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Cancer Care > Cancer Care > Flashcards

Cancer Care Flashcards

1
Q

what do the letters “SPIKES” stand for in breaking bad news

A 
Setting
Perception
Invitation
Knowledge
Empathy
Summary/Strategy
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2
Q

describe the “setting” aspect in the SPIKES model

A

right context, privacy, support

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3
Q

describe the “perception” aspect of the SPIKES model

A

find out how much patient knows and how serious they think the illness is
what their level of understanding is

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4
Q

describe the “invitation” aspect of the SPIKES model

A

find out how much patient wants to know

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5
Q

describe the “knowledge” aspect of the SPIKES model

A

align - find out what they know
educate - changing patient’s understanding in small steps
telling them about: diagnosis, treatment plan, prognosis, support

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6
Q

describe the “empathy” aspect of the SPIKES model

A

address emotions and respond to feelings of patient

observe and give patients time to react

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7
Q

describe the “summary/strategy” aspect of the SPIKES model

A

planning and follow through, tell them what happens next
listen to patient’s problem list
distinguish fixable from non-fixable
incorporate other resources of support

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8
Q

explain some of the potential conflicts doctors may have when taking care of dying patients

A
  • medicine vs. comfort
  • over-treatment and not accepting failure of medicine
  • patients/family members requesting highly aggressive and medically futile measures
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9
Q

what is the AMBER care bundle about?

A

a tool aiming to improve quality of care for patients who are a risk of dying but are still receiving active treatment
(recognise uncertainty between recovery and dying patients)

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10
Q

what does the AMBER care pathway involve

A
  • medical plan
  • escalation decision
  • discussion with patient/family
  • regular review
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11
Q

list some of the physical clues in recognising a patient who is dying

A
  • profoundly weak
  • gaunt
  • drowsy
  • diminished eating/drinking/taking medications orally
  • poor conc
  • abnormal breathing patterns
  • skin colour changes
  • temp changes at extremities
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12
Q

what are the common symptoms in patients at the end of life?

A
  • pain
  • n+v
  • breathlessness
  • restlessness and agitation
  • resp rate secretions
    manage by anticipatory prescribing
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13
Q

how is nausea and vomiting treated in dying patients

A
  • haloperidol, levomepromazine
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14
Q

how is breathlessness treated in dying patients

A
  • midazolam, morphine
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15
Q

how is restlessness/agitation treated in dying patients

A
  • midazolam, haloperidol, levomepromazine
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16
Q

how are resp secretions treated in dying patients

A

glycopyronium

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17
Q

what are the common causes of N+V in palliative patients

A

gastric stasis, medicines, chemical and metabolic disturbances

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18
Q

give the pathway for vomiting

A

CTZ, vagus nerve input and vestibular system feed into the vomiting centre in the brainstem, leading to the vomiting reflex

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19
Q

what is the mechanism of action of domperidone

A

dopamine antagonist

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20
Q

what is the main action site of domperidone

A

gut only

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21
Q

what is the mechanism of action of metoclopramide

A

DA antag, 5HT4 agon

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22
Q

what are the main action sites of metoclopramide

A

central and gut - prokinetic

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23
Q

what is the mechanism of action of haloperidol

A

DA antag

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24
Q

what is the main action site of haloperidol

A

CTZ

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25
Q

what is mechanism of action of cyclizine

A

histamine and ACh antag

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26
Q

what are the main sites of action of cyclizine

A

vestibular system and vomiting centre

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27
Q

what is the mechanism of action of granisetron/ondansetron

A

5ht3 antag

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28
Q

what are the main sites of action of granisetron/ondansetron

A

central gut

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29
Q

what is the mechanism of action of levomepromazine

A

5ht2, da, ach, histamine antagonists

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30
Q

what is the main action site of levomepromazine

A

central - broad spectrum

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31
Q

what is the mechanism of action of hyoscine bromide and glycopyronium

A

ach antag

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32
Q

what is the main action site of hyoscine bromide and glycopyronium

A

vestibular system &VC

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33
Q

why should dopamine antagonist antiemetics not be used together

A

enhanced extrapyramidal side effects

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34
Q

list some of the anticholinergic side effects of certain antiemetics

A

dry mouth, constipation, urinary retention, restlessness

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35
Q

in which patients should anticholinergic antiemetics not be prescribed

A

heart disease or rhythm disturbance

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36
Q

which two antiemetic drugs should not be mixed?

A

cyclizine and metoclopramide

or metaclopramide with IV ondansetron

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37
Q

what are the mechanisms of opioids causing n+v

A

ctz stimualtion, vestibular sensitivity and reduced gut motility

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38
Q

which antiemetics should be used if n+v is caused by impaired gastric empyting

A

prokinetics - metoclopramide and domperidone

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39
Q

what aetiological factor is cml associated with

A

ionising radiation

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40
Q

how do the cells differ between cml and aml

A

the cells retain their ability to differentiate in cml during the chronic phase of the disease

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41
Q

which gene translocation is involved in cml, what is the result

A

translocation on the philadelphia chromosome (t9;22). results in BRC-ABL gene (new fusion gene)

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42
Q

how does the brc-abl gene in cml act

A

as an abnormal tyrosine kinase

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43
Q

what is the blast crisis in cml

A

the cells go through the chronic phase for years, but eventually lose the ability to differentiate normally and enters the blast crisis (treatment aims to prevent this)

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44
Q

what are the symptoms of the chronic phase of cml

A

anaemia, weight loss, splenomegaly. paitents can develop gout.

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45
Q

what happens to the viscosity of blood with cml

A

hyperviscosity - increased wcc

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46
Q

what are the investigations that should be done in patients with suspected cml

A

fbc, blood film, bm, cytogenetics, molecular gneetics, (flow cytometry)

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47
Q

what will investigations for cml show in chronic phase

A

leucocytosis, BM hypercellular, normochromic anaemia

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48
Q

what do investigations for cml show in a blast crisis

A

increased no of blast cells in blood and bm, with anaemia and thrombocytopenia more marked

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49
Q

what is the management of cml in chronic phase

A

1) leukaphoresis - if wcc is very high and there are s+s of hyperviscosity
2) tyrosine kinase inhibitors, e.g. imatinib
3) allogenic stem cell transplant

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50
Q

how do tyrosine kinase inhibitors work in cml

A

bind to the atp-binding site of brc-abl1 and inhibit function of protein

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51
Q

what is the treatment for cml in blast phase

A

imatinib and second gen tyrosine kinase inhibitors, combination chemo

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52
Q

what is the pathophysiology of b cell cll

A

accumulation of mature-looking b cells in the peripheral blood, bm, and lymphatic tissues due to lymphyte clonal expansion through failure to respond to apoptotic signals.

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53
Q

what is the clinical presentation of cll

A

usually indolent
painless lymphadenopahty, anaemia, infection
constitutional symptoms - night sweats, fatigue

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54
Q

what are the clinical presentations of advances cll

A

variable degrees of anaemia, neutropenia and thrombocytopenia

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55
Q

which investigations are undertaken in patients with cll

A

fbc, blood film, bm aspirate and trephine, lymphocyte immunotyping, cytogenetics by fish, abdominal us

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56
Q

how is cll managed

A 
radiotherapy for lymph nodes
chemo
targeted biological therapy
steroids for autoimmune reactions
stem cell and bm transplant
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57
Q

list some inherited conditions that have an associated with acute leukaemia

A

down syndrome, fanconi anaemia, neurofibromatosis, ataxia telangiectasia

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58
Q

list some environmental factors associated with acute leukaemia

A
  • chemical carcinogens
  • ionising radiation
  • chemo drugs
  • infectious agents e.g t cell virus
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59
Q

what is the pathophysiology of acute leukaemias

A

malignant transformation of haemopoetic stem/early progenitor cells leads to rapid proliferation of cells. however there is a failure to differentiate (leads to accumulation of poorly differentiated cells/laukaemic blast cells in marrow and peripherally).

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60
Q

what are clinical presentations of acute leukaemias

A
  • anaemia
  • thrombocytopenic bleeding
  • infections (bacterial, fungal mainly)
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61
Q

what are the features of extramedullary leukaemic infiltration in acute leukaemia

A
  • hepatosplenomegaly
  • lymphadenopathy
  • leukaemic meningitis
  • testicular infiltration
  • skin nodules
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62
Q

what is the commonest cancer in children

A

all

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63
Q

what are the steps of treating patients with all

A

1) induction of remission with chemo and steroids
2) intensification - exposure to new chemo drugs
3) maintenance - chemo drugs

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64
Q

how is high risk all managed

A

intensification of chemo drugs, stem cell transplant

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65
Q

which type of aml is important to identify, as it changes management of patient

A

apl

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66
Q

how are lymphomas classified

A

Hodgkin’s and Non-Hodgkin’s lymphoma
B cell or T cell
Indolent and aggressive types (NHLs)

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67
Q

what are the extranodal presentations of NHL

A

hepatosplenomegaly, as well as other sites such as the gut, testes, thyroid gland, bone, muscle, cns

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68
Q

how is NHL diagnosed

A 
LN biopsy, biopsy of extranodal site,
 cxr, 
ct chest/abdo/pelvis, 
blood count and film, 
BM aspiration and trephine, 
immunophenotyping and cytogenetics
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69
Q

what are the tumour burden markers in NHL

A

LDH

Beta-microglobulin

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70
Q

what is immunophenotyping

A

technique which studies protein expression by cells, done by labelling wbc’s with antibodies directed against surface proteins on their membrane. the labelled cells are then processed through a flow cytometer

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71
Q

how are stage 1 NHL’s managed

A

Involved Field Radiotherapy

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72
Q

how are stage 2/3 NHL’s managed

A

these have a relapsing and remmiting presentation and may be managed with stem cell transplant, rituximab, immunochemotherapy

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73
Q

what is Burkitt’s lymphoma, and how is it managed

A

a highly aggressive non hodgkins lymphoma of the B cells.

it is managed with high-intensity multi agent chemotherapy

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74
Q

which particular viral infection is it important to ask about in the history of a patient with lymphoma - associated with

A

EBV - infectious mononucleosis

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75
Q

what is the hallmark pathological feature of Hodgkin’s lymphoma under a microscope

A

Reed Sternberg Cells

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76
Q

how may Hodgkins lymphoma present

A
  • painless rubbery lymphadenopathy
  • may be generalised lymphadenopathy
  • later spread to liver, lungs, marrow may cause local symptoms
  • B symptoms
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77
Q

list some of the B symptoms in Hodgkins lymphoma

A

fever, night sweats, weight loss

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78
Q

how is Hodgkin’s lymphoma diagnosed

A

lymph node and involved tissue biospy
fine needle aspirate (should not be used alone for diagnosis)
staging with CT neck, chest, abdo, pelvis

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79
Q

how is early stage Hodgkins lymphoma treated (Stages 1a and 2a)

A

involved field radiotherapy

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80
Q

how are stages 2b-4 hodgkins lymphoma managed

A

combination chemotherapy, stem cell transplant may be offered

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81
Q

what is the salvage therapy given for Hodgkin’s lymphoma

A

salvage chemo, monoclonal Ab therapy (not rituximab)

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82
Q

what is the main difference between lymphoma and leukaemia

A

leukaemia is mainly in BM and blood, while lymphoma tends to be in LN and other tissues

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83
Q

which cells proliferate in myeloma

A

plasma cells

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84
Q

how does myeloma affect the bone

A

accumulation of proliferating cells in the BM leads to anaemia and BM failure - and lytic lesions, generalised osteoporosis and pathological fractures

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85
Q

what is MGUS

A

monoclonal gammopathy of unkown cause - increase paraprotein found in blood, similar to myeloma

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86
Q

why is paraprotein increased in myeloma

A

due to excess proliferation of plasma cells

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87
Q

what investigations should be done for a patient with myeloma

A
  • fbc
  • esr/plasma viscosity
  • U+E/Ca2+/albumin
  • electrophoresis and immunofixation
  • light chain in serum, paraprotein levels
  • Bence Jones protein in urine
  • BM aspirate and trephine
  • skeletal survey
  • MRI spine
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88
Q

what is the course of progression of myeloma

A

incurable - runs relapsing and remitting course

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89
Q

how is myeloma treated

A 
analgesia
radiotherapy to areas of bone pain
management of hypercalcaemia
plasma exchange for hyperviscosity
chemo combo therapy
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90
Q

what are myelodysplastic syndromes

A

group of neoplastic conditions where there is dysplastic haemopoesis and peripheral cytopenias.

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91
Q

what type of leukaemia do myelodysplastic syndromes have a tendency to progress to

A

aml

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92
Q

what does bm/peripheral blood look like in patients with myelodysplastic syndromes

A

hypercellular bm with dysplastic morphology and paradoxic peripheral blood cytopenia

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93
Q

what are the clinical features of myelodysplastic syndromes

A

anaemia
thrombocytopenia
recurrent infections
bm failure

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94
Q

what may cause death in myelodysplastic syndromes

A

bm failure, progression to aml

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95
Q

what investigations can be done in patients iwth myelodysplastic syndrome

A
  • fbc
  • blood film
  • bm aspiration/trephine
  • cytogenetics
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96
Q

what is the management of myelodysplastic syndromes

A
  • blood and platelet infusion
  • epo
  • gcsf
  • chemo
  • stem cell transplant
  • hypomethylating agents
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97
Q

what is myelofibrosis

A

myeloproliferative neoplasm in which abnormal cloning of haematopoeitic stem cells in the bm cause fibrosis (replacement of bone marrow with scar tissue)

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98
Q

what are the signs and symptoms of myelofibrosis

A 
splenomegaly, hepatomegaly
bone pain
bruising
cachexia
gout
susceptibility to infection
anaemia
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99
Q

what mutation is associated with myelofibrosis

A

jak2

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100
Q

what is the treatment for myelofibrosis

A
  • stem cell transplant
  • folic acid
  • allopurinol
  • blood transfusions
  • chemo
  • ruxolitinib
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101
Q

what are the three urological emergencies

A

1) loin pain
2) urinary retention
3) testicular pain

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102
Q

list some of the urological causes of loin plain

A
  • ureteric/renal colic

- pyelonephritis/uti

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103
Q

list some non-urological causes of loin pain

A
  • msk
  • gynaecological
  • general surgical
  • vasc - dissecting iliac aneurysm
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104
Q

what are the causes of ureteric colic

A
  • stone
  • clot
  • puj obstruction
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105
Q

where would ureteric colic pain radiate to

A

penis/testis/labia

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106
Q

which stones require intervention

A
  • large
  • renal impairment
  • intractable pain
  • solitary kidney
  • infection
  • failed conservative management
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107
Q

what is a red flag symptom in loin pain on examination

A

septic signs and symptoms - esp temperature/tachy/hypotensive

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108
Q

how is ureteric colic investigated

A
  • fbc/u+e/ca2+/urate/clotting if septic
  • cultures
  • urine dip +/- MSSU for MC+S
  • CT - KUB
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109
Q

