Cancer Care Flashcards
(375 cards)
1
Q
what do the letters “SPIKES” stand for in breaking bad news
A
Setting Perception Invitation Knowledge Empathy Summary/Strategy
2
Q
describe the “setting” aspect in the SPIKES model
A
right context, privacy, support
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
4
Q
describe the “invitation” aspect of the SPIKES model
A
find out how much patient wants to know
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
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
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
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
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)
10
Q
what does the AMBER care pathway involve
A
- medical plan
- escalation decision
- discussion with patient/family
- regular review
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
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
13
Q
how is nausea and vomiting treated in dying patients
A
- haloperidol, levomepromazine
14
Q
how is breathlessness treated in dying patients
A
- midazolam, morphine
15
Q
how is restlessness/agitation treated in dying patients
A
- midazolam, haloperidol, levomepromazine
16
Q
how are resp secretions treated in dying patients
A
glycopyronium
17
Q
what are the common causes of N+V in palliative patients
A
gastric stasis, medicines, chemical and metabolic disturbances
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
19
Q
what is the mechanism of action of domperidone
A
dopamine antagonist
20
Q
what is the main action site of domperidone
A
gut only
21
Q
what is the mechanism of action of metoclopramide
A
DA antag, 5HT4 agon
22
Q
what are the main action sites of metoclopramide
A
central and gut - prokinetic
23
Q
what is the mechanism of action of haloperidol
A
DA antag
24
Q
what is the main action site of haloperidol
A
CTZ
25
what is mechanism of action of cyclizine
histamine and ACh antag
26
what are the main sites of action of cyclizine
vestibular system and vomiting centre
27
what is the mechanism of action of granisetron/ondansetron
5ht3 antag
28
what are the main sites of action of granisetron/ondansetron
central gut
29
what is the mechanism of action of levomepromazine
5ht2, da, ach, histamine antagonists
30
what is the main action site of levomepromazine
central - broad spectrum
31
what is the mechanism of action of hyoscine bromide and glycopyronium
ach antag
32
what is the main action site of hyoscine bromide and glycopyronium
vestibular system &VC
33
why should dopamine antagonist antiemetics not be used together
enhanced extrapyramidal side effects
34
list some of the anticholinergic side effects of certain antiemetics
dry mouth, constipation, urinary retention, restlessness
35
in which patients should anticholinergic antiemetics not be prescribed
heart disease or rhythm disturbance
36
which two antiemetic drugs should not be mixed?
cyclizine and metoclopramide
| or metaclopramide with IV ondansetron
37
what are the mechanisms of opioids causing n+v
ctz stimualtion, vestibular sensitivity and reduced gut motility
38
which antiemetics should be used if n+v is caused by impaired gastric empyting
prokinetics - metoclopramide and domperidone
39
what aetiological factor is cml associated with
ionising radiation
40
how do the cells differ between cml and aml
the cells retain their ability to differentiate in cml during the chronic phase of the disease
41
which gene translocation is involved in cml, what is the result
translocation on the philadelphia chromosome (t9;22). results in BRC-ABL gene (new fusion gene)
42
how does the brc-abl gene in cml act
as an abnormal tyrosine kinase
43
what is the blast crisis in cml
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)
44
what are the symptoms of the chronic phase of cml
anaemia, weight loss, splenomegaly. paitents can develop gout.
45
what happens to the viscosity of blood with cml
hyperviscosity - increased wcc
46
what are the investigations that should be done in patients with suspected cml
fbc, blood film, bm, cytogenetics, molecular gneetics, (flow cytometry)
47
what will investigations for cml show in chronic phase
leucocytosis, BM hypercellular, normochromic anaemia
48
what do investigations for cml show in a blast crisis
increased no of blast cells in blood and bm, with anaemia and thrombocytopenia more marked
49
what is the management of cml in chronic phase
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
50
how do tyrosine kinase inhibitors work in cml
bind to the atp-binding site of brc-abl1 and inhibit function of protein
51
what is the treatment for cml in blast phase
imatinib and second gen tyrosine kinase inhibitors, combination chemo
52
what is the pathophysiology of b cell cll
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.
53
what is the clinical presentation of cll
usually indolent
painless lymphadenopahty, anaemia, infection
constitutional symptoms - night sweats, fatigue
54
what are the clinical presentations of advances cll
variable degrees of anaemia, neutropenia and thrombocytopenia
55
which investigations are undertaken in patients with cll
fbc, blood film, bm aspirate and trephine, lymphocyte immunotyping, cytogenetics by fish, abdominal us
56
how is cll managed
```
radiotherapy for lymph nodes
chemo
targeted biological therapy
steroids for autoimmune reactions
stem cell and bm transplant
```
57
list some inherited conditions that have an associated with acute leukaemia
down syndrome, fanconi anaemia, neurofibromatosis, ataxia telangiectasia
58
list some environmental factors associated with acute leukaemia
- chemical carcinogens
- ionising radiation
- chemo drugs
- infectious agents e.g t cell virus
59
what is the pathophysiology of acute leukaemias
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).
60
what are clinical presentations of acute leukaemias
- anaemia
- thrombocytopenic bleeding
- infections (bacterial, fungal mainly)
61
what are the features of extramedullary leukaemic infiltration in acute leukaemia
- hepatosplenomegaly
- lymphadenopathy
- leukaemic meningitis
- testicular infiltration
- skin nodules
62
what is the commonest cancer in children
all
63
what are the steps of treating patients with all
1) induction of remission with chemo and steroids
2) intensification - exposure to new chemo drugs
3) maintenance - chemo drugs
64
how is high risk all managed
intensification of chemo drugs, stem cell transplant
65
which type of aml is important to identify, as it changes management of patient
apl
66
how are lymphomas classified
Hodgkin's and Non-Hodgkin's lymphoma
B cell or T cell
Indolent and aggressive types (NHLs)
67
what are the extranodal presentations of NHL
hepatosplenomegaly, as well as other sites such as the gut, testes, thyroid gland, bone, muscle, cns
68
how is NHL diagnosed
```
LN biopsy, biopsy of extranodal site,
cxr,
ct chest/abdo/pelvis,
blood count and film,
BM aspiration and trephine,
immunophenotyping and cytogenetics
```
69
what are the tumour burden markers in NHL
LDH
| Beta-microglobulin
70
what is immunophenotyping
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
71
how are stage 1 NHL's managed
Involved Field Radiotherapy
72
how are stage 2/3 NHL's managed
these have a relapsing and remmiting presentation and may be managed with stem cell transplant, rituximab, immunochemotherapy
73
what is Burkitt's lymphoma, and how is it managed
a highly aggressive non hodgkins lymphoma of the B cells.
| it is managed with high-intensity multi agent chemotherapy
74
which particular viral infection is it important to ask about in the history of a patient with lymphoma - associated with
EBV - infectious mononucleosis
75
what is the hallmark pathological feature of Hodgkin's lymphoma under a microscope
Reed Sternberg Cells
76
how may Hodgkins lymphoma present
- painless rubbery lymphadenopathy
- may be generalised lymphadenopathy
- later spread to liver, lungs, marrow may cause local symptoms
- B symptoms
77
list some of the B symptoms in Hodgkins lymphoma
fever, night sweats, weight loss
78
how is Hodgkin's lymphoma diagnosed
lymph node and involved tissue biospy
fine needle aspirate (should not be used alone for diagnosis)
staging with CT neck, chest, abdo, pelvis
79
how is early stage Hodgkins lymphoma treated (Stages 1a and 2a)
involved field radiotherapy
80
how are stages 2b-4 hodgkins lymphoma managed
combination chemotherapy, stem cell transplant may be offered
81
what is the salvage therapy given for Hodgkin's lymphoma
salvage chemo, monoclonal Ab therapy (not rituximab)
82
what is the main difference between lymphoma and leukaemia
leukaemia is mainly in BM and blood, while lymphoma tends to be in LN and other tissues
83
which cells proliferate in myeloma
plasma cells
84
how does myeloma affect the bone
accumulation of proliferating cells in the BM leads to anaemia and BM failure - and lytic lesions, generalised osteoporosis and pathological fractures
85
what is MGUS
monoclonal gammopathy of unkown cause - increase paraprotein found in blood, similar to myeloma
86
why is paraprotein increased in myeloma
due to excess proliferation of plasma cells
87
what investigations should be done for a patient with myeloma
- 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
88
what is the course of progression of myeloma
incurable - runs relapsing and remitting course
89
how is myeloma treated
```
analgesia
radiotherapy to areas of bone pain
management of hypercalcaemia
plasma exchange for hyperviscosity
chemo combo therapy
```
90
what are myelodysplastic syndromes
group of neoplastic conditions where there is dysplastic haemopoesis and peripheral cytopenias.
91
what type of leukaemia do myelodysplastic syndromes have a tendency to progress to
aml
92
what does bm/peripheral blood look like in patients with myelodysplastic syndromes
hypercellular bm with dysplastic morphology and paradoxic peripheral blood cytopenia
93
what are the clinical features of myelodysplastic syndromes
anaemia
thrombocytopenia
recurrent infections
bm failure
94
what may cause death in myelodysplastic syndromes
bm failure, progression to aml
95
what investigations can be done in patients iwth myelodysplastic syndrome
- fbc
- blood film
- bm aspiration/trephine
- cytogenetics
96
what is the management of myelodysplastic syndromes
- blood and platelet infusion
- epo
- gcsf
- chemo
- stem cell transplant
- hypomethylating agents
97
what is myelofibrosis
myeloproliferative neoplasm in which abnormal cloning of haematopoeitic stem cells in the bm cause fibrosis (replacement of bone marrow with scar tissue)
98
what are the signs and symptoms of myelofibrosis
```
splenomegaly, hepatomegaly
bone pain
bruising
cachexia
gout
susceptibility to infection
anaemia
```
99
what mutation is associated with myelofibrosis
jak2
100
what is the treatment for myelofibrosis
- stem cell transplant
- folic acid
