Cellular response to stress and noxious stimuli Flashcards

1
Q

what are the properties of disease

A
  • etiology (cause, risk factors)
  • Pathogenesis
  • Morphologic changes
  • Clinical manifestations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the changes in response to physiological states (adaptations)

A

Hypertrophy
Hyperplasia
Atrophy
Metaplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the increase in the size of cells which

increases the size of the organ

A

hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is an example of hypertrophy

A

fat gaining in adipose tissue (weight gain)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what causes

a) Physiologic hypertrophy
b) Pathologic hypertrophy

A

a) hormones, growth factors

b) work overload e.g. exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are the mechanisms of hypertrophy

A

✓Increased production of cellular proteins
✓Switch of adult to fetal or neonatal forms
✓Re-expression of some shut down genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is hyperplasia

A

increment in the number of cells in an organ or tissue in response to a stimulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

true or false, hypertrophy and hyperplasia cannot occur at the same time

A

false they can

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what kind of cells does hyperplasia only take place

A

in a tissue with cells capable of dividing i.e. not in muscle or nerve cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are the mechanisms of hyperplasia

A

✓Growth factor dependent proliferation of mature cells

✓Increased output of new cells from stem cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the opposite of hypertrophy

A

atrophy (reduction in size of an organ or tissue due to a decrement in cell size & number)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

where is physiological atrophy usually seen

A

in fetuses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the types of pathological atrophy

A
Disuse atrophy
Denervation atrophy
Senile atrophy
Undernourishement
Loss of endocrine stimulus
Continuous pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the mechanisms of atrophy

A
  • Nutrient deficiency or disuse

* autophagy (self-eating)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are residual bodies

A

vesicles containing indigestible materials

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is example of residual bodies

A

Lipofuscin granules in brown atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is metaplasia

A

is a reversible change in which one differentiated cell type is replaced by another cell type which is better able to withstand the adverse environment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are examples of metaplasia

A

✓Columnar epithelium → stratified squamous epithelium
✓Stratified squamous → mucinous epithelium
✓Connective tissue metaplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are mechanisms of metaplasia

A

➢Reprogramming of stem cells
➢Reprogramming of mesenchymal cells in connective tissue
➢Cytokines, growth factors, extracellular matrix components causing gene expression and hence differentiation
➢Retinoic acid regulates progenitors derived from tissue stem cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

when does injury develop

A
  • limits of adaptive responses are exceeded
  • cells exposed to ınjurious agents, stress
  • cells are deprived of essential nutrients
  • compromised by mutations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what does reduction in oxidative phosporylation cause

A

→depleting energy stores (ATP)
→ ion pumps are affected then stop
→causing water influx
→ cells swell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is hypoxia

A

Having low oxygen levels in your tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what can cause hypoxia

A
  • Decreased blood flow (ischemia)
  • Cardiorespiratory failure
  • decreased oxygen carrying capacity of the blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what can cause cell injury and death

A
oxygen deprivation 
physical agents
chemical agents 
infectious agents 
immunologic response
genetic derangements 
nutritional imbalance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
what is the main change that occurs morphologically during reversible injury as seen on a light microscope
cellular swelling
26
what is vacuolar degeneration
cells show small clear vacuoles within the cytoplasm
27
what changes are seen on an electron microscope during reversible injury
▪Plasma membrane alterations; blebbing (protrusions of the cell membrane), blunting, loss of microvilli ▪Mitochondrial changes; swelling, small amorphous densities ▪Dilation of ER; detachement of polysomes, intracytoplasmic myelin figures ▪Nuclear alterations; disintegration of granular & fibrillary elements
28
what is it called when cells are lethally injured
necrosis
29
why do necrotic cells have a glassy homogenous appearance
because of loss of glycogen
30
why do myelin figures appear during cell necrosis
due to enzymes digesting the organelles and dead cell is replaced by whorled phospholipid structures called myelin figures
31
what forms in necrotic cells due to damaged membranes
calcium soaps causing calcification
32
# define these three forms of changes in the nucleus a) Karyolysis b) Pyknosis c) Karyorhexis
a) basophilia of the chromatin fades & DNA is dissolved b) nucleus shrinks, basophilia increases, chromatin condenses into solid shrunken basophilic mass c) pyknotic (irreversible condensation of chromatin) nucleus undergoes fragmentation
33
what are the types of necrosis
1. coagulative necrosis 2. liquefactive necrosis 3. gangrenous necrosis 4. caseous necrosis 5. fat necrosis 6. fibrinoid necrosis
34
what is the localized area of coagulative necrosis called
infarct
35
what happens to the architecture of dead tissues in coagulative necrosis
they are preserved
36
how are necrotic tissues removed in coagulative necrosis
by leucocytes
37
coagulative necrosis can affect everywhere except what organ
the brain
38
what leads to coagulative necrosis
obstructed vessels leading to ischemia (restriction in blood supply to tissues)
39
in coagulative necrosis how long does an anucleated cells persist
days or weeks
40
what process is blocked during coagulative necrosis and hence what does it stain
proteinolysis (due to enzyme denaturing) , eosinophilic
41
what does hypoxic death of cells within central nervous system often manifest as
liquefactive necrosis
42
what forms during liquefactive necrosis and why
pus forms because of tissue digestion
43
where does gangrenous necrosis usually occur
Seen usually in a limb which lost its blood supply
44
what happens when bacteria superimpose and turn to a liquefactive necrosis
wet gangrene
45
in which disease is caseous necrosis usually see
tuberculosis
46
what necrosis is usually associated with trauma to the pancreas
fat necrosis
47
how does fat saponification in fat necrosis occur
when fatty acid combines with calcium forming chalky deposits
48
what happens during fibrinoid necrosis
antigen antibody complexes deposit in the arterial walls causing fibrin deposition
49
what do does fibrinoid necrosis stain
bright eosinophilic
50
what does response to injurious stimuli depend on
the nature of the injury its duration severity
51
what causes hypoxia
Mechanical arterial obstruction
52
what restores blood flow to ischemic tissue and promotes recovery but paradoxically may exacerbate the injury causing cell death
Ischemia-reperfusion
53
what is a complement system
enhances (complements) the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism, promote inflammation, and attack the pathogen's cell membrane
54
what is toxic injury
conversion to toxic metabolites or direct toxicity
55
what is apoptosis
a tightly regulated suicide program within the cell
56
what are apoptotic bodies
fragments containing portions of nuclear & cytoplasmic material formed during apoptosis
57
what enzyme is mainly responsible for apoptosis
caspases
58
what are the mechanisms of apoptosis
1. intrinsic pathway | 2. extrinsic pathway
59
in the intrinsic pathway, what does cytochrome bind to in the cytosol
apoptosis activating factor1 forming an apoptosome which then binds to caspase-9 triggering a cascade of caspases
60
during intrinsic pathway what happens when the outer cell membrane becomes more permeable
release of death inducing pro-apoptotic molecules into the cytoplasm
61
what activates caspase 10 in the extrinsic pathway
Cytoplasmic domain intracellular apoptotic signals. the caspase 10 then activates caspase 8
62
what happens during execution phase
caspase system cleaves cytoplasmic DNAse inhibitor hence cleaving DNA and leading to dead cell removal
63
give 5 morphological changes during apoptosis
cell shrinkage chromatin condensation Formation of cytoplasmic blebs & apoptotic bodies Phagocytosis of apoptotic cells by macrophages Plasma membranes remain intact
64
which type of necrosis has no inflammation
apoptosis
65
what is another name for the extrinsic pathway
death receptor-initiated pathway of apoptosis