Cell degeneration/death (year 2) Flashcards
1
Q
what is homeostasis?
A
cells keeping balance of physiological demands
2
Q
what stimulates cellular adaptation?
A
response to excessive physiological stress of pathological stimuli
3
Q
what does cellular adaptation affect?
A
the growth and differentiation of cells
4
Q
what are some examples of cellular adaptation?
A
hypertrophy, hyperplasia, atrophy, metaplasia
5
Q
what is atrophy?
A
decrease in size and number of cells
6
Q
what is hypoplasia?
A
reduced organ volume because of incomplete cell proliferation
7
Q
what is aplasia?
A
organ absence because of defective cell proliferation
8
Q
define involution
A
a physiological atrophy
9
Q
define atrophy
A
a pathological atrophy
10
Q
give some examples of involution
A
uterus after parturition
thymus after puberty
senescence
11
Q
give some examples of pathological atrophy
A
skeletal muscle disuse
denervation
inadequate nutrition
pressure atrophy
12
Q
define hypertrophy
A
increase in size of cells - no cell division involved
13
Q
what causes hypertrophy?
A
increased functional demand
14
Q
what is an example of physiological hypertrophy?
A
smooth muscle in pregnant uterus
skeletal muscle with training
15
Q
give an example of pathological hypertrophy
A
cardiac myocytes
16
Q
what is hyperplasia?
A
increase in the total number or cells in an organ/tissue
17
Q
what are the two types of physiological hyperplasia?
A
hormonal and compensatory
18
Q
give some examples of hormonal hyperplasia
A
proliferation of mammary and uterine epithelium during pregnancy
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
20
Q
what can cause pathological hyperplasia?
A
excessive hormonal stimulation
attempt at regeneration
viral infection
21
Q
what is metaplasia?
A
reversible change in which one adult cell type is replaced by another adult cell type
22
Q
give an example of metaplasia
A
columnar epithelia replaced by stratified squamous when smoking
23
Q
what are normal cellular constituents?
A
water, lipid, carbohydrate, protein
24
Q
what are the two categories of abnormal intracellular accumulation?
A
exogenous and endogenous
25
name some exogenous abnormal intracellular substances
minerals
| products of infectious agents
26
what is the name for intracellular accumulation of lipids?
steatosis/lipidosis
27
what organ is steatosis common in?
liver cells
28
name some causes of lipidosis
toxins, protein malnutrition, diabetes, obesity
29
describe the normal metabolisms of lipids
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
30
what form of lipid accumulates in hepatocytes?
triglycerides
31
what may cause intracellular protein accumulation?
excess of protein presented to cell
excessive protein synthesis
defects in protein folding
32
where is an example of somewhere that excess proteins can be presented to the cell?
proximal renal tubules during proteinuria
33
where may you see excessive synthesis of proteins?
plasma cells producing high levels of immunoglobulins
34
what may cause abnormal folding of proteins?
```
genetic mutations
ageing
environmental factors
amyloidosis
Alzheimers
```
35
why might defects in protein folding occur?
defective intracellular transport and secretion of critical proteins
toxicity of aggregated abnormally folded protein
36
why may glycogen accumulate intracellularly?
diabetes, glucocorticoid hepatopathy, glycogen storage disease
37
how does glycogen appear in the cell?
clear vacuoles in cytoplasm
38
what are pigments?
coloured substances that can be normal or abnormal constituents of a cell
39
name some normal endogenous pigments of cells
melanin, lipofuscin and haemosiderin, bilirubin
40
name some common abnormal pigments of cells
carbon/coal dust
41
define anthracosis
inhalation of carbon/coal dust
42
where are carbon particles found?
phagocytksed by alveolar macrophages and transported to regional lymph nodes
43
what is is lipofuscin?
insoluble polymers of lipids that are yellow/brown colour
44
what colour is melanin?
brown/black
45
what is haemosiderin?
haemogobulin derived storage form of iron that appears gold/yellow/brown
46
when does haemosiderin appear?
haemorrhage (depredation of haemoglobin)
| end of the lifespan of RBC
47
what is bilirubin?
normal major pigment of bile
48
what colour is bilirubin?
green/blue
49
what does excess bilirubin cause?
jaundice
50
what colour is biliverdin?
green
51
what are the components of bile?
water, cholesterol, bile salts, bile pigment, iron
52
what colour is bile?
yellow/green
53
what can cause jaundice?
excessive haemolysis
severe hepatic injury
obstructed bile flow
54
what may cause cell injury?
```
oxygen deprivation
physical agents
infectious agents
immunological reactions
genetic derangements
nutritional imbalances
chemical agents/drugs
```
55
what intracellular systems are vulnerable to injury?
cell membrane, aerobic respiration, protein synthesis, genetic apparatus
56
what biochemical mechanisms may lead to cellular injury?
