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year 4 CDM 2 > Case 17: gastric and complications > Flashcards

Case 17: gastric and complications Flashcards

1
Q

Investigations gastric cancer

A
  • FBC, LFT
  • diagnosis: endoscopy (gastroscopy) with biopsy
  • staging: CT or endoscopic ultrasound - endoscopic ultrasound has recently been shown to be superior to CT
  • Diffuse gastric cancer on biopsy: signet ring cells
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2
Q

Staging: gastric caner

A
  • CT scanning of the chest abdomen and pelvis is the routine first line staging investigation in most centres.
  • Laparoscopy to identify occult peritoneal disease
  • PET CT (particularly for junctional tumours)
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3
Q

Surgery: gastric cancer

A
  • Partial gastrectomy: Removal of a portion of the stomach, suitable for early-stage, localized tumours
  • Total gastrectomy: Removal of the entire stomach, often necessary for larger or more advanced tumours
  • Lymph node dissection (D1 or D2) should be performed according to tumour stage and location. Minimally invasive techniques, such as laparoscopic or robotic-assisted surgery, may be considered for selected cases.
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4
Q

Indications for different types of gastrectomy and curative treatment for gastric cancer

A
  • Total: tumour is proximal
  • Subtotal: if tumour is antral or treatment is palliative, especially if obstructing

Curative treatment of gastric cancer: gastrectomy plus lymphadenectomy with chemo pre/post op

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5
Q

Chemotherapy gastric cancer

A
  • Neoadjuvant chemotherapy: Administered before surgery to shrink the tumour and improve resectability +/- radiotherapy
  • Adjuvant chemotherapy: Given after surgery to eradicate residual disease and decrease the risk of recurrence +/- radiotherapy
  • Palliative chemotherapy: for metastatic or unresectable disease to control symptoms and prolong survival +/- radiotherapy
  • Common chemotherapeutic agents include fluoropyrimidines (e.g., 5-fluorouracil, capecitabine), platinum compounds (e.g., cisplatin, oxaliplatin), and taxanes (e.g., paclitaxel, docetaxel).
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6
Q

Targeted therapy: gastric cancer

A
  • Anti-HER2 therapy (e.g., trastuzumab, pertuzumab): Effective for HER2-positive tumours, used in combination with chemotherapy
  • Anti-VEGF therapy (e.g., ramucirumab): Targets vascular endothelial growth factor, employed for advanced or metastatic disease
  • Immune checkpoint inhibitors (e.g., pembrolizumab, nivolumab): Effective in some cases of microsatellite instability-high (MSI-H) or PD-L1-positive tumours
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7
Q

Supportive and Palliative are in gastric cancer

A
  • Nutritional supplementation, pain management, psychological support
  • Consider subtotal gastrectomy, chemo
  • endoscopic pyloric stent (plastic tube through tumour)
  • PPIs for bleeding, ulcerating tumours
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8
Q

Gastric cancer complications

A
  • Obstruction: vomiting, malnutrition,dehydration
  • Perforation, Peritonitis and sepsis
  • Metastasis to the liver, lungs and peritoneam
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9
Q

What can cause lymphadenopahty in the supraclavicilur fossa or axilla

A

What can cause lymphadenopathy in the supraclavicular fossa or axilla: breast, lung, oesophagus and stomach.

Most common caner type found in lymph nodes with unknown primary: adenocarcinoma

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10
Q

How do carcinomas of unknown primary present

A
  • clinical absence of primary tumour
  • often multiple sites of involvement
  • unpredictable metastatic pattern
  • greater aggressiveness
  • Median age: 60
  • % of cancer which are from an unknown primary: 4.5%
  • Median survival: 6-9 months
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11
Q

Poor prognostic factors for carcinoma of unknown primary

A
  • number of metastatic sites
  • male
  • poor performance status
  • weight loss more than 10%l
  • lymph node involvement other than supraclavicular fossa
  • Investigation in unknown primary- biopsy lymph node
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12
Q

Chemosensitive and hormone sensitive tumours

A
  • Chemosensitive tumour: Non-Hodgkin’s lymphoma, Germ cell tumours, Neuroendocrine tumours including Small Cell Lung Cancer, Ovarian cancer
  • Hormone sensitive tumour: Breast cancer, Prostate cancer, Endometrial cancer, Thyroid cancer
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13
Q

5 different causes of unknown primary resulting in squamous cell carcinoma of the cervical nodes

A
  • Breast cancer: women with isolated axillary lymphadenopathy often have an occult breast primary
  • Primary peritoneal cancer: papillary carcinoma with elevated CA-125, laparotomy fails to identify a primary. Treat like stage III ovarian cancer
  • Extragonadal germ cell tumours: in young men with pulmonary or lymph node metastases and germ cell tumour markers (AFP and HCG). Cytogenetic analysis will be positive for isochromosome 12p
  • Neuroendocrine tumour: histologically poorly differentiated. Stains are positive for chronogranin or NSE. Often have diffuse hepatic or bone metastasis
  • Head and neck tumours: treat with radical neck dissection and extended field radiotherapy
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14
Q

Investigations for squamous cell carcinoma in lymph nodes

A
  • Meticulous inspection of scalp and skin for primary tumour
  • Ear nose and throat examination, indirect laryngoscopy ± examination under anaesthesia (EUA) with blind biopsies from nasopharynx & base of tongue
  • CT of chest/abdomen/pelvis (lung, cervix)
  • Upper GI endoscopy (oesophageal and gastric)
  • Colposcopy and cervical smear
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15
Q

Treatment for squamous cell carcinoma in cervical lymph nodes

A
  • Aggressive local therapy to the neck: radical neck surgery, high dose radiotherapy or a combination
  • Chemotherapy with cisplatin and 5-FU can improve response
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16
Q

Investigations for anaplastic carcinoma in cervical nodes

A
  • CXR; sputum cytology (most reliable in small cell lung cancer)
  • Thyroid scan + needle biopsy
  • Nasopharyngeal assessment
  • Consider diagnosis of undifferentiated lymphoma (exclude with immunophenotyping)
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17
Q

Investigations for squamous cell carcinoma in inguinal nodes

A
  • Careful examination of legs, vulva, penis, perineum for primary tumour
  • Pelvic examination (exclude vaginal/cervical cancer)
  • Proctoscopy/colposcopy (exclude anal/cervical cancer)
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18
Q

Investigations for metastatic adenocarcinoma

A
  • Oestrogen receptor (ER) and progesterone receptor (PR) expression by tumour in females
  • Serum prostate specific antigen (PSA) and acid phosphatase in males
  • Serum alpha fetoprotein (AFP) and human chorionic gonadotrophin (HCG) (if positive, histology needs review)
  • Consider diagnosis of poorly differentiated lymphoma, exclude with immunophenotyping
  • Adenocarcinomas in higher nodes and patients with lower lymphadenopathy f any histology have poorer prognosis. Managed with local (radiation therapy)
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19
Q

Unknown primary tumour: areas involved and treatment

A
  • Majority do not have a determined cause and response rate to chemo is <20%
  • 2/3rds of unknown primary cancer have metastatic adenocarcinoma with involvement of two or more visceral sites, including liver, lung, lymph nodes, or bone
  • Treat with empirical systemic chemotherapy based on adriamycin, 5-FU or cisplatin. Little response
  • No treatment for metastatic adenocarcinoma in >2 sites
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20
Q

Histological cause of unknown primary

A

60% are adenocarcinoma, 30% poorly differentiated carcinoma, 5% poorly differentiated neoplasm, 5% squamous cell carcinoma

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21
Q

Histological analysis of unknown primary

A
  • Light microscopy
  • Immunocytochemical staining
  • Surface immunophenotype: done through immunohistochemical/immunofluorescent staining or flow cytometry
  • Electron microscopy: can visualise intracellular features
  • Molecular analysis: can see translocations and gene amplifications
22
Q

