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Life Protection > Antibodies and Myeloma > Flashcards

Antibodies and Myeloma Flashcards

1
Q

Vertebral column sections and structure

A 
Cervical 7
Thoracic 12
Lumbar 5
Sacral 5
Coccygeal 4

Intervertebral discs between vertebrae preventing friction and crushing

4 natural curvatures of spine

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2
Q

Function of vertebral column

A

Protects spinal cord
Supports weight of body
Maintains posture
Facilitates movement

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3
Q

Describe the C1 atlas

A

First cervical vertebrae

Articulates w head and occiput of the axis

No vertebral body and no spinous process

Transverse ligament secures the dens (C2) to the axis

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4
Q

Describe the C2 Axis

A

Easily identifiable by the dens

Dens articulates with anterior arch of atlas making the medial atlanto-axial joint and allowing for independent head rotation

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5
Q

Cervical vertebrae

A
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6
Q 
Thoracic vertebrae:
Location
Body
Vertebral foramen
Spinous process
Transverse processes
Functions
A
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7
Q 
Lumbar vertebrae:
Location
Body
Vertebral foramen
Spinous process
Transverse processes
Functions
A
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8
Q

What are the curvatures of the spine?

A
  1. Cervical curvature (lordotic)
  2. Thoracic curvature (kyphotic)
  3. Lumbar curvature (lordotic)
  4. Sacral curvature (kyphotic)

All of these are important for balance, flexibility, stress absorption and distribution.

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9
Q

What are the types of spinal curves?

A

Kyphosis/Kyphotic curve- concave anteriorly and convex posteriorly

Lordosis/Lordotic curve- convex anteriorly and concave posteriorly

KEELING OVER- kyphotic
LIMBBO- lordotic

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10
Q

What is hyperkyphosis?

A

– excessive curvature of the spine (>50 degrees)

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11
Q

What is hyperlordosis?

A

– excessive curvature of the cervical or lumbar regions

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12
Q

Scoliosis

A

– excessive lateral curvature of the spine (mild: 10-24 degrees, moderate: 25-40 degrees, severe: >50 degrees)

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13
Q

Spinal cord structure

A

The spinal cord continues from the medulla oblongata and then travels inferiorly within the vertebral canals

The spinal cord is surrounded by the spinal meninges and CSF

At L2, the spinal cord tapers off to become the conus medullaris

The spinal nerves at the end of the spinal cord bundle together to form the cauda equina

Occupies 2/3 of the vertebral canal

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14
Q

Ventral and dorsal…

A

Anterior (ventral) and posterior (dorsal) roots of the spinal cord

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15
Q 
Type, passing through and innervation of:
Somatic efferent
Somatic afferent
Visceral efferent
Visceral afferent
A
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16
Q

What is lymph?

A

Lymph is formed from interstitialfluid from plasma filtrate

Contains salts, fat, protein, and cells (mainly lymphocytes)

Interstitial fluid drains primarily as lymph rather than venous reabsorption

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17
Q

Function of lymphatic system

A

Maintenance of fluid balance

Supportstissue immunosurveillance and prevention of infection

Facilitates fat transport

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18
Q

How does fluid get pulled into lymphatic system?

A

Lymphatic capillaries are blind ended, all flows in one direction
Gaps between cells (mini valves)
Proteins in lymphatic capillary = higher oncotic pressure compared to venous and arteriole
–> this pulls fluid from interstitial space into lymphatic system, going to greater oncotic pressure

Then pushed through mini valves into larger collecting lymphatics

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19
Q

How is fluid pushed through lymphatic system?

A

No pumps in lymphatics, works via muscle contraction

As you move, muscle contraction squeezes on lymphatics, compresses vessels which pushes lymph up through system

Hence mobility is important for this to occur, and why build up of fluid (lymphoedema) can happen

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20
Q

How does lymph arrive and exit the lymph node?

A

Lymph arrives through the afferent lymphatic vessels

Lymph drains through the sinus spaces allowing it to run through the entire node (to medullary sinus)

B cells and T cells sample the peptide: MHC complexes

Lymph exitsvia the efferent lymphatic vessels

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21
Q

Diapedesis

A

Transmigration, or diapedesis, is the process by which T lymphocytes migrate across venular blood vessel walls to enter various tissues and organs

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22
Q

Differences between:

Isotypic
Allotypic
Idiotypic

A

Isotypic – changes in the constant regions of the heavy and light chains making up the overall class

Allotypic – small genetic variations between individuals/populations (allelic variation)

Idiotypic – the set of epitopes on the variable region of a particular antibody - key for diversity of antibodies

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23
Q

What are the different regions of an antibody

A 
Variable regions at the top- stripey
Constant region0 light parts of Y
Outer part- light chain
Inner part- heavy chain
Fc region- the 'stem' of the Y shape, which binds to receptors on cells
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24
Q

Describe the chain structure of antibodies

A

Each antibody has two heavy chains and two light chains
A light chain has V and J segments
A heavy chain has V, D and J segments
These recombine in different patterns to generate antibody diversity from a small number of genes

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25
Q

Segments of light chain vs heavy chaiin

A

Light: V and J
Heavy: V D J

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26
Q

What are the 2 variations of light chain?

A

Lambda

Kappa

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27
Q

rearrangement of Ig genes

A

Randomly select V region on light chain, and one J region
Join V1 to J2 and the middle section inbetween is lost

Same with heavy chain (random V to random D to random J) everything in middle is cut

Gene segment recombination generates Ab diversity

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28
Q

Define antibodies

A

Antibodies (Ab) = immunoglobulins (Ig) = gammaglobulins

produced in response to foreign structures (antigens, Ag)

the part of an Ag that is recognised by an Ab = epitope, or antigenic determinant

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29
Q

What are the 5 variations of heavy chains?

A 
Mu
Gamma
Alpha
Delta
Epsilon
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30
Q

What holds together the antibody 2 heavy chains and 2 light chains?

A

Disulfide bond

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31
Q

What are the heavy chains associated with each antibody class?

A 
IgG - gamma
IgM - mu
IgA - alpha
IgD - delta
IgE - epsilon
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32
Q

Which immunoglobulins are most prevalent in serum plasma?

A

IgG

then IgA, IgM

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33
Q

Where is the antigen binding site on an antibody?

A

N terminus of Variable region (heavy and light chain)

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34
Q

Linear vs conformational epitopes

A
  • linear epitopes: adjacent amino acid residues (6aa)

- conformational epitopes: non-sequential amino acid residues spatially juxtaposed in the folded protein

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35
Q

Epitope

A

Antigenic determinant- portion of antigen that antibody binds to

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36
Q

Two main function of antibody

A
  1. Recognition of an infinite number of antigens
    - - antigen binding site (Fab)
  2. Effector functions
    - - via Fab - bind and neutralise/block entry of Ags
    - - other effector functions - mainly mediated by Fc portion
    - - interaction with other cells, complement activation –> macrophages, eosinophils have Fc receptors (FcR) => binding of microbes opsonised by Ab
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37
Q

How to achieve recognition of infinite Antigens ?

A

ANTIGEN BINDING SITE (FAB)

VH and VL domains contain three hypervariable regions

hypervariable regions correspond with protruding loops that make contact with Ag

hypervariable regions of heavy and light chain form the antigen-binding surface

hypervariable regions = complementarity-determining regions (CDR1, CDR2, CDR3)

CDR3 has the highest variability due to genetic mechanisms that ensure Ab diversity

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38
Q

CDRs in primary vs tertiary structure?

A

Ig primary structure: CDRs are separated

Ig tertiary (3D) structure: CDRs become adjacent to each other

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39
Q

What type of B cell populates lymph nodes/spleen and why?

A

Naïve B cells- waiting for antigens

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40
Q

Somatic recombination

A

Combinations of gene segments allow generation of a high number of different immunoglobulins

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41
Q

Where is the locus for the heavy chain gene located?