```
ATP depletion
oxygen derived free radicals
loss of Ca homeostasis
defects in membrane permeability
irreversible mitochondrial damage
```
57
what is hypoxia?
a deficiency in oxygen reaching tissue
58
what does lack of oxygen to a tissue result in?
decrease aerobic respiration meaning less ATP leading to reduced activity of the sodium pump
59
what happens as a result of the decreased sodium pump activity?
accumulation of sodium meaning water accumulates in the cell causing swelling
60
what are the consequences of increased intracellular calcium?
activates enzymes such as ATPase, phospholipase, endonuclease, protease
61
what does increased activity if ATPase mean?
less ATP
62
what does increased activity if phospholipase mean?
decreased phospholipids
63
what does increased activity if endonuclease mean?
nuclear chromatin damage
64
what does increased activity if protease mean?
disrupts membranes and cytoskeleton
65
what are some examples of irreversible cell injury?
mitochondrial changes, extensive plasma membrane damage, prominent swelling of lysosomes, massive calcium influx
66
when is cell injury characterised as irreversible?
inability to reverse mitochondrial dysfunction
| profound disturbance in membrane function
67
what are some potential causes of membrane damage resulting in irreversible injury?
loss of membrane phospholipids, cytoskeleton abnormalities, toxic oxygen radicals, lipid breakdown
68
what is a free radical?
extremely unstable highly reactive chemical species with a single unpaired electron in an outer orbit
69
what is the main source of free radicals?
hydrolysis of water into OH and H by ionising radiation
| redox reaction
70
what injuries do free radicals cause?
lipid per oxidation of membranes
lesions in DNA
cross-linking of proteins
71
what is reperfusion injury?
death of cells after the resumption of blood flow
72
why does reperfusion injury occur?
increased generation of oxygen free radicals
| cytokines and adhesion molecules expressed by hypoxic cells - inflammation
73
what are two types of reversible cellular injury?
cellular swelling
| fatty change
74
what are two examples of irreversible cellular injury?
necrosis
| apoptosis
75
what is the medical term used for jaundice?
icterus
76
what is amyloidosis?
pathological accumulation of proteinaceous substance deposited between cells
77
what are the main categories of amyloid?
AA - amyloid associated
AL - amyloid light chain
beta amyloid protein
islet amyloid polypeptide
78
where is AA synthesised?
liver
79
what amyloid is deposited in spongiform encephalopathies?
beta amyloid protein
80
where are islet amyloid polypeptides deposited?
pancreatic islets
81
what are the classification categories of amyloidosis?
systemic
localised
primary
secondary
82
when does primary amyloidosis occur?
with immunocytic disorder
83
when does secondary amyloidosis occur?
with complications of chronic inflammation (AA)
84
define pathological calcification
abnormal deposition of calcium salts
85
define dystrophic
relating to non-viable or dying tissue - necrosis
86
is dystrophic calcification intra or extracellular?
can be either
87
what are the serum calcium levels of animals with dystrophic calcification?
normal
88
what are the two steps of dystrophic calcification?
initiation and propagation
89
what occurs during the initiation phase of dystrophic calcification?
intracellular - Ca accumulate in mitochondira
| extracellular - Ca accumulates by phospholipids in membrane bound vesicles
90
when and where does metastatic calcification occur?
normal tissue with hypercalcaemia
91
when may hypercalcaemia be seen?
increased PTH secretion
bone tissue destruction
vitamin D intoxication
renal failure
92
why is calcium deposited during metastatic calcification?
depending on the pH of a specific area
93
what are the two end points of irreversible cell injury?
apoptosis
| necrosis
94
define necrosis
morphological changes that follow cell death
95
what are the two processes occurring during necrosis?
enzymatic digestion of cell - autolysis or heterolysis
| denaturation of protein
96
what are the two outcomes of necrosis?
phagocytosis
| dystrophic calcification
97
what is autolysis of a cell?
lysosomal enzymes of the dying cell itself
98
what is the gross morphology of necrosis?
focal discoloured (red/white) areas within tissue
99
what are the three appearances of nuclei undergoing necrosis?
pyknosis, karyorrhexis, karyolysis
100
what is pyknosis?
chromatin collapses - nucleus becomes round and condensed
101
define karyorrhexis
fragmentation of the nucleus
102
define karyolysis
complete dissolution of the nucleus
103
what are the types of necrosis?
coagulative
liquefactive
caseous
fat
104
what is the dominant feature of coagulative necrosis?
denaturation
105
when does coagulative necrosis occur?
in hypoxic cell death
106
what type of necrosis preserves the cell outline?
coagulative
107
what is the dominant feature of liquefactive necrosis?
enzymatic digestion
108
when does liquefactive necrosis occur?
focal material/fungal infections
109
what is the end result of liquefactive necrosis?
complete digestion of cells forming a liquid masss
110
when does caseous necrosis occur?
coagulative necrosis in tuberculosis
111
what is fat necrosis?
focal destruction of adipose tissue
112
what is fat necrosis usually due to?
release of pancreatic enzymes with pancreatic necrosis
113
how does fat necrosis appear?
chalky white - fat combines with calcium
114
define apoptosis
programmed cell death
115
what are the biochemical steps of apoptosis?
protein cleavage
protein cross-linking
DNA breakdown
phagocytic recognition
116
what are the phases of apoptosis?
initiation (signalling pathway)
control and integration
execution phase
phagocytosis
117
what are the two ways apoptosis is initiated?
signals transmitted across plasma membrane to intracellular regulatory molecules
signals addressed within target cells
118
what are examples of apoptotic stimuli external to the cell?
hormones, growth factors, cytokine
119
what are intracellular apoptotic stimuli?
heat, radiation, hypoxia, viral infection, glucocorticoids
120
does inflammation occur with apoptosis?
no
121
when may apoptosis occur?
```
embryogenesis
tumours
neutrophils in inflammation
lymphocyte death
cell death by cytotoxic T cells
viral disease
pathological atrophy
ageing
```
