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Infectious disease, Oncology, & Urology > Oncology emergencies > Flashcards

Oncology emergencies Flashcards

1
Q

What are the main oncology emergencies?

A

Hypercalcaemia

Superior Vena Cava Obstruction

Tumour lysis syndrome

Neutropenic sepsis

Spinal cord compression

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2
Q

What is meant by corrected calcium?

A

40% of circulating calcium is bound to albumin, but labs only measured unbound calcium

Corrected calcium is calculated based on serum albumin levels

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3
Q

Your patient is hypercalcaemic.

Their PTH level is also high, what could be the cause?

A

Hyperparathyroidism

High PTH:

  • Increases bone resorption
  • Increases calcium reabsorption in kidneys
  • Converts inactive vit D to active vit D which increases Ca absorption in intestine
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4
Q

What does the body do to correct low calcium?

A

Stimulate parathyroid hormone release

Which increases bone resorption and renal calcium reabsorption.

Also stimulates renal conversion of inactive vit D to active vit D, which increases intestinal calcium absorption.

These mechanisms restore the serum calcium to normal

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5
Q

Your patient is hypercalcaemic.

Their PTH level is normal, what could be the cause?

A

Malignancy

Drugs: thiazide diuretics, vit D

Endocrine: thyrotoxicosis, primary adrenal insufficiency

Granulomatous conditions: sarcoidosis, TB

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6
Q

How does malignancy cause hypercalcaemia?

A

Ectopic production of PTH or PTH-related peptide by tumour cells

Osteolytic (bone mets)

Ectopic calcitriol (active vit D)

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7
Q

Clinical presentation of hypercalcaemia?

A

Bones: pain

Stones: renal stones

Abdominal groans: nausea, constipation

Psychic moans: confusion, drowsy

Also:

  • prologed QT
  • pancreatitis
  • coma
  • muscle weakness
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8
Q

What investigations would you do for hypercalcaemia?

A

Bedside:

  • Obs
  • BMs
  • ECG (Qt interval)

Routine:

  • Bloods: FBC, U+E, Ca, CRP, LFT (esp alk phos), Clotting, PTH, TFTs
  • XR
  • Urine Ca and P

Specialist:

  • CT
  • MRI
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9
Q

Which blood tests are particularly important for hypercalcaemia?

A

Albumin and urea: if raised could indicate dehydration

Alkaline Phosphatase: if raised indicates bony mets, thyrotoxicosis

Calcitonin: if raised indicates possible B cell lymphoma

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10
Q

Acute management of hypercalcaemia in cancer patient?

A
  1. Rehydrate: 0.9% NaCl
  2. Bisphosphonates: pamidronate, zolendronic acid
  3. Treat underlying cause
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11
Q

How do bisphosphonates help in hypercalcaemia?

A

They inhibit osteoclasts so reduce bone absorption and turnover

This reduces Ca levels

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12
Q

How can you manage persistent hypercalcaemia in malignancy?

A

Denosumab: a monoclonal antibody drug which inhibits maturation of osteoclasts

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13
Q

Where does the SVC connect to at either end?

What does it do?

A

It runs from where R and L brachiocephalic veins join to the RA

It’s the venous drainage for the head, neck, upper limbs and upper thorax

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14
Q

What causes SVC obstruction?

A

Inside the vessel:
- thrombus

Inside the vessel wall:
- direct tumour invasion

Outside the vessel:
- tumour (lung cancer, lymphoma)

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15
Q

Clinical features of SVC obstruction?

A 
SYMPTOMS:
Dyspnoea
Chest pain at rest
Cough
Neck and face swelling
Arm swelling
Dizzy
Headache
Visual disturbance
Syncope

SIGNS:
Dilated veins over arms, neck and chest wall
Resp distress
Cyanosis

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16
Q

Investigations of SVC obstruction?

A

Clinical diagnosis

Usual bedside and routine

Specialist:

  • CXR
  • CT scan
  • Contrast venography
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17
Q

Management of SVC obstruction?