A

Chromosome 14

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42
Q

Kappa chain: V, J and C segments

A

35V (variable)
5J (joining)
1C (constant region)

43
Q

Lambda chain: V, J and C segments?

A

30V (variable)
4J (joining)
4C (constant region)

44
Q

Antibodies generation of diversity

A 
Somatic recombination (V-D-J joining)
Addition of N and P nucleotides, transcription and RNA processing in 3 B cell clones

Endonuclease cuts randomly after one D and before one J and then after one V and before DJ (coded by RAG 1 and 2)
The free ends are ligated together to form a functional gene

45
Q

What mediates VDJ recombination?

A

Recombinase enzymes coded for by RAG 1 and RAG 2

recognise recombination signal sequence RSS flanking V, D and J gene segments

46
Q

Junctional diversity

A

increases the number of Ab generated

The enzyme terminal deoxynucleotidyl transferase (TdT) adds random nucleotides (N nucleotides) to the free ends before the joining
=> causes differences in the sequence of antibodies produced

47
Q

Most variable portion of Ig molecule

A

CDR3 – the most variable portion of the Ig molecule is located at the site of D-J (heavy chain) or V-J joining (light chain)

D-J or V-J joining are the sites of N nucleotide addition => maximum variation of Ig sequence corresponds to CDR3

48
Q

T cell receptor chains

A

TCRs made up of 2 polypeptide chains (alpha and beta) with variable chains at ends and constant region

Variable regions produce specificity

49
Q

Ig Gene expression process

A
50
Q

Ways of creating antibody diversity

A

Multiple germ line genes - V,D and J heavy chain and V and J light chain genes

Random recombination of the - V,D and J heavy chain and V and J light chain segments

Imprecise joining of V,D and J segments due to nucleotide deletion or inclusion

Random pairing of different combinations of L and Heavy chain regions in different B cells.

51
Q

Allelic exclusion: heavy chain

A

B cells are diploid ie two alleles of all Ig genes
Heavy chain:
- two alleles
- in theory could make two different heavy chains

This never happens = Allelic exclusion

Mechanism: as soon as one allele rearranges successfully and the heavy chain protein is produced the heavy chain rearrangement is switched off

52
Q

Allelic exclusion: light chain

A

Light chain:

  • 2 alleles for κ chain and 2 alleles for λ chain
  • in theory could make 4 different light chains

This never happens = Allelic exclusion

Mechanism: as soon as one allele rearranges successfully and the light chain protein is produced => switches off light chain rearrangement

Each B cell/B cell clone makes either κ or λ chains never both
Polyclonal B cells are a mixture of cells making κ or λ chains
=> light chain restriction (importance in identifying B cell tumours ie monoclonal)

53
Q

Light chain restriction

A

Each B cell/B cell clone makes either κ or λ chains never both
Polyclonal B cells are a mixture of cells making κ or λ chains
=> light chain restriction (importance in identifying B cell tumours ie monoclonal)

54
Q

Clonal selection

A

Antigen-specific clones of lymphocytes develop before and in the absence of antigens in central (generative) lymphoid organs

lymphocyte clones specific for >107-109 antigens

present before exposure to antigen

B cells leave the ‘central’ lymphoid organ and function in the ‘peripheral’ lymphoid organs

when an antigen enters, it activates (‘selects’) the specific lymphocyte clones that recognise the Ag

generation of Abs specific for that Ag only

expansion of antigen-specific clone

55
Q

What happens to plasma cells after they get rid of antigen?

A

they DIE

56
Q

Why are normal immune responses polyclonal?

A

More than one clone of B-cells is activated

More than one antibody is synthesised

Because

  • Multiple antigens on organism
  • Multiple epitopes on each antigen
  • More than one Ab may recognise the same epitope
57
Q

What generates the switch of B cells to secreted form of antibodies?

