Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

YEAR 4 CANCER CARE > Onco Emergenices (Secondary To Cancer) > Flashcards

Onco Emergenices (Secondary To Cancer) Flashcards

1
Q

What cancers are most likely to get bowel obstruction as a complication?
how does it happen?

A
  • Complication of advanced cancer
  • Cancer in abdomen
  • Ovarian (40%)
  • Bowel
  • Stomach cancer
  • Metastasis

How?
* Cancer grows into nerve supply of bowel and stops muscles working
* Adhesions due to past abdominal surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does bowel obstruction present?

A
  • Stomach pain- colicky
  • Constipation - absolute no wind
  • Vomiting
  • Occurs early in upper GI obstruction and later in lower GI
  • Abdominal distension
  • bloated
  • tinkling bowel sounds -early
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Investigations for bowel obstruction?

A
  • Abdominal X ray: distended loops of bowel.
    Central- upper
    Peripheral- lower
  • CT scan
  • Barium enema

normal limits : 3 cm small bowel
6 cm colon
9 cm caecum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Supportive management of bowel obstruction?

A

If able to go to theatre:
* NBM
* NG decompression/ venting gastrostomy (PEG)
* IV fluids to prevent dehydration

A lot of patients will not be able go to theatre:
* steroids- to reduce odema of bowel wall
* gentle laxatives and anti-emetics- to control N&V
* Control the pain
* reduce volume of intestinal secretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Medical management of bowel obstruction?

A
  • Buscipan- stop muscle spasms and reduce pain
  • Strong painkillers
  • IV antibiotics
  • Antiemetics
  • Octreotide -Reduces fluid that building up in GI tract
  • Steroids to reduce inflammation in bowel
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Surgical management of bowel obstruciton in oncology?

A

Tends to be palliative to relieve pain:
- Resection of damaged bowel-> stoma
- Stent insertion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why might a pt with bowel obstruction become unstable?

complications of bowel osbtruction

A
  • Hypovolaemic shock due to fluid stuck in the bowel rather than the intravascular space (third-spacing)
  • Bowel ischaemia
  • Bowel perforation
  • Sepsis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Full set of bloods is suspect bowel obstrutction: what KEY results expect to find?

A
  • Electrolyte imbalances (U&Es)
  • Metabolic alkalosis due to vomiting stomach acid (venous blood gas)
  • Bowel ischaemia (raised lactate – either on a venous blood gas or laboratory sample)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

causes of Superior vena cava obstruction?

malignant and non malignant

A

Malignancy
* Primary lung cancer e.g. Pancoast tumour
- Small cell
- Non small cell e.g. Squamous (pancoast)
* Lymphoma
* Metastasis
* Kaposi’s sarcoma
* breast cancer

Non malignancy
* aortic aneurysm
* mediastinal fibrosis
* goitre
* SVC thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Pathophysiology of superior vena cava obstruction

A
  • The SVC provides venous drainage for the head, the neck, the upper extremities and the upper thorax
  • Tumour presses on SVC
  • Less blood draining from veins in the brain into the heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Presenentation of SVCO?

A
  • Tachycardia, tachypnoea, hypotension
  • Oedema and errythema of the upper body, extremities and face
  • Jugular venous distension
  • Dilated veins over the arms, neck and anterior chest wall (collaterals )
  • Pemberton sign - positive
  • Engorged conjunctiva.
  • Convulsions and coma.
  • Cyanosis.
  • Severe respiratory distress.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How to ellicit Pembertons sign?

A
  1. Ask patient to raise both arms above head (2-3mins)
  • Normal result: nothing happends
  • SVC syndrome present: facial and neck swelling, cough, SoB, cyanosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Investigation for SVCO

A
  • CXR -widened mediastinum or a mass on the right side of the chest.
  • Doppler scanning: changes seen during the respiratory cycl, evaluate the severity and effect of therapy
  • CT scan with contrast - gold standard
  • detect effusions, metastatic intra- and extrapulmonary manifestations, assessment of collateral vasculature and planning of interventional procedures.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Complications of SVCO

A
  • laryngeal oedema causing laryngeal constriction
  • Tracheal obstruction
  • Resp distress
  • Hypotension (reduced cardiac output) and tachycardia
  • Cyanosis
  • Retinal haemorrhage
  • Stroke
  • Cerebral oedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Management of SVCO

A
  • Head elevation, 02
  • Corticosteroids, diuretics
  • Endovascular surgery - stenting

Palliative care
* Cryotherapy
* Diathermy
* Bronchial stents for central airway
* Endobronchial radiotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How is hypercalacaemia defined?

A

Hypercalcaemia is defined as correct calcium >2.65mmol/L.

