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oncology Flashcards

1
Q

describe the stage of the WHO performance status and the relevance to cancer patients

A

0 - no symptoms, normal activity
1 - symptomatic, able perform daily activities
2 - symptomatic, bedbound <50% day, needs some assistance
3 - symptomatic, bedbound >50% day
4 - bedridden
5 - dead

only consider treating people between 0-2

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2
Q

treatment intents:

  • neo-adjuvant
  • radical
  • adjuvant
  • palliative
A

neo-adjuvant - given before curative (surgery) to shrink it or remove micro metastases that may cause re-occurance

  • radical - curative (mainly surgery) and long term control
  • adjuvant - after curative intent treatment eg chemo/radio - reduce micro-metastases
  • palliative - shrink + control but not get rid - preserve QoL + prolong
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3
Q

how does chemotherapy work

A

broadly by damaging DNA:

  • directly by binding
  • indirectly - affecting replication/miosis
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4
Q

what is radiotherapy

A

is the use of high energy x-rays in carfully measured doses to damage

  • ionising - energetic enough to displace an electiron from its orbit around a nucleus. this electron can go on and interact with other atoms
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5
Q

how is radiotherapy used?

A
  • brachytherapy ?
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6
Q

what is immunotherapy

A

systemic agents that aim to stimulate a patient own immune system to attack cancer cells

  • good for melanoma
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7
Q

s/e of immunotheraopy

A

autoimmune toxicities

- colitis most common eg lots of diarrhoea

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8
Q

what are and name some targeted agents

A

inhibit specif

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9
Q

important things to consider with palliative patients

A

ask them what else they are putting themselves on at the minute - ensure not interacting with actual treatments eg weird diets/pills from internet

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10
Q

treatment related oncological emergencies

A 
cytopenias - neutropenic sepsis
electrolyte disturbance
tumour lysis syndrome
diarrhoea
vomiting
anaphylaxis
extravasation
radiotherapy s/e
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11
Q

in what day of the 3 week cycle are they neutropenic

A

7/8

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12
Q

tumour related oncological emergencies

A 
spinal cord compression
SVCO
upper airway obstruction
brain mets 
bowel obstruction
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13
Q

most appropriate treatment for cancer associated thrombosis?

A

dalteparin first

or rivaroxaban

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14
Q

what do you always pair with dexa when prescribing

A

antiemetic

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15
Q

when does spinal cord end

A

L1

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16
Q

define hypertrophy

A

Increase in size of cells -> increase in size of organ
Physiological (response to functional demand) e.g. cardiac at athletes, pathological (response to abnormal increase demand) e.g. cardiac at hypertension

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17
Q

define hyperplasia

A

Increase in number of cells, may be associated with hypertrophy
Physiological e.g. breast at puberty, pathological e.g. psoriasis

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18
Q

define atrophy

A

Decrease in size of cell/organ due to cessation of growth. Atrophy is an adaptive response (use it or lose it)
Pathological: disuse (post fracture), loss of innervation (nerve transection), loss of blood supply (due to hypoxia e.g. skin at varicose veins), pressure atrophy (tissue compression e.g. bed sore), lack of nutrition, hormone induced (@skin following corticosteroids)

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19
Q

define dysplasia

A

Abnormal increased cell growth with 1) cellular atypia 2) decreased differentiation (pre-malignant, but reversible at early stage)

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20
Q

define metaplasia

A

Transdifferentiation: transformation of one terminally differentiated cell into another e.g. Barrett’s = squamous -> glandular, cigarettes = respiratory to squamous

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21
Q

necrosis vs apoptosis

A

apop
Programmed cell death (individual cell deletion in physiological growth control and in disease.

necro
Death of cells/tissue from ischaemic, metabolic or traumatic cause.
Failure of membrane integrity.

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22
Q

carcinogenesis

A

Transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations

23
Q

benign v malignant

A 
Benign:
Localised
Non-invasive
Closely resemble normal structure
Circumscribed/encapsulated
Nuclear morphology = normal
Necrosis and ulceration rare
Growth exophytic (up and out)
Morbidity/mortality - pressure on adjacent structures, flow obstruction, hormone production, transformation to malignant
malignant:
Invasive
Metastatic
Rapid growth
Variable resemblance to normal structure
Poorly defined border (crablike)
Increased mitotic activity
Necrosis and ulceration common
Growth endophytic (down and in)
Morbidity/mortality - destroy surrounding tissue, metastases, blood loss ulcers, flow obstruction, hormone production, paraneoplastic syndrome
24
Q

names for benign epithelial lesion

A

papilloma

adenoma

25
Q

names for malignant epithelial lesion

A

carcinoma

adenocarcinoma

26
Q

connective tissue benign lesions

A

the OMAs

lipoma, osteoma, angioma, rhabdomyoma (striated), leiomyoma (smooth)

27
Q

connective tissue malignant lesion

A

sarcoma

28
Q

what does poor differentiation mean

A

high grade

29
Q

what does well differentiated mean

A

low grade

30
Q 
what would you expect from these grades of cancers
1
2
4
X
A

Grade 1: cancer cells look like normal cells and are growing slowly
Grade 2: cells look less like normal cells and grow more quickly
Grade 3: cells look abnormal and are growing quickly
Grade X: grade can’t be assessed

31
Q

what is radiotherapy

A

High energy beam of X-rays delivered to precise area using linear accelerator - causes DNA damage. Dose in Grays (1 Gray = 1 J/kg)
May be used as sole treatment or with surgery (before - neoadjuvant, post resection - adjuvant)

32
Q

types of radiotherapy

A

External beam radiation therapy - using CT/MRI to target tumour
Internal radiation therapy - brachytherapy - radiation source placed near target tumour
Stereotactic radiotherapy - involves very accurate treatment, may be good for small discrete lesions

33
Q

complications of radiotherapy

A

Acute (during treatment or <2-3 weeks):
Fatigue (80%)
Skin - Erythema, dry and moist desquamation, irritation
GI - loss of taste, oral mucositis (complicated by yeast/bacterial superinfection), diarrhoea, nausea, vomiting
BM - cytopenias
Lungs - pneumonitis, fever, cough, dyspnoea

Chronic
Infertility
Lymphoedema
Delayed healing
Loss of salivary flow
Transverse myelitis, Lhermitte’s 
Increased risk CV events/stroke
Hypothyroidism
34
Q 
chemotherapy
how given
its target
types
routes
A

Chemotherapy does not tend to be curative (except in leukaemias, lymphomas)
It may be neo-adjuvant (before surgery) or done in combination with surgery if patient is younger/curative cancer
Given in cycles (3 weekly) to allow normal cells to recover
Tends to target fast replicating cells e.g. gut mucosa, hair and bone marrow

types
Alkylating agents
- Chlorambucil, carmustine, darcarbazine
Cytotoxic antibiotics
- Doxorubicin, bleomycin
Antimetabolites
- 5-fluorouracil, methotrexate (NEVER INTRATHECAL)
Topoisomerase inhibitors
- etoposide
Mitotic inhibitors
- Vincristine (vinca alkaloid), paclitaxel (taxane)
Platinum compounds e.g. cisplatin

route
Oral, IM, IV, intrathecal, topical

35
Q

s/e of chemo

A 
side effects:
Myelosuppression - anaemia, infection, bleeding
One week after, FBC prior to admission
Alopecia
Infertility
Nausea, vomiting and diarrhoea
Major cause of distress - use domperidone or metoclopramide
Fatigue
Teratogenicity
Mouth ulcers
36
Q

what is extravasation

mgmt

A

Is a problem with chemotherapy
Associated with pain, redness and inflammation -> may lead to skin necrosis + amputation (dissolving soft tissue). May see brown demarcation of veins
Maintain high index of suspicion with blotching/blistering
Reduce risk by administration by trained personnel
Rx: Topical agents e.g. dimethyl sulfoxide, heat, cold, debridement and grafting may be required

37
Q

biological therapies
how do they work
types

A

Designed to boost body’s defences by:

  1. Stop/slow growth cancer
  2. Stop spread of cancer
  3. Help immune system

types
Monoclonal antibodies
Non-specific immunotherapies - interferons and interleukins
Oncolytic virus therapy - melanoma (T-VEC)
T-cell therapy
Cancer vaccines

38
Q

what do you need to know to consent

A 
Logistics
Benefits (pros)
SE (cons)
Alternatives
Prognosis
39
Q

anaphylaxis
what type of reaction
mgmt

A

t1 hypersensitivity

Stop the drug
Perform ABCDE assessment - if anything is deranged consider anaphylactic reaction rather than strong allergic reaction - airway management, fluid resuscitation, IM adrenaline (0.5mg), IV hydrocortisone + IV chlophenamine/piriton

may recur 4-12 hours so beware

40
Q 
neutropenic sepsis 
why @ risk
suspect when 
def
ix
mgmt
A

why @ risk
Is a risk due to myelosuppression

Suspect with fever in anyone who has had chemotherapy in the last 6W

Defined as neutrophil count of less than 1 per high power field or severe neutropenia = NP < 0.5 x 10^9/L (mod = 0.5-1)
Pyrexia or temp > 37.5 taken at >1 site >1 hour apart
BUT may not get a temperature

Ix
Want to take FBC, LFT, U + Cr, CRP, lactate, blood cultures (multiple sites), urine culture, NOT LP (may introduce infx), swabs and cultures from central line (each part)

mgmt
IV ABX according to local policy -> Beta lactam monotherapy piperacillin and tazobactam (Tazocin), or gentamycin (sometimes) ± G-CSF ± fluconazole (thrush), ± aciclovir (VZV)

41
Q 
spinal cord compression
epi
pres
where
ix
mgmt
A

epi
Occurs in 3-5% of those with known cancer
Occurs in 10% of those with known spinal metastasis (bronchus, breast, prostate, mm)

Presents with PAIN ± sensory loss at level ± weakness below level ± loss of continence

where
70% are thoracic, 20% are lumbosacral, 10% are cervical, below L1/L2 think cauda equina

ix
Perform a peripheral nerve exam + percuss spine
MRI whole spine, refer to neurosurgery/spinal surgery

mgmt
IV DEXAMETHASONE + prevention VTE

42
Q

painful spine mets mgmt

A

Analgesia (NSAID/non-opiate/opiate)

Bisphosphonates if myeloma/breast cancer (lytic lesions)

Palliative radiotherapy

Vertebroplasty

43
Q

DVT/PE in cancer patients

why high risk

A

Both the cancer and its treatment (higher number of platelets and clotting factors)
Surgery and chemotherapy may damage vessel walls (increased clots)
Patients tend to be less active

44
Q

why haemorrhage risk in cancer patients

A

Both chemotherapy and disease process may lead to low platelets
Cancer may cause direct erosion of blood vessels (n.b. major blood vessel = fatal)
Decreased clotting factors with liver metastasis or chemotherapy
Consider NSAIDs for pain, topical tranexamic acids/adrenaline soaks, oral tranexamic acid

45
Q 
hypercalcaemia of malignancy
mechs
def
causes
types
symps
ix
mgmt
A

mechs

  1. Secretion of PTH related peptide by tumour (humoral hypercalcaemia)
  2. Local release of factors increasing osteoclast proliferation (local osteolytic hypercalcaemia) - including PTH-rP
  3. Autonomous production of calcitriol by lymphoma
def
10% of malignancies assoc hypercalcaemia, 20% hypercalcaemias due to malignancy

causes
Humoral - renal, ovarian, breast, endometrial, squamous cell carcinoma
Local osteolytic - breast, multiple myeloma
Calcitriol mediated - lymphoma and granulomatous disease
Ectopic PTH (small cell lung Ca)
20% due to unrelated hyperparathyroidism

