Oncology Flashcards

1
Q

two broad types of lung cancer

A

small cell + non-small cell

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2
Q

small cell + non-small cell lung cancer differentiated by

A

histology

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3
Q

sub classes of non-small cell lung cancer

A

squamous cell, adenocarcinoma, large cell carcinoma

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4
Q

small cell + non-small cell lung cancer worst prognosis?

A

small cell

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5
Q

squamous cell lung carcinoma

A

centrally located, associated with parathyroid hormone related protein secretion (hypercalcaemia), clubbing, hypertrophic pulmonary osteoarthropathy, ectopic TSH secretion (hyperthyroidism)

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6
Q

centrally located, associated with parathyroid hormone related protein secretion, clubbing, hypertrophic pulmonary osteoarthropathy, ectopic TSH secretion

A

squamous cell carcinoma

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7
Q

hypertrophic pulmonary osteoarthropathy is

A

disorder associated with severe clubbing: subperiosteal new bone formation at the distal ends of long bones, metatarsals, metacarpals, proximal phalanges, symmetrical arthropathy of adjacent joints, clubbing, gynaecomastia

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8
Q

disorder associated with severe clubbing: subperiosteal new bone formation at the distal ends of long bones, metatarsals, metacarpals, proximal phalanges, symmetrical arthropathy of adjacent joints, clubbing, gynaecomastia

A

hypertrophic pulmonary osteoarthropathy

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9
Q

lung adenocarcinoma

A

peripherally located, gynaecomastia, hypertrophic pulmonary osteoarthropathy, most common lung cancer in non-smokers (still predominantly smokers affected)

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10
Q

peripherally located, gynaecomastia, hypertrophic pulmonary osteoarthropathy, most common lung cancer in non-smokers

A

adenocarcinoma

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11
Q

large cell lung carcinoma

A

peripherally located, anaplastic, poorly differentiated, poor prognosis, may secrete b-HCG

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12
Q

anaplastic

A

poorly differentiated

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13
Q

peripherally located, anaplastic, poorly differentiated, poor prognosis, may secrete b-HCG

A

large cell lung carcinoma

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14
Q

poorly differentiated cells

A

anaplastic

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15
Q

small cell lung cancer

A

neuroendocrine tumour, centrally located, arise from APUD cells, ectopic ADH (hyponatraemia), ACTH (hypertension, hyperglycaemia, Cushings, bilateral adrenal hyperplasia, hypokalaemic alkalosis) secretion, Lambert-Eaton syndrome, causes majority of paraneoplastic syndrome in lung cancer

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16
Q

APUD cells

A

small cell lung cancer arises from them: amine (high amine content) precursor uptake (high uptake of amine precursors) decarboxylase (high content of the enzyme decarboxylase)

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17
Q

neuroendocrine tumour, centrally located, arise from APUD cells, ectopic ADH, ACTH secretion, Lambert-Eaton syndrome

A

small cell lung cancer

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18
Q

why poor prognosis with small cell lung cancer

A

usually metastatic by time of diagnosis

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19
Q

types of staging for lung cancer

A

TNM and Stage I-IV

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20
Q

TNM staging

A

Tx, T0, Tis, T1 <3cm, T2 3-5cm, T3 5-7cm, T4 >7cm
Nx, N0, N1 hilum, N2 ipsilateral mediastinum, N3
M0, M1a bilateral lung, M1b single area outside of chest, M1c

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21
Q

Lambert Eaton syndrome/Lambert Eaton myasthenic syndrome (LEMS)

A

rare autoimmune disorder (voltage-gated calcium channels) characterised by muscle weakness, paraneoplastic syndrome
Differential diagnosis: myasthenia gravis

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22
Q

rare autoimmune disorder (voltage-gated calcium channels) characterised by muscle weakness, paraneoplastic syndrome

A

Lambert Eaton syndrome/Lambert Eaton myasthenic syndrome (LEMS)

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23
Q

small cell lung cancer management

A

limited disease can be cured with chemotherapy + radiotherapy, advanced disease is managed palliatively

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24
Q

limited lung disease can be cured with chemotherapy + radiotherapy, advanced disease is managed palliatively

A

small cell lung cancer

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25
Q

lung cancer risk factors

A

smoking (x10 risk), asbestos (x5 risk), arsenic, radon, nickel, chromate, aromatic hydrocarbon, cryptogenic fibrosing alveolitis

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26
Q

cryptogenic fibrosing alveolitis aka

A

idiopathic pulmonary fibrosis

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27
Q

idiopathic pulmonary fibrosis aka

A

cryptogenic fibrosing alveolitis

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28
Q

cryptogenic fibrosing alveolitis/idiopathic pulmonary fibrosis is

A

fibrosis of the alveolar walls imparing gas exchange

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29
Q

fibrosis of the alveolar walls imparing gas exchange

A

cryptogenic fibrosing alveolitis/idiopathic pulmonary fibrosis

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30
Q

three investigations for suspected lung cancer

A

chest radiograph, CT scan, broncoscopy + biopsy

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31
Q

additional investigation for non small cell

A

PET scan - establish eligibility for curative treatment

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32
Q

PET scan is an additional investigation for which lung cancer

A

non-small cell

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33
Q

PET scan uses

A

18-fluorodeoxygenase which is taken up by neoplastic tissue

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34
Q

2 week lung referral if

A

suspicious chest radiograph or >40 years + unexplained haemoptysis

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35
Q

suspicious chest radiograph or >40 years + unexplained haemoptysis

A

2 week lung referral

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36
Q

urgent 2 week chest radiograph if >40 years + 2 of the following or smoker + 1 of the following

