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Cell and Tissue Injury Flashcards

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1
Q

Why do human diseases occur?

A

Due to cell / tissue injury

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2
Q

What determines the outcome of cell / tissue injury?

A

Type of Injury
Severity
Duration
and Type of Cell injured

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3
Q

Is cell / tissue injury reversible?

A

Early stages

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4
Q

What are key targets of injury? (2)

A

membranes

mitochondria

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5
Q

What follows cases of irreversible cell / tissue injury?

A

Necrosis / Apoptosis

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6
Q

Pathologic Calcifications =

A

abnormal deposition of calcium salts (together with smaller amount of iron / magnesium / and other minerals)

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7
Q

Two types of pathologic calcifications?

A

Dystrophic

Metastatic

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8
Q

Dystrophic Calcifications

where?

A

occurs in dead or dying tissues

there is an absence of derangements in calcium metabolism

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9
Q

Metastatic Calcifications

where?

A

normal tissues

secondary to derangement in caclium metabolism (hypercalcemia / hyperparathyroidism / Paget disease)

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10
Q

Four main pathways of intracellular accumulations

A
  1. inadequate removal (fatty liver change)
  2. accumulation of abnormal endogenous substance (alpha -1 antitrypsin)
  3. failure to degrade due to inherited enzyme deficiencies (storage diseases)
  4. deposition and accumulation of exogenous substance (anthracosis)
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11
Q

Apoptosis - mechanism and two main pathways?

A

Mechanism - activation of caspases (cystein proteases that cleave proteins after aspartic residues)
Pathways
1. mitochondrial (intrinsic)
2. death receptor (extrinsic)

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12
Q

Apoptosis morphology?

A

apoptotic bodies = membrane bound vesicles of cytosol and organelles

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13
Q

Pathologic causes of apoptosis

A

DNA damage
Misfolded proteins
Cell injury / infection
Pathologic atrophy in obstruction

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14
Q

Physiologic causes of apoptosis

A

Embryogenesis
Hormone deprivation
Cell loss in proliferating populations
Elimination of cells that have served their purpose
Elimination of self-reactive lymphocytes
Cell death induced by cytotoxic T-lymphocytes

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15
Q

can apoptosis and necrosis co-exist?

A

Yes!

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16
Q

What are the four cellular adaptions to stress?

A

hypertrophy
hyperplasia
atrophy
metaplasia

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17
Q

what are the five types of cellular necrosis?

A 
coagulative 
liquefactive 
caseous
fat
fibrinoid
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18
Q

what are two main types of reversible cell injury?

A

cell swelling

fatty change

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19
Q

important sites of membrane damage (3)

A

mitochondria
plasma membrane
lysosome

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20
Q

What determines the damage caused by free radicals?

A

rate of production vs removal

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21
Q

how are free radicals typically removed? (2)

A

spontaneous decay

enzymatic systems

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22
Q

Mechanisms of cell injury (6)

A 
ATP depletion
Mitochondrial damage
Influx of calcium 
Accumulation of ROS
Increased permeability to membranes
Accumulation of damaged DNA and misfolded proteins
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23
Q

ATP depletion / tissue injury?

A

ATP produced via oxphos or glycolysis - tissues with greater glycolytic capacity are better able to withstand inschemic injury

