Lecture 19: Acute Inflammation Flashcards by Niamh Millar

What is inflammation?

“Local physiological response to tissue injury”

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What are the two types of inflammation?

Acute (Initial)
Chronic (Prolonged)

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What can be causes of acute inflammation?

Microbial infection
Hypersensitivity reactions (Sun, Acids, Allergic reactions)

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What are some symptoms of acute inflammation?

Redness
Heat
Swelling
Pain
Loss of function

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What causes redness during inflammation?

Dilation of small blood vessels

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What causes heat during inflammation?

Peripheries
Hyperaemia -> vascular dilation
Fever

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What swelling occurs during inflammation?

Oedema
Exudate
(inflammatory cells)
New connective tissue

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Why does pain occur during inflammation?

Stretching/distortion of tissue
Bradykinin, prostaglandins, serotonin

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Why does loss of function occur during inflammation?

Movement inhibited by pain
Severe swelling

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What are the 3 steps to acute inflammation?

Changes in vessel calibre (and flow)
Increase vascular permeability -> formation of fluid exudate
of cellular exudate

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What allows increased/ diversion of blood flow in acute inflammation?

Opening of precapillary sphincter

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Why is vascular permeability increases during acute inflammation?

Fluid escapes from vessels as does proteins (Fluid exudate) which leads to odema

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What are 3 features of fluid Exudate?

High protein content 50g/L
Contains fibrinogen -> fibrin deposition
High turnover

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How does fluid escape leading to increased vascular permeability in acute inflammation?

Gaps appear between endothelial cells of veins and venules
histamine acts on Contractile proteins (actin)

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What are features of delayed prolonged leakage?

Heat, cold, radiation, bacterial toxins, corrosive chemicals

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What is the mechanism for immediate transient reactions?

Chemical mediators
Histamine, bradykinin, NO, C5a, lecotriene B4, Platelet activating factor

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What is the mechanism for immediate sustained reactions?

Severe direct vascular injury e.g. trauma

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What is the mechanism for delayed prolonged reactions?

Endothelial cell injury

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What is a Diagonostic histological feature of acute inflammation?

accumulation of neutrophil polymorphs within extracellular space (Cellular Exudate)

3 marginations of neutrophils?

Loss of intravascular fluid
Increase of in plasma viscosity
Slowing of flow

How does adhesion of neutrophils occur during acute inflammation?

“pavementing” of neutrophils in venules
Normally random contact does not cause adhesion
Site of inflammation, early process independent of flow
Interaction of adhesion molecules

What happens after adhesion of neutrophils?

Neutrophil Emigration (Diapedesis)

What is Neutrophil Emigration (Diapedesis)?

Migration by active amoeboid movement
Venules and small veins

What might also escape from vessels during acute inflammation aside from fluid and proteins?

Red cells may also escape
Passive process
Hydrostatic pressure

What is chemotaxis?

the attraction of neutrophils towards chemicals

What chemical substances are released by injured tissues early on?

Histamine, thrombin

What does histamine and thrombin release from injured tissue cause?

increase of adhesion molecules on endothelial cells

What cells produce histamine?

Mast cells Basophils Eosinophils Platelets Release stimulated by complement C3a and C5a, neutrophil lysosomal proteins

Repercussions of histamine and thrombin being released from injured cells.

Vasodilation Emigration of neutrophils Chemotaxis Increased vascular permeability Itching and pain

What does plasma contain? (Chemical mediators)

Plasma contains 4 enzymatic cascade systems that produce inflammatory mediators (complement, kinins, coagulation factors, fibrinolytic system)

What do macrophages secrete during an acute response?

Secrete chemical mediators (IL1,TNF-alpha) Effects on endothelial cells Occur after histamine and thrombin E-selectin (adhesion molecule), IL-8 (chemotaxin for neutrophils)

What are the roles of neutrophil polymorph?

Movement (Contraction of microtubules Chemotaxis – directional response to chemical mediators) Adhesion (Opsonised by immunoglobulins or complement Allows for neutrophils to bind) Phagocytosis

Describe phagocytosis?

The process where cells ingest solid particles Adhesion (facilitated by opsonisation) Ingestion (pseudopodia) Phagasome Lysosomes fuse

What are 6 beneficial effects of acute inflammation?

Dilution of toxins – carried away by lymphatics Entry of antibodies – Increased vascular permeability Transport of drugs – Especially antibiotics Fibrin formation – Impedes movement of microorganisms, trapping for phagacyotsis, matrix for granulation tissue Delivery of nutrients and oxygen – Essential for cells with high metabolic activity (neutrophils) Stimulate the immune response – Fluid drains to local lymph nodes with soluble antigens

What are some harmful effects of acute inflammation?

Digestion of normal tissues – collagenases and proteases Swelling – epiglottitis, cranial cavity Inappropriate inflammatory response – type I hypersensitivity

What is resolution?

“complete restoration of tissues to normal after an episode of acute inflammation”

What happens in the body during resolution?

Minimal cell death/tissue damage Occurrence in organ/tissue with regenerative capacity Rapid destruction of causal agent Rapid removal of fluid by vascular drainage

What is suppuration?

Formation of pus

What 5 cells aid suppuration?

Living neutrophils Dead neutrophils Bacteria Cellular debris Globules of liquid

What is an abscess?

Collection of pus, bacteria often inaccessible to antibodies and antibiotics

How can abscesses be drained?

Can form a “point” and burst Cavity collapses -> organisation, fibrosis, scar

What is Empyema?

Empyema = collection of pus in a body cavity e.g. pleural space, gallbladder

What is a fistula?

abnormal connection between 2 mucosal surfaces or a mucosal surface to the skin

What is organisation?

Replacement of tissue by granulation tissue New capillaries grow into the inflammatory exudate Macrophages migrate Fibroblasts proliferate

how does acute inflammation migrate into chronic inflammation?

Causative agent not removed - > progression to chronic inflammation Change in character of exudate Lymphocytes, Plasma cells, macrophages

Can you have chronic inflammation without a period of acute inflammation?

Yes

Systemic effects of inflammation?

Pyrexia Constitutional symptoms (Malaise, anorexia, nausea) Reactive hyperplasia of reticuloendothelial system Enlarged lymph nodes, splenomegaly Haematological changes Increased ESR, leucocytosis, anaemia