A

cough, fatigue, shortness of breath, chest pain, weight loss, apetite loss

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37
Q

cough, fatigue, shortness of breath, chest pain, weight loss, apetite loss should prompt

A

urgent 2 week chest radiograph if >40 years + 2 of the following or smoker + 1 of the following

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38
Q

“consider” urgent 2 week chest radiograph if >40 years and…

A

persistent/recurrent chest infections, clubbing, supraclavicular lymphadenopathy/persistent cervical lymphadenopathy, chest signs, thrombocytosis

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39
Q

persistent/recurrent chest infections, clubbing, supraclavicular lymphadenopathy/persistent cervical lymphadenopathy, chest signs, thrombocytosis should prompt

A

“consideration” of urgent 2 week chest radiograph in >40 years

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40
Q

non-small cell lung cancer management

A

20% eligible for surgery, curative palliative radiotherapy, poor response to chemotherapy

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41
Q

20% eligible for surgery, curative palliative radiotherapy describes management of which lung cancer

A

non-small cell

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42
Q

surgical contraindications for lung cancer resection

A

general health, metastatic disease, FEV1 <1.5L, malignant pleural effusion, tumour near hilum, vocal cord paralysis, superior vena cava obstruction

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43
Q

general health, metastatic disease, FEV1 <1.5L, malignant pleural effusion, tumour near hilum, vocal cord paralysis, superior vena cava obstruction are contraindications for

A

lung cancer surgical resection

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44
Q

recurent laryngeal nerve supplies

A

vocal cords

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45
Q

vocal cords supplied by

A

recurrent laryngeal nerve

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46
Q

recurrent laryngeal nerve damage leads to

A

hoarse voice, difficulty breathing

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47
Q

hoarse voice/difficulty breathing can be caused by

A

recurrent laryngeal nerve/vocal cords damage

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48
Q

superior laryngeal nerve supplies

A

cricothyroid

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49
Q

cricothyroid responsible for

A

voice pitch

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50
Q

voice pitch controlled by

A

cricothyroid

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51
Q

cricothyroid supplied by

A

superior laryngeal nerve

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52
Q

complications of lung cancer

A

superior vena cava obstruction, Horner’s, rib errosion, pericarditis, atrial fibrillation, metastases, ectopic hormone producion

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53
Q

lung metastasises to

A

bone, brain, liver, adrenals

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54
Q

superior vena cava obstruction, Horner’s, rib errosion, pericarditis, atrial fibrillation, metastases, ectopic hormone producion are complications of

A

lung cancer

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55
Q

bone, brain, liver, adrenals sites of metastases for

A

lung cancer

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56
Q

2 week ENT referral for

A

persistent unexplained hoarseness of voice, unexplained neck lump

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57
Q

persistent unexplained hoarseness of voice, unexplained neck lump warrants

A

2 week ENT referral

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58
Q

acanthosis nigricans

A

symmetrical brown velvety plaques often found on neck, axilla, groid

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59
Q

symmetrical brown velvety plaques often found on neck, axilla, groid

A

acanthosis nigricans

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60
Q

acanthosis nigricals is associated with

A

gastrointestinal adenocarcinomas, diabetes mellitus, obesity, polycystic ovary syndrome, acromegaly, Cushing’s, hypothyroidism, familial, Prader-Willi syndrome, oral contraceptive pill, nicotinic acid

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61
Q

gastrointestinal adenocarcinomas, diabetes mellitus, obesity, polycystic ovary syndrome, acromegaly, Cushing’s, hypothyroidism, familial, Prader-Willi syndrome, oral contraceptive pill, nicotinic acid

A

associated with acanthosis nigricans

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62
Q

type of pleural effusion asociated with neoplasm

A

exudative, >30g/L protein (lung cancer, mesothelioma, metastases)

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63
Q

malignancies causing syndrome of innapropriate ADH

A

small cell lung, pancreas, prostate

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64
Q

small cell lung, pancreas, prostate can all cause

A

syndrome of innapropriate ADH production

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65
Q

SIADH biochemistry

A

hyponatraemia, low plasma osmolality, high urine osmololity (retained H2O leads to dilution of blood and concentration of urine)

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66
Q

hyponatraemia, low plasma osmolality, high urine osmololity

A

SIADH

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67
Q

myeloma mneumonic

A

CRAB: hypercalcaemia, renal failure, anaemia (pancytopaenia), bone pain

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68
Q

rouleaux formation

A

stacking of RBC on blood film = myleoma

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69
Q

stacking of RBC on blood film

A

rouleaux formation

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70
Q

multiple myeloma

A

plasma cell neoplasm in bone marrow, 60-70 year olds, bone disease (bone pain, osteoporosis, pathological fractures (vertebral), osteolytic lesions), lethargy, infection, hypercalcaemia, renal failure

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71
Q

plasma cell neoplasm in bone marrow, 60-70 year olds, bone disease, lethargy, infection, hypercalcaemia, renal failure

A

multiple myeloma

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72
Q

investigations for multiple myeloma

A

monoclonal serum proteins (IgG or IgA), urine Bence Jones protein, bone marrow, whole body MRI (bone lesions)

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73
Q

monoclonal serum proteins, urine Bence Jones protein, bone marrow, whole body MRI are investigations for

