inflammation

Question 1

what are the cardinal signs of inflammation

Answer 1

Rubor (redness) – due to vasodilation (↑ blood flow).

Tumor (swelling) – from increased vascular permeability → exudate.

Calor (heat) – from increased blood flow and metabolic activity.

Dolor (pain) – from mediators (bradykinin, prostaglandins) stimulating nerves.

Functio laesa (loss of function) – due to tissue swelling/damage.

Question 2

list causes of acute inflammation

Answer 2

• Infections (bacterial, viral, fungal, parasitic, toxins).
• Tissue necrosis (ischemia, trauma, burns, radiation).
• Foreign bodies (splinters, sutures, urate/cholesterol crystals).
• Immune reactions (hypersensitivity).

Question 3

what are the morphological hallmarks of acute inflammation

Answer 3

• dilation of blood vessels
• activation and recruitment of leukocytes
• active exudation of fluid in the extravascular tissues

Question 4

list mediators in acute inflammation and how they are produced

Answer 4

• vasoavtice amines (histamine) released/produced by mast cells, basophils and platelets
• inflammatory lipids (prostaglandins and leukotrienes) produced by mast cells and leukocytes
• complement (plasma)
• cytokines produced by macrophages, endothelial cells and mast cells
• others: kinins, chemokines, nitric oxide, coagulation cascade

Question 5

what mediators cause vasodilation

Answer 5

inflammatory lipids

Question 6

what mediators of inflammation cause increased vascular permeability

Answer 6

• vasoactive amines
• complement
• inflammatory lipids
• cytokines

Question 7

what mediators cause leukocyte recruitment and activation

Answer 7

• inflammatory lipids
• complement
• cytokine

Question 8

what mediators cause pain

Answer 8

inflammatory lipids

Question 9

what mediators cause tissue damage

Answer 9

neutrophil granule content
ROS

Question 10

outline the sequelae of acute inflammation

Answer 10

1. complete reolution (clearance of offending agent and regeneration)
2. scarring or fibrosis (connective tissue growth into the are of damage or exudate, this occurs after substantial tissue destruction
3. progression to chronic inflammation (unresolved inflammatory process due to either the persistence of inurious agent or some interference with the normal process of healing

Question 11

what are acute phase proteins in inflammation

Answer 11

Produced in liver in response to IL-6, TNF, IL-1.

Functions: opsonization, complement activation, coagulation regulation.

Examples: C-reactive protein (CRP), serum amyloid A (SAA), fibrinogen, haptoglobin.

Question 12

outline the pathophysiology of pyrexia

Answer 12

Exogenous pyrogens (e.g. bacteria).

Endogenous pyrogens: IL-1, TNF, IL-6 → induce PGE₂ in hypothalamus → ↑ body temp via vasoconstriction & shivering.

NSAIDs inhibit PGE₂.

Question 13

what is the difference between exudate and transudate

Answer 13

Exudate: protein- and cell-rich, due to inflammation.

Transudate: protein-poor, due to ↑ hydrostatic or ↓ oncotic pressure.

Question 14

list types of exudates

Answer 14

• serous
• fibrinous
• purulent
• haemorrhagic

Question 15

list causes of chronic inflammation

Answer 15

Failure of acute inflammation to eliminate stimulus.

Resistant microbes (e.g. Mycobacteria).

Autoimmune disease.

Foreign material (sutures, silica).

Question 16

what cells are involved in chronic inflammation

Answer 16

Macrophages: phagocytosis, cytokines, antigen presentation.

M1: pro-inflammatory, ROS, NO, cytokines.

M2: tissue repair, fibrosis, TGF-β, anti-inflammatory cytokines.

Lymphocytes: CD4+ (helper/regulatory), CD8+ (cytotoxic).

Plasma cells: antibodies.

Fibroblasts: collagen deposition → fibrosis.

Endothelial cells: angiogenesis.

Question 17

how do granulomas form

Answer 17

Nodular aggregates of activated macrophages (epithelioid, multinucleated giant cells).

Surrounded by lymphocytes, plasma cells, fibroblasts.

Causes: Mycobacterium bovis, fungi, parasites, foreign bodies.

Types:

TH1 granulomas (caseating necrosis, e.g. TB).

TH2 granulomas (Johne’s disease, parasites).

Pyogranulomas = granulomas with central neutrophils.

Question 18

how does chronic inflammation get repaired

Answer 18

Granulation tissue: fibroblasts + angiogenesis → red, granular tissue.

Fibrosis: collagen replaces lost tissue, can contract organs.

Excess granulation tissue = proud flesh in horses.

Question 19

list the morphological patterns of chronic inflammation

Answer 19

• lymphoplasmacytic
• abscesses
• granulomas
• granulomatous inflammation
• pyogranulomatous inflammation
• granulation tissue
• fibrosis and repair

Question 20

what main cells are present in lymphoplasmacytic inflammation

Answer 20

• lymphocytes
• plasma cells

Question 21

what is lymphoplasmacytic inflammation

Answer 21

very common
- not specific for any one aetiology
- lymphocytes and plasma cells will almot alwys be present to some degree in early stages of chronic inflammation
- very common type of inflammation at mucosal surfaces (chronic gingivities, rhinitis, enteritis
- can be the only cell type present in response to some viral infections

Question 22

what are abscesses

Answer 22

What are they?
Discrete, dense collection of neutrophils surrounded by a rim of connective tissue (fibroblasts, small blood vessels and collagen); nodular
Why do they occur?
When the acute inflammatory response fails
Attempt to wall off the exudate and agent
Can be sterile or septic
Pyogenic bacteria can often be the source
Staphylococcus spp.