- allopurinol
- blood transfusions
- chemo
- ruxolitinib
101
what are the three urological emergencies
1) loin pain
2) urinary retention
3) testicular pain
102
list some of the urological causes of loin plain
- ureteric/renal colic
| - pyelonephritis/uti
103
list some non-urological causes of loin pain
- msk
- gynaecological
- general surgical
- vasc - dissecting iliac aneurysm
104
what are the causes of ureteric colic
- stone
- clot
- puj obstruction
105
where would ureteric colic pain radiate to
penis/testis/labia
106
which stones require intervention
- large
- renal impairment
- intractable pain
- solitary kidney
- infection
- failed conservative management
107
what is a red flag symptom in loin pain on examination
septic signs and symptoms - esp temperature/tachy/hypotensive
108
how is ureteric colic investigated
- fbc/u+e/ca2+/urate/clotting if septic
- cultures
- urine dip +/- MSSU for MC+S
- CT - KUB
109
how is ureteric colic treated
- analgesia
- antiemetic
- iv fluids
- a blocker as explusive therapy for stones
- lasertripsy/lithotripsy
- jj stent
110
how is pyonephritis managed
- call for senior help
- iv access, fluids, O2, IV abx
- blood/urine cultures sent
- abg lactate, base excess
- itu involvement
- needs drainage
111
what antibiotics are given to patients with pyonephritis
gentamicin + tazocin/ coamoxiclav
112
how are patients discharged after pyonephritis
with drain in situ, and readmit
113
what is found in the history of patients with pyelonephritis
chills, fever > 38, loin pain
114
what is the main organism involved in pyelonephritis
e coli
115
what are the less common organisms involved in pyelonephritis
proteus, pseudomonas, klebsiella, enterobacter, serratia, citriobacter
116
what will you find on examination of a patient with pyelonephritis
pyrexia
tachy
tender flank/suprapubic region
117
what would urine dip show in pyelonephritis
blood, wbcs, nitrites
118
what investigations are performed in patients with pyelonephritis
- fbc/u+e
- msu, MC+S
- blood cultures may be done
- renal uss (exclude pyonephritis)
119
what is the management of pyelonephritis
- PO/IV fluids
- PO/IV Abx
- analgesia/antiemetic
- DVT prophylaxis
- urological input if male/complicated/not settling with treatment
120
list the causes of urinary retention
- prostate enlargement
- uti
- constipation
- overdistention e.g. excess iv fluids
- urethral stricture/phimosis
- surgery/anaesthetic effects
- drugs e.g. anticholinergics
121
what are the features of acute urinary retention
- painful
- relieved by drainage
- no upper tract insult
122
what do you assume if elderly man with nocturnal eneuresis presents
chronic retention with overflow incontinence until otherwise proven
123
what are the "storage" symptoms of urinary retention
- frequency
- urgency
- nocturia
- urge incontinence
124
what are the "voiding" symptoms of urinary retention
- hesitancy
- intermittency
- straining
- spraying
- poor flow
- post-mict dribbling
125
what is the management for urinary retention
1) catheter - urethral or suprapubic
2) record residual volume
3) reexamine to make sure mass has disappeared
126
what causes high pressure chronic urinary retention
long term obstruction
127
what causes low pressure chronic urinary retention
failure of detrusor muscle - stroke/ms etc
128
what investigations are performed in patients with chronic retention
- urine dip/MC+S
- Catheter sample
- u+e
- psa
129
how is acute urinary retention managed
- treat cause
- cath
- a blocker e.g. tamsulosin
- 5a reductase inhibitor (BPH)
- TWOC
- turp if fails
130
how is chronic urinary retention treated
- long term indwelling cath
- clean intermittent self cath
- turp if fit
131
list some causes for acute urinary retention
- bph/ca
- paraphimosis
- phimosis
- prolapse
- balantitis, prostatitis, cystitis
132
list some causes of chronic urinary retention
- bph/ca
- drugs
- iatrogenic
- congenital deformities
- trauma, infection
133
list some causes of testicular pain
- torsion!!
- epididymitis/orchitis/epididymoorchitis
- torsion of hytatid of Morgani
- tumour
- trauma
- calculi rarely
134
how do you manage testicular pain
review with senior
| urgent surgical exploration +/- orchidectomy/orchidopexy
135
what age group tends to be affected by testicular torsion
under 20
136
what may be found on examination of a patient with testicular pain
```
pyrexia
tachy
normotensive
difficult/painful movement
erythematous scrotum
exquisistely tender testes
```
137
what is usually the cause of epididymoorchitis in 20-30 yo
sti
138
what is usually the cause of epididymoorchitis in older patients
uti
139
what questions must you ask in a history of a patient with suspected epididymoorchitis
unprotected sex?
uti recently?
urethral instrumentation/cath recently?
MUMPS hx
140
what may be found on examination of a patient with epididymoorchitis
- pyrexial
- tachy
- ?septic
- scrotum erythematous
- enlarged, tender testis
- fluctuant areas if abscess
- reactive hydrocoele may be present
141
what is fournier's gangrene
gangrenous area of scrotal skin in infections etc - is an emergency!!
