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Year 3 > Block 34 Week 7 > Flashcards

Block 34 Week 7 Flashcards

1
Q

Neutropenic sepis?

A
  • occurs 7-14 days after chemotherapy
  • antibiotics must be started immediately, do not wait for the WBC
  • start piperacillin with tazobactam (Tazocin)immediately
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2
Q

Ix for NS?

A

Bedside

  • blood sugar
  • pregnancy test

Bloods

  • VBG / ABG
  • FBC
  • CRP
  • U&Es
  • LFTs
  • Bone profile
  • Clotting
  • Fungal assays(e.g. beta-d-glucan galactomannan)
  • Blood borne virus screen
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3
Q

Cultures for NS?

A
  • blood cultures
  • sputum
  • urine
  • C diff toxin
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4
Q

imaging for nS?

A
  • Chest X-ray
  • Lumbar puncture(meningitis, encephalitis)
  • ECHO(infective endocarditis)
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5
Q

What is purpura?

A
  • describes bleeding into the skin from small blood vessels that produces a non-blanching rash
  • caused by bone marrow failure, certain drugs like antiepileptics, antithrombins, nutritional def like B12, C and folate
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6
Q

Ix for purpura?

A
  • FBC - platelet count and evaluate for thrombocytopenia
  • peripheral blood smear
  • PT, aPTT, fibrinogen levels
  • platelet function assays
  • urinalaysis - haematuria, proteinuria
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7
Q

Myelosuppresion Ix?

A
  • FBC
  • peripheral blood smear
  • bone marrow biopsy/ aspiration
  • iron studies
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8
Q

Outline the long-term effects of cytotoxic chemotherapy?

A
  • cardiotoxicity (leading to heart failure or arrhythmias),
  • pulmonary toxicity (resulting in lung fibrosis or pneumonitis),
  • nephrotoxicity
  • hepatotoxicity
  • peripheral neuropathy.
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9
Q

secondary ? can occur after chemo

A
  • Secondary malignancies - leukemia, solid tumouts
  • can occur years after completion of chemo treatment
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10
Q

infertility & chemo?

A

Long-term effects may include infertility, premature ovarian failure (menopause), and decreased sperm count or quality.

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11
Q

bone side effects of chemo?

A
  • osteopenia/ osteoporosis
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12
Q

hormonal side effects of chemo?

A
  • hypothyroidism
  • adrenal insufficnecy
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13
Q

CV side effects of chemo?

A
  • Certain chemotherapy drugs, particularly anthracyclines and targeted therapies, can increase the risk of cardiovascular complications such as cardiomyopathy, heart failure, and myocardial infarction
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14
Q

acute myeloblastic leukemia is a ?

A
  • 80% adult leukemias
  • incidence increases w age
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15
Q

predisposing factors for AML?

A
  • radiation
  • benzene
  • previous chemo
  • inherited bone marrow failure conditions
  • downs
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16
Q

CF of AML?

A
  • bone marrow failure
  • extramedullary - e.g. gingivitis
  • hyperleukostasis
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17
Q

Peripheral blood film in AML?

A
  • myeloblasts - malignant myeloid cells
  • large nucleus
  • granules in the cytoplasm - can be in rods
  • fibrinogenolysis in acute promyelotic leukemia
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18
Q

Prognosis of AML?

A
  • cytogenetics
  • worse when:
  • complex karyotypes
  • abn chromsome 3, 5, 7
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19
Q

Acute promyelocytic leukemia?

A
  • associated w 15:17 PML: RAR
  • good prognosis - 70% 5 yr survival
  • coagulopathy can be fatal
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20
Q

what is acute promyelocytic leukemia sensitive to?

A
  • sensitive to ATRA and arsenic trioxide
  • doesn’t need chemo
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21
Q

Tx of non-APL AML

A
  • remission induction using anthracycline
  • allogenic stem cell transplant for high risk patients - adverse cytogenetics, relapsed patients
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22
Q

prognosis for AML?

A
  • good risk genetics 65-70% 5 yr survival
  • poor risk genetics 20-30% survival
  • elderly >65 yrs 10%
  • best survival under 40
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23
Q

Acute LL age group?

A
  • 12% of all adult leukemias
  • 60% under 20
  • peaks in the 2-5 yr age group and >50 yrs
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24
Q

ALL can be associated w?

A

Downs

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25
Q

majority of childhood leukemias are?

A

ALL

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26
Q

clinical features of ALL?

A
  • organomegaly
  • lymphadenopathy
  • CNS involvement
  • mediastinal mass -> obstruction of SVC
  • hyperleukostasis
  • hyperuricaemia + tumour lysis syndrome
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27
Q

results for ALL?

A
  • pancytopenia
  • circ lymphoblasts
  • bone marrow - hypercellular largely replaced w immunoblasts
  • lumbar puncture - lymphoblasts if CNS involvement
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28
Q

ALL - good prognosis when?

A
  • hyperdiploidy >50
  • B cell 8:14 translocation
  • 9:12 translocation
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29
Q

Poor cytogenetics in ALL?

A
  • hypodiploidy
  • 9:22 BCR: ABL philadelphia chromosome - very poor in adults
  • t 4:11 MLL rearrangement
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30
Q

Tx of ALL?

A
  • comb chemotherapy w intrathecal methotrexate as induction
  • high dose metho as CNS prophylaxis
  • allogeneic stem cell transplant for high risk
  • maintenance chemo required for up to 2 yrs - not required for B cell ALL
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31
Q

prognosis of ALL?

A
  • V good survival in children
  • poor survival > 40 yrs olds
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32
Q

Most common adult leukemia?

A

CLL

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33
Q

who does CLL affect?

A
  • males> females
  • inc w age - median age 65
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34
Q

features of CLL?

A
  • lymphocytosis, clonal mature B cells
  • lymphadenopathy
  • hepatosplenomegaly
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35
Q

Blood film of CLL?

A
  • peripheral blood B cell lymphocytosis
  • bone marrow infiltration
  • smear cells - smudged and smashed cells
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36
Q

Tx of CLL?

A

no benefit to treating if no symptoms

image

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37
Q

CML?

A
  • rare
  • diagnosed incidentally or following development of systemic symptoms, splenomegaly or gout
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38
Q

CML is characterised by?

A
  • charac by philadelphia chromosome producing constitutive activation of abl kinase
  • risk of transformation to acute leukemia
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39
Q

features of CML?

A
  • basophilia
  • eosinophilia
  • occasional blast
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40
Q

Tx of CML?

A
  • TK inhibitors - e.g. imatinib, nilotinib, bosutinib
  • allogeneic transplantation for resistant or transformed cases
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41
Q

Prognostic index for lymphomas?

A
  • diffuse large B cell lymphoma is the most common type
  • RIPI is the prognostic index
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42
Q

outcome in DLBCL ?

A
  • low risk disease have high chanc of cure
  • germinal centre type has a better prognosis than activated B cell type
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43
Q

Tx of DLBCL?

A
  • localised disease - 3 cycles of chemo
  • followed by radiotherapy to involved sites
  • stage 3/4 disease x6 cycles of chemo
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44
Q

Follicular lymphoma?

A
  • incurable
  • ppl present w lympadenopathy or w constitutional symptoms
  • can occur in the peripheral blood
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45
Q

Tx of follicular lymphoma?

A
  • asymptomatic in many
  • treatment only for symptomatic disease
  • risk of high grade transformation
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46
Q

assessing prognosis of follicular lymphoma?

A
  • FLIPI to assess prognosis
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47
Q

outcome for follicular lymphoma?

A
  • low risk: 5 year survival around 90%
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48
Q

hodgkin lymphoma shows presence of?

A
  • reed-sternberg cells
  • presence of binucleate cells in LNs/ affected cells
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49
Q

staging of HL?

A
  • Ann Arbor staging
  • Hassebclever index for stage 3/4 hodgkin lymphoma
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50
Q

prognosis of HL?

A
  • > 90% cure rate in over 50
  • diff to treat in elderly
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51
Q

Basic principles of radiotherapy?

A
  • uses ionising radiation to target and destroy cancer cells
  • tumour is localised using CT, MRI, PET
  • target delination to accurately define tumor volume and surrounding organs at risk to spare healthy tissue
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52
Q

EBRT =

A

External radiation beams are delivered from a linear accelerator (LINAC) or other external radiation source directed at the tumor from outside the body.

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53
Q

Bracytherapy =

A

Radioactive sources are placed directly into or near the tumor, delivering a high dose of radiation to the target while sparing surrounding tissues.

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54
Q

Stereotactic radiosurgery

A
  • Stereotactic Radiosurgery (SRS) and Stereotactic Body Radiotherapy (SBRT): Highly precise, high-dose radiation is delivered to small targets in the body, typically in one to five treatment sessions.
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55
Q

Fractination =

A
  • fractination: allows for delivery of an effective dose of radiation to the tumor whilst minimising toxicity to surrounding normal tissues by taking advantage of differences in repair capacity between tumor cells and normal tissues.
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56
Q

Immediate radiotherapy side effects?

A
  • skin reactions - erythema, itching and skin dryness within the radiation field
  • fatigue
  • mucositis - pain, dysphagia, oral mucositis
  • nausea and vomiting
  • alopecia in the radiation field
  • if radiation is to the pelvis or bladder they may experience acute urinary symptoms like freq, urgency, dysuria, haematuria
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57
Q

Long term radiotherapy side effects - fibrosis?

A
  • radiation fiborosis -> scarring -> tissue stiffness
  • e.g. skin, subcutaneous tissue, muscles, internal organs
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58
Q

LT side effect of radiotherapy - dermatitos?

A
  • radiation dermatitis e.g. telangiectasia (dilated blood vessels), hyperpigmentation, or hypopigmentation.
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59
Q

radiation enteritis?

A
  • radiation enteritis -> intestinal strictures, bowel obstruction
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60
Q

radiation cystitis?

A
  • radiation cystitis which can lead to incontience
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61
Q

other LT side effects of radiotherapy?

A
  • lymphdema -> inc infection risk
  • pulmonary fibrosis or chronic resp insufficiency
  • secondary malignancies e.g. sarcomas, leukemias, solid tumours
  • CV comps - inc CAD, MI, pericardial disease
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62
Q

what can cause bone pain and abn gait?

A
  • mets bone disease
  • primary bone cancer
  • pathological fractures from cancer related bone weakening
  • SCC
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63
Q

Ix of bone pain and abn gait?

A
  • X rays to identify fractures
  • MRI or CT
  • FBC, ALP, tumour markers
  • bone scans
  • biopsy
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64
Q

benefits of radiotherapy?

A
  • highly effective for local tumour control
  • palliation of symptoms such as pain
  • organ preservation and avoid need for radical surgery by shrinking tumours
  • improved survival
  • curative intent
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65
Q

common types of bracytherapy?

A
  • Common types of brachytherapy include intracavitary (within body cavities such as the uterus or vagina), interstitial (directly into tissues), and surface (applicators placed on the skin) brachytherapy.
  • Brachytherapy may be used alone or in combination with EBRT
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66
Q

proton therapy?

A
  • Proton therapy uses protons instead of photons (X-rays) to deliver radiation to the tumor.
  • Proton therapy can deliver highly conformal radiation to the tumor while minimizing dose to surrounding healthy tissues, potentially reducing side effects.
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67
Q

when is proton therapy useful?

A
  • Proton therapy is particularly useful for treating tumors located near critical structures or in pediatric patients, where minimizing radiation exposure to healthy tissues is crucial.
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68
Q

radioisotope therapy?

A
  • Radioisotope therapy involves administering radioactive substances, either orally or intravenously, that selectively accumulate in tumor cells, delivering radiation directly to the tumor.
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69
Q

when is radioisotope therapy used?

A
  • Examples include radioactive iodine therapy for thyroid cancer and radiopharmaceuticals for treating bone metastases or neuroendocrine tumors.
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70
Q

causes of hypercalcaemia?

A
  • most common causes are malignant hypercalcaemia and primary hyperparathyroidism
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71
Q

malignant hypercalcaemia?

A
  • associated w poor prognosis
  • Hypercalcaemia commonly occurs due to release of parathyroid related peptide (PTHrP), which mimics the action of PTH.
  • Other mechanisms include osteolytic damage to bone or activation of vitamin D.
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72
Q

primary hyperparathyroidism?

A
  • Primary hyperparathyroidism is the most common cause of hypercalcaemia in the general population.
  • It occurs due to excess release of PTH, which leads to bone resorption and excess calcium release.
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73
Q

what is a common cause of primary hyperparathyriodism?

A

parathyroid adenoma

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74
Q

secondary hyperparathyroidism?

A
  • Secondary hyperparathyroidism is characterised by excess PTH production secondary to low serum calcium, typically due to chronic kidney disease or vitamin D deficiency.
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75
Q

tertiary hyperparathyroidism?

A
  • Tertiary hyperparathyroidism is characterised by autonomous PTH excess due to parathyroid hyperplasia in response to longstanding secondary hyperparathyroidism - seen in patients with chronic kidney disease.
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76
Q

how are primary and tertiary hyperparathyroidism similar?

A

both cause hypercalcaemia

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77
Q

which type of hyperparathyroidism causes HYPOcalcaemia?

A

secondary

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78
Q

thyroyoxicosis and hypercalcaemia?

A

Elevated thyroid hormones can lead to thyroid hormone-mediated bone resorption.

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79
Q

hypercalcaemia - Some conditions lead to excess endogenous production of activated vitamin D, which include:

A
  • Granulomatous disorders(e.g. sarcoidosis)
  • Cancers(e.g. lymphoma)
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80
Q

other causes of hypercalcaemia?

A
  • Chronic lithium use: enhances PTH release
  • Thiazide diuretics: lowers urinary calcium excretion
  • Adrenal insufficiency
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81
Q

Hypercalcaemia - features?

A
  • Bones- fragility fractures, bone pain
  • Stones- renal calculi
  • Thrones- polyuria, constipation
  • Abdominal groans- abdominal pain, N&V, pancreatitis
  • Psychic moans- mood disturbance, depression, fatigue, psychosis
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82
Q

signs of hypercalc?

A
  • Dehydration(skin turgor, dry mucous membranes)
  • Hypertension
  • Cardiac arrhythmia(severe disease)
  • Confusion(severe disease)
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83
Q

diagnosis of hypercalcaemia is based on?

A

serum corrected calcium > 2.6 mmol/L.

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84
Q

hypercal + elevated PTH?

A
  • Elevated PTH(i.e. PTH-mediated): suggestive of primary hyperparathyroidism or tertiary hyperparathyroidism
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85
Q

Hypercal and mid to upper normal PTH?

A
  • Mid-to-upper normal PTH(suspected PTH-mediated): in the context of hypercalcaemia this is considered ‘inappropriately high’ and suggestive of hyperparathyroidism
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86
Q

Hyper cal + low to low normal PTH?

A
  • Low or low-normal PTH(i.e. non-PTH mediated): suggestive of malignancy, which needs to be excluded. Hypervitaminosis D also possible.
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87
Q

Mx of hypercal?

A
  • management of symptomatic hypercalcaemia is primarily fluid resus
  • Severe hypercalcaemia requiring inpatient management is typically indicative of a malignant cause.
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88
Q

Mild hypercal Mx?

A
  • Mild (< 3 mmol/L) and asymptomatic/mild symptoms: increase oral fluids and avoid precipitants (e.g. thiazide diuretics, lithium, dehydration).
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89
Q

moderate hypercal Mx?

A
  • Moderate (3-3.5 mmol/L): acute rise requires inpatient admission for intravenous fluids.
  • Chronically raised elevations may not require acute management
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90
Q

Severe hypercal Mx?

A
  • Severe (>3.5 mmol/L): all patients require urgent admission to hospital and treatment.
  • Treatment involves aggressive intravenous fluids and consideration of bisphosphonates, particularly if malignancy is suspected.
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91
Q

when are bisphosphonates used in hypercal

A
  • considered in severe hypercalcaemia particularly if malignancy is suspected
  • Pamidronate or zoledronic acid are typically used.
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92
Q

Alt to bisphosphonates in hypercal?

