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Principles of Disease > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What is acute inflammation?

A

Homeostatic mechanism which sees a series of protective changes in tissue, as a response to injury, in order to maintain the integrity of an organism

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2
Q

What are some signs of acute inflammation?

A

Rubor (redness), Calor (heat), Tumour (swelling) and Dolor (pain)

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3
Q

What is the cause of acute inflammation?

A

Microorganisms (parasites, bacteria etc.), Mechanical trauma to body (physical injury), Chemically unstable environment (extreme pH etc.), Extreme physical environment (extreme weather), Necrosis (dead tissue) or Hypersensitivity

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4
Q

What is the pathogenesis of acute inflammation?

A

Changes in blood flow as a result of changes in BV (blood vessel) permeability. This allows neutrophils to enter tissue from vessel

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5
Q

What are the local effects seen in inflammation?

A

Flush (transient articular contraction), Flare (local arteriolar dilation) and Wheal (relaxation of smooth muscle in vessel). Also seen in increased BV radius (allows more blood to flow to site of infection) and permeability (allows neutrophils/other proteins to enter tissue via blood)

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6
Q

What is exudation and exudate?

A

Exudation - movement of plasma from BV (capillaries) to tissue (as a result of increased BV permeability)
Exudate - the liquid which is moved from BV to tissue

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7
Q

What is an effect of exudation?

A

Oedema - this is the accumulation of fluid in extravascular space and helps to explain swelling during inflammation

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8
Q

Describe the movement of neutrophils during inflammation

A

Migration (movement of neutrophils to the endothelium part of the lumen), Pavementing (attachement of neutrophils to the endothelium of the BV) and Emigration (neutrophils squeezing out of endothelium to enter extravascular space - an ACTIVE process)

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9
Q

What are the benefits of acute inflammation?

A

Rapid process, shows cardinal signs (prioritised in the body), neutrophils will destory the pathogen (phagocytosis) and macrophages will denature antigen. Plasma proteins will localise the process. After this, there will be resolution

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10
Q

What are the roles of neutrophils in acute inflammation?

A

Phagocytosis (recongnise foreign antigen, move towards it (chemotaxis) and adhere to organism), Releasing granules (containing enzymes and free radicals (H2O2))

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11
Q

What happens to neutrophils after they release their contents?

A

They will die and form pus (alongside other proteins; which if leaks into bloodstream, can prolong inflammation)

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12
Q

What is the role of fibrinogen (plasma protein) in inflammation?

A

Aid coagulation (coagulation factor), will form fibrin (structural protein) and clot exudate (which aids in blood clotting)

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13
Q

What is the role of immunoglobin (plasma protein) in inflammation?

A

Will present in plasma for a specific antigen and is part of the humoural immune response

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14
Q

Where can mediators of acute inflammation be found?

A

In plasma, Released from cells, On endothelial membrane surface or Inside of cells

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15
Q

What is the overall effect of mediators within inflammation?

A

Contribute to vasodilation, Increased permeability, Neutrophil adhesion, Itch/pain feeling and chemotaxis

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16
Q

Is the overall effect of mediators pro-inflammatory or anti-inflammatory?

A

Some effects are pro-inflammatory and some are anti-inflammatory - it is all about striking a balance between the two

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17
Q

Describe cell surface mediators

A

ICAM-1 (helps neutrophils to stick to the endothelium) and P-selectin (interacts with neutrophil surface)

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18
Q

Describe serotonin (5-hyrdoxytryptamine) as a mediator released from cells

A

Made in platelets and are released when platelets degranulate in coagulation process - it causes vasoconstriction

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19
Q

Describe histamine as a mediator released from cells

A

Usually released from mast cells, basophils or platelets, has IgE antibody interactions and causes vasodilation and increased permeability in BVs

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20
Q

Describe prostaglandins as a mediator released from cells

A

Released from cells such as endothelium and leukocytes and has similar effects as histamine - increased permeability and vasodilation of the BVs

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21
Q

Describe cytokines and chemokines as mediators released from cells

A

Released from macrophages and endothelium cells and have both pro-inflammatory and anti-inflammatory effects. They are also involved in cell signalling (cytokines)

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22
Q

Describe nitric oxide as a mediator released from cells

A

Released from various cells and causes smooth muscle relaxtion. Also has anti-inflammatory effects as well

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23
Q

Describe free radicals (H2O2, O2-, OH-) as a mediator released from cells

A

Released by neutrophils during phagocytosis and amplify pro-inflammatory effects

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24
Q

What are the systemic effects (whole body/multiple organs) of acute inflammation?