Light microscopy results for different unknown primaries

A
  • Signet ring cells (favour gastric primary)
  • Presence of melanin (favour melanoma)
  • Presence of mucin is common in gut/lung/breast/endometrial cancers, less common in ovarian cancer and rare in renal cell or thyroid cancers
  • Presence of Psammoma bodies (calcospherites) is a feature of ovarian cancer (mucin positive) and thyroid cancer (mucin negative)
23
Q

Electron microscope: different cancers

A
  • Melanoma: Melanosomes
  • Neuroendodermal tumours: Dense core granules
  • Adenocarcinoma: intracellular lumina and surface micorvilli
  • Squamous tumours: desmosomes and prekeratin filaments
  • Carcinoids: Neurosecretory granules
24
Q

Patients with unknown primary definition

A

a biopsy-proven malignancy, where the anatomic origin remains unidentified after history and physical examination including laboratory studies

25
Q

Investigations for patients with unknown primary: depends on cause

A
  • Physical examination: careful palpation of the thyroid, breast, lymph node, testicle, bimanual, liver and prostate.
  • Bedside: PR exam, FIT
  • Bloods: FBC, U&E, LFT
  • CXR, CT TAP (thorax, abdomen and pelvis), Mammography
  • Other: sputum cytology, CT chest, breast US or GI endoscopy
26
Q

How unknown primary presents

A
  • Distant metastasis and lymph node involvement without any primary cancer
  • Supraclavicular lymph nodes with squamous cell carcinoma have poor prognosis
  • Common sites involved: Lung, bone, lymph node and liver
27
Q

Symptoms of Hypercalcaemia of malignancy

A
  • pruritus, lethargy and fatigue
  • Rapid onset nausea, polyuria, polydipsia, dehydration, cardiac arrhythmia’s, costipatin
  • ‘bones, stones, groans and psychic moans’
  • Corneal calcification
  • Shortened QT interval on ECG
  • Hypertension
  • Dehydration, Cardiac arrhythmias
28
Q

Different causes of Hypercalcaemia of malignancy

A
  • THrP from the tumour e.g.squamous cell lung cancer. Caused by squamous cell carcinomas in different areas
  • Due to PTH-rP: NSCLC, Head and Neck, Renal, SCC of oesophagus or cervix. Rare in breast cancer, more commonly due to bone metastasis
  • bone metastases
  • myeloma: due primarily to increased osteoclastic bone resorption caused by local cytokines (e.g. IL-1, tumour necrosis factor) released by the myeloma cells
29
Q

Hypercalcaemia management

A
  • Rehydration with normal saline 3-4 litres/day
  • Post rehydration use Bisphosphonates (maximal effects at 7 days)
  • Calcitonin: quicker effect than bisphosphonates
30
Q

Metastatic Hypercalcaemia due to protein production

A
  • True paraneoplastic hypercalcaemia is due to tumour production of parathyroid hormone-related protein
  • PTH-rP produces hypercalcaemia of malignancy without bone metastasis
  • It is 100-fold more potent than PTH
  • 10% of patients with cancer develop hypercalcaemia
31
Q

Paraneoplatic syndrome definition

A

The clinical manifestations of a non metastatic manifestations of an underlying cancer

32
Q

Hypercalcaemia of malignancy diagnosis

A

Serum Ca2+ > 2.7 mmol/l, serum chloride low, hypercalcuria, high urinary phosphate, low or undetectable plasma parathyroid hormone

33
Q

Paraneoplastic syndrome

A
  • Tumours can produce signs and symptoms at sites distant from the primary tumour or its metastases. Not a direct result of the cancer
  • This can be due to substances produces by the tumour causing distant symptoms, depletion of normal substances or host response to the tumour (immunological)
  • May be the first sign of malignancy. Some paraneoplastic proteins are used as tumour markers. Paraneoplastic symptoms can be more distressing then the cancer
  • Range of symptoms include: Endocrine, Haematological, GI, Renal, Cutaneous, Neurological
34
Q

