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MD2 Rheumatology > Introduction to Inflammation > Flashcards

Introduction to Inflammation Flashcards

1
Q

List 5 components of the innate immune system

A

Physical barriers

Antimicrobial chemicals

Complement

Epithelial cells, phagocytes, NK cells and others

Cytokines

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2
Q

List 3 components of the adaptive immune system

A

Lymphocytes (T cells and B cells)

Antibodies

Cytokines

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3
Q

Compare and contrast the innate and adaptive immune systems

A

Innate: recognises shared molecular patterns associated with “danger”, rapid response, no memory

Adaptive: recognises Ags (microbial and non-microbial) which are “strangers”, slower response, memory

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4
Q

What functions does interaction with PAMPs induce in neutrophils, monocytes, NK cells, eosinophils, basophils and dendritic cells?

A

Neutrophils: phagocytosis

Monocyte/macrophage: phagocytosis

NK cells: binds and kills infected cell, release cytokines

Eosinophils: binds and kills parasites (nematodes)

Basophils: releases inflammatory mediators and cytokines to boost response (esp to parasites)

Dendritic cells: engulfs and presents Ag, releases cytokines

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5
Q

What effector functions are induced by binding of Ag to B cells and T cells?

A

B cells: secrete Abs (block adhesion of EC pathogens)

Abs also: trigger complement (remove EC pathogens), bind to receptors on NK cells and macrophages (activates these cells), bind to receptors on eosinophils and mast cells (removes parasites and boosts immune response)

CD8 T cells: bind cells infected with IC pathogens and release cytokines (kills infected cells)

CD4 T cells: help macrophages, B cells and CD8 T cells and release cytokines

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6
Q

In what context can the innate immune system act on self?

A

If molecular patterns the same as PAMPs are recognised by the PRRs; can result from mimicry as a result of cellular damage due to a disease process or there may be defects in the PRRs

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7
Q

What is the most common context in which self tolerance is broken and autoantibodies form?

A

Advancing age; in suspectible people T cell receptor or Ab-mediated inflammatory processes may result and cause disease

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8
Q

List 9 clinical markers of inflammation

A

Raised ESR

Raised CRP

Raised immunoglobulins

Raised ferritin

Raised caeruloplasmin

Raised WCC

Raised platelet count

Decreased Hb (anaemia of chronic disease)

Decreased albumin

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9
Q

What defines an AI disease?

A

Direct evidence from the transfer of pathogenic Ab or pathogenic T cells

Indirect evidence based on reproduction of AI disease in experimental animals

Circumstantial evidence from clinical clues

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10
Q

List 5 systemic AI diseases

A

SLE

Behcet’s syndrome

Sarcoidosis

Scleroderma

Mixed CTD

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11
Q

Name a respiratory system specific AI disease

A

IPF

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12
Q

List 3 neurological AI diseases

A

MS

Guillian-Barre syndrome

Myasthenia gravis

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13
Q

List 4 AI diseases affecting skin/hair

A

Alopecia areata

Psoriasis

Pemphigoid

Vitiligo

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14
Q

What AI disease affects the salivary/lacrimal glands?

A

Sjogren syndrome

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15
Q

List 4 endocrine AI diseases

A

Hashimoto thyroiditis

Grave’s disease

Addison’s disease

T1DM

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16
Q

Name an AI disease targeting muscle

A

Polymyositis/dermatomyositis

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17
Q

Name an AI disease affecting the kidneys

A

Goodpasture’s syndrome

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18
Q

List 5 AI diseases affecting the haematological system

A

Haemolytic anaemia

Thrombotic thrombocytopaenic purpura (TTP)

Idiopathic thrombocytopaenic purpura (ITP)

Aplastic anaemia

Pernicious anaemia

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19
Q

List 3 RFs for AI disease

A

Specific monogenic or polygenic genotype

Epigenetics (even identical twins don’t have identical immune systems and don’t get the same AI diseases!)

FHx (?combinations of the above)

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20
Q

List 4 possible triggers for AI disease, and give an example of each

A

Infection, e.g. streptococcus and rheumatic fever

Neoplasia, e.g. small cell lung cancer and cerebellar ataxia

Drugs, e.g. tetracyclines and vasculitis

Environmental factors, e.g. gluten and coeliac disease

21
Q

What is the identified target Ag in Goodpasture’s disease?

A

GBM

22
Q

What is the identified target Ag in chronic active hepatitis?

A

Smooth muscle Ags

23
Q

What is the identified target Ag in SLE?

A

dsDNA, snRNP (small nuclear ribonucleic proteins)

24
Q

What is the proposed rationale for higher rates of AI disease in women?

A

Sex hormone receptors are found on immune cells

Cytokine receptors (e.g. IL-1R, IL-18R) has been discovered on hormone-producing tissues

Suggests bidirectional regulation of the immune response

25
Q

List 2 factors which may modify severity and course of AI disease

A

Pregnancy

Intercurrent illness

26
Q

Give some examples for identified environmental triggers for some specific AI diseases

A

Smoking and RA

UV light and SLE

Gluten and coeliac disease

Drugs (e.g. penicillin, cephalosporins) can bind to RBCs and generate a neoAg (as haptens) and stimulate Ab which destroy the RBCs causing haemolytic anaemia

27
Q

Describe the pathogenesis of coeliac disease (AKA gluten enteropathy), including Sx and Dx

A

Sx: association between ingestion of bread/cereal and relapsing diarrhoea

Majority of patients with coeliac disease express the HLA genes DQ2 or DQ8; some non-HLA genes also confer increased risk

Target autoAg is tissue transglutaminase; Ab to transglutaminase, endomysium and gliadin are used clinically for Dx and patient monitoring

28
Q

Describe the clinical features of coeliac disease

A

Association noted between ingestion of bread/cereal and relapsing diarrhoea

Malabsorption: diarrhoea, LOW, nutritional deficiencies (e.g. Fe, B12, folate, vit D)

Abdominal pain (bloating in severe cases)

Dermatitis herpetiformis (pictured)

29
Q

What other clinical manifestations are often seen even in “organ-specific” AI diseases and what is the underlying mechanism of this?

A

Rash, inflammatory joint pains, systemically “unwell” feelings/fatigue

Most likely related to circulating immune complexes which activate complement causing inflammation to occur

30
Q

What is rheumatic fever? Describe the pathogenesis

A

A self-limited AI disease triggered by group A streptococcus infection

Caused by cross-reactivity between a streptococcal Ag and cardiac myosin (“molecular mimicry”)

31
Q

What are the Sx of rheumatic fever?

A

Heart: pericardium, myocardium, endocardium

Joints: inflammatory arthritis

Skin: erythema marginatum

Brain: chorea

32
Q

What is the underlying pathology? Describe the macroscopic findings

A

Chronic rheumatic valvular heart disease

Mitral valve leaflets and chordae are thickened, fibrotic and distorted intercommissural adhesions are present

33
Q

List 5 AI conditions with known infectious triggers

A

Rheumatic heart disease

Reactive arthritis

Guillian-Barre syndrome

Erythema nodosum (usually streptococcal)

Leukocytoclastic vasculitis

34
Q

Describe the macroscopic findings. Dx?

A

Red nodules, indistinct borders

Erythema nodosum

35
Q

List 3 AI conditions with neoplastic triggers (paraneoplastic syndromes)

A

Cerebellar degeneration

Peripheral neuropathy

PMR

36
Q

What cancers are associated with paraneoplastic cerebellar degeneration?

A

Small cell lung

Breast

Ovary

Hodgkin’s lymphoma

37
Q

Give an example of a large, medium and small vessel vasculitis

A

Large: GCA

Medium: microscopic polyangiitis

Small: leukocytoclastic vasculitis

38
Q

Describe the abnormality. What is the possible disease process causing this abnormality?

