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REVISION EXTRAS > BLOCK 9 > Flashcards

BLOCK 9 Flashcards

1
Q

which genes are associated with ovarian cancer?

A

BRCA 1 and 2

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2
Q

which genes are associated with lung cancer/

A

KRAS
TP53
EGFR

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3
Q

which genes are associated with hereditary nonpolyposis colorectal cancer?

A

MSH2 and MLM1

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4
Q

which genes are associated with familial adenomatous polyposis?

A

APC

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5
Q

which genes are associated with breast cancer?

A

BRCA 1

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6
Q

what are aflatoxins?

A

family of toxins produced by certain fungi that are found on agricultural crops such as maize (corn), peanuts, cottonseed, and tree nuts
e.g. aspergillus

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7
Q

what cancer are aflatoxins linked to?

A

liver

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8
Q

what are the 2 characteristics of neoplasia?

A

anaplasia - loss of differentiation and organisation

autonomy

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9
Q

how can tumours cause angiogenesis??

A

they can secrete angiogenic factors which bind epithelial cells and cause formation of new blood vessels

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10
Q

what are some angiogenic factors?

A

vascular endothelial growth factor (VEGF)
fibroblast growth factor 2 (FGF-2)
platelet derived growth factor (PDGF)

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11
Q

how many chromatids are present at the end of G1?

A

46 chromosomes and 46 chromatids

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12
Q

how many chromatids are present at the end of S phase?

A

46

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13
Q

how many chromatids are present at the end of G2?

A

92

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14
Q

when are the 3 checkpoints of cell division?

A

end of G1
end of G2
at the metaphase/anaphase transition in mitosis

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15
Q

whats the specific cyclin and CDK subtype in early G1?

A

cyclin D and CDK4 and 6

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16
Q

whats the specific cyclin and CDK subtype in late G1?

A

cyclin E

CDK 2

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17
Q

whats the specific cyclin and CDK subtype in S phase?

A

cyclin A and CDK 2 and 1

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18
Q

whats the specific cyclin and CDK subtype in G2?

A

cycln B and CDK 1

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19
Q

whats the difference between protooncogenes and oncogenes?

A

proto oncogenes are healthy cells with regulate cell growth and division
oncogenes are the mutated form

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20
Q

how many mutated alleles are needed for an oncogene to cause avoidance of apoptosis?

A

1

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21
Q

how many mutated alleles are needed for an tumour suppressor gene to cause avoidance of apoptosis?

A

both - its recessive

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22
Q

what are examples of oncogenes?

A

RAS

MYC

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23
Q

what are examples of tumour suppressor genes?

A

P53
APC
BRCA 1 and 2

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24
Q

whats the normal function of RAS protein?

A

they are intracellular proteins which sit below the plasma membrane and when activated turn from RAS-GDP to RAS-GTP and induce apoptosis

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25
Q

whats the normal function of MYC?

A

they increase expression of cyclin and CDKs

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26
Q

which gene is found is almost all pancreatic cancers?

A

K-ras

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27
Q

what are examples of gatekeeper genes?

A

p53 and Rb

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28
Q

whats the function of gatekeeper genes?

A

they directly regulate tymour growth

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29
Q

outline the DNA damage response pathway?

A

P53 is normally bound to MDM2
when ATM is released during cell damage, P53 is phosphorylated and released from MDM2
this can then upregulate P21/WAF1 which inhibits cyclinE and CDK2, preventing the transuton from G1 phase to S phase
P53 can also increase transcription of PUMA which inhibits bcl-2 leading to activation of caspases and apoptosis

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30
Q

simply outline pathophysiology behind cervical cancer?

A

HPV protein E6 stimulates ubiquitin attachment to P53 which causes destruction
HPV protein E7 binds to Rb and inhibits it so cell cycle isnt inhibited

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31
Q

what cancers can Rb gene cause?

A

retinoblastoma and osteosarcoma

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32
Q

outline the mechanism of activation of pRb?

A

pRB is usually bound to and inhibits E2F
when its activated by cyclin D CDK4, pRB gets phosphorylated and E2F is released
E2F can then transcribe cyclin E and CDK 2 which prevents G1 to S transition

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33
Q

whats an example of a protein which inhibits apoptosis?

A

BCl-2

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34
Q

whats an example of a protein that promotes cell cycle progression?

