Pathology Flashcards
(189 cards)
1
Q
What does VINDICATE stand for?
A
Vascular Infection/Inflammatory Neoplastic Drugs Intervention/Iatorgenic Congenital/developmental Autoimmune Trauma Endocrine/Metabolic
2
Q
What are some of the bodies responses to injury?
A
Vascular changes, cellular changes, chemical mediators, morphological patterns
3
Q
In inflammation, vessels dilate. What mediates this?
A
Histamine’s and nitrous oxides
4
Q
What mediates white cell rolling along the endothilium?
A
Low affinity binding
Selectins (endothilium) to glycoproteins (WBC)
5
Q
What mediates white cell adhesion to the endothilium?
A
High affinity binding
ICAM/VCAM (endothilium) to integrins (WBC)
6
Q
What does CAM stand for?
A
Cell Adhesion molocule- often glycoproteins on the WBC
7
Q
What is an integrin and what is its function?
A
Protein expressed on WBCs and function mechanically by attaching the cell cytoskeleton to the extracellular matrix and biochemically by sensing whether adhesion has occurred.
8
Q
What does ICAM/VCAM stand for
A
VCAM = vascular cellular adhesion molocule ICAM = intercellular adhesion molocule
9
Q
What will increase selectin expression on the endothilium?
A
Histamine and thrombin from inflammatory cells
10
Q
What will increase ICAM/VCAM expression on the endothilium?
A
TNF alpha and IL1
11
Q
What increases the affinity (increased avidity/strength of binding) of ICAM/VCAM for integrins?
A
Proteoglycans
12
Q
What causes tumor or swelling?
A
Increase vascular permeability => loss of protein => change in osmotic pressure => water leaves vessels and enters tissue
13
Q
What causes an increase in vascular permeability?
A
1) Endothilial contraction due to histamines, bradykinin, substance P => gaps between epithilial cells
2) Direct injury (toxins can burn/damage vessels)
3) Immune response and degranulation can damage host tissue
4) Transcytosis- macromolocules are transported across interior of cell mediated by VEGF
5) New vessel formation (immature) mediated by VEGF
14
Q
What is VEGF?
A
Vascular endothilial growth factor- generates new blood vessels
15
Q
What is chemotaxis?
A
Directional response to a chemical stimuli
16
Q
What are the clinical features of acute inflammation?
A
Rubor, calor, tumor, dolor and loss of function
17
Q
What mediates pain in inflamation?
A
Bradykinin and prostaglandin
18
Q
Which cell type is typical of acute inflammation?
A
Neutrophil with a multilobed nucleus and granules
19
Q
Inflammation is good at damaging tissue. What measures are in place to limit the damage?
A
Mediators of inflammation are short lived
Neutrophils only survive outside the blood vessel for a few hours.
20
Q
What is resolution and what are the features of resolution?
A
Complete restoration of the tissue to normal after the inflammatory response.
Minimal cell death
Occurs in tissues with capacity to repair and replace
Good vascular supply required to deliver inflammatory cells and remove injurious agent
Injurious agent easily removed.
21
Q
What is Suppuration?
A
Formation and collection of puss.
22
Q
What is Pus?
A
A collection of dieing and dead cells. Lots of neutrophils, bacteria and inflammatory deposits like fibrin
23
Q
What is an abscess?
A
Collection of puss which has built up in the tissue of the body
24
Q
What is a empyema?
A
Collection of pus without a vascular supply- normally in the pleural space
Soft and prone to rupture
Antibiotics will not get in
25
What is organization?
Process which leads to scarring
26
Which factors promote organization?
1) Lots of necrosis
2) Lots of fibrin- not easily cleared
3) Poor vascular supply- difficulty removing debris
4) Tissue type which will not regenerate
27
What will happen to an injury to the mucosa which has gone beyond the basement membrane?
Organization as a scaffold is needed for resolution to occur
28
What erosions and abrasions?
Injuries to the mucosa with the basement membrane intact- complete resolution
29
What is an ulcer?
An open sore on an external or internal surface of the body, caused by a break in the skin or mucous membrane which fails to heal and must go beyond the basement membrane
30
When does granulation tissue form?
When an injury goes beyond the basement membrane
31
How does granulation tissue form?
Injury infiltrated by capillaries- VEGF. Allowing fibroblasts to move to the site of injured. Smooth muscle and collagen is deposited => scarring, fibrosis and loss of function of tissue.
32
What is a fibroblast?
Cells that synthesise the extracellular matrix and collagen.
33
Liver has some regenerative capacity but this can be overwhelmed => cirrhosis. What are the consequences of cirrhosis?
Liver failure and loss of function- cannot remove toxins or make new proteins.
Vascular disturbance as blood is not filtered properly as it cannot pass through fibrous tissue
34
Can chronic inflammation occur without preceding acute inflammation?
Yes
35
Chronic inflammation implies nothing about the time period or time period? T of F?
True
36
What factors promote chronic inflammation?
Suppuration
Persistent injury
Infectious agent
Autoimmune injury
37
Which inflammatory cell characterises chronic inflammation?
Lymphocytes and macrohages
38
What is a granuloma?
A mass of granulation tissue produced by a mass of macrophages.
39
When do granulomas occur?
```
Foreign bodies (endogeneous and exogeneous)
Specific infections- paracites, worms, eggs, syphilis and mycobacterium
```
40
What is hypertrophy?
Increased cell size
41
What is Hyperplasia?
Increased cell number
42
What is Atrophy?
Decrease in cell size
43
What is necrosis?
Pathological cell death requiring no energy
44
What is apoptosis?
Programmed cell death requiring energy and stimulus
45
What is coagulative necrosis?
1) Preservation of a cell outline (ghost outine with no nucleus or organelles) for a few days as the cells cannot be digested.
2) Dead cells are consumed by emzymatic processes and inflammatory cells as the microenvironment is to toxic for proteolysis
46
When is coagulative necrosis often seen?
Cardiac muscle following MI
47
What is liquefactive necrosis?
Liquid viscous mass where no cell structure remains.
Suppuration and pus present
Associated with local bacteria/fungal infections
48
When is liquefactive necrosis seen?
In the brain
49
What is caseous necrosis?
Microscopic necrosis usually associated with mycobacterium infections
Granulomatous inflammations with central necrosis
50
What are the physiological causes of apoptosis?
Normal growth esp in embryology
Removal of self reactive lymphocytes
Hormonal dependent involution (menstrual cycle, menopause, regression of lactating breast after weaning)
51
What is involution?
Shrinking or returning of an organ to its normal size
52
What are the pathological causes of apoptosis?
Usually in response to injury eg:
- Cross reacting lymphocytes
- Radiation/sunburn
- Chemotherapy/cancer
- Viral infections
- Graft v host disease post transplant
53
What is graft v host disease?
Attacking of transplanted tissue as it is recognised as non self. Drugs are given to suppress the immune system but this increases the risk of infection post surgery
54
What are the 2 methods of apoptosis?
Extrinsic- signal is from outside the cell
| Intrinsic- signal is from inside the cell
55
What is the extrinsic pathway of apoptosis?
Death receptors linked with TNF and Fas.
1) Fas ligand binds to Fas which activates the caspase cascade => apoptosis
2) TNF induces apoptosis in association with inflammatory conditions
56
What is the intrinsic pathway of apoptosis?
Mitochondrial pathway. Growth sigals promote anti- apoptotic pathway in the mitochondrial membrane. When growth signals are removed they are replaced with Bax/Bak
=> Increased permeability of mitochondria
=> release of proteins eg cytochrome C that stimulate the caspase cascade
57
Which cascade is associated with apoptosis?
Caspase cascade
58
What happens with too much or too little apoptosis?
Too much- neurogenerative diseases
| Too little- cancers and autoimmune diseases
59
How does apoptosis happen in order to prevent an inflammatory response?
1) Pyknosis- cell chrinks
2) Chromatin condensation- nucleus clumps and breaks up
3) Cytoplasmic blebs- cytoplasm breaks up
4) Macrophage comes to digest everything contained in vesicles
60
Are neutrophils present during apoptosis?
No
61
What is pyknosis?
Cell shrinkage
62
Why do cells age?
1) Oxidative stress- free radical damage
2) Accumulation of metabolic byproducts
3) Lipofuscin- pigment granules of lipid containing residues of lysosomal digestion
63
During an MI the Ca++ pump fails leading to increased intracellular calcium. What are the consequences of this?
1) Increasing ATPase
2) Increasing phospholipase => membrane damage
3) Increasing proteases => membrane and cytoskeletal damage
4) Increasing endonucleases => DNA damage and breakdown
5) Increasing mitochondrial permeability => release of proteins which stimulate the caspase cascade eg cytochrome C
64
Post MI- what changes are seen in 0-20 minutes?
No cellular changes in a micro or macroscopic level.
| First signs are redness, pyknosis, nuclear shrinkage and darkening, marginal contraction bands appear
65
Post MI- what changes are seen in 0-24 hours?
Increased perfusion, vasodilation and vascular permeability.
Acute inflammation and coagulative necrosis
Gross changes = redness and cardiac perforation
66
When is the risk of cardiac rupture post MI greatest?
3-7 days post MI
67
Post MI- what changes are seen in 24-48 hours?
Neutrophils replaced by macrophages
| Adaptive immune response- lymphocytes and chronic inflammation
68
What colour does tissue change at autopsy if macrophages are present?
Yellow
69
Why does suppuration not occur following MI?
No persistence of injury
70
Will resolution occur after MI?
No as the blood supply is poor due to ischemia.
| Resolution will occur after angina
71
What cells characterise organization and scarring?
Fibroblasts
72
When does organization and scarring occur post MI?
2-6 weeks
73
Can you date an MI which occurred longer than 6 weeks ago?
No
74
What is pathology?
The study of the causes of disease and the sequence of events steming from the cause to the eventual disease process
75
What is homeostasis?
The maintenance of a constant internal environment.
When the body is subject to different stresses, if they are severer the cell maybe damage (apoptosis/necrosis).
Prior to this there is a period of adaption to change.
76
What is an oesteoblast and an oesteoclast?
Oesteoblast: Cells which lay down bone
Oesteoclast: Cells which remove bone
77
What are the 3 types of growth receptor?
1) Receptors with intrinsic tyrosine kinase activity
2) 7 transmembrane GPCR
3) Receptors without tyrosine kinase activity
78
How is hyperplasia/hypertrophy initiated?
1) The production of more growth factors
| 2) The production of more growth factor receptors
79
Explain the tyrosine kinase pathway?
1) EGF binds to EGFR => activation by phosphorylation
2) Multistep process between the membrane and the nucleus
3) Increased protein synthesis and cell growth, cell proliferation an cell cycle progression and surval and decreased apoptosis
80
Explain how the 7 transmembrane GCPR works?
1) Multistep process between the membrane and the nucleus involving beta catenin and LEF1
2) Protein synthesis and cell growth, cell cycle progression and proliferation and survival and decreased apoptosis
81
Explain how growth receptors with no tyrosine kinase activity work?
1) Cannot phosphorylate themselves
2) Multistep process between membrane and nucleus involving cytokine receptors, JAK and STAT proteins
3) Protein synthesis and cell growth, cell cycle progression and proliferation and survival and decreased apoptosis
82
When are growth receptors with no tyrosine kinase activity important?
Haematological malignancies
83
What are the 4 phases to the cell cycle?
```
G1 = growth pase 1
S = synthesis (DNA replication)
G2 = growth phase 2
M = Mitosis
```
84
What controls and regulates the cell cycle?
Cyclins and cyclin dependent kinases (CDK)
85
What activates a specific CDK?
A specific cyclin. Cyclins vary in concentration throughout the cell.
86
Cyclin D: where does it bind and at what phase of the cell cycle?
CDK4 during G1
87
Cyclin E: where does it bind and at what phase of the cell cycle?
CDK2 during S phase
88
Cyclin A: where does it bind and at what phase of the cell cycle?
CDK2 in the later period of S phase
| CDK1 throughout G2 and M phase
89
Cyclin B: where does it bind and at what phase of the cell cycle?
CDK1 during M phase
90
What happens during G1 and how?
Cells get larger and there is increased protein synthesis
1) CDK4 phosphorylates the retinoblastoma protein
2) Normally Rb is bound to E2F
3) Free E2F stimulates cell division but if bound to Rb cell division is prevented
4) When phosphoylated by CDK4, Rb cannot bind to E2F and cell division begins
91
What happens during S phase and how?
DNA replication
1) E2F stimulates DNA replication
2) E2F increases the levels of cyclin E
3) Cyclin E activates CDK2
4) CDK2 also promotes DNA replication
92
What happes during G2?
Cell gets larger and more protein synthesis.
93
The main check point of the cell cycle is what and when does it occur?
p53 and occurs and the end of G2
1) p53 checks the cell for mistakes
2) If mistakes are found, the cell cycle is paused and repair is attempted
3) If repair is successful then the cell divides
4) If repair is unsuccessful then apoptosis is induced
94
What happens if cells can avoid being checked by p53?
Cell division continues despite faults in the DNA => cancer
95
Can all cells divide?
No eg neurones in the brain.
| Some cells are terminally differentiated
96
What is replicative senesence?
A limitation in the number of times a cell can divide (different for young and old people)
97
Which cells have replicative senesence and how does it work?
All somatic cells except most tumour cells and some stem cells.
Cell division S counting mechanism as a consequence of the telomere shortening hypothesis
98
What is the telomere shortening hypothesis?
Chromosome capped- this provides protectio and stops chromosome ends from fusion and degradation.
Consists of TTAGGG repeats and with every division the number of repeats gets smaller
99
Is hyperplasia reversible and when does it occur?
Yes it is.
Occurs in response to external stimuli and when this is removed hyperplasia will regress. Results in increased organ volume.
100
What are some physiological examples of hyperplasia?
Hormonal- puberty (breast tissue), pregnancy(endometrial lining of uterus), breast feeding (circular mamory glands become star-shapped)
Compensatory- occurs after loss of tissue in the liver and bone marrow
101
What are some pathological examples of hyperplasia?
Prostatic hyperplasia (due to androgens)
Endometrial hyperplasia and menstrual bleeding post menopause (excess oestrogen)
Lymph nodes in response to infection
Cancer cells keep growing in the absence of stimuli
102
Hyperplastic tissue is an at risk site for cancer development. T or F?
True
103
What does unilateral and bilateral lymphadenopathy suggest?
Unilateral => cancer
| Bilateral => infection
104
When does hypertrophy occur?
In conjunction with hyperplasia or in isolation in non dividing cells (muscle and cardiac myocytes)
Often in response to mechanical stress
105
Examples of physiological atrophy?
Menopause, embryological structures, after birth in uterus
106
Examples of pathological atrophy?
Decreased work load = Muscle wasting in cast,
loss of innervation = muscle no longer stimulated
Loss of blood supply in atherosclerosis = decreased brain size with aging
Inadequate nutrition
Pressure due to endogeneous or exogeneous structures
107
What are the mechanisms of atrophy?
Reduced cellular components, protein degredation.
| Components digested in lysosomes often by the ubiquitin protease pathway
108
Which hormones promote growth and which promote degrefation and atophy?
Growth = insulin
| Degradation and atophy = glucocorticoids and thyroid hormone
109
What is cancer?
Uncontrolled cell proliferation and growth that can invade other tissues
110
What is a tumour?
A swelling- benign, malignant or inflammatory
111
What is a neoplasm?
New growth not is response to external stimuli. Can be benign, malignant or premalignant
112
What is a malignancy?
Something with metastatic potential- spreading to other sites. Must go beyond the basement membrane for it to be considered malignant
113
What are the precursor lesions to cancer?
Dysplasia, Metaplasia and hyperplasia
114
What is metaplasia?
Reversible change from one mature cell type to another mature cell type
115
Why does metaplasia occur?
Stress placed on tissues and cells. The original cells are not robust enough to withstand the environments so they transform into another cell type which is more suited
116
If the stimulus for metaplasia is withdrawn, what happens?
Metaplasia will stop
117
Is metaplasia a reversal in appearance of adult cells?
No- its a change in the signals delivered to stem cells causing them to differentiate down a different line
118
What is a noxious stimuli?
An actual or potentially damaging event
119
Why does squamous metaplasia often occur in response to cell injury?
Stratified squamous epithilium is very resistant to noxious stimuli
120
What is Barretts oesophagus?
Columnar lined oesophagus. Results from chronic gastero-oesophageall reflux and is characterised by metastatic replacement of normal squamous cells of the lower oesophagus to columnar epithilium.
121
What is respiratory metaplasia?
Replacement of normal pseudostratified columnar cilliated epithilim with glands to squamous epithilium do to chemicals and heat
122
What is bladder metaplasia?
Replacement of transitional epithilium with squamous epithilium due to persistent injury (long term catheter)
123
When is hyperplasia premalignant?
When it becomes autonomous and no longer requires a signal
124
Why do only obease women get endometrial cancers?
Basic structure of steroid hormones (eg oestrogen) is shared by cholesterol => individuals with high cholesterol are at increased risk
125
What is dysplasia?
Disordered growth which occurs in the absence of a stimulus.
Abnormal cells.
No invasion or growth beyond the basement membrane
126
Dysplasia is often graded. What is low and high grade displasia?
Low grade= most similar to normal
| High grade= most abnormal and closest to becoming cancer
127
What is CiS?
| Carcinoma in Situ?
Dysplasia effecting the whole of the epithilium. High grade dysplasia.
No crossing of the basement membrane
Last stage before invasive cancer
128
Which autosomal dominant mutations can cause cancer?
RB mutations
| FAP- familial adenomatous polyposis. APC gene (100% bowel cancer by 50)
129
What is the double hit hypothesis?
Autosomal recessive conditions- where one working gene is enough. If you have inherited one faulty copy you are at an increased risk of another mutation
130
Cancer syndromes: what are the names of the syndromes caused by mutations in the following genes?
a) p53
b) APC
c) PTCH
d) PTEN
e) RET
f) MLH1
a) p53 = Li Fraumeni syndrome
b) APC = Gardener's syndrome
c) PTCH = Gorlin's syndrome
d) PTEN = Cowden's syndrome
e) RET = MEN (multiple endocrine neoplasia)
f) MLH1 = HNPCC and Muirs Torres (Lynch syndrome)
131
Chemical carcinogens can cause cancer. WHat are initiator and promotors?
```
Initiator = Long lasting DNA damage (not sufficient to cause cancer and must be followed by a promoter
Promoter = Require initiators to have caused damage. Time period after initiation can vary
```
132
What test can be done to bacteria to identify if a carcinogen is present?
Ames test assesses mutogenic potential
133
List 3 chemical carcinogens?
Smoking, Aflotoxins and beta naphthalene's
134
Cigarettes contain over 40 carcinogens. What are 4 of the worst?
Various metals
N-nitrosonornicotine
Polonium
Polycyclic aromatic hydrocarbons (animal fat from meat and smoked meat)
135
What is an aflotoxin?
Carcinogen derived from fungi causing liver cancers. Associated with p53 mutation
136
What is beta naphthalene's?
Carcinogen found in dyes causing bladder cancers
Conjugated in the liver with glucuronic acid and therefore not toxic but is retoxified in the bladder as human urine containes glucuronidase.
Build up of toxin as urine sits in the bladder
137
How does sun damage cause cancer?
UVB causes genetic damage and the formation of pyrimidine dimers in DNA.
Neucleotide excision repair repairs the DNA but is eventually overwhelmed.
138
What is Xeroderma pigmentosa?
A genetic defect in Nucleotide excision repair => lots of skin cancers
139
How does nuclear radiation cause cancer?
Specific radiation causes specific gene abnormalities
| Atomic bomb surivors get leukemia and thyroid cancer
140
Can CT and X ray cause cancer?
X ray = low does radiation
CT = high dose
Associated with increased risk of thyroid cancer and leukemias
141
How does HPV virus cause cancer?
HPV has genes to produce 10 proteins.
1) E7 is an oncogene which will bind to retinoblastoma meaning E2F is ALWAYS free to begin transcription
2) E6 increases destruction of p53.
142
Which cancers are associated with HPV virus?
Cervical and throat cancers
143
Do all people with HPV infection get cancer?
No, there are many types of the virus.
144
The EBV (epstein Barr Virus) causing glandular fever is involved in which tumours?
Burkitt lymphoma, B cell lymphomas, hodgekins lymphoma and nasopharangeal carcinoma
145
How can chronic lymphoma cause cancer?
Causes many lymphomas as there is constant lymphocyte production => increased mutation rate.
Other tumours are formed because the tissue is replicating so often. Often in the context of metaplastic change.
146
What are the Weinburgs Hallmarks of Cancer?
1) Sustained growth signalling- oncogenes
2) Loss of growth inhibition- tumour suppressor genes
3) Unlimited replicative potential
4) Resting apoptosis
5) Inducing angiogenesis
6) Disordered repair mechanisma
7) Evasion of the immune system
8) Activating invasion and metastasis
147
What is MYC?
Last step in the tyrosine kinase pathway before the nucleus.
Nuclear transcriptional factor that promotes growth
Common in lymphoma, neuroblastoma and small cell carcinoma of the lung
Burkitt lymphoma has a MYC translocation that is diagnostic- can use FISH
148
What is P13K?
The most commonly mutated kinase in cancer
149
What are some of the oncogenes in the MAPK/ERK pathway?
EGF, EGFR, RAS, RAF, MEK, MAPK, MYC
150
What are some of the functions of p53 (tumour suppressor gene)?
1) Cell cycle arrest and sensing DNA abnormalities and increase levels of p21 (a CDK inhibator)
2) Phosphorylation of Rb
3) Induce apoptosis via BAX pathway if DNA cannot be repaired
151
What is VHL- von Hippel Lindau?
Tumour suppressor genes
Can be a syndrome associated with renal cancers.
Loss of VHL increases levels of angiogenic growth factors => new blood vessel formation
152
What is PTEN?
Tumour suppressor gene
Increases transcription of p27 which inhibits CDK
Inhibits the P13K/AKT pathway
153
What can cells express to give them unlimited replicative potential and avoid the telomere shortening hypothesis?
Telomerase to renew the length of telomeres. In malignancy there is often a mutation to reactivate telomerase
154
How can cells resist apoptosis?
Bcl2 is an anti apoptotic molocule which binds to BAX or BAK to prevent holes in the mitochondria being created and no initiation of the caspase cascade.
Upregulating Bcl2 decreases apoptosis
155
What causes follicular lymphoma?
Translocation t(14:18) => switch on of Bcl2- antiapoptotic molocule
156
What is angiogenesis?
Formation of new blood vessels
157
What can cause angiogenesis in malignancy?
VEGF- vascular endothilial growth factor is upregulated in some malignancies.
NB: There are VEGF inhibaors for treatment of some cancers
158
What are the cells normal repair genes/mechanisms?
p53
NER- nucleotide excision repair
BRCA good at repairing DNA and arrests cell cycle at the G1/S phase
Mismatch repair proteins- family of proteins that identify faults in the DNA code (MLH1) (abnormal in Lynch syndrome => colorectal carcinomas)
159
What is Lynch syndrome?
```
Abnormal MLH1 (mismatch repair protein)
Causes 3% of colorectal cancers
Detected using immunohistochemistry- all colorectal cancers are screened for mismatch repiar protein abnormality
```
160
Why do we react to our own malignancies?
Malignant cells express foreign proteins eg keratin is expressed abnormally.
Cancers with good inflammatory responses have a better prognosis
161
What is the significance of PDL1 (programmed death ligand 1) in cancer?
This inhibits T cell proliferation
Important in pregnancy so mother doesn't attack fetus.
Tumour cells can over express PDL1 and avade the immune system
162
Which cancers are screened for PDL1?
All lung cancers as you can block PDL1 by targeted treatment
163
How do cancers invade and kill surrounding connective tissue?
Increase expression of matrix metalo proteins which kill surrounding tissue and blood vessels
164
What must a cancer do to be metastatic?
1) Grow uncontrollably and survive
2) Aviod the immune system
3) Extend through the basement membrane and connective tissue
4) Break through vessel wall
5) Survive in blood vessel
6) Aggregate to the vessel wall expressing Integrins and CAM
7) Get back through the vessel wall
8) Anchor to a new organ
9) develop a vascular system, survive and grow
165
Is cancer clonal?
No- the cells come from a single parent cell but they are not identical- its disordered.
This means targeted therapy may work against some but not all daughter cells.
166
How does lineage promiscuity cause treatment resistance?
Not all the cells are the same, some are different.
Recurrence occurs when a cell has a survival advantage over another cell meaning it is not effected by a targeted treatment.
This can limit the effect of 2nd and 3rd line treatments
167
What are the consequences of cancer?
Mass effect and compression of adjacent structures
Loss of function of the organ- warning sign?
Infiltration of other organs and vessels
Paraneoplastic syndromes triggered by an altered immune response to a neopplasm
Immunosupression
Metastasis
168
What is cachexia?
Weight loss- can be due to the energy consumption of the tumour but the tumour may also release molecules that increase metabolism eg TNF
169
What is a fistula?
Abnormal connection between 2 hollow spaces
170
What are the micropathological changes seen in malignancy?
Nuclear cytoplasmic ratio- lots of nucleus and not much cytoplasm
Pleomorphism
Hyperchromasia- lots of clolour
Lots of mitosis and abnormal mitotic bodies and cells with an abnormal number of chromosomes
ecrosis, inflammatory cells
171
Are encapsulated tumours usually benign or malignant?
Bengin- slow growing allowing time for a capsule to form
172
What is meant by 'well differentiated' in terms of tumour cells?
Look similar to the original cells and have some of the same functions
173
What is meant by 'poorly differentiated' in terms of tumour cells?
Difficult to tell the cell of origin and has lost almost all of its oriole functions.
174
If a tumour is poorly differentiated and its type cannot be identified from macro and micro analysis, what other tests can be done?
Genetic tests
Cytogenetics: FISH, karyotype
Molecular genetics: small changes in specific genes (onco or tumour suppressor) Can help with diagnosis, prognosis, therapy.
175
What is immunohistochemistry used for in cancer diagnosis?
To see which preoteins are being produced by the tumour.
176
What does staging of a cancer relate to?
Size or how far through the tissue planes this has progressed
177
How are tumours staged?
TNM
178
What is implied by a high stage tumour?
Slow growing that has been around for ages
179
What is implied by a low stage tumour?
Aggressive and rapidly growing but caught early on
180
What does the grading of a cancer relate to?
How well or poorly differentiated the cells are
181
What is implied by a low grade tumour?
Well differentiated tumour
182
What is implied by a high grade tumour?
Poorly differentiated
183
Epithilial tumours taxonomy: Give the name for a cancer of
a) Glandular tissue
b) Squamous epithilium
c) Transitional epithilium
a) andenocacinoma
b) Squamous cell carcinoma
c) Transitional cell carcinoma or urothilial cell carcinoma
184
Epithilial tumours taxonomy: Give the name for a benign tumour of
a) Glandular tissue
b) Squamous epithilium
a) adenoma
| b) papilloma
185
Mesenchymal (connective tissue) tumours taxonomy: Give the names for cancers of
a) fat
b) bone
c) cartilage
d) Skeletal muscle
e) nerves
f) blood vessels
a) fat = Liposarcoma
b) bone = osteosarcoma
c) cartilage = chondrosarcoma
d) Skeletal muscle = rhabdomyosarcoma
e) nerves = Malignant peripheral nerve shealth tumour
f) blood vessels = Angiosarcoma/Kaposis sarcoma
186
Mesenchymal (connective tissue) tumours taxonomy: Give the names for benign tumours of
a) fat
b) bone
c) cartilage
d) Skeletal muscle
e) nerves
f) blood vessels
a) fat = Lipoma
b) bone = osteoma
c) cartilage = enchondroma
d) Skeletal muscle = Rhabdomyoma
e) nerves = neurofibroma and schwannoma
f) blood vessels = Haemangioma
187
What is the scientific name for a freckle, mole and skin cancer?
Freckle = ephelis
Mole = naevus
Skin cancer = melanoma
188
Give the name of cancers of blood cells?
Leukemias (bone marrow and blood)
| Lymphomas (lymph nodes)
189
Give the name for cancers of the CNS?
Gliomas
