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Disease of Major Organs > Tumours > Flashcards

Tumours Flashcards

1
Q

What two characteristics describe tumour growth?

A

Neoplastic - proliferate/grow independently of normal control mechanims

Malignant- Can invade other tissue/organs

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2
Q

What alterations in cell cycle control elements drive tumour proliferation?

A
  • Abnormal receptor signalling
  • Excessive signalling protiens
  • Loss of inhibitory proteins
  • Excess growth factors
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3
Q

Describe the genetic alterations in cancer

A

Oncogenes
- protooncogene expression is increased coding for proteins that regulate cellular growth processes

Tumour suppressor genes

  • Downregulated as these are cell growth regulation pathways
  • e.g. P53 or BRCA1

DNA repair genes
- DNA repair defects-> cancer predisposition

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4
Q

Describe the different proto-oncogenes and their maturation?

A

5 groups: Growth factors, growth factor receptors, signal transducers, transcription factors, programmed cell death regulators

  • Mutation, gene amplification, or chromosomal re-arrangment or proto-oncogenes -> oncogenes
  • Gain of function mutations
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5
Q

How does cancer develop

A
  • Derives from one single aberrant cell with an inital mutation
  • The normal control of cell division, apoptosis and differentiation is lost due to accummulation fo mutations and epigenetic changes
  • Progression of tumours are slow
  • Example of lost control, telomere shortening in each cycle eventually reaches cell sensecence, but this is avoided in cancer as p53 is mutated.
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6
Q

What is required for metastais?

A
  • Need sufficient vascularisation
  • Changes to adhesion proteins to allow seperation between cells
  • Cleavage of basemement membrane and EXM allows cancer to move freely.
  • The cancer travels via the blood stream or lymphatics to its next target.
  • Cancer will trap in the capillaries of distant organs and penetrate and growth in the distant organ
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7
Q

State some biochemical effects of tumour growth

A

Renal dysfunction, liver failure, bone resorption, exudation (leaky capillaries), bleeding (Gi tract cancer), metabolic change, lipid abnormalities, cachexia

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8
Q

Describe renal dysfunction in cancer

A
  • Common in people with tumours
  • 32% of newly diagnosed cancers exhibit renal insufficiency.

Contributing factors

  • FLuid loss (vomiting, diarrhoea)
  • hypercalaemia
  • hyperuricaemia (tumour destruction)
  • protein deposition (Bence jones protein)
  • glomerular or tubular damge (chemo)
  • Urinary tract obstruction (tumour metastases)
  • Tumour lysis syndrome
  • Immuno-mediated renal disease (nephrotic syndrome)
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9
Q

How does hyponatraemia contribute to renal dysfunction?

A 
Sodium losses
- Fluid loss, adrenal destruction, tumour ADH secretion
Water retention
- Tumour ADH secretion, chemotherapy
Pseudohyponatraemia
- Hyperproteinaemia (myeloma)
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10
Q

In what cancers can SIADH occur?

A

Typically type A occurs in tumours

  • Carcinoma (lung, GI, oropharynx)
  • lymphomas and sarcomas
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11
Q

What physical effects can tumours have?

A

Obstruction

  • Obstructive jaundice: increased bilirubin, ALP, GGT
  • Urethra/ureter/bladder neck: renal failure

Tissue damage

  • Normal tissue destructions releases enzymes: increased LDH and AST
  • Hypopituitarism
  • Diabetes insipidus
  • Hypoadrenalism

Bleeding or exudation

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12
Q

What is the liver invovlement in cancer development?

A

This is a frequent site of secondary tumours manifesting as pain and jaundice.
- Biochemical features are increase in ALT/ASTs. If cholestatic then increase in ALP and GGT

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13
Q

What tumours can secrete placental like ALP

A

e.g. Lung, seminoma of testis and gynaecological malignancy

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14
Q

How is the bone affected by cancer growth

A

Common site for metastasis.

  • osteoclast activation by tumour or cytokine (IL-6, IL-1, TNFalpha)
  • local production of PTHrP - breast cancer secondaries
  • Hypercalcaemia - osteolytic lesions
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15
Q

What pain relief is effective in calcium/bone affected individuals?

