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Medicine - Year 1 > Inflammatory arthritis - Pathology > Flashcards

Inflammatory arthritis - Pathology Flashcards

1
Q

What are the 5 cardinal features of acute inflammation?

A
  • Rubor - redness
  • Calor - heat
  • Dolor - pain
  • Tumor - swelling
  • Functio laesa - loss of function
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2
Q

List 4 causes of acute inflammation?

A
  1. Infections (PAMPS/MAMPS)
  2. Tissue necrosis (DAMPS)
  3. Foreign bodies
  4. Immune reactions (hypersensitivity)
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3
Q

Name 3 cell types which act as sentinel cells in tissues ready to react to invading microogranisms

A
  1. Macrophages
  2. Dendritic cells
  3. Mast cells
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4
Q

What is the main cytokine produced by sentinel cells when they are activated by DAMPS and PAMPS

A

Interleukin 1 (IL-1)

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5
Q

What is the difference between cytokine and chemokine

A
  • Cytokines are proteins produced by many cell types that can mediate and regulate inflammatory reactions.
  • Cyto means cell and kine refers to kinesis or movement.
  • Chemokines are chemotactic cytokines.
  • These are produced as a chemical cloud which spreads out from the source of inflammation and can attract specific white blood cells.
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6
Q

Describe the sequence of inflammation

A
  • PAMPS (small molecules with conserved patterns that are shared amongst many different pathogens) or DAMPS (damage associated molecular patterns) are produced when a cell is injured or when a cell dies
  • This recognises toll-like receptors on sentinel cells - macrophages, dendritic cells + mast cells
  • Cytokines (interleukin 1) produced by sentinel cells
  • Interleukin 1 recruits neutrophils and monocytes
  • Phagocytosis of dead cells or microbes
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7
Q

List the 5 steps of acute inflammation (the 5 R’s)

A
  1. Recognition (of the injurious agent)
  2. Recruitment (of leucocytes)
  3. Removal (of the agent)
  4. Regulation (of the response)
  5. Resolution (of the damage)
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8
Q

List the 5 mediators of acute inflammation

A
  1. Hageman factors (Factor XII)
  2. Complement system
  3. Mast cells
  4. Arachidonic acid metabolites
  5. Toll-like receptors
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9
Q

a) What is the Hageman factor (factor XII)
b) Where is it produced?
c) How is it activated?

A

a) It is an inactive pro-inflammatory clotting protein produced by the liver. It circulates in the blood stream until it is activated by exposure to collagen or microbes
b) Liver
c) Activated by contact with collagen or microbes

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10
Q

What is the link between the clotting system and the inflammatory system

A

Hageman factor activates coagulation cascade and also activates the kinin system

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11
Q

Describe the role of Hageman factor (Factor XII)

A
  • It is an inactive pro-inflamatory clotting protein produced by the liver
  • It is activated by with collagen or microbes
  • It activates the complement system and kinin system activation
  • Hageman factor cleaves plasma kallikrein which acts on HMW kininogen to produce Bradykinin
  • Function of bradykinin: vasodilation (redness and heat), increased vascular permeability (swelling), pain (sensitive nerve endings)
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12
Q

What are the 3 main functions of bradykinin

A
  • Vasodilation (redness and heat)
  • Increased vascular permeability (swelling)
  • Pain (sensitive nerve endings)
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13
Q

What is the complement system?

A

A system of pro-inflammatory serum proteins produced by the liver and circulate blood as inactive precursors until they are activated by 1 of 3 pathways

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14
Q

a) How many pathways is the complement system activated through? List the pathways
b) What do all the pathwyas reuslt in?

