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Microbiology BDS1 > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

what is reversible cell injury?

A

cells adapt to changes in environment and return to normal once stimulus is removed

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2
Q

what is irreversible cell injury?

A

permanent and cell death as consequence

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3
Q

if a cell fails to adapt to stress what happens?

A

it becomes an injured cell

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4
Q

what contributes to cell stress?

A

dose intensity and cell vulnerability

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5
Q

what does reversibility or irreversibility of cell injury depend on?

A

type, duration, severity of injury AND on the susceptibility/adaptability of the cell: nutritional status, metabolic needs

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6
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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7
Q

what is hypoxia?

A

deficiency of oxygen

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8
Q

what does hypoxia cause?

A

anaemia and respiratory failure

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9
Q

what does hypoxia do?

A

disrupt oxidative respiratory processes in cell - decreased ATP but cells can still release energy via anaerobic mechanisms

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10
Q

what is ischaemia?

A

reduced blood supply to tissue, depletion of not just oxygen but also nutrients e.g. glucose

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11
Q

what is ischaemia caused by?

A

blockage of arterial supply or venous drainage

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12
Q

what is the extent of damage caused by ischaemia?

A

it is more rapid/severe damage than hypoxia as anaerobic energy release will also stop

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13
Q

what are the physical agents of cell injury?

A

mechanical trauma, extremes of temperate, ionising radiation, electric shock

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14
Q

what does mechanical trauma affect?

A

cell structure and membranes

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15
Q

what does extreme temperature affect?

A

proteins and chemical reactions

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16
Q

what does ionising radiation damage?

A

DNA

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17
Q

what are the infectious agents that contribute to cell injury?

A

bacteria, viruses, fungi, parasites, protons

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18
Q

what are the different chemicals/drugs that contribute to cell injury?

A

simple chemicals, poisons, environmental, occupational hazards, alcohol, smoking and recreational drug

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19
Q

what do chemicals/drugs do to the cell?

A

disrupts membranes and proteins

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20
Q

how does glucose damage the cell when in excess?

A

causes osmotic disturbance

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21
Q

how does cyanide cause cell injury?

A

blocks oxidative phosphorylation

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22
Q

give an example of an environmental chemical that causes cell injury

A

insecticides

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23
Q

what immunological reactions contribute to cell injury?

A

anaphylaxis, autoimmune reactions

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24
Q

how do immunological reactions cause cell injury?

