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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
Routes of metastasis
Blood vessels | Lymphatics
26
Recognising malignant cells
Increased nuclear to cytoplasmic ration Nuclear pleomorphism and hyperchromasia Irregular chromatin distribution within the nucleus +/- prominent nucleoli Irregular nuclear membrane
27
Recognising benign cells
Low nuclear to cytoplasmic ratio All nuclei of similar size and not hyperchromatic Vesicular, evenly distributed chromatin Smooth nuclear membranes
28
Tumour classification
Histogenetic classification; named after tissue/ cell of origin
29
Tumour grading
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
The higher the tumour grade...
The worse the prognosis
31
Factors influencing tumour invasion
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
Steps of tumour invasion of the basement membrane
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
What do we see in tumour associated fibroblasts
Altered expression of genes that encode extracellular matrix molecules, proteases, protease inhibitors and growth factors
34
Metastasis
Process whereby malignant tumours spreads from the site of origin (1’ tumours) to form other tumours (2’ tumours) at distant sites.
35
Carcinomatosis
Describes extensive metastatic carcinoma.
36
What must cells be able to do to metastasise
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
Seed and soil hypothesis
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
What does detachment/ invasion include
Lymphatics Venules Capillaries
39
What does embolism/ circulation
Interaction w/ platelets, lymphocytes and other blood components
40
Different routes of metastasis
Lymphatic - more typical of carcinoma Haematogenous - more typical of sarcoma Transcoelemic
41
Lymphatic metastasis
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
Which part of the lymph nodes do tumour cells travel to
Subcapsular sinus
43
Transcoelemic metastasis
Metastasis to the peritoneal, pleural and pericardial cavities Can cause ascites
44
How do tumours evade the immune system
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
Tumour staging
Extent of tumour staging | TMN
46
TMN
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
When are clinical effects of tumours inconsequential
If the organ is large relative to the size of the tumour and no vital structure is threatened
48
Local effects of tumours
Destruction Displacement Compression
49
Metabolic effects of tumours
Well-differentiated tumours retain the functional properties of the parent cell e.g. hormone production
50
When can paraneoplastic syndromes result
I§nappropriate secretion of a hormone by a tumour that does not normally secrete the hormone.
51
Systemic effects of cancer
``` Cachexia Warburg effect Neuropathy Myopathy Venus thrombosis Glomerular ```
52
Cachexia
Severe wt loss and debility in a cover pt
53
Warburg effect
Cancer cells have a high rate of glycolysis with formation of lactic acid as opposed to pyruvate in normal cells
54
Mortality associated with neoplasia in lungs
Bronchopneumonia
55
Mortality associated with neoplasia in bone
Hypercalcaemia --> renal failure and cardiac arrhythmias
56
Mortality associated with neoplasia in liver
Electrolyte abnormalities
57
Mortality associated with neoplasia in blood vessels
Haemorrhage or vessel obstruction --> heart failure
58
Mortality associated with neoplasia in brain
Raised intracranial pressure, compressing respiratory centre in brainstem
59
Mortality associated with neoplasia in GI tract
Obstruction → impair nutrition, ulceration/ perforation
60
TMN - T
Tubule formation | The extent to which the tumour forms tubules
61
TMN - T scores
1: >75% of tumour 2: 10-75% of tumour 3: <10% of tumour
62
TMN - N
Nuclear pleomorphism | The size of the nuclei in the cells of the tumour compared to normal nuclei
63
TMN - N scores
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
TMN - M
Mitotic count | How rapidly cells are dividing (depends on microscope field diameter)
65
TMN - M scores
1: Low count (per 10 high power fields) 2: Intermediate count 3: High count
66
Grade 1 tumour scores
Total score 3-5
67
Grade 2 tumour scores
Total score 6-7
68
Grade 3 tumour scores
Total 8-9

MBBS - Year 1 (93 decks)

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