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Principles > Pathology > Flashcards

Pathology Flashcards

1
Q

define necrosis

A
  • death of tissues that does NOT require energy

- always pathological

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2
Q

what are the patterns of necrosis

A
  • caseous
  • colliquative
  • coagulative
  • gangrenous
  • fibrinoid
  • fat necrosis
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3
Q

what is coagulative necrosis

A
  • when proteins coagulate

- preserves cell outline

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4
Q

what is colliquative necrosis

A
  • necrotic material becomes soft and liquefied (PUS)

- no cell structure remains

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5
Q

what is caseous necrosis

A
  • cheese like

- TB

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6
Q

what is gangrenous necrosis

A
  • cell death by necrosis then infection on top of it
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7
Q

what is fibrinoid necrosis

A

fibre deposited

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8
Q

define apoptosis

A
  • programmed cell death that REQUIRES energy
  • defence against inherited and injury
  • pathological OR physiological
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9
Q

give an example of physiological apoptosis and pathological apoptosis

A
  • physiological = normal part of growth

- pathological = injury, chemotherapy

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10
Q

what is the extrinsic pathway for apoptosis

A
  • signal comes from outside cell
  • death receptor initiated which binds to membrane
  • causes caspases
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11
Q

what is the intrinsic pathway for apoptosis

A
  • signal from inside cell
  • often mitochondrial pathway
  • growth signals promote ANTI-apoptotic molecules but when these are removed by BAX/BAK
  • causes caspases
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12
Q

P53 checks at what stage of cell cycle

A

end of G1

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13
Q

why are chromosomes capped with telomeres

A

to prevent degradation or fusion

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14
Q

with every division the number of repeats (telomeres) gets…

A

smaller

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15
Q

what is the job of telomerase

A

adds TTAGG

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16
Q

what do free radicals (particularly O2) cause

A

a chain reaction leading to lipid peroxidation

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17
Q

how are free radicals formed

A
  • drugs
  • O2 toxicity
  • reperfusion injury
  • inflammation
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18
Q

what are some non-lethal cell injuries

A
  • hydropic changes (accumulate H20 in cell)
  • fatty change
  • membrane shedding
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19
Q

define a metabolic disorder

A
  • a biochemical abnormality which may be deleterious by itself but also causes target organ damage
  • may be inherited or acquired
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20
Q

what is the first phase of inflammation

A
  • vascular phase

- dilation and increased permeability of blood vessels

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21
Q

what is the vascular phase of inflammation mediated by

A
  • histamine

- nitric oxide

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22
Q

what does vasodilation during inflammation allow

A
  • blood flow to slow
  • allows WBC to move towards wall of vessel by margination
  • chemical signals cause endothelial cells of vessel to contract so fluid enters surrounding tissues
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23
Q

what proteins do the vessel wall express

A
  • selectins

- ICAM

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24
Q

what proteins do WBC’s express

A
  • glycoproteins

- integrin

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25
Q

selectins bind to ___ on WBC’s

A

glycoproteins

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26
Q

ICAM proteins bind to ___ on WBC’s

A

integrin

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27
Q

what does he binding of WBC proteins to the vessel wall cause

A
  • rolling along the vessel wall

- due to the binding being weak so they constantly break/re-form

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28
Q

what affect do chemokines have on WBC

A
  • they activate it
  • so affinity for integrins increases
    thus WBC binds to vessel wall
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29
Q

once the WBC has bound to the vessel wall what happens

A
  • exits vessel by diapedesis
  • once in extracellular space it migrates to injury site following chemical gradient
  • process = chemotaxis
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30
Q

what are the characteristics of inflammation

A
  • redness
  • heat
  • swelling
  • pain
  • loss of function
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31
Q

surface adhesion molecule expression increased by….

A
  • complement C5a
  • Leukotriene B2
  • TNF
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32
Q

endothelial cell expression of adhesion molecules increased by…

A
  • IL1
  • Endotoxins
  • TNF
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33
Q

what are the responses to inflammation

A
  • suppuration (pus)
  • resolution
  • organisation and repair
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34
Q

what is pus composed of

A

neutrophils, bacteria, cellular debris

35
Q

what is resolution and what must the tissue have

A
  • complete restoration of tissues to normal

- tissue must have good vascular to deliver WBC’s

36
Q

what occurs during organisation and repair and when does it happen

A
  • scar tissue forms
  • occurs when damage goes beyond basement membrane
  • eg erosions and abrasions have membrane in tact so heal with resolution
37
Q

how does healing with a scar take place

A
  • hard to rebuild mucosal membrane so common response =
  • granular tissue formation
  • tissue composed of new capillaries, fibroblasts, collagen
38
Q

when does chronic inflammation occur

A
  • after prolonged or recurrent acute inflammation
39
Q

what are the cells involved in chronic inflammation

A
  • lymphocytes

- macrophages

40
Q

what are the macroscopic appearances of chronic inflammation

A
  • chronic ulcer
  • chronic abscess cavity
  • thickening of fibrous tissue
  • granulomatous
  • NO suppurnation for chronic
41
Q

define differentiation

A

acquisition of specialised function

42
Q

define hyperplasia

A
  • increase in cell number
  • in response to stimulus
  • physiological: breast tissue in puberty
  • pathological: hormonal, oestrogen leads to abnormal periods. hyperplasia of lymph nodes too
43
Q

why are over-weight women at a risk of cancer

A

steroid hormones can induce hyperplasia and cholesterol can change its structure to produce these hormones

