Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Unit 9 > Cell Death & Adaptation > Flashcards

Cell Death & Adaptation Flashcards

1
Q

Cell death: effects on tissue

A

Regenerative capacity and intact ECM
- recovery to normal

Regenerative capacity but ECM damaged
- permanent damage and reduced function

Non-replacing tissue (CNS, cardiac)
- permeant damage and reduced function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Common causes of cellular injury and death

A

Lack of factors essential for normal cell function
- blood (ischaemia)
- oxygen
- nutrients
- hormones/ GF
- neural stimulation

Physical
- trauma

Chemical
- drug injury
- toxins

Inflammation
- appropriate inflammatory responses
- inappropriate inflammatory response eg auto immune

Metabolic and genetic disorders
- diabetes
- obesity
etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Cellular effects of injurious agents

A
  • mitochondrial dysfunction and damage
  • damage to membranes
  • damage to cytoskeleton and cellular proteins
  • DNA damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Clinical recognition of cell injury and death

A

Deranged tissue / organ function

detection of leaked intracellular contents in blood (severe membrane damage)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Pathological recognition of cell injury and death

A

Morphological changes in the tissue
light microscopic changes
gross changes in surgical specimens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Common morphological manifestations of sublethal cell injury

A

Cell swelling:
- all cell types can show this

Fatty changes :
- intracellular accumulation of lipid due to deranged metabolism
- liver most common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Ultrastructural changes of cell swelling

A

Plasma membrane damage
- blebbing, loss of villi

Mitochondrial swelling due to membrane damage

ER damage
- dilated, detached polysomes

Nuclear damage
- disaggregation of granular and fibrillar elements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Reversible fatty changes in liver cells

A
  • intracellular accumulation of lipid due to metabolic derangement
  • disruption of aerobic glycolysis and B-oxidation of fat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Clinical effects of fatty change

A
  • typically little effect on clinically measured LFTs of fatty change alone
  • altered metabolism can stimulate inflammation in liver and lead to cell injury = death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

6 biochemical and morphological features of Apoptosis

A
  • physiological process
  • specific enzymes break down cells
  • neat and tidy
  • typically single cells
  • cell suicide programme
  • activated by some types of injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Cellular changes of Apoptosis

A
  • cell shrinks, cytoplasm stains darker
  • chromatin condenses under nuclear membrane an nucleus fragments
  • cell membrane blebs and cell fragments into membrane bound bodies
  • cells express macrophage attractants and are phagocytosed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

mechanism of Apoptosis

A

INTRINSIC PATHWAY
1) loss of GF/ survival factors, hypoxia, DNA damage, ER stress
2) Bcl2 / BAX
3) inc mitochondrial permeability and release pro-apoptotic proteins
4) caspase activation

EXTINSIC PATHWAY
1) death receptor on cell surface
2) FAS or TNF receptor
3) caspase activation

EXECUTION PHASE OF APOPTOSIS
endonuclease activation-> DNA fragmentation
cytoskeleton breakdown -> cell shrinks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

6 biochemical and morphological features of Necrosis

A
  • not physiological
  • uncontrolled cell breakdown- non specific enzyme activation
  • messy process
  • typically large group of cells
  • mass murder
  • common pattern following injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Coagulative pattern of Necrosis

A
  • most common
  • less rapid distinegration of cells
  • tissue structure transiently preserved but tissue weak and non-functional
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Liquefactive pattern of Necrosis

A

rapid degradation of cells to liquid mass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

nuclear changes of Coagulative necrosis

A
  • non-specific breakdown by degrative enzymes
  • karyolysis = pale nucleus due to endonuclease action
  • pyknosis = shrinkage of nucleus, becomes darker
  • karyorrhexis = nuclear fragmentation
17
Q

cytoplasmic changes in Coagulative necrosis

A
  • cytoplasm steams more darkly than usual
  • cell and tissue architecture preserved
  • severe membrane damage is present but not seen
18
Q

evolution of Coagulative Necrosis

A

1) leakage of cell contents due to membrane breakdown

2) inflammatory cell response

3) leucocyte lysosomal enzymes are major factor in cell digestion

4) attracts macrophages to phagocytose and initiates granulation tissue

19
Q

gross appearances of Coagulative Necrosis

A

Necrotic tissue:
- pale with yellow colour from acute inflammatory cells
- if blood is flowing to tissue- haemorrhage in tissue

Haemorrhaging situations:
- acute inflammation
- infarction due to venous obstruction
- arterial blockage by second blood supply to tissue
- tumour necrosis (due to angiogenesis and leaky vessels)

20
Q

What causes Liquefactive Necrosis?

A

focal material and fungal infections

  • inflammatory cell enzymes present from early stage and rapidly digest tissue
21
Q

Gangrenous Necrosis

A
  • term used when coagulative necrosis involves multiple tissue layers
  • typically used for intestine and limbs
  • massive inflammatory response with circulatory failure
22
Q

Caseous Necrosis

A

pink amorphous granular material with no tissue architecture apparent

  • typcial of TB infection
23
Q

Fat Necrosis

A
  • focal areas of fat destruction

caused by
- physcial damage
- chemical damage
- inflammatory injury

24
Q

Fibrinoid Necrosis

A

seen in immune reactions involving vessels

  • bright pink material seen in vessel wall typically associated with inflammatory cells
  • immune complexes in vessel wall together with fibrin
25
Q

Dystrophic Calcification

A

necrotic cells if not promptly absorbed form a nidus for calcification

26
Q

definition of cell adaptation

A

changes in size, number or pheotype of cells in a tissue in rpesonse to altered physiological demands and environmental stresses

27
Q

hypertrophy

A

increase in cell size due to synthesis of more structural components with also an increase in size of tissue/organ
-does not require cell division
-only response in mature tissues

28
Q

hyperplasia

A

increase in number of cells in organ or tissue with also increase in size of that organ/tissue
-only occurs in tissues capable of division
-labile tissues (hight steady state turnover
-stable tissues

29
Q

pathological hypertrophy

A

chronic pressure or volume load on heart

unwanted effects
-inc metabolic demand
-reduced compliance

-fibrous tissues inc aswell as muscle

30
Q

pathological hyperplasia

A

excess endogenous or exogenous steroid hormone stimulation
viral infections- alter regulation of proliferation cells
> HPV->warts
growth factor mimetic

31
Q

atrophy

A

reduced size of an orison or tissue due to decrease in cell size and number
-dec protein synthesis
-inc protein degradation
-cell death by apoptosis and autophagy
-dec rate of proliferation in renewing tissues

32
Q

what causes atrophy

A

-dec workload
-prolonged physical pressure
-denervation
-dec blood supply
-inadequate nutrition
-loss of endocrine stimulation
-aging

33
Q

Metaplasia

A

one mature cell type is replaced by a different mature cell type
-stimulus is chronic irritation
-mediators: cytokines GF
>act on stem cells in epithelia to tigger a changed differentiation pathway
-predisposed to malignant transformation

34
Q

example of Metaplasia

A
  1. normal respiratory pseudo stratified ciliated epithelium
    > chronic irritation due to cigarette smoke
  2. squamous epithelium
  3. squamous cell carcinoma
  4. loss of ciliated cells- mucous plugging and cough

Unit 9 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions