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Malignant haematology > Chemotherapy > Flashcards

Chemotherapy Flashcards

1
Q

Short term complications chemo

A

Hair loss
Change taste
Loss appetite
Nausea
Fatigue
anaemia, TP, neutropenai
Tumour lysis syydndrome

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2
Q

What can prevent tumour lysis syndroe [re chemo

A

Rasburicase

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3
Q

Long term comps chemmo

A

Peripheral neuropathy
Cardiomyopathy - anthracycline
Hypogammaglobulinaemia - rituximab
Renal damage
Reduced fertility
Risk of secondary malignancy

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4
Q

Low grade lymphomas 30%

A

Indolent clinical behaciour
Non specific symptoms- disseminated
Littel scope for cure
Tend transform to high grade lymphomas

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5
Q

Intermediate and high grade lymphomas features

A

More aggressive but more responsive to chemo
Recurrence more common in first two ears
Relaps or resistance to chemo - poor prognosis <5-10%

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6
Q

Prognosis NHL general

A

2/3 survieve >10 years

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7
Q

IPI score for diffuse large B cell lymphoma

A

Age >60
Poor perfomance status - ECOG
Elevated LDH
>1 exrranodal site
Stage III or IV

FLIPI adds
<12 Hb
>4 nodal sites involvement

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8
Q

Sezary syndrome survival

A

<5 years

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9
Q

Different chemotherapy options

A

Single agent
COmbination
Monoclonal antibodies
Targeted treatments
Steroids

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10
Q

What aim of treatment w chemo

A

Curative
Disease control - keep at bay
Palliative - symptom

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11
Q

How does chemoterhayp work

A

Target different stages of cell cycle to prevent normal replciation of cancer cells
Cancer cells divide more than normal cells hence why targeted by them
Nomral cells affected = side effects

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12
Q

MOA alkylating agents

A

Alkylating agents cause cross links within DNA double helix by adding alkyl groups to guanine bases - DNA damage, cytotoxic in entire cell cycle

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13
Q

Alkylating agents exmaples

A

Cyclophospamide
Bendamustine
Chlorambucil
Melphalan
Ifosfamide

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14
Q

MOA of antimetabolite chemoterhay

A

Interfere w DNA and RNA synthesis act as substitute for normal DNA bases - C, A, T, G
Target S phase of cell cycle - cytotoxic when DNA being synthesised

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15
Q

Examples of antimetabolites

A

Purine analogues -fludarabine, 6-mercaptopurine
Pyrimidine analogues - cytarabine, gemcitabine, azacitadine
Antifolate - methotrexate

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16
Q

Anit-tumour antibiotics MOA

A

1 Intercalate between base pairs
2 Inhibit topoisomerase II
2 Create oxygen free radicals

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17
Q

Examples of anthracyclines

A

Daunorubicin
Doxorubicin
Epirubicin
Idarubicin
Bleomycin

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18
Q

Mitotic inhibitor/plant alkaloid MOA

A

Inhibit microtubule polymerisation
Bind to tubulin protine and inhibit formation, cant form microtubules
Interfere w mitosis phase of cell cycle

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19
Q

Examples of mitotic inhibitors

A

Vincristine, vinblastine

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20
Q

Steroids as chemotherapy MOA

A

Not fully understood

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21
Q

Steroids used in chemo

A

Oral - prednisolone, dexamethasone
IV - dexamethasone, methylprednisolone

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22
Q

Generic chemo side effects

A

Myelosupression - cytopenias
Gut toxicity - sore mouth , change in tast, diarrhoea, neutropenic coliti/typhylitis
N+V
Hair loss
Effect on fertility
Liver toxicity
Teratogenecity
Fatigue

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23
Q

Anthracycline specific side effects

A

Cardiac toxicity
Life tiem dose - cant exceed over life time

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24
Q

Vinca alkaloids side effects

A

Peripheral neuropathy
Constipation

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25
Q

Bleomycin side effects

A

ILD/fibrosis
Avoid in elderly, prev smokers

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26
Q

Ifosfamide side effects

A

Encephalopathy - only as inpatient, usually reversible

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27
Q

Long term chemo side effects

A

Cardiotoxicity, ILD
fertility problems
Bone problemms- steroids
Secondary malignancies incl haematological cancers - MDS,AML - poorer prognosis
Skin cancers

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28
Q

MOA of monoclonal antibodies

A

Target specific cancer cell protein and inducing antibodu depeneent cellular cytotoxicity - ADCC and completment depenent

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29
Q

Monoclonal ABs exmaples

A

Rituximab - CD20 bind (B cells)
Obinutuzumba - 2nd gen CD20
Daratumumab - anti CD38

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30
Q

Side effects of MoABs

A

Infusion related reactions -> fever, hypotension, rash, anaphylaxis
Increased suscetibility to infections - targets helathy B cells

31
Q

How are ibrutinib and acalabrutinib targeted therapies

A

B cell receptro, bruton tyrosine kinase inhibitor - BTKi

32
Q

What can use ibrutinib and acalabrutinib in

A

CLL, mantle cell lymphoma

33
Q

How do imatinib, dasatinib, nilonitib, ponatibin in

A

Tyrosine kinase inhibitors

34
Q

What are imatinib, dasatinib, nilonitib, ponatibin used in

A

CML, Ph + ALL

35
Q

MOA of venetoclax

A

Bcl2 inhibitor (antiapotpic protien inhibited)

36
Q

What use venetoclax in

A

CLL, AML

37
Q

MOA of midostaurin and what use in

A

FLT3i
AML

38
Q

Proteasome inhibitors examples

A

Bortezomib - velcade, ixazomib, carfilozimib

39
Q

Immunomodulatory agents

A

Linalidomide, thalidomide

40
Q

What targeted therapies can be used in myeloma

A

Proteasome is eg bortezomib, ixazomib, carfilzomib
Immunomod- lenalidomide, thalidomide

41
Q

DA regime

A

Daunorubicin + cytarabine
Induction for AML

42
Q

FCR use and what are

A

CLL
Fludarabine, cyclophos

43
Q

VTD + IRD chemo what is and use

A

Myeloma
Velcade
Thalidomide
Dexamethasone

IRD - Izazomib, Revlimid, dexamathasone

44
Q

How do cancer cells most commonly avoid T cell detection

A

PD-1 upregulation
Antibodies still sick but ineffective at killing cell and T cell wont recognise

45
Q

What are Pd-1 inhibitors effective in/used in

A

Good results in hodgkins lymphoma
Used eztensively in solid cancers

46
Q

Side effects of PD1 inhibitors

A

Autoimune disorders due to lack of PD1 on normal cells
Can be life threatening, can affect any organ

47
Q

New approach to targeted haematlogical malignancy therapies

A

Activate T cells to identify tumour cells and -> cell lysis

48
Q

What are CAR-T cells

A

Transfuse own T cells ‘infected’ with vector containing T cell receptor that can recognise antigen that want to target

49
Q

How long does T cell ‘reset’ in CAR-T process take

A

4-5 weeks to get 6 T cells

50
Q

How do bispecific antibodies work?

A

Antibody links T cell via CD3 receptor with target of interest specific antibodies
Brings T cell into proximity w cancer cells

51
Q

CAR-T cells when become effective after transfusion

A

Each CAR-T cell can -> death of >100,000 tumour cells
10 mil when infuse, in 7 days -> 100-200 million

52
Q

Current CAR-T cells available in UK

A

Zuma 1 - 3 transufsions
Tisagenlecleucel

53
Q

ALL relapse what targeted therapy improves prognosis

A

Tisagenlecleucel
V poor prognosis
50% in remission 12 months post therapy
75% survival 12 months later

54
Q

What may develop in first 10-14 days after CAR-T cell therapy

A

Cytokine release syndrome

55
Q

What is cytokine release syndrome

A

Systemic inflam response caused by cytokines released by CAR-T cells and other immune cells -> reversible organ dysfunction

56
Q

Presentation of Cytokine release syndorme

A

Neurologic
Haem - anaemia, TP, neutropenia, lymphopenia, DIC, HLH, coagulopathy etc
Constituational - fevers, rigors, malaise, anorexia, myalgia
CVS - tachy, hypotension, arrhtyhmias, QT prologen, decreased LVDEF
Pulm - hypoxia, tachy RR
Renal - AKI, electrolyte tumour lysis syndrome
N/V, diarrhoea
Elevated CK

57
Q

Why need to give CAR-T cells as inpatient

A

Risk of cytokrine release syndrome

58
Q

Cons of CAR-T cells

A

V expensive - 300,000 [pounds per dose
3-5 weeks to manafacture
Can only give once
Still high mortality rates

59
Q

Potnetial advantages of bispecific antibodies vs CAR-T cells

A

Chepaer
Antibody infusion - multiple repeats
Can be gicen immediately
Toxicity v prediatbale within few hours of transfusion
Only need to stay in hospital for a few days

60
Q

Causes of macrocytic anaemia

A

MDS
B12/foalte deficiency
Haemolytic anaemia

61
Q

What does a positive IgG coombs test suggest

A

Red cells are coated with IgG

62
Q

What does IgG being a warm antibody mean

A

Cant fix to complement
Ass w AIHA

63
Q

Why does a direct positive IgG coombs test suggest extavascular haemolysis

A

Suggests RBC coated in IgG - recognised by macrophages in reticuloendothelial system and -> haemolysis in spleen

64
Q

What does a postive coombs test with complement mean

A

Due to cold IgM antibodies

65
Q

Where does haemolysis take place if direct coombs test complemetn positive

A

Cold IgM - intravascuarly as able recognised by complement therefore takes place intravascuarly

66
Q

What does raised reticulocytes and direct positive IgG coombs test suggest in CLL

A

Extravascular haemolysis is occuring in spleen

67
Q

What haematological malginancy is characterised by progressive failure of the immune system and gradual resistance to chemotherapy interventions

A

CLL

68
Q

How long after splenectomy need antibitoics for and which ones

A

Penicillin or erythromycni
Minmum of two years, pssibly life long

69
Q

What vaccinations shld patietns receive pre splenectomy

A

H.influenzae B
MenC
Pnuemococcus

70
Q

Back pain red flags

A

Weight loss
No improvement after 2 months
Progressive or nocturnal pain
Fever
Pain at rest
Night sweats
Morning stiffness
Neurological disturbance
Sphincter disturbance
History of malignancy

71
Q

What diuretics should you start vs stop in hypercalcemia

A

Start loop diuretics (reduce Ca levels in plasma - NA/K/2Cl ATPase - increased Na excretion->increased K+ secretion -> increased Ca and Mg excretion charge balacne )
Stop thiazide like diuretics - absorb Calcium

72
Q

Most effective bisphosphonate in hypercalcemia

A

Pamidronate
Needs hydration first esp in renal failure

73
Q

How are bisphophonaes used in muliple myeloma

A

-Treat hypercalcemia in emergency
- “bone strengthener” with monthly infusions; they are adsorbed onto bone hydroxyapatite crystals, slowing their rate of growth and dissolution, so bone turnover is reduced.

Malignant haematology (16 decks)

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