A

L subclavian artery stenosis

Could be caused by a large vessel vasculitis (in this case the patient had GCA)

39
Q

What are the commonest features of SLE?

A

Joint pain

Rash (malar)

Mouth ulcers

Serositis

Haematologic abnormalities

NB There is multisystem involvement but this usually occurs sequentially (over years), not contemporaneously

40
Q

What is the screening test used for SLE?

A

Antinuclear Abs (ANA)

41
Q

Describe the hypothesised model for the pathogenesis of SLE

A

Susceptibility genes result in production of B and T cells specific for self nuclear Ags

External triggers (e.g. UV radiation) result in apoptosis of cells, and the cellular debris produced expresses nuclear Ags resembling a PAMP/MAMP which is then recognised by the PRRs on the B and T cells

Antigen-Ab complexes are formed with the cellular debris and ANA, resulting in endocytosis of the complexes and inflammatory signalling which stimulates B cells and DCs to produce persistent high levels of ANA IgG

42
Q

List 6 Ags known to trigger Ab production in SLE. Which of these are thought to be specific for SLE?

A

Ro (SSA) and La (SSB) - ribonucleoproteins

dsDNA (specific)

snRNP core protein (specific)

Thrombin

Phospholipids

Histones (in drug-induced SLE; specific)

43
Q

Describe the mechanism underlying the clinical manifestations of SLE

A

Caused by immune complexes which circulate and deposit in various tissues, probably determined by factors such as size and charge

We know now that some of the Ag implicated in the clinical manifestations are not nuclear in origin

44
Q

Outline the diagnostic criteria for SLE

A

4 of these 11 criteria:

1) Malar rash (fixed erythema over malar eminences, sparing of nasolabial folds)
2) Discoid rash (erythematous raised patches which may scar)
3) Photosensitivity (skin rash as a result of unusual reaction to sunlight)
4) Oral ulcers (usually painless)
5) Arthritis (non-erosive; Jaccoud’s arthropathy)
6) Serositis (pleuritis or pericarditis)
7) Renal disorder (proteinuria >3+ or 0.5g/day, or cellular casts in urine)
8) Neurological disorder (seizures or psychosis)
9) Haematological disorder (haemolytic anaemia or leukopaenia or lymphopaenia or thrombocytopaenia)
10) Immunological disorder (anti-DNA Abs or anti-Sm Abs or anti-phospholipid Abs)
11) ANA (exclude drug causes)

45
Q

Describe the abnormality. What disease process is this consistent with?

A

A) Lupus nephritis class II; light micrograph of glomerulus showing mild mesangial hypercellularity

B) Lupus nephritis class III; light micrograph of a glomerulus with segmental endocapillary hypercellularity, mesangial hypercellularity, capillary wall thickening, and early segmental capillary necrosis (silver stain)

C) Lupus nephritis class IV; endocapillary proliferation, leukocyte influx and apoptotic bodies, double contours, crescent formation with tubular transformation, early sclerosis and disruption of Bowman’s capsule

D) Thrombotic microangiopathy in a patient with SLE and circulating anticoagulant; glomerulus shows severe capillary and arteriolar thrombosis, endothelial cell swelling and necrosis, neutrophil influx, and stasis of erythrocytes, with no signs of immune deposits (silver stain)

46
Q

How is disease activity in SLE monitored?

A

Clinical status

ESR

CRP

MSU: glomerular RBC count, casts, protein

FBE: normocytic normochromic anaemia (i.e. anaemia of chronic disease), specific cytopaenias

Titre of dsDNA Ab

47
Q

Give an example of two AI diseases which have shared genetics

A

Coeliac disease

T1DM

48
Q

What is Jaccoud’s arthropathy?

A

Jaccoud arthropathy (JA) is a deforming non-erosive arthropathy characterised by ulnar deviation of the second to 5th fingers with MCP subluxation

MD2 Rheumatology (5 decks)

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