oncology Flashcards

1
Q

what is the WHO performance status

A

0 - fit and well, no restrictions
1=restricted in physcially streneuous activity but ambulatory and able to carry out light work
2=ambulatory and capable of self care but unable to carry out any work activities. up and about 50% of waking hours
3=capable of limited selfcare, confined to bed or chair for more than 50% of time
4=completely disabled, cannot carry out selfcare, completely confined to bed/chair
5=dead

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2
Q

how does chemo work

A

damages dna
direct - binds
indirect - affects dna replication/mitosis

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3
Q

e.g. chemo agents

A

alkylating
antimetbaolites
anthracyclines
taxanes
platinums
topoisomerase i

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4
Q

how does radiotherapy work

A

use of high energy XR to destroy cancer cells

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5
Q

how does immunotherapy work

A

systemic agents that aim to stimulate a patiejts own immune system to attack cancer cells
e.g. checkpoint i, monoclonal ab

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6
Q

how do targeted agents work and e.g.

A

systemic therapoy
inhibit specific targets involved in cell replication etc
e.g. tyrosine kinase i

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7
Q

what are tx related oncological emergencies

A

cytopenia - neutropenic sepsis
electrolyte disturbance - hypercalcaemia
tumour lysis syndrome
diarrhoea
vomiting
anaphylaxis
extravasation
radiotherapy se

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8
Q

what are tumou related oncological emergencies

A

spinal cord compression
SVCO
upper airway obstruction
brain mets
bowel obstruction

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9
Q

what are cancer cells

A

undergo uncontrolled and unregulated cell proliferation with the abiliity to move to other places in theo body

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10
Q

cell cycle

A

G0 = rest
G1 = pre DNA synthesis
S= DNA synthesis
G2 = post DNA synthesis
M = mitosis

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11
Q

systemic anticancer tx

A

chemo
hormone
molecular - inhibitors, monoclocal ab, immunotherapy

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12
Q

SE chemo

A

HF
immune supprssion
alopecia
renal impairment
skin rashes
bowel upset
peripheral neuropathy
taste changes
hepatic impairment
nasuea

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13
Q

diagnosis neutropenic sepsis

A

temp >38 and neutrophil count <1 x10 to the 9

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14
Q

presentation neutropenic sepsis

A

Any infective symptoms or signs, with or without fever
 Asymptomatic yet febrile
 Suspect in any patients presenting with a new clinical deterioration9 within 6 weeks
of cytotoxic chemotherapy
 Associated risk factors; poor nutritional, mucosal barrier defect, central venous lines,
abnormal host colonisation

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15
Q

ix neutropenic sepsis

A

U+E, creatinine, LFT, CRP/ESR, coag screen
 Septic screen; Blood cultures, clinically relevant swabs or cultures, CXR

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16
Q

mx neutropenic sepsis

A

Initial Antibiotic Therapy: initial empirical antibiotics (Piperacillin with tazobactam) to all patients within 1hr. Do not wait for the results of blood tests before administering antibiotics.

Switch to oral antibiotics after 24-48 hours of IV treatment if the patient is clinically
improving.

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17
Q

prevention neutropenmic sepsis

A

prophylaxis with a fluoroquinolone antibiotics, anti-
fungals or Granulocyte colony-stimulating factor (G-CSF).

 In the palliative setting chemotherapy doses may be reduced with subsequent cycles

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18
Q

causes malignant hypervcalcaemia

A

Osteolysis (lytic bone metastases)
 Humoral (PTHrP in squamous cell lung ca)
 Dehydration
 Other tumour specific mechanisms

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19
Q

presnetation malignant hypercalcaemia

A

BONES, STONES, GROANS AND PSYCHIC MOANS
 GI: abdominal pain, vomiting, constipation, anorexia, weight loss
 GU: polyuria, polydipsia
 Neuro: fatigue, weakness, confusion
 Psych: depression

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20
Q

ix malignant hypercalcaemia

A

Repeat blood sample, PTH
 ECG (shortened QT interval)
 Imaging for bone mets if appropriate

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21
Q

mx malignant hypercalcaemia

A

0.9% saline 4-6L
IV bisphosphonates-zolendronic acid

For persistent or relapsed hypercalcaemia of malignancy
o Denosumab: human monoclonal antibody that inhibits RANK ligand.

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22
Q

causes malignant spinal cord compression

A

Malignancy
o Primary
o Secondary – most common cause e.g. Prostate, Lung, Breast
 Mechanism = Crush fracture, soft tissue tumour extension

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23
Q

presentation malignant spinal cord compression

A

Worsening back pain
 Limb weakness below level of compression
 Sensory loss (sensory level present) below level of compression
 Bowel or bladder dysfunction - LATE sign, do not wait for this
 Radicular pain
 Abnormal neurological examination
o Causes lower motor neurone signs at the level of the lesion and upper motor
neurone signs below that level.14

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24
Q

ix malignant spinal cord compression

A

MRI WHOLE Spine; patient may have multiple levels of compression which require
treatment

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25
Q

mx malignant spinal cord compression

A

High-dose corticosteroids, analgesia, VTE prophylaxis

definitive: surgfery, radio, chemo,

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26
Q

causes superior vena cava obstruction

A

Inside the vessel
o Thrombus
o Intravascular device
 Inside the vessel wall
o Direct tumour invasion
 Outside the vessel
o Tumour; Lung cancer, Lymphoma, Germ cell tumours
o Fibrosing mediastinitis

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27
Q

sx SVCO

A

Dyspnoea
Chest pain, often at rest
Cough
Neck and face swelling
Arm swelling
Others – dizziness, headache, visual
disturbance, nasal stuffiness, syncope

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28
Q

signs SVCO

A

Dilated veins over arms, neck and anterior
chest wall
Oedema of upper torso, arms, neck and face
Severe respiratory distress
Cyanosis
Engorged conjunctiva
Convulsions and coma

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29
Q

ix SVCO

A

May be clinical diagnosis
 CXR (widened mediastinum or a mass on the right side of the heart)
 CT scan

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30
Q

mx SVCO

A

High-dose steroids can be useful in acute SVCO
 Endovascular stenting
 Also consider: Chemotherapy, Radiotherapy, Anticoagulation; if central vein thrombosis is present

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31
Q

what is ionising radiation

A

enough energy to detach electrons damages DNA

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32
Q

what is radiotherapy

A

use of high energy XR/ionising radiation in carefully measured doses to damage and destroy cancer cells

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33
Q

what is a neo-adjuvant

A

aims to decrease the size or extent of disease prior to radical tx

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34
Q

what is an adjunvant

A

aims to target micro-meastatic disease
reduce risk of local recurrnce

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35
Q

what is radical tx

A

aiming for cure
sometimes refers to high/curative dose

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36
Q

general SE radiotherpay

A

sunburn type effects
late = scarring

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37
Q

SE head and neck radiotherapy

A

acute: stomatitis, odynophagia, dysphagia, sore and red broken skin, xerostomia, dysgeusia, fatigue
late: long term xerostomia, dysphagia, skin fibrosis/telangiectasia, dental problems

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38
Q

SE prostate cancer radiotherpay

A

acute: dysuria, urinary freq/urg. diarrhoea, fatigue
late: long term bladder/rectile/erectile dysfunt,

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39
Q

preventing anaphylaxis with chemo

A

high dose steroid
IV/PO antihitamine
slower rate of infusion

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40
Q

mx coronary artery spasm due to chemo

A

stop infusion
nitrates

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41
Q

features coronary artery spsm due to chemo

A

features ACS

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42
Q

common antiemetics used for N+V in chemo

A

metoclopramide, ondansetron

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43
Q

mx constipation caused by chemo

A

excude infection/obstruction
loperamide, laxatives

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44
Q

features bone marrow suppression

A

thrombocytopenia
anaemia
neutropenia

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45
Q

mx fatigue/reduced appetite due to chemo

A

can give steroids but risk

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46
Q

mx alopecia due to chemo

A

cold caps
wigs

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47
Q

late effects of chemo

A

infertility
early menopase
atherosclerosis
heart failure
lung damage
chemo brain
secondary cancers

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48
Q

TNM staging

A

T=tumour size, 1-4
N=nodes
M=metastases

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49
Q

multiple myeloma

A

neoplastic proliferation of bone marrow plasma cells

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50
Q

characteristics multiple myeloma

A

monoclonal protein in serum or urine
lytic bone lesions/CRAB end organ damage
excess plasma cells in bone marrow

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51
Q

common presenting features myeloma

A

tired
bone/back pain +/- fractures
infections
lab: anaemia, renal failure, hypercalcaemia, raised globulins, rasied esr, serum/urien paraprotein

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52
Q

myeloma blood film

A

rouleaux

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53
Q

tx myeloma

A

cytotoxic: radiotherapy, chemo
supportive

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54
Q

what is acute leukaemia

A

proliferation primitve precursor cells usually only found in bone marrow
proliferation without differentiation
replaces normal bone marrow cells

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55
Q

what is acute lymphoblastic leukaemia

A

malignant proliferation of lymphoblasts in bone marrow
affects mainly children

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56
Q

tx acute lymphoblastic leukaemua

A

induction chemo
consolidation chemo +/- craniospinal irradiation
maintenance chemo
bone marrow transplant if relapse

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57
Q

what is acute myeloid leukaemia

A

malignant proliferation of myeloblasts in bone marrow
affects mainly adults

58
Q

chronic lymphocytic leukaemia

A

proliferation mature lymphocytes, usually B cels
affects elderly

59
Q

chronic myeloid leukaemiakey features

A

high white cell count and splenomegaly
philadelphia chromosome
chronic, accelerate, blast crisis

60
Q

tx chronic myeloid leukaemia

A

imatinib
allogeneic stem cell transplant

61
Q

myelodysplasia

A

premalignant condition of haemopoietic precursors
disease of elderly
can be asx or anaemia
can transform to acute myeloid leukaemia

62
Q

tx myelodysplasia

A

support
bone marrow transplant in young

63
Q

presentation hodkin lymphoma

A

painless lymphadenopathy
B sx: sweats, wt loss, fever
15-35y, >55y
reed sternberg cells

64
Q

mx hodgkins lymphoma

A

chemo, radiotherapy, stem cell transplant

65
Q

features low grade non hodgkin lymphoma

A

e.g. follicular
gradual onset
may be asx
incurable

66
Q

features high grade non hodgkin lymphoma

A

e.g. diffuse large B cell
rapidly progressive
sx
potentially curable

67
Q

sx myeloma

A

lytic lesions in bones - pain
hypercalcaemia- thirst, polyurea, confusion, constipation
hyperviscosity
renal failure
anaemia
infections

68
Q

what is lymphoma

A

malignant growth wbc
usually in lymph nodes
also in blood, bone marrow, liver, spleen

69
Q

diagnosing lymphoma

A

blood film and bone marrow
lymph node biopsy
immunophenotyping
PET for staging

70
Q

common presentation acute leukaemia

A

anaemia: tired, fatigue, lightheaded, palpitaiton,s sob
thrombocytopenia: bruising, bleeding
WCC: infection
extramedullary disease
coagulopathy -DIC

71
Q

blood film on acute myeloid leukaemia

A

increased blast cells

72
Q

ix in leukaemia

A

FBC
blood film
haematinics, haemolysis screen, LFTs, U+Es

73
Q

how are brain tumours classified

A

not using tnm
use WHO based on histology
grades using morphology into 4 grades of malignancy

74
Q

most common primary brain tumour

A

gliomas

75
Q

symptoms of brain tumours

A

headache - worse in morning/lying down
seizures
focal neuro sx: weakness, sensory loss, visual/speech disturbance, ataxia
non-focal: personality change/behaviour, memory disturbance, confusion

76
Q

signs of a brain tumour

A

papilloedema
focal neuro deficit - hemiparesis, hemisensory loss, vidual field defect, dysphasia

77
Q

brain tumour red flags

A

headache: features raised ICP or focal neurology
new onset focal seiaure
rapidly progressive focal neurology
past hx cancer

78
Q

ix for brain tumours

A

CT with contrast
MRI
brain biopsy

79
Q

tx brain tumours

A

non curative except grade 1
steroids - reduce oedema
surgery - biopsy or resection
radiotherapy
chemo: temozolamide, pcv

80
Q

effects of pituitary tumours

A

excess hormone production
local effects
inadequate hormone production by remianing pituitary
usually benign and curable

81
Q

neuroepithelial tumours - histological classification 1

A

astrocytic, oligodendrological, ependymal, neuronal and neuro-glial, pineal, embryonal, choroid plexus

82
Q

brain tumours in histological classification 2

A

cranial and spinal nerve tumours
meningeal tumours
lymphomas
germ cell tumours
metastatic tumours

83
Q

astrocytoma grading

A

I-4, worsening prognosis
IV=gliobastoma

84
Q

common cancers that metastasise to the brain

A

lung
breast
melanoma
GI
tract
kidney

85
Q

anatomical effects of a mass lesion

A

local deformity and shift of structures
decreased vol CSF
pressure gradients - internal herniation

86
Q

RF bladder cancer

A

smoking
environemnt: petroleum, phenacetin, cadmium
occupational: leather tanners, shoe workers, asbestos
hormonal: obesity, diethyrlstillbestrol
genetic: VHL, BHD

87
Q

presentation renal cancer

A

triad: mass, haematuria, pain
incidental
haematuria
sx metastatic disease
paraneoplastic sx: PTH, erythropoietin, prolactin
variocele rare

88
Q

upper tract TCC

A

CT CAP
not really curable if gone beyonf kidney
nephroureterectomy

89
Q

tx options for renal cancer

A

surveillance
radical nephrectomy
partial nephrectomy
radiofrequency ablation
cryotherapy
tyrosine kinase inhibitors
cytoreductive nephrectomy
palliative care

90
Q

presentation bladder cancer

A

painless haematuria
LUTS

91
Q

pathology bladder cancer

A

transitional cell carcinoma
increased number epithelial cell layers

92
Q

ix bladder cancer

A

CT
cystoscopy- felxible under LA

93
Q

tx options bladder cancer

A

TURBT
intravesical chemo or immunotheraoy
cystectomy
radiotherapy
chemo
palliative

94
Q

RF testicualr cancer

A

cryptorchidism
germ cell neoplasia - klinefelters
HIV
genetic
maternal oestrogen exposure

95
Q

pathology testicular cancer

A

germ cell tumours - seminomatous and non seminomatous

96
Q

presntation testicular cancer

A

scrotal lump (hard, irregular, non-transilluminable)- painless
scrotal pain due to haemorrhage
sx metastasis - wt loss, lumps in neck, bone main
secondary hydrocele

97
Q

ix testicualr cancer

A

USS
staging - CT CAP
tumour markers - AFP, LDH, hCG, before tx

98
Q

what are sarcomas?

A

Sarcomas are rare tumours of mesenchymal
tissue.

