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EMS > MoD 3 > Flashcards

MoD 3 Flashcards

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
Q

What is the suffix for malignant mesenchymal tumours

A
  • sarcoma

eg. Osteosarcoma, Liposarcoma, Rhabdomyosarcoma, Leiomyosarcoma, Chondrosarcoma, Angiosarcoma

26
Q

What is the benign tumour of melanocytes called

A

Melanocytic Nevus

27
Q

What is the malignant tumour of melanocytes called

A

Melanoma

28
Q

What is a Hamartoma?

A

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
Q

What is a Choristoma

A

a mass of histologically normal tissue in an abnormal location.

eg. normal (non-neoplastic) pancreas nodule in stomach

30
Q

What are genotoxic carcinogens called?

A

Initiators

Mutation induction requires:
Chemical modification of DNA
Replication of modified DNA and mis-incorporation by DNA polymerase

31
Q

What are non-genotoxic carcinogens called?

A

Promoters

induce proliferation and DNA replication

32
Q

What are the two important ways that promoters contribute towards carcinogenesis ?

A

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
Q

What can lead to the epigenetic inactivation of tumour suppressor genes (TSGs)?

A

Aberrent CpG methylation of gene promoters

34
Q

Give an example of a procarcinogen that is metabolically activated

A

Benzopyrene is metabolised into BPDE which is carcinogenic

35
Q

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?

A

Metabolic activation
Detoxification and excretion
DNA repair mechanisms

36
Q

What are the categories of human carcinogens with examples?

A

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
Q

What effect does mutation of a oncogene hve upon cell function?

A

Gain in function

38
Q

What effect does mutation of a tumour suppressor gene have on cell function?

A

Loss of function

39
Q

What produces aflatoxin and what is its carcinogenic effect?

A

Aflatoxin is produced by aspergillus flavus which resides in improperly kept corn

Aflatoxin is a liver carcinogen

40
Q

What is a caretakers?

A

A tumour suppressor gene which maintains genetic stability

  • DNA repair genes
  • Controlling accuracy of mitosis
41
Q

What are gatekeepers?

A

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
Q

Mutation in which TSG is causative of the familial cancer syndrome Retinoblastoma?

A

Retinoblastoma = RB1

43
Q

Mutation in which TSG is causative of the familial cancer syndrome Li-Fraumeni?

A

Li-Fraumeni = p53

causes sarcomas and breast cancer

44
Q

Mutation in which TSG is causative of the familial cancer syndrome Familial adenomatous polyposis?

A

Familial adenomatous polyposis (colorectal) = APC

45
Q

Mutation in which TSG is causative of the familial cancer syndrome familial breast cancer?

A

BRCA1 and BRCA2

also cause ovarian tumours

46
Q

Mutation in which TSG is causative of the familial cancer syndrome Hereditary non-polyposis colorectal cancer?

A

Hereditary non-polyposis colorectal cancer = hMLH1 and hMSH2

also causes endometrial cancer

47
Q

What are proto-oncogenes?

A

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
Q

What is an oncogene?

A

A mutated proto-oncogene which causes increased levels of cell proliferation, survival, angiogenesis and inhibition of apoptosis

49
Q

What are 3 mechanisms of oncogene activation?

A

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
Q

What are the 6 acquired functional capabilities of cancer cells?

A 
Self sufficient in growth signals 
Insensitivity to antigrowth signals 
Evading apoptosis
limitless potential for replication
Sustained angiogenesis
Tissue invasion and metastasis
51
Q

Why might a mutation in the proto-oncogene coding for the protein RAS increase function?

A

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
Q

What is the function or RB protein?

A

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
Q

What example might cause a cell to become resistant to negative growth factors?

A

inactivation of RB gene

54
Q

How do many cancer cells become immortal?

A

Proliferating tumour cells can overexpress the telomerase enzyme to maintain normal telomere length

55
Q

Inactivation of which gene gives cancer cells resistance to apoptosis?

A

Tp53

Inherited mutation in one allele results in Li-Fraumeni cancer syndrome

56
Q

tumours greater that what diameter require a good blood supply?

A

2mm

57
Q

How does hypoxia induce angiogenesis?

A

Hypoxia stabilizes HIF-1 transcription factor, which induces vascular endothelial growth factor (VEGF) – an angiogenic factor

58
Q

What causes epithelial-mesenchymal transition (EMT) and how does this help in metastasis?

A

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
Q

Which serum antigen is raised in ovarian cancer that is used as a marker for diagnosis and response to treatment?

A

CA-125 serum antigen is raised in ovarian cancer

60
Q

Which +ve growth factor receptor is overexpressed in some breast tumours and what drug is used to help treat these patients?

A

HER2 receptor

Herceptin is an antibody drug targeted to HER2 and dampens the effects of an overactive HER2 receptor

EMS (5 decks)

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