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Pathology and Immunity > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

what are the two kinds of cell injury

A

reversible and irreversible

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2
Q

describe reversible cell injury

A

cells will adapt to the changes in environment and returns to normal once stimulus is removed

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3
Q

describe irreversible cell injury

A

permanent and leads to cell death

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4
Q

what does cell injury mean for the body

A

there will be disease

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5
Q

what is cell stress

A

cell injury

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6
Q

what impacts how the cell stress impacts the cell

A

dose intensity and the cell vulnerability - some cells are more sensitive to change than others

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7
Q

what can cell adaptation involve

A

change in cell metabolism or change in cell structure

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8
Q

what is the point of no return for cell injury

A

this is when reversible injury persists for a period of time and no matter how the cell tries to adapt there will be a point where the cell cannot exist in the new environment

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9
Q

what can happen if cell injury is irreversible

A

cell death

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10
Q

what determines if injury will be reversible or irreversible

A

the type, duration and severity of the injury
the susceptibiilty and adaptability of the cell like nutritional status, metabolic needs and cardiac versus skeletal muscle

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11
Q

what is the term used for the causes of cell injury

A

aetiology

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12
Q

what are the causes of cell injury

A

hypoxia
physical agents
chemicals/drugs
infections
immunological reactions
nutritional imbalance
genetic defects

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13
Q

what is hypoxia

A

decreased oxygen supply

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14
Q

describe hypoxia and how it leads to cell death

A

this is oxygen deficiency and causes anaemia and respiratory failure
it disrupts the oxidative respiratory processes in cells to decrease ATP production
however cells can release energy via anaerobic mechanisms but is this limited

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15
Q

what happens to cells when there is hypoxia

A

their supply of energy is greatly diminished

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16
Q

what is ischaemia

A

the reduction in blood supply to tissues and is caused by blockage of arterial supply or venous drainage like atherosclerosis
it means there is a decrease in oxygen and nutrient supply to the tissue like glucose

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17
Q

is ischaemia or hypoxia worse for cells

A

ischaemia as it is more severe and rapid to damage the cells than hypoxia and the anaerobic energy release will also be stopped

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18
Q

what are some physical agents

A

heat electricity and radiation

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19
Q

describe how mechanical trauma impacts cells

A

it affects their structure and cell membranes

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20
Q

describe how extremes of temperature affect cells

A

they affect proteins and chemical reactions

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21
Q

how does ionising radiation impact cells

A

damages DNA

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22
Q

how does electric shock affect cells

A

it burns them

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23
Q

is the damage from radiation immediately apparent

A

no the damage can occur years down the line from the exposure

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24
Q

what is the common form of ulceration

A

traumatic ulcer of the lip

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25
Q

what are some infectious agents that can injure cells

A

bacteria
viruses
fungi
parasites
prions

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26
Q

do infectious agents damage cells through the same basic pathway

A

no they have a variety of different mechanisms that bring about the damage

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27
Q

what is an example of a simple host chemical that can cause damage to the body

A

glucose - when in excess it can affect many different organ systems

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28
Q

what is a poison that injures cells

A

cyanide blocks oxidative phosphorylation

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29
Q

what are occupational hazards that can injure cells

A

asbestos can cause inflammation

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30
Q

what do chemicals and drugs to do damage cells

A

they disrupt cell membranes and proteins

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31
Q

how does glucose cause damage in excess

A

it leads to osmotic disturbances

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32
Q

what are some immunological reactions that can damage cells

A

anaphylaxis
auto immunity
inflammation

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33
Q

summarise anaphylaxis

A

closure of airways due to type 1 hypersensitivity mediated by IgE immunoglobin

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34
Q

summarise how autoimmunity affects the cells in the body

A

type 2 hypersensitivity where antibodies are directed toward host antigens
type 3 hypersensitivity where there is formation of antigen antibody complexes can cause damage to cells

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35
Q

summarise inflammation and cell injury

A

inflammation from complement, clotting and the products of neutrophils can damage cells

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36
Q

what can too little nutrient intake lead to

A

either generalised deficiency or specific nutrient deficiency can affect the body

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37
Q

what is generalised nutrient deficiency associated with

A

anorexia

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38
Q

what is specific nutrient defiency associated with

A

scurvy and rickets

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39
Q

what can lead to excessive nutrient imbalance

A

hypervitaminosis where people are taking too much vitamin A or D
or obesity

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40
Q

what is HbS

A

sickled haemoglobin

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41
Q

describe how genetic defects can affect cells

A

there are some big changes in genetic makeup or more subtle changes that can lead to effects on cells - to do with DNA

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42
Q

give examples for genetic defects and their impacts on cell health

A

sickle cell anaemia can lead to clotting in blood vessels.
people with the trait develop sickling when exposied to low oxygen tension like whenunder general anaesthesia
inborn errors of metabolism can cause cell injury such as through the lack of an enzyme which can cuase build up of the enzyme substrate

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43
Q

what is disrupted in cells during reversible injury

A
  • aerobic respiration and ATP synthesis due to mitochondrial damage
  • plasma membrane integrity
  • enzyme and structural protein synthesis
  • DNA maintenance
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44
Q

what can the cells look like if there has been reversible injury

A

there can be cloudy swelling or fatty change

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45
Q

what leads to the cloudy swelling appearance of cells when there is reversible injury

A

the cells are incapable of maintaining ionic and fluid homeostasis whcih leads to failure of energy dependent ion pumps in the cell membrane
there is loss of ATP so the energy dependent sodium pump will influx sodium and water, which combined with build up of intracellular metabolites leads to swelling

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46
Q

is cloudy swelling an irreversible damage to cells

A

no it can be reversed

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47
Q

what does this image show

A

cloudy swelling in kidney tubules due to reversible cell injury

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48
Q

what causes the fatty change effect seen in some cells with reversible injury

A

accumulation of lipid vacuoles in the cytoplasm caused by the disruption of fatty acid metabolism so that triglycerides cannot be released from the cell, especially in the liver.

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49
Q

in what type of reversible cell injury does fatty change occur

A

toxic and hypoxic injury like in alcohol abuse, diabetes and obesity.

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50
Q

what can the liver look like when the cells undergo fatty change due to alcohol abuse

A

can become enlarged and pale due to the accumulation of lipid droplets in the cells

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51
Q

what is the main cause of fatty change

A

alcohol abuse

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52
Q

what are some reversible changes that can happen to injured cells

A
  • dilation of organelles
  • ribosome disaggregation
  • blebbing
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53
Q

what happens at the point of no return in cell injury

A

mitochondrial high amplitude swelling
mitochondrial matrix densities
violent blebbing

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54
Q

what are examples of irreversible changes that occur in the cell following the point of no return

A
  • membrane rupture, dispersal of organelles
  • breakdown of lysosomes
  • activation of inflammatory response
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55
Q

what is blebbing

A

this is when bits of the cell breaks off from the cytoskeleton

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56
Q

why does cell necrosis lead to inflammation

A

because the cell will burst and release its constituents into the surrounding space which recruits immune cells like macrophages to arrive and remove them by phagocytosis

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57
Q

what occurs in necrosis and what is it

A

cell death that usually occurs due to pathology.
occurs when there is irreversible cell injury, and intracellular protein denaturation and lysosomal digestion of the cell
disrupted cell membrane leaks the cell contents to trigger an inflammatory response

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58
Q

when can histopathological changes occur after necrosis

A

not necessarily immediately, they could take some time to appear

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59
Q

why are lysosomes released during necrosis

A

to digest the cell

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60
Q

what are the three stages to nuclear changes in necrosis

A
  • pyknosis
  • karyorrhexis
  • karyolysis
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61
Q

what is pyknosis

A

this is when the nucleus shrinks and the nucleus will stain darker here

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62
Q

what is karyorrhexis

A

this is when the nucleus breaks up and fragments are produced

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63
Q

what is karyolysis

A

this is when the blue staining DNA in the nucleus is digested by endonucleases and the blue staining fades away

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64
Q

what is the end result of the nuclear changes that occur during necrosis

A

loss of the blue staining nucleus, which is a useful sign to show that the cell is necrotic

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65
Q

what happens to the cytoplasm during necrosis

A

the cytoplasm appears paler and swollen, and becomes more pink due to an increase in eosphinophilicness, this occurs due to denaturation of both cytoplasmic structural proteins and enzymes

66
Q

what happens to the colour of the cytoplasm during necrosis

A

becomes paler and more pink (eosinophilic)

