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NEUROLOGY > Rx for Blood Malignancies > Flashcards

Rx for Blood Malignancies Flashcards

1
Q

What does chemo and radiotherapy do?

A
  • damages the DNA of cancer cells as it divides
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2
Q

What is the protein P53 responsible for?

A

protein in the cell nucleus

- involved in programmed cell death (cell recognises it’s damaged and DIES by process of apoptosis)

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3
Q

What occurs to a normal cell with exposure to LOW dose chemo or RT?

A
  • fewer side efx…duh

> apoptosis; formation of blebbing> cell breaks apart into several apoptotic bodies> phagocytosed

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4
Q

What effect does a BIGGER dose of chemo or RT have on normal cells?

A
  • causes necrosis of the cell
    > cell will SWELL
    > plasma membrane RUPTURE
    > cellular and nuclear lysis > inflammation
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5
Q

Why do CLL/ lymphoma, and acute leukaemia respond well to chemo - and radio- than other cancers?

A
  • lymphocytes are KEEN to undergo apoptosis in the normal lymph node
  • —lymphoma and CLL can be triggered to undergo apoptosis READILY with chemo- or radio-
  • acute leukaemia will be dividing very quickly and are therefore affected by chemo
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6
Q

Immediate side effects of chemo?

A
  1. immediate: hair loss/ N.V/ neutropenic infection

- VERY TIRED

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7
Q

Long term side effects of chemo?

A
  • heart damage
  • lung damage
  • other cancers
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8
Q

What is involved in supportive rx of CLL and lymphoma?

A
  1. rx of neutropenic fever/ infection
  2. broad spectr. antibiotics
  3. red cell and platelet transfusion
  4. growth factors
  5. prophylactic antibiotics and antifungals to prevent infection occuring in the 1st oplace
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9
Q

How is death anti-fungals rare nowadays?

A
  • prophylactic antifungal drugs are given to ALL at risk to prevent infection
  • ex: ITRACONAZOLE or POSACONAZOLE
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10
Q

When is high dose chemo and rt given?

A
  • to those who need it

- accept the incr. side effects

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11
Q

What helps us in chemotherapy?

A

PET scan

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12
Q

What does it mean is PET scan was still positive despite 6 cycles of chemo?

A
  • very high chance of RELAPSE
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13
Q

How to avoid side effects of chemotherapy?

A
  • miss out bleomycin in cycles 3-6 !
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14
Q

Name 3 examples of targeted therapy.

A
  1. monoclonal antibodies
  2. Biological agents
  3. Molecularly targeted treatments
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15
Q

How do monoclonal antibodies help treat leukaemia?

How effective is it?

A
  • immune treatment
  • affects ONLY cells which posses target protein
  • avoid side effects
  • –MORE EFFECTIVE than CHEMO !
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16
Q

What is given to treat low grade and mantle cell NHL?

A
  • maintenance Rituximab

- —prolongs survival and time to next rx

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17
Q

What improves and cures patients with HIGH grade B cell NHL?

A

RCHOP

18
Q

What is given to elderly pts with NHL?

A

R-mini-CHOP

19
Q

Apart from rituximab, what arre other Anti-B cell Abs?

A
  • Ofatumunab
  • Obinutumab
  • —more direct kill of malignant B cells
20
Q

What best as rx of CLL in less fit patients?

A
  • Ofatumunab
  • Obinutumab
  • —with gentle chem (chlorambucil)
21
Q

What is the MOA of brentuximab vedotin?

A
  • CHEMOTHERAPY tagged anti-CD 30 Ab

- —-“targeted chemo”

22
Q

Where is CD30 found?

A

on Hodgkin’s cells

- some Tcell NHL

23
Q

How are biological rx diff. from chemotherapies?

A
  • don’t affect cells as they divide
  • —many MOA
  • not targeted to malignant cells
  • —ex: PROTEOSOME inhibitors and IMIDs
24
Q

Where are biological rx used?

A
  • in MULTIPLE myeloma

- evaluated in LYMPHOMA

25
Q

What are proteosome inhibitors?

A
  • aka the DUSTBIN for the old proteins inside the cells

- —breaks them down to A.A

26
Q

Consequence of blocking the proteosome inhibitor?

A

-allows for accumulation of toxic proteins

27
Q

What is CHOP?

A
  • a combination of drugs used to treat NHL and CLL

- MADE UP OF :— cyclophosphamide/ vincristine/ doxorubicin/ prednisolone

28
Q

When may i tbe ideal to give IMIDs?

A
  • pts with LOW grade NHL and CLL, no longer responding to chemo !
29
Q

How should MIDs be given to a pt with mantle cell NHL?

A
  • IMIDS are slightly better in combination with chemo (CHOP) than chemo alone—
30
Q

S.e of IMIDs?

A
  • risk to fetus
  • effect on blood counts
  • other CANCERs
31
Q

What are the derivatives of IMIDs?

A
  • derivative of thalidomide (LENALIDOMIDE)
32
Q

How effective is molecular therapy?

A
  1. target pathway specific to the cancer cells
  2. avoid side effects
  3. more EFFECTIVE than chemo
33
Q

How is the CML prognosis,when the pt is on tyrosine kinase inhibitors?

A
  • blood counts should be normal
    —chromosomes normal (BCR-ABL NOT detected in blood.
    STOP trials
    —-most well tolerated; SOME side effects.
34
Q

What are side effects for administering tyrosine kinase?

A
  • s.e: diarrhoea= FLUID IN LUNG, NEUTROPN=ENIA
35
Q

What drugs affect the B-cell signalling pathways?

A

Ibrutinib and Idelaisib

—-effective in LOW grade NHL and Bcell CLL ——ones that DON’T respond to RITUXIMAB and chemo

36
Q

What mutations make ti difficult for the pt to respond to chem/rt in CLL?

A
  • P53 mutation
37
Q

When is Idelalisib approved for CLL?

A
  • Idelalisib is given for use in CLL with P53 mutation

- —-HUGE improvement (previously no/ little resp. to chemo)

38
Q

What are the s.e of Ibrutinib?

A

fever/ low platlets/ anaemia/ shortness of breath

39
Q

What are the s.e of Idelalisib?

A
  • diarrhoea, rash, fatigue, liver abnormality, fever !
40
Q

Name a checkpoint inhibitor.

And its MOA?

A

NIVOLUMAB
- more effective in LYMPHOMA/ esp. hodgkin’s

—-when receptor is stimulated the immune system cell is swtiched off and ignores the tumour

41
Q

How does immune evasion occur Hodgkin’s?

A
  • when cancer cells EVADE the immune system
  • PD-1 receptors, found on the surface of cells of the immune system, when stimulated by chems released by the tumor cells, is SWTICHED OFF and ignores the tumor
42
Q

How do check point inhibitors work?

A

NIVOLUMAB
sticks to the chemical released by cancer cells. preventing it to bind to the effector cells
—immune system remains “on” and ATTACKS the cancer cell

NEUROLOGY (36 decks)

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