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Pathology > Cell degeneration/death (year 2) > Flashcards

Cell degeneration/death (year 2) Flashcards

1
Q

what is homeostasis?

A

cells keeping balance of physiological demands

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2
Q

what stimulates cellular adaptation?

A

response to excessive physiological stress of pathological stimuli

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3
Q

what does cellular adaptation affect?

A

the growth and differentiation of cells

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4
Q

what are some examples of cellular adaptation?

A

hypertrophy, hyperplasia, atrophy, metaplasia

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5
Q

what is atrophy?

A

decrease in size and number of cells

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6
Q

what is hypoplasia?

A

reduced organ volume because of incomplete cell proliferation

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7
Q

what is aplasia?

A

organ absence because of defective cell proliferation

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8
Q

define involution

A

a physiological atrophy

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9
Q

define atrophy

A

a pathological atrophy

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10
Q

give some examples of involution

A

uterus after parturition
thymus after puberty
senescence

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11
Q

give some examples of pathological atrophy

A

skeletal muscle disuse
denervation
inadequate nutrition
pressure atrophy

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12
Q

define hypertrophy

A

increase in size of cells - no cell division involved

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13
Q

what causes hypertrophy?

A

increased functional demand

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14
Q

what is an example of physiological hypertrophy?

A

smooth muscle in pregnant uterus

skeletal muscle with training

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15
Q

give an example of pathological hypertrophy

A

cardiac myocytes

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16
Q

what is hyperplasia?

A

increase in the total number or cells in an organ/tissue

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17
Q

what are the two types of physiological hyperplasia?

A

hormonal and compensatory

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18
Q

give some examples of hormonal hyperplasia

A

proliferation of mammary and uterine epithelium during pregnancy

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19
Q

give an example of compensatory hyperplasia

A

in symmetrical organs with functional loss of one such as kidney
partial loss of parenchyma such as partial hepatectomy

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20
Q

what can cause pathological hyperplasia?

A

excessive hormonal stimulation
attempt at regeneration
viral infection

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21
Q

what is metaplasia?

A

reversible change in which one adult cell type is replaced by another adult cell type

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22
Q

give an example of metaplasia

A

columnar epithelia replaced by stratified squamous when smoking

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23
Q

what are normal cellular constituents?

A

water, lipid, carbohydrate, protein

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24
Q

what are the two categories of abnormal intracellular accumulation?

A

exogenous and endogenous

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25
Q

name some exogenous abnormal intracellular substances

A

minerals

products of infectious agents

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26
Q

what is the name for intracellular accumulation of lipids?

A

steatosis/lipidosis

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27
Q

what organ is steatosis common in?

A

liver cells

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28
Q

name some causes of lipidosis

A

toxins, protein malnutrition, diabetes, obesity

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29
Q

describe the normal metabolisms of lipids

A

free fatty acids transported to liver where they form triglycerides, phospholipids, cholesterol, ketone bodies
triglycerides are then associated with apoproteins and form lipoproteins that enter circulation

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30
Q

what form of lipid accumulates in hepatocytes?

A

triglycerides

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31
Q

what may cause intracellular protein accumulation?

A

excess of protein presented to cell
excessive protein synthesis
defects in protein folding

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32
Q

where is an example of somewhere that excess proteins can be presented to the cell?

A

proximal renal tubules during proteinuria

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33
Q

where may you see excessive synthesis of proteins?

A

plasma cells producing high levels of immunoglobulins

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34
Q

what may cause abnormal folding of proteins?

A 
genetic mutations
ageing
environmental factors
amyloidosis 
Alzheimers
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35
Q

why might defects in protein folding occur?

A

defective intracellular transport and secretion of critical proteins
toxicity of aggregated abnormally folded protein

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36
Q

why may glycogen accumulate intracellularly?

A

diabetes, glucocorticoid hepatopathy, glycogen storage disease

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37
Q

how does glycogen appear in the cell?

A

clear vacuoles in cytoplasm

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38
Q

what are pigments?

A

coloured substances that can be normal or abnormal constituents of a cell

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39
Q

name some normal endogenous pigments of cells

A

melanin, lipofuscin and haemosiderin, bilirubin

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40
Q

name some common abnormal pigments of cells

A

carbon/coal dust

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41
Q

define anthracosis

A

inhalation of carbon/coal dust

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42
Q

where are carbon particles found?

A

phagocytksed by alveolar macrophages and transported to regional lymph nodes

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43
Q

what is is lipofuscin?

A

insoluble polymers of lipids that are yellow/brown colour

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44
Q

what colour is melanin?

A

brown/black

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45
Q

what is haemosiderin?

A

haemogobulin derived storage form of iron that appears gold/yellow/brown

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46
Q

when does haemosiderin appear?

A

haemorrhage (depredation of haemoglobin)

end of the lifespan of RBC

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47
Q

what is bilirubin?

A

normal major pigment of bile

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48
Q

what colour is bilirubin?

A

green/blue

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49
Q

what does excess bilirubin cause?

A

jaundice

50
Q

what colour is biliverdin?

A

green

51
Q

what are the components of bile?

A

water, cholesterol, bile salts, bile pigment, iron

52
Q

what colour is bile?

A

yellow/green

53
Q

what can cause jaundice?

A

excessive haemolysis
severe hepatic injury
obstructed bile flow

54
Q

what may cause cell injury?

A 
oxygen deprivation
physical agents
infectious agents
immunological reactions
genetic derangements
nutritional imbalances
chemical agents/drugs
55
Q

what intracellular systems are vulnerable to injury?

A

cell membrane, aerobic respiration, protein synthesis, genetic apparatus

56
Q

what biochemical mechanisms may lead to cellular injury?

A 
ATP depletion
oxygen derived free radicals
loss of Ca homeostasis
defects in membrane permeability
irreversible mitochondrial damage
57
Q

what is hypoxia?

A

a deficiency in oxygen reaching tissue

58
Q

what does lack of oxygen to a tissue result in?

A

decrease aerobic respiration meaning less ATP leading to reduced activity of the sodium pump

59
Q

what happens as a result of the decreased sodium pump activity?

A

accumulation of sodium meaning water accumulates in the cell causing swelling

60
Q

what are the consequences of increased intracellular calcium?

A

activates enzymes such as ATPase, phospholipase, endonuclease, protease

61
Q

what does increased activity if ATPase mean?

A

less ATP

62
Q

what does increased activity if phospholipase mean?

A

decreased phospholipids

63
Q

what does increased activity if endonuclease mean?

A

nuclear chromatin damage

64
Q

what does increased activity if protease mean?

A

disrupts membranes and cytoskeleton

65
Q

what are some examples of irreversible cell injury?

A

mitochondrial changes, extensive plasma membrane damage, prominent swelling of lysosomes, massive calcium influx

66
Q

when is cell injury characterised as irreversible?

A

inability to reverse mitochondrial dysfunction

profound disturbance in membrane function

67
Q

what are some potential causes of membrane damage resulting in irreversible injury?

A

loss of membrane phospholipids, cytoskeleton abnormalities, toxic oxygen radicals, lipid breakdown

68
Q

what is a free radical?

A

extremely unstable highly reactive chemical species with a single unpaired electron in an outer orbit

69
Q

what is the main source of free radicals?

A

hydrolysis of water into OH and H by ionising radiation

redox reaction

70
Q

what injuries do free radicals cause?

A

lipid per oxidation of membranes
lesions in DNA
cross-linking of proteins

71
Q

what is reperfusion injury?

A

death of cells after the resumption of blood flow

72
Q

why does reperfusion injury occur?

A

increased generation of oxygen free radicals

cytokines and adhesion molecules expressed by hypoxic cells - inflammation

73
Q

what are two types of reversible cellular injury?

A

cellular swelling

fatty change

74
Q

what are two examples of irreversible cellular injury?

A

necrosis

apoptosis

75
Q

what is the medical term used for jaundice?

A

icterus

76
Q

what is amyloidosis?

A

pathological accumulation of proteinaceous substance deposited between cells

77
Q

what are the main categories of amyloid?

A

AA - amyloid associated
AL - amyloid light chain
beta amyloid protein
islet amyloid polypeptide

78
Q

where is AA synthesised?

A

liver

79
Q

what amyloid is deposited in spongiform encephalopathies?

A

beta amyloid protein

80
Q

where are islet amyloid polypeptides deposited?

A

pancreatic islets

81
Q

what are the classification categories of amyloidosis?

A

systemic
localised
primary
secondary

82
Q

when does primary amyloidosis occur?

A

with immunocytic disorder

83
Q

when does secondary amyloidosis occur?

A

with complications of chronic inflammation (AA)

84
Q

define pathological calcification

A

abnormal deposition of calcium salts

85
Q

define dystrophic

A

relating to non-viable or dying tissue - necrosis

86
Q

is dystrophic calcification intra or extracellular?

A

can be either

87
Q

what are the serum calcium levels of animals with dystrophic calcification?

A

normal

88
Q

what are the two steps of dystrophic calcification?

A

initiation and propagation

89
Q

what occurs during the initiation phase of dystrophic calcification?

A

intracellular - Ca accumulate in mitochondira

extracellular - Ca accumulates by phospholipids in membrane bound vesicles

90
Q

when and where does metastatic calcification occur?

A

normal tissue with hypercalcaemia

91
Q

when may hypercalcaemia be seen?

A

increased PTH secretion
bone tissue destruction
vitamin D intoxication
renal failure

92
Q

why is calcium deposited during metastatic calcification?

A

depending on the pH of a specific area

93
Q

what are the two end points of irreversible cell injury?

A

apoptosis

necrosis

94
Q

define necrosis

A

morphological changes that follow cell death

95
Q

what are the two processes occurring during necrosis?

A

enzymatic digestion of cell - autolysis or heterolysis

denaturation of protein

96
Q

what are the two outcomes of necrosis?

A

phagocytosis

dystrophic calcification

97
Q

what is autolysis of a cell?

A

lysosomal enzymes of the dying cell itself

98
Q

what is the gross morphology of necrosis?

A

focal discoloured (red/white) areas within tissue

99
Q

what are the three appearances of nuclei undergoing necrosis?

A

pyknosis, karyorrhexis, karyolysis

100
Q

what is pyknosis?

A

chromatin collapses - nucleus becomes round and condensed

101
Q

define karyorrhexis

A

fragmentation of the nucleus

102
Q

define karyolysis

A

complete dissolution of the nucleus

103
Q

what are the types of necrosis?

A

coagulative
liquefactive
caseous
fat

104
Q

what is the dominant feature of coagulative necrosis?

A

denaturation

105
Q

when does coagulative necrosis occur?

A

in hypoxic cell death

106
Q

what type of necrosis preserves the cell outline?

A

coagulative

107
Q

what is the dominant feature of liquefactive necrosis?

A

enzymatic digestion

108
Q

when does liquefactive necrosis occur?

A

focal material/fungal infections

109
Q

what is the end result of liquefactive necrosis?

A

complete digestion of cells forming a liquid masss

110
Q

when does caseous necrosis occur?

A

coagulative necrosis in tuberculosis

111
Q

what is fat necrosis?

A

focal destruction of adipose tissue

112
Q

what is fat necrosis usually due to?

A

release of pancreatic enzymes with pancreatic necrosis

113
Q

how does fat necrosis appear?

A

chalky white - fat combines with calcium

114
Q

define apoptosis

A

programmed cell death

115
Q

what are the biochemical steps of apoptosis?

A

protein cleavage
protein cross-linking
DNA breakdown
phagocytic recognition

116
Q

what are the phases of apoptosis?

A

initiation (signalling pathway)
control and integration
execution phase
phagocytosis

117
Q

what are the two ways apoptosis is initiated?

A

signals transmitted across plasma membrane to intracellular regulatory molecules
signals addressed within target cells

118
Q

what are examples of apoptotic stimuli external to the cell?

A

hormones, growth factors, cytokine

119
Q

what are intracellular apoptotic stimuli?

A

heat, radiation, hypoxia, viral infection, glucocorticoids

120
Q

does inflammation occur with apoptosis?

A

no

121
Q

when may apoptosis occur?

A 
embryogenesis
tumours
neutrophils in inflammation
lymphocyte death
cell death by cytotoxic T cells
viral disease
pathological atrophy
ageing

Pathology (17 decks)

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