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WEEK 10 SEM 4 > CLINICAL WORKSHOP- MYELOMA Histopathology > Flashcards

CLINICAL WORKSHOP- MYELOMA Histopathology Flashcards

1
Q

What is the appearance of the skull in the skull X ray (see slide 2 of pp)?

A

can see multiple lytic lesions

appearance is called - pepperpot appearance

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2
Q

What is pepperpot appearance?

A

when multiple tumour deposits have replaced parts of the skull

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3
Q

What is the cause of the pepperpot appearance?

A

either because the tumour has stimulated osteoclast activity (which break down bone)
OR
the tumour is putting pressure on the bone causing its atrophy

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4
Q

What is the differential diagnosis for multiple lesions on bone?

A

metastatic carcinoma of breast, lung, prostate, thyroid

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5
Q

What do you take from the bone to diagnose myeloma?

A

bone marrow aspirates (ie a small bone marrow sample) and bone marrow trephines (a small cylinder of bone marrow) are taken from a patient for diagnosis

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6
Q

Which one out of bone marrow aspirates and bone marrow trephines give the final diagnosis of myeloma?

A

bone marrow aspirates may not be taken from areas of plasma cell malignancies, and thus trephines are used to make a final diagnosis

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7
Q

Under light microscopes, what do normal plasma cells look like?

A

Under light microscopy, normal plasma cells have an eccentric nucleus (nucleus not in the centre of the cell), with chromatin condensation, and a pallor showing rough endoplasmic reticulum

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8
Q

What is an active plasma cell?

A

making antibody

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9
Q

What is a neoplastic plasma cell?

A

cancerous cell

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10
Q

Why do we need to stain the kappa and lambda chains?

A

because it is hard to tell the difference between active plasma cells and neoplastic plasma cells

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11
Q

What happens if there is an excess of one chain (kappa/lambda)?

A

myeloma indicative= daughter cells produce same light chains as parent so in cancer keep replicating one chain

If the plasma cells were making antibodies for inflammation, there would have been a large number of diverse immunoglobulins secreted by a large number of plasma cells, and they would include both kappa and lambda chains

a neoplasm such as myeloma is clonal, ie is derived from a single mutated parent cell

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12
Q

Where are osteoclasts derived from?

A

bone marrow monocytes

which proliferate and fuse to form multinucleate osteoclasts

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13
Q

What inactivates an osteoclast?

A

calcitonin

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14
Q

What does active osteoclast look like?

A

ruffled border
round
bigger in size

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15
Q

What happens in paget’s disease?

A

osteoclasts get overactivated and grow in size

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16
Q

What do myeloma cells do to bone?

A

secrete hormones and cytokines to stimulate osteoclast activity

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17
Q

Other than in myeloma, which other disease also has high osteoclast?

A

osteoporosis

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18
Q

What do osteoclasts do?

A

osteoclast:
resorb bone
when active- release calcium into bone

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19
Q

Where are osteoclasts derived from?

A

derived from bone marrow monocytes- proliferate and fuse to form multinucleate osteoclasts

20
Q

What do osteoclasts activate?

A

activates TGF= which stimulates bone deposition by osteoblasts

21
Q

What do osteoblasts do?

A

produce bone

22
Q

Where are osteoblasts derived from?

A

periosteum

bone marrow stromal cells

23
Q

What suppresses osteoclasts?

A

calcitonin

medically: bisphosphonates

24
Q

Where is calcitonin from?

A

C cells in the thyroid

25
Q

How does the RANK ligand work?

A

there is a receptor called RANK which is present on osteoclasts and bone marrow stromal cells

−when the RANK ligand binds to the RANK receptor, it causes progenitor cells to fuse and become osteoclasts

26
Q

How do osteoblasts regulate osteoclasts?

A

osteoblasts can upregulate osteoclasts activity
osteoblasts begin to secrete monocyte CSF and RANK ligand in response to parathyroid hormone

osteoblasts can also downregulate osteoclast activity
osteoblasts can secrete osteoprotogerin in response to calcitonin which blocks the RANK receptor-OPG (osteoprotogerin) is a secreted glycoprotein and is thought to be a member of the TNF super family

27
Q

How do myeloma cells act on osteoclasts?