A

multiple myeloma

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74
Q

multiple myeloma diagnostic requirements

A

1 major + 1 minor or 3 minor with signs/symptoms

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75
Q

1 major + 1 minor or 3 minor with signs/symptoms are dfiagnostic criteria for

A

multiple myeloma

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76
Q

major diagnostic criteria for multiple myeloma

A

plasmacytoma, 30% plasma proteins in bone marrow, high M protein in blood/urine

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77
Q

plasmacytoma, 30% plasma proteins in bone marrow, high M protein in blood/urine

A

major diagnostic criteria for multiple myeloma

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78
Q

minor diagnostic criteria for multiple myeloma

A

10-30% plasma cells on bone marrow, minor increase in M protein in blood/urine, osteolytic lesions, low antibody

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79
Q

plasmacytoma

A

discrete solitary mass of neoplastic monoclonal plasma cells in bone or soft tissue

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80
Q

discrete solitary mass of neoplastic monoclonal plasma cells in bone or soft tissue

A

plasmacytoma

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81
Q

10-30% plasma cells on bone marrow, minor increase in M protein in blood/urine, osteolytic lesions, low antibody

A

minor diagnostic criteria for multiple myeloma

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82
Q

CA125

A

monoclonal antibody for ovarian cancer (+? elevated in cholangiocarcinoma)

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83
Q

monoclonal antibody for ovarian cancer

A

CA125

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84
Q

CA19-9

A

monoclonal antibody for pancreatic cancer (+ 80% of cholangiocarcinomas)

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85
Q

monoclonal antibody for pancreatic cancer

A

CA19-9

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86
Q

CA15-3

A

monoclonal antibody for breast cancer

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87
Q

monoclonal antibody for breast cancer

A

CA15-3

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88
Q

PSA

A

tumour antigen for prostate cancer

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89
Q

tumour antigen for prostate cancer

A

PSA (prostate specific antigen)

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90
Q

AFP (alpha-fetoprotein)

A

tumour antigen for hepatocellular cancer + teratomas/germ cell tumours e.g. testicular

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91
Q

tumour antigen for hepatocellular cancer + teratomas

A

AFP (alpha-fetoprotein)

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92
Q

CEA (carcinoembryonic antigen)

A

tumour antigen for colorectal cancer (+ ?elevated in cholangiocarcinoma)

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93
Q

tumour antigen for colorectal cancer

A

CEA (carcinoembryonic antigen)

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94
Q

S-100

A

tumour antigen for melanoma + schwannomas

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95
Q

tumour antigen for melanoma + schwannomas

A

S-100

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96
Q

bombesin

A

tumour antigen for small cell lung cancer, gastric cancer + neuroblastoma

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97
Q

tumour antigen for small cell lung cancer, gastric cancer + neuroblastoma

A

bombesin

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98
Q

commonest causes of hepatocellular carcinoma

A

hepatitis B and C infection

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99
Q

hepatitis B and C infection are the commonest cause of what cancer

A

hepatocellular

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100
Q

risk factors for hepatocellular carcinoma

A

cirrhosis (secondary to hepatitis B/C, alcohol, haemachromatosis, primary billiary cholangitis), alpha-1-antitrypsin deficiency, hereditary tyrosinosis, glycogen storage disorder, aflatoxin, oral contraceptive pill, anabolic steroids, porphyria cutanea tarda, male sex, diabetes mellitus, metabolic syndrome

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101
Q

primary biliary cholangitis aka

A

primary biliary cirrhosis

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102
Q

cirrhosis, alpha-1-antitrypsin deficiency, hereditary tyrosinosis, glycogen storage disorder, aflatoxin, oral contraceptive pill, anabolic steroids, porphyria cutanea tarda, male sex, diabetes mellitus, metabolic syndrome are risk factors for what cancer

A

hepatocellular

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103
Q

primary biliary cirrhosis aka

A

primary biliary cholangitis

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104
Q

primary biliary cholangitis/cirrhosis

A

autoimmune destrucion of small bile ducts leading to cholestasis, leading to fatigue, pruitis and jaundice

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105
Q

autoimmune destrucion of small bile ducts leading to cholestasis, leading to fatigue, pruitis and jaundice

A

primary biliary cholangitis/cirrhosis

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106
Q

aflatoxin

A

poisonous carcinogen produced by certain moulds (causes HCC)

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107
Q

poisonous carcinogen produced by certain moulds

A

aflatoxin (causes HCC)

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108
Q

polyphoria cutanea tarda

A

blistering of sun exposed skin

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109
Q

blistering of sun exposed skin

A

polyphoria cutanea tarda

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110
Q

hepatocellular carcinoma presentation

A

often late, jaundice, ascites, RUQ pain, hepatomegaly, splenomegaly, pruitis

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111
Q

jaundice, ascites, RUQ pain, hepatomegaly, splenomegaly, pruitis are presentations of

A

hepatocellular carcinoma

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112
Q

screening for hepatocellular carcinoma is offerend to

A

people with liver cirrhosis secondary to hepatitis B/C or haemachromatosis or alcohol (males)

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113
Q

people with liver cirrhosis secondary to hepatitis B/C or haemachromatosis or alcohol (males) are entitles to

A

screening for hepatocellular carcinoma

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114
Q

management of hepatocellular carcinoma

A

surgery, transplantation, radiofrequency ablation, transarterial chemoembolisation, sorafenib (multikinase inhibitor)
DON’T BIOPSY! risk of seeding

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115
Q

surgery, transplantation, radiofrequency ablation, transarterial chemoembolisation, sorafenib is the management of