67
Q

what makes a dead cell obvious

A

lack of nucleus

68
Q

what are the types of necrosis

A
  • coagulative necrosis
  • liquefactive necrosis
  • caseous necrosis
  • fibrinoid necrosis
69
Q

describe coagualative necrosis

A
  • no proteolysis of the dead cells due to denaturation of enzymes
  • the architecture of tissues is preserved for some days, but there is no nucleus
  • firm in texture
  • cells are digested by lysosomes of leukocytes
70
Q

why is the architecture of the tissue preserved for a few days during coagulative necrosis

A

this is because the enzymes are denatured so there isnt any proteolysis

71
Q

what are the dark dots on histological imaging of coagulative necrotic tissue

A

inflammatory cells

72
Q

what is an infarction

A

localised area of coagulative necrosis

73
Q

describe liquefactive necrosis

A

this is when there is digestion of dead tissues which mean the tissue is in a liquid viscous state
caused by focal bacteria or fungal infections and leads to an abscess
the necrotic material is thick and pale yellow in colour

74
Q

what is the necrotic material produced from liquefactive necrosis

A

pus

75
Q

what is an abscess

A

an accumulation of pus

76
Q

what does the necrosis of the CNS as a result of hypoxia usually manifest as

A

liquefactive necrosis

77
Q

what is colliquative necrosis

A

this is the liquefactive necrosis that causes pus production

78
Q

what makes up pus

A

a mixture of tissue and pathogens

79
Q

describe caseous necrosis

A

this is mostly seen in tuberculosis infections and causes the tissue to have a friable white appearance resembling cheese
microscopically it appears as granuloma fragmented cells and granular debris surrounded by apoptosis

80
Q

where is there granular debris in caseous necrosis

A

mass apoptosis

81
Q

what makes up the lesion in caseous necrosis

A

masses of granulation tissue made up of chronic inflammatory cells and multinucleated giant cells and fibroblasts

82
Q

what is the appearance of caseous necrotic material

A

firm and crumbly lesion that looks like cheese

83
Q

what is gangrenous necrosis

A
  • occurs when blood supply to a limb is restricted and it will undergo coagulative necrosis
  • also used when a limb undergoes liquefactive due to extensive bacterial infection - degradative enzymes due to infection causes the “wet gangrene”.
  • two pathways linked to this name then
84
Q

describe fat necrosis

A

this is when focal areas of fat are destroyed. the fat cells may be liquified by activated pancreatic enzymes like in acute pancreatitis
can laed to calcium salts being deposited within them

85
Q

describe fibrinoid necrosis

A

this is a special type of necrosis seen in immune reactions in blood vessels
antibody antigen complexes are deposited in artery walls together with fibrin that leaks out of the vessels
bright pink and amorphous substances in H&E

86
Q

what type of necrosis is often seen in blood vessels

A

fibrinoid necrosis

87
Q

what are the effects of necrosis

A
  • functional and it depends on the organ and tissue and how severe it was
  • inflammation
  • release of cell contents to activate inflammation which are then phagocytosed
  • the necrotic areas is replaced by a scar and if the remains are not removed then calcium salts may be deposited in the necrotic tissue
88
Q

when may calcium salts be deposited in necrotic tissue

A

if the cell remains are not removed by phagocytosis

89
Q

what does a denatured cytoplasm indicate

A

coagulative necrosis caused from hypoxia and free radicals

90
Q

what does a hydrolysed cytoplasm indicate

A

liquefaction necrosis caused by strong acids, snake venom, clostridia and neutrophils

91
Q

what does mass apoptosis indicate

A

caseous necrosis from fungi or tuburculosis

92
Q

what does saponified cytoplasm indicate

A

enzymatic fat necrosis by lipase

93
Q

what does exposure to free radicals lead to

A

coagulation necrosis

94
Q

what does acute pancreatitis lead to

A

enzymatic fat necrosis

95
Q

what is apoptosis

A

this is genetically programmed cell death and orderly elimination of unwanted cells.
it can occur in pathological situations and requires energy.
there are distinct pathways involved but it does not cause inflammation
there is a different morphology compared to necrosis

