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ICS/GP/ILA > Atherosclerosis, Apoptosis, Cell Definitions, Cancer Pathology > Flashcards

Atherosclerosis, Apoptosis, Cell Definitions, Cancer Pathology Flashcards

1
Q

Definition of atherosclerosis?

A

formation of fibrolipid plaques in the intima of systemic arteries

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2
Q

When do plaques develop?

A

teens - fatty streaks
30s-50s - established plaques
40s-80s - complications of plaques

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3
Q

What is plaque composed of?

A

central lipid core and cap of fibrous tissue. Inflammatory cells such as lymphocytes reside in cap

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4
Q

Where does plaque tend to form?

A

arterieal branching points

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5
Q

What leads to plaque formation?

A

chronic or episodic exposure of arterial wall due to endothelial cells being easily damaged

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6
Q

How is plaque formed? (4 steps)

A
  1. damaged endothelial cells are more permeable and have increased adhesion - allows lipids and inflammatory cells to accumulate
  2. macrophages and lymphocytes accumulate - macrophages undergo apoptosis and leak lipids
  3. growth factors secreted by platelets and endothelium stimulate smooth muscle cells which form fibrous cap
  4. haemorrhage results from rupture of vessels within plaque - this causes expansion
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7
Q

What are common risk factors for atherosclerosis?

A

hypercholesterolaemia, hyperlipidaemia, hypertension, smoking, diabetes, male gender, increasing age

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8
Q

Why is smoking a risk factor for atherosclerosis?

A

increases blood pressure and damages endothelial wall due to free radicals, nicotine and CO

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9
Q

What are some complications of atherosclerosis?

A
  • lumen narrowing due to stenosis
  • atherothrombotic occlusion
  • embolism and ruptured abdominal aorta
  • cerebral/myocardial infarction
  • peripheral vascular disease
  • gangrene
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10
Q

Definition of apoptosis?

A

programmed cell death

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11
Q

Why is apoptosis needed?

A

for development and cell turnover

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12
Q

What disease can a lack of apoptosis cause?

A

cancer - mutation of p53 gene

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13
Q

What disease can too much apoptosis cause?

A

HIV - kills antibodies (CD4 helper cells) so no defense

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14
Q

What is apoptosis normally triggered by?

A

DNA damage, eg. single/double strand break, base alteration, or cross-linkage

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15
Q

Does apoptosis require energy?

A

Yes - energy dependent mechanism

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16
Q

What are some inhibitors of apoptosis?

A

growth factors, extracellular matrix, sex steroids

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17
Q

What are some inducers of apoptosis?

A

growth factor withdrawal, loss of matrix, glucocorticoids, free radicals, ionising radiation

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18
Q

What does the intrinsic apoptosis mechanism use?

A

Bcl2 (induces) and Bax (inhibits) ratio determine cell’s susceptibility to apoptotic stimuli and whether a cell expands tissues or dies

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19
Q

What does the p53 protein do in apoptosis?

A

induces cell cycle arrest and initiates dividing of cells. however if damage is difficult to repair then p53 can induce apoptosis

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20
Q

What is the extrinsic mechanism of apoptosis?

A

specific mechanism by ligand-binding at death receptors on the cell surface

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21
Q

What receptors are used in extrinsic apoptosis?

A

tumour necrosis factor receptors (TNFR), eg. TNFR1 and Fas

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22
Q

What does ligand binding promote in extrinsic apoptosis?

A

clustering of receptor molecules and initiation of signal –> transduction cascade activates caspases

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23
Q

What are caspases?

A

cell death enzymes

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24
Q

Which pathway do intrinsic and extrinsic apoptosis both lead to?

A

Cytotoxic/Common/Execution

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25
Q

What produces active caspases in sytotoxic apoptosis?

A

activation of intiator caspases cleaves pro-caspases

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26
Q

What do active caspases cause the degradation of?

A

cytoskeletal framework and nuclear proteins

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27
Q

What is the last stage of cytotoxic apoptosis?

A

dead cells fragment into small membrane-bound apoptotic bodies - this triggers inflammatory response

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28
Q

Definition of necrosis?

A

death of most or all cells in organ tissue due to disease, injury, or failure of blood supply

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29
Q

How does necrosis induce inflammation and repair?

A

rupture of plasma membrane spills cell contents and some of these are immunostimulatory

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30
Q

What are some examples of necrosis?

A

infarction, pancreatitis, frostbite, toxic venom, avascular necrosis of bone (eg. femur)

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31
Q

What is caseous necrosis?

A

soft cheese appearance due to tuberculosis

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32
Q

Definition of Hypertrophy?

A

Increase in size of an organ due to increase in size of constituent cells

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33
Q

Where does hypertrophy occur?

A

In organs where cells cannot divide eg. skeletal muscle in bodybuilders and athletes

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34
Q

Definition of Hyperplasia?

A

Increase in size of an organ due to increase in number of constituent cells

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35
Q

Where does hyperplasia occur?

A

In organs where cells can divide, eg. benign prostatic hyperplasia, endometrial hyperplasia

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36
Q

What is mixed hypertrophy/hyperplasia?

A

Increase in size of an organ due to both the size and number of constituent cells increasing

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37
Q

Where does mixed hypertrophy/hyperplasia occur?

A

In organs where cells can divide eg. smooth muscle cells of uterus in pregnancy

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38
Q

Definition of atrophy?

A

Decrease in size of an organ due to decrease in size or number of constituent cells

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39
Q

Examples of atrophy?

A

Alzheimier’s dementia, quadriceps muscle following knee injury

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40
Q

How does atrophy occur?

A

Naturally by apoptosis, eg. regression of wolfian or mullerian ducts

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41
Q

What is atrophy often a result of?

A

decreased function, loss of innervation, lack of nutrition

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42
Q

Definition of metaplasia?

A

Change in cell differentiation from one fully differentiated type to another

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43
Q

What is metaplasia usually caused by?

A

Consistent change in environment of epithelial surface

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44
Q

Three examples of metaplasia?

A
  1. Smoking: bronchial epithelium from ciliated respiratory –> squamous
  2. Barrett’s Oesophagus: squamous epithelium –> glandular
  3. Puberty: uterine cervix from columnar –> squamous
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45
Q

Definition of dysplasia?

A

Imprecise term for morphological changes that are seen in cells in development of cancer

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46
Q

How is dysplasia classified?

A

Spectrum from mild to sever, carcinoma in situ, and invasive cancer

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47
Q

Example of dysplasia?

A

Bronchial epithelium in smokers: metaplasia from ciliated to squamous, then dysplasia in squamous

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48
Q

What is ageing?

A

Cells in the body divide continuously during life (eg. skin and gut lining) or stop dividing shortly after birth (eg. neurones)

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49
Q

What is the Hayflick limit?

A

limit to how many times a human cell can divide

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50
Q

Why do skin cells divide less in older people?

A

Telomere (non-coding) region becomes too short after repeated cell division

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51
Q

Why can’t chromosomes divide in ageing people?

A

Telomere length too short to engage with DNA polymerase

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52
Q

Is telomere length maternally or paternally inherited?

A

Paternally

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53
Q

How can ageing be accelerated?

A

Due to mutations in the cell membrane proteins which make cell division impossible

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54
Q

What are non-dividing cells?

A

Cells that can’t replace themselves by dividing so they die once they have accumulared a certain amount of damage

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55
Q

What factors cause damage to cells and contribute to ageing? (7)

A
  • cross-linking of DNA or proteins
  • damage to mitochondrial DNA, loss of DNA repair mechanism
  • loss of calcium controls, peroxidation of membranes
  • free radical generation
  • time-dependent activation of death genes
  • telomere shortening
  • accumulation of toxic by-products
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56
Q

Definition of prolonging life?

A

Anything that reduces damage to cells can reduce defects of ageing

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57
Q

What are methods for delaying ageing?

A

local measures for specific parts of the body, eg. sun protection to reduce UV cross-linking of proteins in the dermis

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58
Q

How is skin affected by ageing?