types
humoral
local osteolytic hypercalcaemia
calcitriol mediated

symps
Dehydration + bones, stones, abdominal moans, thrones, psychic overtones
Poor skin turgor/dry mucous membranes (DEHYDRATION)
Bone pain (BONES)
Abdominal pain (STONES)
Constipation, loss of appetite, nausea (ABDOMINAL MOANS)
Polyuria + polydipsia (THRONES)
Confusion + fatigue (PSYCHIC OVERTONES)

ix
total calc
serum ionised calc
serum albumin
resting ECG
serum PTH
serum PTHrP
serum phos
serum calcitiriol
skeletal survery
mgmt
avoid meds that worsen:
Thiazide diuretics
Calcitriol
Calcium supplementation
Antacids
Lithium
if mild/asymp - supportive
if mod/severe
IV normal saline (reverses dehydration secondary to hypercalcaemia induced nephrogenic diabetes insipidus)
IV bisphosphonates/denosumab (pamidronate, zoledronic acid) - block osteoclastic bone resorption
Furosemide to avoid fluid overload
46
Q 
SVC obstruction
where
what surrounded by
patho
symps
ix
mgmt
A

where
SVC from junction of L + R brachiocephalic to RA

surrounding stuff
Located in middle mediastinum
Surrounded by trachea, right bronchus, aorta, pulmonary artery, perihilar LNs

patho
SVC obstruction initiates collateral venous return to heart - most important is azygous system (azygous, hemiazygous, intercostals), second is internal mammary venous system

symps
Oedema of face and upper extremities (80%)
Dyspnoea (60%) - worse leaning forward
Facial plethora (venous engorgement)
Cough
Distended neck veins + chest veins - worse leaning forward
Hoarse voice
? Blurred vision + sev = laryngeal oedema, cyanosis, mental changes
FIXED (non-pulsatile) + RAISED JVP

ix
Chest x-ray (widened mediastinum or mass in lung),
CT thorax with contrast (collat vess, loc, sev, path),
USS upper extremities (dilated SVC, thrombus)

mgmt
Acute airway obstruction?
1. Secure airway (intubate/surgical) + local radiotherapy + corticosteroids (dexamethasone 10mg IV bolus + 4mg every 6 hours) OR
2. Secure airway + percutaneous endovascular stent (bleeding risk, patency)

Malignant (usually gradual)
Treat malignancy - often cancers are radiosensitive (thymoma = radio/chemo resistant)
+ palliative radiotherapy/ dexamethasone (for thymoma/lymphoma)

47
Q 
tumour lysis syndrome
def
common when
pres
patho
ix
mgmt
A 
def
Combination of metabolic and electrolyte abnormalities occurring spontaneously following initiation of cytotoxic treatment in patients with cancer. Characterised by excessive cell lysis.

common when
In highly prolif, chemosensitive malignancies e.g. lymphoma and leukaemia esp NHL/ALL

pres
in lab:
- 2 of hyperuricaemia, hyperphosphataemia, hyperkalaemia, hypocalcaemia
Lab + increased serum creatinine, arrhythmia (K+, PO4, hypoCa), seizure (hypoCa + muscle cramps + tetany)

patho
Malignant cells have high turnover. Produce high nucleic acid products (-> uric acid) + phosphate.
Ability of kidney to eliminate large amounts is saturated
Hyperuricaemia + reduced urinary flow -> uric acid crystals, renal tubule obstruction and decline in renal func (AKI)
Hyperphosphataemia -> calcium phosphate crystals -> nephrocalcinosis and urinary obstruction
Secondary hypocalcaemia due to hyperphosphataemia
Hyperkalaemia from cell degradation
AKI -> fluid overload and pulmonary oedema
Main mechanism of AKI is uric acid nephropathy + calcium phosphate deposition

rfs
Haematological malignancy, large tumour burden (*high lactate dehydrogenase, WBC and uric acid pre-treatment), chemosensitive, renal impairment, dehydration