(Normal range 2.2-2.51 mmol/l)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Ca and albumin link

A

Can be free or bound to albumin
* Adjusted for how much albumin in blood
* If low albumin – may be low calcium as decreased binding of calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are common causes of hypercalcaemia related to malignancy?

A
  • often in disseminated disease- poor prognosis
  • Humoral cause (80%) (tumour derived PTHrP)
  • Bone invasion
  • myeloma
  • Tymour calcitriol release
  • immunotherapies and hormonal therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

non malignancy causes of hyercalcaemia?

A
  • Primary hyperparathyroidism
  • Granulomatous diseas : sarcoidosis/ TB
  • vitamin D intoxication
  • acromegaly
  • thyrotoxicosis
  • Milk-alkali syndrome
  • drugs: thiazides, calcium-containing antacids, Lithium
  • Addison’s disease
  • Paget’s disease of the bone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

humoral cause of hypercalcaemia?

(blood related - relating to, proceeding from, or involving a bodily humor (such as a hormone))

A
  • PTH-related protein released by certain cancers
  • E.g. paraneoplastic feature of lung cancer – SCC
  • Increased release of calcium from bone and increase uptake from kidneys
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Risk factors for hypercalcaemia?

(i.e. which malignancies can cause high calcium)

A

Breast cancer
SCC (NSCLC)
Renal
Myeloma
Lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How does bone invasion cause hypercalcaemia?

A

Osteolytic metastases with local release of cytokines -> increased bone reportion and therefore calcium release from bone into blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Presentation of hypercalcaemia?

A

Bones, stones, groans and psych moans (painful bones, kidney stones, abdominal groans and psych moans)
* Nausea
* Anorexia
* Thirst
* Constipation
* Kidney stones
* Confusion
* Polydipsia and polyuria
* Fatigue and weakness
* Bone pain
* Neurological
* Cardiac

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

hypercalcaemia and neurological symptoms?

(what neurological symptoms present with hypercalcemia?)

A

Seizures
Poor coordination
Change in personality
cognitive dysfunction
depressin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

hypercalcaemia and cardiac symptoms?

A

Bradycardia
HTN
Shortened QT interval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Revision calcium homeostasis

A

Reduction in calcium detected by the PTH gland
* Increase PTH secretion
* Increase PTH in plasma
reabsorption of Ca from bone – increases plasma Ca2+

Kidney:
* Calcium reabsorption in nephron increases
* Reduced excretion of calcium
* Reduced reabsorption + increased excretion of phosphate
o Low plasma phosphate= higher calcium in plasma (inversely proportional)

Vitamin D
* PTH increases 1,25 dihydroxycholecalciferol (active vitamin D ) in the kidney
* more Ca absorption from intestine
* Increase plasma calcium

RESULT:
Restore plasma calcium to normal – negative feedback to PTH gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How does calcitonin effect ca?

A

a peptide released from the thyroid- has an opposite effect to PTH
- when PT detects high calcium- calcitonin released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Investigations of hypercalcaemia ?

A
  • ECG
  • LFTs
  • U+Es
  • Bone profile (calcium, phosphate, albumin, total protein, ALP)
  • PTH (parathyroid hormone)

Further investigation depends on the suspected diagnosis:
* Urinary Bence-Jones proteins and plasma electrophoresis (for myeloma)
* FBC (myeloma)
* Chest x-ray (myeloma, sarcoid, TB)
* 24 hour urinary calcium (familial hypocalciuric hypercalcaemia)
* Bone scan/PET Scan (malignancy)
* USS neck

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

ECG findings in hypercalcaemia?

A
  • Osborn wave
  • ST segment elevation
  • Biphasic T waves
  • Prominent U waves
  • Shortened QT interval
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How is hypercalcaemia managed?

A

Treating the immediate complications and reduce calcium release into the blood:

  1. Aggressive IV fluids - 3-4 litres/day. (corrects dehydration, protects the kidneys and increases calcium excretion)
  2. Bisphosphonates
    * (inhibits osteoclast activity reducing calcium release)
    * e.g. IV pamidronate or zolendronic acids - renal failure so must ensure properly rehydrated first
    * Denosumab for refractory hypercalcaemia
  3. Further management to prevent recurrence (depending on the cause):
    * Chemotherapy (malignancy)
    * Surgical resection (malignancy)
    * Radiotherapy (malignancy)
    * Steroids (sarcoidosis)
    * Calcitonin
    * Furosemide - reduce reabsortion of calcium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

VTE and malignancy
common?
why do they happen in malignancy?
RIsk for cancer vs other patients?

A
  • VTE in cancer patients is a common cause of mortality
  • Hypercoagulable state is a hallmark of cancer
  • Increased risk 2-3X the normal population
  • Complicated managing risk of thrombocytopenic bleeding and risk of clots
  • People with cancer who undergo surgical resection are at higher risk than patients who undergo surgery for non-malignant disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Pathophysiology of VTE and malignancy

A

Hypercoagulable state induced by specific prothrombotic properties of cancer cells that activate blood clotting

Activation of:
* Platelets
* Leukocytes
* Endothelial cells / damage
endothelium activation by anti-cancer drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

High risk cancers for VTE?

A

Pancreatic
Gastric
Lung cancers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Patient and cancer treamtent RF for VTE?

A

Patient RF
* CVD
* Smoking
* Obesity
* COCP/HRT
* inactivity / immobility

Cancer treatment RF
* Cisplatin
* Tamoxifen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Presentation of VTE

A

DVT
* Redness
* unilateral warm, swollen calf or thigh
* Tenderness
* pain on palpation of deep veins
* Pitting oedema
* Collateral superficial veins

PE
* SoB
* Chest pain
* Cough
* Tachycardia
* Cyanosis
* Dizziness and fainting
* sweating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

investigations for VTE

A
  • D-dimer raised in cancer so not used as a predictor
  • DVT- US of leg
  • PE- CTPA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

AR of Wells Score for DVT

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Wells score for DVT result that makes DVT likely

A

2 or more = DVT likely
1 or less = DVT unlikely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Management of VTE

A

DOAC +/- LMWH, warfarin, LMWH alone

DOACS
* Apixaban
* Rivaroxaban
* Dabigatran
* Edoxaban

LMWH
* Dalteparin
* Enoxaparin

Pt w/active cancer should be anticoagulated for at least 3-6 months. Unprovoked DVTs 6 months

DR Barbara said - she would do LMWH as easier to reverse than DOAC. Safer.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Reducing risk of blood clots whilst in hospital

A
  • Anticoagulants
  • Antiembolic stockings
  • Compression devices
  • Keeping moving
  • Stopping COCP or HRT
  • Keeping hydrated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

GI bleeding and cancer: what patients get it?

A
  • patients with solid cancers and also those with bone cancers due to thrombocytopenia
  • Problem in advanced cancers mostly
  • Divided into Upper and lower GI bleed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Causes of bleeding secondary to cancers

A
  • Local tumour invasion
  • Thrombocytopenia
  • Abnormal tumour vasculature
  • Oesophagitis secondary to radiation
  • Liver cancer- portal hypertension (oesophageal varices)
  • Tumor regression
  • Radiation or chemotherapy or immunotherapies
  • Steroid therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Causes of upper GI bleed?

A
  • Gastric ulcer (splenic artery erosion)
  • Duodenal ulcer
  • Oesophageal varices
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Presentation of upper GI bleed?

A

Haematemesis
* Coffee ground vomiting- digested blood

Melaena
* tar like, black greasy and offensive stools caused by digested blood- oxidised

Haemodynamic instability

Epigastric pain

raised urea

Tacchy / hypovolaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Scoring systems for Upper GI bleed

A

Glasgow-Blatchford score and Rockall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

When is the Glasgow- blatchford score used?

A

It scores patient based on their clinical presentation with upper GI Bleed.

The Glasgow-Blatchford score is preferred by NICE pre-endoscopy for deciding upon timing of the procedure.

used to plan: e.g. those scoring<0 may be suitable for outpatient OGD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What parameters does the Galsgow blatchford score look at?

A
  • Urea
  • Haemoglobin (different for men and women)
  • Systolic blood pressure

Other paremeters:
* Tachycardia
* Clincally observed malaena
* Syncope
* Liver disease
* Heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

When is Rockall score for upper GI bleed used?

A

Used in pts that have had an endoscopy to calculate their risk of rebleeding and overall mortility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What parameters for the Rockall score look at?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Compare Glasgow - blatchford and Rockall scores

A

Glasgow- blatchford
* establishes risk of having an upper GI bleed in order to make a plan e.g. discharge them or not

Rockall
* calculates risk of rebleeding and overall mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Management of an upper GI Bleed

A

ABATED
A – ABCDE approach to immediate resuscitation
B – Bloods / fluids
A – Access (ideally 2 large bore cannula)
T – Transfuse (group and save, if varices 4 units blood cross-matched))
E – Endoscopy (arrange urgent endoscopy within 24 hours)
D – Drugs (stop anticoagulants and NSAIDs)

Bloods:
* Haemoglobin (FBC)
* Urea (U&Es)
* Coagulation (INR, FBC for platelets)
* Liver disease (LFTs)
* Crossmatch 2 units of blood
* Transfusion blood, platelets (if <50) and prothrombin complex concentrate (if on warfarin) in patients with massive hameorrhage

Definitive investigation/treatment:
* Esophagogastroduodenoscopy (OGD) (within 12h)– stops bleedings

V PPI may also be initiated.
In variceal bleeding, IV terlipressin and a

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

GI Ulcers
Pathophysiology

A

Erosion of blood vessels supplying upper GI tract
- Lesser curve of stomach (20%)
- Posterior duodenum (40%)

Gastroduodenal artery most common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

RF for ulcers?

A

Ulcer disease
H pylori positive
NSAIDS
Steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Investigations for ulcers?
(peptic ulcer)

A

Erect CXR if suspect peptic ulceration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Management of peptic ulcers

A
  • A to E
  • Injection of adrenaline and cauterisation of bleeding
  • High dose IV PPI therapy (e.g. IV 40mg of omeprazole) to reduce acid secretion
  • +/- H.Pylori eradication therapy if necessary
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is oesophagitis?

A

Inflammation of intraluminal epithelial layer of the oesophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Causes of oesophagitis ?

A
  • GORD
  • Infections e..g candia albicans
  • Medication (bisphosphonates)
  • Radiotherapy
  • Ingestion of toxic substance
  • Crohns disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Pathophysiology of oesophageal varicies

A
  • Dilation of portosystemic venous anastomoses in oesophagus
  • portal HTN
  • Thin, swollen and dilated- prone to rupture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Risk factors for oesophageal varices

A
  • Alcoholic liver disease
  • liver cancer or metastatic liver cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Risk factors for oesophageal varices

A
  • Alcoholic liver disease
  • liver cancer or metastatic liver cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Variceal rupture management

A
  • ABC
    resuscitation before endoscopy i.e. blood transfusion
  • correct clotting: FFP, vitamin K, platelet transfusions may be required
  • vasoactive agents: terlipressin
  • prophylactic IV antibiotics- quinolones
  • Endoscopy: endoscopic variceal band ligation
  • Sengstaken-Blakemore tube if uncontrolled haemorrhage
  • Transjugular Intrahepatic Portosystemic Shunt (TIPSS) if above measures fail (connects the hepatic vein to the portal vein exacerbation of hepatic encephalopathy is a common complication_
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Lower GI bleeding main symptoms?

A

rectal bleeding (haemtochezia)
- passage of fresh blood per rectum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

causes of lower GI bleed

A
  • Ischaemic or infective colitis
  • Haemorrhoids
  • Malignancy
  • IBD
  • Radiation proctitis
  • Diverticular disease
64
Q

History taking for lower GI bleed

A
  • Nature of bleeding, including duration, frequency, colour of the bleeding, relation to stool and defecation
  • Associated symptoms, including pain (especially association with defaecation), haematemesis, PR mucus, or previous episodes
  • Family history of bowel cancer or inflammatory bowel disease
65
Q

Examination for lower GI bleed

A

abdomen
* localised tenderness / masses palpable.

PR examination
* every patient presenting with haematochezia
* assess for any rectal masses and ongoing presence of blood

66
Q

Investigation for lower GI bleed

A
  • Bloods- FBC, U&Es, LFT, clotting
    Acute bleed may not show reduced Hb levels
  • Group and save
  • Stool culture

Haemodynamically unstable:
* stabilise before undergoing urgent CT angiogram to find source of bleeding

Haemodynamically stable:
* Flexible sigmoidoscopy (exclude left colonic pathology)- can be outpatient

PR bleeding but no abnormality found on colonoscopy
* look for upper GI bleed- OGD

67
Q

management of unstable lower GI bleed

A

Standard A to E
- IV fluid
- Blood products
- Hb <70 requires transfusion of packed red blood cells (unless pt has CVD, then Hb <80 used)
- Reversal of any anti-coagulation

Potential management
* Endoscopic haemostasis methods -Injection (diluted adrenaline)
* Mechanical therapies (endoscopic clips and band ligation)
* Arterial embolization possible in those with identified bleeding point (termed a ‘blush’ of sufficient size on angiogram

**Surgery **
* Rarely required
* May be considered in pt with ongoing GI bleeding (requiring continued transfusion), where endoscopic and radiographic treatment has failed

68
Q

What is ascites?

A

Pathological accumulation of ascitic fluid in the peritoneal cavity

Peritoneum makes up ascitic fluid -> if it builds up -> ascites

69
Q

Causes of ascites?

A
  • Portal hypertension (cirrhosis, heart failure, liver cancer)
  • Non-portal hypertension
    –> Hypoalbinemia, malignant, infection
70
Q

Pathophysiology of ascites in cancer patients

A

Cancer of the liver
* Portal HTN forces fluid out of nearby blood vessels
* Damage to the liver reduces albumin production -> reduced hydrostatic pressure

Metastasis to the peritoneum
* Makes it leaky- malignant ascites

71
Q

presentation of ascites

A
  • Swollen / distended of the abdomen
  • Tightness
  • Feeling full when eating
  • Nausea
  • SoB

If infected
* Pain
* Fever
* rigors

72
Q

investigations for ascites?