A

Differential splicing of exons

  • secreted IgG doesn’t have hydrophobic transmembrane portion like membrane IgG does so can be released
58
Q

Production of secreted IgG

A

Primary transcript has membrane coding sequence- this is spliced out for secreted IgM and so whole molecule is instead secreted

59
Q

Antibody actions

A

Bind to extracellular microbes and toxins:

  • neutralise (block adherence/entry)
  • eliminate
  • opsonisation = ↑ phagocytosis
  • complement activation = opsonisation, lysis
60
Q

Antibody isotope switching

A

During an immune response B cells become capable to produce Abs of different classes but without changing specificity (respond to the same Ag)

  • ability to perform different effector functions
  • can deal better with pathogens
  • isotype switch needs signals from helper T cells
  • does NOT alter specificity or alter light chain
61
Q

What does IgM switch to?

A

IgG, IgA, IgE

62
Q

What does IgG switch to?

A

IgA, IgE

63
Q

How do T cells help with isotope switching?

A
  1. CD40L on T cell interacts with CD40 on B cells
  2. cytokines produced by T cell
    - IFN-gamma => switch to IgG1, IgG3
    - IL-4 => switch to IgE

TGF-beta (and other cytokines) => switch to IgA

64
Q

Isotope switching process

A

Between constant regions are switch regions that allow splicing out of different constant region genes

Done via endonucleases like activation induced cytidine deaminase (AID)

Sequence with variable part and different heavy chain classes of genes along chromosome → so if B ell switches from IgM to IgG3 then Cmu and Cdelta cut out = Cgamma 3 (produced from class switch)

then to produce IgA from Cgamma 3, switch out Cgamma 1 and 3 for Calpha 1

ALL MEDIATED BY TGF BETA

65
Q

What happens in patients with AID immunodeficiency?

A

AID: activation induced cytidine deaminase

DONT HAVE

  1. Class switch recombination (CSR)
  2. Somatic hypermutation (SHM)
66
Q

Polymeric pentameric IgM

A 
J chain (joining chain present in all polymeric Igs)
Pentameric IgM: high avidity for Ag – 10 Ag binding sites

1st Ab produced in a primary immune response
very efficient at complement activation
–Leading to promotion of opsonisation and lysis

67
Q

IgG properties

A

Highest concentration in circulation

monomeric
complement activation
promotes opsonisation and lysis
neutralises/blocks entry microbes and toxins

Only Ab to cross placenta -> neonatal protection

68
Q

IgA dimer properties

A

J chain (joining chain present in all polymeric Igs)

In circulation: mostly monomer

Major Ab in mucosal secretions
GI / respiratory tract, breast milk

Dimer (polymer) – has a J chain
Prevents adherence and entry of pathogens

69
Q

How are IgA antibodies secreted?

A 
Found in lamina propria
Produce IgA attaching via J chain 
Then attach via poly Ig receptors
Pass into mucosal epithelial cells
Proteolytic cleavage -> secreted into lumen where they function
70
Q

IgE properties

A

very low levels in healthy individuals

monomeric
Fc receptors on eosinophils, mast cells- degranulation
Defence against particles
Responsible for allergies (type 1 hypersensitivity)

71
Q

IgD properties

A

Monomer

Mainly B cell receptor together with IgM

72
Q

Co expression of IgM and IgD

A

IgD is co-expressed with IgM (works as Ag receptor)

IgM is the 1st immunoglobulin to be produced
IgD is produced at the same time with IgM
Mechanism: differential splicing

Exons for Cμ and Cδ are transcribed as part of a single precursor RNA
Differential splicing can remove Cμ exons => now Cδ exons are used => IgD (same VDJ as IgM joined to Cδ)

73
Q

Myeloma pathogenesis

A

Clonal expansion of immunoglobulin secreting, heavy-chain class switched, terminally differentiated B cells

Bone marrow based disease associated with lytic bone disease, anaemia and bone marrow failure