A

osteoclast inhibitors, e.g. bisphosphonates, relieves pain and reduce fracture risk

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16
Q

Describe two situations where cancers increase osteoclastic bone resorption?

A

Humoral hypercalcaemia of malignancy (squamous carcinoma)

  • PTHrP main mediator. Binds to PTH receptors to increase 25OH Vit D hydroxylation
  • PTH secretion by tumour is rare

Local osteolytic hypercalcaemia

  • results form boney metastasis
  • promote local resoprtion via increased osteoclast activity e.g. myeloma (TNFbeta, IL1 and 6)
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17
Q

Symptoms of hypercalcaemia of malignancy

A

Bones, stones, abdominal groans, polyuria and polydipsia

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18
Q

Biochemical features of hypercalcaemia of malignancy

A

Increased

  • Ca
  • ALP-bone

Decreased

  • phosphate
  • K
  • PTH
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19
Q

Treatment of hypercalcaemia of malignancy

A

Rehydration
Tumour removal
Reducing bone resorption (bisphosphonates)
Steroids (myelpma)

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20
Q

What is exudation?

A

Leaky capillaries in malignancies

- patients form ascites in peritoneal carcinomatosis, hepatic metastasis

21
Q

Biochemistry of exudates

A
  • High total protein >30-35g/L
  • Fluid:serum protein>0.5
  • Fluid:serum LDH> 0.6
  • Pleural fluid LDH >2/3 URL for plasma LDH
  • high cholesterol
22
Q

What does bleeding imply?

A

Manifestation of Gi tract cancers

- May be present in iron deficicent anaemia and IBD

23
Q

Test for GI cancer

A

Test for faecal blood

  • immunochemical tests
  • Guaiac test (detect peroxidase activity of intact heam, upper and lower GI tract bleeding)
  • Detection of haem derived porphyrins
24
Q

WHat is the national bowel cancer screening program?