A
  • US
  • Needle aspiration- paracentesis
    Looking for: WBC, blood, cancer cells, bacteria
  • serum ascites albumin gradient (SAAG) to determine cause (subtract the ascitic albumin concentration from the serum albumin concentration.)
  • Examination- shifting dullness

SAAG > 11g/L (indicates portal hypertension) e.g. cirrhosis .<11g/L - hypoalbuminaemia, malignant peritoneal

73
Q

The causes of ascites can be grouped into those with a serum-ascites albumin gradient (SAAG) <11 g/L or a gradient >11g/L .

Give causes of ascites with HIGH serum- ascites albumin gradinet and LOW

A
74
Q

Management of ascites?

A
  • Address the underlying cause
  • Salt restricted diet
  • Fluid restriction
  • Spironolactone
  • diuretic e.g. furosemide if spironolactone is insufficient.
  • refractory acites -therapeutic paracentesis- fluid is drained from the abdomen over a few hours.
  • prophylactic antibiotics to reduce the risk of spontaneous bacterial peritonitis e.g. oral ciprofloxacin
75
Q

What is a plueral effusion?

A

Pathological accumulation of pleural fluid in the pleural cavity

76
Q

Causes of plueral effusion

A

Lung infections
Heart failure

Metastatic cancer
* Lung cancer
* Breast cancer
* Ovarian cancer
* Lymphomas

Primary cancers
* Mesothelioma (cancer of the pleura)

77
Q

Presentation of pleural effusion

presnting and examination signs

A
  • Breathlessness
  • Cough
  • Chest pain

Examination
* Stony dullness
* Trachea pushed away from effusion

78
Q

Investigations and definitive diagnosis for pleural effusion

A
  • Chest X-ray
  • Test fluid for: WBC, cancer cells, culture for bacteria
  • ECG
  • Bloods: FBC, U&E’s, LFT’s, CRP, Bone profile, LDH, clotting
  • ECHO (if suspect heart failure)
  • Staging CT(with contrast) if suspect exudative cause

Definitive diagnosis
* US guided pleural aspiration -
Biochemistry (protein, pH, LDH, Cytology, Microbiology)
* If no tracheal deviation then pathology may be a mixture of atelectasis and effusion (pull + push = no deviation)
* Bedside US to determine if fluid or collapse

79
Q

Caution when managing a pleural effusion?

A
  • Never inset a chest drain unless diagnosis is well established e.g. known metastatic lung cancer
  • draining fluid may hinder opportunity to obtain pleural biopsies
80
Q

Management of plueral effusions

complications as well

A
  1. Chest drain
    * Complications: blocked drain, infected drain, pneumothorax, recurrence
  2. Management of Recurrent plueral effusions :
    * Catheter insertion
    * Pleurodesis –> Fusion of 2 pleural layers
81
Q

Management of plueral effusions

complications as well

A
  1. Chest drain
    * Complications: blocked drain, infected drain, pneumothorax, recurrence
  2. Management of Recurrent plueral effusions :
    * Catheter insertion
    * Pleurodesis –> Fusion of 2 pleural layers
82
Q

Causes of Transudate effusions (pleural protein <30 g/L)

A

Common:
- Heart failure
- Cirrhosis
- Hypoalbuminaemia (nephrotic syndrome or peritoneal dialysis)

Less common:
- Hypothyroidism, mitral stenosis, pulmonary embolism

Rare:
- Constrictive pericarditis, superior vena cava obstruction, Meig’s syndrome

83
Q

Causes of Exudative effusions (pleural protein >30 g/L)

A

Common:
- Malignancy
- Infections – parapneumonic, TB, HIV (kaposi’s)

Less common:
- Inflammatory (rheumatoid arthritis, pancreatitis, benign asbestos effusion, Dressler’s, pulmonary infarction/pulmonary embolus), Lymphatic disorders, Connective tissue disease

Rare:
- Yellow nail syndrome, fungal infections, drugs

84
Q

Lights criteria for plerual effusion : transudative or exudative

A
85
Q

Why might a cancer pt get raised ICP

A

Principle cause of RICP in cancer patients is
- Space-occupying tumour
- Obstructive hydrocephalus

86
Q

Presentation of a SOL

A
  • N and V
  • Dizziness
  • Changes in eyesight
  • Behaviour changes
  • Worse on cough
  • Worse on leading forwards

Neurological problems:
* Eyesight
* Weakness and numbness
* Coordination problems
* Arthralgia
* Reduced consciousness

Coning symptoms- emergency
* Bradycardia
* High blood pressure
* Abnormal breathing

87
Q

Investigations of RICP

A

CT scan +- MRI with and without contrast

Fundoscopy
- Papilledema
- Loss of retinal venous pulsation

Lumbar puncture-> to determine CSF pressure and look for cancer cells

88
Q

Management of RICP

A

Dexamethasone to shrink tumour

Antibiotics if infective cause

Cancer treatment if SoL:
* Debulking surgery
* Radiation therapy
* Intrathecal chemotherapy- given via lumbar puncture

Surgery:
* Cerebral shunts placed tp drain CSF and lower ICP
* CSF is drained from brain to the abdomen

89
Q

Why are cancer pts at greater risk of seizures?