96
Q

does necrosis use energy

A

no

97
Q

does apoptosis use energy

A

yes

98
Q

what necrosis cause inflammation

A

yes

99
Q

does apoptosis cause inflammation

A

no

100
Q

what colour do cells stain as they undergo apoptosis

A

dark stain

101
Q

what are some pathological triggers of apoptosis

A
  • hypoxia or ischaemia
  • viral infection
  • dna damage
102
Q

why does hypoxia/ischaemia lead to apoptosis

A

there is protein misfolding and the cell will undergo apoptosis

103
Q

why does viral infection lead to apoptosis

A

cytotoxic t lymphocytes contain enzymes which can then induce apoptosis

104
Q

why does dna damage cause apoptosis

A

p53 will activate caspases to trigger apoptosis
the cell contents are degraded by enzymes activated by the cell

105
Q

what is p53

A

guardian of the genome

106
Q

what are the physiological roles of apoptosis

A
  • deletion of cell populations during embryogenesis
  • hormone change dependent involution from the uterus breast and ovary
  • cell deletion in proliferating cell populations to maintain the constant number of cells
  • deletion of inflammatory cells after inflammation
  • deletion of self reactive lymphocytes in the thymus
107
Q

what does too much apoptosis lead to

A

degenerative diseases

108
Q

what does too little apoptosis lead to

A

cancer

109
Q

describe the morphology of apoptosis

A
  • cell will shrink
  • chromatin will condense to package the nucleus
  • cell membrane remains intact with the formation of cytoplasmic blebs
  • blebs break off to form apoptotic bodies
  • cell phagocytosed by there is no widespread inflammation
110
Q

why is there no inflammation in apoptosis

A

the fragments of the apoptotic cell are encased in the cell membrane and this does not cause inflammation this way
the cell is taken up by phagocytosis

111
Q

describe the cell size in necrosis vs apoptosis

A

enlarged and swelling in necrosis
reduced from shrinkage in apoptosis

112
Q

describe the nucleus in necrosis vs in apoptosis

A

in necrosis it undergoes pyknosis, karyorrhexis and karyolysis
in apoptosis there is fragmentation into nucleosome size fragments

113
Q

describe the cell membrane in necrotic vs apoptotic cells

A

disrupted in necrotic, intact with altered lipid orientation in apoptotic

114
Q

describe the cellular contents in necrotic vs apoptotic cells

A

enzymatic digestion that could leak out of the cell during necrosis, could be released in apoptotic bodies but otherwise intact in apoptosis

115
Q

is there adjacent inflammation in necrosis or in apoptosis

A

frequently seen in necrosis

116
Q

is the role of necrosis pathologic or physiologic

A

invariably pathologic due to a culmination of irreversible cell injury

117
Q

is the role of apoptosis pathological or physiological

A

often it is physiological as a means of eliminating unwanted cells, but it may be pathologic after some forms of cell injury, especially DNA damage

118
Q

what is intracellular accumulation

A

this is the accumulation of abnormal substances in cells

119
Q

what are some forms of intracellular accumulation

A
  • excessive normal cellular constituent
  • abnormal endogenous / exogenous material
120
Q

what are some normal cellular constitutents that can accumulate

A

water
lipids in fatty change
glycogen

121
Q

what are some abnormal contents that can accumulate in cells

A

carbon
silica
metabolites
cholesterol

122
Q

is accumulation in cells always permanent

A

no it can be temporary depending if it is cytoplasmic or nuclear

123
Q

why does atherosclerosis occur

A

due to lipid deposition in the walls of blood vessels
cholesterol accumulation in macrophages and smooth muscle cells in blood vessel walls

124
Q

where is cholesterol accumulation found

A

in atherosclerosis and at sites of haemorrhage and necrosis

125
Q

why do macrophages get called foam cells at sites of cholesterol accumulation

A

they look like foam due to large size and pale colour, and when there are many packed together they look like foamy bubbles

126
Q

why does cholesterol appear as empty spaces on stainings

A

it disappears when you prepare the slides

127
Q

what is amyloid

A

a fibrillar protein material that is deposited as a result of pathologic processes

128
Q

why is there a lot of amyloid found at sites of pathology

A

it is deposited as a result of pathologic processes to its production is increased when there is infection.
it is deposited in extracellular location mostly on the basement membrane, in various tissues and organs
the proteins can be produced by the body de novo or due to infection, inflammation or malignancy