A

a) 3 pathways

  1. Classical pathway
  2. Alternative pathway
  3. Mannose-binding lectin

b) All result in the formation of C3 convertase which activates leukocytes using anaphyltoxins, phagocytosis and forms membrane attack complex

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15
Q

Name the 3 complement system activation pathways and explain how they are activated

A
  1. Classicle pathway - antigen binds IgG or IgM which activates C1 (complement protein)
  2. Alternative pathways - activated by microbial components directly (does not need antigen-antibody components for activation)
  3. Mannose- binding lectin pathway where mannose-binding lectin (MBL) binds to mannose in bacterial surface
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16
Q

List 4 consequences of complement system activation

A
  1. Formation of anaphylatoxins (C3a, C4a +C5a) - Causes histamine to be released from mast cells. C5a is a chemotatic and activation agent for neutrophils, monocytes, eosinophils and basophils
  2. Opsonisation - C3b is the main opsinin that coats the wall of a microbe. Neutrophils and macrophages have C3b receptors enabling phagocytosis
  3. Cell lysis (MAC) - The final stage in the cascade results in formation of a membrane attack complex (C5b, C6, C7, C8 and C9) flooding the cell with water and ions, causing lysis
  4. Immunoglobulin clearance - removal of immune complexes from circulation
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17
Q

List 3 ways mast cells are activated

A
  1. Complement proteins 3a + C5a
  2. Tissue trauma
  3. Crosslinking of cell surface IgE by antigen
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18
Q

Describe the consequences of mast cell activation

A
  • Mast cells contain pre-formed histamine granules which can be quickly relesed causing vasodiation and blood to leak
  • Mast cells also cause a delayed response by producing leukotrienes
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19
Q

What are TLRs? and describe the role

A
  • TLRs are receptors resent on cells of the innate immune system including macrophages and dendritic cells and adaptive immunity e.g., lymphocytes
  • They are ctivated by PAMPs, CD14 (co-recptor for LTR4) on macrophages recognises lipopolysaccharide
  • TLR activation upregulates Nuclear Factor Kapa Beta - activates immune response genes producing cytokines which can amplify reaction
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20
Q

Describe the role of arachidonic acid metabolites in acute inflammation

A
  1. Membrane phospholipids converted to arachidonic acid by pohspholipase A2
  2. Arachidonic acid acted on by COX-1 and 2 to form prostaglandins (PG) or by 5-lipoxygenase to form leukotriences (LT)
  3. PGI2 and D2 cause vasodilation and increased vascular permeability and PGE2 causes pain and fever
  4. LTC4, LTD4, LTE4 mediate vasoconstriction, bronchospasm and increased vasular permeability and LTB4 is important in neutrophil attraction + activation
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21
Q

How is arachidonic acid produced?

A

Membrane phospholipids are converted to arachidonic acid by the enzyme Phospholipase A2

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22
Q

What enzyme is required to generate arachidonic acid from membrane phospholipids and what drug class can stop this reaction?

A

Phospholipase A2 and steroids

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23
Q

What can arachidonic acid be acted on by? and to form what?

A

Arachidonic acid may be acted on by cyclooxgenase 1 and 2 (COX-1 and 2) to form prostaglandins

or

can be acted by 5-lipoxgenase to form leukotrienes

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24
Q

What enzymes are required to generate Prostaglandins from Arachidonic acid and name 2 drugs which can block these enzymes?

A

Cyclooxygenase 1+2 (COX 1+2) and Aspirin/Non-steroidal anti-inflammatory drugs (NSAIDS)

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25
Q

Which cells produce prostaglandins?

A
  • Mast cells
  • Macrophages
  • Endothelial cells + many other cell types
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26
Q

What is produced when 5-lipooxygnease acts on Arachidonic acid?

A

Leukotrienes

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27
Q

a) Describe the role of prostaglandin I2 and D2
b) Describe the role of prostaglandin E2

A

a) Causes vasodilation and increased vascular permeability
b) Causes pain and fever by raising the temperature set point in the hypothalamus

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28
Q

List 4 effects of prostaglandin production in the context of acute inflammation

A
  1. Vasodilation.(I2 and D2)
  2. Increased vascular permeability (I2 and D2)
  3. Pain (PGE2).
  4. Fever (PGE2).
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29
Q

What are leukotrienes produced by?