A

epileptic seizures increase in cancer patients due to
* Brain metastases and
* Primary brain tumour

90
Q

How is status epilepticus defined?

A

Status epilepticus is defined as:
* a single seizure lasting >5 minutes, or
* >= 2 seizures within a 5-minute period without the person returning to normal between them

91
Q

Risk factors for status epilepticus in cancer pts

A
  • Slow growing , low grade tumour
  • Tumour is in one of the lobes of the cerebrum or meninges
92
Q

Pathophysiology of status epilepticus in cancer pts

A
  • Due to abnormal development of cells around the tumour
  • May be due to imbalance of chemicals in the brain caused by tumour
  • Leads to altered electrical activity in the brain -> epilepsy
93
Q

managemetn of frequent seizures in cancer patients?

A

Management
* Anti-epileptics

Frequently used anti-convulsants include:
* levetiracetam (Keppra®)
* sodium valproate (Epilim®)
* lamotrigine (Lamictal®)
* clobazam
* carbamazepine (Tegretol®)
* topiramate
* phenytoin (Epanutin®).

Surgery- neurosurgery

94
Q

status epilepticus emergency management

A

Start timer
1) After 5 mins give
- Lorazepam IV or if in community midazolam buccally/rectally

2) After 10 mins
- Lorazepam IV
- Prepare second line medication

3) At 15 mins
- Levetiracetam
- Phenytoin
- Phenobarbital

4) At 20 mins
- Intubate or administer further alternatives to the second line drugs (Levetiracetam, phenytoin, phenobarbital)

5) If this does work
Rapid sequence induction of anaesthesia using thiopental sodium

95
Q

What is? metastatic spinal cord compression? (MSCC )

how many people does it affect? where exactly is cord compressed?

A
  • Spinal cord compression is an oncological emergency and affects up to 5% of cancer patients.
  • Extradural compression accounts for the majority of cases, usually due to vertebral body metastases.
  • Increasingly common due to prolonged survival
96
Q

Which cancers have highest risk of Metastatic spinal cord compression (MSCC )

A
  • lung
  • breast
  • prostate cancer
97
Q

Pathophysiology of MSCC

and causes, mets from which cancer?

A

Occurs when dural sac and its contents are compressed at the level of the cord or cauda equina

Causes
* Collapse of vertebral body due to bony mets causing brittle bones
* Metastasis in the epidural space (paraspinal area)
–> Especially lymphoma

98
Q

Stages of damage to the spinal cord in MSCC

A

1) Reversible initial stages
- Initially oedema
- Venous congestion
- Demyelination

2) Prolonged compression
- Vascular injury
- Cord necrosis
- Permanent damage

99
Q

Presentation of MSCC?

A
  • Back pain
  • Motor symptoms (upper motor neuronee signs)
  • Sensory loss
  • Sphincter dysfunction
  • Diminishing performance status/generally unwell
100
Q

Presentation of MSCC: back pain
elaborate on its features

A
  • Often for 2-3 months
  • Poorly responsive to analgesia
  • Radiation around chest- band like
  • Radicular –> Exacerbated by neck flexion, SLR, coughing, sneezing, straining
  • Pain at night/ wakes up
101
Q

Presentation of MSCC: motor symptoms
elaborate on its features

A
  • (upper motor neuronee signs)
  • Affects >75%,
  • Reduced power, difficulty standing, walking, climbing stairs, often symmetrical
  • (high cervical scc causes poor truncal balance)
102
Q

Presentation of MSCC:
Sensory loss
how common?

A

Affects >50%, but may be unaware until examined

103
Q

Presentation of MSCC: Sphincter dysfunction
elaborate on its features

A
  • Urinary hesitancy, frequency, then urinary retention with overflow, faecal incontinence
104
Q

examination findings of a patient with MSCC?

A
  • Acute onset -> Flaccid paralysis
  • Progressive (UMN):
    a. - Spasticity (increased tone, clonus, hyperreflexia in limbs below level of MSCC)
    b. - Plantar reflexes up-going - Babinski (not cauda equina- LMN)
    c - Palpable bladder (urinary retention)
    d. - Sensory loss with well defined dermatomal levels
  • Cauda equina
105
Q

Common areas of spine involved in MSCC?

A
  • Thoracic commonest site
  • 30-50% - >1 areas involves
  • Below L2 vertebra= cauda equina(compression of peripheral nerve and not spinal cord)
106
Q

investigation for MSCC?

A
  • MRI of the whole spine
  • Routine blood
  • If high chance of surgery- Group and save and clotting screen
107
Q

When to refer if suspect MSCC>

A

Referral
- Pain suggestive of spinal mets – MRI within 1 weeks
- Signs MSCC, MRI within 24 hours

108
Q

UMN vs LMN signs

A

UMN
- Spinal cord compression
o Hypertonia
o Hyperreflexia
o Babinskis sign
o clonus

LMN
- Cauda equina
- Peripheral nerve compression

109
Q

Initial management of MSCC?

A
  • Admit and treat within 24 hours of diagnosis
  • Bed rest / log-roll (preserve spinal stability and prevent neuro deterioration)
  • Dexamethasone 16mg + PPI
  • Adequate analgesia

If >48hrs no motor function -> supportive care
- Analgesia
- Laxative
- Care of pressure areas
- Bladder
- Monitor BMs
- VTE prophylaxis
- Physiotherapy
- OT

110
Q

Surgical management of MSCC?

first line surgery , best suited for which cancers?

A

Surgery
- First line treatment- Balloon kyphoplasty

Best suited:
* Multiple myeloma
* Lymphoma
* Breast
* Prostate
* Renal

111
Q

Which patients are good candidates for surgery for MSCC?
AIM of surgery

A

Good motor function at presentation
* Good performance status
* Limited comorbidity
* Single level spinal disease
* Absence of visceral mets
* Long interval from primary diagnosis
* Helpful for biopsy/ stabilisation

Aim:
* Relive compression
* Remove tumours
* Stabilise spine
* Preserve greater degree of mobility

112
Q

What partients recieve radiotherapy for MSCC?
How does it work?

A
  • Majority receive this (due to extensive disease- multi spinal level disease, mets and/or compression and poor performance status when MSCC occurs)
  • Delivered within 24 hours

MOA:
- Targets abnormal area plus 1-2 vertebra either side

113
Q

Aim of radiotherapy for MSCC?

life expectancy ?

A
  • Relieve compression of the spine and nerve roots by causing cell death in the rapidly dividing tumour tissue
  • Relives pain and stabilises neurological deficict
  • Life expectancy often measured in months
114
Q

When might chemotherapy be considered for MSCC?

A

Urgent chemotherapy
- May be considered if very sensitive tumours e.g. lymphoma /SCLC

115
Q

Causes of cauda equina?

A

Causes
- Disc herniation
- Trauma
- Neoplasm
a. Primary or metastatic:
b. Most common cancers that spread to spinal vertebrae: thyroid, breast, lung, renal and prostate)
- Infection
- Chronic spinal inflammation
- Iatrogenic

116
Q

Where does the lesion have to be to be called cauda equina? what fibres involved?

A

Caused by compression of the spinal cord
- Below L2
- Peripheral nerves (LMN), containing motor and sensory fibres

117
Q

presentation of cauda equina?

A

LMN signs
- Reduced lower limb sensation (often bilateral)
- Hyporeflexia
- Bladder or bowel dysfunction:
a. Perianal (saddle) numbness
b. Loss of anal tone
c. Urinary retention
- Lower limb motor weakness
- Severe back pain
- Impotence

118
Q

Investigations for cauda equina?

A

PR examination
Post-void bladder scan
Lumbar-sacral spine MRI

119
Q

Management of cauda equina syndrome?

A

Management
- Surgical decompression within 48 hours
- Radiotherapy and/or chemotherapy

  • In patients where malignancy is demonstrated on MRI, or in patients where clinical suspicion is high, administration of dexamethasone 16 mg daily in divided doses (with PPI cover) is indicated.
120
Q

What are common causes of Nausea and Vomitting in pts with cancer?

surgical sieve e.g. infection

A
121
Q

AR the mechanisms / pathophysiology of nausea and vomitting

A
122
Q

Recap: which anti-emetics work on which recpetors to combat nausea and vomitting?

A
123
Q

Chemical cause of N&V:
1. what would be clinical features?
2. What is best antiemetic?

A
124
Q

Gastric stasis is cause of N&V
1. clinical features?
2. treatment?

A
125
Q

Bowel obstruction is the cause of N&V
1. clincial features
2. treatment?

A
126
Q

Raised ICP is cause of N&V
1. clinical features
2. treatment

A
127
Q

Psychological factors causing N&V
1. features
2. treatment

A
128
Q

Post op / RT causes of N&V
1. features
2. treatment

A
129
Q

Constipation causes N&V
1. clincial features
2. treatment

A
130
Q

How many cancer pts get N&V?

