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MBBS - Year 1 > Pathology - Viral Diseases > Flashcards

Pathology - Viral Diseases Flashcards

1
Q

Outcomes of acute infl

A

Resolution and healing
Continued acute infl
Abcess infl
Chronic infl

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2
Q

Resolution and healing as a result of acute infl

A

Macrophages produce anti-infl cytokines

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3
Q

Anti infl cytokines

A

IL-10

TGF-beta

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4
Q

Continued acute infl as an outcome of acute infl

A

Persistent pus formation

Macrophages produce IL-8, which recruits additional neutrophils

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5
Q

Abcess formation as an outcome of acute infl

A

Acute infl surrounded by fibroids

Macrophages produce fibrogenic growth factors and cytokines

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6
Q

Chronic infl as an outcome of acute infl

A

Macrophages present antigen to activate CD4+ T-helper cells, which secrete cytokines promoting chronic infl

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7
Q

Chronic infl

A

Response of prolonged period e.g. weeks or months

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8
Q

What is the response causing chronic infl due to

A

Persistence of a stimulus, causing disordered homeostasis

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9
Q

Causes of chronic infl

A

Persistent infection - most common
Autoimmune disease
Foreign materials
Carcinoma

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10
Q

How does persistent infection cause chronic infl

A

Causes delayed type sensitivity

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11
Q

Chronic infl cells

A

Macrophages
Lymphocytes
Plasma cells

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12
Q

Macrophages as chronic infl cells

A

Dominant chronic infl cells
Phagocytosis
Display antigen to T-cells and respond to T cell signals and production of cytokines
Lifespan is several months or years

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13
Q

Macrophage activation pathways

A

Classical

Alternative

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14
Q

Classical macrophage activation pathways

A

M1 macrophages produce No and ROS and up regulate lysosomal enzymes, killing ingested organisms
They secrete cytokines and stimulate infl

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15
Q

How is the classical macrophage activation pathway induced

A

Induced by bacterial products which engage toll-like receptors or by interferon-gamma produced by T cells

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16
Q

How is the alternative macrophage activation pathway induced

A

By cytokines other than interferon-gamma e.g. IL-4 and 13, from T-cells

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17
Q

Alternative macrophages activation pathway

A

M2 macrophages secrete growth factors promoting angiogenesis, fibroblast activation and collagen synthesis
Principal function is tissue repair

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18
Q

T lymphocytes in acute infl

A

T-cell receptor undergoes gene rearrangement and progenitor cells become CD4+ or CD8+
T cells use TCR complex for antigen surveillance
Th1, Th2 and CD8+ all are activated

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19
Q

Th1 cells in acute infl

A

Secreet interferon-gamma to recruit macrophages

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20
Q

Th2 cells in acute infl

A

Involved in allergies

Can recruit eosinophils and cause B-lymphocytes to produce IgE

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21
Q

CD8+ T cells in acute infl

A

Either release perforin and granzymes or bind FAS-ligand to FAS on target cells

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22
Q

Perforin

A

Creates pores allowing granzyme to enter cell

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23
Q

B lymphocytes in acute ink

A

Produced in bone marrow + undergo immunoglobulin gene rearrangement to become naïve B-cells, expressing IgM and IgD
Antigen binds to IgM or IgD, causing maturation of plasma cells

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24
Q

Granuloma

A

Collection of activated macrophages or epithelioid histiocytes. Can be caseating or non-caseating

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25
Conditions associated w/ granulomatous infl
``` Foreign material Sarcoidosis Crohn’s disease Cat scratch disease Mycobacterial and fungal infection – caseating granulomas ```
26
Granuloma formation
Macrophages process and present antigen on surface in association w/ MHC-II molecules to CD4+ helper T-cells Macrophages secrete IL-2 causing CD4+ helper T-cells to differentiate into the Th1 subtype Th1 cells secrete interferon gamma converted macrophages into epithelioid histiocytes and giant cells
27
How is TB diagnosed
Clinical detection of interferon-gamma
28
When is wound healing initiated
When infl begins
29
What is replacement of damaged tissue dependent on
Regenrative capacity of the tissue
30
Subtypes of tissue
Labile Stable Permanent
31
Labile tissues
Possess stem cells that continuously cycle to regenerate tissue e.g. bowels (stem cells in mucosal crypts), skin (basal layer)
32
Stable tissues
Cells that are quiescent (G0) but can re-enter cell cycle to regenerate tissue when necessary e.g. hepatocytes
33
Permanent tissues
Lack significant regenerative potential e.g. myocardium
34
Repair of damaged tissue
Replacement of damaged tissue w/ fibrous scar
35
When does repair of damaged tissue occur
When regenrtauve stem cells are lost or when tissue lacks retentive capacity
36
Initial stage of repair
Granulation
37
What is granulation tissue comprised of
Proliferated capillaries (providing nutrients), fibroblasts (which deposit type III collagen) and myofibroblasts (which cause wound contraction)
38
What happens in scar formation
Type III collagen is replaced w/ type I collagen | Collagenase removes type III collagen
39
Type III collagen
Pliable | Present in embryonic tissue, granulation tissue and keloids
40
Type I collagen
Has a high tensile strength | Present in skin, bone, tendons and in most organs
41
How are mechanisms of tissue regeneration and repair mediated
Via paracrine signalling by growth factors (macrophages secrete growth factors which target fibroblasts)
42
What does interaction of growth factors w/ receptors result in
Gene expression and cellular growth
43
Mediators of repair
``` TGF - alpha TGF - beta Platelet Derived Growth Factors (PDGF) Fibroblast Growth Factor (FGF) Vascular Endothelial Growth Factor (VEGF) ```
44
Function of TGF - alpha
Epithelial and fibroblast growth
45
Function of TGF - beta
Fibroblast growth and inhibition of infl
46
Function of PDGF
Growth of endothelium, smooth muscles and fibroblasts
47
Function of FGF
Angiogenesis and skeletal development
48
Function of VEGF
Angiogenesis
49
Phases of wound healing
Coagulation phase Infl phase Proliferative/ granulation tissue phase Remodelling phase
50
Hypertrophic scar
Excess production of scar tissue localised to wound
51
Keloid scar
Exuberant prediction of scar tissue that is out of proportion to the wound size. Excess type III collagen
52
Reasons for delayed wound healing
``` Vitamin C and copper deficiency Zinc deficiency Infections Ischaemia Diabetes Malnutrition ```
53
Why are vitamin C and Cu needed in wound healing
Collagen cross-linking
54
Why is zinc needed in wound healing
Replacement if type II collagen w/ type I collagen
55
Hypersensitivity reaction
Excessive immune reactions
56
Causes of hypersensitivity
Autoimmunity – failure of self-tolerance Reaction against environmental antigens – genetic predisposition Reactions against microbes
57
Reactions against microbes causing hypersensitivity
Excessive reaction forming excess immune complexes T – cell responses against persistent microbes T – cells or antibodies to microbes cross-react w/ host tissues Normal reaction to virally infected cells
58
Different hypersensitivity reactions
Type I Type II Type III Type IV
59
Type I hypersensitivity reaction
Anaphylaxis Allergy Asthma
60
Type II hypersensitivity reaction
(Cytotoxic) | Haemolytic anaemia
61
Type III hypersensitivity reaction
(Immune complex mediated) | SLE
62
Type IV hypersensitivity reaction
(T-cell mediated) RhA Psoriasis
63
What are autoimmune disorders characterised by
Immune mediated damage of self tissues Involves loss of self-tolerance Clinically progressive w/ relapses and remissions
64
Aetiology of autoimmune disorders
Likely to be an environmental trigger in genetically susceptible individuals
65
Where can self-reactive lymphocytes develop
Central (thymus and bone marrow) or peripheral tolerance
66
What does central tolerance in the thymus lead to
T-cell apoptosis or generation of regulatory T-cell – stop autoimmunity by blocking T – cell activation and producing anti-infl cytokines
67
What does central tolerance in the bone marrow lead to
Receptor editing or B-cell apoptosis
68
What does peripheral tolerance lead to
Energy or apoptosis of T and B cells
69
Anergy
Functional inactivation rather than death

MBBS - Year 1 (93 decks)

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