Apoptosis and Necrosis Flashcards

1
Q

What is Apoptosis

A

Programmed Cell Death without the release of harmful products

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2
Q

What does apoptosis with mitosis allows

A

Continuous renewal of cells

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3
Q

What are the characteristics of apoptosis

A
  • It is energy dependant

- Enzymatic digestion of nuclear/cytoplasmic contents

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4
Q

How is apoptosis different to necrosis

A
  • Necrosis cell death is unintended caused by cellular injury
  • Apoptosis suppresses inflammation and responds to necrosis
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5
Q

Why is defective apoptosis clinically significant

A

Allows for neoplasia like cancer cells living longer

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6
Q

Why is apoptosis important in AIDs

A

HIV proteins activate CD4 on T-helper lymphocytes causing apoptosis
cause immunodepleting and dysfunction

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7
Q

What are the inhibitors of apoptosis

A

Growth factors
Ex. cellular matrix
Sex steroids
Viral proteins

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8
Q

What are the inducers of apoptosis

A
Lack of Growth factor
Loss of matrix attachment
Glucocorticoids
Free radicals
Ionising radiation
DNA damage
Ligand bind at death receptors
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9
Q

What are the two pathways of apoptosis

A

Intrinsic

Extrinsic

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10
Q

What members of the BCL-2 family does the intrinsic apoptosis pathway use

A

BCL-2 inhibits the factors that induce apoptosis (no apoptosis)
Bax forms Bax-Bax dimers that enhance apoptosis stimuli (yes apoptosis)

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11
Q

What stimuli does the intrinsic factor respond to

A
Growth factors
Biochemical stress (DNA damage)
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12
Q

What is the p53 gene

A

A protein that induces cell cycle arrest and initiates DNA damage repair

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13
Q

When is apoptosis activated by pro-apoptotic members of the Bcl-2 family

A

When DNA damage is too difficult to repair

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14
Q

How is the extrinsic apoptosis pathway induced

A

Ligand binding at Tumour Necrosis Factor Receptors on cell surface

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15
Q

What receptors act as death receptors

A

TNFR1

Fas (CD95)

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16
Q

What is the result of ligand binding

A

Promotes clustering of receptor molecules
Initiates signal transduction cascade = CASPASES activation
Lymphocyte elimination

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17
Q

What are CASPASES

A

Cell death enzymes

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18
Q

What happens when apoptosis is triggered

A
  • Activation of initiator caspases
  • Other pro-caspases cleaved
  • Active caspases cause degradation of cytoskeletal framework and nuclear proteins
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19
Q

What is necrosis

A

Traumatic cell death which induces inflammation and repair

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20
Q

What is necrosis characterised by

A

Bioenergetic failure

Loss of plasma membrane integrity

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21
Q

How does necrosis induce inflammation and repair

A

Ruptured plasma membrane
Cell content spillage
Inflammatory response and repair

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22
Q

What happens to a cell during coagulative necrosis after ischaemia

A

Cell retains shape as protein coagulates but metabollic processes shut down
Tissue goes from firm to soft as macrophages digest (can cause ventricular rupture if the tissue is the myocardium)

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23
Q

Where does liquefactive necrosis occur

A

In the brain because

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24
Q

what is caseous necrosis

A

Cheese like structured tissue

Most likely Tuberculosis

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25
What is gangrene
Bacteria caused tissue rotting (black) Likely caused by clostridia Black = deposition of iron sulphide from degraded haemoglobin
26
What is a congenital disease
PRESENT AT BIRTH - Chromosomal - genetic diseases
27
What is a genetic disease
Inherited | Spontaneous
28
What are inherited genetic disorders
``` Cystic Fibrosis- AR Sickle cell anaemia -AR Familial adenomatous polyposis- AD Colour blindness -X Huntington’s - Adulthood ```
29
What are spontaneous genetic disorders
Down’s - trisomy 21 Edward’s - trisomy 18 Palau’s -trisomy 13
30
What are non genetic disorders
Environmentally acquired | -fetal alcohol syndrome
31
What are acquired diseases
Not environmentally acquired - Tuberculosis - lung cancer - bone fracture - AIDS
32
What are multi factorial diseases
Due to many factors - neural tube defects - cleft palate
33
What are some neural tube defects
Spina bifida - exposed spinal cord Anencephaly - major brain absence Hydrocephalus - fluid build up in brain Folate deficiency
34
What is hypertrophy
Increase in cell size without cell division
35
what is hyperplasia
Increase in cell number by mitosis
36
when a nd what stimulates Uterine smooth muscle hypertrophy
Oestrogens | during Puberty and Pregnancy
37
What are two examples of muscular hypertrophy
Skeletal muscle- limb response to increase activity | Left ventricle- Sustained outflow resistance
38
What two cells can hyperplasia not happen in
Myocardial | Nerve
39
Whic growth factor causes brain marrow hyperplasia for people living in high altitudes
Erythropoeitin
40
Is hyperplasia of prostate smooth muscle an issue
Can be benign/malignant
41
What is atrophy
Reduction in organ/tissue size/cell number by apoptosis
42
When is there natural atrophy in the development of the GI tracts
Wollfian (males) Mullerian (females) There is no more use for them
43
When can atrophy cause disease
Lack of function - immobilisation by pain/cast Innervation loss = muscle atrophy Lack of nutrition
44
What is metaplasia
The change in differentiation of a differentiated cell
45
What can cause metaplasia
smoking - ciliated respiratory epithelium to squamous epithelium stones - duct epithelium of salivary gland/pancreas,bile duct to squamous stomach acid - columnar epithelium of oesophagus to squamous epithelium
46
What is Barrett's Oesophagus
stomach acid - columnar epithelium of oesophagus to squamous epithelium
47
What is dysplasia
Cell changes in the PROGRESSION to cancer | or a lack of development (i.e bones)
48
What is the trend between ageing and cell division
Cell division decreases with ageing
49
Which cells have the greatest potential for cell division
Fetal cells
50
What is ageing influenced by
Genetic and Environmental factors
51
What causes deafness
Loss of hair cells
52
What causes senile dementia
Nerve cells cannot replicate = brain atrophy
53
What causes cataracts
UV light damage = cross linking proteins in eye
54
What causes osteoporosis
Lack of Vitamin D and oestrogen in earlier life
55
What causes dermal elastosis (wrinkling)
UV light damage = less collagen = less elastin
56
Why do the elderly have impaired immunity
Less production of Immune cells
57
What is carcinogenesis
Transform normal cells to neoplastic cells by permanent genetic mutations (malignant)
58
What is neoplasm
A lesion from autonomous abnormal growth
59
What is neoplasia
Autonomous Abnormal Persistent New growth
60
Why can neoplasms areise from erythroblasts but not erythrocytes
Because erythrocytes have no nucleus
61
Why does the probability of cancer increase with age
Chance of neoplastic transformations increase with the number of cell divisions a cell undergoes