Immunopathology Associations Flashcards by Tiarnán Byrne | Brainscape

Q

Attacks synovial joints

A

Rheumatoid Arthritis, often progresses to synovial joint destruction. Also targets tendon sheathes and bursae

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Q

Autoimmune form of arthritis

A

Rheumatoid Arthritis

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Q

Arthritis that peaks age 40, but can become symp in 40’s

A

Rheumatoid Arthritis

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Q

Arthritis, more common in females than males

A

Rheumatoid Arthritis

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Q

HLAB4 is a haplotype of this arthritis.

A

Rheumatoid Arthritis

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Q

Type of arthritis that increase in prevalence with increase in latitute?

A

Rheumatoid Arthritis

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Q

Histological Pathogenesis of Rheumatoid Arthritis.

A

Synovial edema and sparse mononuclear infiltrate.
Synovial aggregates of mononuclear cells, CD4+ THELPER Cells, Plasma cells, Dendritic cells, Macrophages
Synovial hyperplasia with villous change
Increased synovial vascularity
Organising fibrin on synovial surface and neurtophils on synovial surface and in joint space.
Osteoclast activation = osteoporosis, junta-articular erosions, sub-chondral cysts.
Mass of boggy inflammed synovium PANNUS, can erode cartilage, bone and ligament.
Joint destroyed. Loss of articular cartilage. Fibrous ankylosis or Unstable

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Q

Mass of boggy inflammed synovium that can erode cartilage, known as what? Seen in What?

A

PANNUS

Rheumatoid Arthritis

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Q

Signs and symptoms of PANNUS/Rheumatoid Arth?

A

(4 basic signs of inflammation)

Calor
Rubor (
Tumour (swelling)
Dolar (pain)

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Q

Common site to observe synovial joint destruction

A

Metacarpal/interphalangeal joints

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Q

HLA-DRB1

A

Rheumatoid Arthritis.

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Q

TH17

A

Neutrophil recruitment – Rheumatoid Arthritis

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Q

TH1

A

Interferon Gamma (y) – Rheumatoid Arthritis

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Q

Cartilage Matric Metalloproteases

A

Rheumatoid Arthritis

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Q

Immune Complexes

A

Rheumatoid Arthritis

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Q

RANKL

A

Rheumatoid Arthritis

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Q

TNF

A

Rheumatoid Arthritis

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Q

Stiffness WORSE in the Morning

A

Rheumatoid Arthritis

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Q

Pain on movement of joint

A

Rheumatoid Arthritis

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Q

Small non-weight bearing joints (Hands and Feet, C-Spine)

A

Rheumatoid Arthritis

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Q

Important test pre-intubation

A

Sign of RA on the Neck = X-Ray, Lateral and an AP. Shows narrowing, bony erosions etc.

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Q

Treatment for Rheumatoid arthritis?

A

Total Joint Replacement

Joint Fusion.

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Q

Arthritis usually sparing hips and rest of spine?

A

Rheumatoid Arthritis

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Q

Symmetrical arthritis

A

Rheumatoid Arthritis

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Q

Z-deformities (thumb)

A

Sign of Joint Destruction in Rheumatoid Arthritis

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Q

Boutoniere deformities (V at interphalageal joint)

A

Sign of Joint Destruction in Rheumatoid Arthritis

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Q

Swan neck deformities

A

Sign of Joint Destruction in Rheumatoid Arthritis

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Q

Ulnar deviation (fingers towards little finger)

A

Sign of Joint Destruction in Rheumatoid Arthritis

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Q

Volar subluxation (enlargement at knuckles caused by tendon slip)

A

Sign of Joint Destruction in Rheumatoid Arthritis

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Q

Joint Effusions

A

Sign of Joint Destruction in Rheumatoid Arthritis

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Q

Juxta-articular osteopaenia

A

Sign of Joint Destruction in Rheumatoid Arthritis

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Q

Erosions

A

Sign of Joint Destruction in Rheumatoid Arthritis

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Q

Joint Space Narrowing

A

Sign of Joint Destruction in Rheumatoid Arthritis

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Q

Subluxations

A

Sign of Joint Destruction in Rheumatoid Arthritis

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Q

Secondary Amyloidosis

A

Protein Misfolding. Seen in…

Rheumatoid Arthritis.

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Q

Serosistitis

A

Inflammation of the serosa. Seen in…

Rheumatoid Arthritis

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Q

Caplans Syndrome

A

Rheumatoid arthritis (RA) and pneumoconiosis combination.

Manifests as intrapulmonary nodules, which appear homogenous and well-defined on chest X-Ray

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Q

Felty’s Syndrome

A

Combination of heumatoid arthritis, splenomegaly and neutropenia.

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Q

Sicca’s (Sjogrens) Syndrome

A

Chronic autoimmune disease in which the body’s white blood cells destroy the exocrine glands, specifically the salivary and lacrimal glands, that produce saliva and tears, respectively.[2] The immune-mediated attack on the salivary and lacrimal glands leads to the development of xerostomia (dry mouth) and keratoconjunctivitis sicca (dry eyes), which takes place in association with lymphocytic infiltration of the glands.

