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MoD 3 Flashcards

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1
Q

What happens in the group of conditions known as porphyrias?

A

Porphyrins, which are normally used to synthesize haem, instead accumulate in the body

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2
Q

What accumulates in patients with urea cycle defects?

A

Ammonia

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3
Q

What are the two main buffering systems in the body?

A

Haemoglobin and Bicarbonate

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4
Q

What is the normal range of pH for the body?

A

pH = 7.45 - 7.35

H+ conc = 35nmol/L - 45nmol/L

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5
Q

What causes right shift in the oxygen dissociation curve?

A 
Right shift with 
Increased 
2,3 diPG
H+ Acidosis 
Temperature
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6
Q

What are the bodies 3 main compensatory mechanisms for acid-base disturbances?

A

Respiratory
Renal bicarbonate regeneration
Hepatic shift between urea synthesis and ammonia excretion

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7
Q

Respiratory acidosis

A

High H+
High CO2
Low Oxygen

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8
Q

Respiratory alkalosis

A

Low H+
Low CO2
High Oxygen

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9
Q

Metabolic acidosis

A

High H+
Low CO2
High Oxygen

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10
Q

Metabolic alkalosis

A

Low H+
High CO2
Low Oxygen

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11
Q

What is involution?

A

Involution is physiological atrophy by apoptosis

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12
Q

What is agenesis

A

the incomplete development or total absence of a body part

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13
Q

What is neoplasm?

A

Lesion resulting from the autonomous growth or relatively autonomous abnormal growth of cells that persists in the absence of the initiating stimulus

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14
Q

What is anaplasia?

A

poorly differentiated cells in a tissue

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15
Q

What are sentinel nodes?

A

The first node in a regional lymphatic basin that receives lymph flow from the primary tumour.
Identified by injecting radiolabelled tracers or coloured dyes.

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16
Q

What is the stroma of a tumour?

A

The connective tissue framework that neoplastic cells are embedded in. It provides mechanical support, Intercellular signalling, nutrition

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17
Q

What is desmoplasia and its significance to tumours?

A

Desmoplasia is the growth of fibrous or connective tissue. Tumours cause a desmoplastic reaction where there is:
Fibrous stroma formation due to induction of connective tissue
Fibroblast proliferation by growth factors from the tumour cells

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18
Q

What does the stroma around a tissue contain?

A 
Stroma contains:
Cancer-associated fibroblasts 
Myofibroblasts 
Blood vessels
Lymphocytic infiltrate
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19
Q

What is histogenesis?

A

The differentiation of cells into specialised tissues and organs during growth from undifferentiated cells (the 3 primary germ layers)

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20
Q

Benign tumour of surface epithelium

A

Papilloma

Further classified by cell type of origin eg. Squamous cell papilloma

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21
Q

Benign tumour of glandular epithelium

A

Adenoma

Further classified by the name of glanular tissue of origin eg. Pancreastic cystadenoma

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22
Q

Malignant epithelial tumours are called

A

Carcinoma

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23
Q

Malignant epithelial tumours derived from glandular/ductal epithelium are called

A

Adenocarcinoma

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24
Q

What is the suffix for benign mesenchymal tumours

A
  • oma

eg. Osteoma, Lipoma, Rhabdomyoma, Leiomyoma, Chondroma, Angioma

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25
What is the suffix for malignant mesenchymal tumours
- sarcoma | eg. Osteosarcoma, Liposarcoma, Rhabdomyosarcoma, Leiomyosarcoma, Chondrosarcoma, Angiosarcoma
26
What is the benign tumour of melanocytes called
Melanocytic Nevus
27
What is the malignant tumour of melanocytes called
Melanoma
28
What is a Hamartoma?
A hamartoma is a benign, focal malformation that resembles a neoplasm in the tissue of its origin. This is not a malignant tumor, and it grows at the same rate as the surrounding tissues. It is composed of tissue elements normally found at that site, but which are growing in a disorganized mass. eg. Lung hamartoma
29
What is a Choristoma
a mass of histologically normal tissue in an abnormal location. eg. normal (non-neoplastic) pancreas nodule in stomach
30
What are genotoxic carcinogens called?
Initiators Mutation induction requires: Chemical modification of DNA Replication of modified DNA and mis-incorporation by DNA polymerase
31
What are non-genotoxic carcinogens called?
Promoters induce proliferation and DNA replication
32
What are the two important ways that promoters contribute towards carcinogenesis ?
Firstly, they can stimulate the two rounds of DNA replication required for mutation fixation Secondly, they can stimulate clonal expansion of mutated cells, which enables the accumulation of further mutations
33
What can lead to the epigenetic inactivation of tumour suppressor genes (TSGs)?
Aberrent CpG methylation of gene promoters
34
Give an example of a procarcinogen that is metabolically activated
Benzopyrene is metabolised into BPDE which is carcinogenic
35
Genetic polymorphisms in genes encoding for enzymes with what three functions may confer greater or lesser susceptibility persons susceptibility to the effects of carcinogenic exposure?
Metabolic activation Detoxification and excretion DNA repair mechanisms
36
What are the categories of human carcinogens with examples?
Chemicals e.g. Polycyclic aromatic hydrocarbons (PAHs), nitrosamines Infectious agents e.g. human papilloma virus, Helicobacter pylori Radiation e.g. UV light, radon Minerals e.g. asbestos, heavy metals Physiological e.g. oestrogen, androgens Chronic inflammation – free radicals and growth factors
37
What effect does mutation of a oncogene hve upon cell function?
Gain in function
38
What effect does mutation of a tumour suppressor gene have on cell function?
Loss of function
39
What produces aflatoxin and what is its carcinogenic effect?
Aflatoxin is produced by aspergillus flavus which resides in improperly kept corn Aflatoxin is a liver carcinogen
40
What is a caretakers?
A tumour suppressor gene which maintains genetic stability - DNA repair genes - Controlling accuracy of mitosis
41
What are gatekeepers?
TSGs which play important roles in regulating normal growth: - Negative regulators of the cell cycle and proliferation - Positive regulators of apoptosis - Positive regulators of cell differentiation
42
Mutation in which TSG is causative of the familial cancer syndrome Retinoblastoma?
Retinoblastoma = RB1
43
Mutation in which TSG is causative of the familial cancer syndrome Li-Fraumeni?
Li-Fraumeni = p53 causes sarcomas and breast cancer
44
Mutation in which TSG is causative of the familial cancer syndrome Familial adenomatous polyposis?
Familial adenomatous polyposis (colorectal) = APC
45
Mutation in which TSG is causative of the familial cancer syndrome familial breast cancer?
BRCA1 and BRCA2 also cause ovarian tumours
46
Mutation in which TSG is causative of the familial cancer syndrome Hereditary non-polyposis colorectal cancer?
Hereditary non-polyposis colorectal cancer = hMLH1 and hMSH2 also causes endometrial cancer
47
What are proto-oncogenes?
Proto-oncogenes promote cell proliferation, survival, angiogenesis and negative regulation of apoptosis Mutations can lead to activated versions or increased expression of proto-oncogenes, this gain in function makes it a oncogene
48
What is an oncogene?
A mutated proto-oncogene which causes increased levels of cell proliferation, survival, angiogenesis and inhibition of apoptosis
49
What are 3 mechanisms of oncogene activation?
Translocation of a proto-oncogene from a low transcriptionally active site to an active site - aberrant expression of the oncogene Point mutation - substitution of a single base pair can alter an amino acid in the protein causing it to become hyperactive Amplification by insertion of multiple copies of an oncogene – increased expression
50
What are the 6 acquired functional capabilities of cancer cells?
``` Self sufficient in growth signals Insensitivity to antigrowth signals Evading apoptosis limitless potential for replication Sustained angiogenesis Tissue invasion and metastasis ```
51
Why might a mutation in the proto-oncogene coding for the protein RAS increase function?
RAS is a G-protein involved in signal transduction. A mutation in the protein may lead to it losing its ability to cleave the phosphate off GTP to make GDP, leaving it in the activated state constantly This is an example of self sufficiency in growth signals.
52
What is the function or RB protein?
RB protein is a key regulator of cell cycle by preventing progression from G1 to S phase. -ve Growth Factors such as TGF-beta inhibit progression of the cell cycle by activating RB protein
53
What example might cause a cell to become resistant to negative growth factors?
inactivation of RB gene
54
How do many cancer cells become immortal?
Proliferating tumour cells can overexpress the telomerase enzyme to maintain normal telomere length
55
Inactivation of which gene gives cancer cells resistance to apoptosis?
Tp53 Inherited mutation in one allele results in Li-Fraumeni cancer syndrome
56
tumours greater that what diameter require a good blood supply?
2mm
57
How does hypoxia induce angiogenesis?
Hypoxia stabilizes HIF-1 transcription factor, which induces vascular endothelial growth factor (VEGF) – an angiogenic factor
58
What causes epithelial-mesenchymal transition (EMT) and how does this help in metastasis?
loss of E-cadherin through mutation/hypermethylation of the gene Mesenchymal cells are motile and secrete proteases - allows them to break through basement membrane and invade the underlying stroma
59
Which serum antigen is raised in ovarian cancer that is used as a marker for diagnosis and response to treatment?
CA-125 serum antigen is raised in ovarian cancer
60
Which +ve growth factor receptor is overexpressed in some breast tumours and what drug is used to help treat these patients?
HER2 receptor Herceptin is an antibody drug targeted to HER2 and dampens the effects of an overactive HER2 receptor

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