Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Haem - pathology > 1 > Flashcards

1 Flashcards

1
Q
  1. Q. What occurs in multiple myeloma?
A

A. Accumulation of malignant plasma cells (B lymph) in the bone marrow leading to progressive bone marrow failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q
  1. Q. What is the common presentation of multiple myeloma?
A

A. Tiredness and malaise, bone/back pain + fractures, infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
  1. Q. What characteristic product is produced in multiple myeloma?
A

A. Paraprotein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q
  1. Q. What systems are affected in multiple myeloma?
A

A. Renal failure

B. Destructive bone disease and hypercalcaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q
  1. Q. How does multiple myeloma effect bone density? Which cells are involved?
A

A. Increase bone resorption (osteoclasts), Decreased bone production (osteoblasts)
B. Uncoupling of resorption/production = rapid bone loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
  1. Q. Name 2 osteoclast activating factors and osteoblast inhibitory factor
A

A. Osteoclast activating factors: RANKL, MIP1-alpha, IL-3

B. Osteoblast inhibitory factors: Dkk-1, sFRP-3, HGF, TGF-beta1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why is there renal impairment in multiple myeloma?

A

renal impairment –

  1. Malignant cells secrete/produce monoclonal proteins of varying types most commonly immunoglobulins (antibodies) and free light chains, resulting in abnormally high levels of proteins in the blood. The delicate structure of the kidney can be damaged by tubulopathtic effects of proteins or light chains.
  2. Hypercalcemia = nephrocalcinosis = leading to kidney failure
  3. Amyloidosis: high levels of amyloid protein, amyloid is excreted via the kidney – may cause damage
  4. (Hyperuricemia, recurrent infections, local infiltration of tumour cells, drug induced kidney failure may also contribute)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
  1. Q. Which neuro symptoms may be multiple myeloma and why?
A

A. Anaemia/hypercalcemia – may manifest weakness, confusion and fatigue
B. Hyperviscosity of blood due to paraprotein – may manifest headache, visual and retinopathy
C. Spinal cord compression and infiltration of amyloid in peripheral nerves – may result in radicular pain, loss of bowel/bladder control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
  1. Q. What imaging techniques are used in MM?
A

A. CT: first-line
B. MRI: good definition of bone/anatomy used to clarify ambiguous lesions, myeloma ‘pepper pot skull’, also used to assess spinal cord leisons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
  1. Q. What are the three overlapping aims of treatment for MM?
A

A. Anti-myeloma treatment
a. combination chemotherapy e.g. CTD, MPT, HD-ASCT
B. Prevention and treatment of bone and tissue damage
a. Bisphosphonates, renal dialysis, MSCC treatment (radiotherapy, surgery), pain
C. Improve quality of life and survival
a. Infection prophylaxis and treatment, anaemia (EPO, transfusion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
  1. Q. What is lymphoma and where does it occur?
A 
A.	Malignant growth of WBCs
B.	Predominatly in lymph nodes
C.	Bone marrow, blood
D.	Liver, spleen
E.	Can occur anywhere
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
  1. Q. How does lymphoma present?
A

A. In a variety of ways: depending on system affected
B. Weight loss, night sweats, most commonly nodal disease
C. Also extra-nodal disease (malignant WBCs in other places)
D. Compression syndromes (DVT/swollen leg due to compression)
E. Systemic symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
  1. Q. How is lymphoma diagnosed?
A

A. Blood film & bone marrow
B.

Lymph node biopsy (often image guided)
C. Immunophenotyping
D. Cytogenetics: karyotype analysis, FISH
E. Blood film & bone marrow
F. i.e. diagnosis is complex
G. Staging: blood tests, CT scan, bone marrow biopsy, PET

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q
  1. Q. What are the two main types of lymphoma?
A

A. Hodgkin’s lymphoma

B. Non-Hodgkin’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
  1. Q. Name the presentation of Hodgkin’s lymphoma
A

A. Painless lymphadenopathy, B symptoms (sweats, weightloss)
B. Diagnosis: Reed-Sternberg cell
C. Incidence: Hodgkin’s lymphoma affects younger people at a higher rate and has a bimodal peak rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
  1. Q. Name some long-term effects of Hodgkin’s lymphoma
A 
A.	Infertility
B.	Cardiomyopathy
C.	Lung damage
D.	Peripheral neuropathy
E.	Second cancer
F.	Psychological issues
17
Q
  1. Q. Name a monoclonal antibody, what is their mechanism of action?
A

A. Binds to cancer-specific antigens and induce an immune response against the target cancer cell
B. Rituximab
C. Targets CD20 expressed on cell surface of B-cells

18
Q

A. Chronic myeloid leukaemia (CML):

A

A. Chronic myeloid leukaemia (CML): basophil, neutrophil, eosinophil mutation

19
Q

A. Chronic myelomonocytic

A

A. Chronic myelomonocytic leukaemia (CMML): monocyte mutations

20
Q

Acute myeloid leukaemia (AML)

A

Acute myeloid leukaemia (AML): common myeloid progenitor mutations

21
Q

Chronic lymphocyic leukaemia (CLL):

A

Chronic lymphocyic leukaemia (CLL): B lymph (most common leukaemia)

22
Q

Acute lymphoblastic leukaemia (ALL):

A

A. Acute lymphoblastic leukaemia (ALL): Lymphoblast mutations (mostly paeds) - platelets

23
Q
  1. Q. How does chronic leukaemia most commonly present?
A

A. Usually 40-60 yrs age, slow onset, sometimes incidental finding, splenomegaly, metabolic features - maturation, haemocytoblasts (large nucleus, little cytoplasm)

24
Q
  1. Q. Describe the diagnosis of leukaemia
A

A. Blood tests
B. Bone marrow aspirate ad trephine biopsy
a. Increasing in blasts >20% (acute leukaemia)
b. Background abnormalities to suggest pre-exsiting bone marrow abnormalities
c. Cytogenetics for prognosis
d. Molecular genetics for prognosis
e. Immunophenotyping (confimatory/prognosis)
C. Cytogenetics
D. Minimal residual disease monitoring
E. Molecular

25
Q
  1. Q. Name three side effects of chemotherapy
A

A. Nausea/vomiting, diarrhea/constipation, hair loss, reduced fertility, anaemia, loss of platelets, loss of appetite, fatigue, allergic reactions, bystander organ damage (kidneys, liver etc)

26
Q
  1. Q. Describe the ‘related organ or tissue involvement’ CRAB of multiple myeloma
A

A. Calcium increase - due to overexpression of RANKL: bone resorption (osteoclasts) – hypercalcemia

B. Renal impairment – renal impairment –

C. Anaemia– normal bone marrow is replaced by infiltrating tumour cells and normal haematopoiesis is inhibited by cytokines. Lack of Hb.

D. B – lytic lesions, overexpression of receptor activator for RANKL by bone marrow stroma, activates osteoclasts (bone resorption). Results in B-lytic bone leisons (these cause breakdown). This breakdown in bone leads to calcium release leading to hypercalcemia and associated symptoms.

Haem - pathology (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions