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Y4 Cancer > Acute cancer > Flashcards

Acute cancer Flashcards

1
Q

What is the superior vena cava?

A

found in middle of mediastinum surrounded by trachea, R bronchus, aorta, pulmonary aorta
- drains from head, neck, upper extremities
- thin walls

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1
Q

What is the pathophysiology of SVCO?

A

extrinsic or intrinsic via thrombus
if gradual obstruction, collaterals recruited, which contribute to oedema and dilated veins in obstruction

  • commonly with small cell lung cancer, lymphoma, metastatic seminoma, kaposi’s sarcoma, any mets like breast, colon, oesophageal
  • other causes: aortic aneurysm, mediastinal fibrosis, goitre
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2
Q

How might SVCO present?

A

dyspnoea, tachypnoea
stridor
thoracic or neck vein distention, facial plethora, non-pulsatile JVP
central or peripheral cyanosis

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3
Q

What is the Pemberton manoeuvre?

A

lift both arms until they touch side of face and if positive there will be facial congestion, cyanosis and respiratory distress after 1 min

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4
Q
A
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4
Q

How might you manage SVCO?

A

emergency - secure airway!
endovascular stenting - may push thrombus into RA and lung
radical chemo or radio
oral dexamethasone to reduce oedema

supportive - elevate head, loose restrictive clothing, benzo and opioids, o2 if needed
underlying cancer mx

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4
Q

What are some complications of SVCO?

A
  • life threatening
  • laryngeal oedema
  • acute airway obstruction
  • stenting related - thrombosis, migration of stent, SVC dissection or perforation, infection, volume overload or acute HF due to sudden increase in venous return post obstruction
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5
Q

What is the pathophysiology of pleural effusion?

A
  • abnormal build up of fluid and cancer cells that collects between the chest wall and the lung, when the cancer has spread to pleural space causing an increased production of pleural fluid and decreased absorption due to inflammation
  • this affects patient ability for lung expansion
  • seen in lung cancer, breast cancer, lymphoma, mesothelioma or from stomach, kidney, ovaries and colon metastatic spread
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6
Q

How might pleural effusion present?

A
  • SOB at rest or with activity
  • chest pain or pressure
  • cough
  • pleuritic pain
  • fever
  • fatigue
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7
Q

How might you manage pleural effusion?

A
  • management of underlying malignancy
  • thoracentesis - drain
  • pleurodesis - lung stuck to chest wall preventing buildup of fluid
  • indwelling pleural catheter - repeated drainage allowed at home
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8
Q

what is the pathophysiology of bowel obstruction in the context of malignancy?

A
  • cancer in abdominal area causing direct compression
  • metastatic spread from lung or breast
  • spread into nerve supply causing muscle inactivity
  • solid mass indigestible material collecting in bowel
  • malignancy induced hypercalcaemia and constipation
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9
Q

how might bowel obstruction present?

A
  • bloated
  • colicky abdominal pain
  • nausea
  • vomiting - undigested food or bowel fluid
  • absolute constipation
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10
Q

how is bowel obstruction investigated?

A
  • blood - FBC
  • urine tests
  • tumour markers
  • CT scan
  • abdominal XR
  • USS
  • MRI
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11
Q

how is bowel obstruction managed?

A
  • drip and suck - NGT for decompression, to reduce risk of aspiration
  • nil by mouth
  • incase surgical input needed
  • stenting
  • medication to stop muscle spasms and reducing pain
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12
Q

what kind of malignancies can cause a GI bleed?

A

upper - oesophageal, gastric
lower - colorectal

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13
Q

how might a GI bleed present?

A
  • haematemesis
  • PR bleeding
  • dizziness and syncope
  • altered bowel habits
  • haematochezia
  • malaena
  • confusion
  • dehydration
  • pallor
  • anaemia from occult
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14
Q

how is GI bleeds investigated?

A

*observations
- stool cultures, faecal calprotectin
- ECG
- FBC, CRP, U&E, LFT, G&S, CM
- haematinics, clotting, ABG
- CT angio, endoscopy, colonoscopy

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15
Q

how is a GI bleed managed?

A
  • A-E
  • cause dependent
  • blood products
  • surgery? clips?
  • thermal coagulation with adrenaline
  • tranexemic acid
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16
Q

how would you define hypercalcaemia?

A

defined as a corrected serum calcium >2.6mmol/L - 10% of patients

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17
Q

what is the pathophysiology of hypercalcaemia? - use benign vs malignant!

A

benign: hyperparathyroidism, dietary, medications

malignant: local osteolytic, paraneoplastic PTrH, bony mets

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18
Q

how might hypercalcaemia present?

A
  • polydipsia
  • polyuria
  • N+V
  • abdominal pain
  • constipation
  • sudden confusion
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19
Q

how is hypercalcaemia investigated?

A
  • FBC
  • U&E
  • bone profile for adjusted calcium
  • LFT
  • ECG
  • confusion screen
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20
Q

How would you manage hypercalcaemia?

A
  • assess fluid balance
  • IVF: 24h with 0.9% saline 3-4L but check U&E daily and Mg2+
  • bisphophonates
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21
Q

How do you take bisphosphonates?

A
  • Tablets should be swallowed whole with plenty of water while sitting or standing
  • to be given on an empty stomach at least 30 minutes before breakfast (or another oral medication)
  • patient should stand or sit upright for at least 30 minutes after taking tablet

*take 2-3 days to work with maximal effect being seen at 7 days

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22
Q

what is the pathophysiology of ascites?

A
  • over-production of ascitic fluid made by peritoneum when cancer cells spreads to peritoneum causing inflammation leading to fluid production
  • lymph node blockage and impaired drainage
  • liver metastases causing portal hypertension
  • liver unable to make enough proteins and hence reduced oncotic pressure
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23
Q

what cancers commonly present with ascites?

A

ovarian, breast, bowel, stomach, pancreatic, mesothelioma, lung, liver, endometrial

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24
Q

how does ascites present?

A
  • clothes feel tighter
  • discomfort or pain in abdomen
  • nausea
  • loss of appetite
  • indigestion
  • fatigue
  • constipation
  • needing to pass urine often
  • SOB
  • difficulty sitting comfortable and moving around
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25
Q

how is ascites investigated?

A
  • USS
  • bloods - renal function and liver function
  • CT scan CAP
  • paracentesis - ascitic tap and sample
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26
Q

how is ascites managed?

A
  • low salt diet
  • ascitic drain
  • long term drainage catheter
  • peritoneovenous shunt
  • diuretics
  • chemo for underlying
  • manage sx
27
Q

what is the pathophysiology of metastatic spinal cord compression?

A

by direct pressure or vertebral collapse as a result of metastatic spread and may cause neurological deficit and paralysis

*lung cancer, prostate, breast, haematological malignancies, GI, kidney

28
Q

what is the presentation of MSCC?

A
  • new, severe, progressive pain
  • localised spinal tenderness
  • worsening limb weakness
  • sensory loss (saddle parasthaesia)
  • bladder or bowel dysfunction
  • tingling in lower limbs - most likely suggestive of SCC as sensory involvement
29
Q

what investigations would you do in MSCC?

A
  • examination: neuro exam, temp, pulse, BP, RR, sats, EWS, AVPU
  • FBC, U&E, LFT, G&S
  • Ca as anaesthesia effect
  • MRI spine within 24h of arrival
30
Q

how is MSCC managed?

A
  • high dose dexamethasone with PPI
  • urgent surgical decompression within 24h
  • analgesia
  • MDT discussion with neuro, spinal surgeons, oncologist
  • lesion biopsy if first cancer presentation
  • radiotherapy to decrease burden
31
Q

what can cause raised ICP in a malignancy setting?

A
  • primary tumours
  • mets from melanoma, lung, breast, kidney
  • CSF flow blockage
  • meningitis
  • cerebral haemorrhage, oedema
  • radiation therapy side effects
32
Q

how might raised ICP present?

A
  • vomiting, headache worse on leaning forwards
  • cushings triad: bradycardia, widened pulse pressure, irregular respirations
  • papilloedema
  • reduced consciousness
  • false localising cranial nerve palsies
33
Q

how do you investigate raised ICP?

A
  • fundoscopy - papilloedema and loss of retinal venous pulsation on fundoscopy
  • CT head
  • MRI head
34
Q

how is raised ICP managed?

A
  • position head elevated
  • dexamethasone IV 8mg repeating 4h if needed
    • omeprazole
  • mannitol if not response to steroids?
  • cyclizine for N+V
  • definitive - surgery, radiotherapy
  • cerebral shunt
35
Q

what is status epilepticus?

A
  • seizure activity lasting more than 5 minutes with impaired neurological function, or recurrent seizures without baseline return
  • caused by primary brain tumours or metastases or even adverse effects of treatment
36
Q

how does status epilepticus present?

A
  • stiff
  • convulsions - jerking motions, grunting, drooling, rapid eye movement
  • tongue biting
  • urinary incontinence
  • post-ictal confusion, fatigue etc
37
Q

how is status epilepticus managed?

A
  • ABC
    • airway adjunct
    • oxygen
    • blood glucose check
  • first line is benzo
    • prehospital setting PR diazepam or buccal midazolam
    • hospital IV lorazepam
    • repeat after 5-10 mins
  • ongoing start second line like levetiracetam, phenytoin or sodium valproate
  • if refractory within 45 min of onset - induction of general anaesthesia or phenobarbital
38
Q

how is VTE exacerbated in malignancy?

A
  • 2nd leading cause of death in cancer patients with 4-7 fold increased risk of VTE compared to those without cancer
    • disruption to Virchow’s triad - venous stasis with immobility and compression from tumours, hyper-coagulability with adhesions molecules expressed on surface and cytokine secretion
39
Q

how might VTE present?

A

PE

  • SOB
  • tachycardia
  • pleuritic chest pain
  • cough
  • DVT Sx

DVT

  • swelling
  • oedema
  • pain
  • redness
  • warmth
40
Q

how is VTE managed?

A

prophylaxis

  • aspirin, unfractionated heparin, LMWH

treatment

  • LMWH
  • DOAC
  • 6m treatment with 3 monthly re-evaluations
41
Q

what is neutropenic sepsis?

A
  • temperature of >38c
  • or temp >37.5 on 2 occasions 1h apart
  • neutrophil count ≤1.0×109/L
  • clinical signs of sepsis in someone who received chemo within past 6w
42
Q

how would you qualify neutropenia?

A
  • Severe Neutropenia <0.5×10*9/L
  • Very severe neutropenia <0.2×10*9/L
43
Q

what are some risk factors for neutropenic sepsis?

A

duration of neutropenia, co-morbidities, type of disease, other treatments, elderly, frequent hospitalisations, malnutrition, indwelling vascular devices

44
Q

what is the common pathogen seen in neutropenic sepsis?

A

coagulase-negative, gram-positive most common eg: staph epidermidis due to indwelling lines

45
Q

how might neutropenic sepsis present?

A
  • temperature - high or low
  • shivers, sweating
  • tachycardia
  • hypotension
  • confusion
  • rashes
  • diarrhoea
46
Q

how might neutropenic sepsis be investigated?

A
  • blood cultures and line cultures before Abx
  • MSU cultures
  • FBC - neutropenia
  • U&E - renal function
  • LFT - hepatic function
  • CRP
47
Q

how is neutropenic sepsis managed?

A
  • antibiotics!! within first 30 mins
    • broad spectrum like tazocin with gentamicin for gram negative cover
    • if not responding consider alternative Abx or fungal causes
  • supportive care
  • G-CSF may be indicated in some
48
Q

What is tumour lysis syndrome?

A

breakdown of the tumour cells and the subsequent release of chemicals from the cell
It leads to a high potassium and high phosphate level in the presence of a low calcium, faster than the kidneys can remove them

49
Q

What can trigger tumour lysis?

A

induction of combination chemo or even steroids
high proliferation rate
large tumour burden

50
Q

What are some complications of tumour lysis?

A
  • AKI
  • cardiac dysrhythmias
  • seizures
  • cardiac arrest
  • death
51
Q

how might tumour lysis present?

A

*develop within first 72h following treatment initiation but can be up to 7 days post treatment
- lethargy
- N+V
- diarrhoea
- anorexia
- muscle cramps
- syncope
- pruritis
- arthritis
- fluid overload
- haematuria
- tetany & paraesthesia (polycaemia)
- bronchospasm (wheezing)

52
Q

what are investigations carried out for tumour lysis?

A

*renal function, electrolytes, serum urate

  • urine dip
  • urine microscopy - crystals
  • serum lactate
  • LDH
  • ECG
  • cardiac monitoring
53
Q

how does Cairo-bishop define TLS?

A

Laboratory tumor lysis syndrome
- abnormality in two or more of the following, occurring within three days before or seven days after chemotherapy
- high uric acid, phosphate, potasisum and low calcium

clinical
- increased serum creatinine (1.5 times upper limit of normal)
- cardiac arrhythmia or sudden death
- seizure

54
Q

how is TLS managed?

A
  • IV fluids
  • higher risk patients - allopurinol or rasburicase
  • rasburicase -> converts uric acid to easily excreted form

*not together

55
Q

How does Rasburicase affect TLS?

A

a recombinant version of urate oxidase, an enzyme that metabolizes uric acid to allantoin
Allantoin is much more water-soluble than uric acid and is, therefore, more easily excreted by the kidneys

*generally preferred now for patients at a higher risk of developing TLS

56
Q

what is the pathophysiology of immune related colitis?

A

immune checkpoint inhibitor induced colitis
- as these stimulate body’s immune system this may cause the immune system to attack own organs

57
Q

how might immune mediated colitis present?

A
  • diarrhoea
  • blood or mucus in stool
  • malaena
  • severe pain, tenderness, cramping
  • fever
  • abdominal distension
58
Q

How is immune related colitis investigated?

A
  • stool studies for infectious causes
    • C.diff
    • ova/ parasites
    • calprotectin
  • FBC - CRP
    • metabolic panel
    • HIV
  • tissue transglutaminase immunoglobulins as rare side effect
  • colonoscopy or flexible sigmoidoscopy
59
Q

How is immune related colitis managed?

A

*depends on level of hydration

  • IV methylprednisolone
    • taper off over 4-6w
  • IV fluids
  • biologic therapies?
60
Q

what is radiation mucositis?

A
  • acute inflammation of the oral mucosa following systemic cancer therapy or radiotherapy
  • lesions are often very painful, may compromise nutrition and oral hygiene, increases risk of local systemic infection
61
Q

What are some risk factors for radiation mucositis?

A

intensive chemo, radiotherapy to oral cavity, chemoradiation, genetic polymorphisms in drug metabolite enzymes

62
Q

how does radiation mucositis present?

A
  • erythema to patchy or confluent ulceration with superficial pseudomembranous membrane
  • oral pain
  • dietary impairment
  • diarrhoea
  • fever
63
Q

how is radiation mucositis investigated?

A
  • FBC
  • blood cultures
  • fungal cultures
64
Q

how is radiation mucositis managed?

A
  • preventative treatment include palifermin
  • low level laser therapy
  • ice chips during chemo infusion therapy
  • topical mouthwash - viscous lidocaine
65
Q

what is the pathophysiology of thrombocytopenia?

A
  • caused by bone marrow failure
  • or even by management options such as chemo drugs, radiation therapy
    • chemo caused in usually temporary but can cause serious loss of blood and damage to internal organs
  • hypersplenism causes this due to pooling
  • viral infections
  • fast breakdown: ITP
  • bleeding etc
66
Q

how does thrombocytopenia present?

A
  • bruising
  • petechiae
  • unusual bleeding from gums or nose
  • long-lasting bleeding from wounds
  • haematuria
  • malaena or haematochezia
  • PV bleeding
  • constant headache, blurred vision, changes in consciousness
67
Q

how is thrombocytopenia investigated?

A
  • FBC - plt levels
  • Clotting profile
  • G&S and cross-match
  • blood film
  • antibody test
  • BM aspiration and biopsy for underlying cause in unknown
68
Q

how is thrombocytopenia managed?

A
  • avoid brushing too hard
  • no hard contact sport if hypersplenism
  • manage bleeds
  • blood or platelet transfusion
  • ITP - steroids, immunoglobulins
  • plasma exchange for TTP
69
Q

What are some complications of thrombocytopenia?

A
  • life threatening haemorrhage
  • stroke
  • MI

Y4 Cancer (15 decks)

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