A

myc

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35
Q

what does vinyl chloride become once its been biotransformed in the liver and what can this cause?

A

vinyl chloride epoxide

liver cancer

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36
Q

what does the hallmark of cancer ‘cell immortalisation’ mean?

A

increased telomerase activity in cells which allows them to divide indefinitly

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37
Q

what is xeroderma pigmentosum?

A

an autosomal recessive condition

mutation in XP genes involved in DNA repair

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38
Q

what is familial adenomatous polyposis?

A

an autosomal dominant condition

APC gene mutation which usually suppresses beta-catenin proteins

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39
Q

what infection is Kaposis sarcoma associated with?

A

human herpesvirus 8

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40
Q

what infection is gastric cancer associated with?

A

H.pylori

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41
Q

what infection is Burkitts lymphoma associated with?

A

epstein barr virus

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42
Q

what infection is Hodgkins lymphoma associated with?

A

epstein barr virus

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43
Q

what infection is nasopharyngeal cancer associated with?

A

epstein barr virus

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44
Q

what infection is cervical and penile cancer associated with?

A

human papilloema 16 and 18

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45
Q

which virus is hepatocecllular carcinoma associated with?

A

hep B and C

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46
Q

which cancers can contraceptive pill reduce risk of?

A

endometrial, ovarian, and colorectal cancers

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47
Q

which cancers can contraceptive pill increase risk of?

A

breast and cervical

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48
Q

which cancer is most strongly linked to occupational exposure?

A

bladder cancer

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49
Q

whats the precursor to colorectal cancer?

A

adenomatous polyp formation

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50
Q

what is the most common acute lymphoid leukaemia?

A

B cell ALL

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51
Q

which mutation is B-ALL associated with?

A

t(12,21)

t(9,22)

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52
Q

what mutation is T-ALL associated with?

A

NOTCH1 mutation

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53
Q

what are the risk factors for acute leukaemia?

A

young age
downsyndrome
radiation exposure

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54
Q

what mutation is acute promyelocytic leukaemia associated with?

A

t(15,17) - disruption of retinoic acid receptor so prmyelocytes accumulate

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55
Q

whats the risk factor for acute myeloid leukaemia?

A 
age around 60
radiation
chemotherapy
downsyndrome
myeloproliferative disorders
56
Q

what is acute leukaemia?

A

uncontrolled proliferation of blast cells (partially developed WBCs) hich build up in the blood

57
Q

what is acute leukaemia?

A

uncontrolled proliferation of blast cells (partially developed WBCs) hich build up in the blood

58
Q

what can haematopoeitic stem cells become?

A

myeloblasts or lymphblasts

59
Q

what can myeloblasts become?

A

erythrcytes
thrombocyte
monocyte
granulocyte (neutrophil, basophil and eosinophil)

60
Q

what can lymphoblasts become?

A

B cells

T cells and NK cells

61
Q

what is the Philadelphia chromosome?

A

t(9,22)

62
Q

what are the types of AML?

A 
AML without maturation
AML with minimal maturation
AML with maturation
acute promyelocytic leukaemia
acute myelomonocytic leukaemia
acute monocytic leukaemia
acute erythroid leukaemia
acute megakaryoblastic leukaemia
63
Q

what is myelodyplastic syndrome?

A

defective maturation of myeloid cells and build up of blasts in the bone marrow
this is a syndrome that can lead to AML

64
Q

outline the pathology of acute leukaemia?

A

blood cells lose their ability to differentiate so they get stuck in the blast stage and don’t function effectively
it causes blast cells to divide uncontrollably which takes up a lot of space in the bone marrow
this makes other blood cells get crowded out - causing cytopenias
eventually blast cells spill out into the blood. Some settle into organs and tissues.

65
Q

why can thymus and lymph nodes enlarge in T cell ALL?

A

because pe-T cells can migrate to these areas, settle down here an cause these structures to enlarge

66
Q

which type of acute leukaemia can cause disseminated intravascular coagulation and why?

A

acute promyelocytic leukaemia

as it can activate the clotting process (along with already low platelets)

67
Q

which type of acute leukaemia can cause swelling of gums and why?

A

acute myelomonocytic leukaemia because we get monocytic infiltration

68
Q

what would you expect the percentage of blast cells to be in acute leukaemia?

A

from 1-2% to >20%

69
Q

how can you differentiate AML from ALL?

A

blood smear:
myeloblasts are larger than lymphoblasts
myeloblasts have finer chromatin and auer rods
lymphoblasts have coarse chromatin and glycogen granules

immunophenotying
TdT - lymphocytes
CD10- pre-B cells

70
Q

how is acute leukaemia treated?

A

chemo
biological therapy
stem cell transplants and bone marrow transplants

acute promyelocytic leukaemia can be treated with all-trans-retinoic acid

71
Q

what mutation is 30% of AML associated with?

A

FLt3

72
Q

whats the cause of chronic myeloblastic leukaemia?

A

translocation of 9;22 to form BCR-ABL gene (Philadelphia chromosome)
This codes for the BCR-ABL protein which is a tyrosine kinase that is always on. This causes myeloid cells to divide faster, increasing mutation risk

73
Q

whats the cause of chronic lymphoblastic leukaemia?

A

not entirely known specifically but known that B cells constantly interact with their B cell receptors, activating tyrosine kinases constantly which prevents the maturation of cells and cell death

74
Q

which is chronic lymphoid leukaemia also known as?

A

small lymphocytic lymphoma

75
Q

what would you see on a blood smear in chronic myeloid leukaemia?

A

increased granulocytes and monocytes

76
Q

what would you see on a blood smear in chronic lymphoid leukaemia?

A

smudge cells - immature B cells broken during the smear

77
Q

what are receptor tyrosine kinases?

A

plasma membrane receptors with enzymatic activity that catalyses the transfer of phosphate groups

78
Q

whats an example of a tyrosine kinase inhibitors?

A

imatinib

79
Q

what is imatinibs moa?

A

targets the BCR-ABL tyrosine kinase to inhibit the cell proliferation driven by this as well as inducing apoptosis

80
Q

what is tretinoin? what is it used to treat?

A

a naturally occuring derivative of vitamin A

acute promyelocytic leukaemia

81
Q

what is tretinoins moa?

A

binds to alpha beta and gamma retinoid acid receptors which are associated with the development of acute promyelocytic leukaemia

82
Q

what is cefuroxime and what is its moa?

A

a transpeptidase inhibitor

similar to penicillin - inhibits cell wall synthesis

83
Q

what type of drug is vancomycin? whats its moa? whats it used for?

A

a peptidoglycan inhibitor (antibiotic)
used for gram negative, mycobacteria and fungi
incorporates NAM and NAG peptide subunits Into the peptidoglycan matrix forming the major structural component of cell walls

84
Q

what type of drug is fusidic acid? whats its moa?

A

a translocation inhibitor (antibiotic)

inhibits translocation of EF_G from the ribosome, leading to inhibition of protein synthesis

85
Q

what type of drug is amprenavir?

A

protease inhibitor

86
Q

what type of drug is zidovudine?

A

a nucleoside reverse transcriptase inhibitor used to treat HIV-1 - its a structural analog of thymidine so competes for incorporation into viral DNA

87
Q

what type of drug is pyrimethamine?

A

folate antagonist - anti parasitic

88
Q

what type of drug is artemether?

A

a peroxide antimalarial

89
Q

what type of drug is griseofulvin?

A

a fungal mitosis inhibitor

90
Q

what type of drug is clobetasone?

A

a glucocorticoid nuclear hormone receptor agonist

91
Q

what type of drug is dacarbazine?

A

an alkylating agent

92
Q

what type of drug is cyclophosphamide?

A

an alkylating agent

93
Q

what type of drug is rituximab?

A

B cell CD20 antibody (monoclonal)

94
Q

what type of drug is doxorubicin?

A

a DNA/RNA synthesis inhibitor (cytotoxic Anthracyclines antibiotic)

95
Q

what type of drug is paclitaxal??

A

a microtubule stabilisation agent (taxed antineoplastic)

96
Q

what type of drug is 5-fluorouracil?

A

a pyridine analogue

97
Q

what type of drug is etoposide?

A

a DNA topoisomerase 2 inhibitor

98
Q

what type of drug is vinblastine?

A

a tubulin polymerase inhibitor (vinca alkaloid)

99
Q

can viruses contain both DNA and RNA?

A

no they only contain 1 type

100
Q

whats the function of reverse transcriptase?

A

RNA -> DNA

101
Q

whats the virus envelope made of?

A

lipid and proteins derived from the host cell membrane

102
Q

what type of antibiotics can inhibit nucleic acid synthesis?

A

quinolines (inhibit topoisomerase 2 aka gyrase)

103
Q

what is the function of gyrase?

A

bacterial enzyme that catalyzes the ATP-dependent negative super-coiling of double-stranded closed-circular DN

104
Q

whats the earliest manifestation of AKI?

A

reduced urine output

105
Q

what is phenylketonuria?

A

a rare inherited disorder that causes an amino acid called phenylalanine to build up in the body. PKU is caused by a change in the phenylalanine hydroxylase (PAH) gene

106
Q

what does it mean if the ALT is raised markedly compared to ALP?

A

primarily a hepatocellular pattern of injury

107
Q

what does it mean if ALP is raised markedly compared to ALT?

A

this is primarily a cholestatic pattern of injury

108
Q

other than liver disease, when else will ALP be raised?

A

in bone disease

109
Q

whats the difference between gout and pseudogout?

A

gout involves uric acid crystals and pseudogout involves pyrophosphate crystals
gout involves smaller joints e.g. the big toe than pseudogout

110
Q

what nerve is responsible for gag reflex?

A

glossopharyngeal

111
Q

what type of vaccine is BCG?

A

live attenuates

112
Q

is GFR determines by systemic bp?

A

no iits usually independat of it de to autoregulatuon

113
Q

whats the difference betwene mono and bifunctional alkylating agents?

A

monofunctional alkylating agents, implying reactions with only one strand of DNA, or bifunctional alkylating agents, which cross-link two strands of DNA.

114
Q

whwhats an exampke of a monofunctional alkylating agent?

A

procarbazine

115
Q

what are examples of bifunctional alkylating agents?

A

nitrogen mustards
platinum drugs
nitrosureas

116
Q

what are anthravyclines moa?

A

topisomerase inhibitors

117
Q

what type of drug is cimetidine?

A

a H2 antagonist

118
Q

what type of drug is indomethacin?

A

NSAID

119
Q

what is lipopolysaccharise?

A

an endoxtoxin which is weakly toxic and common to all gram negative bacteria

120
Q

where do femoral hernias protrude?

A

below the inguinal ligament through the femoral canal below and lateral to the pubic tubercle

121
Q

what are anti-mitochondrial antibodies a marker of?

A

primary biliary cirrhosis

122
Q

whats antinuclear antibodies a marker of?

A

lupus

123
Q

what antibodies may be present in type 1 diabetes?

A

GAD65

islet cell antibodies

124
Q

what antibodies are associated with psoriatic arthritis?

A

anti-LL-37 antibodies

125
Q

what antibody is associated with graves disease?

A

thyrotropin receptot antibody

126
Q

which antibody is associated with hashimotos disease?

A

thyroid peroxidase antibodies

127
Q

what are some causes of microcytic anaemia?

A

iron deficiency
anaemia of inflamation and chronic disease
thalassemias
sideroblastic

128
Q

what are some causes of normocytic anaemia?

A 
bone marrow suppression
CKD
haemorrhage
haemolysis
sickle cell
G6PD deficiency
proxysmal noctural haemoglobinuria
129
Q

what are the 2 types of macrocytic anaemia?

A

megaloblastic and non-megaloblastic

130
Q

what are the main causes of megaloblastic anaemia?

A

vitamin B12 or folate deficiency

131
Q

whats the difference in pathology between megaloblastic and non-megaloblastic macrocyctic anemia?

A

megaloblastic is caused by impaired DNA synthesis during RBC production which caues continued cell growth without division
whilst non-megaloblastic anaemia does not have DNA replication issues

132
Q

whats the difference between graves and hashimotos disease?

A

graves disease - autoimmune disease causing hyperthyroidism

hashimotos disease - autoimmune disease causing hypothyroidism

133
Q

in which species are exotoxins found?

A

both gram neg and pos

134
Q

whats more heat stable, endotoxins or exotoxins?

A

endotoxins

135
Q

whats more toxic, endotoxins or exotoxins

A

exotoxins

REVISION EXTRAS (7 decks)

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