129
Q

where is amyloid often found in the body

A

the kidney heart liver and on the tongue

130
Q

what are the types of amyloidosis

A

AL
AA
Abeta
AF
SSA

131
Q

what is AL

A

primary amyloidosis, caused by disorder of the plasma cells produced too many immunoglobins.
amyloid light chain that is derived from light chain immunoglobins is the abnormal protein that will then deposit around organs

132
Q

what is AA

A

asecondary amyloidosis, due to infection or inflammation. produces amyloid A which deposits.
myloid associated which is derived from proteins synthesised in the liver

133
Q

what is Abeta amyloid associated with

A

alzheimers disease

134
Q

what is the stimulus for amyloid deposition

A

chronic inflammation
multile myeloma
ageing
drug abuse

135
Q

describe the histological appearance of amyloid

A

pink hyaline appearance that is difficult to identify with H&E so congo red staining is used instead
this is due to the beta pleated sheets in amyloid proteins, which stain pink or red depending on the staining used.

136
Q

how can amyloid impact the kidney

A

affects the structure of the glomerulus and thickens the walls of the tubules which compromises the function of the kidney

137
Q

describe pathological pigmentation

A

occurs due to a build up of pigmented substances in the cytoplasm
there is endogenous and exogenous pigmentation

138
Q

describe endogenous pigmentation

A

occurs due to lipfuscin cellular lipid breakdown products such as:
- melanin
- haemosiderin localised bruising
- bilirubin
all appear brown

139
Q

why are bruises different colours

A

due to the breakdown of red blood cells

140
Q

when are melanocytes more active

A

when we are out in the sun

141
Q

describe exogenous pathological pigmentation

A

carbon deposition is the most common
- in macrophages there is alveoli of the lungs
- black pigment suggests anthracosis
- inhaled soot or smoke
- can be severe in coal workers

142
Q

what are other examples of exogenous pigmentation aside from carbon

A

tattoos
heavy metal salts like lead
pigmentation associated with intravascular drug use

143
Q

what is pneumoconiosis

A

fibrosis in the lungs due to carbon build up

144
Q

why is there pigmentation in people who inject recreational drugs

A

it is not sterile and often foreign objects can be injected alongside the drug

145
Q

what are the two kinds of pathological calcification

A

dystrophic and metastatic

146
Q

describe dystrophic calcification

A

this is when there are deposits of calcium phosphate in necrotic tissue
the levels of serum calcium are normal in this kind

147
Q

what is an example of dystrophic calcification

A

valvular heart disease - calcification of valves

148
Q

describe metastatic calcification

A

deposits of calcium salts in normal, vital tissue with raised serum calcium levels
often seen in connective tissues of blood vessels
can compromise the function of tissue

149
Q

which type of calcification leads to increased calcium levels

A

metastatic

150
Q

what can cause hypercalcaemia

A
  • increased PTH due to a tumour in the gland
  • destruction of bone tissue
  • excessive vitamin D
  • renal failure
151
Q

what can cause destruction of bone tissue

A

leukemia
metastasis to bone
immobilisation

152
Q

what is the cause of secondary hyperparathyroidism

A

renal failure

153
Q

after how many days does the nucleus disapear from a cell when it is undergoing necrosis

A

1-2 days

154
Q

what does the breakdown of lysosomes during necrosis lead to

A
  • digestion of cells
  • includes those produced from neutrophils in the inflammatory response
155
Q

why does hypoxia cause apoptosis

A

leads to the formation of abnormal proteins due to misfolding

156
Q

what happens in amyloidosis

A

the removal mechanism for abnormally formed proteins is impaired
amyloid proteins will build up on the organs and eventually damage them

157
Q

where can lipofuscin be seen

A

surrounding the nucleus, seen in the liver and heart of ageing patients and patients with severe malnutrition or cachexia

158
Q

how can intravascalar drug use cause pigmentation

A
  • soot and foreign particles that enter the skin when the drug is cooked and enter via the needle
  • post inflammaotry pigmentation around old needle sites
159
Q

what is AF

A

familial amyloidosis that occurs due to inherited mutations causing mutated proteins being produced from the liver

160
Q

what is SSA

A

senile systematic amyloidosis, deposits transthyretin protein which aggregates and deposits in the heart of older men

161
Q

what is amyloidosis

A

deposition of abnormal proteins in the body that can go onto multiple organs and lead to organ failure

Pathology and Immunity (16 decks)

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