Chronic Inflammation

Question 1

Define chronic inflammation

Answer 1

• When inflammation persists and lacks resolution
• If it persists for weeks/months/years with ongoing tissue damage,
• when tissue is infiltrated by lymphocytes, plasma cells and macrophages.
• It can be the initial response to certain viral/fungal infections

Question 2

What are the cells involved in chronic inflammation

Answer 2

• Macrophages,
• Plasma cells
• Lymphocytes

(cells of acute is neutrophil polymorphs)

Question 3

Describe the appearence of plasma cells on a histology slide

Answer 3

• Round/oval shape
• Dark cytoplasm
• Clock-face pattern nucleus (lots of spots) which is dark
• Can be di/trinuclear

Question 4

Describe the appearence of a lymphocyte

Answer 4

• Dark purple. Have a very large dark nuclei and little cytoplasm

Question 5

Describe the appearence of a neutrophil, basophil and eosinophil and platelets

Answer 5

Neutrophil - segmented nucleus of 2-5 lobes and a pale blue nucleus.
Basophil - Bilobed or S shape dark blue nucleus with a pale blue nucleus.
Eosinophil - Bilobed nucleus with pale pink granular cytoplasm
Platelets - Very small, no nucleus and purple

Question 6

Describe the appearence of a macrophage

Answer 6

Oval in shape, abundant pale blue nucleus. Called monocytes in blood

Question 7

What is the function of macrophage products?

Answer 7

They can be involved in tissue destruction by activating proteases, arachidonic acid metabolites, nitric oxide and coagulation factors or fibrosis by activating growth factors, fibrogenic cytokines, angiogenesis factors and remodelling collagenases.

Question 8

What is granulomatous inflammation?

Answer 8

It is a distinctive pattern of chronic inflammatory reactions.
- Predominant cell types are epithelioid macrophages (Activated macrophages with a modified appearence) and giant cells (fused epithelioid macrophages). These cells form granulomas

Question 9

Granulomas within lung tissue without necrosis suggests?

Answer 9

Pulmonary sarcoidosis (not TB due to lack of necrosis that accompanies granulomas)

Question 10

Chronic granulomatous inflammation can be due to?

Answer 10

• Infectious agents: TB, leprosy or toxoplasmosis,
• Foreign material,
• Sarcoidosis or crohn’s disease,
• Response to a tumour (Hodgkin’s lymphoma)

Question 11

What cells are involved in chronic granulomatous inflammation?

Answer 11

• Epithelioid macrophages (Mainly have a secretory role, giant cells form where material is hard to digest)
• Lymphocytes (CD4 which produces interferon gamma which can activate more macrophages and CD8)
• Formation of granulomas can be a manifestation of T cell mediated immune reactions

Question 12

What is healing by primary and secondary intention?

Answer 12

Primary - Healing of a simple wound were the edges are closely opposed. Minimal granulation tissue is needed to close gap.
Secondary - Healing of the wound with a larger surface defect in the edges or one that is dirty/infected. Abundant granulation tissue is needed.

Question 13

What are the phases of healing a tissue wound?

Answer 13

• Formation of blood clot,
• Formation of granulation tissue (new connective tissue),
• Cell proliferation and collagen deposition,
• Scar formation,
• Wound contraction,
• CT remodelling,
• Recovery of tensile strength

Question 14

Describe the basic overview of fracture healing

Answer 14

Inflammatory
Repair
Remodeling

Question 15

Describe the inflammatory stage of fracture healing

Answer 15

• Haematoma forms at the site of fracture,
• Prostaglandins recruit neutrophil polymorphs, macrophages, lymphocytes and fibroblasts to injury.
• Granulation tissue, ingrowth of new vessels and migration of mesenchymal cells occurs.
• Nutrients and oxygen are supplied by the exposed bone and muscle.

Question 16

Describe the repair stage of fracture healing

Answer 16

• Fibroblasts lay down stroma to support ingrowing vessels,
• Collagen matrix is laid down,
• Osteoid (bone tissue) is secreted and mineralised leading to soft callus formation.
• Callus ossifies after 4-6 weeks by forming bridge of woven bone between fracture fragments.

Question 17

Describe the remodelling phase of fracture healing

Answer 17

• Occurs slowly over months and years
• Returns bone to its original shape, structure and mechanical strength
• Facilitated by mechanical stress

Question 18

What are factors that facilitate wound healing?

Answer 18

Local factors - Type, size, location, movement within wound, infection, presence of foreign bodies, irritation and poor blood supply.
Systemic - Age, nutrition, systemic diseases, drugs and smoking

Question 19

Name and describe a chronic inflammatory disease

Answer 19

• Rheumatoid Arthritis. There is destruction of articular cartilage leading to infiltration of inflammatory cells causing increased vascularity, aggregation of fibrin and pannus formation leading to erosion of cartilage and bone.

Question 20

Describe the role of inflammation in atherosclerosis

Answer 20

• Macrophages play a key role as they ingest LDL and become foam cells.
• Lymphocytes release chemical mediators

Question 21

Describe features of chronic granulomatous diseases

Answer 21

• X-linked defect in NADPH oxidase system within phagocytes.
• Inability to kill intracellular organisms so patients have repeated infections and develop granulomata of the lymph nodes, skin, lungs, liver and GI tract.

Question 22

What is hypereosinophilia syndrome?

Answer 22

A genetic mutation which drives excess production of clone eosinophils. This driver inflammatory processes within the myocardium which damages myocytes in a subendocardial distribution.
Fibrosis ensues and patient presents with clinically with restrictive cardiomyopathy

Question 23

How does syphilis present histologically?

Answer 23

With plasma cell rich infiltrate

Question 24

What is systemic mastocytosis?

Answer 24

• Excessive mast cells. Results in lots of histamine release. The mast cells can infiltrate the bone marrow, spleen, liver and lymph nodes which can supress their normal function. It is a CD117 mutation which can be treated with imatinib