A

they cause damage as a result of inflammation

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25
deficiency of what nutrient causes scurvy?
vitamin C
26
deficiency of which nutrient causes rickets?
Vitamin D
27
what problems can arise from an inadequate intake of nutrients?
scurvy, rickets (specific nutrient deficiency) , anorexia (generalised)
28
what problems can arise from an excessive intake of nutrients?
hypervitaminosis (specific) and obesity
29
what genetic defects contribute to cell injury?
sickle cell anaemia, inborn error of metabolism, cancer, more subtle variations in genetic makeup an determine susceptibility too
30
what are the disruptions made to the cell in reversible injury?
disruptions to aerobic respiration/ATP synthesis, plasma membrane integrity, enzyme and structural protein synthesis, DNA maintenance
31
what do the cells appear as histologically when they are going through reversible injury?
cloudy swelling, fatty change
32
why do the cells take on cloudy swelling in reversible injury?
cells are incapable of maintaining iconic and fluid homeostasis, energy dependent Na pump leads to influx of Na and water, there is also a build of up intracellular metabolites
33
why do cells in reversible injury undergo fatty change?
accumulation of lipid vacuoles in cytoplasm caused by disruption of fatty acid metabolism so triglycerides cannot be released from the cell
34
what type of cell injury does fatty change in cell structure in
toxic and hypoxic injury (alcohol abuse, diabetes, obesity)
35
what are the reversible changes of cell injury?
dilation of organelles, ribosome disaggregation, blebbing
36
what changes to the cell occur at the point of no return?
mitochondrial high amplitude swelling, mitochondrial matrix densities, violent blebbing
37
what changes occur to the cell in irreversible injury?
membrane rupture, dispersal of organelles, breakdown of lysosomes, activation of inflammatory response
38
what results in the digestion of cells and those that are produced from the neutrophils at inflammatory response?
breakdown of lysosomes
39
what is necrosis?
cell death
40
what causes necrosis?
pathology
41
what type of cell injury is necrosis?
irreversible cell injury
42
what happens to the cell during necrosis?
intracellular protein denaturation and lysosomal digestion of cell
43
what does the disrupted cell membrane during necrosis lead to?
leakage of cell contents
44
what happens to the surrounding tissue of necrotic tissue?
inflammatory response
45
how are the cell remains of a necrotic tissue removed?
by phagocytosis
46
what are the nuclear microscopic changes of necrosis?
nucleus shrinks, blue staining DNA in nucleus is digested by endonucleases and the blue staining fades away
47
what is a useful sign that a tissue is necrotic?
histologically, the end result is the loss of the blue staining nucleus showing necrotic tissue is present as endonucleases digest the blue staining DNA
48
what does pyknosis mean?
nucleus shrinks
49
what does karyorrhexis mean?
nuclear fragments
50
what is karyolysis?
endonucleases digesting blue staining DNA
51
what are the cytoplasmic changes that take place in necrosis?
appears paler, become swollen or more eosinophilic (pinker) because of denaturation of cytoplasmic structural and enzyme proteins
52
how long does it take the nucleus of a necrotic cell to disappear?
1-2 days
53
what are the 3 types of necrosis?
coagulative necrosis, liquefactive necrosis, caseous necrosis
54
what happens in coagulative necrosis?
no proteolysis of dead cells as enzymes are denatured, cells digested by lysosomes of leukocytes, there is no nucleus by instead are eosinophillic cells
55
what does coagulative necrotic tissue appear as?
grossly, firm in texture
56
what is a localised area of coagulative necrosis called?
an infarct
57
what happens in liquefactive necrosis?
digestion of dead tissues so tissue is in liquid viscous state
58
what does liquefactive necrosis appear as?
focal bacterial or fungal infections (abscess)
59
what does liquefactive necrosis appear as?
grossly, necrotic material is thick, pale yellow in colour (pus)
60
what does caseous necrosis appear as?
grossly, friable white appearance (like cheese)
61
what is caseous necrosis mostly seen in?
TB infection
62
what is caseous necrosis like microscopically?
granuloma-fragmented cells and granular debris surrounded by inflammatory cells
63
what is gangrenous necrosis?
coagulative necrosis with superimposed bacterial infection - liquefactive necrosis
64
what is fat necrosis?
focal areas of fat destruction, fat cells may be liquefied by activated pancreatic enzymes
65
what is fibrinoid necrosis?
special type of necrosis seen in immune reactions in blood vessels
66
what happens in fibrinoid necrosis?
immune complexes are deposited in artery walls together with fibrin that leaks out of the vessels
67
what are the functional effects of necrosis dependent on?
the organ/tissue
68
what are the inflammatory steps of necrosis?
release of cell contents activates inflammation, cell remains are phagocytosed, necrotic area is replaced by a scar (repair or organisation)
69
what happens if the cell remains of a necrotic tissue are not removed?
calcium salts ma be deposited in necrotic tissue
70
what tells you whether the cell has died
the sate of the nuclei =, pyknosis, karyorrhexis and karyolysis = DEAD
71
what tells you how cells have died?
cytoplasm
72
what is apoptosis?
genetically programmed cell death, orderly elimination of unwanted cells
73
what apoptosis require?
energy
74
what are the pathological triggers of apoptosis?
hypoxia/ischaemia, viral infection, DNA damage, caspases
75
what happens in apoptosis?
cell contents are degraded by enzymes activated by the cell
76
what are the physiological roles of apoptosis?
deletion of cell populations during embryogenesis, hormone change depended involution, cell deletion in proliferating cell populations to maintain constant number of cells, deletion of inflammatory cells are an inflammatory response, deletion of self reactive lymphocytes in the thymus
77
what does too much apoptosis cause?
degenerative disease
78
what does too little apoptosis cause?
cancer
79
what is the morphology of apoptosis?
cell shrinkage, chromatin condensation - packaging up of nucleus, cell membrane remains intact with formation of cytoplasmic blebs, break off to form apoptotic bodies, phagocytosed but no widespread inflammation
80
what are the two types of accumulation of abnormal substances in cells?
excessive normal cellular constituent and abnormal endogenous/exogenous material
81
what is excessive normal cellular constituent made of?
water, lipid, glycogen
82
what is abnormal endogenous/exogenous material made of?
carbon, silica, metabolites, cholesterol
83
what is atherosclerosis?
accumulation of cholesterol in macrophages and smooth muscle cells in blood vessel walls, also found at sites of haemorrhage and necrosis
84
what is amyloid?
a fibrillar proteins that is deposited as a result of pathologic processes leading to increased production of these proteins
85
where is amyloid deposited?
in extracellular locations in various tissues and organs
86
whar are the 3 types of amyloid?
AL (amyloilight chain from immunoglobulins), AA (amyloid associated, from proteins in liver), Abeta (alzheimers disease)
87
what are the stimuli of amyloid deposition?
chronic inflammation, multiple myeloma, ageing, drug abuse
88
what does amyloidosis do?
prevent the degradation/removal of abnormally formed proteins
89
what is pathological pigmentation?
build up of pigmented substances in cytoplasm and can be either endogenous pigmentation or exogenous pigmentation
90
what occurs in endogenous pigmentation?
lipfuscin (cellular lipid breakdown products), melanin, haemosiderin (localised brusing), bilirubin all appear as brown
91
what are the types of exogenous pathological pigmentation?
carbon deposition, tattoos, heavy metal salts, pigmentation associated with intravascular drug use
92
how does carbon deposition occur?
it is in macrophages in alveoli of lungs, black pigment, inhaled soot/smoke, in coal workers and can be severe and lead to fibrosis = pneumoconiosis
93
what is dystrophic pathologic calcification?
deposits of calcium phosphate in necrotic tissue, serum calcium is normal
94
what is metastatic pathologic calcification?
deposits of calcium salts in normal vital tissue with raised serum calcium levels, often seen in connective tissue of blood vessels, can compromise function of tissue
95
what are the causes of raised calcium?
1 - increased levels of parathyroid hormone, parathyroid gland tumour , 2 - destruction of bone tissue, leukaemia, metastasis to bone, immobilisation, 3 - excess vitamin D, 4 - renal failure, causes secondary hyperparathyroidism

Microbiology BDS1 (20 decks)

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