142
what are the investigations for epididymoorchitis
- FBC/U&E/cultures
- MSU, MC+S
- scrotal USS if ?abscess isnt settling
143
what is the management for epididymoorchitis
```
abx via local guidelines (cipro/doxy often used)
analgesia
recue non essential activity
sti clinic
uti further investigations
```
144
what are the symptoms that are "voiding" luts
- dysuria
- poor stream
- hesitancy
- terminal dribbling
- incomplete voiding
145
list the zones of the prostate
- central
- peripheral
- transitional
146
which gene is associated with prostate cancer
brca2 (ask about female relatives with breast cancer)
147
what is the significance of prostate intrapeithelial neoplasia
recognised precursor to prostate cancer
148
what is the gleason score out of
2-10
149
how is the gleason score calculated
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
150
what gleason score is poor prognosis
usually above 8
151
how does prostate cancer metastasise to bone
through the vertebral plexus of veins
152
what are the symptoms of prostate cancer
often asymptomatic
- frequency
- hesitancy
- terminal dribble
- poor stream
- nocturia
- haematospermia
- erectile dysfunction
- systemic symptoms e.g. malaise, weight loss
153
what are some of the signs and symptoms of prostate cancer metastasis
- bone/back pain
- path fractures
- hypercalcaemia
154
what may be felt on pr examination of a patient with prostate ca
hard craggy nodule or diffusely infiltrating abnormality
| typically loss of midline sulcus of prostate gland
155
what is the problem with the use of psa as a tumour marker
sensitive but relatively non-specific for prostate ca therefore poor screening test
156
list the investigations that should be performed in a suspected prostate cancer
- PSA
- Routine bloods - esp excluding hyperCa2+ and uraemia
- IV urography
- CT scan
- TRUS (most sensitive)
- Biopsy/resection
- MRI (local tissue)
- Isotope bone scan
157
what are the T-stages of prostate cancer
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
what is active surveillance in prostate cancer
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
how do LHRH agonists work in prostate cancer
block release of testosterone (after initial surge); given with antiandrogens initially
160
how do LHRH antagonists work in prostate cancer
block testosterone release (testosterone promotes prostate cancer)
161
list the hormone-related therapies for prostate cancer
- bilateral orchidectomy
- antiandrogen drugs
- GnRH analogue/antag
162
what is the difference between LHRH agonists/antagonists and antiandrogens
antiandrogens work peripherally
163
what are the surgical options for prostate cancer treatment
- TURP
- Radical prostatectomy (removal of entire prostate, adjacent bladder neck, seminal vesicles, vas deferens, surroudnign fascia)
164
what should happen to the PSA levels following radical prostatectomy?
undetectbale - if they are there, even at a low level - it indicates that there is some residual prostatic tissue present (i.e. mets)
165
what is brachytherapy in prostate cancer
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
what is the palliative management for prostate cancer
GnRH analogue/oral antiandrogen
| chemo/pred for relapses
167
what are the side effects of antiandrogens
hot flushes, loss of libido, gynaecomastia, impotence
168
what is tumour lysis syndrome
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
what are the ways in which tumour lysis syndrome can present
usually 3-7 days post chemo
- oliguric/anuric renal failure
- cardiac arrhythmias/arrest
- primary presentation of malignancy; lab blood abnormalities
170
what are the patient-specific risk factors for tumour lysis syndrome
- preexisting renal dysfunction/disease
- hypovolaemia e.g. diuretic use pretreatment
- pretreatment LDH high
- urinary tract obstruction from tumour
171
what are the tumour-specific risk factors for tumour lysis syndrome
- high grade lymphomas, burkitt's lymphoma
- rapidly dividing cancers
- all
- myeloma
- germ cell tumours
- sclc
- breast (inflammatory)
172
how can tumour lysis syndrome be prevented
prehydration and vigorous hydration throughout treatment
| monitoring of electrolytes and treat promptly if disturbances
173
how is tumour lysis syndrome managed
- 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
what are the symptoms of SVCO
- swelling of face/neck/arm(s)
- distended neck and chest wall veins (non collapsible)
- sob
- headache (intracranial venous congestion)
- drowsiness
175
what are the investigations you would do for SVCO
- cxr - mediastinal mass
- ct scan
- needle biopsy
- peripheral LN sampling
176
what is the management for SVCO
- consider anticoag and steroids
- stent insertion
- radiotherapy/chemo for treatment of underlying cause of obstruction
177
what are the causes of hypercalcaemia in cancer
- osteolytic lesions
- PTHrP tumour production
- calcitriol tumour production
178
which cancer types are especially assoc with hypercalcaemia
lung, breast, myeloma, lymphoma
179
what are the symptoms of hypercalcaemia
- nausea, dehydration, anorexia
- polydipsia, polyuria
- confusion, poor conc, drowsiness
- constipation
- bone pain
180
what are the investigations to do in hypercalcaemia
```
calcium (2.1-2.6), corrected for albumin
pth/pthrp
u+e
phosphate
(+/- myeloma screen)
```
181
what is the treatment for hypercalcaemia in malignancy
- correct dehyd: IV saline +/- diuretics to promote calcium loss (loop - not thiazide!)