99
Q

early SE chemo

A

Anaemia, thrombocytopenia, neutropenia

Mouth ulcers, thrush

N&V

Constipation

Neurotoxicity – peripheral neuropathy, encephalopathy

Nephrotoxicity – also haemorraghic cystitis

Hair loss

Tiredness

100
Q

late SE chemo

A

Cardiotoxicity

Nephrotoxicity

Neurotoxicity

Osteopenia

Fertility

Second malignancies

101
Q

mx localised sarcomas

A

surgery

Addition of radiotherapy improves local control rates,

102
Q

mx advanced sarcomas

A

usually palliative
surgery, chemo, radiotherapy

103
Q

back pain red flags

A

thoracic pain, non mechanical, Hx of malignancy, saddle anaesthesia, incontinence, leg weakness, systemic features <20 or >55 years

104
Q

mx spinal metastases

A

Analgesia (pain ladder, specialist pain teams)
Palliative radiotherapy
Vertebroplasty/spinal stabilisation surgery
Bisphosphonates – only if involvement from breast or prostate cancer or myeloma

105
Q

mx spinal cord compression

A

Refer to neurosurgery for MRI whole spine
Give IV dexamethasone and VTE prophylaxis

106
Q

pathophysiology humoralhypercalcaemia of malignancy

A

Humoral is caused by secretion of parathyroid hormone related peptide by tumour, activating osteoclasts suppressing osteoblasts, releasing Ca

107
Q

causes hypercalcaemia of malignancy

A

Ca renal, ovarian, breast, endometrial, squamous cell
Release of factors by bony mets increasing osteoclasts: Myeloma, Breast bony mets
Calcitriol production: Lymphoma
Ectopic hyperparathyroidism: Small cell lung cancer

108
Q

hypercalcaemia sx

A

Dehydration!
Bones, stones, groans, thrones and psychic moans: Bone pain, Increased risk of kidney stones, Abdominal pain, nausea, Constipation, polyuria (+polydipsia), Confusion, fatigue

109
Q

hypercalcaemia mx

A

REHYDRATE, MONITOR U+ES
Treat malignancy, support and monitor, avoid meds that worsen hypercalcaemia (Thiazides, calcitriol/calcium supps, antacids, lithium)
If severe: IV bisphosphonates/denosumab, Furosemide

110
Q

what is tumour lysis syndrome

A

Metabolic and electrolyte abnormalities and renal impairment – due to lysis of rapidly dividing cancer cells, releasing intracellular contents into circulation
Usually hours/days into chemotherapy
Usually chemosensitive lymphoma/leukaemia
Cancer cells have high turnover, produce lots of uric acid and phosphate, renal ability for excretion is saturated

111
Q

who is at risk of tumour lysis syndrome

A

dehydrated, renal impairment, prechemo high urate and lactate

112
Q

what does renal saturation in tumour lysis syndrome cause

A

Hyperuricaemia – can cause uric acid nephropathy and AKI
Hyperphosphataemia – can cause calcium phosphate deposition and obstruction
Secondary hypocalcaemia (from high phosphate)
Hyperkalaemia (from cell degradation)

113
Q

presentation tumour lysis syndrome

A

Syncope/chest pain/dyspnoea
Seizures
Nausea, D+V
Muscle weakness and cramps

114
Q

ix tumour lysis syndrome

A

25% INCREASE in uric acid, phosphate, potassium
25% DECREASE in calcium
High creatinine and LDH

115
Q

mx tumour lysis syndrome

A

Prevention is key
Prechemotherapy IV fluids, avoid nephrotoxic meds, use allopurinol (blocks conversion to uric acid)
Treating – hydrate, correct high potassium, give rasburicase (oxidises uric acid), give aluminium hydroxide (phosphate binder)

116
Q

benign tumours

A

can put pressure on structures, obstruct flow, produce hormones
Localised, non invasive
Closely resemble normal structures
Circumscribed
Normal morphology

117
Q

malignant tumours

A

destroy tissue, cause blood loss
Invasive, metastatic
Rapid growth down and in
Variable resemblance to normal structures
Poorly defined border, increased mitosis

118
Q

papilloma

A

benign epithelial neoplasm

119
Q

adenoma

A

benign epithelial neoplasm of glandular/secretory

120
Q

carcinoma

A

malignant tumour of epithelial cells

121
Q

adenocarcinoma

A

malignant tumour of glandular/secretory epithelium

122
Q

tumour invasion steps

A

Normal tissue
Carcinogenesis
Dysplasia
In situ neoplasia
Invasive malignancy
Metastatic cascade (intravasation, evasion, adherence, angiogenesis)
Metastatic disease
Death

123
Q

tumour grading

A

1 – looks like normal cells, growing slowly
2 – less like normal cells, quicker growth
3 – abnormal fast growing cells
T0-3 (extent of tumour) N0-3 (presence/extent of regional lymph nodes) M0-1 (presence of metastases)

124
Q

cancer and thrombosis

A

Cancers are prothrombotic so VTE prophylaxis important
Can cause higher number of platelets and clotting factors
Surgery/chemo can damage vessels and cause increased clots
Cancer and chemo can also lead to low platelets
Cancer can directly erode blood vessels
Clotting factors decrease with chemo or liver involvement

125
Q

endocrine paraneoplastic syndromes

A

Syndrome of inappropriate antidiuretic hormone (SIADH): Mostly small cell lung cancer
Cushing’s syndrome – overproduction of ACTH precursors: Mostly small cell lung cancer, non SCLC, carcinoids
Hypercalcaemia – most caused by bony mets, this is humoral hypercalcaemia of malignancy: Squamous cell – NSCLC, head/neck, renal

126
Q

neuro paraneoplastic syndromes

A

Peripheral neuropathy: SCLC, myeloma, Hodgkin’s, breast, GI
Encephalomyelopathies: SCLC
Cerebellar degeneration: SCLC, breast, Hodgin’s
Lambert-Eaton myasthenic syndrome : SCLC

127
Q

haem paraneoplastic syndromes

A

anaemia, leukocytosis, thrombocytosis – mostly renal, lymphomas, leurkaemias, lung squamous cell

128
Q

derm paraneoplstic syndromes

A

pruritus, pigmentation, erythema, bullous pemphigus – mostly lymphoma/leukaemia, some GI

129
Q

what is carcinoid syndrome

A

Due to secretion of serotonin and kinins from neuroendocrine tumours : Gastric carcinoma, bronchial adenoma, pancreatic carcinoma – often liver mets

130
Q

features carcinoid syndrome

A

Flushing, diarrhoea, wheeze, abdo pain

131
Q

mx carcinoid syndrome

A

resection, octreotide (somatostatin analogue)

132
Q

what are neuroendocrine tumours

A

Neoplasms arising from endocrine or nervous system
Commonly in the intestine (can be called carcinoid tumours), Also in pancreas, lung (SCLC)

133
Q

what is a sarcoma

A

Cancer of connective tissue, some associated with specific gene mutations

134
Q

presentation sarcoma

A

soft tissue swelling and pain

135
Q

types of sarcoma

A

Liposarcoma
Leiomyosarcoma (uterine bleed)
Fibrosarcoma
GIST (acute abdomen, bleed)
Synovial sarcoma
Kaposi’s sarcoma (AIDS related)

136
Q

ix sarcoma

A

Ix: CT/MRI of the mass shows heterogeneous mass with central necrosis, patchy contrast enhancement
CT chest for mets, HIV test, biopsy and histology, genetic testing

137
Q

mx sarcoma

A

wide local excision with pre and post of radiotherapy
Possible chemo but not very sensitive

138
Q

what is lymphoedema

A

Chronic progressive swelling of tissue with protein rich fluid as a consequence of developmental or acquired disruption of lymphatic system
Majority malignancy or cancer treatment

139
Q

mechanisms lymphoedema

A

Inflammation and increased vascular permeability
Lymphatic obstruction of drainage
Hypoalbuminaemia decreased oncotic pressure
Venous oedema from increased venous pressure

140
Q

mx lymphoedema

A

Skin care, compression bandaging, elevation, exercise, weight loss, psych support
If filiariasis = diethylcarbamazine or albendazole