Endocrine manifestation of Paraneoplastic syndrome: ACTH

A
  • Patients with ectopic ACTH syndrome have a much higher ratio of ACTH precursors to endogenous ACTH
  • Overproduction of ACTH precursors: ACTH and MSH, b-lipotropin, endorphins, encephalins, propiomelanocortin (POMC)
  • Cancer types: SCLC (50% of cases of ectopic ACTH), NSCLC, pancreatic, thymic and carcinoid tumours, phaemochromocytoma, medullary carcinomaof the thyroid
  • Rapid onset
  • May develop Cushing’s syndrome: Truncal obesity, hypertension, fatigue, depression, weakness, hirsutism, hypokalaemia, metabolic alkalosis, hyperpigmentation, oedema, diabetes millitus
35
Q

Ectopic ACTH: diagnosis and treatment

A
  • Diagnosis: Clinical features, esp. hyperpigmentation, marked weakness secondary to proximal myopathy. Metabolic disturbances i.e. hypoglycaemia, hypokalaemia and metabolic alkalosis; high 24hr urinary cortisol, high plasma ACTH/precursors, no response to high-dose dexamethasone suppression or corticotropin-releasing hormone stimulation
  • Treatment: Specific anti-tumour treatment. Decrease cortisol secretion either surgically (bilateral adrenalectomy) or medically (octreotide, ketoconazole, aminogluthethamide)
36
Q

Paraneoplatic syndrome inappropriate diuresis

A
  • The most common endocrine paraneoplastic syndrome, due to inappropriate secretion of ADH
  • Results in SIADH
  • Causes are normally pulmonary, CNS, drugs
  • Cancer types: SCLC, pancreatic, prostate, NHL, HD
  • Presentation: often asymptomatic, CNS toxicity (fatigue,headache, progressing to altered mental state, confusion and seizures)
  • Diagnosis: exclude non malignant causes, pulmonary disease and drug induced
  • Treatment: fluid restriction (0.5-1L/day), democlocycline
37
Q

Laboratory criteria for diagnosis of SIAD

A
  • Hyponatremia Na+ <130 mmol/L
  • Normal serum albumin and glucose
  • Serum hypo-osmolarity <275 mosm/Kg
  • Urine osmolarity > serum osmolarity
  • Urinary sodium >25mmol/L
  • Non-suppressed ADH
38
Q

Paraneoplastic syndrome: Gonadotrophins

A
  • Causes raised b-hCG, causes gynaecomastia in men
  • Investigations: testicular exam, CXR/CT scan- exclude lung cancer
  • Secretions occur in pituitary tumours, gestational trophoblastic tumours (women), germ cell tumours, hepatoblastomas in children and lung tumours
  • Extragonadal tumours which secrete b-hCG: lung, adrenal, Hepatoma, GI tract tumours, GU tumours
39
Q

Encephalomyopathies

A
  • Due to antibodies generates against tumour antigens
  • Perivascular inflammation and neuronal degeneration at several levels of the nervous system
  • Can affect the limbic system, brainstem and spinal cord. Loss of neurons in the amygdala, hippocampus and insular cortex gliosis, lymphocyte cuffing of blood vessels, microglial nodules
  • Cancer types: SCLC (75% of cases), breast, ovary, NHL
40
Q

Encephalomyopathies: presentation, diagnosis, treatent

A
  • Presentation: Slow, subacute onset; progressive, loss of short term memory, hallucinations, fits, personality changes
  • Diagnosis: LP- CSF (raised protein/IgG level, pleocytosis), Serum (anti-Hu antibody), MRI
  • Treatment: Anti-tumour therapy (cure cancer). Sometimes even when cancer is treated symptoms persist.
41
Q