A

hepatocellular carcinoma

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116
Q

liver primaries make up what percentage of liver malignancies

A

5%

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117
Q

cholangiocarcinoma

A

bile duct neoplasm, jaundiuce

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118
Q

you shouldn’t biopsy

A

suspected hepatocellular carcinoma for risk of seeding

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119
Q

bile duct neoplasm, jaundiuce

A

cholangiocarcinoma

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120
Q

risk factors fo cholangioncarcinoma

A

primary sclerosing cholangitis/sclerosis, typhiod, liver flukes

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121
Q

primary sclerosing cholangitis/sclerosis, typhiod, liver flukes are risk factors for

A

cholangiocarcinoma

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122
Q

Pemberton sign

A

PT to raises arms until they touch side of face, cyanosis/worsening SOB = +ve test

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123
Q

PT to raises arms until they touch side of face, cyanosis/worsening SOB = +ve test

A

Pemberton’s sign

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124
Q

PSA can be falsely elevated by

A

BPH, prostatitis, UTI, ejaculation, vigorous exercise, urinary retention, instrumentation of the urinary tract, prostate biopsy, DRE

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125
Q

BPH, prostatitis, UTI, ejaculation, vigorous exercise, urinary retention, instrumentation of the urinary tract can cause, prostate biopsy, DRE

A

false elevation of PSA

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126
Q

causes of a superior vena cava obstruciton

A

non-small cell lung cancer, lymphoma, metastatic seminoma, Kaposi’s sarcoma, breast cancer, aortic aneurysm, mediastinal fibrosis, goitre, SVC thrombosis

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127
Q

non-small cell lung cancer, lymphoma, metastatic seminoma, Kaposi’s sarcoma, breast cancer, aortic aneurysm, mediastinal fibrosis, goitre, SVC thrombosis are all potential causes of

A

SVCO

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128
Q

SVCO management

A

dexamethasone, balloon venoplasty, stenting, chemotherapy, radiotherapy

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129
Q

dexamethasone, balloon venoplasty, stenting, chemotherapy, radiotherapy to manage

A

SVCO

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130
Q

aniline dyes

A

carcinogen, causes transitional cell carcinoma of the bladder

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131
Q

carcinogen, causes transitional cell carcinoma of the bladder

A

aniline dye

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132
Q

asbestos

A

causes mesothesioma and bronchial carcinoma

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133
Q

causes mesothesioma and bronchial carcinoma

A

asbestos

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134
Q

nitrosamines

A

carcinogen used in the manufacture of cosmetics, pesticides + rubber produciton causing oesophageal and gastric cancer

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135
Q

carcinogen causing oesophageal and gastric cancer

A

nitrosamine

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136
Q

vinyl chloride

A

carcinogen used in the manufacture of PVC causing hepatic angiosarcoma

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137
Q

carcinogen causing hepatic angiosarcoma

A

vinyl chloride

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138
Q

normal range for PSA

A

<4

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139
Q

<4

A

normal range for PSA

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140
Q

PSA can be falsely elevated by

A

BPH, prostatitis, UTI, ejaculation, vigorous exercise, urinary retention, instrumentation of the urinary tract

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141
Q

BPH, prostatitis, UTI, ejaculation, vigorous exercise, urinary retention, instrumentation of the urinary tract can cause

A

false elevation of PSA

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142
Q

wait how long after UTI/prostatitis treatment to measure PSA

A

1 month

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143
Q

wait 1 month to measure PSA after

A

UTI/prostatitis treatment

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144
Q

wait how long after ejaculation/vigorous exercise to measure PSA

A

48 hours

145
Q

wait 48 hours to measure PSA after

A

ejaculation/vigorous exercise

146
Q

Gleasdon score

A

used to grade prostate cancer, graded 3-5 based on the characteristics of the two most prevelent cell type e.g. 3+3 is lowest grade

147
Q

score used to grade prostate cancer

A

Gleasdon score

148
Q

prostate cancer is usually an

A

adenocarcinoma

149
Q

rish factors for developing prostate cancer

A

age, obesity, Afro-Caribean origin, family history

150
Q

age, obesity, Afro-Caribean origin, family history are risk factors for developing

A

prostate cancer

151
Q

prostate cancer tends to originate in what part of the prostate

A

periphery > centrally therefore can be asymptomatic as obstruction symptoms don’t develop until the tumour size is advanced

152
Q

symptoms of prostate cancer

A

asymptomatic, obstruciton, haematuria, haematospermia, pain

153
Q

asymptomatic, obstruciton, haematuria, haematospermia, pain could be symptoms of

A

prostate cancer

154
Q

hormone therapy for prostate cancer includes

A

synthetic GNRH agonist (goserelin/Zoladex), antiandrogen (cyproterone acetate)

155
Q

locally advanced prostate cancer is T…

A

T3/T4

156
Q

flutamide should be used as pretreatment for

A

goserelin in hormone therapy for prostate cancer

157
Q

active monitoring, watchful waiting, radical prostatectomy, external beam radiotherapy, brachytherapy are management options for

A

T1/T2 prostate cancer

158
Q

management options for T3/T4 prostate cancer

A

hormone therapy, radical prostatectomy, external bean radiotherapy, brachytherapy

159
Q

hormone therapy, radical prostatectomy, external bean radiotherapy, brachytherapy are management options for

A

T3/T4 prostate cancer

160
Q

management options for metastatic prostate cancer

A

medical/surgical castration

161
Q

medical/surgical castration is the management of

A

metastatic prostate cancer

162
Q

watchful waiting in prostate cancer is suitable for

A

elderly patients, multiple comorbidities, low Gleason score

163
Q

elderly patients, multiple comorbidities, low Gleason score are suitable for

A

watchful waiting

164
Q

active surveillance in prostate cancer is suitable for

A

stage T1c, 3+3, PSA density <0.15, cancer in <50% of 10 biopsies (+ at least 1 rebiopsy) with <10mm of any core involved

165
Q

stage T1c, 3+3, PSA density <0.15, cancer in <50% of 10 biopsies (+ at least 1 rebiopsy) with <10mm of any core involved patients are suitable for

A

active surveillance

166
Q

radiotherapy side effects in prostate cancer

A

radioation proctitis, rectal malignancy

167
Q

radioation proctitis, rectal malignancy are side effects of

A

radiotherapy in prostate cancer

168
Q

side effects of a radical prostatectomy

A

erectile dysfunction

169
Q

erectile dysfunction is a side effect of

A

a radical prostatectomy

170
Q

hormone therapy for prostate cancer includes

A

synthetic GNRH agonist (goserelin/Zoladex), antiandrogen (cyproterone acetate)

171
Q

when commencing goserelin treatment pretreat with

A

flutamide (antiandrogen) to prevent initial flair of prostate cancer symptoms when commencing on a GNRH agonist

172
Q

flutamide should be used as pretreatment for

A

goserelin in hormone therapy for prostate cancer

173
Q

wait how long after prostate biopsy to do a PSA

A

6 weeks

174
Q

wait 6 weeks to measure PSA after

A

prostate biopsy

175
Q

wait how long after DRE to do PSA

A

1 week

176
Q

wait 1 week to measure PSA after

A

DRE

177
Q

3 weeks concurrent treatment with goserelin

A

cyproterone acetate (antiandrogen) to prevent tumour flare

178
Q

cyproterone acetate is prescribed for how long in hormonal management of prostate cancer

A

3 weeks concurrently with goserelin, start 3 days before

179
Q

thrombocytosis

A

high platelets

180
Q

high platelets

A

thrombocytosis

181
Q

two main origin cell types of breast cancer

A

ductal and lobar

182
Q

ductal and lobar describe the

A

cell type origin of the two most common breast cancers

183
Q

ductal and lobar can then be further divided into

A

in situ and invasive disease

184
Q

tumours compatible with wide local excision

A

solitary lesions, peripheral tumours, small lesion in large breasts, DCIS <4cm, PT choice

185
Q

solitary lesions, peripheral tumours, small lesion in large breasts, DCIS <4cm, PT choice are indications for

A

wide local excision

186
Q

tumours compatible with a mastectomy

A

multifocal tumours, central tumours, large lesion in small breast, DCIS >4cm, PT choice

187
Q

multifocal tumours, central tumours, large lesion in small breast, DCIS >4cm, PT choice are indications for

A

mastectomy

188
Q

breast cancer risk factors

A

BRCA (40% lifetime risk of breast/ovarian), 1st degree premenopausal relative, nuliparity, 1st pregnancy >30, early menarche, late menopause, HRT, COCP, previous breast cancer, not breastfeeding, ionising radiation, p53 gene mutation, obesity, previous surgery for benign breast lesion

189
Q

BRCA (40% lifetime risk of breast/ovarian), 1st degree premenopausal relative, nuliparity, 1st pregnancy >30, early menarche, late menopause, HRT, COCP, previous breast cancer, not breastfeeding, ionising radiation, p53 gene mutation, obesity, previous surgery for benign breast lesion

A

breast cancer risk factors

190
Q

Nottingham prognostic index

A

indication of survival using tumour size, LN, grade

191
Q

indication of survival (breast cancer) using tumour size, LN, grade

A

Nottingham prognostic index

192
Q

two types of breast reconstruction

A

latissimus dorsi, subpectoralis implants

193
Q

latissimus dorsi, subpectoralis implants

A

types of breast reconstructive surgery

194
Q

breast cancer screening programme

A

women 47-73, 3 yearly mammogram

195
Q

hormone therapies

A
tamoxifen (pre and perimenopausal women), increase risk of endometrial cancer, VTE, menopausal symptoms
aromatase inhibitors (postmenopausal women)
196
Q

tamoxifen and aromatase inhibitors

A

hormone therapies for breast cancer

197
Q

biological therapy

A

herceptin for HER2 positive breast cancers

198
Q

herceptin

A

biological breast cancer treatment for HER2 positive tumours

199
Q

most common type of breast cancer

A

invasive ductal carcinoma aka NST no special type

200
Q

NST

A

no special type = invasive ductal carcinoma

201
Q

Modified Bloom + Richardson

A

grading system for breast cancer

202
Q

grading system for breast cancer

A

Modified Bloom + Richardson

203
Q

anastrozole

A

aromatase inhibitor

204
Q

aromatase inhibitor

A

anastrozole

205
Q

ovarian cancer risk factors

A

family history, BRCA, early menarche, late menopause, nuliparity
COCP is protective

206
Q

family history, BRCA, early menarche, late menopause, nuliparity
COCP is protective

A

ovarian cancer risk factors

207
Q

CA125 can be falsely elevated due to

A

endometriosis, benign ovarian cyst

208
Q

CA125 should be performed if

A

abdominal distension, bloating, early satiety, loss of appetite, pelvic/abdominal pain, increased urinary urgency +/ frequency

209
Q

abdominal distension, bloating, early satiety, loss of appetite, pelvic/abdominal pain, increased urinary urgency +/ frequency