- IV bisphosphanates
- others: calcitonin, corticosteroids, systemic management of malignancy
182
which tumour types are commonly assoc with metastatic SC compression
bronchus, breast, prostate, kidney, haem (multiple myeloma, NHL)
183
which anatomical part of a vertebra are mets most likely to go to
vertebral body
184
what are the clinical symptoms of a cancer patient with SC compression
- back pain
- radicular pain
- weakness
- sensory deficit
- autonomic dysfunction
- proprioception, light touch, pin prick sensation disturbance
unilat or bilat
185
what investigations should be done for a cancer patient with SC compression
MRI
whole body imaging
CT/PET
186
what is the treatment for SC compression in cancer patients
- 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
what is neutropenic sepsis
cancer patients with low wcc (<1 x 10^9) and who have either temperature > 38 deg or other s+s of sepsis
188
who is particularly at risk of neutropenic sepsis in cancer
- 5-10 days post chemo
- extensive field radiotherapy
- haematological malignancies with neutropenia e.g. leukaemia
- certain drugs
189
what is the management of neutropenic sepsis in cancer
a - e
empirical abx (tazocin/meropenem)
fluid resus, consider cath, involve seniors
GCSF in profoundly neutropenic
190
how can future neutropenic sepsis episodes be avoided
consider changing chemo cycles to reduce dose
give GCSF prophylactically
educate patients to look for signs
191
what is GCSF
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
what is the epidemiology of breast cancer
affects 1 in 8 women
| commonest cause of cancer death in women
193
what are the risk factors for developing breast cancer
- high bmi
- high fat intake
- high alcohol intake
- lack of exercise
- BRCA genes
- hrt/cocp
- oestrogen exposure, especially unapposed
194
list some of the ddx for breast cancer
- galactocoele
- haematoma
- fibradenoma
- duct papilloma
- breast abcess, cyst
- fat necrosis
195
what is male breast cancer assoc with
strong fhx, inherited BRCA genes
196
how may breast cancer present
- 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
list the commonest sites to with breast ca spreads
- bone
- lungs
- liver
- skin
198
how are breast cancers classified, and what are the different types
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
what is the role of atypical ductal hyperplasia
confers increased risk of developing breast cancer
200
describe paget's disease of the breast
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
what is paget's disease like under a microscope
paget cells in the epidermis
202
how does inflammatory carcinoma present
ill-defined erythema, tenderness, induration and oedema of the breast. aggressive
203
are bilateral breast cancers common
no - assoc with strong fhx of breast ca
| lesions tend to be solitary and not multifocal in breast ca also
204
what are "basal cancers" in breast cancer
triple negative - oestrogen receptor negative, progesterone receptor negative, her-2 negative
205
what is the triple assessment for breast cancer
examination, mammography (x rays) and sonography
206
what are the different investigations done for breast cancer once the triple examination is done
```
mri
nipple cd cytology
fine needle aspiration biopsy
needle biopsy
excision biopsy
```
207
what would be seen on mammography which would suggest malignancy
irregular mass with calcification
208
what does breast uss tell us about a mass
can assess whether cystic or solid, and can also assist in retrieving biopsy
209
what is fine needle aspiration cytology
looking at a sample of cells from breast mass under microscope
210
what is needle/core biopsy of breast
under LA, a core of tissue is taken for histological examination (in situ, invasive types determined), determine hormone receptor status
211
what is the contribution of excision biopsy in breast cancer
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
what cancers does presence of BRCA 1/2 genes increase the risk of
breast, ovarian, fallopian tube
213
what are the side effects of antioestrogen drugs like tamoxifen, faslodex
hot flushes, fluid retention, vaginal dryness/dc, uterine bleeding, vte
214
what are the side effects of aromatase inhibitor drugs like anastrozole, letrozole
hot flushes, fluid retention, vaginal dryness/dc, uterine bleeding, vte
increased cholesterol, osteoporosis, joint pains
215
what are the side effects of medroxyprogesterone/megestrol drugs used to treat breast ca
nausea, fluid retention, weight gain
216
what are the protective risk factors for breast ca
- oopherectomy <35 yo
- increasing parity
- young age at 1st pregnancy
- breastfeeding
- regular exercise
217
how does tamoxifen work
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
how does herceptin work
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
how do aromatase inhibitors work for breast cancer
block the enzyme aromatase peripherally, to prevent peripheral activation of oestriol/oestrone to oestrodiol
220
what tests cay be done to look for metastatic disease in breast ca
ct breast/thorax/abdo/pelvis
isotope bone scan
serum ca125
serum calcium (bone mets)
221
what are the different stages of breast ca
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
what is the role of radiotherapy in breast cancer
indicated in all patients having breast-conserving surgery
treatment of choice for mets/bone involvement
brachytherpay is an option
223
what is the role of chemotherapy/hormonal therapy in breast cancer
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
what are the different srugical procedures for breast cancer
- wide total excision for localised smaller tumours
- simple mastectomy
- modified radical mastectomy
- radical mastectomy
225
what is the difference between modified radical mastectomy and radical mastectomy
modified radical: breast + ln's removed and pec major spared
| radical: breast + ln's + pectoralis muscles removed
226
what are the different axillary procedures that can be done in breast cancer
- sentinel ln mapping + biospy
- axillary sampling
- axillary disection/clearance
227
what is sentinel ln mapping
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
what are the risk factors for local recurrence of breast cancer
- t3/4 tumours
- poorly differentiated
- lymphovascular invasion
- involved axillary ln's
- incomplete excision
229
list some of the complications of breast mets
- fungating tumours: infections, dc, bleeding
- brachial plexopathy and lymphoedema
- sc compression, path fractures
- pleural effusions, lymphangitis
- svco, oesophageal compression, laryngeal nerve palsy
- DIC
230
what are some of the complications related to radiotherapy treatment of breast ca
erythema, swelling, skin irritation, tenderness, temporary skin breakdown
lymphoedema if axillary radiation
231
what is the current screening programme for breast cancer in the UK
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
what happens to those with strong fhx of breast cancer in terms of management
screening starts earlier
genetic counselling referral, risk assessemnt and counselling
some may choose to have double mastectomy
233