Lambert-Eaton myasthenic syndrome

A
  • Disorder of the neuromuscular junction; reduced pre-synaptic calcium-dependent acetylcholine release
  • Similar symptoms to Graves disease
  • About 60% of patients have underlying cancer
  • Cancer types: SCLC (60-70%), breast, thymus, GIT cancers
  • Presentation: Proximal muscle weakness, Classical myaesthenia gravis affects bulbar muscles; LEMS does not, yet 30% will have dysphagia
42
Q

Diagnosis and treatment of LEMS

A
  • Diagnosis: EMG: normal conduction velocity with low amplitude compound muscle action potential that enhance to near normal following exercise
  • Treatment: Cancer treatment, corticosteroids, plasma exchange (high response rate), cholinesterase inhibitors usually ineffective
43
Q

Paraneoplatic syndrome: Dermatomyositis/polymyositis

A
  • Inflammatory myopathies, often present prior to cancer diagnosis
  • Cancer types: NSCLC, SCLC, breast, ovary, GIT cancers, associated with cancer in only 10% of cases
  • Presentation: proximal myopathy, skin changes, other systemic features: cardiopulmonary conditions, arthralgias, retinopathy
  • Skin: heliotrope salmon pink rash surrounding the eyes. Gottron’s papules on the extensor surface of joints, ancanthon nigrans
  • 40% of people with Dermatomyositis have an underlying cancer
44
Q

Parenoplastic syndrome: Dermatomyositis diagnosis and treatment

A
  • Diagnosis: Serum: (high CK, LDH, aldolase). Muscle biopsy (myositis and inflammatory degeneration) EMG (fibrillation, insertion irritability, short polyphasic motor units)
  • Treatment: Search for and treat tumour; corticosteroids, azathioprine, inconsistent course, independent of tumour
  • Progression of skin condition can correlate to cancer course
45
Q

Paraneoplastic syndrome: Haematological manifestations

A
  • Erythrocytosis: can cause polycythaemia
  • Anaemia
  • Granulocytosis/granulocytopenia
  • Thrombocytosis/thrombocytopenia: increased due to inflammation, decreased due to bone marrow infiltration
  • Thrombophlebitis
  • Coagulopathies and disseminated intravascular coagulation
  • Nonbacterial thrombotic endocarditis
46
Q

Types of lung cancer

A
  • Small cell lung cancer (20%)
  • Non small cell lung cancer (80%)
  • Non small cell lung cancer can be split into: Adenocarcinoma (40%), squamous cell carcinoma (20%), Large cell carcinoma (10%)
47
Q

Small cell lung cancer

A
  • Arise in large airways, tend to be more central. Associated withsmoking
  • Present with systemic disease and frequently metastasises via haematogenous routes to the liver, skeleton, bone marrow, brain and adrenal glands
  • Can cause Cushing’s syndrome (ACTH) and SIAD
  • 80% have mutations in RB1 and TP53
48
Q

Non small cell lung cancer

A
  • Arise from epithelial cells from the central bronchi to the terminal alveoli
  • Squamous cell carcinoma: obstructive lesion of the bronchus causing infection. Grow slowly, spread locally and disseminate late. Can cause cavitating lesions. Associated with smoking
  • Adenocarcinoma: arise from the bronchial mucosal gland and occur in the periphery. High risk of metastasis, originate in scar tissue. Most common in non-smokers
  • Large cell carcinoma: present as a large peripheral mass on x-ray. Have paraneoplastic features. Poorly differentiated, grow rapidly and metastasise early
49
Q

Lung cancer epidemiology

A
  • Lung cancer is the most common malignant solid tumour in the UK
  • Smoking is most commonly associated with SCLC
  • 60-70 year old males
50
Q

Lung cancer spread

A

spreads to ipsilateral peri bronchial and hilar nodes followed by mediastinal, contralateral hilar and supraclavicular nodes

year 4 CDM 2 (39 decks)

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