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Q

Vasculitis

A

Rheumatoid Arthritis

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Q

Pneumonitis

A

Rheumatoid Arthritis

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Q

Rheumatoid Nodules

A

Rheumatoid Arthritis

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Q

Serology of Rheumatoid Arthritis

A

Rheumatoid factor (80%)
non-specific
Antibodies (usually IgM) against IgG Fc portion
Marker for activity
APCA (anti-citrullinated peptide antibodies)
Specific for RA

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Q

Rheumatoid Factor

A

Seen in 80% of Rheumatoid Arthritis
non-specific
Antibodies (usually IgM) against IgG Fc portion
Marker for activity

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Q

Anti-Citrullinated Peptide Antibodies (ACPA) (AKA ACCP)

A

Rheumatoid Arthritis (Specific)

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Q

ACR/EULAR 2010 Criteria

A

Rheumatoid Arthritis
Points for:
	Joint Involvement
	Serology
	Acute phase reactants
	Duration of symptoms

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Q

Degenerative arthritis

A

Osteoarthritis

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Q

Arthritis affecting articular cartilage, with a periarticular bone response

A

Osteoarthritis

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Q

Mechanical degradation of joints

A

Osteoarthritis

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Q

Arthritis associated with old age?

A

Osteoarthritis

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Q

COL2A1 gene

A

Familial Osteoarthritis

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Q

WNT signalling, Prostaglandin pathways

A

Osteoarthritis

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Q

Local factors affecting loading and wear (point loading)
“Secondary Osteoarthritis”
	Injury
	Obesity
	Instability
	Hypermobility
	Joint dysplasia
	Neuropathy

A

Secondary Osteoarthritis

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Q

Chondrocyte Proliferation?

A

Osteoarthritis

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Q

Stages of osteoarthritis?

A

Chondrocyte Proliferation
Mediator Release
Cartilage Remodelling
Secondary Changes in Bone and Synovium
(Cystic Changes)
Loss of cartilage with subchondral bony change

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Q

Loss of cartilage with subchondral bony change

A

Osteoarthritis

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Q

Cystic Changes in Bone and Synovium

A

Osteoarthritis

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Q

Arthritis in PIP’s, 1sr MCP and 1st MTP joints

A

Osteoarthritis

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Q

Arthritis in Lumbar and Cervical Spine

A

Osteoarthritis

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Q

Deep, achy pain
Worsens with use
Short-lived morning stiffness

A

Osteoarthritis

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Q

Crepitus

A

Osteoarthritis

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Q

Decreased range of movement

A

Osteoarthritis

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Q

Subchondral Sclerosis

A

Osteoarthritis

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Q

Subchondral Cysts

A

Osteoarthritis

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Q

The Secondary Osteoarthritis.

A

Metabolic – Gout &
Pseudogout (Chondrocalcinosis)
Infectious / Septic Arthrits

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Q

The Seronegative immune mediated joint disorders

A

Ankylosing spondylitis
Reactive arthritis/Reiter syndrome
Enteropathic arthritis
Psoriatic arthritis

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Q

Joint disorder common in 6wks

A

Juvenile Idiopathic Arthritis

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Q

6wks affecting fewer than 4, mostly larger joints, ANA positive?

A

Oligoarthritis (Juvenile Idiopathic Arthritis Subtype)

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Q

6wks affecting more than 4, mostly smaller joints, RF+ positive? With poorer prognosis

A

Polyarthritis (Juvenile Idiopathic Arthritis Subtype)

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Q

ANA

A

Oligoarthritis (Juvenile Idiopathic Arthritis Subtype)

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Q

RF+

A

Polyarthritis (Juvenile Idiopathic Arthritis Subtype)
Ddx
10% of Psoriatic Arthritis

Sjogrens (75%)

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Q

Stills Disease

A

Systemic Onset JIA

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Q

Joint pain in 5yo

A

Systemic Onset JIA. Also...
Fever
Rash (salmon-pink)
Lymphadenopathy
Organomegaly
Serositis / Hepatitis

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Q

Joint pain and inflammation
Fever
Rash (salmon-pink)
Lymphadenopathy
Organomegaly
Serositis / Hepatitis

Patient 5yo and more likely female

A

Systemic Onset JIA or Stills Disease

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Q

Seronegative destruction of articular cartilage and bony ankylosis

A

Ankylosing spondylitis.

Usually affect sacro-iliac and apophysial joints

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Q

Arthropathy in sacro-iliac and apophysial (facet joints)

A

Ankylosing spondylitis

Ddx
HLA-B27+ Enteropathic Arthritis

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Q

Seronegative arthritis more common in males, average more common in mid-20’s

A

Ankylosing spondylitis

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Q

Question mark spine

A

Ankylosing spondylitis

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Q

Schober’s test (limited flexion (

A

Ankylosing spondylitis

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Q

Uveitis

A

Ankylosing spondylitis

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Q

Aortitis

A

Ankylosing spondylitis

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Q

HLA-B27

A

95% w/Ankylosing spondylitis are HLA-B27+
8% of Caucasian population = HLA-B27+

80% w/Reactive Arth/Reiters are HLA-B27+

Enteropathic Arthritis w/sacroiliitis or spondylitis

Psoriatic Arthritis

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Q

Arthritis (sausage finger, bony spurs)
\+
Nongonococcal urethritis/cervicitis (+/- circinate balanitis)
\+
Conjunctivitis

A

Reactive Arthritis/Reiter Syndrome
Also,
+/- oral ulceration, heart block, aortic regurgition

50% is chronic and resembles Ankylosing Spondylitis.

