- 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)

3 - Chronic Inflammation + Histological Interpretation Flashcards by Dinah Mandell

What happens after acute inflammation

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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What is chronic inflammation

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

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How does chronic inflammation arise

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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How does chronic inflammation arise

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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Histological features of chronic inflammation

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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Monocyte vs macrophage

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

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Macrophage appearance

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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Macrophage function (3)

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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Lymphocyte appearance

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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T cell vs B cell

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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Plasma cell appearance (histology)

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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Plasma cell function

These are fully differentiated B lymphocytes
produces antibodies

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

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

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Eosinophil function

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

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What are giant cell

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

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

What type of cell is specifically seen in tuberculosis

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

Cell types in chronic inflammation

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

Effects of chronic inflammation

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

What are the two types of idiopathic inflammatory bowel disease

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

Ulcerative vs Crohn’s

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

Liver cirrhosis

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

Granulomatous inflammation

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)

What is a granuloma + it’s types

☞ 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

Causes of granulomatous inflammation

**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

Mycobacterium granulomata + caseous necrosis

- 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

How do pathologist interpret images

- **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.

Haematoxylin + eosin

**haematoxylin** - Purple/blue - Nuclei **eosin** - Pink/red - Cytoplasm + extracellular matrix

Histology vs cytology

**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

Neutrophil vs eosinophil histology

- 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

Epithelium

- 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

Where does carcinoma arise from

Epithelium

Benign vs malignant neoplasms (tumours)

**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

Histology features of malignant neoplasm

- **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

Adenocarcinoma

- Cancer arising from glandular epithelium - Eg bowel cancer