PC secrete monoclonal protein. IgG (60%), IgA (20-25%), light chains only (15-20%)

74
Q

Tests required to diagnose myeloma

A

Lab tests:
FBC and blood chemistry
SPEP (Serum protein electrophoresis) and UPEP (Urine protein electrophoresis)
- looking for abnormal light chains

Bone marrow biopsy
–> flow cytometry

Imaging: CT, MRI, PET

75
Q

MM diagnostic criteria

A

At least 10% bone marrow cells being clonal abnormal plasma cells or biopsy of bone proving a clonal plasma cell disorder

Must also demonstrate patient has one or more SLiM CRAB criteria

76
Q

MGUS diagnosis

A

Less than 10% clonal plasma cells or less than 30g light chain/paraprotein and NONE SLiM CRAB criteria

77
Q

SLiM criteria stands for:

A

S- BM >60% clonal plasma cells
Li- SFLC (light chain) ratio >100
M- 2 or more lesions on MRI

78
Q

Myeloma prognostication

A

Abnormalities like 17p deletion or translocation of 4;14 puts them in a high risk group

79
Q

What pattern characterises multiple myeloma?

A

Remission and relapse

Patients become symptomatic so have first line therapy
→ longest period of remission before disease relapses and need further treatment
→ with each relapse time the remission becomes shorter until = refractory disease and they succumb to their illness

80
Q

What is pain due to in MM?

A
  • Bone pain
  • Nerve pain - nerve root, spinal cord compression

Pain as a complication of the treatment
- Peripheral neuropathy

81
Q

NICE recommendations for MM imaging

A

Offer imaging to all people with a plasma cell disorder suspected to be myeloma.

Consider whole‑body MRI as first‑line imaging.

Consider whole‑body low‑dose CT as first‑line imaging if whole‑body MRI is unsuitable or the person declines it.

Only consider skeletal survey as first‑line imaging if whole‑body MRI and whole‑body low‑dose CT are unsuitable or the person declines them.

Do not use isotope bone scans to identify myeloma‑related bone disease in people with a plasma cell disorder suspected to be myeloma.

82
Q

Why do bone scans have low sensitivity in myeloma?

A

Bone scans have low sensitivity in myeloma due to low osteoblastic activity

83
Q

Common sites for bone involvement in MM

A

Skull
Spine
Pelvis
Long bones

84
Q
A

Skeletal lesions in MM

pepper pot

85
Q
A

Lytic bone disease

bone weakened, little stress can cause pathological fracture

86
Q
A

T2 weighted MRI showing myeloma- related fractures at L3 and L4

87
Q

Common cause of back pain in MM patients?

A

Vertebral compression fracture

75% of the patients have bone pain1

55-70% have VCFs or history of vertebral body abnormalities.2

Back pain in patients correlates with Vertebral Compression Fracture (VCF) in >50% of patients at time of diagnosis1

88
Q

Why does the bone pain occur?

A

Origin of pain from sensory and sympathetic neurones in medulla of bone

Marrow contains rich plexus of nerves

Cancer cells release cytokines sensitizing neurones. This can lead to up regulation of pain receptors, central sensitization in spinal cord and long-term potentiation

89
Q

Cause of MM bone disease

A

RANK is protein receptor found on osteoclast precursor cells
RANKL is a protein expressed by bm stromal cells - binds to RANK and promotes osteoclast differentiation
OPG decoy receptor - inhibits binding of RANK and RANKL.
In myeloma RANKL expression upregulated and OPG switched off – promotes osteoclast activity

RANK Ligand upregulated by myeloma cells + downregulation of its natural antagonist OPG = increased interaction of RANKL and RAN on osteoclasts with upregulation of osteoclasts
= bone reabsorption and imbalance of osteoclasts and osteoblasts

90
Q

MM treatment goals

A

Induce remission, if possible
Prevent immune suppression
Prevent hematologic abnormalities (anemia, low platelets)
Prevent end-organ damage
Prevent fractures
Maintain function, quality of life, control symptoms

91
Q

Painkillers to use in MM patients

A

Act on different receptors Ca2+ - Gabapentin
opioid - Opiates/ Fentanyl GABA - Benzodiazepines

Effect may be synergistic

Potential toxicities:
Nausea/ constipation, opiate induced hyperanalgesia, metabolite toxicity, potential immunosuppression

92
Q

Novel drugs that have helped myeloma patients

A

Proteasome inhibitors
HDAC inhibitors
VEGF inhibitors

93
Q

When do we need orthopaedic input?