A

do a CA125

210
Q

ovarian cancer staging

A

stage 1 = tumour confined to ovary
stage 2 = tumour outside ovary, but within pelvis
stage 3 = tumour outside pelvis but within abdomen
stage 4= distant metastasis

211
Q

bladder cancer risk factors

A

smoking (even up to 20 years after quitting), hydrocarbons, aniline dye, rubber production, cyclophosphamide

212
Q

smoking (even up to 20 years after quitting), hydrocarbons, aniline dye, rubber production, cyclophosphamide are risk factors for

A

bladder cancer

213
Q

bladder cancer TNM staging

A
T1 = subepithelial connective tissue, T2 = muscularis propria, T3 = perivesicular fat, T4 = further invasion
N1 = single regional LN in true pelvis, N2 = multiple regional LN in true pelvis, N3 = common iliac LN
M1 = metastasis
214
Q

true pelvis

A

space between pelvic inlet and pelvic outlet

215
Q

space between pelvic inlet and pelvic outlet

A

true pelvis

216
Q

inflammatory breast cancer

A

progressive erythema, odema, in the absence of infection

217
Q

breast: progressive erythema, odema, in the absence of infection

A

inflammatory breast cancer

218
Q

T1/T2 prostate cancer is

A

local disease

219
Q

T3/T4 prostate cancer is

A

locally advanced

220
Q

CML symptoms

A

young PT, fatigue, weight loss, early satiety, splenomegaly, leucocytosos (basophils, eosinophils), night sweats, LUQ pan (splenic infarction), hepatomegaly, easy bruising, lymphadenopathy

221
Q

young PT, fatigue, weight loss, early satiety, splenomegaly, leucocytosos (basophils, eosinophils), night sweats, LUQ pan (splenic infarction), hepatomegaly, easy bruising, lymphadenopathy are symptoms of

A

CML

222
Q

CML is

A

a myeloproliferative DZ, of pluripotent haemopoietic stem cells, >90% of cases caused by Philadelphia ch

223
Q

a myeloproliferative DZ, of pluripotent haemopoietic stem cells, >90% of cases caused by Philadelphia ch

A

CML

224
Q

AML is

A

BM malignancy where blood cell precursors are arrested in an early stage of development, continue to proliferate w/i BM leading to pancytopaenia

225
Q

PTs who have received an organ transplant are at risk of what type of ca

A

skin, particularly SCC, due to long term immunosuppression, therefore should avoid sun exposure

226
Q

cyclophasphamide SE

A

haemorrhagic cystitis, myelosuppression, TCC

227
Q

bleomycin SE

A

L fibrosis

228
Q

doxorubicin SE

A

cardiomyopathy

229
Q

methotrexate SE

A

myelosuppression, mucositis, liver fibrosis, L fibrosis

230
Q

fluorouracil (5-FU) SE

A

myelosuppression, mucositis, dermatitis

231
Q

6-mercaptopurine SE

A

myelosuppression

232
Q

cytarabine SE

A

myelosuppression, ataxia

233
Q

vincristine SE

A

peripheral neuropathy (reversible), paralytic ileus

234
Q

vinblastine SE

A

myelosppression

235
Q

docetaxal SE

A

neutropaenia

236
Q

cisplatin SE

A

ototoxicity, peripheral neuropathy, hypomagnesaemia

237
Q

hydroxyurea/hydroxycarbamide SE

A

myelosuppression

238
Q

common tumours that cause bone mets

A

prostate > breast > L

239
Q

common sites for bone mets

A

spine > pelvis > ribs > skull > long bones

240
Q

schistosomiasis is associated with

A

SCC of the bladder

241
Q

SCC of the bladder is associated with

A

schistosomiasis

242
Q

nasopharyngeal ca is associated with

A

EBV infection

243
Q

EBV infection is associated with

A

nasopharyngeal ca

244
Q

reduce the incidence of haemorrhagic cystitis in cyclophosphamide use

A

hydration + mesna

245
Q

ABL is associated with

A

CML

246
Q

c-MYC is associated with

A

Burkitt’s lymphoma

247
Q

n-MYC is associated with

A

neuroblastoma

248
Q

BCL-2 is associated with

A

follicular lymphoma

249
Q

RET is associated with

A

MEN types II + III

250
Q

RAS is associated with

A

many ca, esp pancreatic

251
Q

erb-B2/HER2/neu is associated with

A

breast, ovarian ca

252
Q

CML gene mutation

A

ABL

253
Q

Burkitt’s lymphoma gene mutation

A

c-MYC

254
Q

neuroblastoma gene mutation

A

n-MYC

255
Q

follicular lymphoma gene mutation

A

BCL-2

256
Q

MEN types II + III gene mutation

A

RET

257
Q

breast/ovarian ca gene mutation

A

erb-B2/HER2/neu

258
Q

ALL is the most common malignancy among

A

children

259
Q

peak incudence of ALL

A

2-5 y.o.

260
Q

features of ALL

A

anaemia (lethargy, pallor), neutropaenia (f/severe infections), thrombocytopaenia (easy bruising, petechiae), bone pain (2’ to BM infiltration), hepatosplenomegaly, testicular swelling

261
Q

Wilms’ tumour is

A

most common renal tumour in children

262
Q

features of Wilms’ tumour

A

abdo mass, painless haematuria, flank pain, anorexia, fever, ux

263
Q

Wilms’ tumour management

A

nephrectomy, chemotherapy, radiotherapy

264
Q

prognosis in Wilms’ tumour

A

good

265
Q

common sites of CRC

A

rectal > signmoid > descending colon > transverse colon > ascending colol + caecum

266
Q

CRC screening program

A

2 yearly FOBT for men + women 60-74, via post, abnormal results have colonoscopy

267
Q

types of CRC

A

sporadic (95%), HNPCC, FAP

268
Q

HNPCC is

A

an autosomal dominant condition, poorly differentiated, highly aggressive CRC, also at risk of endometrial ca

269
Q

criteria used to indicate HNPCC

A

Amsterdam criteria

270
Q

Amsterdam criteria consists of

A

3 family members with CRC, over 2 generations, 1 of which <50 y.o.

