Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

In what cancers can SIADH occur?

A

Typically type A occurs in tumours

  • Carcinoma (lung, GI, oropharynx)
  • lymphomas and sarcomas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What tumours can secrete placental like ALP

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Symptoms of hypercalcaemia of malignancy

A

Bones, stones, abdominal groans, polyuria and polydipsia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Biochemical features of hypercalcaemia of malignancy

A

Increased

  • Ca
  • ALP-bone

Decreased

  • phosphate
  • K
  • PTH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Treatment of hypercalcaemia of malignancy

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

What are some causes for false positive is the guaic based faecal occult blood test?

A
  • 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
Q

What are some causes for false negatives is the guaic based faecal occult blood test?

A
  • Large dose of vit D

- Failure to collect multiple samples (condition only produce blood sporadicallly)

27
Q

What are some biochemical markers of tumours increased cellular activity/growth?

A
  • 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
Q

Describe the metabolic changes associated with tumour growth?

A
  • 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
Q

How is the lipid system affected by tumour growth?

A

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
Q

What is the tissue reponse to injury in cancer growth?

A

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
Q

Trace metal abnormalities seen in cancer development due to the tissue response to injury

A

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
Q

What is cachexia and what biochemical features are associated?

A

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
Q

What are paraneoplastic syndromes?

A

clinical syndromes associated with a tumour, but not directly resulting from the primary tumour mass or metastasis

34
Q

What tumours are not included in causing paraneoplastic syndrome?

A

Tumours of the endocrine gland

35
Q

How does tumour removal affect paraneoplastic syndromes?

A

The syndromes will disappear as the tumour was the cause

36
Q

What are some examples of paraneoplastic syndromes?

A

Hypercalcaemia
SIADH
Cushings syndrome

37
Q

How does Cushings syndrome form from a tumour?

A

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
Q

How does hypoglycaemia form due to tumours

A

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
Q

How are the IGF concs affected in tumour-inudced hypoglycaemia? and its effect on GH response?

A

IGF-1 decrease
IGFII normal/increase
IGF1:IGF2 decrease
IGFBP-3 decrease

Results in attenuated GH response

40
Q

How is tumour induced hypoglycaemia treated?

A

GH, prednisolone

41
Q

Describe gonadal dysfunction as a neoplastic syndrome

A

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
Q

What may a patient at risk of gonadal dysfunction choose to do?

A

Protect ovarian function using GnRH analogues to suppress oocyte maturation

Sprem banking/embryo stage

43
Q

How are androgens target in therapy?

A

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
Q

State some electrolyte disturbances of paraneoplastic syndromes in tumours

A
  • 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
Q

How does hepatic dysfunction occuring in cancer treatment?

A

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
Q

What is tumour lysis syndrome?

A

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
Q

What are the biochemical features of tumour lysis syndrome?

A
  • Hyperkalaemia
  • Hyperuricaemia
  • Hyperphosphataemai - Hypocalcaemia
  • Tachyarrhytmias or sudden cardiac death
  • Increased LDH
  • Cause acute renal failure
48
Q

How is tumour lysis syndrome prevented?

A
  • Maintenance of adequate hydration
  • Allopurinol
  • monitoring of fluids and liquids
  • urinary alkalinisation
  • renal dialysis
49
Q

State some other pathology specialities

A
  • 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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions