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MBBS - Year 1 > Pathology - Bone Pain > Flashcards

Pathology - Bone Pain Flashcards

1
Q

What are metabolic bone disorders

A

Altered Ca or phosphate or disordered homeostasis

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2
Q

Primary osteoporosis

A

Senile OP

Post-menopausal OP

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3
Q

Secondary OP

A

Endocrine disorders e.g. hypeyerparathyroidism
GI disorders e.g. malnutrition
Drugs e.g. corticosteroids

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4
Q

Pathogenesis of OP

A 
Age-related changes 
Reduced physical activity 
Genetic factors 
Ca nutritional status 
Hormonal influences
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5
Q

Age related changes leading to OP

A

Osteoblasts in older people have reduced proliferative and biosynthetic availability and don’t respond to growth factors as well as they used to

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6
Q

Reduced physical activity leading to OP

A

Mechanical factors stimulate normal bone remodelling

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7
Q

Hormonal influences leading to OP

A

Oestrogen deficiency after menopause increases secretions of infl cytokines —> osteoclast recruitment and activation

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8
Q

Complications of OP fractures

A

Fractures
PE - DVT due to lack of movement after fracture
Pneumonia

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9
Q

Non-skeletal effects of infl

A

Induction of immune cell differentiation and enhanced infl

Inhibition of tumour cell proliferation, induces differentiation and inhibits angiogenesis

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10
Q

What is cancer caused by

A

DNA mutations either induced by exposure to mutagens or spontaneously

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11
Q

Hallmarks of cancer

A 
Sustaining proliferative signalling 
Evading growth suppressors 
Resisting cell death 
Enabling replicative immortality 
Inducing angiogenesis 
Reprogramming energy metabolism
Evading immune destruction 
Activating invasion/ metastasis
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12
Q

What causes the hallmarks of cancers

A

Underlying genome instability causing genetic diversity

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13
Q

Tumour microenvironment

A

Normal cells recruited by the tumour cells to help the development of these hallmark traits

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14
Q

Oncogene categories

A

Growth factors or growth factor receptors – these induce cell growth
Signal transducers – relay receptor activation to the nucleus
Nuclear regulators
Cell cycle regulators

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15
Q

Regulators of apoptosis

A

Prevent apoptosis in normal cells and promote it when mutated cells have DNA that cant be released
BCL2

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16
Q

BCL2

A

Normally stabilises the mitochondrial membrane blocking release of cytochrome c but can be disrupted by malignant cells

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17
Q

Why do cancers upregylate telomerase

A

Telomeres normally shorten w/ serial cell divisions, eventually causing cell senescence

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18
Q

Angiogenic factors produced by cancers

A

FGF and VEGF

New blood vessel formation is needed for tumour survival and growth

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19
Q

Dysplasia

A

Disordersed cell growth
Theoretically reversible w/ alleviation of the inciting stress
If stress persists, dysplasia can progress to carcinoma (irreversible)

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20
Q

Neoplasia

A

Growth that is unregulated, clonal and irreversible

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21
Q

What causes neoplasia

A

The autonomous/ relatively autonomous abnormal growth of cells that persists in the absence of the initiating stimulus

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22
Q

Characteristics of benign tumours

A

Remain localised
Slow growing
Closely resemble tissue from which they arise
Often circumscribed or encapsulated

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23
Q

Characteristics of malignant tumours

A

Invade the surrounding tissues and many have the capacity to metastasize
Often rapidly growing
Vary in their resemblance to the tissue of origin
Usually have an irregular margin

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24
Q

In-stu carcinoma vs invasive carcinoma

A

In situs carcinomas are epithelial neoplasms exhibiting all of the cellular features associated w/ malignancy, but which has not yet invaded through the epithelial basement membrane

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25
Q

Routes of metastasis

A

Blood vessels

Lymphatics

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26
Q

Recognising malignant cells

A

Increased nuclear to cytoplasmic ration
Nuclear pleomorphism and hyperchromasia
Irregular chromatin distribution within the nucleus +/- prominent nucleoli
Irregular nuclear membrane

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27
Q

Recognising benign cells

A

Low nuclear to cytoplasmic ratio
All nuclei of similar size and not hyperchromatic
Vesicular, evenly distributed chromatin
Smooth nuclear membranes

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28
Q

Tumour classification

A

Histogenetic classification; named after tissue/ cell of origin

29
Q

Tumour grading

A

How closely the tumour resembles the tissue from which is arises (differentiated)
Indicator of how aggressive the tumour is likely to be
Grade 1 tumours are well differentiated and closely resemble the origin tissue, but Grade 3 tumours do not

30
Q

The higher the tumour grade…

A

The worse the prognosis

31
Q

Factors influencing tumour invasion

A

Decreased cell adhesion – cells must be able to separate and disperse integrin receptors allowing tumour cell matric adhesion
Secretion of proteolytic enzymes – to enter vessels
Increased cell motility

32
Q

Steps of tumour invasion of the basement membrane

A

Loosening of intercellular junctions due to loss of cadherins (down regulated) and increased expression/ distribution of integrins
Degradation of the extracellular matrix due to proteolytic enzymes
Migration and invasion – cleavage of basement membrane proteins generate molecules that bind to receptors on tumour cells and stimulates locomotion

33
Q

What do we see in tumour associated fibroblasts

A

Altered expression of genes that encode extracellular matrix molecules, proteases, protease inhibitors and growth factors

34
Q

Metastasis

A

Process whereby malignant tumours spreads from the site of origin (1’ tumours) to form other tumours (2’ tumours) at distant sites.

35
Q

Carcinomatosis

A

Describes extensive metastatic carcinoma.

36
Q

What must cells be able to do to metastasise

A

Detach tumour cells from the neighbours
Invade the connective tissue to reach lymphatics and blood vessels
Intravasate into the lumen of vessels
Evade host defence mechanism e.g. NK cells and T lymphocytes
Adhere to endothelium as a remote location
Extravasate the cells of the vessel lumen into the tissue
Survive and grow in the new environment

37
Q

Seed and soil hypothesis

A

Primary tumour
Proliferation/ angiogenesis
Detachment/ invasion Embolism/ circulation
Transport
Arrest in organs
Adherence to vessel wall
Extravasation and establishment of a microenvironment
Proliferation/ angiogenesis –> metastasis

38
Q

What does detachment/ invasion include

A

Lymphatics
Venules
Capillaries

39
Q

What does embolism/ circulation

A

Interaction w/ platelets, lymphocytes and other blood components

40
Q

Different routes of metastasis

A

Lymphatic - more typical of carcinoma
Haematogenous - more typical of sarcoma
Transcoelemic

41
Q

Lymphatic metastasis

A

Tumour cells travel through afferent lymphatics to enter lymph nodes
Cause lymph nodes to enlarge and become firm
May extend lymph node and causes adherence
Interrupts lymphatic flow

42
Q

Which part of the lymph nodes do tumour cells travel to

A

Subcapsular sinus

43
Q

Transcoelemic metastasis

A

Metastasis to the peritoneal, pleural and pericardial cavities
Can cause ascites

44
Q

How do tumours evade the immune system

A

Destruction by selection of antigen negative clones
Loss of MHC molecules
Expression of transforming growth factor beta or PD1 ligands by the tumour cells

45
Q

Tumour staging

A

Extent of tumour staging

TMN

46
Q

TMN

A

T - primary tumour, suffixed by number denoting size, or anatomical extent
N - lymph node spread, suffixed by number denoting no. lymph nodes or group of lymph nodes containing metastases
M: anatomical extent of distant metastases

47
Q

When are clinical effects of tumours inconsequential

A

If the organ is large relative to the size of the tumour and no vital structure is threatened

48
Q

Local effects of tumours

A

Destruction
Displacement
Compression

49
Q

Metabolic effects of tumours

A

Well-differentiated tumours retain the functional properties of the parent cell e.g. hormone production

50
Q

When can paraneoplastic syndromes result

A

I§nappropriate secretion of a hormone by a tumour that does not normally secrete the hormone.

51
Q

Systemic effects of cancer

A 
Cachexia 
Warburg effect 
Neuropathy 
Myopathy 
Venus thrombosis 
Glomerular
52
Q

Cachexia

A

Severe wt loss and debility in a cover pt

53
Q

Warburg effect

A

Cancer cells have a high rate of glycolysis with formation of lactic acid as opposed to pyruvate in normal cells

54
Q

Mortality associated with neoplasia in lungs

A

Bronchopneumonia

55
Q

Mortality associated with neoplasia in bone

A

Hypercalcaemia –> renal failure and cardiac arrhythmias

56
Q

Mortality associated with neoplasia in liver

A

Electrolyte abnormalities

57
Q

Mortality associated with neoplasia in blood vessels

A

Haemorrhage or vessel obstruction –> heart failure

58
Q

Mortality associated with neoplasia in brain

A

Raised intracranial pressure, compressing respiratory centre in brainstem

59
Q

Mortality associated with neoplasia in GI tract

A

Obstruction → impair nutrition, ulceration/ perforation

60
Q

TMN - T

A

Tubule formation

The extent to which the tumour forms tubules

61
Q

TMN - T scores

A

1: >75% of tumour
2: 10-75% of tumour
3: <10% of tumour

62
Q

TMN - N

A

Nuclear pleomorphism

The size of the nuclei in the cells of the tumour compared to normal nuclei

63
Q

TMN - N scores

A

1: Similar in size to benign epithelial cells
2: 1.5 - 2x size of benign epithelia; cells
3: >2x size of benign epithelial cells

64
Q

TMN - M

A

Mitotic count

How rapidly cells are dividing (depends on microscope field diameter)

65
Q

TMN - M scores

A

1: Low count (per 10 high power fields)
2: Intermediate count
3: High count

66
Q

Grade 1 tumour scores

A

Total score 3-5

67
Q

Grade 2 tumour scores

A

Total score 6-7

68
Q

Grade 3 tumour scores

A

Total 8-9

MBBS - Year 1 (93 decks)

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