1 Cell Injury Flashcards
*Q: What does lethal cell injury lead to? What does sublethal cell injury lead to?
A: cell death
injury may not amount to cell death but may be reversible/progress to cell death
*Q: Define hypertrophy.
A: stress that makes cells adapt and become bigger
Consequently increasing organ size
Trophy= size
*Q: What are the 8 types of cell injury?
A: oxygen deprivation- v common
infectious agents- inc drugs
chemical agents
genetic defects
immunological reactions- autoimmune
nutritional imbalances
physical agents- eg lightning, gunshot
ageing
DICGINPA
*Q: What does the cellular response injurious stimuli depend on? (3)
A: type of injury, severity, duration
Q: What are the 4 intracellular mechanisms particularly vulnerable to cell injury? Why are they important? Relationship?
A: cell membrane integrity (allows distinguishing from self and non self cells) ATP generation (important in maintaining cell integrity) Protein synthesis (affect cell membrane) Integrity of genetic apparatus (can lead to malfunction in protein synthesis)
integrally related that multiple secondary effects rapidly occur//if one is damaged then leads to problems in others (all feed into eachother)
*Q: What kills the cell first: Morphological changes or loss of function?
A: loss of function
*Q: Define atrophy. Example.
A: shrinking of size of cell (or organ) by loss of cell substance
Dementia brain = smaller due to smaller cells
*Q: What can cause hypertrophy? (2)
A: increased functional demand
Specific hormonal stimulation
*Q: What is hyperplasia? Can be? (2) Describe each.
A: plasia= number
Increase in number of cells in organ
Can be physiological or pathological
Physiological can be hormonal or compensatory
pathological is usually due to excessive hormonal or growth factor stimulation
*Q: What is an example of hormonal physiological hyperplasia?
A: oestrogenic wave of proliferation of the endometrium (mucous membrane lining the womb/inside on uterus)
(proliferative endometrium stimulated by oestrogen)
*Q: What is an example of pathological hyperplasia?
A: carcinoma
*Q: What is tremendous hyperplasia?
A: lots of mitosis
*Q: Define metaplasia. May be? (2) Give an example.
A: reversible change in which one adult cell type is replaced by another
physiological or pathological
when you spoke, columnar epi goes to squamous (returns back when smoking stops)
*Q: Give an example of metaplasia.
A: Barrett’s oesophagus- get columnar epithelium instead of squamous lined epithelium due to acid reflu
*Q: What is dysplasia?
A: precancerous cells which show genetic and cytological features of malignancy but not invading the underlying tissue (basal lamina)
key features: increased mitoses and increased nuclear cytoplasmic ratio
Q: What is the connection between metaplasia and dysplasia in terms of cancer?
A: metaplasia doesn’t give increased risk of cancer but once you’ve got metaplasia, then you may go on to have dysplasia
*Q: What are 2 light microscopic changes associated with reversible injury? Examples of?
A: fatty change (fat accumulation is seen as holes in images)
Cellular swelling
examples of degenerative changes (ie damage associated with cell and tissue damage)
Q: What is necrosis? What’s it associated with being?
A: confluent (cells near eachother) cell death associated with inflammation
Whole areas of cells die not just single cell
Associated with being pathological
*Q: What are the 4 types of necrosis? (light microscope changes associated with irreversible change)
A: coagulative
Liquefactive
Caseous
Fat
Q: Describe fat necrosis by aid of an example.
A: Associated with acute pancreatitis where you get the release of lipases which digests fats and hydrolyses triglycerides -> free FA and glycerol
Free FA combine with calcium in the extra cellular fluid and deposits
Each deposit (appears as white part on real life image) are areas of fat necrosis
Q: What is apoptosis?
A: programmed cell death of single cells not associated with inflammation
Active cell death that needs energy
Can be pathological or physiological
Q: How does apoptosis occur?
A: nucleus shrinks
Little bits of the cell break off (lined by cytoplasm)
Nothing from inside cell is exposed to outside so there is no inflammation
It is phagocytosed by macrophages
*Q: What are the differences between apoptosis and necrosis? (4)
A: A may be physiological
A is an active energy dependent process
N is what happens when ATP runs out
A is not associated with inflammation
N includes a damaged plasma membrane
N is a response to severe injury
A is a response to mild injury
Q: Describe the stress triangle involving a normal cell.
A: can stress the normal cell and it will adapt -> adapted state (eg heart cells work harder when low bp)
normal cell-> too much stress -> cell injury which leads to cell death (eg. myocardial infarction where blood supply is cut off)
adapted state-> continually put pressure on -> reach point where no longer adapt -> cell injury …
Q: What are the 2 types of cell injury?
A: lethal and sublethal
Q: Describe the 2 types of stress exerted on cells.
A: physiological- that healthy people have eg. when exercising
pathological- associated with a diseased state eg. HBP
*Q: What do the consequences of an injurious stimulus depend on? (4)
A: type of cell (some are more susceptible to injury)
status (cell that is dividing is more vulnerable)
adaptability
genetic makeup
*Q: Define hypertrophy. Can be? (2)
A: increase in cell size and consequently an increase in the size of the organ
pathological or physiological
*Q: What’s an example of physiological hypertrophy? pathological?
A: uterus is larger during pregnancy (more fibres)
HBP
Q: Describe an alcoholic fatty change? Ballooning degeneration?
A: -single metabolic consequence
- (liver disease)
- reversible change
- fluid leaks in
- cells are much bigger as are swollen
Q: How does necrosis occur?
A: contents are released-> attract neutrophils and cause necrosis (membrane is damaged)
*Q: What are 5 causes of apoptosis that are normal physiological processes?
A: embryogenisis (separate fingers)
deletion of auto reactive T cells in the thymus
hormone dependent physiological involution
cell deletion in proliferating populations
variety of mild injurious stimuli that cause irreparable DNA damage that triggers cell suicide pathways
Q: What’s a third type of cell death? Describe. Circumstance?
A: necroptosis
programmed cell death associated with inflammation
only in pathological circumstances eg viral infections
*Q: Define ulcer.
A: open sore on an external or internal surface of the body, caused by a break in the skin or mucous membrane which fails to heal
*Q: Define degeneration.
A: process by which tissue deteriorates and loses its functional ability due to traumatic injury, aging and wear and tear
Q: Describe caseous necrosis. What is it associated with?
A: ‘cheesy’ necrosis
Necrotic area is granular (that’s what makes it caseous)
Associated with pulmonary TB
Q: Describe liquefactive necrosis using an example. Identified?
A: brain has totally liquified
Is an empty space and can only identify cells by looking at cells around the cyst
Q: Describe coagulative necrosis. (3) Appearance? Example.
A: cell shape does not change- tissue keeps structure
Nuclei are gone
Loss of cell substance
On images- see inflammatory cells between
In images appear like ‘ghost cells’ due to loss of proteins etc so stain isn’t picked up as much
myocardal infarct (dead cells are still recognisable)
