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Malignant haematology > Chemotherapy > Flashcards

Chemotherapy Flashcards

(73 cards)

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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
Bleomycin side effects
ILD/fibrosis Avoid in elderly, prev smokers
26
Ifosfamide side effects
Encephalopathy - only as inpatient, usually reversible
27
Long term chemo side effects
Cardiotoxicity, ILD fertility problems Bone problemms- steroids Secondary malignancies incl haematological cancers - MDS,AML - poorer prognosis Skin cancers
28
MOA of monoclonal antibodies
Target specific cancer cell protein and inducing antibodu depeneent cellular cytotoxicity - ADCC and completment depenent
29
Monoclonal ABs exmaples
Rituximab - CD20 bind (B cells) Obinutuzumba - 2nd gen CD20 Daratumumab - anti CD38
30
Side effects of MoABs
Infusion related reactions -> fever, hypotension, rash, anaphylaxis Increased suscetibility to infections - targets helathy B cells
31
How are ibrutinib and acalabrutinib targeted therapies
B cell receptro, bruton tyrosine kinase inhibitor - BTKi
32
What can use ibrutinib and acalabrutinib in
CLL, mantle cell lymphoma
33
How do imatinib, dasatinib, nilonitib, ponatibin in
Tyrosine kinase inhibitors
34
What are imatinib, dasatinib, nilonitib, ponatibin used in
CML, Ph + ALL
35
MOA of venetoclax
Bcl2 inhibitor (antiapotpic protien inhibited)
36
What use venetoclax in
CLL, AML
37
MOA of midostaurin and what use in
FLT3i AML
38
Proteasome inhibitors examples
Bortezomib - velcade, ixazomib, carfilozimib
39
Immunomodulatory agents
Linalidomide, thalidomide
40
What targeted therapies can be used in myeloma
Proteasome is eg bortezomib, ixazomib, carfilzomib Immunomod- lenalidomide, thalidomide
41
DA regime
Daunorubicin + cytarabine Induction for AML
42
FCR use and what are
CLL Fludarabine, cyclophos
43
VTD + IRD chemo what is and use
Myeloma Velcade Thalidomide Dexamethasone IRD - Izazomib, Revlimid, dexamathasone
44
How do cancer cells most commonly avoid T cell detection
PD-1 upregulation Antibodies still sick but ineffective at killing cell and T cell wont recognise
45
What are Pd-1 inhibitors effective in/used in
Good results in hodgkins lymphoma Used eztensively in solid cancers
46
Side effects of PD1 inhibitors
Autoimune disorders due to lack of PD1 on normal cells Can be life threatening, can affect any organ
47
New approach to targeted haematlogical malignancy therapies
Activate T cells to identify tumour cells and -> cell lysis
48
What are CAR-T cells
Transfuse own T cells 'infected' with vector containing T cell receptor that can recognise antigen that want to target
49
How long does T cell 'reset' in CAR-T process take
4-5 weeks to get 6 T cells
50
How do bispecific antibodies work?
Antibody links T cell via CD3 receptor with target of interest specific antibodies Brings T cell into proximity w cancer cells
51
CAR-T cells when become effective after transfusion
Each CAR-T cell can -> death of >100,000 tumour cells 10 mil when infuse, in 7 days -> 100-200 million
52
Current CAR-T cells available in UK
Zuma 1 - 3 transufsions Tisagenlecleucel
53
ALL relapse what targeted therapy improves prognosis
Tisagenlecleucel V poor prognosis 50% in remission 12 months post therapy 75% survival 12 months later
54
What may develop in first 10-14 days after CAR-T cell therapy
Cytokine release syndrome
55
What is cytokine release syndrome
Systemic inflam response caused by cytokines released by CAR-T cells and other immune cells -> reversible organ dysfunction
56
Presentation of Cytokine release syndorme
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
Why need to give CAR-T cells as inpatient
Risk of cytokrine release syndrome
58
Cons of CAR-T cells
V expensive - 300,000 [pounds per dose 3-5 weeks to manafacture Can only give once Still high mortality rates
59
Potnetial advantages of bispecific antibodies vs CAR-T cells
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
Causes of macrocytic anaemia
MDS B12/foalte deficiency Haemolytic anaemia
61
What does a positive IgG coombs test suggest
Red cells are coated with IgG
62
What does IgG being a warm antibody mean
Cant fix to complement Ass w AIHA
63
Why does a direct positive IgG coombs test suggest extavascular haemolysis
Suggests RBC coated in IgG - recognised by macrophages in reticuloendothelial system and -> haemolysis in spleen
64
What does a postive coombs test with complement mean
Due to cold IgM antibodies
65
Where does haemolysis take place if direct coombs test complemetn positive
Cold IgM - intravascuarly as able recognised by complement therefore takes place intravascuarly
66
What does raised reticulocytes and direct positive IgG coombs test suggest in CLL
Extravascular haemolysis is occuring in spleen
67
What haematological malginancy is characterised by progressive failure of the immune system and gradual resistance to chemotherapy interventions
CLL
68
How long after splenectomy need antibitoics for and which ones
Penicillin or erythromycni Minmum of two years, pssibly life long
69
What vaccinations shld patietns receive pre splenectomy
H.influenzae B MenC Pnuemococcus
70
Back pain red flags
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
What diuretics should you start vs stop in hypercalcemia
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
Most effective bisphosphonate in hypercalcemia
Pamidronate Needs hydration first esp in renal failure
73
How are bisphophonaes used in muliple myeloma
-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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