A 
Stabilisation of pathological fracture
Decompression of cord
Vertebroplasty
Balloon kyphoplasty
Radiotherapy
94
Q

Role of bisphosphonates

A

Role in treatment of malignant hypercalcaemia and bone pain

Inhibitors of osteoclastic bone resorption

Reduction in vertebral and non vertebral fractures in MRC myeloma VI trial

95
Q

How do bisphosphonates work?

A

High affinity to bone – rapidly absorbed onto bone surface and ingested by osteoclasts
2 classes of bisphosphonate – work in different ways

Non-nitrogen containing (eg clodronate) metabolised by osteoclast and disrupt cell metabolism leading to apoptosis

Nitrogen containing (aminobisphosphonates) eg pamidronate and zoledronic acid and some orals eg alendronate and ibandronate) – induce apoptosis and inhibit osteoclast function by disrupting signalling of key regulatory proteins

96
Q

What is a complication of using bisphosphonates long term?

A

Osteonecrosis of jaw

Exposed bone in maxillofacial area often in association with dental surgery (ONJ can also happen spontaneously), with no evidence of healing

97
Q

What are the different causes of peripheral neuropathy when associated with MM?

A

Disease related: Amyloid, cryoglobulin, nerve root compression, POEMS, autoimmune

Co-morbidities: Diabetes, EtOH, weight loss and malnutrition

Drug related: Thalidomide, IMiDs, proteosome inhibitors, platinum,

98
Q

Assessment and management of neuropathic pain

A

Peripheral neuropathy is associated with newer agents thalidomide and bortezomib

Assessment through use of neurotoxicity assessment tool, neurological examination and EMG studies, antibody studies, biopsies

Management includes dose reduction, pharmacological agents, massage, patient education

99
Q

Incidence of neuropathic pain in patients with multiple myeloma

A
  • 11-20% of newly diagnosed patients
  • 83% in relapsed, refractory patients
  • High incidence due to neurotoxic drugs used including vincristine, platinum, thalidomide, bortezomib
100
Q

Management of neuropathic pain in a MM patient?

A

Close monitoring of patients (neurology assessment/ tools)

Actively seeking out symptoms through asking appropriate questions

Prompt action (dose reduction, switching to alternatives)

Symptom relief (amitriptyline, duloxetine, gabapentin or pregabalin )

101
Q

12/23 rule

A

Only a Ig gene segment with a 12 base spacer RSS can be joined to an Ig gene segment with a 23 base spacer

In heavy chain never just join a V segment to a J segment- so because both V and J have 23 they cant join together due to 12/23 rule,

(needs to be V 23 and D 12, or D 12 and J 23- needs to be in right order so 12 first)

102
Q

Joining segments in heavy chains

A

There are V, D and J segments in a heavy chain
A D segment will be randomly selected and joined with a J
The DJ segment will then be randomly joined with a V segment
The 12/23 base spacer rule makes sure that V joins to a D and a D joins to a J

103
Q

How does rearrangement occur in light chians?

A

V and J segments will randomly join to generate a VL domain

There are specific recombinases (RAG enzymes) which recognize the RSSs and allow joining

There will be a coding joint generated between the V and J domain that has been randomly selected

There will also be a signal joint which is the lost intervening piece of DNA

There may also be receptor editing of the light chain genes

104
Q

Antibody structural regions are…

A

1 Fc fragment region + 2 Fab fragment regions

Life Protection (10 decks)

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