A

Up to 75% of all cancer patients will experience chemotherapy related emesis

131
Q

What are some increased risks for N&V when have cancer?

A
  • Increased risk associated with specific chemo
    agents
    female gender
    age <50 years
    past Hx
    of N&V (pregnancy, prior chemotherapy use,
    motion sickness)
132
Q

features of N+V caused by chemotherapy

A

persistent, often severe nausea, unrelieved by vomiting, aggratated by sight/smell of food

133
Q

Management after sickness inducing chemotherapy

A
  • Metoclopramide
  • Dexamethasone
  • Ondansetron

Non-pharmacological management:
* Advice and realistic aims
* Smell
* Taste - small appropriate meals
* Hypnosis?
* Acupuncture?

134
Q

timings wise how can chemotherapy induced nausea and vomitting present?

A

Acute, delayed, anticipatory

135
Q

management of route and regime in a patient with nausea and vomtiing

A

Route and regime:
* Oral absorption likely to be poor
* Consider SC route for at least 24 hours
* Regular anti-emetic
* Consider alternative if not improving
* Control of symptoms using one antiemetic is possible in ~60% of patients
* 1/3 require concurrent use of a second antiemetic
* Combine anti-emetics with different mechanisms of action
* Consider switch to oral if improving
* Cause resolves…?stop

136
Q

which symptoms except pain may be need to be managed in a cancer pt?

A
  • Nausea and vomiting
  • Intractable breathlessness
  • Constipation
  • Psychological distress, depression and anxiety
  • Confusion and delirium
137
Q

Clinical features of constipation?
What can it lead to?

A
138
Q

causes of constipation?

A
139
Q

Give examples of laxatives, their class, and their mechanism of action

A
  • Laxido and Movicol popular in oncology
  • Rarely use lactulose because poorly tolerated due to sweetness, except encephalopathy
140
Q

Which cancer pts get malignant bowel obstruction

A
  • Effects up to 15% of cancer patients
  • Ovarian (20-50%)
  • Colon (10-29%)
141
Q

Pathophysiology of malignant bowel osbtruction?

A
  • Mechanical (tumour within gut lumen or outside bowel wall)
  • Functional: (infiltration of myenteric plexus +/or gut musculature)
  • Combination of mechanical + functional
  • Gradual onset common
142
Q

How to treat malignant bowel obstruction

A
143
Q

How to treat inoperable bowel obstruction?

A
144
Q

If inoperable malignant bowel obstruction is NOT resolving despite initial interventions. What can you do next?

A
145
Q

SUMMARY SLIDE : N&V causes and treatment!

A
146
Q

compare cyclizine and metoclopramide

A

The oppose each in other !

  • metoclopramide -> prokinetic
  • good for nausea and vomiting caused by chemo/ cancer
  • Cyclizine -> antikinetic (opposite affect to meto)
  • good for bowel obstruction
147
Q

presentation of breathlessness

A
  • Patient-centred symptom
  • Cannot be inferred from physical examination or investigation- must ask about it
148
Q

treatable causes of breathlessness i.e. give examples and how they are treated

A
149
Q

Prevalenceof breathlessness?

A
150
Q

Pathophysiology of breathlessness

A
  • neurophysiology of breathlessness is related to but distinct from the control of the respiratory system
  • Breathlessness is a MISMATCH between the pts percieved need to breathe (respiratory drive) and their ability to do so (physiological capacity)
151
Q

Non drug management of intractable breathlessness?

A
  • Aim to reduce the perception
  • Patients can quickly detect lack of HCP confidence- calm, positive, logical approach needed
  • Position patient using gravity and not hinder weak diaphragm/ chest wall muscles
  • Air flow across face: fan or open a window
  • Trial of oxygen (if hypoxic)
  • Non-drug approaches if feasible
152
Q

Intractable breathlessness : drug management

A
153
Q

what is intractable breathlessness?

A

sustained severe breathlessness in patients who have not obtained relief from conventional treatment.

154
Q

Causes of hypercalcaemia?

capsule

A

Most common:
* primary hyperparathyroidism i.e. parathyroid adenoma / MENI/II

Hypercalcaemia of malignancy
Sarcoidosis
thryrotoxicosis
thiazide diuretic

155
Q

Signs and symptoms of hypercalacaemia

capsule onoclogy

A

Abdo pain
nausea and vomiting
constipation
polyuria
polydipsia
depression
confusion
renal stones
renal failure

156
Q

Which cancers commonly causes bony tumour deposits?

capsule oncology

A

breast
prostate
lung
thyroid
renial
myeloma
melanoma

YEAR 4 CANCER CARE (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions