Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Resolution and healing as a result of acute infl

A

Macrophages produce anti-infl cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Anti infl cytokines

A

IL-10

TGF-beta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Continued acute infl as an outcome of acute infl

A

Persistent pus formation

Macrophages produce IL-8, which recruits additional neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Abcess formation as an outcome of acute infl

A

Acute infl surrounded by fibroids

Macrophages produce fibrogenic growth factors and cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Chronic infl

A

Response of prolonged period e.g. weeks or months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the response causing chronic infl due to

A

Persistence of a stimulus, causing disordered homeostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Causes of chronic infl

A

Persistent infection - most common
Autoimmune disease
Foreign materials
Carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does persistent infection cause chronic infl

A

Causes delayed type sensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Chronic infl cells

A

Macrophages
Lymphocytes
Plasma cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Macrophage activation pathways

A

Classical

Alternative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Alternative macrophages activation pathway

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Th1 cells in acute infl

A

Secreet interferon-gamma to recruit macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Th2 cells in acute infl

A

Involved in allergies

Can recruit eosinophils and cause B-lymphocytes to produce IgE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

CD8+ T cells in acute infl

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Perforin

A

Creates pores allowing granzyme to enter cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Granuloma

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Conditions associated w/ granulomatous infl

A 
Foreign material 
Sarcoidosis 
Crohn’s disease 
Cat scratch disease 
Mycobacterial and fungal infection – caseating granulomas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Granuloma formation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How is TB diagnosed

A

Clinical detection of interferon-gamma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

When is wound healing initiated

A

When infl begins

29
Q

What is replacement of damaged tissue dependent on

A

Regenrative capacity of the tissue

30
Q

Subtypes of tissue

A

Labile
Stable
Permanent

31
Q

Labile tissues

A

Possess stem cells that continuously cycle to regenerate tissue e.g. bowels (stem cells in mucosal crypts), skin (basal layer)

32
Q

Stable tissues

A

Cells that are quiescent (G0) but can re-enter cell cycle to regenerate tissue when necessary e.g. hepatocytes

33
Q

Permanent tissues

A

Lack significant regenerative potential e.g. myocardium

34
Q

Repair of damaged tissue

A

Replacement of damaged tissue w/ fibrous scar

35
Q

When does repair of damaged tissue occur

A

When regenrtauve stem cells are lost or when tissue lacks retentive capacity

36
Q

Initial stage of repair

A

Granulation

37
Q

What is granulation tissue comprised of

A

Proliferated capillaries (providing nutrients), fibroblasts (which deposit type III collagen) and myofibroblasts (which cause wound contraction)

38
Q

What happens in scar formation

A

Type III collagen is replaced w/ type I collagen

Collagenase removes type III collagen

39
Q

Type III collagen

A

Pliable

Present in embryonic tissue, granulation tissue and keloids

40
Q

Type I collagen

A

Has a high tensile strength

Present in skin, bone, tendons and in most organs

41
Q

How are mechanisms of tissue regeneration and repair mediated

A

Via paracrine signalling by growth factors (macrophages secrete growth factors which target fibroblasts)

42
Q

What does interaction of growth factors w/ receptors result in

A

Gene expression and cellular growth

43
Q

Mediators of repair

A 
TGF - alpha 
TGF - beta 
Platelet Derived Growth Factors (PDGF)
Fibroblast Growth Factor (FGF)
Vascular Endothelial Growth Factor (VEGF)
44
Q

Function of TGF - alpha

A

Epithelial and fibroblast growth

45
Q

Function of TGF - beta

A

Fibroblast growth and inhibition of infl

46
Q

Function of PDGF

A

Growth of endothelium, smooth muscles and fibroblasts

47
Q

Function of FGF

A

Angiogenesis and skeletal development

48
Q

Function of VEGF

A

Angiogenesis

49
Q

Phases of wound healing

A

Coagulation phase
Infl phase
Proliferative/ granulation tissue phase
Remodelling phase

50
Q

Hypertrophic scar

A

Excess production of scar tissue localised to wound

51
Q

Keloid scar

A

Exuberant prediction of scar tissue that is out of proportion to the wound size. Excess type III collagen

52
Q

Reasons for delayed wound healing

A 
Vitamin C and copper deficiency  
Zinc deficiency 
Infections 
Ischaemia 
Diabetes 
Malnutrition
53
Q

Why are vitamin C and Cu needed in wound healing

A

Collagen cross-linking

54
Q

Why is zinc needed in wound healing

A

Replacement if type II collagen w/ type I collagen

55
Q

Hypersensitivity reaction

A

Excessive immune reactions

56
Q

Causes of hypersensitivity

A

Autoimmunity – failure of self-tolerance
Reaction against environmental antigens – genetic predisposition
Reactions against microbes

57
Q

Reactions against microbes causing hypersensitivity

A

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
Q

Different hypersensitivity reactions

A

Type I
Type II
Type III
Type IV

59
Q

Type I hypersensitivity reaction

A

Anaphylaxis
Allergy
Asthma

60
Q

Type II hypersensitivity reaction

A

(Cytotoxic)

Haemolytic anaemia

61
Q

Type III hypersensitivity reaction

A

(Immune complex mediated)

SLE

62
Q

Type IV hypersensitivity reaction

A

(T-cell mediated)
RhA
Psoriasis

63
Q

What are autoimmune disorders characterised by

A

Immune mediated damage of self tissues
Involves loss of self-tolerance
Clinically progressive w/ relapses and remissions

64
Q

Aetiology of autoimmune disorders

A

Likely to be an environmental trigger in genetically susceptible individuals

65
Q

Where can self-reactive lymphocytes develop

A

Central (thymus and bone marrow) or peripheral tolerance

66
Q

What does central tolerance in the thymus lead to

A

T-cell apoptosis or generation of regulatory T-cell – stop autoimmunity by blocking T – cell activation and producing anti-infl cytokines

67
Q

What does central tolerance in the bone marrow lead to

A

Receptor editing or B-cell apoptosis

68
Q

What does peripheral tolerance lead to

A

Energy or apoptosis of T and B cells

69
Q

Anergy

A

Functional inactivation rather than death

MBBS - Year 1 (93 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions