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EMS > Lecture 19: Acute Inflammation > Flashcards

Lecture 19: Acute Inflammation Flashcards

1
Q

What is inflammation?

A

“Local physiological response to tissue injury”

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2
Q

What are the two types of inflammation?

A

Acute (Initial)
Chronic (Prolonged)

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3
Q

What can be causes of acute inflammation?

A

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

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4
Q

What are some symptoms of acute inflammation?

A
  • Redness
  • Heat
  • Swelling
  • Pain
  • Loss of function
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5
Q

What causes redness during inflammation?

A

Dilation of small blood vessels

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6
Q

What causes heat during inflammation?

A

Peripheries
Hyperaemia -> vascular dilation
Fever

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7
Q

What swelling occurs during inflammation?

A

Oedema
Exudate
(inflammatory cells)
New connective tissue

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8
Q

Why does pain occur during inflammation?

A

Stretching/distortion of tissue
Bradykinin, prostaglandins, serotonin

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9
Q

Why does loss of function occur during inflammation?

A

Movement inhibited by pain
Severe swelling

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10
Q

What are the 3 steps to acute inflammation?

A
  1. Changes in vessel calibre (and flow)
  2. Increase vascular permeability -> formation of fluid exudate
  3. of cellular exudate
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11
Q

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

A

Opening of precapillary sphincter

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12
Q

Why is vascular permeability increases during acute inflammation?

A

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

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13
Q

What are 3 features of fluid Exudate?

A

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

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14
Q

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

A

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

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15
Q

What are features of delayed prolonged leakage?

A

Heat, cold, radiation, bacterial toxins, corrosive chemicals

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16
Q

What is the mechanism for immediate transient reactions?

A

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

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17
Q

What is the mechanism for immediate sustained reactions?

A

Severe direct vascular injury e.g. trauma

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18
Q

What is the mechanism for delayed prolonged reactions?

A

Endothelial cell injury

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19
Q

What is a Diagonostic histological feature of acute inflammation?

A

accumulation of neutrophil polymorphs within extracellular space (Cellular Exudate)

20
Q

3 marginations of neutrophils?

A

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

21
Q

How does adhesion of neutrophils occur during acute inflammation?

A

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

22
Q

What happens after adhesion of neutrophils?

A

Neutrophil Emigration (Diapedesis)

23
Q

What is Neutrophil Emigration (Diapedesis)?

A

Migration by active amoeboid movement
Venules and small veins

24
Q

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

A

Red cells may also escape
Passive process
Hydrostatic pressure

25
Q

What is chemotaxis?

A

the attraction of neutrophils towards chemicals

26
Q

What chemical substances are released by injured tissues early on?

A

Histamine, thrombin

27
Q

What does histamine and thrombin release from injured tissue cause?

A

increase of adhesion molecules on endothelial cells

28
Q

What cells produce histamine?

A

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

29
Q

Repercussions of histamine and thrombin being released from injured cells.

A

Vasodilation
Emigration of neutrophils
Chemotaxis
Increased vascular permeability
Itching and pain

30
Q

What does plasma contain? (Chemical mediators)

A

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

31
Q

What do macrophages secrete during an acute response?

A

Secrete chemical mediators (IL1,TNF-alpha)
Effects on endothelial cells
Occur after histamine and thrombin

E-selectin (adhesion molecule), IL-8 (chemotaxin for neutrophils)

32
Q

What are the roles of neutrophil polymorph?

A

Movement (Contraction of microtubules
Chemotaxis – directional response to chemical mediators)

Adhesion
(Opsonised by immunoglobulins or complement
Allows for neutrophils to bind)

Phagocytosis

33
Q

Describe phagocytosis?

A

The process where cells ingest solid particles

Adhesion (facilitated by opsonisation)

Ingestion (pseudopodia)

Phagasome

Lysosomes fuse

34
Q

What are 6 beneficial effects of acute inflammation?

A

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

35
Q

What are some harmful effects of acute inflammation?

A

Digestion of normal tissues
– collagenases and proteases

Swelling
– epiglottitis, cranial cavity

Inappropriate inflammatory response
– type I hypersensitivity

36
Q

What is resolution?

A

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

37
Q

What happens in the body during resolution?

A

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

38
Q

What is suppuration?

A

Formation of pus

39
Q

What 5 cells aid suppuration?

A

Living neutrophils
Dead neutrophils
Bacteria
Cellular debris
Globules of liquid

40
Q

What is an abscess?

A

Collection of pus, bacteria often inaccessible to antibodies and antibiotics

41
Q

How can abscesses be drained?

A

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

42
Q

What is Empyema?

A

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

43
Q

What is a fistula?

A

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

44
Q

What is organisation?

A

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

45
Q

how does acute inflammation migrate into chronic inflammation?

A

Causative agent not removed - > progression to chronic inflammation

Change in character of exudate
Lymphocytes, Plasma cells, macrophages

46
Q

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

A

Yes

47
Q

Systemic effects of inflammation?

A

Pyrexia

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

EMS (54 decks)

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