A

Pyrexia (fever), Malaise (feeling unwell, weight loss), Vomiting & nausea (in children), raised WBC (neutrophilia - produced in the bone marrow)

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25
Q

What are the longer term effects of acute inflammation?

A

Lymphadenopathy (enlargement of lymph nodes), Weight loss (as it is a catabolic process), Aneamia (bone marrow cannot be produced), Supparation (formation of pus (which is made up from dead cells and tissue) with a membrane surrounding it - this can lead to abscess formation)

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26
Q

What causes septic shock?

A

Mediators are released from cells causing vasodilation and, as a result, system vascular resistence (SVR) is decreased. This results in release of catecholamine which causes increased HR (tachycardia) to maintain CO (cardiac output). Bacterial leukin (interleukin-1) is released which causes pyrexia (fever) and activation of coagulation, causing haemorrhagic skin rash

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27
Q

What are the complications of acute inflammation?

A

Granulation tissue (used for healing and repair) may lead to scar formation

28
Q

What is the function of granulation tissue within acute inflammation?

A

It is used for healing and repair, may undergo fibrosis and lead to scar formation

29
Q

Describe the process of scar formation

A

Capillaries grow (angiogenesis) as part of inflammatory response which allows recruitment of macrophages from blood to tissue. Fibroblasts lay down collagen as this replaces exudate at site of inflammation. Necrotic tissue (dead tissue) is replaced as collagen pulls together to close gap at site of wound. Fibrous tissue is then formed (scar)

30
Q

What can problematic fibrosis lead to?

A

Chronic inflammation

31
Q

How can process of acute inflammation be altered to detriment of patient?

A

Dissemination

32
Q

Describe the process of dissemination

A

Process by which bacteria spreads around the body - Bacteraemia (bacteria in the blood), Septacaemia (growth of bacteria in the blood), Toxicaemia (toxic products in the blood)

33
Q

Describe septic shock in acute inflammation

A

Pyrexia (fever), Peripheral Vasodilation, Low BP, High HR, Haemorrhagic skin rash

34
Q

What is a possible outcome of acute inflammation?

A

Organisation - granulation tissue is formed to allow healing and repair to occur, scar is formed through fibrosis

35
Q

What is the outcome of septic shock?

A

It is fatal and can cause hypoxia (cell death), can lead to haemorrhage and urgent intervention & support is required. Patient should be admitted to hospital ASAP (to prevent organ failure and hypoxia)

36
Q

What happens when compensation fails?

A

Increased HR due to increased CO - so the SVR and BP is low - this can lead to hypoxia and organ failure

37
Q

What is chronic inflammation?

A

Inflammation where most of the cell population consists of macrophages, lymphocytes and plasma cells and there are signs of loss of function in organs/tissue and necrosis (dead tissue). There may be signs of healing and repair by presence of granulation tissue, alongside scarring fibrosis.

38
Q

What are the main causes of chronic inflammation?

A

Acute inflammation or Primary lesion (no acute phase seen, just chronic changes)

39
Q

How can chronic inflammation arise from acute inflammation?

A

Failure to remove debris from site of infection, Large amount of damage from wound and No sign of resolution from acute insult (inital wound)

40
Q

How a primary lesion arise?

A

Autoimmune disease, Materials which resist digestion therefore producing a response (mycobacteria, viruses), Exogenous substances (metals, plastics, sutures etc.), Endogenous substances (keratin, hair - cannot be phagocytosed)

41
Q

What cells are involved in chronic inflammation?

A

Lymphocytes, plasma cells, macrophages, fibroblasts and giant cells

42
Q

What is the role of lymphocytes within chronic inflammation?

A

They are involved in immune response and immunological memory.
May be T cell or B cell

43
Q

What is the role of B cells in chronic inflammation?

A

Differentiate into plasma cells and secrete antibodies; this contributes to immunological memory
Act alongside macrophages (as they have antigen presenting qualities to them)

44
Q

What is the role of T cells in chronic inflammation?

A 
Produce cytokines (which attract and hold macrophages and increase permeability of that area)
Produce interferons (which have antiviral effects)
Release granules which lyse (kill) cells and destroy antigen (similar to NK cells)
45
Q

What is the role of NK cells during chronic inflammation?

A

Release granule proteins to destroy antigen/cells (similar to T cells)

46
Q

What is the role of fibroblasts in inflammation?

A

Metabolically active cells which lay down structural proteins such as COLLAGEN

47
Q

What are the effects of chronic inflammation?

A

Scarring & fibrosis and granuloma formation

48
Q

What is a granulamatous inflammation?

A

Inflammation which is characterised by the presence of granulomas (brought about by indigestible antigen)

49
Q

What is a granuloma?

A

A structure containing a mass of fragments of epitheliod macrophages in tissue
Contains neutrophils and eosinophils and are a response to indigestible antigen
Mostly type IV hypersensitivity reaction
May contain giant cells or be surrounded by dead material or lymphocytes

50
Q

What are some examples of granulomatous infections?

A

Tuberculosis (mycobacterium tuberculosis)
Leprosy (mycobacterium leprae)
Syphillus (trapenoma pallidum)

51
Q

What are giant cells?

A

Mass of fused cells (histocytes/macrophages) to form larger cells

52
Q

What is the structure of giant cells?

A

Larger cytoplasm

Multiple nucleui

53
Q

What are some examples of giant cells?

A 
Langhans type (TB linked, large eosinophillic cytoplasm, nucleui on periphery)
Foreign body type (granulation tissue, pus, neutrophils and shows organisation)
Silicone associated (ruptured silicone implants, vacuoles containing silicone)
Warthin-fikeldy type (central cluster of nucleui)
54
Q

What are some examples of non-infective granulomatous infections?

A 
Rhuematoid disease (autoimmune disease)
Sarcoidosis 
Crohns disease (chronic inflammatory bowels disease)
55
Q

What factors contribute to wound healing?

A

Granulation tissue formation
Angiogenesis
Fibrosis and scar formation

56
Q

Describe surgical wound healing

A 
Healed by primary intention (no tissue loss)
Small wound with small gap and blood clot
Presence of (a little) granulation tissue and small scar present
57
Q

Describe healing of larger defects

A

Healed by secondary intention (tissue loss)
Granulation tissue ingrowth
Scarring present

58
Q

Describe the sequence of events involved in healing and repair

A

Injury will occur and blood clot will form
Fibrin is laid down at site of wound
Growth factors and cytokines get involved in process
Angiogenesis will allow recruitment of macrophaages and other cells
Fibrin is phagocytosed
Myofibroblasts lay down collagen as wound is healed up
Scar forms as e-epithelialisation occurs

59
Q

What factors favour wound healing?

A

Good hygiene
Sound nutrition and metabolism
Apposition of edges (wound closure)
Normal inflammation/coagulation processes occurring

60
Q

What factors impair wound healing?

A

Large unclean wound
Large haematoma (swollen blood clot in tissue)
Poor nutrition and lack of vitamin A & C
Metabolic abnormalities (diabetes)
Lack of/inhibition of angiogenesis

61
Q

What contributes to healing and repair?

A

Wound healing

Fracture healing

62
Q

What are the sequence of events in fracture healing?

A

Trauma to the body and bone fracture
Haematoma will form as well around dead bone and tissue
Acute inflammation occurs
Organisation occurs
Granulation tissue is formed (containing osteoblasts and fibroblasts)
Macrophages remove debris

63
Q

What is a callus?

A

Bone healing tissue formed at ends of broken bones

64
Q

Describe callus formation

A

Osteoblasts lay down on woven bone
Nodules of cartilage are present
Osteoclasts remove damaged bone tissue and replace with lamellar bone
Trabecular and cortical bone are reformed

65
Q

Describe the role of angiogenesis

A

Formation of new blood vessels into capillary buds
Vascular endothelial growth factor (VEGF) are released by hypoxic cells (cells deprived of oxygen) to stimulate proliferation

66
Q

What is a benefit of angiogenesis?

A

Allows blood supply to reach damaged tissue (allows recruitment of macrophages, neutrophils etc)

67
Q

Give some examples of angiogenesis in action

A

Thrombosis (prevent thrombus propogation (could lead to blockage of blood vessels) and allows blood to flow again)
Malignant tumours (angiogenesis occurs as tumour grows, this can contribute to therapeutic control)
Fibrosis and scarring in artherosclerosis

Principles of Disease (2 decks)

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