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Pathology Flashcards

1
Q

What are the 3 types of growth receptor?

A

tyrosine kinase receptors; GPCRs and receptors without tyrosine kinase activity

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2
Q

What are the main stages of the cell cycle?

A

G1, S, G2 and M

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3
Q

What controls the steps of the cell cycle?

A

cyclin dependent kinases that activate each other and other enzymes

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4
Q

What is the main cyclin expressed during metaphase?

A

cyclin B

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5
Q

What happens in G1?

A

cell gets bigger with increased protein synthesis

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6
Q

What CDK is actiavted during G1?

A

CDK4

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7
Q

What is the effect of CDK4?

A

phosphorylates the retinoblastoma protein

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8
Q

What cyclin activates CDK4?

A

cyclin D

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9
Q

What is the retinoblastoma protein usually bound to?

A

E2F

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10
Q

What is the function of E2F?

A

stimulates cell division

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11
Q

What is the function of the phosphorylation of Rb?

A

Rb can’t bind to E2F so E2F is able to stimulate cell disivion

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12
Q

What cyclin does E2F increase the levels of?

A

cyclin A

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13
Q

What CDK does cyclin A actiavte?

A

CDK2

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14
Q

What is the function of CDK2?

A

promotes DNA replication

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15
Q

What should be present at the end of S phase in the cell?

A

2 copies of genome

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16
Q

What is the main chekcpoint protein at the end of G2?

A

p53

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17
Q

What is the function of p53?

A

checks for DNA mistakes

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18
Q

Give an example of a cell which is terminally differentiated (can’t divide) or exhibit replicative sensence?

A

neurons

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19
Q

What is the function of telomeres?

A

provides protection and stops chromosome ends from degradation and fusion

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20
Q

Where does hypertrophy occur in isolation without hyperplasia?

A

in non-dividing cells eg cardiac myocytes and SK muscle

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21
Q

Which hormones promote degradation and atrophy?

A

glucocorticoids and thyroid hormone

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22
Q

What pathway are proteins often degraded by?

A

ubiquitin proteasome pathway

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23
Q

What is vasodilation in inflammation mediated by?

A

histamine and nitric oxide

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24
Q

What allows white cell margination?

A

vascular dilatation which slows rate of flow

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25
Q

What do selectins bind to?

A

proteoglycans on white cellls

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26
Q

Where are integrins found?

A

surface of white cells

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27
Q

what do integrins bind to?

A

ICAM

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28
Q

What factors increase selectin expression?

A

histamine and thrombin

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29
Q

What factors increase cell expression of VCAM and ICAM?

A

TNF and IL1

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30
Q

What is the function of chemokines on the endothelial cell surface?

A

bind to proteoglycans to increase the affinity of VCAMs and ICAMs for integrins

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31
Q

What substances cause endothelial contraction?

A

histamine; bradykinin; substance P; leukotrienes

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32
Q

What mediates transcytosis?

A

VEGF

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33
Q

What is chemotaxis?

A

cells follow a chemical gradient

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34
Q

What is pain in inflammation mediated by?

A

prostaglandins and bradykinin

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35
Q

What is resolution?

A

complete restoration of the itssue to nomral after removal of inflammatory components

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36
Q

What is required for resolution?

A

tissue capacity for repair; good vascular supply; scaffold

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37
Q

What healing is favoured if damage goes beyond the basemenet membrane?

A

organisation and repair

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38
Q

What happens after granulation tissue?

A

defect is slowly infiltrated by capillaries and then myofibroblasts which deposit collagen and SM

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39
Q

When is chronic inflammation favoured?

A

suppuration; persistence of injury and types of injury e.g autoimmune

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40
Q

Waht is chronic inflammation characterisedby?

A

lymphocytes and macrophages

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41
Q

What are the outcomes of acute inflammation?

A

resolution; suppuration; repair organisation and fibrosis; chornci inflammation

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42
Q

What does increased calcium in the cell stimulate?

A

ATPase; phospholipase; proteases; endonucleases; mitochondrial permeability

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43
Q

What is pyknosis?

A

irreversible condensation of chromatin in a cell undergoing necrosis or apoptosis

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44
Q

What are the first signs of necrosis?

A

cells shrink; become red; darkened nucleus and marginal contraction bands appear

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45
Q

What is diapedesis?

A

passage of blood cells thorugh endothelium

46
Q

What are hte types of necrosis?

A

caseous; liquefactice; coagulative

47
Q

What is seen with coagulative necrosis?

A

cell death with some structure of cells left as ghost outline before complete phagocytosis

48
Q

When is the greatest risk of cardiac rupture following an MI?

49
Q

What colour does the presence of macrophages cause?

50
Q

What happens in restitution?

A

macrophages are replaced by fibroblasts

51
Q

What is the difference between neoplasia and hyperplasia?

A

neoplasia is new growth not in response to a stimulus

52
Q

What is the only part of the body not to undergo neoplasia?

A

lens of the eye

53
Q

What is metaplasia?

A

reversible change from one mature cell to another mature cell type

54
Q

What causes metaplasia?

A

change in signals delivered to stem cells causing them to differentiate down a different line

55
Q

Why is squamous metaplasia commonly encountered in response to injury?

A

very resistant to noxious stimuli

56
Q

What is dysplasia?

A

disordered growth

57
Q

What are Weinberg hallmarks?

A

specific genes/proteins with specific functions that enable cellular progression to malignancy

58
Q

What is the affected gene in FAP?

59
Q

What is the double hit hypothesis?

A

need two faulty copies to have a functional problem

60
Q

What disease is associated with p53 mutation?

A

Li Fraumeni syndrome

61
Q

What mutation is associated iwth MEN1?

62
Q

What mutations are associated with aflatoxins?

63
Q

What problem does radiation cause?

A

formation of pyrimidine dimers in DNA

64
Q

What is the defect in xeroderma pigmentosa?

A

defect in nucleotide excision repair

65
Q

What virus is E7 associated with?

66
Q

What does E7 do?

A

binds to retinoblastoma which results in free E2F

67
Q

What is the function of E6?

A

increases destruction of p53

68
Q

Waht type of UV radiation is really bad?

69
Q

What are the effects of vitamin D on the skin?

A

increase cell differentiation and apoptosis and decrease angiogenesis

70
Q

What type of cancer is especially asssocaited iwth RAS mutations?

71
Q

What cancer is assocaited with Braf mutations?

72
Q

What cancer is associated with C-KIT?

A

GI stromal tumours

73
Q

What is Myc?

A

a nuclear transcription factor that promotes growth

74
Q

What is the most commonly mutated kinase in cancer?

75
Q

How does p53 pause the cell cycle?

A

increases levels of p21 which inihibts CDK

76
Q

How does p53 induce apoptosis?

A

via BAX pathway

77
Q

What is the fucntion of Bcl-2?

A

binds bax/Bak to stop holes being punched in mitochondria- anti-apoptotic molecule

78
Q

What is the function of MLH1?

A

mismatch repair protein

79
Q

What syndrome has an abnormal MLH1?

A

lynch syndrome

80
Q

What are microsatellites?

A

segments of repeated DNA codes specific to an individual

81
Q

What is microsatellite instability?

A

microsatellites are full of errors- indicates a problem with DNA repair

82
Q

What is the function of PD-L1?

A

inhibits T cell proliferation

83
Q

How do cancers destroy surrounding tissues?

A

increase expression of matrix metalloproteinases

84
Q

what substance is produced by tumours that results in increased metabolism?

85
Q

What are the histological features of a malignant cell?

A

increased N:C ratio; pleomorphism; hyperchromasia; mitoses; necrosis;

86
Q

What is th restul of advanced glycation end products in DM?

A

abnormal crosslinking in vessel walls

87
Q

What are the steps in atherosclerosis?

A

priamry endothelial injury; accumulation of lipids and macrophages; migration os SM; increase in size

88
Q

Why does endothelial injury result in atheroma?

A

increased permeability and increased white cell adhesion- monocytes migrate through wall and beomce macrophages

89
Q

Where does smooth muscle migrate from in atheroma?

A

from media to intima

90
Q

what does the presence of smooth muscle chagne about the atheroma?

A

from fatty streak to fibrofatty plaque

91
Q

What forms the centre of hte plaque in atheroma?

A

pool of extracellular cholesterol

92
Q

Waht is arterial systole?

A

narrowing of arterial lumen; reduced elasticity; reduced flow in systole and tissue ischaemia

93
Q

What is anaplasia?

A

malignant cells which are very undifferentiated (can’t tell cell of origin)

94
Q

How do G cells in the stomach appear?

95
Q

What do chief cells in the stomach secrete?

A

pepsinogen

96
Q

What is the function of parietal cells in the stomach?

A

secrete HCl

97
Q

What is the risk factor for endometrial hyperplasia?

98
Q

What is endometrioid cancer associated with?

A

endometrial hyperplasia- obesity

99
Q

What cancers are associated with HNPCC?

A

colorectal; endometrial; ovarian and TCC

100
Q

What type of colorectal cancer is seen with HNPCC?

A

sessile (flat)

101
Q

Where in the colon are tumours in HNPCC found?

A

right-side (normally left side is a lot more common)

102
Q

What is the other name for a leiomyoma?

103
Q

What age groups get sarcoma?

104
Q

What is a histiocyte?

A

stationery phagocytic cell in connective tissue

105
Q

What is the response to foreign bodies?

106
Q

What cell is assocaited with granulomas?

A

histiocytes

107
Q

Why do adenocarcinomas appear as signet ring?

A

mucin is pushing the nucleus to the edge

108
Q

What is the prognosis of an adenocarcinoma with signet ring morphology?

109
Q

What does pink blobs on pathology indicate?

A

keratin- SCC

110
Q

What is a psamomma body?

A

abnormal calcification in papillary cancer as well as serous ovarian carcinoma

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