A
  • An alternative to bisphosphonates is denosumab, which is a monoclonal antibody that binds to RANK ligand and inhibits the action of osteoclasts.
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93
Q

Mx of hypercal - steroids?

A
  • Corticosteroids: may be used in hypervitaminosis D.
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94
Q

Mx of hypercal - surgery?

A
  • Surgery: able to provide a cure in primary hyperparathyroidism. Potential option in tertiary hyperparathyroidism
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95
Q

Mx of hypercal - cinacalcet?

A
  • Cinacalcet: calcimimetic that mimics the action of calcium on calcium-sensing receptors. May be utilised in primary hyperparathyroidism if surgery has failed or not an option. Also used in secondary/tertiary hyperparathyroidism.
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96
Q

Dialysis in Mx of hypercal?

A
  • Dialysis: may be reserved for severe, refractory hypercalcaemia.
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97
Q

Indications for primary radiotherapy?

A
  • Indications for primary radiotherapy include early-stage cancers, inoperable tumors, or cases where surgery is not feasible due to tumor location or patient factors.
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98
Q

Adjuvant radiotherapy?

A
  • adjuvant - after surgery to reduce risk of reccurence
  • indications: high risk features such as positive surgical margins, lymph/ vascular invasion
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99
Q

Neoadjuvant radiotherapy?

A
  • neoadjuvant therapy - before surgery to downstage the tumor, improve resectability and facilitate surgical resection
  • indications: locally advanced tumors, large tumours requiring downsizing for organ preservation
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100
Q

Palliative radiotherapy?

A
  • palliative therapy - relief of symptoms, pain alleviation, improved QOL
  • Indications for palliative radiotherapy include symptomatic relief of pain, bleeding, obstruction, neurological symptoms, or other cancer-related symptoms.
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101
Q

curative intent radiotherapy?

A
  • curative intent therapy - comb w other treatments such as surgery, chemo, or targeted therapies
  • indications: localized cancers w potential for cure such as early stage non small cell lung cancer, CC, prostate cancer
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102
Q

indications of radiotherapy other than cancer?

A
  • non cancerous conditions - e.g. benign tumours, vascular malformations, autoimmune
  • aim to control symptoms, improve functional outcomes, or prevent disease progression.
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103
Q

bone mets are most commonly from?

A
  • breast
  • bronchus
  • thyroid
  • prostate
  • kidney
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104
Q

Osteoblastic bone mets?

A

consequence of prostate cancer, Hodgkin’s lymphoma and small cell lung cancer

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105
Q

Osteolytic bone mets?

A

renal cell cancer, thyroid cancer, melanoma, non-small cell lung cancer and non-Hodgkin’s lymphoma

106
Q

mixed osteoblastic and osteolytic bone mets?

A

GI and breast cancers

107
Q

CFs of bone mets?

A
  • pain - severe, often wakes them from sleep
  • classicaly described as gnawing
  • weight loss
  • reduced motility
  • pathological fracture
  • paralysis and weakness rarely if SCC
108
Q

Bone mets can lead to symptoms of ?

A
  • hypercalcaemia
  • Bone pain, muscle weakness, thirst, excessive urination, confusion, malaise.
109
Q

Ix of bone mets?

A
  • bone scintigraphy scan - inc uptake or assymetical
110
Q

Bone mets - imaging modality used if the ppt presents with pain and features of nerve involvement?

A
  • If the patient presents withpain and features of nerve involvementsuch as weakness or paralysis, it would be more appropriate to consider a CT or MRI scan as it is easier to visualise soft tissues and if there is any nerve compression.
  • If bone metastases are found in one area, thewhole body should be scanned using bone scintigraphyto find any other areas affected.
111
Q

Bloods for bone mets?

A
  • FBC - can show anemia
  • U&Es
  • LFTs - inc ALP
  • CRP
  • hypercalcamia
  • MM screen
  • tumour markers screen
112
Q

Mx of bone mets?

A
  • Treatment may include surgery to stabilise affected bones, radiotherapy, chemotherapy, or hormone therapy
  • denosumab - osteoclast inhibition, monoclonal ab that slows progression of bone mets
  • analgesia
  • bisphosphonates
113
Q

What are the symptoms of SCC?

A
  • Weakness/ numbness of limbs
  • bladder/ bowel dysfunction
  • sensory loss
  • noctural spinal pain
114
Q

Patients with signs of spinal cord compression should be treated as a

A

medical emergency and require an urgent MRI.

115
Q

Cancers inc risk of malignant spinal cord comp?

A
  • Prostate
  • lung
  • breast
  • renal
  • MM
116
Q

Red flag featuresof back pain that may suggest MSCC (particularly in patients with a known cancer diagnosis) include:

A
  • Thoracic or cervical pain
  • Progressive lumbar pain
  • Spinal pain aggravated by straining
  • Localised spinal tenderness
  • Nocturnal pain preventing sleep
117
Q

symptoms of SC compression

A
  • Limb weakness (e.g. the limb feeling “heavy” or “stiff”, difficulty climbing stairs)
  • Loss of coordination
  • Sensory disturbance
  • Autonomic dysfunction (e.g. urinary retention, faecal incontinence due to loss of anal tone, constipation)
  • cauda equina syndrome
118
Q

Symptoms of cauda equina syndrome?