A

Wrinkling (dermal elastosis) caused by UV-B light causing cross-linking of proteins, especially collagen

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59
Q

How can skin ageing be reduced?

A

Avoiding too much sun exposure and using sun protection

60
Q

How are eyes affected by ageing?

A

Cataracts caused by UV-B cross-linking of proteins in lens causing opacity

61
Q

How can catarcats be prevented?

A

Wearing sunglasses and treated by replacing lens

62
Q

How are bones affected by ageing?

A

Osteoporosis - loss of bone matrix predominantly in women post menopause

63
Q

How is osteoporosis prevented?

A

HRT and calcium, C, D supplements

64
Q

How is the brain affected by ageing?

A

Dementia - Alzheimer’s or vascular. Plaques and neurofibrillary tangles occur in brain

65
Q

What are some preventative and risk factors for dementia?

A

Preventative: genetic and lifestyle factors, eg. exercise
Risk: high blood pressure, hyperlipidaemia

66
Q

How is muscle affected by ageing?

A

Sarcopaenia - muscle loss caused by reduced levels of growth hormones and testosterone

67
Q

How is sarcopaenia prevented?

A

Regular exercise

68
Q

How is hearing affected by ageing?

A

hair cells in cochlear do not divide and replace so will die if too damaged. Prevented by avoiding high volume sounds throughout life

69
Q

How is immunity affected by ageing?

A

Immunological changes result in less production of immune cells

70
Q

Definition of carcinogenesis?

A

The transformation of normal cells to neoplastic cells through permanent gene mutations

71
Q

What kind of process is carcinogenesis?

A

multistep - applies to malignant and benign

72
Q

What is oncogenesis?

A

Refers to both benign and malinant tumours

73
Q

What is a carcinogenic?

A

Agents known or suspected to cause tumours

74
Q

Carcinogenic Vs Oncogenic Vs Mutagenic?

A

cancer causing, tumour causing, acts on DNA

75
Q

What percentage of caner risk is environmental?

A

85%

76
Q

What are some limitations of diagnosing environmental carcinogens? (3)

A
  • latent interval between exposure and development
  • complex environment
  • ethical constraints
77
Q

What are some examples of epidemiological or occupational risks?

A
  • hepatocellular common in countries with high rates of hepatitis
  • scrotal cancer has increased incidence in chimney sweeps
78
Q

Why do we screen new drugs, food, and pollutants?

A

Carcinogens not united by common physical or chemical properties

79
Q

What is an ehtical issue of using animals or bacteria to test potential carcinogens?

A

animals might metabolise differently, bacteria might mutate in cultures

80
Q

Properties of chemical carcinogens? (4)

A
  • no common structure
  • some act directly
  • most require metabolic conversion from pro-carcinogens to ultimate
  • enzymes required may be ubiquitous or confined
81
Q

Are viral carcinogenics a common cause of cancer?

A

No (10-15%). Most oncogenic viral infections don’t result in cancer

82
Q

Which population of people are viral carcinogenics more common in?

A

Those who are immunosuppressed

83
Q

How does non-ionising radiation act as a carcinogenic?

A

UV light - UVA or UVB increases risk of basal/squamous cell carcinoma and melanoma

84
Q

Does ionising radiation have a short or long term effect?

A

Long term

85
Q

What are some examples of hormones that can be carcinogenics?

A

Oestrogen (mammary/endometrial cancer) and anabolic steroids (hepatocellular)

86
Q

What type of cancer does shistosoma parasite cause?

A

bladder cancer

87
Q

Example of a mycotoxin that can act as a carcinogenic?

A

Aflatoxin B1 causes hepatocellular cancer

88
Q

What role does race and ethnicity place as a host factor for cancer?

A

hard to define. Eg. increase in oral cancer in SE Asia due to reverse smoking. Decrease in skin cancer in darker skin due to melanin

89
Q

How does diet/lifestyle play as a host factor for cancer?

A

high fat/red meat contributes to colorectal cancers, alcohol contributes to breast or oesophageal, sexual behaviour to HPV-related cancers

90
Q

What are some constitutional factors that act as a host factor for cancer?

