Immunology: Autoimmunity Flashcards

1
Q

Type II autoimmunity

A

IgG

cell surface/ECM antigens

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2
Q

Type III autoimmunity

A

IgG

immune complex deposition

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3
Q

Type IV autoimmunity

A

mediated by T cells

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4
Q

autoimmune hemolytic anemia

A

type II (IgG and IgM): Rh blood group or I antigen
destruction of RBC by classical complement (MAC and C3b) and phagocytes (with Fc receptor (IgG) or C3b)
anemia
Dx: Direct Coomb’s
Tx: corticosteroids

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5
Q

autoimmune thrombocytopenia purpura

A

type II: platelet integrin, gpIIb:IIIa
inhibition of enzyme that cleaves vWF (links platelets and vessels with clots) = excessive platelet adhesions (occlude small vessels)
damage: kidney, liver, brain
abnormal bleeding, neurological symptoms, low platelets, bruises
Dx: microangioplastic hemolytic anemia
Tx: plasmaphoresis

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6
Q

Goodpasture’s syndrome

A

type II: collagen type IV of BM
classical (then alternative) complement and phagocytes cause damage
glomerulonephritis, pulmonary hemorrhage
symptoms: loss of appetite, weakness, fatigue
Dx: anti-GBM
Tx: plasma exchange and antiinflammatory drugs

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7
Q

pemphigus vulgaris

A

type II: epidermal cadhedrin: proteins desmoglein 1 and 3
blistering of skin
Dx: punch biopsy of lesion with immunofluorescent stain (IgG4 Ab = pathogenic)
Tx: corticosteroids, anti-inflammatory drugs, rituximab

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8
Q

acute rheumatic fever

A

type II: GAS (S. pyogenes) cell wall antigens; molecular mimicry (Ab cross-react with cardiac muscle)
arthritis, myocarditis, late scarring of heart valves
symptoms: chest pain, shortness of breath, fever, joint pain, endocarditis

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9
Q

Grave’s disease

A

type II: TSH receptor (agonist)
hyperthyroidism
symptoms: heat intolerance, nervous, irritable, warm moist skin, weight loss, enlarged thyroid, bulging eyes, characteristic start (eye muscle inflammation)
Pregnant women: pass IgG to fetus and fetus will have condition
Tx fetus: plasmaphoresis to remove Ab and thyroid function is restored

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10
Q

Myasthenia gravis

A

type II: Ach receptor (antagonist: endocytosed and degraded)
progressive weakness
symptoms: facial muscles (esp. eyes and eyelids) first: diplopia, ptosis; progresses to generalized muscle weakness
Tx: anti-inflammatory, pyridostigmine

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11
Q

Type 2 diabetes (insulin-resistant diabetes)

A

type II: insulin receptor (antagonist)

hyperglycemia, ketoacidosis

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12
Q

Hypoglycemia

A

type II: insulin receptor (agonist)

hypoglycemia

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13
Q

Scleroderma

A

type II: destruction of vascular endothelial cells of arterioles and sm. muscle cells; replaced with collagen and fibrous material
localized or systemic symmetrical skin thickening; hard, smooth, ivory skin
damage: kidney, vessels, liver, brain
Dx: ANA (anti-nuclear Ab), ATA (anti-topoisomerase Ab), ACA (anti-centromere Ab)
Tx: increase blood flow to extremities

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14
Q

rituximab

A

B cell marker CD20 specific mAb: Ab results in NK ADCC to B cells
Tx: pemphigus vulgaris and RA (doesn’t make sense if T cell mediated)

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15
Q

pyridostigmine

A

inhibits cholinesterase

Tx: myasthenia gravis

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16
Q

subacute bacterial endocarditis

A

type III (IgG complex): S. viridans (normal flora) antigen = inflammation of endocardium (typically previous damage to heart valves- rheumatic fever or congenital)
mediated by phagocytes that recognize opsonized bacteria (IgG and C3b) and anaphylatoxins
glomerulonephritis

17
Q

mixed essential cryoglobulinemia

A

type III (IgG complex): rheumatoid factor IgG complexes (with or without HCV antigens)
most often: pt with B cell proliferative disorder (multiple myeloma or Waldenstrom macroglobulinemia)
systemic vasculitis
Meltzer’s triad: purpura, arthralgia, myalgia

18
Q

systemic lupus erythematous

A

type III (IgG complex): DNA, histones, ribosomes, snRNP, scRNP
glomerulonephritis, vasculitis, arthritis, neurological
symptoms: fever, malais, joint pain, myalgias, fatigue, butterfly facial rash
Tx: anti-inflammatory
women, Asian and African descent
highly variable severity
*positive direct Coomb’s, blood in urine, reduced in complement C1 levels

19
Q

cryoglobulins

A

immunoglobulins that become insoluble at reduced temperature

sometimes only light chains (Bence Jones proteins)

20
Q

Type 1 diabetes (insulin-dependent DM)

A

type IV: pancreatic beta cells
Beta cell destruction
CTL effectors
European descent
untreated symptoms: many and can lead to coma and death
Tx: pig/bovine insulin (immune responses directed against foreign insulin can cause an immune complex hypersensitivity) or human recombinant insulin

21
Q

Rheumatoid arthritis

A
type IV: unknown synovial joint antigen
auto reactive T cell
Anti-CCP
joint inflammation and destruction
Dx: production of IgG, IgM, and IgA (rheumatoid factor) specific for the Fc region of Ab molecules (rheumatoid factor not req. for Dx)
most common rheumatic disease
Tx: infliximab and rutiximab
22
Q

Multiple sclerosis

A

type IV: myelin basic protein, proteolipid protein
TH1 effector cells directed at myelin sheath (macrophages)
sclerotic plaques in white matter of CNS
brain degeneration, paralysis
symptoms: motor weakness, impaired vision, lack of coordination, spasticity
Dx: oligoclonal bands of IgG in CSF
Tx: immunosuppressive drugs and IFN-b1

23
Q

infliximab

A

anti-TNF-alpha
– TNF-alpha made by TH1 effector cells
Makes sense to treat RA

24
Q

Sjogren’s syndrome

A

type IV: exocrine glands that produce saliva and tears
symptoms: dry eyes and mouth, sometimes skin, nose and vaginal dryness
can also effect kidney, blood vessels, liver, brain
Dx: Schirmer test to measure tear production, ANA, and rheumatoid factor
second most common rheumatic disease (rheumatoid factor not req. for Dx)
Tx: artificiae tears, goggles

25
Q

Guillain Barre

A

type II: gangliosides
demyelination
molecular mimicry: Camplobacter jejuni
symptoms: symmetrical weakness of lower limbs, rapidly ascends to upper limbs and face, difficulty swallowing and breathing, drooling (usually regain most motor function with Tx)
Tx: plasma exchange with immunosuppressive drugs

26
Q

Miller-Fisher

A

form of Guillain Barre

starts with facial muscles and descends

27
Q

Wegener’s Granulomatosis

A

type II: molecular mimicry: viral or bacterial infection that cross-reacts with neutrophil determinants
ANCAs (anti-neutrophil cytoplasmic antibodies) pind to neutrophils -> activate them -> up regulate adhesin molecules-> bind vascular endothelial cells->degranulate-> vasculitis
symptoms: rhinitis and conjunctivitis; lung infiltrates, rapidly progressing kidney dysfunction leading to glomerulonephritis, granulomas found in all infected tissue
Tx: plasma exchange and anti-inflammatory drugs