how may breast ca be prevented
maintain normal bmi, exercise, moderate alcohol drinking, stop smoking
234
what are the different stages of cell division
```
G0 - rest phase
G1 - cell growth
S - cell duplicates DNA
G2 - cell grows more
M - mitosis (prophase, prometaphase, metaphase, anaphase, telophase and cytokinesis)
```
235
what does growth fraction of cells mean
represents the percentage of cells actively progressing through the cell cycle
236
list some of the mechanisms by which cancer cells become resistant
- decreased cell uptake
- increased efflux
- increased dna repair
- altered drug target
- increased catabolism
- increased drug detoxification
237
what are the porperties of cancer cells
- self sufficient growth signals
- insensitive to antigrowth signals
- evade apoptosis
- sustained angiogenesis
- limitless replicative potential
- tissue invasion and mets
238
what factors of the person need to be taken into account before prescribing chemotherapy
- body weight, surface area
- liver function
- kidney function (narrow therapeutic window)
239
list some LUTS
- frequency, urgency, hesitancy
- dysuria, haematuria, reduced flow, dribbling
- nocturia, incontinence
- pelvic pain
240
list the questions you would ask about in the history of a patient with loin pain
- speed of onset
- colicky/sharp
- severity
- unilat/bilat
- relieving/precipitating
- previous episodes
- assoc systemic/LUTS
241
what may be found on examination of a patient with epididymoorchitis
```
may be pyrexial or even septic
scrotum erythematous
testes/epididymis enlarged, tender
fluctuant areas if abscess
reactive hydrocoele
```
242
what is the management for epididymoorchitis
local abx (ciprofloxacin/doxycycline)
analgesia
reduce non essential activity
sti/gum clinic referral
243
which factors increase risk of prostate cancer
increases with age
first degree relative affected
breast cancer in the family - BRCA2 carriers
afrocaribbean
244
which zone of the prostate is most commonly affected by prostate cancer
peripheral zone
245
what is the histological type of prostate cancer
adenocarcinoma
246
describe gleason score
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
what gleason score has a bad prognosis
8 or above especially, but the higher the score the worse the prognosis generally
248
what is the natural history of prostate cancer
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
what are the symptoms of prostate cancer
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
what are the signs of prostate cancer
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
what are the investigations you would do in a patient with prostate cancer
- PSA (sensitive but non-specific)
- routine bloods
- DRE
- CT/MRI
- IV urography
- TRUS + needle biopsy
- TURP + biopsy
252
why would you do an isotope bone scan on someone with prostate cancer
look for bone mets - shows up as increased areas of uptake
253
what stages are there of prostate cancer
- stage 1/2 = confiend to prostate
- stage 3 = extended through capsule of gland
- stage 4 = invasion of rectum/other structures
254
describe the different hormone therapy options for prostate cancer
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
what is flutamide
antiandrogen
256
what is the palliative management of prostate cancer
hormone therapy to achieve response eg GnRH analogue/antiandrogen
chemo
prednisolone
257
what are the treatment options for prostate cancer
- hormone therapy
- radical radiotherapy, brachytherapy
- radical prostatectomy
- post op radiotherapy in some
- active surveillance, watchful waiting
258
what is the difference between watchful waiting and active surveillance for prostate cancer
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
what is brachytherapy
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
what is usuallu irradiated in prostate cancer
prostate, seminal vesicles, local lymph nodes
261
what stage of cancer is radical prostatectomy suitable for
t1/2
262
what is the procedure in radical prostatectomy
removal of the entire prostate gland, both seminal vesicles, adjacent bladder neck, vas deference and surrounding fascia
263
what are some of the complications of a radical prostatectomy
impotence, occassional urinary incontinence if nerve supply affected
264
describe what the PSA levels should be like after a radical prostatectomy
undetectable - anything above would indicte mets or residual prostatic tissue and is an indication for post op radiotherapy
265
who is active surveillance most suitable for
small tumour, indolent, confined to prostate
| gleason score <7
266
what regular tests are done in active surveillance of prostate cancer
3-monthly PSA, repeat biopsies every 2 years
| if PSA rises above threshold/velocity increases -> introduce treatment
267
what are some of the complications of prostate cancer
obstructive hydronephrosis, urianry obstruction/chronic retention
increased ca and scc in bony mets
268
is bladder cancer more common in males or females
males
269
what are the risk factors for bladder cancer
- smoking
- occupational exposure e.g. rubber and plastics manufacture, crude oil handling, painters, hair dressers
- chronic irritation
- schistosomiasis
270
what is the presentation of bladder cancer
dipstick (painless) haematuria (microscopic usually),
| frequency, dysuria, urgency may also be present
271
what is the treatment of bladder cancer
- Transurethral Resection of Bladder Tumour
- intravesical chemo/immunotherapy in low grade
- higher risk cancers = neoadjuvant chemo, cystectomy + ileal conduit, reconstruction
272
what is the palliative treatment for bladder cancer
chemo/radiotherapy
273
what are the investigations for bladder cancer
```
IV urography (filling defect), urine cytology, CT/MRI
CXR / isotope scan for mets
```
274
list some urological causes for haematuria
cancer (renal cell cancer, transitional cell cancer)
advanced prostate cancer (also bph)
infections
275
list some nephrological causes for haematuria
glomerulonephirites
renal calculi
infections
276
list the investigations you would do in a patient with haematuria
```
- egfr, albumin:creatinine ratio
uss
urine cytology, MC+S
flexi cystoscopy
CT chest/abdo/pelvis in ?mets
```
277
which populations is penile cancer rare in
those who practice circumcision
278
what are the pathological features of penile cancer
papilloferous or solid growth on shaft or glans which can also develop insidiously below the foreskin. May ulcerate
Squamous cell cancer
279
what are some of the differentials for penile cancer
lymphogranulomata venereum, condylomata acunimata, chancroid, traumatic ulceration, leukoplakia, bowen's disease
280
what are the investigations you would in the diagnosis of penile cancer
biopsy/cytological scrapings
FNA of enlarged nodes
CT for inguinal node involvement
281
what are the signs and symptoms of penile cancer
usually asymptomatic, but lesion often obvious
can have dc or odour
+/- enlarged local LN's
may interfere with micturition or potency
282
what is the treatment for penile cancer
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
what are the risk factors for testicular cancer
undescended testes!
| previous orchiitis, first deg relative, genetic causes may all be possible associations
284
what is the pathology of testicular cancer
2 main types: seminoma (germ cell) or teratoma
| seminomas tend to be solid lesions, teratomas tend to be haemorrhagic and cystic
285
what is the natural history of testicular cancer
invade locally into tunica vaginlis and along spermatic cord
LN spread - paraortic nodes
blood spread commonly to lungs and liver
286
what are the signs and symptoms of testicular cancer
- 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
what are the tests done in the diagnostic work up for testicular cancer
```
fbc, liver, renal function
AFP, bHCG, LDH
Alk phos (seminoma)
USS for nodes
CT pelvis/abdo
```
288
what are the differentials for testicular cancer
benign hydrocoele
testicular torsion
lymphadenopathy from other cause e.g. infection
289
what is the marker for pancreatic cancer
CA19-9
290
what is the treatment for testicular cancer
stage 1: inguinal orchidectomy, radiotherapy to paraortic nodes, surveillance
stage 2/3/4: proceed to chemo, radiotherapy of paraortic/pelvic nodes
lymphadenectomy
291
list some of the rarer pathological types of testicular tumours
yolk sac, sertoli cell, intestinal cells
292
what is the screening for testicular cancer
none - self examination and patient education
293
list some of the treatment-related complications for testicular cancer
chemo: alopecia, peripheral neuropathy (cisplatin), skin changes (bleomycin), impaired fertility
radiotherapy: peptic ulcers
294
what is the aetiology of renal cell cancers
```
smoking
cadmium exposure
HLA types
von Hippel Landau disease
Horseshoe kidney
adult PKD
```
295
what is the most common pathological type of renal cancer
adenocarcinoma - clear cell characteristic
| varying degrees of differentiation
296
what is te natural history of renal cell tumours
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
what are the signs and symptoms of renal cell tumours
- 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
what are the ddx of renal cell carcinoma
```
benign renal adenoma
tumour of renal pelvis
renal calculi
bladder tumour
hydronephrosis
```
299
what are the investigations for renal cell carcinoma
bloods - fbc, polycythaemia
cxr showing cannon ball mets
us/ct to image tumour and look at renal vein/ivc
ct abdo/thorax
300
why may there be polycythemia assoc with renal cell carcinoma
tumour production of Epo-like substance
301
which part of the kidney does renal cell carcinoma arise from
proximal convoluted tubule
302
is renal function usually impaired with renal cell carcinoma
usually no, unless other kidney is affected by disease
303
what is von hippel lindau syndrome
genetic condition which confers predisposition to variety of cancers including renal cell carcinoma, phaeochromocytoma, islet tumours, pancreatic cysts
304
what is fanconi anaemia
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
which congenital abnormalities carry risk for acute leukaemia
down syndrome
neurofibromatosis
fanconi anaemia
ataxia telangectasia
306
list some environmental risk factors for acute leukamia
chemical carcinogens e.g. benzene, ionising radiation, chemo/radiotherapy,
infectious agents e.g. ebv, t cell laukaemia virus
307
what are the common ways in which acute leukamias present
as the quickly-growing blasts take over the marrow and cause pancytopenia - tiredness, fever, sweats, pallor, sob, infection, bleeding/bruising
dic in some
308
what are the symptoms of acute leukaemias if they infiltrate different organs
- hepatomegaly
- splenomegaly
- pulm infiltrates
- bone pain
- gum hypertrophy
- renal failure
- cns signs
309
what are the supportive treatments for acute leukaemias
fluids, abx
| allopurinol, rasburicase
310
what are the investigations and their findings in acute leukamia
- 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
what is a hallmark of AML on blood film
Auer Rods
312
what is the management of acute lymphoblastic leukaemia
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
what are the factors that would determine how well a patient will do if they have been diagnosed with AML
age, performance status, subtype APL
314
how is treatmetn different if a patient with AML has the subtype APL
include another drug: ATRA to the treatment (treated as a separate entity)
315
what is the treatment for AML
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
what is the pathology of CML
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
what are the changes that occur after Philadelphia Chromosome translocation in CML
creates a new fusion genes: BRC-abl1
| this codes for abnormal tyrosine kinase which drives proliferation
318
what are the phases of CML
chronic phase -> accelerated phase -> blast crisis
319
what is the blood like in CML
hyperviscous due to raised wcc, reduced rbcs, platelets usually preserved
320
what are the symptoms of hyperviscosity of blood
headache, tinnitus, coma, retinal haemorrhages
321
what investigations would you do in CML and what would they show
- 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
what is the treatment for CML
allopurinol
hydroxycobalamine
BRC-abl inhibitors/tyrosine kinase inhibitors: Imatinib, Dasatinib, Nalotinib
(leucophoresis out of favour)
323
what is the main subtype of CLL
B-CLL (98%)
324
what is the age group commonly affected by CLL
late-middle aged and old age - most common leukaemia
325
what is the pathology of B-CLL
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
what are the immune effects of CLL
reduced repetoire of antibodies
altered T cell immunity
autoimmune phenomena e.g. ITP, AIHA
327
how does CLL usually present
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
what is transformation of CLL to high grade lymphoma called
Richter's transformation
329
what are the investigations and findings for CLL
- 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
what is the hallmark of CLL seen on blood film
smear cells
331
what is the treatment of CLL
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
what is survival like for CLL
variable - usually many years though it depends on when it was first picked up
333
what infection history increases risk of hodgkins lymphoma
EBV
334
what is the usual age of presentation of hodgkins lymhoma
20-30
335
what is the hallmark of hodgkins lymphoma on blood film
binucleate reed sternberg cells
336
what is special about Hodgkines lymphoma subtype NLPHL
b cell lineage - expresses cd20
337
what is the presentation of hodgkins lymphoma
painless rubbery lymphadenopathy, generalised lymphadenopathy
B symptoms of fever, night sweats, weight loss
338
what is the diagnostic investigation for hodgkins lymphoma
lymph node and involved tissue biopsy
+/- FNA
CT neck/chest/abdo/pelvis
339
what is the pathology of hodgkins lymphoma
disease spreads from one lymph node group to another, and to involve other tissues
340
what is the name of the staging for hodgkins lymphoma
ann arbor
341
list the ann arbor stages for hodgkins lymphoma
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
what is the management for hodgkins lymphoma
stage 1A/2A = 2-4 courses of chemo, involved field radiotherapy
stage 2B and above = 6-8 cycles of chemo +/- monoclonal Ab therapy
343
what is the most common type of NHL
B cell
344
what are the differences between low grade and high grade NHL
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
what are the clinical features of NHL
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
what are the investigations used to diagnose NHL
LN biopsy/biopsy involved extranodal site
immunohistiochemistry, cytogenetics,
CT chest/abdo/pelvis
cxr
blood count and film
tumour burden markers: LDH, B microglobulin
347
what are the tumour burden markers of NHL
LDH B microglobulin
348
what is the staging for NHL
modified Ann Arbor
349
what is the management for NHL
low grade types: if low stage - involved field radiotherapy; if high stages: incurable, relapse and remit
high grade types: intense multiagent chemo
350
what is an important high grade type NHL
Burkitt's lymphoma
351
what is the pathology of myeloma
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
what is mgus
monoclonal gammopathy of undetermined significance
increased paraprotein found in blood, resembles myeloma,
usually no symptoms or problems - few progress to myeloma
353
what autoimmune condition is myeloma assoc with
systemic amyloidosis
354
what are the clinical features of myeloma
anaemia, bone resorption, bone pain, increased Ca2+, path #
355
what are the investigations and findings in myeloma
- 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
what is the management for myeloma
- 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
what is the pathology of myelofibrosis
abnormal cloning of haematopoeitc stem cells in BM causes fibrosis, replacement of BM with scar tissue therefore reducing haematopoeisis
358
what are the signs and symptoms of myelofibrosis
bone pain, bruising, anaemia, infections
hepatosplenomegaly
gout
359
which gene mutation is assoc with myelofibrosis
JAK2
360
what is the pathology of myelodysplastic syndromes
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
what does myelodysplastic syndrome tend to progress to
aml
362
what are the clinical features of myelodysplastic syndrome
symptomatic anaemia, bleeding, bruising, recurrent infections
363
what is the management of myelodysplastic syndrome
blood and platelet transfusion
EPO, GCSF
chemo for aml type
allogenic stem cell transplant
364
what is the management for myelofibrosis
```
stem cell transplant
folic acid
allopurinol
blood tranfusions
thalidomide, ruloxitinib
```
365
what is BM failure
condition where there is ineffective/no production/reduced release of cells from BM - either of specific lineage or all lineages
366
what are the investigations you would do for BM failure
```
FBC, reticulocyte count,
B12, folate
infection screen
LFTs, ue, tfts
BM: aspirate and trephine
```
367
what are the causes of BM failure
- congenital e.g. fanconi anaemia
| - acquired e.g. infections, drugs, immune related, radiation, vitamin deficiency, idioapthic
368
what is the treatment for BM fialure except treating the cause
```
supportive: manage infections, transfusions,
haemopoeitic progenitor
antithymocyte globulin
antilymphocyte globulin
ciclosporin
```
369
what advances care plans are there that must be found and considered before making a decision about the patient's care
- advance statements
- advanced decision to refuse treatment
- appointment of a personal welfare Last Power of Attorney (LPA)
370
what are the medications given for restlessness and confusion at end of life
midazolam, haloperidol
371
what are the treatments given for breathlessness at the end of life
fan/fresh air to stimulate breathing
| glycopyronium, hyoscine hydrobromide
372
what is a syringe driver
SC infusion set up for those unable to take PO meds
| can give morphine, anitemetics, midazolam, glycopyrronium
373
what are the side effects of morphine
drowsiness, constipation, nasuea, resp depression, antitussive, hyptension, tolerance, addiction
374
how regularly are zomorph and oramorph taken in end of life
```
zomorph = bd
oramorph = prn up to 6 times daily
```
375
what is the way in which TTOs are written out
"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)