A

inherited predisposition, increasing age, gender

91
Q

What is a premalignant legsion?

A

Identifiable local abnormality associated with increased risk of malignancy at that site. Eg. colonic polyps

92
Q

What is another host factor of carcinogenics (2)?

A
  • premalignant lesions
  • transplacental exposure
93
Q

How does invasion and metastasis occur?

A

A single cell acquires mutations to become cancerous, this divides until all healthy cells have been replaced by cancerous cells

94
Q

What is carcinoma in situ?

A

A malignant epithelial neoplasm that hasn’t yet invaded through the original basement membrane

95
Q

What is a micro-invasive carcinoma?

A

A carcinoma that has breached the basement membrane but hasn’t invaded far from the original carcinoma

96
Q

What is an invasive carcinoma?

A

A carcinoma that has breached the basement membrane so can now spread elsewhere

97
Q

Definition of invasion?

A

Defining feature of malignant neoplasm that allows neoplastic cells to spread directly through tissue and gain access to vessels and lymphatic channels

98
Q

What is invasion dependent upon?

A

Decreased cellular adhesion, abnormal cellular motility, and production of enzymes with a lytic effect

99
Q

Definition of metastasis?

A

Process by which a malignant tumour spreads from its primary site to produce secondary tumours at distant sites

100
Q

Where can metastasis occur?

A

via blood vessels, nerves, lymphatics, across body cavities

101
Q

What type of growth factors does metastasis use at site?

A

autocrine

102
Q

What are the 7 stages of metastatic cascade?

A
  1. detachment
  2. invasion
  3. intravasation
  4. evasion of host defences
  5. arrest
  6. extravasation
  7. vascularisation
103
Q

What happens specifically in intravasation?

A

collagenases and cell motility: tumour cell derived motility factors and breakdown products of extracellular matrix

104
Q

What happens in evasion of host defences? (3)

A
  • aggregation with platelets
  • shedding of surface antigens
  • adhesion to other tumour cells
105
Q

What is haematogenous route of metastasis?

A

By blood stream - secondary tumours form in organs perfused by blood that has drained from a tumour

106
Q

What is lymphatic route of metastasis?

A

By lymph channels - forms secondary tumours in regional lymph nodes

107
Q

What is trans-coelomic route of metastasis?

A

pericardial and peritoneal cavities where it results in neoplastic effusion

108
Q

Definition of angiogenesis?

A

Tumour begins to grow it’s own blood supply after reaching ~1mm in diameter

109
Q

Promoters of angiogenesis?

A

endothelial growth factors, fibroblast growth factors

110
Q

Inhibitors of angiogenesis?

A

angiostatin, endostatin, vasculostatin

111
Q

Examples of common metasases?

A
  • sarcomas and other common –> lung
  • colon, stomach, pancreatic, intestinal –> liver
  • breast, lung, thyroid, kidney, prostate –> bone
112
Q

What is a tumour used to describe?

A

any swelling including: neoplasm, inflammation, hypertrophy, hyperplasia

113
Q

Definition of neoplasm?

A

a NEW GROWTH or lesion resulting from the AUTONOMOUS or relatively autonomous ABNORMAL growth of cells which PERSISTS after the initiating stimulus has been removed

114
Q

What do neoplasms arise from?

A

Single cells that have transformed by cumulative mutational events

115
Q

Why can’t neoplasms arise from erythrocytes?

A

They don’t have a nucleus but can arise from their precursors

116
Q

When does the probability of neoplastic transformation increase?

A

Increases with the number of cell divisions experiences by a cell

117
Q

What proportion of the population get neoplasms and how many deaths?

A

25% of population and 20% of all deaths

118
Q

What are the 3 main structural components of a neoplasm?

A
  1. neoplastic cells
  2. stroma
  3. tumour angiogenesis
119
Q

What do neoplastic cells derive from?

A

nucleated cells and are usually monoclonal - growth pattern and synthetic activity realte to parent cell

120
Q

What is the function of the stroma of a neoplasm?

A

connective tissue framework, mechanical support, and nutrition

121
Q

What are the cell and tissue types that make up the stroma of a neoplasm?

A

fibroblasts and collagen

122
Q

What is the growth of a tumour dependent on in terms of blood supply?

A

Stroma always contains blood vessels which perfuse the tumour, so growth is dependent on its ability to induce blood vessels to perfuse

123
Q

What is angiogenesis induced by?

A

endothelial growth factors

124
Q

Why do we classify neoplasms?

A

To determine appropriate treatment and provide prognostic information

125
Q

What are the two methods of classification for neoplasms?

A

Behavioural (benign or malignant) or histigenetic

126
Q

What is histogenesis?

A

Specific cell of origin of a tumour

127
Q

What is the difference in localisation of benign and malignant neoplasms?

A

benign: localised and non-invasive
malignant: metastasise and invasive

128
Q

What is the difference in growth rate and mitotic activity of benign and malignant neoplasms?

A

benign: slow growth rate and low mitotic activity
malignant: rapid growth rate and increased mitotic activity

129
Q

What is the difference in appearance of benign and malignant neoplasms?

A

benign: circumscribed or encapsulated
malignant: poorly defined or irregular border

130
Q

Difference in nuclei between benign and malignant neoplasms?

A

benign: nuclear morphometry is normal
malignant: hyperchromatic or pleomorphic nuclei

131
Q

Is necrois and ulceration common or rare in benign neoplasms?

A

rare in benign, common in malignant

132
Q

Difference between exophytic (benign) and endophytic (malignant) growth?

A

Exophytic grows out from mucosal surface whereas endophytic grows underneath

133
Q

Why can benign neoplasms still cause morbidity and mortility?

A
  • puts pressure on adjacent structures
  • obstruct flow
  • produce hormones
  • can transform into malignant
  • cause anxiety
134
Q

Why do malignant neoplasms cause morbidity and mortality?

A
  • destruction of adjacent tissue
  • metastases
  • blood loss from ulcers
  • obstruct flow
  • produce hormones
  • paraneoplastic effects
  • anxiety and pain
135
Q

How are neoplasms organised by nomenclature?

A

may arise from epithelial cells, connective tissues, and lymphoid/haematopoietic organs so suffix depends on cell type

136
Q

What is a papilloma?

A

benign tumour of non-glandular, non-secretory epithelium

137
Q

What is an adenoma?

A

benign tumour of glandular or secretory epithelium

138
Q

What is a carcinoma?

A

malignant tumour of epithelial cells

139
Q

What is an adenocarcinoma?

A

carcinomas of glandular epithelium

140
Q

Examples of benign neoplasm of connective tissue?

A
  • lipoma in adipocytes
  • osteoma in bone
  • chondroma in cartilage
  • angioma in vasculature
  • rhabdomyoma in striated muscle
  • leiomyoma in smooth muscle
  • neuroma in nerves
141
Q

Examples of malignant neoplasms of connective tissue?

A

Same as benign connective tissue neoplasms but with sarcoma suffix as opposed to just -oma

142
Q

How are carcinomas and sarcomas further classified?

A

By degree of differentiation as this strongly correlates with prognosis

143
Q

Is a poorly-dffierentiated or well-differentiated tumour more aggressive?

A

poorly differentiated are more aggressive because well-differentiated more closely resemble parent tissue

144
Q

What is an anaplastic neoplasm?

A

A tumour where the cell-type of origin is unknown

145
Q

What are 4 exceptions of neoplasm classification rules?

A
  1. Not all ‘omas’ are neoplasms, eg. granuloma
  2. not all malignant tumours are carcinomas or sarcomas, eg. melanoma
  3. Named after the person who first found it, eg. Burkitt’s lymphoma
  4. Teratoma is neplasm of germ cell eg. embyonal tumours
146
Q

What is the uncontrolled proliferation and indefinite lifespan enabled by?

A

autocrine growth stimulation, reduced apoptosis, prevention of telomeric shortening

ICS/GP/ILA (9 decks)

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