A
  • bladder/bowel dysfunction
  • saddle anaesthesia
  • leg weakness
  • gait disturbance
  • back pain
119
Q

Ix of malignant SCC?

A
  • any patients w malignant SCC should be referred for urgent MRI of the spine within 24 hrs
  • If an MRI is contraindicated (e.g.pacemakers and metallic foreign bodies), the next best imaging modality is CT.
120
Q

Other Ix of SCC?

A
  • bladder scan to assess for urinary retention
  • baseline bloods
  • bone profile - hypercalcamia
  • LDH
  • myeloma screen if the ppt doesn’t have a known cancer diagnosis
  • Tumour markers
121
Q

Mx of SCC - reducing inflammation?

A
  • Dexamethasone to reduce inflammation and oedema
122
Q

other Mx techniques in SCC?

A
  • Omeprazole (or alternativePPI) for stomach protection
  • Low molecular weight heparin (or alternative) forthromboprophylaxis
  • Immobilise the spine if instability is suspected
  • Analgesia
123
Q

Definitive Mx of SCC?

A
  • surgical decompression followed by radio
  • radiotherapy - particularly those with multiple medical comorbidities, rapidly progressive neurological deficits and radiosensitive tumours (e.g. myeloma)
124
Q

acute radiotherapy side effects

A
125
Q

Late radiotherapy side effects

A
126
Q

Pain characteristics suggesting spinal metastases:

A
  • severe unremitting back pain
  • progressive back pain
  • mechanical pain (aggravated by standing, sitting or moving
  • back pain aggravated by straining (for example, coughing, sneezing or bowel movements)
  • night-time back pain disturbing sleep
  • localised tenderness
  • claudication (muscle pain or cramping in the legs when walking or exercising).
127
Q

What should be done if there are signs of compression?

A
  • immediately contact the MSCC co-ordinator if signs of compression
128
Q

Causes of hypoglycaemia can be remembered by the mnemonic EXPLAIN

A
  • Exogenous drugs (typically sulfonylureas or insulin)
  • Pituitary insufficiency
  • Liver failure
  • Addison’s disease
  • Islet cell tumours (insulinomas)
  • Non-pancreatic neoplasms
129
Q

Where is folate abs?

A

Folate is predominantly absorbed in the duodenum and proximal jejunum and so absorption would not be affected by ileocaecal resection - ileocaecal resection causes B12 def

130
Q

Tumour marker in medullary thyroid cancer?

A

Calcitonin is a tumour marker in medullary thyroid cancer

131
Q

Follicular/Papillary thyroid cancer tumour marker?

A

thyroglobulin

132
Q

ovarian cancer marker?

A

CA 125

133
Q

hypercal Sx

A
134
Q

when to act - hypercal

A
135
Q

pancreatic cancer TM?

A

ca19-9

136
Q

breast cancer marker?

A

CA 15-3

137
Q

prostate cancer marker?

A

PSA

138
Q

Alpha-feto protein (AFP)?

A

Hepatocellular carcinoma,teratoma

139
Q

CEA tumour marker?

A

Carcinoembryonic antigen (CEA) Colorectal cancer

140
Q

S-100 tumour marker?

A

melanoma

141
Q

Bombesin tumour marker?

A
  • Small cell lung carcinoma
  • gastric cancer,
  • neuroblastoma
142
Q

what type of electrolyte abn is seen in cushings syndrome?

A

hypokalaemic metabolic alkalosis

143
Q

Subclinical hyperthyroidism is associated with ?

A

atrial fibrillation, osteoporosis and possibly dementia

144
Q

causes of CES?

A
  • lumbar disc herniation - most common ause
  • degenerative lumbar canal stenosis
  • neoplastic space occupying lesion
  • spinal trauma
145
Q

CFs of cauda equina syndrome?

A
  • bladder dysfunction - urinary retention at first which progresses to overflow incontenence which is a late sign
  • bowel - constipation or faecal incontienence
  • sexual
  • peri-anal sensory loss - saddle anaesthesia
146
Q

reflexes

neuro symptoms of CES?

A
  • unilateral or bilateral
  • Lower back painwith or without sciatica
  • Lower limb sensory loss
  • Lower limb lower motor neurone signs: most notably weakness, hypotonia and hyporeflexia
147
Q

Acute vs chronic CES presentation?

A
  • Acute:Sudden onset, rapidly progressing symptoms which worsen over several hours or days
  • Chronic:insidious onset with slow progression of symptoms
148
Q

how do CES symptoms start in most patients?

A
  • most patients start with lower back pain, may be present with or without sciatica
149
Q

Ix for CES?

A
  • urgent MRI scan
  • if unavailable, CT is the next best method
150
Q

Mx of CES?

A
  • spinal decompression
  • dexamethasone
  • emergency surgery - espec if evidence of bladder dysfunction
151
Q

SCC Mx?

A
  • immobilisation
  • pain management
  • physical therapy
  • corticosteroids - dexamethasone
  • bisphosphonates
  • radiotherapy
152
Q

diagnostic vs therapeutic X rays?

A
  • kilovoltage - diagnostic X rays
  • megavoltage - therapeutic X rays
153
Q

Mechanism of XR production?

A
  • Breaking radiation - electron enters the atom and passes through the nucleus due to opposite charge, bends the electron and loses energy
  • most common form
  • characteristic X ray -e- strikes an electron orbiting an atom
154
Q

indications for curative radio?

A
  • curative = early stage, prostate, cervic, VC, skin e.g. non melanoma
  • curative before or after surgery
155
Q

indications for curative w chemo radiotherapy?

A
  • curative w chemo - advance H&N cancer, lymphoma
156
Q

indications for palliative radio?

A
  • palliative - pain control, control bleeding, SC compression - cauda equina, reduce tumour mass so relieving the mass effects
157
Q

dose of curative radiotherapy?

A
  • curative: 60-70 Gy
  • palliative: 8 Gy in one fraction/ 20 over a week
158
Q

when is secondary cancer most common after radio?

A
  • secondary cancer is more common in children and growing adolescents
159
Q

late side effects of radiotherapy in children and growing adolescents?

A
  • growth retardation
  • hypoplasia of organ irradiated
  • secondary cancer
160
Q

mechanism of action of radiation

A
  • OH- radical production
  • reacts w DNA -> cell death
161
Q

Tumour induced hypercalcaemia - serum calcium is bound to albumin so?

A

measurements should be adjusted for serum albumin

162
Q

mechanisms of tumour induced hypercalcaemia - 3?

A
  • paraneoplastic syndrome
  • sectretion of PTHr protein: enhances osteoclast activation and bone resoprtion
  • inc renal tubular calcium reabs
  • sign bone lysis directly by the tumour - e.g. multiple myeloma
163
Q

examination and Ix for TIHC?

A
  • gen + abdo
  • urine output
  • other cancer related signs and symptoms
  • other electromytes: albumin, ALP
  • T3 and T4
  • ECG
164
Q

Causes of hypercal - lung?

A

squamous and small cell

165
Q

cancers that cause hypercal?

A
  • any advanced sq cell cancer - head and neck, bladder, anal canal, vulva
  • MM
  • renal cell cancer - release of PTHr
  • advance breast cancer
166
Q

Mx of tumour induced hypercalcaemia?

A
  • rehydrate 2-4 litres of 0.9% saline IV over 24 hrs
  • mobilize
  • IV bisphosphonate
167
Q

caution of fluid resus in hypercalcaemia?

A
  • caution: elderly, cardiac history, obst uropathy, renal failure
168
Q

Glucocorticoids in the Mx of hypercal?

A
  • glucocorticoids: inhibit 1,25-hydroxyvit D production
169
Q

resistant tumour induced hypercal?

A
  • in resistant cases, consider calcitonin
170
Q

other causes of hypercal?

A
  • primary hyperparathyroidism
  • sarcoidosis
  • vit d intox
  • thyrotoxicosis
  • meds
171
Q

side effects of bisphosphonates?

A
  • can cause kidney damage
  • flu like symptoms
  • hypocalcemia
  • jaw necrosis w long term use
172
Q

monitoring after tumour induced hypercalcaemia?

A
  • repeat bloods
  • check other electrolytes and renal function
  • pain control
  • if not for anti-cancer treatment, involve palliative care
173
Q

blood results in malignant hypercalcaemia?

A
  • parathyroid hormone (PTH) levels are typically low or suppressed.
  • This is because malignant hypercalcemia is usually caused by cancer-induced overproduction of parathyroid hormone-related protein (PTHrP) or by direct bone destruction from metastatic cancer
174
Q

prostate cancer is the?

A
  • most common cancer in males in the UK
  • most diagnosed at 65+
  • age standardised incidence rate: 173 per 100000 in 2016
175
Q

RF for prostate cancer?

A
  • age
  • highest in african americans > white americans> asians
  • red meat diet
  • FHx
  • genetic mutation: BRCA-2: 5x higher risk
176
Q

what can transiently elevate PSA?

A
  • prostatitis
  • ejaculation
  • urinary retention
  • after endoscopic urethral manipulation
  • prostatic biopsy
177
Q

PC arises in which zone of the prostate?

A
  • PC commonly arises in the peripheral zone
  • 5-10% in the transitional zone
  • 5% central
178
Q

Sx of prostate cancer - obstruction?

A
  • urinary hesitancy
  • decreased force of urine stream
  • intermittency
179
Q

Sx of PC - irritation?

A
  • urinary freq
  • nocturia
  • urgency
  • urge incontinence
180
Q

Sx of PC - obstruction of ejaculatory duct?

A
  • haematospermia
  • dec in ejaculate volume
181
Q

Sx of PC - extension to NV bundle?

A

ED

182
Q

features of metastatic PC?

A
  • bone pain
  • anaemia
  • leg oedema
  • leg weakness
  • fracture
  • weight loss
  • asymptomatic
183
Q

Ix of PC?

A
  • DRE
  • PSA - repeat
  • transrectal US guided biopsy - to confirm cancer
184
Q

How is pC staged?

A
  • MRI/ CT - staging
  • MRI preferred but CT used if suspected spread to lymph nodes or other organs
185
Q

when should a bone scan for PC be done?

A
  • bone scan if PSA>10 or Gleason score > 7
  • routine bloods - ALP etc
186
Q

T staging of PC?

A
  • T1-T2c: cancer remains within prostate capsule
  • T3-T4: cancer has infiltrated
187
Q

Gleason scoring?

A

gleason score - higher gleason the more poorly differeniated the cancer. The more diff it looks to normal, the higher the score.

188
Q

Low risk prostate cancer?

A

PSA<10, gleason 6, T2a

189
Q

intermediate risk PC?

A

Gleason 7, PSA 10-20, T2b

190
Q

high risk PC?

A

T3a+, gleason =>8, PSA>20

191
Q

Localised PC Mx?

A

surgery + radiotherapy

192
Q

locally advanced PC Mx?

A

radiotherapy, ADT

193
Q

mX of metastatic PC?

A

Chemo

194
Q

acute side effects of radiotherapy to the prostate?

A
  • diarrhoea
  • dysuria/ freq
  • rectal soreness/ bleeding
  • fatigue
  • anal fissure: GTN cream
  • exacerbation of haemorrhoids
195
Q

LT side effects of radiotherapy to the prostate?

A
  • 6-12 months after radiotherapy
  • bleeding
  • urethra/ bladder neck stenosis
  • rectal ulcer/ weak sphincter
  • haematuria
196
Q

most common LT side effect following radiotherapy to the prostate?

A

ED

197
Q

comps of prostatectomy?

A
  • ED - most common
  • urinary incontience
  • loss of ejaculation - permanent
  • shrinkage of penis
198
Q

Prognosis of PC?

A
  • low risk: 80-90%
  • high risk: 30-50% 10 yr control
  • metastatic - median 5 yrs or 3 yrs if ADT/ castrate resistant
199
Q

PC - androgen dependent therapy?

A
  • means of testosterone deprivation:
  • removal of source/ decrease section of testosterone/ block test receptors
200
Q

PC - ADT side effects

A
201
Q

PC - if the cancer progresses despite following all available Tx

A
  • progressive weight loss
  • anaemia and thrombocytopenia
  • skeletal related events
  • dec mobility/ independence
  • pain
202
Q

Bony metastases usually present as pain but may also present as:

A
  • pathological fracture
  • spinal cord compression
  • hypercalcaemia
  • symptoms of nerve root compression
  • swelling / deformity / loss of mobility
203
Q

What to ask abt for bony mets?

A
  • the nature of the pain
  • exacerbating factors
  • radiation to other areas
  • loss of function
  • timescale
  • relief with simple analgesia
  • disturbance of sleep
  • a history of trauma
  • existing metastatic disease
  • loss of weight
204
Q

concerning features in a pain history?

A
  • progresses over time
  • does not respond to simple analgesia
  • disturbs sleep
  • is associated with bony tenderness +/or weight loss
205
Q

summary of Mx of bone mets?

A
  • bisphosphonates or denosumab
  • sugical fixation if instability
  • chemo
  • vertebroplasty
  • radioactive isotopes
206
Q

BM - Vertebroplasty?

A

percutaneous technique for spinal metastases

207
Q

Radioactive isotopes seek out the bone mets and irradiate them selectively – work best for?

A

PC

208
Q

Alpha-1 antitrypsin deficiency is a risk factor for

A

HCC

209
Q

kidney cancer prev?

A
  • comprises 3% of all cancers in men, 2% in women
  • 8th most common cancer in men
  • overall mortality 40%
210
Q

Types of kidney cancer?

A
  • 85% occur in renal parenchyma (renal cell carcinoma (RCC))
  • 6% occur in renal pelvis (transitional cell carcinoma (TCC))
  • 6% occur in ureter (transitional cell carcinoma)
211
Q

RF for kidney cancer?

A
  • age
  • sex - male > female
  • obesity
  • smoking
  • HTN
  • diet - poor intake of fruit and veg
  • radiotherapy for prev testicular/ gynae cancer
212
Q

what inc risk of KC by 3-4x?

A

adult polycystic kidney disease

213
Q

what inc risk of kidney cancer by 7x?

A
  • renal dialysis - inc risk 7x after 10 yrs dialysis
214
Q

FHx of ? inc risk of kidney cancer?

A

bon Hippel Lindau disease

215
Q

and which renal cancer?

drugs inc risk of KC?

A

phenacetin - inc risk of TCC of renal pelvis

216
Q

Most common histological subtype of kidney cancer?

A
  • conventional (aka clear cell) RCC 75-80%
217
Q

How is clear cell RCC graded?

A
  • graded histologically according to Fuhrman classification
  • Fuhrman 1 (well differentiated) -> Fuhrman 4 (poorly differentiated)
218
Q

other histological types of RCC?

A
  • papillary (aka chromophilic) RCC 10-15%
  • chromophobic RCC 5%
  • collecting duct RCC 1%
  • unclassified
219
Q

Most common way renal cancer presents?

A

*asymptomatic – incidental discovery on imaging done for other reasons (commonest)

220
Q

Symptoms of RC?

A
  • haematuria (blood in urine) – visible and non-visible (dipstick, microscopic)
  • palpable mass
  • weight loss/ night sweats
  • anaemia
  • bone pain/ fracture from mets
221
Q

Paraneoplastic syndromes from renal cell cancers?

A

renal cell cancers can inappropriately secrete ectopic peptide hormones e.g. EPO, PTH

222
Q

staging of renal cancer?

A
  • US and CT for formal staging
223
Q

RC - observation for?

A

small tumours in elderly or those w sig medical co-morbidity

224
Q

Tx of localised kidney disease?

A
  • surgery (nephrectomy)
  • radiofreq ablation or cryotherapy
225
Q

Tx of metastatic kidney disease?

A
  • cytoreductive nephrectomy
  • can inc resp to subsequent biological therapy
  • biological therapy
  • interferon-alpha
  • TKI
226
Q

survival from kidney cancer?

A
  • 10th highest cause of cancer deaths in men in the UK, 12th in women
  • 10 yr survival = 43%
227
Q

prev of bladder cancer?

A
  • 4th commonest cancer in men, 11th in women
  • overall mortality approx 50%
228
Q

gender affected more by bladder cancer?

A
  • M:F = 5:2
229
Q

RF for bladder cancer?

A
  • SMOKING
  • occupation - analine dyes - paint, hair dye, textile and pesticide industries
  • hair dyes
  • pelvic irradiation
  • caucasian males
  • dietary factors
230
Q

drugs inc rate of bladder cancer?

A

phenacetin, cyclophosphamide

231
Q

chronic UTI predisposes to which type of bladder cancer?

A

squamous cell carcinoma

232
Q

Schistosomiasis predisposes to?

A

sq cell carcinoma espec in the Middle East

233
Q

histology of bladder cancer?

A
  • 90-95% are transitional cell carcinomas (TCC)
  • 3-4% are squamous cell carcinomas
  • 1-2% are adenocarcinomas
234
Q

Most common type of bladder cancer?

A

TCC

235
Q

grading and staging of bladder cancer?

A
  • graded according to degree of cytological atypia
  • 1 (well differentiated, low grade) to 3 (poorly differentiated, high grade)
  • staging based on TNM
236
Q

Three features

presentation of BC?

A
  • haematuria
  • irritative lower urinary tract symptoms (frequency, urgency)
  • recurrent UTI (SCC)
237
Q

symptoms of advanced/ metastatic bladder cancer?

A
  • general – weight loss, lethargy
  • bone pain/fracture
  • pelvic pain
  • lower limb/genital oedema from pelvic lymphadenopathy
238
Q

Ix of bladder cancer?

A
  • cytoscopy
  • CT/ MRI for staging
239
Q

initial treatment of bladder cancer?

A
  • initial: TURBT - transurethral resection of bladder tumour
  • removes primary tumour and allows formal histological grading and staging
240
Q

?% of bladder cancers are muscle invasive

A
  • 75% of tumours are non muscle invasive, 25% are muscle invasive from the outset
241
Q

Low grade non-muscle invasive bladder cancer ->

A

Cystoscopic surveillance x5-10 years

242
Q

Moderate/high grade non-muscle invasive BC(including carcinoma-in-situ) ->

A

Intravesical chemotherapy (Mitomycin C) or intravesical immunotherapy (BCG) + Cystoscopic surveillance

243
Q

muscle invasive bladder cancer ->

A

Radical cystectomy or radiotherapy ± neoadjuvant Cisplatin-based systemic chemotherapy

244
Q

metastatic bladder cancer ->

A

Palliative chemotherapy ± palliative radiotherapy for local symptom control

245
Q

what is the most common cancer in men?

A

PC, * accounts for nearly 25% of all newly diagnosed cancers in men

246
Q

2nd most common cause of cancer death in men?

A
  • PC, 1st is lung
  • overall mortality approx 25-30%
247
Q

Why is PC being diagnosed more?

A
  • increasing use of serum PSA (prostate specific antigen) test has led to increase in diagnosis of prostate cancer and detection of prostate cancers at earlier stage
248
Q

RF for PC?

A
  • age - 80% OF OVER 80
  • Fhx
  • ethnic origin -2-3x inc risk in black Africans/ Caribbean
  • dietary - lycopenes and selenium protective
249
Q

PC - 98% are ?

A

adenocarcinomas

250
Q

Ix of PC

A
  • histological material obtained via prostate biopsy or from TURP shaings
  • transrectal prostate biopsy performed if clinical suspicion of prostate cancer (↑ PSA or abnormal-feeling prostate on rectal examination)
251
Q

CP of PC?

A
  • asymptomatic (through PSA testing)
  • local disease
  • haematuria
  • lower urinary tract symptoms (identical to those cause by BPH)
252
Q

Advanced prostate cancer symptoms?

A
  • general – weight loss, lethargy
  • bone pain/fracture - mets
  • pelvic pain
  • lower limb/genital oedema from pelvic lymphadenopathy
253
Q

other tests for PC?

A
  • PSA level
  • pelvic MRI
  • isotope bone scan
254
Q

Tx of low risk PC

A
  • active surveillence
  • bracyhtheapy, prostatectomy, radio, waiting
255
Q

Tx of medium risk PC

A
  • radical prostatectomy
  • radical radiotherapy
256
Q

Tx of high risk PC?

A
  • radical prostatectomy
  • radical radiotherapy w neoadjuvant hormone therapy
257
Q

Main Tx of metastatic PC?

A
  • hormone manipulation - PALLIATIVE
258
Q

hormone manipulation in PC?

A
  • prostate cancer initially dependent on testosterone
  • therapy aims at blocking testosterone production or testosterone metabolism by
  • prostate cancer cell (and inducing castrate status)
259
Q

How can hormone manipulation be done?

A
  • surgically – bilateral scrotal orchidectomy
  • medically – anti-androgens, LHRH analogues, oestrogens
  • average response to 1st line therapy = 2-3 years
260
Q

side effects of hormone manipulation (PC)

A

hot flushes, breast enlargement/tenderness, weight gain, osteoporosis, loss of libido, impotence

261
Q

Castration resistant PC?

A
  • systemic chemotherapy (Taxotere)
  • new agents (Abiraterone, Enzalutamide)
  • median survival 18-24 months
262
Q
A

Year 3 (45 decks)

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