Treatments and complications Flashcards

1
Q

Surgery in cancer uses

A

Curative approach - WLE, mastectomy, Whipples, anterior resection

Biopsy - lobectomy, mediastinoscopy

Palliative surgery - defunctioning stoma, gastrojejunostomy

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2
Q

Surgery in cancer considerations

A

Bleeding, infection

Anaesthetic risks

Specific complications and risks

Recovery time

Pre and post operative fitness

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3
Q

Radiotherapy

A

High energy ionising radiation to treat malignant disease

Treatment options - radiotherapy alone, with surgery, with SACT, with hormonal treatment

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4
Q

Radiotherapy mechanism of action

A

Direct action: radiation → DNA damage → cell death

Indirect action: radiation → free radicals → DNA damage → cell death

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5
Q

Radiotherapy types

A

External beam

Brachytherapy - used as a boost treatment/can be primary treatment

  • prostate & cervical cancers

Systemic treatments - radioactive substance (injected/swallowed)

Aims: deliver the highest dose possible to the tumour & minimise dose to surrounding ‘normal tissue’

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6
Q

Radiotherapy intent

A

Radical radiotherapy is used to treat cancer as part of a curative strategy - neoadjuvant, adjuvant & definitive

Can be used to control/improve symptoms - palliative

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7
Q

Radiotherapy acute toxicity

A

Within 3/12

Hair loss

Fatigue

N&V

Dysphagia, sore throat, oral mucositis

Erythema

Lymphoedema

Low blood counts

Dysuria - radiation cystitis

Diarrhoea

Sterility

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8
Q

Radiotherapy late toxicity

A

After 3/12

Skin - pigmentation, necrosis, telangiectasia, ulceration

Bone - necrosis, fracture, impaired growth (children)

Mouth - ulceration, xerostomia

Eyes - cataracts, loss of sight

Lung fibrosis

Heart - cardiomyopathy, pericardial fibrosis

Gonads - infertility, menopause

Bowel - strictures, adhesions, fistulas

Secondary malignancy

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9
Q

Cytotoxic chemotherapy

A

Cytotoxic drugs that destroy cancer cells

Single/combination of agents that can be combined with other treatment modalities

Treatment intent - neoadjuvant, adjuvant, palliative

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10
Q

Alkylating agents

A

Cyclophosphamide, ifosfamide, temozolamide

Methylation of DNA bases causing cross linking of DNA strands

Leads to inhibition of DNA replication

Used in breast, sarcoma

Cyclophosphamide SEs - haemorrhagic cystitis

Ifosfamide SEs - encephalopathy, haemorrhagic cystitis

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11
Q

Taxanes

A

Paclitaxel, docetaxel, cabazitaxel

Bind to and stabilise tubulin in microtubules which inhibits anaphase

SEs - alopecia, peripheral neuropathy, hypersensitivity reactions

Used in breast, lung, prostate

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12
Q

Vinka alkaloids

A

Vinorelbine, vincristine

Prevents polymerisation of tubulin to form microtubules so failure of mitotic spindle

SEs - peripheral neuropathy

Used in lung, mesothelioma, sarcoma

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13
Q

Platinums

A

Cisplatin, carboplatin, oxaliplatin

Cause cross linking of DNA strands and stop DNA replication

SEs: emetogenic, ototoxic, peripheral neuropathy, nephrotoxic

Used in breast, lung, colon, HPB, H&N

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14
Q

Antimetabolites

A

5FU, capecitabine, methotexate, gemcitabine, pemetexed

Interfere with DNA synthesis through various mechanisms

Toxicity - palmar plantar erythema, diarrhoea, mucositis

Used in colon, HPB, breast, sarcoma, lung

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15
Q

Topoisomerase I inhibitors

A

Irinotecan, topotecan

Inhibits topo I (involved in DNA replication)

SEs - alopecia, diarrhoea

Used in colon, HPB, lung

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16
Q

Topoisomerase II inhibitors

A

Anthracyclines - doxorubicin, epirubicin

Inhibits topo II disrupting DNA replication → free radical generation to cause DNA damage

SEs - cardiomyopathy, alopecia, vesicant

Used in breast, sarcoma

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17
Q

Prescribing chemotherapy

A

Individual dosing - surface area/BMI, drug handling ability (LFTs, U&Es), performance status

Routes of administration - IV, PO, intralesional, intrathecal, topical, IM

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18
Q

Bowel obstruction

A

Due to mechanical obstruction (partial or complete) of the bowel lumen and/or peristaltic failure

Commonly occurs with carcinoma of the ovary or bowel

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19
Q

Bowel obstruction clinical features

A

Abdominal pain - colicky or cramping in nature

Vomiting

Abdominal distension

Constipation

O/E - evidence of underlying cause, abdominal distension, tinkling bowel sounds

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20
Q

Bowel obstruction ix

A

Urgent bloods - G&S, U&Es, venous blood gas

CT scan with IV contrast of the abdomen & pelvis

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21
Q

Bowel obstruction mx

A

Urgent IV fluid resuscitation

NG tube & urinary catheter

Surgery - remove the blockage; may need colostomy/ileostomy afterwards

Stent - can help relieve symptoms caused by the obstruction

Drugs - hyoscine butylbromide (Buscopan): stops muscle spasms and reduces pain, analgesia, octreotide: reduces amount of fluid that builds up in GI tract, steroids: reduce inflammation & help control sickness

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22
Q

Malignant hypercalcaemia

A
  • serum calcium > 2.6 mmol/L, secondary to a malignant process
  • most common cause of hypercalcaemia in the inpatient population
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23
Q

Malignant hypercalcaemia pathophysiology

A

Most common malignancies associated with hypercalcaemia are breast, multiple myeloma, lymphoma & lung cancer (SCC)

Three main mechanisms - osteolytic metastasis, PTHrP secretion, increased 1,25-dihydroxyvitamin D production

1) PTHrP secretion - solid tumours such as breast & non-Hodgkin’s lymphoma are common causes, less likely to lead to activation of vitamin D

2) osteolytic metastasis - most commonly associated with breast cancer, deposition of tumour cells within bone → local production of inflammation cytokines → stimulates osteoclasts causing bone resportion

3) 1,25-dihydroxyvitamin D production - increased activated vitamin D levels leads to increased absorption of calcium, most common in Hodgkin’s lymphoma

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24
Q

Malignant hypercalcaemia clinical features

A

Frequently asymptomatic

Bones - fragility fractures, bone pain,

Stones - renal calculi

Thrones - polyuria, constipation

Psychic moans - mood disturbance, fatigue/malaise

Abdominal groans - abdo pain, pancreatitis

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25
Q

Malignant hypercalcaemia ix

A

Bloods - bone profile, myeloma screen

CT C/A/P

26
Q

Malignant hypercalcaemia mx

A

IV hydration - normal saline

Calcitonin - can be given to a patient with moderate/severe hypercalcaemia → promotes urinary calcium excretion

Bisphosphonates - provide calcium-lowering effects over a prolonged period

27
Q

Ascites

A

Build up of fluid within the peritoneal cavity in the abdomen due to underlying malignancy

28
Q

Ascites causes

A

Ovarian cancer

Breast cancer

Bowel cancer

Stomach cancer

Pancreatic cancer

Lung cancer

Liver cancer

29
Q

Ascites pathophysiology

A

Tumour cells irritate the peritoneum and cause it to produce too much fluid

Lymph glands in the abdomen get blocked & can’t drain fluid properly

Cancer has spread to the liver → raises pressure in blood vessels → forces fluid out

Liver can’t produce enough albumin → fluid leaks out of veins into the cavity

30
Q

Ascites clinical features

A

Abdominal distension

Abdominal pain

Back pain

Loss of appetite

Indigestion

Breathlessness

31
Q

Ascites ix

A

Bloods - FBC, U&Es, LFTs, clotting, bone profile, CRP

Abdominal ultrasound

Ascitic tap - fluid sent to lab & tested

32
Q

Ascites mx

A

Abdominal paracentesis - reduces swelling & makes patient more comfortable

Long term drain may be required if fluid builds up again

Drugs - diuretics, chemotherapy into abdomen

33
Q

Pleural effusion

A

Build up of fluid in the pleural cavity with underlying malignancy

34
Q

Pleural effusion clinical features

A

Shortness of breath

Dru cough

Pain

Feeling of chest heaviness/tightness

Inability to lie flat

Inability to exercise

Generally feeling unwell

35
Q

Pleural effusion causes

A

Cancer - breast cancer, lung cancer, lymphoma, mesothelioma, ovarian cancer

Cancer treatments - radiotherapy, chemotherapy, lung surgery

36
Q

Pleural effusion ix

A

CXR

CT scan

Ultrasound

Thoracentesis - needle that removes fluid from pleural space for cytology

37
Q

Pleural effusion mx

A

Most common treatment is to drain the malignant pleural fluid

Thoracentesis - needle is inserted to remove the fluid

Tube thoracostomy - tube inserted to drain the fluid, typically stays in for a day or longer until enough of the fluid has drained; after this pleurodesis is done → stick the edge of the lung to the chest wall which decreases the chance that the fluid will return

Tunneled pleural catheter - can be left in long term for ongoing draining

Shunt - inserted during surgery, and used to bypass and divert excess fluid from one place to another

Chemotherapy

38
Q

Malignant spinal cord compression

A

defined by radiological evidence of indentation of the thecal sac

39
Q

MSCC aetiology

A

Usually occurs secondary to metastatic deposits within the spinal column

Lung, breast, kidney, prostate and thyroid cancers are associated with cord compression secondary to metastatic disease

Primary malignancies → primary bone tumours, CNS malignancies

Other causes → trauma, intervertebral disc prolapse, haematoma, epidural abscess, cervical spondylitic myelopathy

40
Q

MSCC pathophysiology

A

A tumour invades into the epidural space and compresses the thecal sac

More extensive the compression of the thecal sac & thus the spinal cord → more likely there will be significant neurological symptoms

Most cases occur secondary to metastatic extension from the vertebral bodies → pressure on the thecal sac occurs anteriorly

41
Q

MSCC clinical features

A

Pain - usually precedes the development of neurological symptoms by several weeks

Weakness, typically, symmetrical → progressive with development of disturbed gait & eventually paralysis

UMN lesions → increased tone → positive Babinski

Cauda equina symptoms

42
Q

MSCC ix

A

MRI scan - investigation of choice in suspected MSCC

Other possible ix: myelography, CT, bone scan & plain radiographs

43
Q

MSCC mx

A

Surgical emergencies requiring prompt recognition and treatment

General measures - receive adequate analgesia utilising WHO ladder, TED stockings & prophylactic LMWH

Glucocorticoids - normally high dose dexamethasone

Definitive procedures

  • external bean radiotherapy may be used as an adjuvant to surgery/a definitive stand-alone therapy in those unable to undergo surgical intervention
  • surgical management options include surgical decompression and reconstruction, vertebroplasty & kyphoplasty
44
Q

SVCO

A

Obstruction to the flow of blood through the superior vena cava secondary to a cancer

SVC = provides venous drainage for the upper limbs, head and beck

45
Q

SVCO aetiology

A

Lung cancer (70-80%) - NSCLC

NHL (10%) - may occur due to mediastinal nodes

Other - thymic, breast, mediastinal germ cell tumours

46
Q

SVCO clinical features

A

Symptoms

  • dyspnoea
  • facial swelling
  • head ‘fullness’
  • symptoms exacerbated by bending forwards/lying down
  • cough
  • dysphagia

Signs

  • facial swelling
  • distended neck and chest wall veins
  • upper limb oedema
  • facial plethora
  • cyanosis
  • cognitive dysfunction
  • coma
  • Pemberton’s sign - patient is asked to elevate both arms above the head for 1-2 minutes
    • positive = congestion, cyanosis or respiratory distress
    • occurs due to increased venous return from the upper extremities exacerbating any obstruction
47
Q

SVCO ix

A

CXR - mediastinal widening & pleural effusion

CT chest with contrast

Duplex US

Histology if malignant cause is suspected

48
Q

SVCO mx

A

Relieving the obstruction & treatment of the underlying cause

Elevation of the head and neck & oxygen titrated to saturations

Medical therapy - radiotherapy & chemotherapy

Surgical therapy - endovenous stent

49
Q

SVCO prognosis

A

Average life expectancy of six months → reflects the extent of tumour or lymphadenopathy necessary to develop obstruction of the SVC

50
Q

Neutropenic sepsis

A

a fever > 38 or features or sepsis in a patient with a neutrophil count of < 0.5 x 10^9

51
Q

Neutropenic sepsis causative organisms

A

Bacteria most commonly isolated organisms in neutropenic sepsis

  • gram negative:
    • E. coli
    • Klebsiella spp
    • Pseudomonas aeruginosa
  • gram positive:
    • coagulase-negative staphylococci
    • staph aureus
    • strep pneumoniae
  • other:
    • c. difficile

Viral - more common in high-risk patients

  • usually part of the human herpes family

Fungal - more common in high-risk patients

  • candida & aspergillus typically
52
Q

Neutropenic sepsis hx

A

Date of last chemo and which agent

Symptoms of infection

Ask about lines

Drugs and allergies

53
Q

Neutropenic sepsis clinical features

A

May present with signs of symptoms of a specific infection

Should be considered in any patient at risk of neutropenia presenting with clinical features of infection → patient receiving or having recently received chemotherapy

54
Q

Neutropenic sepsis ix

A

Looking for source of infection

Bedside - observations, blood sugar, pregnancy test

Bloods - VBG/ABG, FBC (urgent), CRP, U&Es, LFTs, bone profile, clotting, fungal assays, blood borne virus screen

  • don’t wait for results of FBC to start the abx

Cultures - blood cultures, line cultures, sputum MC&S, urine cultures, stool MC&S, c. diff toxin, viral PCR, wound swabs

Imaging - CXR, LP, echo (infective endocarditis)

55
Q

Neutropenic sepsis mx

A

Require antibiotics < 1 hour

Sepsis 6 bundle should be completed in all patients

Additional efforts should be made to identify the source of infection

56
Q

TLS

A
  • metabolic disturbances arising from the breakdown of malignant cells following the initiation of treatment for malignancy
  • rapid cellular breakdown leads to the release of intracellular components resulting in a series of electrolyte abnormalites:
    • hyperkalaemia
    • hyperphosphataemia
    • hypocalcaemia
    • hyperuricaemia
  • AKI, arrhythmias & sudden death can occur as a consequence
57
Q

TLS pathophysiology

A

Cytotoxic-mediated lysis of tumour cells lead to the release of intracellular components → potassium, phosphate and nucleic acids

Hypocalcaemia develops secondary to hyperphosphataemia with the precipitation of calcium in soft tissues

Development of hyperuricaemia and hyperpsophataemia can lead to an AKI through the precipitation of uric acid and calcium phosphate within the renal tubules

58
Q

TLS clinical features

A

Tend to develop within the first 72 hours following the initiation of treatment but can occur up to 7 days post-treatment

Generally related to the metabolic abnormalities that occur

Symptoms

  • lethargy
  • N&V
  • diarrhoea
  • anorexia
  • muscle cramps
  • syncope
  • pruritus
  • arthritis

Signs

  • fluid overload
  • haematuria
  • tetany & paraesthesia
  • bronchospasm
59
Q

TLS ix

A

U&Es, serum urate (serum urate levels taking in patients treated with rasburicase should be sent to lab on ice to prevent falsely low levels)

Urine dip

Urine microscopy

Serum lactate

LDH

ECG

Cardiac monitoring

60
Q

TLS diagnosis

A

Cairo-Bishop definition, clinical and laboratory

Laboratory - presence of two or more abnormal serum values that occur three days prior to or seven days after beginning treatment (25% increase in everything except calcium which is 25% decrease)

Clinical - patient who meets the lab diagnosis with the presence of one or more of the following features:

  • serum creatinine > 1.5 ULN
  • cardiac arrhythmia/sudden death
  • seizure
61
Q

TLS mx

A

Centres around the treatment of hyperphosphataemia, hyperkalaemia, hypocalcaemia & renal impairment

Calcium gluconate, insulin/dextrose

Hypouricaemic agents - allopurinol, rasburicase

Phosphate binders

IV hydration