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My1 Principles > pathology > Flashcards

pathology Flashcards

1
Q

what are some signs of inflammation

A

redness, heat, swelling, pain and loss of function

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2
Q

what can cause inflammation

A

infection, trauma, foreign body, immune response

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3
Q

describe transendothelial migration

A

blood slows and vasodilation, white blood cells move to side of vessel. neutrophils activate CAM 1 which are adhesion molecules and histamine and thrombin increase their affinity. the white blood cells roll along vessel until they stick, chemokines from site of injury also increase affinity. Blood vessels become leaky and cells pass through (diapedesis) follow chemical gradient ‘chemotaxis’, neutrophils then phagocytose

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4
Q

what causes the release of histamine

A

mast cells, eosinophils, basophils

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5
Q

what receptors on phagocytes (neutrophils) let them recognise bacteria

A

mannose receptors

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6
Q

describe phagocytosis

A

pseudopods extend from phagocyte to form a phagosome, it joins with lysosome to form a phagolysosome and cytotoxic granules kill bacteria

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7
Q

how else can neutrophils kill

A

reactive oxygen species which requires NAPDH

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8
Q

what is resolution

A

complete restoration of tissue to normal, minimal cell death, tissue must have capacity to repair ie good blood supply and bad agents easily removed

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9
Q

what is suppuration

A

formation of pus which contains dead/ dying cells, neutrophils, bacteria and fibrin

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10
Q

organisation of tissue happens when?

A

lots of necrosis and fibrin isn’t cleared properly, often with poor blood supply.

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11
Q

what replaces normal tissue in organisation

A

granulation, myofibroblasts deposit collagen which leads to scarring and fibrosis

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12
Q

what is a granuloma

A

a collection of macrophages in response to swelling

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13
Q

which cells are involved in chronic inflammation

A

lymphocytes, plasma cells and macrophages

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14
Q

what are some characteristics of chronic inflammation

A

chronic ulcer, scarring, granulomas, abscess, thickening of walls

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15
Q

what is infarction

A

cell death due to a lack of o2

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16
Q

how long is the reversible time frame in myocardium

A

20 mins

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17
Q

in what 2 processes are cells killed

A

apoptosis and necrosis

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18
Q

what is necrosis

A

premature cell death

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19
Q

what is apoptosis

A

programmed cell death

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20
Q

why are free radicals dangerous and what can stop them

A

they cause chain reactions leading to lipid peroxidation, protection by anti-oxidants

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21
Q

what are liable cells

A

constantly dividing eg bone marrow

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22
Q

what are stable cells

A

only divide when needed eg liver

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23
Q

what are the 2 types of metabolic disorders

A

inherited or acquired

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24
Q

what is the cell cycle controlled by

A

CDK’s, activated by specefic cyclin

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25
Q

what are the 4 stages of the cell cycle

A

G1, S, G2, M

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26
Q

how is G1 activated

A

CDK4 activated by cyclin D

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27
Q

how does cell growth happen in G1

A

CDK4 actiavtes retinoblastoma (Rb) which releases transcription factor E2F.

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28
Q

how is S phase activates

A

CDK2 and cyclin A

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29
Q

what happens in S phase

A

DNA replication

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30
Q

what is G0

A

insufficient cyclin so cell does not divide (stable cells)

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31
Q

what is p53

A

a G1 checkpoint protein that checks for mistakes, can pause cell cycle and try to repair or kill cell

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32
Q

what is M stage

A

mitosis - cell division

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33
Q

what happens to telomeres during division

A

telomeres on chromosomes are capped, every-time they divide cap gets smaller, once hayflick limit reached they die

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34
Q

what happens to telomeres in stem cells

A

telomerase adds caps so cell can divide indefinitely

35
Q

is p53 is under active what can happen

A

cancer

36
Q

if p53 is overactive what can happen

A

degenerative disease

37
Q

what 2 pathways can apoptosis kill abnormal cells by

A

intrinsic and extrinsic (death signals)

38
Q

what is the morphology of apoptosis or

A

1) cell shrinks (pyknosis) 2) chromatin condensation 3) cytoplasmic blebs (cytoplasm breaks up), 4) macrophages hover up

39
Q

what are the main types of necrosis (3)

A

coagulative (MI), liquefactive (brain) and caseous (TB)

40
Q

when does fibrinoid necrosis occur

A

blood vessels, possible due to hypertension

41
Q

which requires energy apoptosis or necrosis

A

apoptosis

42
Q

which can be physiological apoptosis or necrosis

A

apoptosis

43
Q

what is hyperplasia

A

fast cell division - more cells

44
Q

what is hypertrophy

A

cells get bigger but don’t reply, normally in response to stress

45
Q

what is atrophy

A

reduction in cell size

46
Q

what is hypoplasia

A

reduced size of an organ that never full developed

47
Q

which is non-reversible

A

hypoplasia

48
Q

what is metaplasia and an example

A

change of one cell type to another in response to stress/ stimuli eg barrett’s oesophagus

49
Q

what is dysplasia

A

presence of abnormal cells in tissue - no invasion beyond basement membrane

50
Q

what is a carcinoma in situ

A

last stage before invasive, affects whole of epithelium

51
Q

what is an oncogene

A

a gene that promotes cell division eg PDGF, ras, src

52
Q

name some autosomal dominant oncogenes

A

retinoblastoma and FAP

53
Q

what is BRCA, what do mutations do

A

a tumour suppressor, can increase chances of cancer

54
Q

name some initiators that can cause genetic damage that may lead to cancer

A

smoking, aflatoxins (fungus), polycyclic aromatic hydrocarbons (meat + fish)

55
Q

what virus is associated with cancer

A

EBV

56
Q

what are growth receptors

A

receptors with or without tyrosine kinase activity, 7 transmembrane G-receptor proteins

57
Q

what is the most commonly mutated kinase in cancer

A

P13K

58
Q

what is Myc

A

nuclear transcription factor promoting growth

59
Q

what are tumour supressors

A

stop growth eg p53, VHL, BRCA and PTEN

60
Q

what can malignancy do to telomerase

A

reactivate it so cancer cells can never die

61
Q

what do Bcl-2 proteins do

A

stop bax/ bak attackin cell in apoptosis

62
Q

what is angiogenesis

A

cancer grows it’s own blood supply to grow, increases VEGF

63
Q

what proteins are responsible for identifying faults in code

A

mismatch proteins

64
Q

how can tumour evade the immune system

A

inhibiting PDl1, and T cell proliferation, they over express

65
Q

describe the stages of cancer formation

A

1) increase growth receptors eg P13K, 2) inhibit tumour supressors eg p53, 3) divide 4) resist apoptosis (Bcl2) 5) angiogenesis, 6) repair 7) evade immune system 8) adhere to new vessel

66
Q

describe the lineage of cancer

A

each daughter cell is different, makes it harder to treat, immortal

67
Q

what do benign tumours normally look like

A

smooth, symmetrical, encapsulated

68
Q

what do malignant cancers normally look like

A

irregular, no capsule, high nucleus: cytoplasm (N:C)

69
Q

what has a better prognosis highly or poorly differentiated cells

A

highly

70
Q

what are some cancer cell characteristics

A

pleomorphism (variety), hyperchromasia (big nuclei), mitosis and necrosis

71
Q

what is a malignant epithelial called

A

carcinoma

72
Q

what is a malignant and benign glandular called

A

adenoma, adenocarcinoma

73
Q

what is a malignant and benign squamous called

A

papilloma, squamous cell carcinoma

74
Q

what is a malignant and benign connective tissue called

A

mesenchyme, sarcoma

75
Q

what is a malignant and benign fat called

A

lipoma, liposarcoma

76
Q

what is a malignant and benign bone called

A

osteoma, osteosarcoma

77
Q

what is a malignant bladder cancer called

A

transitional cell carcinoma

78
Q

what is blood cancer called

A

leukaemia

79
Q

what is the stage of a cancer? (TNM)

A

how far it’s spread, has it invaded lymph nodes, has it metastasised

80
Q

describe T1-T4

A

T1: invasion of submucosa
T2: invasion of musclaris proproa
T3: invasion of tissue
T4: invasion of organ

81
Q

describe N0-2

A

N0; no lymph nodes
N1: 1-3
N2: 4+

82
Q

describe M0/1

A

M0: no mets
M1: mets

83
Q

what is meant by the grade of the cancer

A

how differentiated it is, poor differentiation = high grade

My1 Principles (12 decks)

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