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Q

Arthritis within weeks after shigella, salmonella, yersinia, campylobacter or chlamydia.

A

Reactive Arthritis/Reiter Syndrome

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Q

Arthritis of mostly men 20-40

A

Reactive Arthritis/Reiter Syndrome
Or
Ankylosing Spondylitis

Ddx
Possible Rheumatoid (early)

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Q

Less severe symptoms that reiter but nonetheless following infection?

A

Enteropathic Arthritis

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Q

Arthritis found in 10-15% of IBD patients

A

Enteropathic Arthritis

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Q

Asymmetrical arthritis of lower limb

A

Enteropathic Arthritis

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Q

Seronegative (in 90%) arthritis associated with psoriasis 20-40yo?

A

Psoriatic Arthritis (10% RF+)

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Q

HLA-CW6

A

Psoriatic Arthritis

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Q

Arthritis usually DIP, dactylitis, sausage finger/TOE 33%.
Also sometimes ankles, knees, hips, SI and facet joints
Asymetric, Histo resembling RA but not as destr.

A

Psoriatic Arthritis

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Q

“telescopic fingers” “whittling”

A

Arthritis mutilans due to osteolysis seen in 5% of Psoriatic Arthritis cases

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Q

“Pencil in cup”

A

Erosive but central not peripheral

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Q

Iritis and conjunctivitis

A

Psoriatic Arthritis

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Q

Hyperuricaemia

A

Gout (w/intraarticular sodium urate chrytals)

10% have hyperuricaemia, only 0.5% have gout

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Q

Intraarticular sodium urate chrystals

A

Gout (w/hyperuricaemia)

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Q

Arthritis of elderly with heavy male predominance.

A

Gout

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Q

Pathogenesis of Gout

A

Hyperuricemia
Urate precipitates in joints forming crystals

Activation of complement and kinen system
Neutrophil chemotaxis
Release LTB4, prostaglandins and free radicals causes tissue inflamm.
Neutrophils phagocytose crystals, causing lysis of neutrophils .
Release of lysosomal enzymes leads to tissue inflaCammation.
Phagocytosis by macrophages
Leads to release of IL-1Beta and other cytokines in joint (resulting in further neutrophil chemotaxis)
Release of proteases leads to tissue inflammation.

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Q

Podgara

A

Acute Arthritis Gout

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Q

Gouty Tophi

A

Chronic Arthritis Gout

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Q

Large cause of mortality in gout?

A

Gouty nephropathy (20% of gout mortality)

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Q

Uurate overproduction due to:
Diet
Enzyme defects (known and unknown)
Decreased excretion

A

Primary Gout (90%)

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Q

Overproduction of Urate

Increased cell turnover
Inborn errors of metabolism

Reduced excretion
-Chronic renal failure

A

Secondary Gout (10%)

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Q

Chrystal Arthritides

A

Pseudogout

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Q

Calcium pyrophosphate dihydrate deposition disease

A

Pseudogout

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Q

Acute pain and swelling in knee, wrist or shoulder

A

Pseudogout

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Q

Chondrocalcinosis

A

(Calcification of fibro and hyaline cartilage)

= Pseudogout

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Q

Calcification of fibro and hyaline cartilage

A

Pseudogout

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Q

Low Phosphate

A

Pseudogout

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Q

Low Magnesium

A

Pseudogout

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Q

Increase PTH

A

Pseudogout

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Q

Arthropathy associated with Wilsons disease?

A

Pseudogout

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Q

Arthropathy associated with Haemachromatosis?

A

Pseudogout

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Q

Arthropathy associated with Alkaptonuria disease?

A

Pseudogout

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Q

Weakly positively birefringent rhomboid crystals on polarisation.
May be cloudy and associated with fever and ↑ peripheral WCC

A

Result from joint aspirate

=Pseudogout

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Q

Treatment for Pseudogout

A

Supportive

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Q

Should be excluded first in Dx of pseudogout?

A

Septic Arthritis

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Q

Negatitive birefringment

A

Gout

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Q

Hot, Red, one joint?

A

Septic Arthritis

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Q

Routes to septic arthritis?

A

Direct inoculation through injury
Direct spread from adjacent infection
Haematogenous spread

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Q

Common causative organisms in Septic Arthritis?

A

Haemophilus influenzaepredominates in children under age 2 years,

Staph. Aureus:older children and adults,

Gonococcus: young adulthood. mainly in sexually active women

Individuals with sickle cell disease are prone to infection withSalmonellaat any age.

Gram negative bacilli (elderly),

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Tests in Septic Arthritis?

A

Aspirate
Stain
Culture

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Q

HLA-B8

A

Sjogrens

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Q

HLA-DR3

A

Sjogrens

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Q

Sjograns w/o RA?

A

Primary Sjogrens

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Q

Salivary gland enlargement F>M

A

Sjogrens

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Q

Risk lymphoma 1.16 (MALTOMA)

A

Sjogrens

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Q

Investigations in Sjogrens?

A

Lip biopsy

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Q

Lip Biopsy in Sjogrens

A

Periductal and perivascular CD4+ TH cells, B cells, plasma cells , fibrosis

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Q

Anti-Ro

A

Sjogrens (90%) also RF (75%)

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Q

Schirmer Tear Test

A

Sjogrens

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Q

Syndrome common in Turkey, Iran and Japan?