271
Q

FAP is

A

a rare autosomal dominant condition which leads to the formation of hundereds of polyps by 30-40 y.o., ineviatably develop carcinoma

272
Q

guidelines for 2/52 referral to colorectal services

A

> 40 y.o. + unexplained weight loss + abdo pain
50 y.o. + unexplained PR bleeding
60 y.o. + Fe deficiency anaemia or change in bowel habits
+ve FOBT

273
Q

consider 2/52 referral to colorectal services if

A

PR/abdo mass, unexplained anal mass/ulceration, <50 y.o. + PR bleeding + abdo pain/change in bowel habits/weight loss/Fe deficiency anaemia

274
Q

FOBT should be offered to

A

> 50 y.o. + unexplained abdo pain or weight loss
<60 y.o. + change in bowel habit or Fe deficiency anaemia
60 y.o. + anaemia

275
Q

how to stage for CRC

A

CT CAP, colonoscopy/CT colonography, ?MRI rectum

276
Q

CRC management

A

Sx, chemotherapy, neoadjuvent RT (rectal ca), palliation (stents, bypass, diversion stomas)

277
Q

Sx for caecal, ascending, proximal transverse CRC

A

R hemicollectomy

278
Q

Sx for distal transverse, desceding CRC

A

L hemicollectomy

279
Q

Sx for sigmoid CRC

A

high ant resection

280
Q

Sx for rectal CRC

A

ant resection

281
Q

Sx for anal verge CRC

A

abdo-perineal excesion of rectum

282
Q

an autosomal dominant condition, poorly differentiated, highly aggressive CRC, also at risk of endometrial ca describes

A

HNPCC

283
Q

Amsterdam criteria is used to indicate

A

HNPCC

284
Q

3 family members with CRC, over 2 generations, 1 of which <50 y.o. are the criteria for

A

Amsterdam criteria

285
Q

a rare autosomal dominant condition which leads to the formation of hundereds of polyps by 30-40 y.o., ineviatably develop carcinoma describes

A

FAP

286
Q

> 40 y.o. + unexplained weight loss + abdo pain
50 y.o. + unexplained PR bleeding
60 y.o. + Fe deficiency anaemia or change in bowel habits
+ve FOBT

A

require 2/52 referral to colorectal services

287
Q

PR/abdo mass, unexplained anal mass/ulceration, <50 y.o. + PR bleeding + abdo pain/change in bowel habits/weight loss/Fe deficiency anaemia

A

consider 2/52 colorectal services referral

288
Q

> 50 y.o. + unexplained abdo pain or weight loss
<60 y.o. + change in bowel habit or Fe deficiency anaemia
60 y.o. + anaemia

A

offer FOBT

289
Q

R hemicollectomy is used to resect

A

caecal, ascending, proximal transverses CRC

290
Q

L hemicollectomy is used to resect

A

distal transverse, descending CRC

291
Q

high ant resection is used to resect

A

sigmoid CRC

292
Q

ant resection os used to resect

A

rectal CRC

293
Q

abdo-perineal excision of rectum is used to resect

A

anal verge CRC

294
Q

gastric ca peak age

A

60-70 y.o.

295
Q

gastric ca most common in which countries

A

Japan, China, Finland, Colombia

296
Q

gastric ca on histology

A

signet ring cells

297
Q

gastric ca associations

A

H. pylori infection, blood group A, gastric adenomatous polyps, pernicious anaemia, smoking, salty, spicy, nitrate-rich diet

298
Q

gastric ca features

A

dyspepsia, N, V, anorexia, weight loss, dysphagia

299
Q

gastric ca investigations

A

endoscopy + biopsy, CT/endoscopic US, laparoscopy, PET CT

300
Q

gastric ca management

A

Sx, lymphadenectomy, chemo

301
Q

signet ring cells seen on histology indicate

A

gastric ca

302
Q

H. pylori infection, blood group A, gastric adenomatous polyps, pernicious anaemia, smoking, salty, spicy, nitrate-rich diet are associated with

A

gastric ca

303
Q

dyspepsia, N, V, anorexia, weight loss, dysphagia are features of

A

gastric ca

304
Q

types of oesophageal ca

A

adenocarcinoma, squamous cell carcinoma

305
Q

risk factors for oesophageal ca

A

smoking, EtOH, GORD, Barrett’s oesophagus, achalasia, Plummer-Vinson S

306
Q

features of oesophageal ca

A

dysphagia, anorexia, weight loss, V, odynophagia, hoarseness, melaena, cough

307
Q

odynophagia

A

pain on swallowing food

308
Q

oesophageal ca investigations

A

endoscopy, CT CAP, laproscopy, PET CT

309
Q

oesophageal ca management

A

Sx, chemo, palliation

310
Q

smoking, EtOH, GORD, Barrett’s oesophagus, achalasia, Plummer-Vinson S are risk factors for

A

oesophageal ca

311
Q

dysphagia, anorexia, weight loss, V, odynophagia, hoarseness, melaena, cough are features of

A

oesophageal ca

312
Q

pain on swallowing food

A

odynophagia

313
Q

AML features

A

anaemia, pallor, lethagy, neutropenia (ECC may be high, functioning neutrophils low), f infections, thrombocytopenia, bleeding, splenomegaly, bone pain

314
Q

poor prognostic features for AML

A

> 60 y.o., >20% blast cells after 1st course of chemo, ch 5 or 7 dels

315
Q

Burkitt’s lymphoma is

A

a high grade B-cell neoplasm

316
Q

two forms of Burkitt’s lymphoma

A

sproadic = abdo, endemic (African) = maxilla + mandible

317
Q

sporadic Burkitt’s lymphoma is > common in PTs with

A

HIV

318
Q

endemic/African form of Burkitt’s lymphona is associated with

A

EBV infection

319
Q

Burkitt’s lymphoma on microscopy

A

‘stary sky’ apearance

320
Q

management of Burkitt’s lymphoma

A

chemo

321
Q

risk associated with treating Burkitt’s lymphoma

A

tumour lysis S

322
Q

complications of tumour lysis S

A

hyperkalaemia, hyperphosphataemia, hypocalcaemia, hyperuricaemia, acute renal failure

323
Q

CLL is caused by

A

monoclonal proliferation of well differentiated lymphocytes which are almost always B-cells

324
Q

features of CLL

A

asymptomatics, anorexia, weight loss, bleeding, infection, lymphadenopathy

325
Q

complications of CLL

A

hypogammaglobulinaemia leading to recurrent infections, warm AI haemolytic anaemia, transformation to high grade lymphoma

326
Q

CLL investigations

A

blood film, immunophenotyping

327
Q

CLL on blood film

A

smudge cells

328
Q

CLL transformation to high grade lymphoma aka

A

Richter’s transformaiton

329
Q

indications that Richter’s transformaiton has happened

A

LN swelling, fever w/o infeciton, weight loss, night sweats, N, abdo pain

330
Q

Hodgkin’s lymphoma is characterised by the presence of

A

Reed-Sternberg cells

331
Q

features of HL

A

lymphadenopathy (painless, non-tender, asymetrical), weight loss, pruitis, night sweats, fever, alcohol pain, normocytic anaemia, eosinophillia, raised LDH

332
Q

HL staging

A

CT CAP

333
Q

management of HL

A

chemo, radiotherapy

334
Q

HL is linked to

A

EBV infeciton

335
Q

myelodysplasia is

A

acquired neoplastic disorder of haematopoietic SC, pre-leukaemia, may progress to AML

336
Q

myelodysplasia presentation

A

anaemia, neutropaenia, thrombocytopenia

337
Q

anaemia, pallor, lethagy, neutropenia (ECC may be high, functioning neutrophils low), f infections, thrombocytopenia, bleeding, splenomegaly, bone pain are features of

A

AML

338
Q

a high grade B-cell neoplasm describes

A

Burkitt’s lymphoma

339
Q

‘stary sky’ apearance on microscopy

A

Burkitt;s lymphoma

340
Q

monoclonal proliferation of well differentiated lymphocytes which are almost always B-cells

A

CLL

341
Q

asymptomatics, anorexia, weight loss, bleeding, infection, lymphadenopathy are features of

A

CLL

342
Q

hypogammaglobulinaemia leading to recurrent infections, warm AI haemolytic anaemia, transformation to high grade lymphoma are complications of

A

CLL

343
Q

smudge cells on blood film

A

CLL

344
Q

Richter’s transformaiton is when

A

CLL transforms to a high grade lymphoma

345
Q

LN swelling, fever w/o infeciton, weight loss, night sweats, N, abdo pain are features of

A

Richter’s transformation

346
Q

Reed-Sternberg cells are characteristic of

A

HL

347
Q

lymphadenopathy (painless, non-tender, asymetrical), weight loss, pruitis, night sweats, fever, alcohol pain, normocytic anaemia, eosinophillia, raised LDH are features of

A

HL

348
Q

acquired neoplastic disorder of haematopoietic SC, pre-leukaemia, may progress to AML describes

A

myelodysplasia

349
Q

anaemia, neutropaenia, thrombocytopenia describes the presentaiton of

A

myelodysplasia

350
Q

Waldenstrom’s macroglobulinaemia is

A

uncommon, lymphoplasmacytoid malignancy, characterised by the secretion of IgM

351
Q

features of Waldenstrom’s macroglobulinaemia

A

monoclonal IgM paraproteinaemia, weight loss, lethargy, visual disturbances, hepatosplenomegaly, lymphadenopathy, Raynaud’s

352
Q

uncommon, lymphoplasmacytoid malignancy, characterised by the secretion of IgM

A

Waldenstrom’s macroglobulinaemia

353
Q

monoclonal IgM paraproteinaemia, weight loss, lethargy, visual disturbances, hepatosplenomegaly, lymphadenopathy, Raynaud’s are features of

A

Waldenstrom’s macroglobulinaemia

354
Q

NHL presentation

A

55-60 y.o., painless widespread lymphadenopathy, raised LDH, paraprotein, AIHA

355
Q

most common form of NHL

A

diffuse large b cell lymphoma

356
Q

55-60 y.o., painless widespread lymphadenopathy, raised LDH, paraprotein, AIHA describes the presentation of

A

NHL

357
Q

Reed-Sternberg cells look like

A

large multinucleated cells with prominent eosinophilic nucleoli

358
Q

poor prognosis is HL associated with

A

weight loss (>10% in 6/12), fever (>30’c), night sweats