A

Leukocytes and mast cells

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30
Q

a) Describe the role of leukotriene C4, D4, E4
b) Describe the role of leukotriene B4

A

a) Mediates vasoconstrition, bronchospasm and increased vascular permeabiliy
b) Leukotriene B4 - important neutrophil attraction and activation

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31
Q

List 4 consequences of leukotriene production in the context of acute inflammation

A
  1. Vasoconstriction (LTC4, LTD4, LTE4)
  2. Bronchospasm (LTC4, LTD4, LTE4)
  3. Increased vascular permeability (LTC4, LTD4, LTE4)
  4. Attraction and activation of neutrophils (LTB4).
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32
Q

How do steroids reduce inflammation?

A

Corticosteroids are broad-spectrum anti-inflammatory agents that reduce the transcription of genes encoding phospholipase A2, COX-2, proinflammatory cytokines (interleukin-1 and tumour necrosis factor) and iNOS.

33
Q

a) How does rubor (redness) and calor (heat) occur in acute inflammation
b) List 4 mediators of redness and heat (rubor and calor)?

A

a) Due to vasodilation, causing increased blood flow
b) Mediated by histamine, prostoglandins, bradykinin and nitric acid

34
Q

What causes fever in the context of acute inflammation

A
  • Pyrogens (e.g., lipopolysaccharide) causes macrophages to release IL-1 and TNF. This increases COX activity in perivascular cells of the hypothalamus
  • COX acts on archidonic acid to produce prostaglandins. PGE2 causes pain and fever by raising temperature set point
35
Q

a) What causes swelling (tumor) seen in acute inflammation
b) What is it mediated by?

A

a) Histamine (from mast cells) causes endothelial cells to contract and endothelial cells can also be disrupted. This results in leakage of fluid from post-capillary venules into the interstitial space.
b) Mediated by histamine (endothelial cell contraction) and tissue damage (endothelial cell distruption)

36
Q

What is oedema?

A
  • An excess of fluid in the interstitial tissue or serous cavities.
  • Can be an exudate (a fluid high in protein containing cell debris) or a transudate (a fluid low in protein).
37
Q

What is pus?

A
  • A purulent exudate which is an inflammatory exudate rich in leucocytes (mostly neutrophils), the debris of dead cells and in many cases microbes.
38
Q

What causes pain in the context of acute inflammation

A

Bradykinin and PGE2 sensitive sensory nerve endings

39
Q

Which inflammatory cell predominates in acute inflammation and which can be raised in a full blood count in the setting of acute inflammation, such as in the setting of an acute bacterial infection?

A

Neutrophils

40
Q

List the steps which netrophils follow to get from the post-capillary venule to the site of infection and then removing the pathogen

A
  1. Margination
  2. Rolling
  3. Adhesion
  4. Transmigration
  5. Chemotaxis
  6. Phagocytosis
  7. Desctruction of phagocytosised material
  8. Resolution
41
Q

Describe the 5 steps which neutrophils follow to get from the post-capillary venule to the site of infection

A
  1. Margination - vasodilation slows blood-flow in post-capillary venules, cells marginate from centre of flow to periphery
  2. Rolling- selectins cause neutrophil to slow down and to roll along the endothelial surface
  3. Adhesion - Mediated by adhesion molecules e.g., ICAM and VCAM strongly binding to integrins on neutrophils. IL-1 and TNF induce the expression of selectins and adhesion molecules
  4. Transmigration - Histamine contracts endothelial cells allowing neutrophils to squeeze through the gaps, helped by PECAM1 (CD31)
  5. Chemotaxis - Neutrophils are attracted by bacterial products, IL-8, C5a and LTB4.
42
Q

Describe the steps involved in phagocytosis (neutrophls)

A
  1. Consumption of pathogens is enhanced by opsonins (eat me signals) (IgG and C3b).
  2. Pathogen binds to receptor on neutrophil membrane and is engulfed to form a phagosome
  3. Phagosome fuses with phagocytic vacuoles with lysosomes to form a phagolysosome
  4. Ingested particles within phagolysosome is destroyed by lysosomal enzymes and oxyen and nitrogen species
43
Q

Which cell dominates 3 days after acute inflammation begins?

