, resulting in reduced glands)
  • stimulation of immune response antigen presentation
20
Q

What are the two types of idiopathic inflammatory bowel disease

A

Ulcerative colitis + Crohn’s Disease
☞ weight loss, abdominal pain, altered bowel motion, rectal bleeding

21
Q

Ulcerative vs Crohn’s

A

crohn’s
- Can affect all of the GI tract (from mouth to anus)
- Discontinuous patches of inflammation (skip lesions)
- Inflammation affects full thickness of bowel wall (transmural) → causes strictures (narrowing, obstruction) + fistulae (abnormal connections between bowel + bladder etc)
- Can sometimes find granulomata
- Less likely to have rectal bleeding

ulcerative colitis
- Only affects large bowel
- Continuous inflammation
- Inflammation affects superficial layers of bowel wall on mucosa and submucosa
- No granulomata
- More likely to have rectal bleeding

22
Q

Liver cirrhosis

A
  • Liver has a nodular appearance (nodules are due to trying to regenerate)
  • End stage damage to liver
  • Can be caused by alcohol, hepatitis, drugs, toxins, fatty liver disease (caused by obesity, alcohol + diabetes)
  • Bands of fibrosis in between nodules
23
Q

Granulomatous inflammation

A
  • Specific type of chronic inflammation
  • chronic inflammation + granuloma
  • One or more granuloma
  • Multiple = granulomata
  • May sometimes see a giant cell sitting within a granuloma
  • Several different causes (sep card)
24
Q

What is a granuloma + it’s types

A

☞ a collection of epitheloid histiocytes (macrophages that look like epithelial cells)
☞ have pale pink cytoplasm
☞ may or may not have a rim of surrounding lymphocytes
☞ may or may not have giant cell sitting within a granuloma

foreign body
- Destruction + removal of foreign material (eg splinter or suture)
- Few lymphocytes

immune mediated
- Could be due to destruction + removal of pathogens
- Can be idiopathic
- Can undergo central necrosis (big areas of necrosis in middle of granulomata)
- Many lymphocytes

25
Q

Causes of granulomatous inflammation

A

infections of mycobacterium
- Mycobacterium tuberculosis + m. leprae
- These give rise to tuberculosis + leprosy
- Tuberculosis tends to affect top of lung, forming mass that looks like cancer
- Forms caseous necrosis (different card)

chron’s disease
- In GI tract
- Non-necrotising granulomatas
sarcoidosis
- In skin, lymph nodes + lungs
- Non-necrotising granulomatas

26
Q

Mycobacterium granulomata + caseous necrosis

A
  • Cheese-like necrosis that forms in centre of granulomata
  • Specific to tuberculosis (often at top of lung, forms a mass that looks like a tumour)
  • Looks bright pink on H+E histology
  • Surrounded by epitheloid histocytes (macrophages)
  • No inflammatory cells around it
27
Q

How do pathologist interpret images

A
  • biopsy thin core of tissue collected by needle. Usually done to diagnose a disease process, or monitor disease process.
  • resection surgeon takes out part of organ/whole organ. Usually done after biopsy – to cure someone of disease or symptoms.
  • H+E to stain + identify different structures
  • special tests eg immunohistochemistry (antibody labelling), immunofluorescence (used in kidney disease), electron microscopy (to see intracellular components)
  • low power/high power low = zoomed out, high = zoomed in.
28
Q

Haematoxylin + eosin

A

haematoxylin
- Purple/blue
- Nuclei

eosin
- Pink/red
- Cytoplasm + extracellular matrix

29
Q

Histology vs cytology

A

histology
Solid tissue ie biopsy or resection
- Good for tissue structure
- Looking for specific things (ie tumour invasion, tumor grade + special testing)
- Cons: Expensive, timely, invasive
- Pros: More accurate

cytology
Collected as fluid aspirate
- Looking at individual cells
- Can only query benign or malignant (nothing else)
- Cons: less accurate
- Pros: less invasive, cheap, quicker

30
Q

Neutrophil vs eosinophil histology

A
  • Neutrophil is multi-lobed nucleus
  • Neutrophil has paler pink cytoplasm
  • Eosinophil ‘tomato wearing sunglasses’
  • Eosinophil is bi-lobed nucleus
  • Eosinophil has granular cytoplasm that stains darker red
31
Q

Epithelium

A
  • Lines all mucosal surfaces
  • Has specific job (protection, secretion, absorbtion)
  • Easily damaged but can repair
  • Many different types eg simple squamous / cuboidal / columnar, stratified squamous / cuboidal, pseudostratified columnar + transitional
32
Q

Where does carcinoma arise from

A

Epithelium

33
Q

Benign vs malignant neoplasms (tumours)

A

benign
- Well circumscribed
- Doesn’t invade into other structures
- Uniform nuclear features
- Few mitoses
- No necrosis

malignant
- Irregular borders
- Invade into other tissues
- Nuclear pleomorphism
- Abnormal mitoses
- Necrosis

34
Q

Histology features of malignant neoplasm

A
  • pleomorphism where nuclei all look different
  • enlarged nuclei → raised nuclear:cytoplasm ratio
  • **mitoses* → high cell turnover suggest that the tumor is rapidly growing
  • hyperchromasia where the cell is darker
  • High grade neoplasms (ie the ones that are more serious) show more of these features
35
Q

Adenocarcinoma

A
  • Cancer arising from glandular epithelium
  • Eg bowel cancer

PP (4 decks)

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