A

Behcet’s Syndrome

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Q

HLA-B51

A

Behcet’s Syndrome

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Q

Genital ulcers
Eye: Uveitis (anterior or posterior) Retinal vasculitis
Skin: Erythema nodosum, Pseudofolliculitis, Papulopustular lesions

Pathergy
Minor skin injury precipitates pustules in a couple of days
±Constitutional symptoms

A

Behcet’s Syndrome

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Q

Anti-La

A

Sjogrens (60-90%)

SLE (10-15%)

Q

MPO-ANCA

A

Anti-myeloperoxidase ANCA

=Microscopic PolyAngiitis
&
=Churg-Strauss Δ
- necrotising vasculitis
- asthma
- allergic rhinitis
- pulmonary infiltrates
- increased circulating eosinophils
- necrotizing granulomas (extrvascular)

Q

necrotising vasculitis
asthma
allergic rhinitis
pulmonary infiltrates
increased circulating eosinophils
necrotizing granulomas (extrvascular)

A

Churg Strauss Syndrome

Q

PR3-ANCA

A

Anti-proteinase-3 ANCA
= Wegener’s Granulomatosis
- Upper airways (necrotising granulomas)
- Necrotising granulomatous vasculitis (small-medium vessels)
- Necrotising glomerulonephritis

Q

Upper airways (necrotising granulomas)
Necrotising granulomatous vasculitis (small-medium vessels)
Necrotising glomerulonephritis

A

Wegners Granulomatosis

Q

Autologous

A

Self Organ Donation (graft etc)

Q

Syngeneic

A

Monozygotic (identical) siblings

Q

Allogeneic

A

Living or Cadaveric (Another genetically different person donor)

Q

Umbilical Cord Blood

A

Cord blood is collected because it contains stem cells, which can be used to treat hematopoietic and genetic disorders.

Q

Xenograft

A

From animal e.g. Pig heart valves

Q

Issues in Organ Transplant besides rejection

A

Technical
Cold ischaemia time
Reperfusion injury
Functional status and co-morbidity of recipient
Rejection/Immunosuppression (Infection, Post-transplant-lymphoproliferative disease PTLD (EBV- mediated), Neoplasia - HPV SCC, HHV8 -Kaposi, Lymphoma)
Recurrence (viral, primary FSGS, mesangiocapillary GN, diabetic and IgA nephropathy)

Q

Rate of 5-10y graft survival?

A

(80%)

Q

Rate of 10-20y graft survival?

A

(50%)

Q

Definition of transplant rejection?

A

Aka HOST versus graft
“A process whereby the transplant recipient’s immune system recognizes the graft as foreign and attacks it with potential adverse effects on its viability and function”

Q

Rejection Antigens?

A

MHC (Minor HC antigens account for GVHD in Human Leucocyte Antigen - identical Bone Marrow Transplant)
ABO
Others

Q

MHC

A

Major Histocompatability Complex
Mediated Graft Versus Host disease in HLV identical BMT

Seen in Hyperacute rejection (MHC1)

Q

ABO

A

Most important blood type system (or blood group system) in human blood transfusion. The associated anti-A and anti-B antibodies are usually IgM antibodies, which are produced in the first years of life by sensitization to environmental substances, such as food, bacteria, and viruses.

Q

No HLA, but ABO compatibility required?

A

Cardiac and Liver transplant

Q

HLA and ABO compatibility min requirement?

A

Pancreas Transplant

Q

Extensively matched 
ABO (ABO mismatched are possible)
\+
HLA (mostly DR)
\+
X-matched for preformed antibodies

A

Kidney Transplant

Q

ABO Compatibility Essential

HLA as possible

A

Bone Marrow Transplant

Q

T-Cell Mediated Rejection?

A

Cellular Rejection (as opposed to humeral)

Cytotoxic T-Cells
\+
Cytokine Sectreting CD4+ T-Cells
\+
Activated Microphages.

Q

Role of Cytotoxic T-cells in transplant rejection (HVGD)

A

Kill cells in the grafted tissue, causing parenchymal and, perhaps more importantly, endothelial cell death (resulting in thrombosis and graft ischemia).

Q

Role of Cytokine Secreting CD4+ T-Cells in transplant rejection (HVGD)?

A

Trigger DTH (delayed type hypersensitivity), with increased vascular permeability and local accumulation of mononuclear cells (lymphocytes and macrophages).

Q

Role of Activated Macrophages in transplant rejection (HVGD)?

A

Injure graft cells and vasculature.

Q

DTH

A

Trigger DTH (delayed type hypersensitivity), with increased vascular permeability and local accumulation of mononuclear cells (lymphocytes and macrophages).

Q

Autoimmune reaction resulting in rejection of graft?

A

Humeral Rejection
Type II (Autoantibody)  immune response.

Q

Classification of Transplant Rejection?

A

Hyperacute
(Accelerated Acute)
Acute
Chronic

Q

Cyanotic, mottled and flacid graft on removal of vascular clamps in Operating Room?

A

Hyperacute Rejection

Q

Rejection involving complement fixing

A

Hyperacute Rejection

Q

Graft rejection in less

A

Hyperacute Rejection

Q

Treatment or hyperacute rejection?

A

Organ Removal

Q

Rejection involving preformed antibodies? Name the antibody types?

