cell pathology Flashcards

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1
Q

what do our bodies react to

A
  • physiological stress or pathological stimuli
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2
Q

what do cells to accommodate for extracellular stresses

A

change structure and function. also maintain normal homeostasis

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3
Q

what type of process can cell death be

A

normal or abnormal processes

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4
Q

what are examples of reversible changes

A
  • number
  • size
  • phenotype (observable characteristics)
  • function
  • metabolic activity
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5
Q

what are the two types of adaptive responses

A

physiological and pathological adaptations

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6
Q

name some adaptive responses

A
  • hypertrophy
  • atrophy
  • hyperplasia
  • metaplasia
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7
Q

what is hypertrophy

A

this is the increased size of cells and organs.

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8
Q

why can hypertrophy occur

A

it can occur because of an increased amount of proteins and organelles and in cells that don’t divide

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9
Q

what type of adaptive response can hypertrophy be

A

can be physiological and pathological

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10
Q

what other adaptation can hypertrophy occur at the same time as

A

hyperplasia

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11
Q

what is hyperplasia

A

this is the increased number of cells and increased organ size

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12
Q

in what type of cells does hyperplasia occur in

A

in cells that are able to replicate

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13
Q

with what other adaptation can hyperplasia also occur with at the same time

A

hypertrophy

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14
Q

what type of adaptive response can hyperplasia be

A

can be physiological or pathological

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15
Q

give an example of hyperplasia

A

gingival hyperplasia

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16
Q

what can gingival hyperplasia be caused by

A

phenytoin

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17
Q

what is atrophy

A

this is the reduces size of cells and organs

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18
Q

what can be the cause of atrophy

A
  • decreased work load
  • loss of innervation (supply of nerves)
  • diminished blood supply
  • not enough nutrition
  • loss of endocrine stimulation
  • ageing
  • reduces protein synthesis (because of lowered metabolic activity)
  • increased protein degradation
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19
Q

what is metaplasia

A

this is a reversible change in phenotype (observable characteristic). this is as it’s replaced with a cell type that can withstand the environment better

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20
Q

where does metaplasia arise from

A

genetic reprogramming of stem cells

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21
Q

what are some causes of cell injury

A
  • physical trauma
  • hypoxia below normal level of O2 in blood)
  • infectious and chemical agents
  • genetic defects
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22
Q

give an example of metaplasia in real life

A

epithelial metaplasia in smokers. this is where specialised ciliated columnar epithelial cells are exchanged with hardy squamous epithelial cells. this change helps survival but protective mechanisms are lost.

23
Q

what are reversible cell changes in injury

A
  • cell swelling
  • swelling of organelles
  • loss of microvilli
  • surface blebs
  • clumping of chromatin
24
Q

what are irreversible cellular changes in injury

A
  • severe cell swelling
  • membrane damage
  • nuclear changes
  • lysosomal enzyme release
  • protein digestions
25
Q

what can irreversible cell changes lead to

A

cell death

26
Q

what are cellular changes we can see with a microscope

A
  • necrosis (pathological cell death)
  • membrane blebbing
  • nuclear changes
  • cloudy swelling
27
Q

what are cellular changes we can’t see

A
  • endoplasmic reticulum swelling
  • loss of ribosomes
  • loss of specialised membrane structures
  • vacuolisation of mitochondria
28
Q

what is cell death

A
  • the cell membrane, mitochondria, DNA are the main targets for cell injury
  • the inability to divide
  • loss of normal structure and function
  • biochemical changes due to changes to structure
  • cell death can be through necrosis (pathological) or apoptosis (physiological)
29
Q

what happens in necrosis cell death

A
  • small blebs start to form which causes a structural change in the nucleus
  • the blebs fuse together causing it to become bigger and the organelles move to the middle
  • the membrane swells causing it to rupture, releasing the contents of the cell
  • ends in inflammation
30
Q

what are the types of nuclear changes in cell death

A
  • pyknosis = nuclear shrinkage
  • karyolysis = nuclear fading
  • karyorrhexis = nuclear fragmentaion
31
Q

what is necrosis caused by

A

caused by external factors such as infections, toxins or trauma

32
Q

what causes loss of cell membrane integrity and uncontrolled release of components

A

autolysis (self-destruction through it’s own enzymes)

33
Q

what does necrosis cause in the surrounding tissue

A

inflammation

34
Q

what is the tissue response to necrosis

A

haemorrhage

35
Q

what are the two types of tissue response to necrosis

A

resolution and repair

36
Q

what is resolution in tissue response to necrosis

A
  • site (where), type and extent of injury
  • means when it’s resolved which is done by replacing cells with other cells
  • if can’t resolve, the body tries to repair
37
Q

what is repair in tissue response to necrosis

A
  • if tissue can’t resolve it removes dead tissue by using neutrophils and macrophages.
  • Also granulation tissue forms (tissue that forms during healing process)
38
Q

what are the 5 types of necrosis

A
  • coagulative
  • liquefaction (colliquative)
  • caseating
  • fat
  • gangrenous
39
Q

what is the most common type of necrosis

A

coagulative

40
Q

what is coagulative necrosis

A
  • affects solid organs eg, heart
  • the organs are are firm and pale
  • artery occlusion (blockage of blood flow in an artery) is due to ischemia (loss of blood flow)
  • associated with people with cardiovascular and diabetes
41
Q

what is liquefactive necrosis

A
  • semi liquid
  • the degradation (tissue broken down) of cellular and extracellular components by hydrolytic enzymes
  • there are cystic cavities that contain fluid and cell debris
  • main causes are cerebral infarction (stroke) and bacterial infection
  • there’s also loss of neurons and neuroglia cells
  • many macrophages to remove cell debris
42
Q

what is caseating necrosis

A
  • soft and white (cream cheese)
  • soft degradation
  • there’s unstructured protein mass
  • associated with tuberculosis
43
Q

what is fat necrosis

A
  • hard, yellow tissue that’s found in dead adipose tissue (tissue made of fat cells)
  • when have pancreatitis (inflammation of pancreas) proteolytic and lypolytic enzymes are released
  • when have breast trauma fatty acids are released which causes inflammatory response
44
Q

what is calcification of necrotic tissue

A

Dystrophic calcification
- lots of calcium enter the cells
- calcium is combined with phosphate to form calcium phosphate crystals
- extracellular calcification can also occur
- eg, in heart valves which prevents them from working properly

45
Q

is gangrene a distinctive type of necrosis

A

no

46
Q

what is gangrene

A
  • the blackening of dead tissue
  • associated with severe atherosclerosis, diabetes
  • ischaemia (loss of blood flow) is irreversible
47
Q

what are the types of gangrene

A

dry, wet, gas

48
Q

what type of necrosis is associated with dry gangrene

A

coagulative necrosis

49
Q

what type of necrosis is associated with wet gangrene

A

liquefactive necrosis

50
Q

what is gas gangrene

A
  • when bacteria release toxins which release gas into tissue
  • occurs after an infection with clostridium welchii (gram positive bacteria).
  • bacteria invades injuries with damaged blood supply
  • skin appears grey to to purplish red also has bubbles which make crackling noise when pressed
51
Q

what is dry gangrene

A

coagulative necrosis form ischaemic injury (loss of blood flow)

52
Q

what is dry gangrene caused by

A

poor circulation

53
Q

what type of process is dry gangrene

A

slow, gradual process

54
Q
A