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pathology Flashcards

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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
what are the 4 stages of the cell cycle
G1, S, G2, M
26
how is G1 activated
CDK4 activated by cyclin D
27
how does cell growth happen in G1
CDK4 actiavtes retinoblastoma (Rb) which releases transcription factor E2F.
28
how is S phase activates
CDK2 and cyclin A
29
what happens in S phase
DNA replication
30
what is G0
insufficient cyclin so cell does not divide (stable cells)
31
what is p53
a G1 checkpoint protein that checks for mistakes, can pause cell cycle and try to repair or kill cell
32
what is M stage
mitosis - cell division
33
what happens to telomeres during division
telomeres on chromosomes are capped, every-time they divide cap gets smaller, once hayflick limit reached they die
34
what happens to telomeres in stem cells
telomerase adds caps so cell can divide indefinitely
35
is p53 is under active what can happen
cancer
36
if p53 is overactive what can happen
degenerative disease
37
what 2 pathways can apoptosis kill abnormal cells by
intrinsic and extrinsic (death signals)
38
what is the morphology of apoptosis or
1) cell shrinks (pyknosis) 2) chromatin condensation 3) cytoplasmic blebs (cytoplasm breaks up), 4) macrophages hover up
39
what are the main types of necrosis (3)
coagulative (MI), liquefactive (brain) and caseous (TB)
40
when does fibrinoid necrosis occur
blood vessels, possible due to hypertension
41
which requires energy apoptosis or necrosis
apoptosis
42
which can be physiological apoptosis or necrosis
apoptosis
43
what is hyperplasia
fast cell division - more cells
44
what is hypertrophy
cells get bigger but don't reply, normally in response to stress
45
what is atrophy
reduction in cell size
46
what is hypoplasia
reduced size of an organ that never full developed
47
which is non-reversible
hypoplasia
48
what is metaplasia and an example
change of one cell type to another in response to stress/ stimuli eg barrett's oesophagus
49
what is dysplasia
presence of abnormal cells in tissue - no invasion beyond basement membrane
50
what is a carcinoma in situ
last stage before invasive, affects whole of epithelium
51
what is an oncogene
a gene that promotes cell division eg PDGF, ras, src
52
name some autosomal dominant oncogenes
retinoblastoma and FAP
53
what is BRCA, what do mutations do
a tumour suppressor, can increase chances of cancer
54
name some initiators that can cause genetic damage that may lead to cancer
smoking, aflatoxins (fungus), polycyclic aromatic hydrocarbons (meat + fish)
55
what virus is associated with cancer
EBV
56
what are growth receptors
receptors with or without tyrosine kinase activity, 7 transmembrane G-receptor proteins
57
what is the most commonly mutated kinase in cancer
P13K
58
what is Myc
nuclear transcription factor promoting growth
59
what are tumour supressors
stop growth eg p53, VHL, BRCA and PTEN
60
what can malignancy do to telomerase
reactivate it so cancer cells can never die
61
what do Bcl-2 proteins do
stop bax/ bak attackin cell in apoptosis
62
what is angiogenesis
cancer grows it's own blood supply to grow, increases VEGF
63
what proteins are responsible for identifying faults in code
mismatch proteins
64
how can tumour evade the immune system
inhibiting PDl1, and T cell proliferation, they over express
65
describe the stages of cancer formation
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
describe the lineage of cancer
each daughter cell is different, makes it harder to treat, immortal
67
what do benign tumours normally look like
smooth, symmetrical, encapsulated
68
what do malignant cancers normally look like
irregular, no capsule, high nucleus: cytoplasm (N:C)
69
what has a better prognosis highly or poorly differentiated cells
highly
70
what are some cancer cell characteristics
pleomorphism (variety), hyperchromasia (big nuclei), mitosis and necrosis
71
what is a malignant epithelial called
carcinoma
72
what is a malignant and benign glandular called
adenoma, adenocarcinoma
73
what is a malignant and benign squamous called
papilloma, squamous cell carcinoma
74
what is a malignant and benign connective tissue called
mesenchyme, sarcoma
75
what is a malignant and benign fat called
lipoma, liposarcoma
76
what is a malignant and benign bone called
osteoma, osteosarcoma
77
what is a malignant bladder cancer called
transitional cell carcinoma
78
what is blood cancer called
leukaemia
79
what is the stage of a cancer? (TNM)
how far it's spread, has it invaded lymph nodes, has it metastasised
80
describe T1-T4
T1: invasion of submucosa T2: invasion of musclaris proproa T3: invasion of tissue T4: invasion of organ
81
describe N0-2
N0; no lymph nodes N1: 1-3 N2: 4+
82
describe M0/1
M0: no mets M1: mets
83
what is meant by the grade of the cancer
how differentiated it is, poor differentiation = high grade

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