A

MHC 1 or ABO, mothers, previous transfusions and transplants)

Q

Fibrinoid necrosis of vessels and Cortical Infarction in transplant rejection?

A

Hyperacute Rejection

Q

Process which has reduced the incidence of hyperacute transplant rejection?

A

Cross Matching

Q

Monitoring of query “Hyperacute rejection’?

A

U/S Doppler ofr BF or Duplex

Q

Transplant rejection over 1-5 days

A

Accelerated Acute Rejection

Q

Non-complement fixing rejection

A

Accelerated Acute Rejection

Q

FcR-bearing cells (T-Cells – primarily Cytotoxic)

A

Accelerated Acute Rejection

Q

Rejection, can be humeral or cell mediated, but is more commonly cell mediated?

A

Accelerated Acute Rejection

Q

Rejection that often relapses?

A

Accelerated Acute Rejection

Q

Treatment for Accelerated Acute Rejection?

A

Immosuppression, but only partially effective.

Transplant removal often required.

Q

Rejection between 6-90 days?

A

Acute Rejection

Q

Type of rejection, common (10-30%) in Kidney transplants?

A

Acute Rejection

Q

Anti-CD20

A

Treatment used in humoral acute rejection.
On CD4 staining.
Also seen = Polyconal Immunoglobulin, Plasmapharesis

Q

Plamaphaesis

A

Treatment in humoral acute rejection. On CD4 staining. Also used = Plasmapharesis and Anti-CD20

Q

Polyconal Immunoglobulin

A

Treatment in humoral acute rejection.
On CD4 staining.
Also used = Polygonal Immunoglobulin and Anti-CD20

Q

ATG (Anti-Thymocyte Globulin)

A

Anti-thymocyte globulin is used in the treatment of vascular acute rejection. Along with ALG.

Q

ALG (Anti-lymphocyte globulin)

A

ALG is used as a treatment for vascular acute transplant rejection. Along with ATG

Q

Treatment for acute transplant rejection?

A

Cellular
	Steroids
Vascular
	ATG, ALG
Humoral
	C4 staining 
	Polyconal immunoglobulin, plasmapharesis, antiCD20

Q

Rejection characterised by loss of function w/o fever?

A

Acute Rejection.

Q

Pathogenesis an Tx targets of Acute Rejection?

A

Endothelium is main target of pathology
CD4+ and CD8+ infiltrate (glomerular and tubular damage and endothelitis)
Necrosis
Heart: Lymphocyte infiltrate and myocyte damage
Vascular response may be subacute proliferation and fibrosis
Responds to aggressive immunosuppression (particularly anti-T cell strategies)

Progression to chronic rejection common

Q

Rejection marked by an interstitial mononuclear cell infiltrate with associated edema and parenchymal injury,

A

Cellular Acute Rejection

Q

Rejection marked by necrotizing vasculitis with thrombosis (when less acute mimics arterioscleotic thickening)

A

Humeral Acute Rejection (Antibody medicated)

Q

Rejection over months/years

A

Chronic Rejection

Q

Obliterative intimal fibrosis
Glomeruli
Coronary arteries

A

Vascular damage associated with Chronic Rejection

Q

Interstitial fibrosis
Tubular atrophy
Vanishing bile duct syndrome
Bronchiolitis obliterans
Gross scarring and shrinkage

A

Chronic Rejection

Q

Relatively refractory with progressive loss of graft function

A

Chronic Rejection

Q

Why are chronic rejections the most common?

A

Immunosuppresents so good it drags rejection out

Q

Suspected mechanism behind chronic rejection?

A

Recipient cells present MHC from the recipient organs

Q

Difference between direct and indirect cellular rejection?

A

Own (indirect) versus donor (direct) antigen presenting cells (APC’s) which are presenting the MHC (always from donor).

Q

Indirect cellular rejection

A

Usually chronic rejection

Q

Methods for improving graft survival?

A

Better Matching

2. Immunosuppression

Q

Better HLA matching improves Graft survival?

A

Yes but….

As drugs for immunosuppression have improved, HLA matching is not even attempted in some situations, such as heart, lung, and liver transplantation; in these cases, the recipient often needs a transplant urgently.

Q

Cyclosporine (FK506)

A

Immunosuppressant

Q

Anti lymphocyte Globulins

A

Immunosuppressant

Q

Monoclonal Antibodies (e.g. Monoclonal Anti-CD3)

A

Immunosuppressant

Q

Squamous cell carinoma a side effect of which type of drug?

A

Immunosuppressants

Q

Kaposi sarcoma a s/e of what drugs? Where else seen?

A

Immunosuppressants/HIV progression to AID’s

Q

Lymphomas as s/e?

A

Immunosuppressants

Q

Presensitisation?

A

Now Countered by cross-matching
Irradiated to leucocyte deplete

Questionable increase in tolerance

Q

Tx for Aplasia/neoplasias/Herediatary immunodeficineies or metablic abnormalities?

A

Bone Marrow Transplantation

Q

Mortality in BMT patients?

A

20-40%

Q

BMT graft sources

A

Allogenic (Match sibling or unrelated doner)

Autologous

Q

BMT graft types

A

Bone Marrow
Peripheral Stem Cells (mat. T-cells)
Cord Stem Cells

Q

Graft manipulation for BMT

A

T-Cell Depletion (less GVHD, Less successful engraftment, Less graft v tumour)
Stem Cell (CD34+) Enrichment

Q

Sequence for BMT Transplantation

A

Matchining (fully matched sibling can be used whole)
Viral Status (esp. CMV)
Conditioning of Recipient (eliminate residual immune system. Note: not required in Sever Combined Immune Deficiency (SCID).
Immunosuppression
Growth factor support.
Supportive blood products (CMV-)

Q

Low Risk CMV group in BMT

A

CMV- Recipient, CMV- Donor

Q

High Risk CMV group in BMT

A

CMV+ Recipient

w/wo CMV+ Donor

Q

Lenght of post BMT neutropenia?

A

Should lift be 21 days

Q

Time to NK cells post BMT?

A

1 month

Q

Time to T-Cells post BMT?

A

Depends on T-Cell
1-24 for most.
Some never return.
Depends too on immunosuppression

Q

Time to B-Cells post BMT?

A

Slow production for 1st 3months

If rapid in 1st 3mts then suspect autologous reconstitution or lymphoproliferative disease.

Plateaus out at between 6-9 months

Q

IgM, IgG, IgA normalisation post BMT?

A

6-24 months

Q

Vaccination post BMT?

A

Follow guidelines

No BMT.

Q

Immunocompetent donor T-cells recognize a mismatch with recipient HLA and initiate an immune response against an immunologically vulnerable host

A

Graft Versus Host Disease (GVHD)

Q

Rate of GVHD in BMT?

A

30-50%

Q

Transplants associated with GVHD?

A

BMT (30-50%)
Blood Transfusion
Solid Organs, commonly LIVER (immune organ CD4+8 cells, transplanted a lot) (others =occasionally)

Q

Minor histocompatibility antigens
Non-MHC encoded polymorphisms
Cytokine polymorphisms

A

Mechanism of GVHD which avoid “Matching”

Occasionally seen in autologous transplants die t re-emergence of autoreactive t-cells

Q

Rejection in

A

Acute GVHD

Q

Maculopapular rash +

Hepatosplenomegaly

A

Acute GVHD

Q

Treatment for Acute GVHD?

A

Aggressive and early

Steroids + Anti-T-Cell agents + Anti-TNFalpha

Q

Types of Chronic GVHD?

A

Progressive (worst Px)
Interrupted
De novo (best Px)

Q

Similar in appearance to systemic scleosis and Sjogrens?

A

Chronic GVHD

Q

Tightening of skin around the mouth
Portal system of the liver
White out lung disease (acute vascular information)
GI fibrosis and dysmotilty

A

Chronic GVHD

Q

Granulomatous arteritis of the aorta and larger vessels with a predilection for the extracranial branches of the carotids

A

Giant Cell Arthritis

Q

Older person

Unilateral Headache, facial pain and scalp tenderness.

A

Giant Cell Arthritis

Q

Arteritis far more common in the elderly (>50) and affect F>M, 2:1?

A

Giant Cell Arthritis

Q

Commonest primary systemic vasculitis

A

Giant Cell Arthritis

Q

ESR adjusted for age and CRP if this condition is suspected.

A

Giant Cell Arthritis

Q

25% of those with this go blind?

A

Giant Cell Arthritis

Q

Tx in Giant Cell Arthritis affecting eye

A

Corticosteroids can reduce initial inflammation.

Q

Skip Lesions

Often associated with polymyalgia rheumatica

A

Giant Cell Arthritis

Q

Bilateral neck, shoulder and low back
pain and stiffness. 
Worse in the morning
Malaise, tiredness, weight loss, depression and fever. 
Elevated ESR and CRP.

A

Polymyalgia Rheumatica

Q

Tx for Polymyalgia rheumatica?

A

Responsive to steroids

Q

HLA-DRB1*04

A

Polymyalgia Rheumatica

Q

HLA-DRB1*01

A

Polymyalgia Rheumatica

Q

Arthritis with temporal relationship to outbreaks of…

Parainfluenza
Parvovirus B19
Mycoplasma
Chlamydia

A

Polymyalgia Rheumatica

Q

Association between GCA and polymyalgia rheumatica?

A

50% of patients with Giant Cell Arteritis have symptoms of PMR and up to 20% of PMR patients have biopsy findings of GCA

Q

Pulseless Syndrome

A

Takayasu Arteritis

Q

Patient in upper limbs may have a weak or absent pulse

A

Takayasu Arteritis

Q

Granulomatous thickening of the aortic arch, which primarily affects the brachial artery yeilding a pulsless upper limb

A

Takayasu Arteritis

Q

Arthritis affecting young adults?

A

Polyarteritis Nodosa

Q

Artritis affecting mostly small and medium arteries?

A

Polyarteritis Nodosa

Q

Artritis associated with
Abdo pain and melaena
Renal Disease (renal artery affected)
Rash

A

Polyarteritis Nodosa

Q

Virus associated with Polyartritis Nodosa?

A

Hepatitis B

Q

Necrotising Vasculitis?

A

Polyartrirs Nodosa

Q

Histological signs of Polyartritis Nodosa?

A

Fibrinoid Necrosis

Multiple Thrombosis

Q

Erythema of hands and fee (cutaneous) and of eyes and mouth (muco) t, e in children?

A

Query Kawasaki disease.

Q

Artritis affecting large, small and medium arteries in children?

A

Kawakaski

Q

Sex affected more by kawasaki?

A

Male

Q

Lymph and Cardiac Signs of Kawasaki Disease?

A

Lymph = Cervical Lymphadenopathy

Coronary Arteries = Aneurysm and MI

Q

Anti-endothelial and smooth muscle antibodies

A

Kawakaski

Q

Young men

A

Buerger’s Disease(Thromboangitis Obliteran)

Q

Small Vesses Vasculitis?

A

Microscopic Polyangitis
Wegner’s Granulomatosis
Churg-Straus
Henoch-Schonlein Purpura

Q

P-ANCA, purpura, lungs, kidneys, cvs, git, necrotizing glomerular nephritis, exogenous antigens from drugs , blood and infections.

A

Microscopic Polyangitis

Q

Triad:
Renal Disease
Chronic Sinusitis
Pneumonitis

ANCA+

A

Wegner’s Granulomatosis (Tx = Rapid Immunosup)

Q

Typically affects vessels of respiratory tract, strongly associated with asthma, eosinophilia and pulmonary infiltrates. May also have GI Sx (e.g. colitis, bleeding) +/- cardiac +/- peripheral neuropathy Sx’s.

P-ANCA+ and IgE

A

Churg-Straus Syndrome (Tx = Glucocortiocids +Support)

Q

Small vessel IgA & immune complex mediated vasculits often following upper-RTI in young children

Giveaway is lesions on the buttocks and legs

A

Henoch-Schonlein Purpura

Q

Ability of a test to indicate a negative result in the absence
of disease.

A

Specificity

Q

Ability of a test to indicate a positive result in the presence
of disease.

A

Sensitivity

Q

Immune complex mediated disease affecting any organ with diverse manifestations and variable prognosis?

A

Systemic Lupus Erythematous

Q

SLE affects who?

A

Females x9 more
20-30’s
60% Concordance in Twins.

Q

Varients of SLE limited only to the skin?

A

Discoid lupus erythematosus

Subacute cutaneous lupus

Q

Butterfly rash

A

Systemic Lupus Erythematous

Q

Arthralgia and arthritis with skin and haematological abnormalities?

A

Systemic Lupus Erythematous

Q

Haematological features of SLE?

A

Immune thrombocytopaenia
Haemolytic anaemia
Autoimmune neutropaenia

Q

Anti-nuclear antibody (ANA)
Anti-dsDNA antibody
ENA antibodies
Anti-RBC antibody
Anti-cardiolipin & lupus anticoagulant

A

All auto-antibodies of Systemic Lupus Erythematous

Q

Inflammation & organ dysfunction due to Immune Complex deposition in the vasculature of affected organs

A

SLE

Q

Dx for SLE?

A

Clinical Hx & examination
Urinalysis & urine microscopy
Assess function of potentially involved organs.

Autoantibodies (Indirect immunofluoresence)

DIFF= Skin /Renal

Q

Detection of Anti-Nuclear Antibodies?

A

Indirect Immunofluoresence

Q

ANA patterns

A

Homogenous
Speckled
Centromere
Nucleolar

Q

ANA reactivity clarification?

A

ELISA, RIA and Immunoblotting

Q

Anti-bodies to double stranded DNA?

A

Highly Specific for SLE

Q

Anti-Sm (30%)
Anti-Ro (30%)
Anti-La

A

30% specific (except La) each for SLE

All are anti-ENA (extractable nuclear antigen).

Q

ELISA meaning?

A

Enzyme Linked ImmunoSorbant Assay

Q

Jo-1

A

30% of Polymyosistitis

Q

RNP

A

100% Mixed Connective Tissue Disease

Q

Scl-70

A

A poor prognostic indicator for Scleroderma.

Q

Most common glomerular disease?

A

IgA nephropathy.

Q

IgA immune complexes deposited in mesangium.

A

IgA nephropathy.

Q

Anti-GBM antibody

A

Goodpastures

Q

Anti-CCP

A

Rheumatoid Arthritis

Q

DR4 and DR1

A

Rheumatoid Arthritis

Q

Citrulline

A

Rheumatoid Arthritis

Q

Principle Antibodies in Rheumatoid Arthritis

A

Anti CCP (Specific 97%, sensitive 88%)
RF (Specific 65%, Sensitive 50-90%)

Q

Anti-PR3+

A

Granulomatosis with Polyangitis (GPA)

Q

Treatment for Granulomatosis with Polyangitis?

A

Cyclophosphamide

Q

Anti-ACHr (receptor)

A

Myasthenia Gravis

Q

Anti-MUSK (muscle specific tyrosine kinase)

A

Found in some anti-AchR negative MG

Q

IgA EMA

A

Coeliac (90-100% sensitive and specific)
Dermatitis herpetiformis (50-70% sensitive, 90-100 specific)

False negative – gluten free diet

Q

Commonest malignant disorder of plasma cells

A

Multiple Myeloma

Q

Age of onset in Multiple Myeloma?

A

After age 50 yrs

Q

> 20% Abnormal looking BM plasma cells

A

Multiple Myeloma

Q

Paraprotein in blood and/or urine

A

Multiple Myeloma

Q

Bone destruction with osteoporosis or lytic lesions

A

Often seen in Multiple Myeloma

Q

Test for paraproteins?

A

Electrophoresis

Q

Dx of Multiple Myeloma

A

Monoclonal expansion of paraprotein secreting plasma cells in bone marrow

IgG 60% of cases
IgA 20% of cases
Light chains alone 15-20% of cases

Q

X-Chromosome (males) defect in B-Cell Maturation. Presents in early childhood.

A

XLA/Brutons Tyrosine Kinase Defect/X-linked agammaglobulinaemia

Q

btk

A

Brutons Tyrosine Kinase
Vital in maturation of Pro-BCell to Pre-Bcell
Defect = agammaglobulinaemia = IgA, IgG and IgM def

Q

Recurrent infections – RTIs (lungs & ears chronic OM)

Meningitis and septic arthritis

A

Agammaglobinaemia.

Q

Complications and Tx of X-linked Agammaglobinaemia?

A

IVIg and antibiotics

Complications…
Bronchiectasis
Chronic Sinus Damage

Q

Antibody deficiencies

A

XLA
CVID
Hyper-IgM
IgA
Specific antibody deficiency
Transient hypogammaglobulinaemia

Q

Infections soon after birth

Recurrent bacterial
Persistent Viral
Opportunistic
Persistent Thrush

A

Severe Combined Immunodeficiency (SCID)

Q

Absence of T cells (

A

Severe Combined Immunodeficiency (SCID)

Q

Treatment of SCID?

A

Isolation in +pressure
Antibiotics
Bone Marrow Transplant, possibly gene therapy.

Q

X-linked (young men) Typically presents as a skin infection with +ve organisms (staph aureus, fungi, tc) with deep abscess formation

A

Chronic Granulomatous Disease

Q

NADPH oxidase (Phox)

A

Chronic Granulomatous Disease

Q

Treatment for chronic granulomatous disease?

A

Prophylaxis (co-trimoxasole, itraconasole)

BMT

Q

CD11a, 11b, 11c and CD18

A

Adhesion molecules (Neutrophil Function Disorder)

Q

Failure in inactivation of complement and kinin systems
Angioedema (deep tissue swelling)
Any part of body
Airway & gut (recurrent abdominal pain)
No urticaria or itch (tingling described)
Late childhood or teenage years

A

Hereditary Angioedema.

Q

Treatment for hereditary angioedema

A

Treatment
C1-Inh replacement (acute attacks)
Modified androgens (danazol or stanazol)
Bradykinin receptor anatagonists

Q

Atophy

A

Type 1 IgE mediated allergy (most common allergy)
10% population. 
- Asthma
- Hay Fever
- Eczema
- Foods
- Urticaria and angioedema 
- Anaphylaxis

Q

Type 2 Allergy

A

Autoantibody

Q

Type 4

A

Patch Test (Angry Back Syndrome)

Q

Important consideration in IgE allergies

A

Sensitisation does not mean necessarily mean clinical allergy!
Negative result does not exclude allergy
Patient may need a challenge test

Negative SPT does not exclude allergy

Q

Investigation for Anaphylaxis?

A

Mast cell tryptase 
Demonstration of mast cell degranulation
Elevated levels seen from 1-12 hrs after rxn
90% specific
Sensitivity less good

Usually IgE-mediated
Food allergy
Other stimuli not excluded

Q

Gold Standard in Allergen Dx

A

Allergen Challange

Q

Tx for Allergens

A

Avoid allergen – if possible

Anti-histamines
Self injectable adrenaline
Steroids – onset of action 6hrs
Individualised plan
life threatening reaction?
Chance of re-exposure?

Desensitisation – venoms, pollens

Q

Indications for Glucocorticoids

A

Significant Acute Inflammation

Q

Cortisol

A

Main Natural Glucocorticoid

Q

Aldosterone

A

Main Natural Glucocorticoid

Q

Prednisone and Cortisone

A

Biologically inactive synthetic
11 keto group requires activation to the 11-hydroxy group before having effect on cytosolic receptor.

Activated forms = Prednislone, Cortisol.

Q

Long Acting Glucocorticoid?

A

Dexmethasone

Q

Short Activng Glucocorticoid?

A

Prednisolone
Hydrocortisone
Methylprednisolone
Tramcinolone.

Q

Steroid Dosing

A

High (20-40mg p/day)
Medium
Low (250mg given every 24-48 hrs

Q

MEDICATION TO AVOID IN STEROIDS?

A

NSAIDS

Q

Graft Rejection Pathophysiology

A

APC-TCR = CD4 proliferation, release of IL2 and recruitment of Cytotoxic CD8+Tcells

Q

Agents used in Transplant Immunosuppression

A

Glucocorticoids
Calcineurin Inhibitors (Cyclosporine, Tacrolimus)
Antiproliferative/antimetabolic agents
Monclonal Antibody Therapies (cell specific)

Q

Calcineurin Inhibitors

A

Cyclosporine, Tacrolimus (100x more potent).
Intracell signalling pathways to block IL2.
Mainstay of organ transplant.

S/E’s Nephrotoxicity, Neurotixcity.

Q

Sirolimus

A

TOR (Target of Rapamycin) inhibition.

Thereby blocking IL2

Q

Cell Cycle Inhibitors

A

Mycophenolate Mofetil
Inhibits Inosine, needed for nucleotide synthesis
Used in SLE

Azathioprine
Metabolised to 6MP in the liver.

Q

Anti-IL2-Receptor Antibodies.

A

Daclizumab and Basiliximab

Prophylaxis against organ rejection.