Pathology Flashcards
(83 cards)
1
Q
define necrosis
A
- death of tissues that does NOT require energy
- always pathological
2
Q
what are the patterns of necrosis
A
- caseous
- colliquative
- coagulative
- gangrenous
- fibrinoid
- fat necrosis
3
Q
what is coagulative necrosis
A
- when proteins coagulate
- preserves cell outline
4
Q
what is colliquative necrosis
A
- necrotic material becomes soft and liquefied (PUS)
- no cell structure remains
5
Q
what is caseous necrosis
A
- cheese like
- TB
6
Q
what is gangrenous necrosis
A
- cell death by necrosis then infection on top of it
7
Q
what is fibrinoid necrosis
A
fibre deposited
8
Q
define apoptosis
A
- programmed cell death that REQUIRES energy
- defence against inherited and injury
- pathological OR physiological
9
Q
give an example of physiological apoptosis and pathological apoptosis
A
- physiological = normal part of growth
- pathological = injury, chemotherapy
10
Q
what is the extrinsic pathway for apoptosis
A
- signal comes from outside cell
- death receptor initiated which binds to membrane
- causes caspases
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
12
Q
P53 checks at what stage of cell cycle
A
end of G1
13
Q
why are chromosomes capped with telomeres
A
to prevent degradation or fusion
14
Q
with every division the number of repeats (telomeres) gets…
A
smaller
15
Q
what is the job of telomerase
A
adds TTAGG
16
Q
what do free radicals (particularly O2) cause
A
a chain reaction leading to lipid peroxidation
17
Q
how are free radicals formed
A
- drugs
- O2 toxicity
- reperfusion injury
- inflammation
18
Q
what are some non-lethal cell injuries
A
- hydropic changes (accumulate H20 in cell)
- fatty change
- membrane shedding
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
20
Q
what is the first phase of inflammation
A
- vascular phase
- dilation and increased permeability of blood vessels
21
Q
what is the vascular phase of inflammation mediated by
A
- histamine
- nitric oxide
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
23
Q
what proteins do the vessel wall express
A
- selectins
- ICAM
24
Q
what proteins do WBC’s express
A
- glycoproteins
- integrin
25
selectins bind to ___ on WBC's
glycoproteins
26
ICAM proteins bind to ___ on WBC's
integrin
27
what does he binding of WBC proteins to the vessel wall cause
- rolling along the vessel wall
| - due to the binding being weak so they constantly break/re-form
28
what affect do chemokines have on WBC
- they activate it
- so affinity for integrins increases
thus WBC binds to vessel wall
29
once the WBC has bound to the vessel wall what happens
- exits vessel by diapedesis
- once in extracellular space it migrates to injury site following chemical gradient
- process = chemotaxis
30
what are the characteristics of inflammation
- redness
- heat
- swelling
- pain
- loss of function
31
surface adhesion molecule expression increased by....
- complement C5a
- Leukotriene B2
- TNF
32
endothelial cell expression of adhesion molecules increased by...
- IL1
- Endotoxins
- TNF
33
what are the responses to inflammation
- suppuration (pus)
- resolution
- organisation and repair
34
what is pus composed of
neutrophils, bacteria, cellular debris
35
what is resolution and what must the tissue have
- complete restoration of tissues to normal
| - tissue must have good vascular to deliver WBC's
36
what occurs during organisation and repair and when does it happen
- scar tissue forms
- occurs when damage goes beyond basement membrane
- eg erosions and abrasions have membrane in tact so heal with resolution
37
how does healing with a scar take place
- hard to rebuild mucosal membrane so common response =
- granular tissue formation
- tissue composed of new capillaries, fibroblasts, collagen
38
when does chronic inflammation occur
- after prolonged or recurrent acute inflammation
39
what are the cells involved in chronic inflammation
- lymphocytes
| - macrophages
40
what are the macroscopic appearances of chronic inflammation
- chronic ulcer
- chronic abscess cavity
- thickening of fibrous tissue
- granulomatous
- NO suppurnation for chronic
41
define differentiation
acquisition of specialised function
42
define hyperplasia
- 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
why are over-weight women at a risk of cancer
steroid hormones can induce hyperplasia and cholesterol can change its structure to produce these hormones
44
define hypertrophy
- increase in cell size
| - often as a result of mechanical stress eg gym
45
define atrophy
- reduction in cell size
- physiological: uterus shrinks after birth
- pathological: decreased workload... after cast taken off have muscle wastage
46
define cancer
uncontrolled proliferation of cells
47
define tumour
swelling, can be benign or malignant
48
deine malignant
has capacity to spread
49
define metastases
spreads to other sites
50
define metaplasia
- 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
define dysplasia (disordered growth)
- when cell gains mutation s
| - pre-malignant process
52
define CIS (carcinoma in situ)
- means dysplasia affecting whole epithelium
| - last stage before malignant
53
neoplasia (new growth) are what type of cells
monoclonal
| derived from a single common ancestor
54
what are the properties for a benign tissue/cell
- no necrosis and well differentiated
- N:C ratio normal
- minimal polymorphism (change in shape/size)
- encapsulated as going slowly so can form one
55
adenoma
benign glandular cell
56
papilloma
benign squamous cell
57
osteoma
benign bone cell
58
leiomyoma
benign smooth muscle cell
59
rhabdomyoma
benign skeletal muscle cell
60
endochondroma
benign cartilage cell
61
hemangioma
benign blood vessel
62
what are the properties of a malignant tissue/cell
- necrosis is common and poorly differentiated
- N:C ratio increased
- pleomorphic
- usually rough and irregular cells
63
carcinoma
malignant epithelial cell
64
leiomyosarcoma
malignant smooth muscle cell
65
adenocarcinoma
malignant glandular cell
66
chondosarcoma
malignant cartilage cell
67
osteogenic sarcoma
malignant bone cell
68
rhabdomyosarcoma
malignant skeletal muscle cell
69
angiosarcoma
malignant blood vessel
70
lymphomas and leukemias
tumours of blood
71
weight loss due to cancer is called
cachexia
72
what is the double hit hypothesis
- 1 working gene is enough
- 1 faulty gene puts person at increased risk
- 2 faulty mutated genes will result in a functional problem
73
what are the 5 chemical carcinogenesis
- 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
what do classical oncogenes do
- stimulate cell proliferation
- inhibit cell death
- dominant
75
what do classical tumour suppressors do
- inhibit cell proliferation
- stimulate cell death
- recessive
76
what are the 7 traits for a cancer cell to develop
- sustained cell proliferation
- loss of growth inhibition
- induce angiogenesis
- disordered DNA repair
- evade apoptosis
- evade immune system
- achieve immortality
77
what are common mutations to sustain growth signalling
- RAS (GTP binding)
- BRAF (melanoma)
- Myc (lymphoma, small cell cancer in lung)
- P13K (most common kinase mutation)
78
what are common mutations for loss of growth inhibition
- PTEN (prevents p27 proliferation)
79
what are common mutations to induce angiogenesis
- up regulation of Vascular Endothelial Growth Factor
80
what are common mutations for disordered DNA repair
- BRCA1 + BRCA2 (breast cancer)
81
what are common mutations to evade apoptosis
- BCl2 binds to BAX/BAK to stop apoptosis
82
inherited metabolic disorders are usually...
autosomal recessive
83
acquired metabolic disorders are usually...
- diabetes
| - obesity