A

Macrophage

44
Q

a) When do macrophages peak in acute inflmmation
b) How do macrophages kill organisms?

A

a) Peak 2-3 days after acute inflammation beings
b) Follow the margination, rolling, adhesion and transmigration sequence. They ingest via phagocytosis helped by opsonins (C3b) and destroy phagocytosed material using enzymes (lysozyme) in secondary granules (Oxygen-independent killing).

45
Q

a) In an infection, you will have systemic effects. Which cytokines are the mediators of this?
b) Describe the role of pyrogens such as lipoplysaccharide from bacteria

A

a) IL-1, IL-6 and TNF
b) Pyrogens such as lipopolysaccharide from bacteria cause macrophages to produce IL-1 and TNF, which increase COX activity in perivascular cells of the hypothalamus. This leads to PGE 2 raising the temperature set point

46
Q

List 3 organs which mediate the systemic protective effects seen in acute inflammation and the cytokines which mediate these effects.

A
  1. Brain. Fever (mediated by TNF IL-1 and IL-6).
  2. Liver. Production of acute phase proteins (mediated by IL-1 and IL-6).
  3. Bone marrow. Leukocyte production (mediated by TNF, IL-1 and IL-6).
47
Q

Describe the role of TNF and IL-1 in systemic pathological effects of an infection

A

TNF can accelerate atherosclerosis and promote thrombosis. TNF and IL-1 can cause insulin resitance promoting type 2 diabetes

48
Q

Describe the outcomes of acute inflammation

A
  1. Resolution and healing - mediated by IL-10 and TGF-beta (transforming growth factor 10)
  2. Continued acute inflammation - mediated by IL-8 with persistent pus
  3. Abscess formation
  4. Chronic inflammation - macrophages present antigen to activate CD4+ helper T cells
49
Q

What is chronic inflammation?

A

It is a response of prolonged period due to persistence of a stimulus, causing disordered homeostasis

50
Q

List the 5 causes of chronic inflammation

A
  1. Persistent infection (most common)
  2. Infection with viruses, mycobacteria, parasites and fungi
  3. Autoimmune disease
  4. Foreign materials
  5. Carcinoma
51
Q

List the cell mediators that are involved chronic inflammation

A
  • Plasma cells
  • B lymphocytes
  • T lymphocytes
52
Q

a) Where are macrophages derived from?
b) What do the circulate as?
c) Where can they be found?

A

a) Derived from hematopoetic stem cell
b) Monocytes
c) Connective tissue, liner (Kupffer cells), spleen, lymph nodes (sinus histiocytes), central nervous system (microglia) and lungs (aveolar macrophages)

53
Q

Compare the life span of a monocyte to tissue macrophages

A

Half-life of a monocyte is about a day, where as life span of tissue macrophages is several months or years

54
Q

Describe classical and alternative macrophage activation and the outcomes for each of these pathways

A

In classical macrophage activation, M1 macrophages are activated by bacteria or by T-cells (via interferon gamma) killing the bacteria and secreting cytokines which stimulate inflammation.

In alternative macrophage activation, M2 macrophages are activated by T-cells (producing IL-4 + 13). These M2 macrophages promote tissue repair by secreting growth factors which promote angiogenesis, fibroblast proliferation and collagen synthesis.

55
Q

Sate the role of macrophage subtype M1 and M2

A

M1 - stimulates inflammation

M2 - Stimulates repair

56
Q

What are the molecules which pathogens and damaged cells produce which can acitivate cells of the innate immune system

A
  • PAMPS (Pathogen associated molecular patterns)
  • DAMPS (Damage associated moleclar patterns)
57
Q

Describe the origin and activation of B-cells

A
  1. Produced in bone marrow + undergo immunoglobulin gene rearrangement to become naïve B-cells, expressing IgM and IgD
  2. If the antigen is T independent , then it can directly bind to B cells to activate it
  3. T-dependant antigens (most antigens) are presented to helper T-lymphocytes to activate B lymphocytes. This occurs by:
    * Antigen binds to IgM or IgD on B-cells, causing maturation of IgM or IgD-secreting plasma cells
    * The CD40 receptor on the B cell then binds CD40 ligand on helper T-cells which provides the second activation signal
58
Q

Which immunoglobulins do naive B cells express?

A

IgM and IgD

59
Q

What is the receptor that is found on B cell that is involved in the activation of the second activation signal, whereby helper T cells are activated?

A

CD40 receptor

60
Q

What does hypermutation in the variable region of the antibody determine?

A

Hypermutation in the variable region of the antibody, determines the affinity of the antibody for the particular antigen

61
Q

Describe the origin and activation of CD4+ Helper T-cells

A
  • T cells are produced in the bone marrow and mature in the thymus
  • Extracellular antigens are ingested and processed by APCs and presented on MHC II on the cell surface
  • B7 on the APC membrane is the molecule which provides the second activation signal for T helper cells
  • The T-cell receptor complex binds to antigen on MHC II and CD28 binds to B7, providing the second signal
  • T-helper cell 1 – secrete interferon gamma to recruit macrophages
  • T-helper cell 2 – involved in allergy in that they recruit eosinophils and cause B-lymphocytes to produce lgE
62
Q

Describe the roles of T- helper cell 1 and 2

A

T-helper cell 1 – secrete interferon gamma to recruit macrophages

T-helper cell 2 – involved in allergy in that they recruit eosinophils and cause B-lymphocytes to produce lgE

63
Q

Describe the activation of CD8+ Cytotoxic T-cells

A
  • Intracellular antigens (proteins derived from proteins in the cytoplasm) are presented on MHC class I (which are expressed by all nucleated cells and platelets)
  • The cytotoxic T-cell receptor with its CD8 co-receptor binds to MHC I
  • IL-2 produced by CD4+ T helper 1 cells provides the second activation signal
  • Kill occurs by:

Secretion of perforin and granzymes. Perforin creates pores and granzymes enter and destroy target cell

By binding FAS ligand to FAS on a target cell. The cell is attacked by apoptosis or programmed cell death

64
Q

What is granuloma inflammation?

A

A form of chronic inflammation which the body uses to get rid of pathogens which are difficult to eliminate

65
Q

What is a granuloma?

A

A collection of activated macrophages/epitheloid histiocytes. Granulomas may be caseating or non-caseating i.e., may show caseous necrosis or not

66
Q

List 6 causes of granulomatous inflammation

A
  1. Foreign bodies
  2. Sarcoidosis (Non-caseating granulomas)
  3. Crohns disease
  4. Cat sractch disease
  5. Myobacterial infection (tuberculosis
  6. Fungi infection
67
Q

How are granulomas formed?

A
  1. Macrophages process and present antigen on surface in association with MHC-II molecules to CD4+ helper T cells
  2. Macrophages secrete IL-12 which CD4+ helper T-cells to different into the TH1 subtytpe
  3. TH1 cells secrete interferon gamma (can be detected clinically - diagnosis of TB) which converts macrophages into epitheloid histiocytes and giant cells
68
Q

Replacement of damaged tissue with native tissue depends on the regenerative capacity of the tissue. List the 3 types of tissue based on their regenerative capacity and give examples of each tissue type.

A
  1. Labile - Labile tissues have stem cells that continuously cycle. Bowel mucosa, skin and bone marrow.
  2. Stable - Normally quiescent but can regenerate if necessary. Liver.
  3. Permanent - Lack significant regenerative potential. Myocardium, skeletal muscle and neurons.
69
Q

What is repair and when does it happen?

A
  • Repair is replacement of damaged tissue with a collagen rich or fibrous scar
  • This occurs when regenerative stem cells are lost or when the tissue which is injured lacks regenerative capacity e.g., heart muscle which undergoes ishaemic necrosis
70
Q

What is granulation tissue?

A
  • Granulation tissue formation is seen in the initial phase of repair
  • Granulation tissue consists of proliferated capillaries (which provide nutrients) and fibroblasts (which deposit type 3 collagen and myofibroblasts (which mediate wound contraction)
71
Q

What are the layers of an ulcer?

A
  • The first layer of an ulcer contains neutrophils, fibrin, and red blood cells
  • Deep to this layer there is a layer of granulation tissue which comprises a proliferation of blood vessels and fibroblasts.
  • These fibroblasts secrete collagen and the layer beneath the granulation tissue layer comprises predominantly fibroblasts with associated collagen representing scar tissue.
72
Q

List the 5 important growth factors which are necessary for repair and their actions

A
  1. Transforming growth factor (TGF) alpha - Epithelial and fibroblast growth
  2. Transforming growth factor (TGF) beta - Fibroblast growth and inhibition of inflammatation
  3. Platelet derived growth factor (PDGF) - Growth of endothliym, smooth muscles and fibroblasts
  4. Fibroblast growth factor (FGF) - Angiogenesis and skeletal development
  5. Vasclar endothelial growth factor (VEGF) - Angiogenesis
73
Q

What are the four phases of wound healing?

A
  1. Coagulation phase
  2. Inflammatory phase
  3. Proliferative/granulation tissue phase
  4. Remodelling phase
74
Q

What is the difference between wound healing by primary and secondary intention?

A

In primary intention, wound edges are brought together with sutures which leads to minimal scarring.

In secondary intention, the edges are not brought together and granulation tissue will fill the gap and then myofibroblasts contract the wound in which case scar tissue will form.

75
Q

Describe the three wound healing intentions

A
  1. Primary intention healing - wounds brought together (suturing) leads to minimal scarring
  2. Secondary intention - Edges brought together. Granulation tissue fills the gap, the myofibroblasts contract the wund. Scars form
  3. Tertiary intention healing - occurs when there is a need to delay wound close e.g., if the tissue is infected and antibiotics are used to treat the in
76
Q

What is the difference between hypertrophic scar and a keloid scar?

A

A hypertrophic scar is defines as excess production of scar tissue that is localised to the area of the wound

A keloid scar is exuberant production of scar tissue that is out of proportion to the wound size. Keloids are associated wuth excess type 3 collagen deposition.

77
Q

Name one vitamin and two minerals which are important for wound healing and how these contribute to the wound healing process

A
  • Vitamin C and copper needed for collage crosslinking
  • Zinc needed to replace type III collagen with type I collagen
78
Q

List 7 reasons for impaired wound healing

A
  1. Vitamin C and copper deficiency
  2. Zinc deficiency
  3. Presence of foreign bodies
  4. Infection
  5. Poor blood supply
  6. Diabetes
  7. Malnutriton
79
Q

Describe the pathogenesis of the 4 types of hypersensitivity reaction and give one example of a disease caused by each type.

A

Type I hypersensitivity reactions - immediate allergic reactions that are caused by preformed IgE antibodies activating mast cells and basophils. E.g., anaphylaxis, food or pollen allergies and asthma.

Type II hypersensitivity reactions -referred to as cytotoxic, as they involve antibodies that are specific to particular tissues within the body and cause destruction of cells in these tissues E.g., autoimmune haemolytic anaemia (where red cells are the target) and pemphigus vulgaris (where desmosomes are attacked).

Type III hypersensitivity reactions - immune complex-mediated with tissue damage caused by antigen-antibody complex deposition. E.g., SLE, glomerulonephritis and vasculitis.

Type IV hypersensitivity reactions -delayed and cell-mediated and are the only hypersensitivity reaction that involves sensitized T-lymphocytes rather than antibodies. E.g., RhA, psoriasis and allergic contact dermatitis.

Medicine - Year 1 (61 decks)

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