pres
Syncope/chest pain/dyspnoea
Seizure
Nausea/vomiting/diarrhoea
Muscle weakness/cramps

ix
Serum uric acid (25% increase), phosphate (25%), potassium (25%), calcium (25%) decrease
FBC - elevated WCC, serum creatinine (x 1.5 upper limit), lactate dehydrogenase (elevated), serum urea (high at AKI), ECG

mgmt
low risk - monitor + avoid nephrotoxic drugs
inter - prechemo IV hydration, reg monitor, aluminium hydroxide as phosphate binder, allopurinol
high risk - prechemo IV hydration, reg monitor, phosphate binder, rasburicase
acute - Treat hyperkalaemia
Intense fluid resuscitation
Phosphate binder
Rasburicase
Sodium bicarbonate

48
Q

paraneoplastic syndromes
what is it
mediators
common which with cancers?

A

A syndrome that is the consequence of cancer in the body, but unlike mass effect is not due to local presence of cancer cells.
Mediated by humoral factors - hormones/cytokines secreted by cancer cells, or by immune response to tumour
Common with breast, lung, ovarian or lymphoma

49
Q 
lambert-eaton myasthenic syndrome
def
mech
pres
ix
mgmt
A 
def
Rare AI disorder of NM junction associated with SCLC (50%) + smoking + AI disease

mech
Circulating antibodies against VGCaC, impair NM transmission by inhibiting calcium current and release of Ach to synaptic cleft.
SCLC cells contain high concentrations of VGCaC (induce production of VGCaC antibodies)

pres
Limb weakness (proximal legs + arms)
Dry mouth (xerostomia + metallic taste) - autonomic
Weakness (Limb girdle + waddling gait)
Dysarthria, ptosis, diplopia, impotence
ix
Nerve conduction studies - doubling of compound muscle action potential post exercise
Anti VGCaC - positive
Anti AChR - negative
Chest CT - ? malignancy
Serial LuFT - low FVC - ? resp crisis

mgmt
No resp/bulbar weakness -> treat cause + amifampridine ± pred
Severe resp/bulbar weakness -> intubation and ventilation + plasma exchange/IVIG

50
Q 
carcinoid syndrome
pres
patho
dx
mgmt
comps
A

Commonly presents with flushing/diarrhoea (± wheeze, palpitations, telangiectasia, abdo pain)
Symptoms due to secretion of serotonin and kinins (vasoactive peptides) from neuroendocrine tumours (gastric carcinoma, bronchial adenoma - carcinoid type, pancreatic carcinoma). Often seen in pts with liver mets
Diagnose by elevated urinary-5-hydroxyindoleacetic acid (24 hr)
Treatment - medical therapies (octreotide - somatostatin analogue) + surgical resection
Complications - carcinoid heart disease (fibrosis on R valves) and crisis at times of stress (surgery = hypotension and wheeze)

51
Q

which cancers to bone?

A 
reast - lytic or sclerotic
Prostate - sclerotic
Bronchus - lytic
Myeloma - lytic
Thyroid - lytic
52
Q

familial cancer syndromes

A

MEN - see endocrine
NF - see endocrine
Retinoblastoma - associated with sarcoma (Rb1, Ch13)
Ataxia telangiectasia - AR - assoc lymphoma and leukaemia
HBOC (hereditary breast/ovarian cancer) - AD by BRCA
HNPCC/Lynch syndrome - AD - endometrial, stomach, ovarian, small bowel, pancreas
FAP - AD - 100% penetrance
Li Fraumeni - AD (Tp53 gene) - soft tissue sarcoma, osteosarcoma, breast, brain, leukaemia
VHL - Von Hippel Lindau - AD - benign and malignant. CNS and retinal hemangioblastoma, clear cell renal, phaeo, pancreatic

53
Q

places where chemo doesnt reach well? what are these called

A

A sanctuary site is an area that chemotherapy does not reach well e.g. brain and scrotum in ALL

finals (17 decks)

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