Brainscape's Knowledge GenomeTM

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


See full index

Haematology > Haem: Lymphomas 2 - CLL and quiz > Flashcards

Haem: Lymphomas 2 - CLL and quiz Flashcards

1
Q

Why do we need to check LDH and B2 microglobulin in lymphomas?

A

Give an indication about how aggressive the lymphoma is and cell turnover (LDH is a marker of cell turnover

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

Why do you need a HIV serology in lymphomas?

A

as loss of T cell function can increase the incidence of B cell lymphomas

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

Why do you need a Hep B serology in lymphomas?

A

If B cell depleting therapy is carried out and the patient is a carrier of Hepatitis B, they may run risk of fatal liver failure due to reactivation of Hepatitis B

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

How will women normally present with HL?

A

Nodular sclerosing subtype

Cervical and mediastinal lymphadenopathy

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

How can HL present in general?

A

Patients present with PAINLESS enlargement of lymph node/nodes
This may cause obstructive symptoms/ signs
Great vessels (IVC, SVC, etc.)
Tracheal obstruction
Oesophageal obstruction
Bile duct obstruction
Constitutional symptoms (B symptoms):
Fever
Night sweats (drenching)
Unexplained weight loss (10% in 6 months)
+ pruritis may be present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the 4 subtypes of classical HL (cHL)?

A

Nodular sclerosing
Mixed cellularity
Lymphocyte rich
Lymphocyte depleted

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

How is cHL staged?

A

FDG-PET/CT scan leading to Ann-Arbor staging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does cHL spread?

A

Contiguously

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the different stages in cHL?

A

1 - One group of nodes
2 - >1 group of nodes same side of diaphragm
3 - Nodes above and below the diaphragm
4 - Extra nodal spread

A - If no systemic symptoms
B - If you have FLAWS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How is HL treated?

A

Chemotherapy - ABVD

Follow up with PET CT to see how effective treatment has been

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the long term side effects of cHL?

A

Pulmonary fibrosis

Cardiomyopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Why is radio AND chemo not advised in terms of treatment?

A

Combined modality treatment (radiotherapy AND chemotherapy) leads to a VERY HIGH risk of secondary malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Is the risk of relapse a bigger risk than secondary malignancy after treatment?

A

Until 10 years post treatment, risk of relapse is bigger, then secondary malignancy is the bigger risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the 3 subtypes of NHL in terms of prognosis?

A

Very aggressive - Easier to treat lol
Aggressive
Indolent - Harder to treat lmao

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the main difference in the way HL and NHL present?

A

Hodgkin’s tends to be contiguous and patients present with mediastinal masses. NHL is more widespread.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are some very aggressive NHL?

A

Burkitt’s

B or T cell lymphoblastic leukaemia/lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are some aggressive NHL?

A

Diffuse large B cell (DLBCL)

Mantle cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are some indolent NHL?

A

Follicular
CLL
MALT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How is DLBCL treated?

A

6-8 cycle of R-CHOP

If they relapse consider autologous stem cell transplant

20
Q

What is follicular NHL associated with?

A

t 14:18 translocation resulting in over espression of bcl-2

21
Q

How is follicular NHL treated?

A

Watch and wait
Only treat if clinically indicated like:
- compression due to nodes e.g. bowel, ureter, vena cava
- massive painful nodes, recurrent infections

22
Q

What is Extranodal Marginal Zone Lymphoma?

A

A marginal zone NHL involving extranodal lymphoid tissue e.g. MALT

23
Q

What are some conditions associated with Extranodal Marginal Zone Lymphomas?

A

Sjogren’s syndrome- parotid lymphoma
Hashimoto’s thyroiditis- thyroid MZL
Psittaci infection- lacrimal gland
H. pylori- gastric MALToma

24
Q

Where do Hy Pylori gastric MALTs usually arise and how don they present?

A

In the stomach

Usually present with dyspepsia, epigastric pain, ulceration, or bleeding

25
Q

What is Enteropathy Associated T cell Lymphoma (EATL) and how does it present?

A

T cell NHL associated with Coeliac disease

26
Q

What cells does EATL involve and where does it occur?

A

Mature T cells

Small intestine

27
Q

How does EATL present?

A

Abdominal pain, obstruction, perforation, GI bleeding
Malabsorption
Systemic symptoms
Responds poorly to chemotherapy

28
Q

What cells does CLL involve and what kind of mutation is it associated with?

A

Mature B cells

Acquired sporadic mutation

29
Q

What are the lab findings in CLL?

A

LYMPHOCYTOSIS between 5-300 x 109/L
Smear cells present- Artefactual problems as the cells break down (damaged by smearing)
Normocytic normochromic anaemia
Thrombocytopaenia
Bone marrow lymphocytic replacement of normal marrow elements- due to lots of infiltration

30
Q

What cell markers do normal mature B cells express?

A

CD19

31
Q

What cell markers do normal mature T cells express?

A

CD 3
CD 5
Cd 4 or 8 depending on whether its a cytotoxic cell or helper cell

32
Q

What cell markers do CLL B cells express?

A

CD 5 - Should never be expressed by B cells

CD 19

33
Q

What indicated poor prognosis in CLL?

A

CD 38 expression
IgH unmutated
Deleted 17p (TP53)

34
Q

What causes increased risk of infection in CLL?

A

Malignant and non functional mature B cells cannot secrete polyclonal immunoglobulins, leading to hypogammaglobulinaemia

35
Q

What causes bone marrow failure in CLL?

A

Proliferation of B cells in bone marrow causing effacement of bone marrow

36
Q

What causes lymphadenopathy and splenomegaly in CLL?

A

B cells circulating to nodes, spleen and blood

37
Q

What is Richter transformation and what causes it in CLL?

A

Transformation into a higher grade lymphoma

Further acquired mutations cause this

38
Q

What other diseases can CLL cause?

A

Autoimmune diseases such as haemolytic anaemia

39
Q

Which vaccines are not given to CLL patients?

A

Live vaccines such as VZV vaccine

40
Q

What supportive treatments can be given to CLL patients?

A

Vaccines

Acyclovir

Pneumocystis jiroveci pneumonia prophylaxis with pentamidine for those who are immunosuppressed

IVIg recommended for those with hypogammaglobulinaemia and recurrent bacterial infections

41
Q

What are the treatment options for CLL

A

Chemo if possible otherwise watch and wait

42
Q

What is the aim of treatment?

A

Establish remission

43
Q

What are the indications for treatment?

A

Progressive lymphocytosis (count doubling < 6 months)
Progressive bone marrow failure
Hb < 100
Platelets < 100
Neutrophils < 1
Massive or progressive lymphadenopathy/ splenomegaly
Systemic symptoms (B symptoms)
Autoimmune cytopaenias (treat with steroids)

44
Q

How does venetoclax cure CLL?

A

BCL 2 protein inhibitor

45
Q

How does Rituximab cure CLL?

A

Targets CD20 Ag on B cells

46
Q

How does Ibrutinib cure CLL?

A

BCR kinase inhibitor

Haematology (10 decks)

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