how is ureteric colic treated

A
  • analgesia
  • antiemetic
  • iv fluids
  • a blocker as explusive therapy for stones
  • lasertripsy/lithotripsy
  • jj stent
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110
Q

how is pyonephritis managed

A
  • call for senior help
  • iv access, fluids, O2, IV abx
  • blood/urine cultures sent
  • abg lactate, base excess
  • itu involvement
  • needs drainage
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111
Q

what antibiotics are given to patients with pyonephritis

A

gentamicin + tazocin/ coamoxiclav

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112
Q

how are patients discharged after pyonephritis

A

with drain in situ, and readmit

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113
Q

what is found in the history of patients with pyelonephritis

A

chills, fever > 38, loin pain

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114
Q

what is the main organism involved in pyelonephritis

A

e coli

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115
Q

what are the less common organisms involved in pyelonephritis

A

proteus, pseudomonas, klebsiella, enterobacter, serratia, citriobacter

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116
Q

what will you find on examination of a patient with pyelonephritis

A

pyrexia
tachy
tender flank/suprapubic region

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117
Q

what would urine dip show in pyelonephritis

A

blood, wbcs, nitrites

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118
Q

what investigations are performed in patients with pyelonephritis

A
  • fbc/u+e
  • msu, MC+S
  • blood cultures may be done
  • renal uss (exclude pyonephritis)
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119
Q

what is the management of pyelonephritis

A
  • PO/IV fluids
  • PO/IV Abx
  • analgesia/antiemetic
  • DVT prophylaxis
  • urological input if male/complicated/not settling with treatment
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120
Q

list the causes of urinary retention

A
  • prostate enlargement
  • uti
  • constipation
  • overdistention e.g. excess iv fluids
  • urethral stricture/phimosis
  • surgery/anaesthetic effects
  • drugs e.g. anticholinergics
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121
Q

what are the features of acute urinary retention

A
  • painful
  • relieved by drainage
  • no upper tract insult
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122
Q

what do you assume if elderly man with nocturnal eneuresis presents

A

chronic retention with overflow incontinence until otherwise proven

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123
Q

what are the “storage” symptoms of urinary retention

A
  • frequency
  • urgency
  • nocturia
  • urge incontinence
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124
Q

what are the “voiding” symptoms of urinary retention

A
  • hesitancy
  • intermittency
  • straining
  • spraying
  • poor flow
  • post-mict dribbling
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125
Q

what is the management for urinary retention

A

1) catheter - urethral or suprapubic
2) record residual volume
3) reexamine to make sure mass has disappeared

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126
Q

what causes high pressure chronic urinary retention

A

long term obstruction

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127
Q

what causes low pressure chronic urinary retention

A

failure of detrusor muscle - stroke/ms etc

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128
Q

what investigations are performed in patients with chronic retention

A
  • urine dip/MC+S
  • Catheter sample
  • u+e
  • psa
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129
Q

how is acute urinary retention managed

A
  • treat cause
  • cath
  • a blocker e.g. tamsulosin
  • 5a reductase inhibitor (BPH)
  • TWOC
  • turp if fails
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130
Q

how is chronic urinary retention treated

A
  • long term indwelling cath
  • clean intermittent self cath
  • turp if fit
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131
Q

list some causes for acute urinary retention

A
  • bph/ca
  • paraphimosis
  • phimosis
  • prolapse
  • balantitis, prostatitis, cystitis
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132
Q

list some causes of chronic urinary retention

A
  • bph/ca
  • drugs
  • iatrogenic
  • congenital deformities
  • trauma, infection
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133
Q

list some causes of testicular pain

A
  • torsion!!
  • epididymitis/orchitis/epididymoorchitis
  • torsion of hytatid of Morgani
  • tumour
  • trauma
  • calculi rarely
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134
Q

how do you manage testicular pain

A

review with senior

urgent surgical exploration +/- orchidectomy/orchidopexy

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135
Q

what age group tends to be affected by testicular torsion

A

under 20

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136
Q

what may be found on examination of a patient with testicular pain

A 
pyrexia
tachy
normotensive
difficult/painful movement
erythematous scrotum
exquisistely tender testes
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137
Q

what is usually the cause of epididymoorchitis in 20-30 yo

A

sti

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138
Q

what is usually the cause of epididymoorchitis in older patients

A

uti

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139
Q

what questions must you ask in a history of a patient with suspected epididymoorchitis

A

unprotected sex?
uti recently?
urethral instrumentation/cath recently?
MUMPS hx

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140
Q

what may be found on examination of a patient with epididymoorchitis

A
  • pyrexial
  • tachy
  • ?septic
  • scrotum erythematous
  • enlarged, tender testis
  • fluctuant areas if abscess
  • reactive hydrocoele may be present
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141
Q

what is fournier’s gangrene

A

gangrenous area of scrotal skin in infections etc - is an emergency!!

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142
Q

what are the investigations for epididymoorchitis

A
  • FBC/U&E/cultures
  • MSU, MC+S
  • scrotal USS if ?abscess isnt settling
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143
Q

what is the management for epididymoorchitis

A 
abx via local guidelines (cipro/doxy often used)
analgesia
recue non essential activity
sti clinic
uti further investigations
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144
Q

what are the symptoms that are “voiding” luts

A
  • dysuria
  • poor stream
  • hesitancy
  • terminal dribbling
  • incomplete voiding
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145
Q

list the zones of the prostate

A
  • central
  • peripheral
  • transitional
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146
Q

which gene is associated with prostate cancer

A

brca2 (ask about female relatives with breast cancer)

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147
Q

what is the significance of prostate intrapeithelial neoplasia

A

recognised precursor to prostate cancer

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148
Q

what is the gleason score out of

A

2-10

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149
Q

how is the gleason score calculated

A

pattern of growth is seen under microscopy - the sum of the two most common grades of cell differentiation is recorded. e.g. grade 3+4 are the two most common therefore sum of 7

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150
Q

what gleason score is poor prognosis

A

usually above 8

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151
Q

how does prostate cancer metastasise to bone

A

through the vertebral plexus of veins

152
Q

what are the symptoms of prostate cancer

A

often asymptomatic

  • frequency
  • hesitancy
  • terminal dribble
  • poor stream
  • nocturia
  • haematospermia
  • erectile dysfunction
  • systemic symptoms e.g. malaise, weight loss
153
Q

what are some of the signs and symptoms of prostate cancer metastasis

A
  • bone/back pain
  • path fractures
  • hypercalcaemia
154
Q

what may be felt on pr examination of a patient with prostate ca

A

hard craggy nodule or diffusely infiltrating abnormality

typically loss of midline sulcus of prostate gland

155
Q

what is the problem with the use of psa as a tumour marker

A

sensitive but relatively non-specific for prostate ca therefore poor screening test

156
Q

list the investigations that should be performed in a suspected prostate cancer

A
  • PSA
  • Routine bloods - esp excluding hyperCa2+ and uraemia
  • IV urography
  • CT scan
  • TRUS (most sensitive)
  • Biopsy/resection
  • MRI (local tissue)
  • Isotope bone scan
157
Q

what are the T-stages of prostate cancer

A

T1 - asymptomatic/incidental finding - cannot be felt
T2 - tumour confined to capsule of gland
T3 - tumour extension beyond capsule of gland
T4 - invasion of rectum and other pelvic structures

158
Q

what is active surveillance in prostate cancer

A

those with low gelason score and low psa who have indolent disease, are monitored with 3-monthly PSA levels. biopsies are repeated every 2 years. treatment can be introduced if PSA rises above threshold/increased velocity of PSA increase.

159
Q

how do LHRH agonists work in prostate cancer

A

block release of testosterone (after initial surge); given with antiandrogens initially

160
Q

how do LHRH antagonists work in prostate cancer

A

block testosterone release (testosterone promotes prostate cancer)

161
Q

list the hormone-related therapies for prostate cancer

A
  • bilateral orchidectomy
  • antiandrogen drugs
  • GnRH analogue/antag
162
Q

what is the difference between LHRH agonists/antagonists and antiandrogens

A

antiandrogens work peripherally

163
Q

what are the surgical options for prostate cancer treatment

A
  • TURP
  • Radical prostatectomy (removal of entire prostate, adjacent bladder neck, seminal vesicles, vas deferens, surroudnign fascia)
164
Q

what should happen to the PSA levels following radical prostatectomy?

A

undetectbale - if they are there, even at a low level - it indicates that there is some residual prostatic tissue present (i.e. mets)

165
Q

what is brachytherapy in prostate cancer

A

form of radiotherapy where a source of radiation in placed inside or next to the area requiring treatment - implanted. entered through the perineum to gain access to prostate

166
Q

what is the palliative management for prostate cancer

A

GnRH analogue/oral antiandrogen

chemo/pred for relapses

167
Q

what are the side effects of antiandrogens

A

hot flushes, loss of libido, gynaecomastia, impotence

168
Q

what is tumour lysis syndrome

A

group of metabolic abnormalities that occur as a complication during treatment of cancer, where large amounts of tumour cells are lysed at the same time by treatment, therefore releasing their contents into the blood stream

169
Q

what are the ways in which tumour lysis syndrome can present

A

usually 3-7 days post chemo

  • oliguric/anuric renal failure
  • cardiac arrhythmias/arrest
  • primary presentation of malignancy; lab blood abnormalities
170
Q

what are the patient-specific risk factors for tumour lysis syndrome

A
  • preexisting renal dysfunction/disease
  • hypovolaemia e.g. diuretic use pretreatment
  • pretreatment LDH high
  • urinary tract obstruction from tumour
171
Q

what are the tumour-specific risk factors for tumour lysis syndrome

A
  • high grade lymphomas, burkitt’s lymphoma
  • rapidly dividing cancers
  • all
  • myeloma
  • germ cell tumours
  • sclc
  • breast (inflammatory)
172
Q

how can tumour lysis syndrome be prevented

A

prehydration and vigorous hydration throughout treatment

monitoring of electrolytes and treat promptly if disturbances

173
Q

how is tumour lysis syndrome managed

A
  • allopurinol for hyperuricaemia
  • rasburicase which converts uric acid to allantoin for secretion
  • avoid thiazides
  • haemodialysis for persistentrenal failure despite adequate treatment
  • treat electrolyte imbalances e.g. salbutamol nebs, calcium gluconate, phosphate binders, sodium bicarb to alkalinise urine and increase clearance of potassium and phosphates
174
Q

what are the symptoms of SVCO

A
  • swelling of face/neck/arm(s)
  • distended neck and chest wall veins (non collapsible)
  • sob
  • headache (intracranial venous congestion)
  • drowsiness
175
Q

what are the investigations you would do for SVCO

A
  • cxr - mediastinal mass
  • ct scan
  • needle biopsy
  • peripheral LN sampling
176
Q

what is the management for SVCO

A
  • consider anticoag and steroids
  • stent insertion
  • radiotherapy/chemo for treatment of underlying cause of obstruction
177
Q

what are the causes of hypercalcaemia in cancer

A
  • osteolytic lesions
  • PTHrP tumour production
  • calcitriol tumour production
178
Q

which cancer types are especially assoc with hypercalcaemia

A

lung, breast, myeloma, lymphoma

179
Q

what are the symptoms of hypercalcaemia

A
  • nausea, dehydration, anorexia
  • polydipsia, polyuria
  • confusion, poor conc, drowsiness
  • constipation
  • bone pain
180
Q

what are the investigations to do in hypercalcaemia

A 
calcium (2.1-2.6), corrected for albumin
pth/pthrp
u+e
phosphate
(+/- myeloma screen)
181
Q

what is the treatment for hypercalcaemia in malignancy

A
  • correct dehyd: IV saline +/- diuretics to promote calcium loss (loop - not thiazide!)
  • IV bisphosphanates
  • others: calcitonin, corticosteroids, systemic management of malignancy
182
Q

which tumour types are commonly assoc with metastatic SC compression

A

bronchus, breast, prostate, kidney, haem (multiple myeloma, NHL)

183
Q

which anatomical part of a vertebra are mets most likely to go to

A

vertebral body

184
Q

what are the clinical symptoms of a cancer patient with SC compression

A
  • back pain
  • radicular pain
  • weakness
  • sensory deficit
  • autonomic dysfunction
  • proprioception, light touch, pin prick sensation disturbance
    unilat or bilat
185
Q

what investigations should be done for a cancer patient with SC compression

A

MRI
whole body imaging
CT/PET

186
Q

what is the treatment for SC compression in cancer patients

A
  • supportive care e.g. bladder care, laxatives etc
  • initiate high dose glucocorticoids e.g. dexamethasone
  • surgery + radiotherapy (especially if single vertebral level affected)
  • urgent chemo for sensitive cancer
187
Q

what is neutropenic sepsis

A

cancer patients with low wcc (<1 x 10^9) and who have either temperature > 38 deg or other s+s of sepsis

188
Q

who is particularly at risk of neutropenic sepsis in cancer

A
  • 5-10 days post chemo
  • extensive field radiotherapy
  • haematological malignancies with neutropenia e.g. leukaemia
  • certain drugs
189
Q

what is the management of neutropenic sepsis in cancer

A

a - e
empirical abx (tazocin/meropenem)
fluid resus, consider cath, involve seniors
GCSF in profoundly neutropenic

190
Q

how can future neutropenic sepsis episodes be avoided

A

consider changing chemo cycles to reduce dose
give GCSF prophylactically
educate patients to look for signs

191
Q

what is GCSF

A

granulocyte colony -stimulating factor: stimulates BM to produce granulocytes and stem cells and release them into the bloodstream
(used in neutropenic sepsis, stem cell transplants…)

192
Q

what is the epidemiology of breast cancer

A

affects 1 in 8 women

commonest cause of cancer death in women

193
Q

what are the risk factors for developing breast cancer

A
  • high bmi
  • high fat intake
  • high alcohol intake
  • lack of exercise
  • BRCA genes
  • hrt/cocp
  • oestrogen exposure, especially unapposed
194
Q

list some of the ddx for breast cancer

A
  • galactocoele
  • haematoma
  • fibradenoma
  • duct papilloma
  • breast abcess, cyst
  • fat necrosis
195
Q

what is male breast cancer assoc with

A

strong fhx, inherited BRCA genes

196
Q

how may breast cancer present

A
  • usually painless lump
  • nipple changes, inversion
  • skin dimpling
  • distortion of breast
  • skin changes, rash
  • blood stained nipple dc
  • signs of assoc lymphadenopathy, peu d orange
197
Q

list the commonest sites to with breast ca spreads

A
  • bone
  • lungs
  • liver
  • skin
198
Q

how are breast cancers classified, and what are the different types

A

invasive or non invasive, ductal or lobar, or diffuse/other

non-invasive: dcis, lcis (can be precursors to invasive malignancy)

invasive: invasive ductal carcinoma, invasive lobar carcinoma, mucinous, papillary, medullary
misc - pyhlloides, lypmhoma, angiosarcoma

199
Q

what is the role of atypical ductal hyperplasia

A

confers increased risk of developing breast cancer

200
Q

describe paget’s disease of the breast

A

breast malignancy-associated condition affecting the nipple and areola where there is dryness, fissuring, erythema +/- exudate. almost always unilat.
patients most often have assoc underlying breast cancer

201
Q

what is paget’s disease like under a microscope

A

paget cells in the epidermis

202
Q

how does inflammatory carcinoma present

A

ill-defined erythema, tenderness, induration and oedema of the breast. aggressive

203
Q

are bilateral breast cancers common

A

no - assoc with strong fhx of breast ca

lesions tend to be solitary and not multifocal in breast ca also

204
Q

what are “basal cancers” in breast cancer

A

triple negative - oestrogen receptor negative, progesterone receptor negative, her-2 negative

205
Q

what is the triple assessment for breast cancer

A

examination, mammography (x rays) and sonography

206
Q

what are the different investigations done for breast cancer once the triple examination is done

A 
mri
nipple cd cytology
fine needle aspiration biopsy
needle biopsy
excision biopsy
207
Q

what would be seen on mammography which would suggest malignancy

A

irregular mass with calcification

208
Q

what does breast uss tell us about a mass

A

can assess whether cystic or solid, and can also assist in retrieving biopsy

209
Q

what is fine needle aspiration cytology

A

looking at a sample of cells from breast mass under microscope

210
Q

what is needle/core biopsy of breast

A

under LA, a core of tissue is taken for histological examination (in situ, invasive types determined), determine hormone receptor status

211
Q

what is the contribution of excision biopsy in breast cancer

A

performed if aspiration cytology/core needle biopsy has not been performed
done under GA and frozen section produced and examined immediately - then according to results +/- excision

212
Q

what cancers does presence of BRCA 1/2 genes increase the risk of

A

breast, ovarian, fallopian tube

213
Q

what are the side effects of antioestrogen drugs like tamoxifen, faslodex

A

hot flushes, fluid retention, vaginal dryness/dc, uterine bleeding, vte

214
Q

what are the side effects of aromatase inhibitor drugs like anastrozole, letrozole

A

hot flushes, fluid retention, vaginal dryness/dc, uterine bleeding, vte
increased cholesterol, osteoporosis, joint pains

215
Q

what are the side effects of medroxyprogesterone/megestrol drugs used to treat breast ca

A

nausea, fluid retention, weight gain

216
Q

what are the protective risk factors for breast ca

A
  • oopherectomy <35 yo
  • increasing parity
  • young age at 1st pregnancy
  • breastfeeding
  • regular exercise
217
Q

how does tamoxifen work

A

antioestrogen - is a prodrug which is activated in the liver and has a high affinity for oestrogen receptors. it acts as an antagonist to oestrogen receptors causing inhibition transcription of oestrogen-responsive genes

218
Q

how does herceptin work

A

HER-2 are receptors on the cell surface which communicate molecular signals from outside the cell to turn genes on and off. down the line, these stimulate cell proliferation.
HER-2 is overexpressed in some cancers, causing the cells to reproduce uncontrollably.
Herceptin arrests this proliferation

219
Q

how do aromatase inhibitors work for breast cancer

A

block the enzyme aromatase peripherally, to prevent peripheral activation of oestriol/oestrone to oestrodiol

220
Q

what tests cay be done to look for metastatic disease in breast ca

A

ct breast/thorax/abdo/pelvis
isotope bone scan
serum ca125
serum calcium (bone mets)

221
Q

what are the different stages of breast ca

A

1- tumour <2 cm and not spread outside breast
2- 2-5cm / spread to neighbouring LN
3- spread to ln/neighbouring tissues
4- spread to other parts of the body

222
Q

what is the role of radiotherapy in breast cancer

A

indicated in all patients having breast-conserving surgery
treatment of choice for mets/bone involvement
brachytherpay is an option

223
Q

what is the role of chemotherapy/hormonal therapy in breast cancer

A

used in inoperable tumours, palliation, soft tissue mets (not useful for bone spread)
adjuvant to surgery/radio to kill off any remaining cells

hormonal therapy is receptor positive cancers, or in metastatic disease

224
Q

what are the different srugical procedures for breast cancer

A
  • wide total excision for localised smaller tumours
  • simple mastectomy
  • modified radical mastectomy
  • radical mastectomy
225
Q

what is the difference between modified radical mastectomy and radical mastectomy

A

modified radical: breast + ln’s removed and pec major spared

radical: breast + ln’s + pectoralis muscles removed

226
Q

what are the different axillary procedures that can be done in breast cancer

A
  • sentinel ln mapping + biospy
  • axillary sampling
  • axillary disection/clearance
227
Q

what is sentinel ln mapping

A

dye is injected to look for the nearest ln’s to the tumour, which would therefore highlight the ones most likely for cancer to spread to. these can then be removed

228
Q

what are the risk factors for local recurrence of breast cancer

A
  • t3/4 tumours
  • poorly differentiated
  • lymphovascular invasion
  • involved axillary ln’s
  • incomplete excision
229
Q

list some of the complications of breast mets

A
  • fungating tumours: infections, dc, bleeding
  • brachial plexopathy and lymphoedema
  • sc compression, path fractures
  • pleural effusions, lymphangitis
  • svco, oesophageal compression, laryngeal nerve palsy
  • DIC
230
Q

what are some of the complications related to radiotherapy treatment of breast ca

A

erythema, swelling, skin irritation, tenderness, temporary skin breakdown
lymphoedema if axillary radiation

231
Q

what is the current screening programme for breast cancer in the UK

A

47-73 year olds get a 3-yearly mammogram to screen for cancer. can also get mammogram on request
if known gene mutation, e.g. BRCA1/2 start at 30
of TP53 gene mutation, start at 20

232
Q

what happens to those with strong fhx of breast cancer in terms of management

A

screening starts earlier
genetic counselling referral, risk assessemnt and counselling
some may choose to have double mastectomy

233
Q

how may breast ca be prevented

A

maintain normal bmi, exercise, moderate alcohol drinking, stop smoking

234
Q

what are the different stages of cell division

A 
G0 - rest phase
G1 - cell growth 
S - cell duplicates DNA
G2 - cell grows more
M - mitosis (prophase, prometaphase, metaphase, anaphase, telophase and cytokinesis)
235
Q

what does growth fraction of cells mean

A

represents the percentage of cells actively progressing through the cell cycle

236
Q

list some of the mechanisms by which cancer cells become resistant

A
  • decreased cell uptake
  • increased efflux
  • increased dna repair
  • altered drug target
  • increased catabolism
  • increased drug detoxification
237
Q

what are the porperties of cancer cells

A
  • self sufficient growth signals
  • insensitive to antigrowth signals
  • evade apoptosis
  • sustained angiogenesis
  • limitless replicative potential
  • tissue invasion and mets
238
Q

what factors of the person need to be taken into account before prescribing chemotherapy

A
  • body weight, surface area
  • liver function
  • kidney function (narrow therapeutic window)
239
Q

list some LUTS

A
  • frequency, urgency, hesitancy
  • dysuria, haematuria, reduced flow, dribbling
  • nocturia, incontinence
  • pelvic pain
240
Q

list the questions you would ask about in the history of a patient with loin pain

A
  • speed of onset
  • colicky/sharp
  • severity
  • unilat/bilat
  • relieving/precipitating
  • previous episodes
  • assoc systemic/LUTS
241
Q

what may be found on examination of a patient with epididymoorchitis

A 
may be pyrexial or even septic
scrotum erythematous
testes/epididymis enlarged, tender
fluctuant areas if abscess
reactive hydrocoele
242
Q

what is the management for epididymoorchitis

A

local abx (ciprofloxacin/doxycycline)
analgesia
reduce non essential activity
sti/gum clinic referral

243
Q

which factors increase risk of prostate cancer

A

increases with age
first degree relative affected
breast cancer in the family - BRCA2 carriers
afrocaribbean

244
Q

which zone of the prostate is most commonly affected by prostate cancer

A

peripheral zone

245
Q

what is the histological type of prostate cancer

A

adenocarcinoma

246
Q

describe gleason score

A

in prostate cancer - score of 2-10 which is the sum of the sum of the two most common grade of cell differentiation found on microscopy. e.g. 4 is the most common and 3 is the second most common, gives a gleason score of 7 in total

247
Q

what gleason score has a bad prognosis

A

8 or above especially, but the higher the score the worse the prognosis generally

248
Q

what is the natural history of prostate cancer

A

local growth results in infiltration of the prostate gland and surrounding tissues. extracapsular spread can result, involving pelvic ln’s. can eventually get blood-bourne spread, bone mets, (soft tissue mets uncommon)

249
Q

what are the symptoms of prostate cancer

A

usually asymptomatic and incidental

  • obstructive symptoms of freq, hestitancy, poor stream, terminal dribble, nocturia
  • haematospermia
  • erectile dysfunction
  • general malaise, weight loss, anorexia
  • symptoms of spread e.g. bone pain
250
Q

what are the signs of prostate cancer

A

tumour may be palpable PR
prostate hard and nodular mass or diffusely nodular, enlarged
typically loss of midline sulcus
signs of spread e.g. fractures

251
Q

what are the investigations you would do in a patient with prostate cancer

A
  • PSA (sensitive but non-specific)
  • routine bloods
  • DRE
  • CT/MRI
  • IV urography
  • TRUS + needle biopsy
  • TURP + biopsy
252
Q

why would you do an isotope bone scan on someone with prostate cancer

A

look for bone mets - shows up as increased areas of uptake

253
Q

what stages are there of prostate cancer

A
  • stage 1/2 = confiend to prostate
  • stage 3 = extended through capsule of gland
  • stage 4 = invasion of rectum/other structures
254
Q

describe the different hormone therapy options for prostate cancer

A

aim to reduce testosterone, for primary tumour or metastatic

  • LHRH agonists: these intially increase release of testosterone before function is disabled (given in conjunction with antitestosterone)
  • GnRH antagonists - suppress testosterone without initial surge
  • bilat orchidectomy
  • antiandrogens
  • GnRH analogue
255
Q

what is flutamide

A

antiandrogen

256
Q

what is the palliative management of prostate cancer

A

hormone therapy to achieve response eg GnRH analogue/antiandrogen
chemo
prednisolone

257
Q

what are the treatment options for prostate cancer

A
  • hormone therapy
  • radical radiotherapy, brachytherapy
  • radical prostatectomy
  • post op radiotherapy in some
  • active surveillance, watchful waiting
258
Q

what is the difference between watchful waiting and active surveillance for prostate cancer

A

active surveillance = men with localised prostate cancer who can still have treatment to cure it in the future. regular testing
watchful waiting = men who are less able to deal with radical treatments are assessed less regularly, and management is aimed at symptom control rather than curative

259
Q

what is brachytherapy

A

a form of radiotherapy indicated for those with disease localised to the pelvis where a sealed source of radiation is placed inside next to the area requiring treatment - more direct form of radiotherapy

260
Q

what is usuallu irradiated in prostate cancer

A

prostate, seminal vesicles, local lymph nodes

261
Q

what stage of cancer is radical prostatectomy suitable for

A

t1/2

262
Q

what is the procedure in radical prostatectomy

A

removal of the entire prostate gland, both seminal vesicles, adjacent bladder neck, vas deference and surrounding fascia

263
Q

what are some of the complications of a radical prostatectomy

A

impotence, occassional urinary incontinence if nerve supply affected

264
Q

describe what the PSA levels should be like after a radical prostatectomy

A

undetectable - anything above would indicte mets or residual prostatic tissue and is an indication for post op radiotherapy

265
Q

who is active surveillance most suitable for

A

small tumour, indolent, confined to prostate

gleason score <7

266
Q

what regular tests are done in active surveillance of prostate cancer

A

3-monthly PSA, repeat biopsies every 2 years

if PSA rises above threshold/velocity increases -> introduce treatment

267
Q

what are some of the complications of prostate cancer

A

obstructive hydronephrosis, urianry obstruction/chronic retention
increased ca and scc in bony mets

268
Q

is bladder cancer more common in males or females

A

males

269
Q

what are the risk factors for bladder cancer

A
  • smoking
  • occupational exposure e.g. rubber and plastics manufacture, crude oil handling, painters, hair dressers
  • chronic irritation
  • schistosomiasis
270
Q

what is the presentation of bladder cancer

A

dipstick (painless) haematuria (microscopic usually),

frequency, dysuria, urgency may also be present

271
Q

what is the treatment of bladder cancer

A
  • Transurethral Resection of Bladder Tumour
  • intravesical chemo/immunotherapy in low grade
  • higher risk cancers = neoadjuvant chemo, cystectomy + ileal conduit, reconstruction
272
Q

what is the palliative treatment for bladder cancer

A

chemo/radiotherapy

273
Q

what are the investigations for bladder cancer

A 
IV urography (filling defect), urine cytology, CT/MRI
CXR / isotope scan for mets
274
Q

list some urological causes for haematuria

A

cancer (renal cell cancer, transitional cell cancer)
advanced prostate cancer (also bph)
infections

275
Q

list some nephrological causes for haematuria

A

glomerulonephirites
renal calculi
infections

276
Q

list the investigations you would do in a patient with haematuria

A 
- egfr, albumin:creatinine ratio
uss
urine cytology, MC+S
flexi cystoscopy
CT chest/abdo/pelvis  in ?mets
277
Q

which populations is penile cancer rare in

A

those who practice circumcision

278
Q

what are the pathological features of penile cancer

A

papilloferous or solid growth on shaft or glans which can also develop insidiously below the foreskin. May ulcerate
Squamous cell cancer

279
Q

what are some of the differentials for penile cancer

A

lymphogranulomata venereum, condylomata acunimata, chancroid, traumatic ulceration, leukoplakia, bowen’s disease

280
Q

what are the investigations you would in the diagnosis of penile cancer

A

biopsy/cytological scrapings
FNA of enlarged nodes
CT for inguinal node involvement

281
Q

what are the signs and symptoms of penile cancer

A

usually asymptomatic, but lesion often obvious
can have dc or odour
+/- enlarged local LN’s
may interfere with micturition or potency

282
Q

what is the treatment for penile cancer

A

NO recognised chemo
surgery: partial or complete amputation unless small lesion on prepuce where circumcision can be done
penile reconstruction after surgery
external beam radiotherapy/brachytherapy, involved nodes irradiated

283
Q

what are the risk factors for testicular cancer

A

undescended testes!

previous orchiitis, first deg relative, genetic causes may all be possible associations

284
Q

what is the pathology of testicular cancer

A

2 main types: seminoma (germ cell) or teratoma

seminomas tend to be solid lesions, teratomas tend to be haemorrhagic and cystic

285
Q

what is the natural history of testicular cancer

A

invade locally into tunica vaginlis and along spermatic cord
LN spread - paraortic nodes
blood spread commonly to lungs and liver

286
Q

what are the signs and symptoms of testicular cancer

A
  • testicular swelling (+/- hydrocoele), discomfort
  • gynaecomastia from excess HCG secretion form tumour
  • backache from elanrged paraortic nodes
  • central abdo mass from palpable nodes
  • lesion may be felt in testes
287
Q

what are the tests done in the diagnostic work up for testicular cancer

A 
fbc, liver, renal function
AFP, bHCG, LDH
Alk phos (seminoma)
USS for nodes
CT pelvis/abdo
288
Q

what are the differentials for testicular cancer

A

benign hydrocoele
testicular torsion
lymphadenopathy from other cause e.g. infection

289
Q

what is the marker for pancreatic cancer

A

CA19-9

290
Q

what is the treatment for testicular cancer

A

stage 1: inguinal orchidectomy, radiotherapy to paraortic nodes, surveillance
stage 2/3/4: proceed to chemo, radiotherapy of paraortic/pelvic nodes
lymphadenectomy

291
Q

list some of the rarer pathological types of testicular tumours

A

yolk sac, sertoli cell, intestinal cells

292
Q

what is the screening for testicular cancer

A

none - self examination and patient education

293
Q

list some of the treatment-related complications for testicular cancer

A

chemo: alopecia, peripheral neuropathy (cisplatin), skin changes (bleomycin), impaired fertility
radiotherapy: peptic ulcers

294
Q

what is the aetiology of renal cell cancers

A 
smoking
cadmium exposure
HLA types
von Hippel Landau disease
Horseshoe kidney
adult PKD
295
Q

what is the most common pathological type of renal cancer

A

adenocarcinoma - clear cell characteristic

varying degrees of differentiation

296
Q

what is te natural history of renal cell tumours

A

tumour invades kidney and surrounding tissues, renal vein/ivc
renal hilar node invasion and progress to paraortic chain
blood bourne mets to lung and liver

297
Q

what are the signs and symptoms of renal cell tumours

A
  • painless haematuria
  • loin pain if enlarging tumour
  • paraneoplastic e.g. hypercalcaemia, polycythaemia
  • general e.g. malaise and weight loss
  • mass felt in loin
  • some have assoc fever
298
Q

what are the ddx of renal cell carcinoma

A 
benign renal adenoma
tumour of renal pelvis
renal calculi
bladder tumour
hydronephrosis
299
Q

what are the investigations for renal cell carcinoma

A

bloods - fbc, polycythaemia
cxr showing cannon ball mets
us/ct to image tumour and look at renal vein/ivc
ct abdo/thorax

300
Q

why may there be polycythemia assoc with renal cell carcinoma

A

tumour production of Epo-like substance

301
Q

which part of the kidney does renal cell carcinoma arise from

A

proximal convoluted tubule

302
Q

is renal function usually impaired with renal cell carcinoma

A

usually no, unless other kidney is affected by disease

303
Q

what is von hippel lindau syndrome

A

genetic condition which confers predisposition to variety of cancers including renal cell carcinoma, phaeochromocytoma, islet tumours, pancreatic cysts

304
Q

what is fanconi anaemia

A

rare genetic disorders, common in Ashkenazi jews, where there is a defect in the genes responsible for dna repair
most develop cancer - often AML, BM failure
(cafe au lait spots)

305
Q

which congenital abnormalities carry risk for acute leukaemia

A

down syndrome
neurofibromatosis
fanconi anaemia
ataxia telangectasia

306
Q

list some environmental risk factors for acute leukamia

A

chemical carcinogens e.g. benzene, ionising radiation, chemo/radiotherapy,
infectious agents e.g. ebv, t cell laukaemia virus

307
Q

what are the common ways in which acute leukamias present

A

as the quickly-growing blasts take over the marrow and cause pancytopenia - tiredness, fever, sweats, pallor, sob, infection, bleeding/bruising
dic in some

308
Q

what are the symptoms of acute leukaemias if they infiltrate different organs

A
  • hepatomegaly
  • splenomegaly
  • pulm infiltrates
  • bone pain
  • gum hypertrophy
  • renal failure
  • cns signs
309
Q

what are the supportive treatments for acute leukaemias

A

fluids, abx

allopurinol, rasburicase

310
Q

what are the investigations and their findings in acute leukamia

A
  • fbc: normocytic, normochrmoic anaemia, low platelets, wcc levels vary
  • coag profile + d-dimer + fibrinogen
  • film: blasts found often; AUER RODS in AML
  • BM: hypercellular, packed with blasts
  • flow cytometry
  • cytogenetics/FISH: assess riskiness
311
Q

what is a hallmark of AML on blood film

A

Auer Rods

312
Q

what is the management of acute lymphoblastic leukaemia

A

1) induce remission: vincristine, steroids, L-asparginase used in combination
2) intensification: exposure to new chemo drugs, Intrathecal methotrexate or cns irradiation to tackle leukaemia cells hiding in cns
3) maintenance: cyclical chemo and steroids
+/- intrathecal prophylaxis/cranial irradiation

some may require stem cell transplant, antibody treatment

313
Q

what are the factors that would determine how well a patient will do if they have been diagnosed with AML

A

age, performance status, subtype APL

314
Q

how is treatmetn different if a patient with AML has the subtype APL

A

include another drug: ATRA to the treatment (treated as a separate entity)

315
Q

what is the treatment for AML

A

if older, generally not suitable for intensive treatment - so treated with low dose chemo agents
chemotherapy with 3 drugs to achieve induction, and may trial adding another drug

allogenic stem cell transplant

316
Q

what is the pathology of CML

A

philadelphia chromosome translocation
mutated haematopoetic stem cell produces abnormla clones which invade the BM. these cells then differentiate during the chronic phase to produce lots of different blood cell types

317
Q

what are the changes that occur after Philadelphia Chromosome translocation in CML

A

creates a new fusion genes: BRC-abl1

this codes for abnormal tyrosine kinase which drives proliferation

318
Q

what are the phases of CML

A

chronic phase -> accelerated phase -> blast crisis

319
Q

what is the blood like in CML

A

hyperviscous due to raised wcc, reduced rbcs, platelets usually preserved

320
Q

what are the symptoms of hyperviscosity of blood

A

headache, tinnitus, coma, retinal haemorrhages

321
Q

what investigations would you do in CML and what would they show

A
  • FBC - normocytic, normochromic anaemia
  • wcc - increased (50-400)
  • cytogenetics: t (9;22), BRCA-abl fusion
  • platelets often normal
  • film
  • high B12
  • BM: hypercellular but not as many blasts as acute leukaemias (if blast count is high then it indicates progression)
322
Q

what is the treatment for CML

A

allopurinol
hydroxycobalamine
BRC-abl inhibitors/tyrosine kinase inhibitors: Imatinib, Dasatinib, Nalotinib
(leucophoresis out of favour)

323
Q

what is the main subtype of CLL

A

B-CLL (98%)

324
Q

what is the age group commonly affected by CLL

A

late-middle aged and old age - most common leukaemia

325
Q

what is the pathology of B-CLL

A

accumulation of mature-looking B cells in the peripheral blood, BM and lymphatic tissues
there is lymphocytic clonal expansion as the CLL cells resist apoptopsis and survive, proliferate and accumulate in peripheral tissues

326
Q

what are the immune effects of CLL

A

reduced repetoire of antibodies
altered T cell immunity
autoimmune phenomena e.g. ITP, AIHA

327
Q

how does CLL usually present

A

often chance finding on fbc as it is usually indolent
painless lymphadenopathy, anaemia, infections
fatigue, sob, hepatosplenomegaly, susceptibility to infection
night sweats in advances

328
Q

what is transformation of CLL to high grade lymphoma called

A

Richter’s transformation

329
Q

what are the investigations and findings for CLL

A
  • fbc: normocytic, normochromic anaemia
  • normal or low platelets
  • increased lymphocyte count with smear cells
  • neutropenia
  • BM: infiltrated, nodular
  • immunophenotyping, cytogenetics: FISH for chromosomal changes
330
Q

what is the hallmark of CLL seen on blood film

A

smear cells

331
Q

what is the treatment of CLL

A

only when clinically-indicated such as low platelet or hb count, infections, autoimmune phenomena etc
chemotherapy - combined
antibody treatment
transplant/local LN radiotherapy trials

332
Q

what is survival like for CLL

A

variable - usually many years though it depends on when it was first picked up

333
Q

what infection history increases risk of hodgkins lymphoma

A

EBV

334
Q

what is the usual age of presentation of hodgkins lymhoma

A

20-30

335
Q

what is the hallmark of hodgkins lymphoma on blood film

A

binucleate reed sternberg cells

336
Q

what is special about Hodgkines lymphoma subtype NLPHL

A

b cell lineage - expresses cd20

337
Q

what is the presentation of hodgkins lymphoma

A

painless rubbery lymphadenopathy, generalised lymphadenopathy
B symptoms of fever, night sweats, weight loss

338
Q

what is the diagnostic investigation for hodgkins lymphoma

A

lymph node and involved tissue biopsy
+/- FNA
CT neck/chest/abdo/pelvis

339
Q

what is the pathology of hodgkins lymphoma

A

disease spreads from one lymph node group to another, and to involve other tissues

340
Q

what is the name of the staging for hodgkins lymphoma

A

ann arbor

341
Q

list the ann arbor stages for hodgkins lymphoma

A

1 - single LN/single extralymphatic site
2 - 2 or more LN group on same side of diaphragm/1 LN group with contiguous spread to extralymphatic site
3 - LN regions on both sides of diaphragm affected +/- spleen, or contiguous extralymphatic site
4 - disseminated involvement of one or more extralymphatic organs
- A = no systemic symptoms
- B = systemic symptoms
- E = extranodal
- S = splenic

342
Q

what is the management for hodgkins lymphoma

A

stage 1A/2A = 2-4 courses of chemo, involved field radiotherapy
stage 2B and above = 6-8 cycles of chemo +/- monoclonal Ab therapy

343
Q

what is the most common type of NHL

A

B cell

344
Q

what are the differences between low grade and high grade NHL

A

low grade: indolent, relapse and remit but incurable, with indestructible growth patterns
high grade: aggressive, fatal without treatment, curable in many, destructible growth patterns. cns and extranodal involvement common

345
Q

what are the clinical features of NHL

A

low grade have slow growing nodes, high grade have fast growing nodes
hepatosplenomegaly
extranodal sites e.g. gut, cns, bone
systemic symptoms: weight loss, fever, signs of spread to extranodal sites

346
Q

what are the investigations used to diagnose NHL

A

LN biopsy/biopsy involved extranodal site
immunohistiochemistry, cytogenetics,
CT chest/abdo/pelvis
cxr
blood count and film
tumour burden markers: LDH, B microglobulin

347
Q

what are the tumour burden markers of NHL

A

LDH B microglobulin

348
Q

what is the staging for NHL

A

modified Ann Arbor

349
Q

what is the management for NHL

A

low grade types: if low stage - involved field radiotherapy; if high stages: incurable, relapse and remit
high grade types: intense multiagent chemo

350
Q

what is an important high grade type NHL

A

Burkitt’s lymphoma

351
Q

what is the pathology of myeloma

A

increased proliferation of monoclonal plasma cells -> paraprotein excess
they accumulate and lead to anaemia and BM failure, causing bone resorption and lytic lesions (path #)

352
Q

what is mgus

A

monoclonal gammopathy of undetermined significance
increased paraprotein found in blood, resembles myeloma,
usually no symptoms or problems - few progress to myeloma

353
Q

what autoimmune condition is myeloma assoc with

A

systemic amyloidosis

354
Q

what are the clinical features of myeloma

A

anaemia, bone resorption, bone pain, increased Ca2+, path #

355
Q

what are the investigations and findings in myeloma

A
  • fbc, esr/ plasma viscosity: hyperviscosity
  • xr - lytic lesions, skeletal survey/mri
  • U+E, ca2+, albumin
  • serum/urine paraproteins/light chains, Bence Jones urine protein
  • electrophoresis
  • BM aspirate and trephine
356
Q

what is the management for myeloma

A
  • incurable - relapse and remit
  • analgesia
  • radiotherapy for boens
  • management of increased Ca2+ and renal impairement (dialysis)
  • plasma exchange for correction of hyperviscosity
  • chemo combos, thalidomide trialled
357
Q

what is the pathology of myelofibrosis

A

abnormal cloning of haematopoeitc stem cells in BM causes fibrosis, replacement of BM with scar tissue therefore reducing haematopoeisis

358
Q

what are the signs and symptoms of myelofibrosis

A

bone pain, bruising, anaemia, infections
hepatosplenomegaly
gout

359
Q

which gene mutation is assoc with myelofibrosis

A

JAK2

360
Q

what is the pathology of myelodysplastic syndromes

A

neoplastic disorder of BM which causes dysplastic haemopoeisis and peripheral blood cytopenias due to ineffective production of cell lines.
the BM is hypercellular, with dysplastic morphology

361
Q

what does myelodysplastic syndrome tend to progress to

A

aml

362
Q

what are the clinical features of myelodysplastic syndrome

A

symptomatic anaemia, bleeding, bruising, recurrent infections

363
Q

what is the management of myelodysplastic syndrome

A

blood and platelet transfusion
EPO, GCSF
chemo for aml type
allogenic stem cell transplant

364
Q

what is the management for myelofibrosis

A 
stem cell transplant
folic acid
allopurinol
blood tranfusions
thalidomide, ruloxitinib
365
Q

what is BM failure

A

condition where there is ineffective/no production/reduced release of cells from BM - either of specific lineage or all lineages

366
Q

what are the investigations you would do for BM failure

A 
FBC, reticulocyte count, 
B12, folate
infection screen
LFTs, ue, tfts
BM: aspirate and trephine
367
Q

what are the causes of BM failure

A
  • congenital e.g. fanconi anaemia

- acquired e.g. infections, drugs, immune related, radiation, vitamin deficiency, idioapthic

368
Q

what is the treatment for BM fialure except treating the cause

A 
supportive: manage infections, transfusions, 
haemopoeitic progenitor
antithymocyte globulin
antilymphocyte globulin
ciclosporin
369
Q

what advances care plans are there that must be found and considered before making a decision about the patient’s care

A
  • advance statements
  • advanced decision to refuse treatment
  • appointment of a personal welfare Last Power of Attorney (LPA)
370
Q

what are the medications given for restlessness and confusion at end of life

A

midazolam, haloperidol

371
Q

what are the treatments given for breathlessness at the end of life

A

fan/fresh air to stimulate breathing

glycopyronium, hyoscine hydrobromide

372
Q

what is a syringe driver

A

SC infusion set up for those unable to take PO meds

can give morphine, anitemetics, midazolam, glycopyrronium

373
Q

what are the side effects of morphine

A

drowsiness, constipation, nasuea, resp depression, antitussive, hyptension, tolerance, addiction

374
Q

how regularly are zomorph and oramorph taken in end of life

A 
zomorph = bd
oramorph = prn up to 6 times daily
375
Q

what is the way in which TTOs are written out

A

“Supply x amount (x amount written in words) of x drug x mg (tablets/capsule/total patches etc)”

e.g. Supply 20 (twenty) Zomorph 30mg capsules

(take 30mg Zomorph BD, PO, for 10 days)

Cancer Care (1 decks)

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