cancer care Flashcards

things important

1
Q

neutropenic sepsis abx

A

Tazocin

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2
Q

neutropenic sepsis time, presentation, differentials

A

10-14 days after chemo
diagnosis=
<0.5 x 10 ^9 + fever OR clinical sepsis

malignancy related fever
chemo related fever
Pulmonary embolism!

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3
Q

microbes neutro seps

A
usually line infection with commensals 
ent infection also common
uti
staph aureus
epidermidis
enterococcus
streptococcus
MRSA 
VRE
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4
Q

ix for neutr sepsis

A

FBC, CRP, blood culture, lactate, urine output - dipstick and mcs, u&es, LFTs,
swabs from lines
cxr/axr/mri
blood film, d-dimer and fibrinogen (to rule out DIC)

NEED TO CALL SpR and Consultant
Give Abx within one hour
fluids
O2 if desats

IF HYPOTENSIVE NEEDS URGENT ATTENTION
call itu outreach
consider escalation from ward care

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5
Q

prevention of neut sepsis

A

Patient information - hygiene, food be careful
Patient education: written and oral information, including how and when to contact 24-hour specialist oncology advice and seek emergency care
 Antibiotic prophylaxis (versus increased antibiotic resistance)
 Consider for future chemotherapy cycles  Dose reduction (palliative chemo)
 Prophylactic GCSF (curative/adjuvant)
 ?stop treatment

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6
Q

common ca that cause spinal chord compression

A

breast
prostate
lung
myeloma

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7
Q

when is spinal chord compression cauda equina

A

when below L2

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8
Q

what is the criteria for mri with suspected spinal chord compression

A

urgent mri within 24 hours if bone pain + abnormal neurology

otherwise within weekish

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9
Q

prevent scordc?

A

educate pts

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10
Q

spinal cord compression rx

A

admit + log roll
analgesia
steroids - dexamethasone 16mg STAT IV then 8mg BD, ppi for gastroprotection
neurosurgery review
if prog for cancer is >3months, consider surgery +/- radio +/- chemo

supportive therapy includes:

analgesia, managing pressure sores, laxatives, bladder (catheter), monitor BM, VTE prophylaxis, physiotherapy

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11
Q

common causes of hypercalcaemia

A
PTHrp
Osteolytic mets - Breast, prostate, lung, kidney mets to bone 
multiple myeloma
Lymphomas (can produce vit D)
thiazide diuretics
ca/vit d supplements misuse??
Addisons disease
Acromegaly
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12
Q

why can lymphomas cause hypercalc

A

Lymphomas (can produce vit D)

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13
Q

which cancers metastasise to bone

A

Breast, prostate, lung, kidney mets to bone

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14
Q

rx hypercalcaemia

A
iv fluids
iv zolendronic acid
if refractory, rankal (which is needed by osteoclasts) inhibitor = Denosumab
calcitonin
steroids
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15
Q

tumour lysis parameters

3 up, 1 down

A

urea up
phosphate up
potassium up
calcium down

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16
Q

symptoms of tumour lysis syndrome

A
n+v
dehydration
AKI
diarrhoea
oliguria
heart failure
seizures
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17
Q

why can tumour lysis syndrome cause aki?

A

because capo4 crystals in kidney and also uric acid crystals

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18
Q

treatment for tumour lysis syndrome

A

allopurinol - xanthine oxidase inhibitor (reduces produc of uric acid)

Rasburicase (recomb uric oxidase enzyme), breaks down uric acid - also given prophylactically

manage other imbalances too
if bad, haemodialysis

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19
Q

when does tumour lysis present?

A

day 1-5 after chemo or radio

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20
Q

how to prevent tumour lysis syndrome?

A

Educate
Hydrate
monitor u&es

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21
Q

small bowel obstruction in cancer management

A

operate if operable
venting gastrostomy to decompress
switch oral meds to iv/subcut (NBM)
ppi

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22
Q

large bowel obstruction cancer rx

A

diverting stoma
chemo / radio
segmental resection
stent

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23
Q

Metoclopramide

moa

A

Acts on D2, 5HT4, 5HT3 both centrally in the chemoreceptor trigger zone (CTZ) and peripherally in the gut wall

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24
Q

metoclopramide indication

A

Indication
• Gastric stasis
• Ileus
• Chemotherapy related nausea/vomiting

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25
Q

metoclopramide adrs

A
Undesirable effects
•	Extra-pyramidal / antidopaminergic effects:
o	Tardive dyskinesia
o	Acute dystonic reaction (young women)
o	Akathesia
o	Parkinsonism
o	Neuroleptic malignant syndrome
•	Abdominal colic
•	Diarrhoea
•	Cardiac arrhythmias (when given intravenously (IV) in combination with HT3 antagonist (eg ondansetron)
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26
Q

Haloperidol moa

A

Haloperidol

Acts on D2 in the CTZ

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27
Q

Haloperidol indication for nv

A
  • Opioid induced nausea and vomiting
  • Metabolic disturbance (hypercalcaemia)
  • Chemical – other drug causes
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28
Q

Haloperidol

adrs

A
  • QT prolongation/Torsades de pointes
  • Extra-pyramidal effects
  • Neuroleptic malignant syndrome
  • Sedation
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29
Q

Levomepromazine

moa and indication

A

Broad spectrum antiemetic. Acts on 5HT2 and H1 in the vomiting centre, and the D2 and alpha 1 adrenergic receptor in the CTZ and gut wall

  • Nausea of unknown aetiology
  • Bowel obstruction
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30
Q

Levomepromazine

adrs

A
  • QT prolongation/Torsades de pointes
  • Extrapyramidal effects
  • Neuroleptic malignant syndrome
  • Sedation
  • Anticholinergic side effects
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31
Q

Ondansetron moa

indications

A

5HT3 in the CTZ and gut wall

• Used for chemotherapy induced nausea and vomiting

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32
Q

ondansetron adrs

A
  • Constipation
  • Headache
  • Dizziness
  • Nervousness
  • Tremor
  • Ataxia
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33
Q

Cyclizine

indication and moa

A

Acts on H1 in vomiting centre, vestibular area

  • Raised intracranial pressure
  • Vestibular causes
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34
Q

cyclizine adrs

A
Cyclizine
Acts on H1 in vomiting centre, vestibular area	•	Raised intracranial pressure
•	Vestibular causes	•	Anticholinergic side effects:
o	Dry mouth
o	Confusion/delirium
o	Postural hypotension
o	Blurred vision
o	Constipation
o	Urinary retention
o	Arrhythmias
•	Drowsiness
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35
Q

colon cancer is now screened by what instead of faecal occult blood sampling?

A

FIT

faecal immunochemical testing?

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36
Q

colon ca screening programme

A

60-74 years
every 2 years send poop
if + colonoscopy

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37
Q

SE of bleomycin

A

pulmonary fibrosis

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38
Q

SE of cisplatin

A

othotoxicity, nephrotoxicity

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39
Q

SE of cyclophosphamide

A

haemorrhagic cystitis, nephrotox, SiADH

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40
Q

SE of doxorubicin

A

Cardiotoxicity

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41
Q

SE of vinchristine

A

Christ my nerves

nerve damage

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42
Q

SE of vinblastin

A

Blast my bones - myelosuppresion

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43
Q

SE of mtx

A

myelosuppor

nephrotoxic

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44
Q

Tamoxefen hormone therapy SEs

A

menopausal symptoms
DVt
Endo ca
vaginal discharge
osteoporosis in pre-meno, no added risk in post menop
teratogenecity hence need barrier contraceptives

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45
Q

cytotoxic chemo SEs

A
myelosuppresion
nv
mucositis
oral ulcers
diarrhoea
weight loss
infertility
46
Q

immunotherapy SEs

A

may not occur straight away

organs inflamed

47
Q

radio SEs

A

burns, desquamation, erythema, radiation fibrosis

further ca risk
rectal proctitis

48
Q

WHO status

A

0-5

0 = fit and well

1 = can do work, but not strenous activity

2 = can do ADLs, but not work. Up and about >50% of the day.

3 = limited self-care, up and about <50% of the day.

4 = bed bound, disabled, unable to ADLs

5 = dead

49
Q

what is different about haem chemo in neutropaenia

A

the nadir (low point) is usually deeper and prolonged

50
Q

what should chemo pts have?

A

All patients should be issued with an alert card with
24 hour contact numbers.
Chemo units should rehearse situations with patients to ensure that they understand when and who they should contact if they have a proble

51
Q

spin chord compres pathophysic

A

Usually caused by the collapse or compression of a vertebral body that contains metastatic disease (arterial seeding)
 10% by direct tumour (paraspinal mass) extension into the vertebral column
 Compression of cord initially causes oedema, venous congestion and demyelination which are reversible
 Prolonged compressionvascular injury, cord necrosis and permanent damage

52
Q

features of spin chord compre

A

 >90% have back pain
 Frequently first symptom and prolonged
 Spinal or radicular pain (8/10)
 Exacerbated by straight leg raising, coughing, sneezing or straining
 > 75% have Limb weakness
 >50% have sensory level (not cauda equina)
 > 40% have bladder and anal sphincter dysfunction
 Diminishing performance status/generally unwell

53
Q

hcg as tumour marker

A

testicular
placental choriocarcinomas
hydatidiform moles

54
Q

alpha foetoprotein in cancer

A

foetus - albumin

in ca 
pancreatic
biliary/hcc
gastric
bronchial
55
Q

ca19-9

A

mucin in epithelium of foetal git

used to monitor response to rx in pancreatc, gastric, mucinous ovarian

56
Q

lead bias

A

detected earlier via screening

false illusion improved survival

57
Q

lag bias

A

slower growing tumour detected

false illusion

58
Q

demeclcycline is used for…

A

siadh

59
Q

pembrolizumab

A

Nsclc targeted therapy:
 Selective, humanized monoclonal anti-PD-1 antibody agaonst programmed death (PD) inhibitor
 Blocks the interaction of PD-1 on T-cells with its
ligands, PD-L1 and PD-L2, to reactivate anti-tumor
immunity
 Dual ligand blockade of PD-1 pathway

60
Q

aml definition

characteristic blood film finding

A

accumulation of immature myeloblasts in blood and bone marrow

auer rods

61
Q

gingival hyperplasia which blood ca

A

aml - monocytic infiltration into gums

62
Q

where does aml infiltrate

A

lung bladder skin sinus

63
Q

serious complication of aml presentation

A

leukostasis

64
Q

Leukostasis management

A
too many blasts in blood
impairment of microvasc perfusion
hypoxia
mi
stroke
bowl inschaemia
renal failure
priapism

treat with hydroxyurea, chemo, leukopheresis

65
Q

what is a particularly aggressive type of aml in young people

A

acute promyelocytic leukemia

but

responds to all trans retinoic acid (ATRA)

66
Q

age of aml

A

> 40yo

rarely <4

67
Q

features of aml

A

paradoxical bleeding and thrombosis
b marrow failure
b symptoms
bone pains

68
Q

ix for ?AML

A
FBC - pancytopaenia with blasts
deranged LFTs
CXr infection
coag - dic (ddimer)
bone marrow ex
69
Q

Myelofibrosis aetiology

A
abnormal proliferation of all myeloid cells
megakaryocytes start to release PDGF
this over time leads to fibrosis of BM
may even lead to failure
results in EXTRAMEDULLARY HAEMATOPOESIS
70
Q

Symptoms of myelofibrosis

A
MASSIVE hepatosplenomegaly (+ assoc symp)
fever
fatiguability
sob
hyperuricaemia
bm failure
71
Q

signs of myelofibrosis

A
pallor
plethora
petechiae/ecchymoses
febrile/b symptoms
cachexia
72
Q

ix for ?myelofibrosis

A
fbc 
blood film TEAR DROP RBC pathognomonic
bizarre platelets
PCR/FISH for Bcr-abl
Serum urate/ldh
73
Q

key treatment of myelofibrosis

A
patient education
support rx
anaemia management
manage thrombocytopaenia
splenectomy
hydroxyurea
RUXOLITINIB - Jak1/2 inhibitor
74
Q

causes of massive splenomegaly

A
CML/CLL
Myelofibrosis
Hairy cell leukemia
Marginal zone lymphoma
Sarcoidosis
Gaucher disease
Kala-azar
75
Q

if kidney normal, what is an increased beta microbulin a sign of?

A

lymphoma

76
Q

Physiological polycythaemia causes

A
smoking
high altitude
kidney issues that cause ^EPO e.g. ca or polycystic kidney disease
sleep apnoea
congenital heart disease
ida
77
Q

polycythaemia rubra vera define and symptoms

A

too many RBC, platelets, basophils, mast cells (hence aquagenic pruritis)

symptoms of hyperviscosity - cns(lethargy confusion headaches), visual disturbances, gout, arterial/venous thrombosis AND haemorrhage, burning fingers/toes, splenomegaly

78
Q

poly rubra vera key mutation and rx

A

JAK2 - activates EPO and thromboEPO receptors

rx: clots reduce, venesection, aspirin,

if needed, chemo - hydroxycarbamide (decreases DNA synthesis)

79
Q

Essential thrombocythaemia ix findings

A

fbc - thrombocythaemia
jak2/calr/mpl
BM - large megakaryocytes

80
Q

Essential thrombocythaemia rx

A

aspirin
hydroxycarbamide
interferon alpha

81
Q

myelodysplastic syndrom is FABULOUS

A

FAB classification

RA - refractory anaemia
RAS - “ with sideroblasts in BM
RAEB - refractory anaemia with >5% blasts but not enough to become a leukemia <20%

82
Q

ix to do when ?MDS

A

FBC, bm t and a with cytogenetics and immunophenotyping to exclude AML
LDH/urate

rule out other causes:
B12/folate, UEs, LFTs, infections - HIV, Hep, EBV

83
Q

what is a ring sideroblast a sign of?

A

x-linked sideroblastic anaemia
low grade mds

could also be alcohol abuse and lead poisoning

84
Q

aplastic anaemia aetiology

A

immune response to initial bone marrow insult that causes damage to HPC

= pancytopaenia

= ATG, ALG and supportive rx + transfusions

prog <6 months without rx!

85
Q

Active euthanasia
Witholding rx
Assisted suicide

difference

A

Active euthanasia = the doctor intention to end a patients life
 WWT = intention is not to shorten life
 Assisted suicide = a doctor helps a patient to
bring about their own death

86
Q

Aprepitant

A

Aprepitant
NK1 antagonist; acts mainly centrally Used for more emetogenic chemo; augments
5HT3 and dex
S/E; constipation, headache

87
Q

Metoclopramide

A
Metoclopramide
 Prokinetic
D2 blocker (CTZ- some central activity)
Can help gastric stasis
10mg TDS orally or 30mg/24 hrs SCSD
Avoid long term use
S/E; extra-pyramidal (may include muscle spasms and tardive dyskinesia
 Parkinsonian
88
Q

Haloperidol

A

Haloperidol
D2 blocker
Acts at CTZ
Good for metabolic and drug causes of N&V 0.5-5mg in 24 hrs orally or SC
S/E; extra-pyramidal , restlessness, sedation
 Parkinsonian

89
Q

Cyclizine

A

Cyclizine
Anti-cholinergic and H1 antagonist
Blocks conduction in vestibular-cerebellar pathway and acts at VC
Good for ICP, motion sickness, pharyngeal stim, BO
50mg TDS orally or 150mg/24hrs via SCSD
Avoid in cardiac failure
S/E; hypotension, urinary retention, dry mouth, constipation, restlessness

90
Q

Ondansetron

A

Ondansetron
5HT3 antagonist; peripheral (vagal N) and central (CTZ) action
Serotonin release triggered by bowel injury, chemo, RT
Primarily used for acute CINV
Can help in BO and renal failure
S/E; constipation, headache
4-8mg BD-TDS orally or 8-16mg/24hr SCSD Reduce dose in hepatic failure

91
Q

levomepromazine

A

May consider levomepromazine „Domestos‟ of anti-emetics
A phenothiazine
Acts at vomiting centre and CTZ Drowsiness main dose limiting S/E 6.25mg – 12.5mg SC/orally

92
Q

how to treat chemotherapy induced nausea and vomitign

A

CINV
N&V frequently cited as the most distressing side-effects of chemotherapy
Up to 75% of all cancer patients will experience chemotherapy-related emesis
Increased risk associated with specific chemo agents, female gender, age <50 years, past Hx of N&V (pregnancy, prior chemotherapy use, motion sickness)
Acute, delayed, anticipatory 5HT3, NK1, dexamethasone

93
Q

Factor V Leiden

A

Factor V Leiden

Factor V Leiden (activated protein C resistance) is the most common inherited thrombophilia, being present in around 5% of the UK population.

It is due to a gain of function mutation in the Factor V Leiden protein. The result of the mis-sense mutation is that activated factor V (a clotting factor) is inactivated 10 times more slowly by activated protein C than normal. This explains the alternative name for factor V Leiden of activated protein C resistance,

94
Q

random fact about cholangiocarcinoma

A

as w primary sclerosing cholangitis - a rare complication of ulcerative colitis

95
Q

what is percutaneous transhepatic cholangiography? PTC

A

Needle passed through skin into dilated extrahepatic bile duct under uss

contrast injected into biliary tree
cholangiogram obtained

96
Q

Lynch syndrome

A

autosomal dom
DNA mismatch repair gene mutation

Hereditary non-polyposis colon cancer

HNPCC

97
Q

FAP

A

rare autosomal dom
APC tumour suppressor gene mutation

affected individuals develop multiple polyps, inevitably one will transform into cancer (accumulation of mutations)
prophylactic surgical excision of colon and rectum is advised in young adults

98
Q

Peutz-jeghers syndrome

A

v similar to FAP
STK11 tumour suppressor gene
multiple bowel hamartomas
cancer

99
Q

Duke Staging for colorectal cancer

A

a - within bowel lumen 90% survival
b - breached in to bowel wall 70%
c - lymph nodes 40%
d - distant mets

100
Q

Bowel cancer screening

A

60-75
every 2 years
faecal immunochemical test (FIT)

101
Q

EGFR monoclonal ab

A

colorectal ca

102
Q

TTP

A
Pentad of Features:
Haemolytic anaemia
Thrombocytopenia
Renal impairment
Fever
Neurology: Hallucinations, behavioural change, headaches

Path: Antibody against a metalloprotease
Reduces function of Von Willebrand’s factor

Mx: Plasmapheresis (removes antibody) and FFP

Cx: Fatal without treatment, 20% mortality with treatment

103
Q

Modified hartmans explain

A

Operation for L sided pathology
when making anastamosis is unsafe

excise lesion, cross-staple the rectal stump, bring out the proximal part into a colostomy.

can reverse at later date.

104
Q

Prostate ca

A

Local t1-2
Radical prostatectomy
Robotic if under 70 and thin
Or radio - brachy or external beam

Hormones via watchful waiting or active surveillance

Palliative with hormones

Locally advanced t3-4 gone through capsule
Radical radiotherapy plus hormones
Or watchful waiting

Metastatic

If fit, neoadjuvant docetaxil
Hormones
4 weeks of anti androgen + LHRH long term

Last resort steroids

105
Q

Taxanes and vinca alkaloids moa

A

spindle poisons

106
Q

doxorubicin, daunorubicin moa

A

dna intercalating agents

prevents transcription and replication

107
Q

bleomycin moa

A

scission of DNA strands

108
Q

Cisplatin moa

A

covalently binds DNA
Forms DNA-DNA adducts + cross-linking
physical disruption of DNA therefore no replication

109
Q

Give two examples of antimetabolites

A

Purine analoge - 6-mercaptopurine

Pyrimidine analogue - 5FU, inhibits thymidilate synthase

110
Q

moa of methotrexate in chemo

A

binds to DHFR

interferes with folate metabolism which is key to DNA synthesis

111
Q

SEs of chemo

A

Mucositis, alopecia, Diarrhoea, NV, pulmonary fibrosis, cardiotoxicity, renal failure, myelosuppresion, phlebitis, myalgia, sterility, DIC