A

Elevation of head
Oxygen therapy

High dose steroids

Endovascular stenting

Anti-coagulation if thrombosis

Treat tumour: chemo, radiotherapy

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18
Q

What is tumour lysis syndrome?

What causes it?

A

The abrupt release of large quantities of cellular components into the bloodstream following rapid lysis of the malignant cell

Caused by treatment

Or spontaneously, this commonly occurs in haematological malignancies like ALL, Burkitt’s lymphoma

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19
Q

What are the risk factors for tumour lysis syndrome?

A

Treatment sensitive tumours

Volume depletion (bleeding, dehydration)

Renal impairment

High pre-treatment lactate, urate, LDH levels

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20
Q

Clinical features of tumour lysis syndrome?

A

Weakness

Paralytic ileus: constipation, vomiting, abdo pain

Arrhythmias: palpitations, chest pain, collapse

Seizures

AKI: reduced UO, lethargy, nausea

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21
Q

What investigations would you do in suspected tumour lysis syndrome?

A

Bedside:

  • UO
  • Urinalysis

Routine:
- Bloods: FBC, U+E, serum LDH, urate, phosphate, Ca

22
Q

What is LDH?

A

Lactate dehydrogenase

An enzyme the body uses in respiration (glucose -> energy)

Found in muscles, liver, heart, pancreas, kidneys, brain, blood cells

23
Q

What would you see in bloods of someone with tumour lysis syndrome?

A

HypERuricaemia

HypERphosphataemia

HypERkalaemia

HypOcalcaemia

AKI: so raised creatinine, urea

24
Q

Why does tumour lysis syndrome cause AKI.

A

Tumour lysis syndrome causes release of allsorts into the blood, including uric acid and Ca phosphate crystals

Deposition of both these in the renal tubules causes AKI

25
Q

How can you prevent tumour lysis syndrome?

When should you think about doing this?

A

Before starting chemotherapy in an at-risk patient

  • IV fluids
  • Rasburicase: catalyses uric acid -> allantoin which is more soluble
  • Allopurinol: blocks conversion of xanthines to uric acid
26
Q

Management of tumour lysis syndrome?

A

Vigorous hydration

Correct high potassium:

  • calcium gluconate
  • IV insulin + dextrose
  • salbutamol

Rasburicase: uric acid -> soluble allantoin

Acetazolamide: alkalinise urine b/c uric acid more soluble at higher pH

Phosphate binders

Dialysis in severe cases

27
Q

What’s the treatment for raised potassium?

A

Fluids

Calcium gluconate

IV insulin + dextrose

Salbutamol nebs

28
Q

Where does the spinal cord terminate and the cauda equina start?

Which important nerves does the cauda equina contain?

A

L1

Lumbar, sacral and coccygeal nerves

29
Q

Which nerve roots control these reflexes?

Knee jerk
Ankle jerk

Which nerve roots control anal sphinchter?

A

L3, 4 keeps foot off the floor (knee jerk)

S1 (ankle jerk)

S2,3,4 keeps poo off the floor

30
Q

What things can cause spinal cord compression?

A

Malignancy, more commonly secondary

Trauma

Disc prolapse

Inflammatory arthritis

Spinal infection

Haematoma

31
Q

Clinical features of spinal cord compression?

A

Depends on where the lesion is

Radicular pain

Sensory loss below level

UMN signs:

  • hypertonia
  • weakness
  • brisk reflexes

Only LMN signs if compression on the spinal nerves, so they’re often present at the level of the lesion only

32
Q

What are UMN and LMN signs?

Which are UMN and LMN?

A

UMN (spinal cord)

  • hypertonia
  • brisk reflexes
  • weakness
  • no wasting or fasciculations

LMN (spinal nerves, all other nerves)

  • hypotonia
  • weakness
  • absent reflexes
  • wasting
  • fasciculations
33
Q

Signs of cauda equina?

A

Lower back pain

Perineal numbness

Loss of anal sphincter tone

Urinary retention

34
Q

Where are the spinal nerves?

A

The nerves that come out of the spinal cord at each level, C1-L1

35
Q

Investigations of possible spinal cord compression?

A

Urgent MRI of whole spine (within 24hrs)

Bloods: FBC, U+E, LFTs (could indicate liver and bone mets)

36
Q

What are the red flag signs of cord compression?

A

Insidious onset

Gait disturbance
Clumsy, weak hands
Loss of sexual, bladder or bowel function

UMN signs in lower limbs

LMN signs in upper limbs

Sensory changes

Lhermitte’s sign: electric shocks

37
Q

Management of spinal cord compression?

A

Analgesia

High dose corticosteroids: dexamethasone

Surgery, radiotherapy, chemo

Bisphosphonate for bone pain caused by mets

VTE prophylaxis

Manage bladder and bowel, catheterise

Refer to spinal rehab

38
Q

Which cancer causes sclerotic bone mets?

What do these look like on XR?

A

Prostate

They look white and bright

39
Q

Which cancers commonly metastasise to bone?

A

BLT + KP

Breast
Lung
Thyroid
Kidney 
Prostate
40
Q

A patient has is 9 days into their chemotherapy for breast cancer. They present with a fever and feeling generally unwell. What do you think?

A

Neutropenic sepsis!

41
Q

What is neutropenic sepsis?

A

Chemotherapy can cause myelosupression

  • leukopenia
  • thrombocytopenia
  • low red cell count

Neutropenia is low neutrophil count

Makes patients susceptible to serious infections

42
Q

On what day of chemo is neutropenia most likely to happen?

A

Day 7-14

43
Q

At what neutrophil count does a patient become susceptible to sepsis?

A

Below 1x10^9/L

44
Q

Patients should be treated for neutropenic sepsis if they meet criteria, what criteria?

A

They have a temperature over 38
OR
A temp over 37.5 for two consecutive readings for two hours

AND

A neutrophil count below 1x10^9 or expected to fall below

45
Q

Clinical features of neutropenic sepsis?

A

Fever

Any infective signs

Can have no symptoms except fever

Suspect it in all patients with new deterioration within 6 weeks of cytotoxic chemo

46
Q

What infections can patients get when they’re neutropenic?

A 
Meningitis
Encephalitis
Chest: pneumonia, empyema
Liver abscess
Gastroenteritis
Pyelonephritis
UTI
Skin: cellulitis etc.

LINE INFECTION

47
Q

Investigations of neutropenic sepsis?

A

Bedside:

  • BM
  • Obs
  • Urinalysis
  • ABG, VBG

Routine:

  • Bloods: FBC, LFTs, U+E, lactate, CRP, ESR, Coag
  • Cultures: blood, urine, faecal, sputum, swab
  • CXR

Do a full septic screen

48
Q

Management of neutropenic sepsis?

A

ANTIBIOTICS, do not wait until confirmed
Start within an hour of arrival at hosp

Empirical abx: tazocin +/- gentamicin

Low risk patients: oral abx, observe for 24hrs as inpatient

High risk: IV abx and review daily as inpatient, can switch to oral after 24-48hrs if improvement

Monitor for complications: AKI, DIC, organ failure

Supportive tx

49
Q

How long should you give abx for in neutropenic sepsis?

A

When neutrophils have normalised, patient has been afebrile for 24 hours and cultures are negative

If patient is still neutropenic but they’ve been asymptomatic for 5-7 days abx can be stopped

50
Q

How can you prevent neutropenic sepsis?

A

Prophylactic abx: a fluroquinolone (like cipro)

G-CSF: stimulate bone marrow to produce WBCs

Reduce chemo if palliative setting

51
Q

What is the name of the drug which stimulates bone marrow to produce WBCs?

A

G-CSF

Granulocyte colony-stimulating factor

Infectious disease, Oncology, & Urology (11 decks)

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