44
Q

define hypertrophy

A
  • increase in cell size

- often as a result of mechanical stress eg gym

45
Q

define atrophy

A
  • reduction in cell size
  • physiological: uterus shrinks after birth
  • pathological: decreased workload… after cast taken off have muscle wastage
46
Q

define cancer

A

uncontrolled proliferation of cells

47
Q

define tumour

A

swelling, can be benign or malignant

48
Q

deine malignant

A

has capacity to spread

49
Q

define metastases

A

spreads to other sites

50
Q

define metaplasia

A
  • reversible change from one mature cell type to another mature cell type in response to stress
  • changes in signals to stem cells to differentiate
  • metaplastic tissue at risk site for cancer
51
Q

define dysplasia (disordered growth)

A
  • when cell gains mutation s

- pre-malignant process

52
Q

define CIS (carcinoma in situ)

A
  • means dysplasia affecting whole epithelium

- last stage before malignant

53
Q

neoplasia (new growth) are what type of cells

A

monoclonal

derived from a single common ancestor

54
Q

what are the properties for a benign tissue/cell

A
  • no necrosis and well differentiated
  • N:C ratio normal
  • minimal polymorphism (change in shape/size)
  • encapsulated as going slowly so can form one
55
Q

adenoma

A

benign glandular cell

56
Q

papilloma

A

benign squamous cell

57
Q

osteoma

A

benign bone cell

58
Q

leiomyoma

A

benign smooth muscle cell

59
Q

rhabdomyoma

A

benign skeletal muscle cell

60
Q

endochondroma

A

benign cartilage cell

61
Q

hemangioma

A

benign blood vessel

62
Q

what are the properties of a malignant tissue/cell

A
  • necrosis is common and poorly differentiated
  • N:C ratio increased
  • pleomorphic
  • usually rough and irregular cells
63
Q

carcinoma

A

malignant epithelial cell

64
Q

leiomyosarcoma

A

malignant smooth muscle cell

65
Q

adenocarcinoma

A

malignant glandular cell

66
Q

chondosarcoma

A

malignant cartilage cell

67
Q

osteogenic sarcoma

A

malignant bone cell

68
Q

rhabdomyosarcoma

A

malignant skeletal muscle cell

69
Q

angiosarcoma

A

malignant blood vessel

70
Q

lymphomas and leukemias

A

tumours of blood

71
Q

weight loss due to cancer is called

A

cachexia

72
Q

what is the double hit hypothesis

A
  • 1 working gene is enough
  • 1 faulty gene puts person at increased risk
  • 2 faulty mutated genes will result in a functional problem
73
Q

what are the 5 chemical carcinogenesis

A
  • polycyclic aromatic hydrocarbons (smoking/meat)
  • aflatoxins (p53 mutations from fungus/peanuts)
  • beta napthylines (dye industry)
  • nitrosamines (food preservatives)
  • radiation (UVB can cause pyrimidine dimers in DNA)
74
Q

what do classical oncogenes do

A
  • stimulate cell proliferation
  • inhibit cell death
  • dominant
75
Q

what do classical tumour suppressors do

A
  • inhibit cell proliferation
  • stimulate cell death
  • recessive
76
Q

what are the 7 traits for a cancer cell to develop

A
  • sustained cell proliferation
  • loss of growth inhibition
  • induce angiogenesis
  • disordered DNA repair
  • evade apoptosis
  • evade immune system
  • achieve immortality
77
Q

what are common mutations to sustain growth signalling

A
  • RAS (GTP binding)
  • BRAF (melanoma)
  • Myc (lymphoma, small cell cancer in lung)
  • P13K (most common kinase mutation)
78
Q

what are common mutations for loss of growth inhibition

A
  • PTEN (prevents p27 proliferation)
79
Q

what are common mutations to induce angiogenesis

A
  • up regulation of Vascular Endothelial Growth Factor
80
Q

what are common mutations for disordered DNA repair

A
  • BRCA1 + BRCA2 (breast cancer)
81
Q

what are common mutations to evade apoptosis

A
  • BCl2 binds to BAX/BAK to stop apoptosis
82
Q

inherited metabolic disorders are usually…

A

autosomal recessive

83
Q

acquired metabolic disorders are usually…

A
  • diabetes

- obesity

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