A

Screening for ages 60-74

  • Test uses guaic based faecal occult blood test
  • relies on chemical reaction to produce a colour change
  • restrict meds before
  • Dietary restrictions
25
What are some causes for false positive is the guaic based faecal occult blood test?
- Condition causing bleeding,e.g. dental procedure - bleeding of gums - Other sources of haemoglobin - Other substances react with the FOB test (eating fish, turnips, horseradish). - Menstrual bleeding
26
What are some causes for false negatives is the guaic based faecal occult blood test?
- Large dose of vit D | - Failure to collect multiple samples (condition only produce blood sporadicallly)
27
What are some biochemical markers of tumours increased cellular activity/growth?
- Urate increases (nucleic acid breakdown) - LDH increases (tissue destruction) - Lactic acidosis (anaerobic respiration - metabolic disease) - Pseudohyperkalaemia (WBC destruction during venepucture and centrifuge release K) (leukaemia with high white blood cells) - Common in leukaemias, lymphomas and small cell cancer of lung.
28
Describe the metabolic changes associated with tumour growth?
- hyperglycaemia - hypoglycaemia in insulomas - lactic acidosis (metastatic disease) - increased glucose turnover (TNF alpha) - abnormal glucose tolerance (insulin resistance) - increased glucose transport into tumour cells
29
How is the lipid system affected by tumour growth?
Some tumours will utilise lipids as energy source via FFA mobilisation - Decrease in cholesterol - Hypercholesterolaemia that normalises following therapy (3.g. HCC) - Hypertriglyceridaemia in some cancers such as myeloma, carcinoma of colon - Abnormal lipid composition in malignant cells and unusual lipid synthesis
30
What is the tissue reponse to injury in cancer growth?
Cancaer induces tissue damage invoking an acute phase response, using cytokines like IL-6, TNF alpha Acute phase proteins - positive: A1AT, haptoglobin, C3, CRP - negative: albumin, transferrin
31
Trace metal abnormalities seen in cancer development due to the tissue response to injury
Increased - copper (due to increase in caeroloplasmin) Decreased - Zinc (decreased albumin, increase excretion and metalloproteinases) - Iron (decreasesd transferrin and increased ferritin in APR) - Selenium
32
What is cachexia and what biochemical features are associated?
Cachexia is also called wasting syndrome. Describes the waste in the processess associated with utilistation of lipid, carbohydrates and proteins. - weight loss - anorexia: loss of appetite, premature satiety - anaemia - insulin resistance - hypoalbuminaemia - increased glycolysis, lipolysis, protein catabolism
33
What are paraneoplastic syndromes?
clinical syndromes associated with a tumour, but not directly resulting from the primary tumour mass or metastasis
34
What tumours are not included in causing paraneoplastic syndrome?
Tumours of the endocrine gland
35
How does tumour removal affect paraneoplastic syndromes?
The syndromes will disappear as the tumour was the cause
36
What are some examples of paraneoplastic syndromes?
Hypercalcaemia SIADH Cushings syndrome
37
How does Cushings syndrome form from a tumour?
This occurs in neuroendocrine tumours causing uncontrolled ACTH secretion by tumours - Include small cell carcinoma of lung, bronchial carcinoids, pheochromocytoma - Biochemical features are: increased cortisol, hypokalaemic metabolic alkalosis, glucose intolerance
38
How does hypoglycaemia form due to tumours
Occurs in large mesodermal tumours and carcinomas of the adrenal cortex. There is an unregulated overproduction of IGF-II. - IGFII (proliferation) occurs at greater conc than insulin-> hypoglycaemic potential. - IGFII - Biochemical features are decreased insulin and C-peptide in the presence of hypoglycaemia
39
How are the IGF concs affected in tumour-inudced hypoglycaemia? and its effect on GH response?
IGF-1 decrease IGFII normal/increase IGF1:IGF2 decrease IGFBP-3 decrease Results in attenuated GH response
40
How is tumour induced hypoglycaemia treated?
GH, prednisolone
41
Describe gonadal dysfunction as a neoplastic syndrome
Can occur in treatment using radiotherapy or chemotherapy. This affects spermatogensis and ovarian follicle formation. - may be direct effect on germ cells or indirect suppression of GnRH - Sperm production may not be recovered - Temp cessation of menstruation (high LH & FSH, low E2.
42
What may a patient at risk of gonadal dysfunction choose to do?
Protect ovarian function using GnRH analogues to suppress oocyte maturation Sprem banking/embryo stage
43
How are androgens target in therapy?
Androgens stimulate prostate cancer growth, whilst oestrogens stimulate breast cancer growth so these are potential therapy points - androgen suppression via LHRH analogues e.g. goserelin
44
State some electrolyte disturbances of paraneoplastic syndromes in tumours
- Drug induced nausea and vomiting (hyponatraemia and hypercalacaemia) - Chemo is nephrotoxic - acute oliguric renal failure - renal magnesium wasting (can cause hypokalaemia) - Hypokalaemia - hypocalcaemai - hyponatraemia
45
How does hepatic dysfunction occuring in cancer treatment?
Drugs are metabolised by the liver, making them extra susceptible to damage - Damage is usually asymptomatic and mild - moderate increase in AST/ALT - Fatty changes and intra-hepatic cholestatis common (increased ALP/GGT)
46
What is tumour lysis syndrome?
This is quite uncommon distoder that occurs post-treatment. Can be fatal. Where there is a constellation of metabolic disturbances that occurs when large numbers of neoplastic cells are killed rapidly - release of intracellular ions and metabolic byproducts into the systemic circulation.
47
What are the biochemical features of tumour lysis syndrome?
- Hyperkalaemia - Hyperuricaemia - Hyperphosphataemai - Hypocalcaemia - Tachyarrhytmias or sudden cardiac death - Increased LDH - Cause acute renal failure
48
How is tumour lysis syndrome prevented?
- Maintenance of adequate hydration - Allopurinol - monitoring of fluids and liquids - urinary alkalinisation - renal dialysis
49
State some other pathology specialities
- evaluation of risk e.g. BRCA1 mutation in breast and ovarian cancer - early diagnosis (mutant p53 and/or ras oncogenes) - prognosis and staging (e.g. reverse transcriptase-PCR) - Genomic medicine

Disease of Major Organs (14 decks)

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