A

myeloma cells can secrete TNF alpha, IL1, IL6= all upregulate the secretion of RANK ligand from osteoblasts = more osteoclast activity= result in osteoporosis

myeloma cells are constantly expanding= put pressure on the bone =create lytic lesions
when these lytic lesions are repaired, osteoclast activity outweighs osteoblast activity, leading to much more lysis of the bone

28
Q

What pharmacological agents can depress osteoclast acitivty?

A

denosumab
bisphosphonates
pamidronate and zoledronic acid
non nitrogenous bisphosphonates

29
Q

What is denosumab?

A

monoclonal antibody
binds to the RANK ligand
blocks its binding to RANK on osteoclasts thus mimicking OPG (osteoprotogerin)

30
Q

What do bisphosphonates do?

A

bind calcium in bone

when osteoclasts take up calcium, they get poisoned and die prematurely

31
Q

What do pamidronate and zoledronic acid do?

A

induce OPG secretion by osteoblasts thus blocking the RANK ligand

32
Q

What do non nitrogenous bisphosphonates do?

A

induce apoptosis in the osteoclasts, whilst nitrogenous bisphosphonates interfere with actin or cytoskeletal elements important for activation of inactive osteoclasts

33
Q

What are renal complications that arise from myeloma?

A

renal calculi
myeloma protein deposition
amyloidosis

34
Q

What are renal calculi?

A

kindey stones
occur due to hypercalcaemia
calcium binds with phosphate and precipitates out (calcium phosphate stones)

35
Q

What are the consequences of renal calculi?

A

obstruct urine flow- cause stagnation- UTI

36
Q

What can infected urine lead to in the kidneys?

A

infected urine may reflex into the kidney due to back pressure causing acute or chronic pyelonephritis sepsis

37
Q

What does obstruction of urine flow by renal calculi cause?

A

back pressure causes:
hydronephrosis (fluid in nephron) = this pressure may cause atrophy of the kidney (renal parenchyma which consists of the filter system of the kidney)

38
Q

What can a failing kidney cause?

A

hypertension via RAAS

39
Q

What colour does myeloma protein stain?

A

dark pink

40
Q

What can myeloid protein in the renal tubules cause?

A

rupture tubules
so inflammatory cells come in
cause inflammatory response (CALLED INTERSTITIAL NEPHRITIS)

41
Q

What is amyloid?

A

glycoprotein with beta pleated sheet
mixture of protein and starch
accumulate in interstitial space (between cells)
compress cell but expand organ

42
Q

Explain the staining of amyloid:

A

starch like component of amyloid allows it to stain blue/black with Lugol’s iodine

looking at this stain through polarized light will allow one to see an apple green stain on the amyloid-this is because amyloid is a glycoprotein with a beta pleated sheet structure-the anti-parallel sheets mean that the amyloid can refract light, producing an apple gree colour-

43
Q

How is amyloid formed?

A

partial degradation of light chains by macrophages-

44
Q

What is commonly seen in amyloid?

A

substance P is common in several types of amyloid, and is being used to map the extent of amyloid deposition and in treatment

45
Q

What causes localised lytic lesions?

A

the pressure of the expanding clones of myeloma cells can push on the bone causing pressure atrophy

46
Q

What is myeloma protein?

A

precipitation of free light chains

47
Q

What are the consequences of renal failure?

A
  • Obstruction to urine flow causes stagnation of urine and infection can easily develop. Infected urine can reflux back up into the kidney causing acute or chronic pyelonephritis.
  • Back pressure from obstructed urine can lead to hydronephrosis and pressure atrophy of the renal parenchyma
  • Failing kidney may cause hypertension via action of RAAS
  • Death by chronic renal failure or by the complications of hypertension (e.g. stroke)

WEEK 10 SEM 4 (8 decks)

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