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24
Q

Susceptibility of neurons, cardiac myocytes, and soft tissue to ischemic injury

A

neurons - 3-5 min
cardiac myocytes - 30min-2hr
soft tissue - many hours

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25
what happens when there is mitochondrial damage / dysfunction?
failure of oxphos --> ATP depletion and increased formation of ROS - loss of membrane potential - release of proteins that activate apoptosis
26
What leads to influx of calcium?
ischemia and toxins --> release of calcium from intracellular stores and increased influx across PM
27
Accumulation of ROS - cell injury involved damage by free radicals - two major pathways
1. all cells during redox reactions | 2. phagocytic leukocytes (neutrophils and macrophages)
28
Immune reaction in which complexes of antigens and antibodies are deposited in the walls of arteries? / Deposited immune complexes combine with fibrin and produce a bright pink amorphous appearance on H&E?
fibrinoid necrosis
29
When do we usually see fibrinoid necrosis?
Vasculitis
30
Fat necrosis?
Fat destruction, typically resulting from release of activated pancreatic lipases (following acute pancreatitis or trauma) Fats hydrolyzed into free fatty acids which precipitate with calcium tor produce a chalky gray material
31
Caseous necrosis?
Necrosis characteristic of tuberculosis infection Caseous derived from the white appearance of the area of necrosis Microscopically the necrotic area appears as a collection of fragmented or lysed cells and amorphos granular debris enclosed with a distinctive inflammatory border (granulomatous inflammation)
32
Which necrosis is characteristic of tuberculosis infection
Caseous
33
Liquefactive Necrosis
Seen in focal bacterial or occasional fungal infections Microbes stimulate the accumulation of inflammatory cells and leukocyte enzymes digest the tissue Also seen in hypoxia in CNS
34
Coagulative necrosis
Tissue architecture preserved for at lease several days (due to damage to both structural proteins and enzymes) Dead cells remain - pale "ghost like" Characteristic of infarcts - classically seen in heart following myocardial infarction - can be seen in any solid organ following ischemia
35
What is gangrenous necrosis?
subset of coagulative necrosis in which multiple tissue layers are involved
36
Cytoplasmic changes seen in irreversible injury ?
increased eosinophelia - inceased binding of eosin to denatured cytoplasmic proteins - and loss of RNA basophilia in cytoplasm
37
Nuclear changes in irreversible injury
Pyknosis Karyorrhexis Karyolysis
38
Pyknosis
nuclear shrinkage and increased basophilia (DNA condenses)
39
Karyorrhexis
pyknotic nucleus fragments
40
Karyolysis
dissoluation of nucleus (basophilia of chromatin fades secondary to deoxyribonuclease activity - breakdown of denatured chromatin)
41
Irreversible cell injury (2)
necrosis | apoptosis
42
Intracellular changes associated with reversible injury (4)
Plasma membrane blebing mitochondrial changes (swelling) dilation of ER with ribosomal detachment nuclear alterations (chromatin clumping)
43
Fatty changes?
accumulation of lipid in hepatocytes (or other cells) Reversible Due to increased entry and synthesis of FFAs and decreased FA oxidation
44
Cell swelling?
Early (reversible) - failure of energy dependent ion pumps in plasma membrane - disrupted ionic and fluid homeostasis inschemic injury can see surface blebs and increased eosinophilia of cytoplasm and cell swelling
45
What are some common causes of cell injury and death?
``` oxygen deprivation chemical agents infectious agents immune reactions genetics nutrition ```
46
Reversible cell injury
Recoverable if damaging stimulus is removed | Injury has not progressed to severe membrane damage and nuclear dissolution
47
Irreversible injury (cell death) (2)
necrosis | apoptosis
48
What is it called when there is reversible change in which one adult/differentiated cell type is replaced by another adult / differentiated cell type?
metaplasia | - cell type sensitive to a particular stress is replaced by another cell type better able to withstand particular stress
49
Barrett esophagus is an example of?
metaplasia
50
What is it called when there is a decrease in size and functional capacity of a cell
atrophy
51
example of physiologic atrophy
loss of hormone stimulation in menopause - decreased workload - aging
52
pathologic atrophy e.g.
denervation or diminished blood supply
53
mechanism of atrophy
decreased protein syntehsis and increased protein degradation (ubquitin proteasome pathway)
54
what is it called when there is an increase in teh number of cells in response to stimulus or injury?
hyperplasia
55
physiologic hyperplasia, e.g.
hormonal (female breast) | compensatory (liver)
56
pathologic hyperplasia e.g.
excessive hormonal or GF stimulation (e.g. endometrial hyperplasia, BPH) If stimulation removed, hyperplasia should abate (contrast with cancer)
57
what is it called when there is an increase in size of cells resulting in increase in size of organ (functional demand or growth factor or hormonal stimulation)
Hypertrophy
58
what is an example of physiologic hypertrophy
gravid uterus
59
what is an example of pathologic hypertrophy
left ventricular hyperplasia in HTN
60
Can hypertrophy and hyperplasia occur together?
yes
61
what characterizes cellular adaptations to stress?
reversible changes in number, size, phenotype, metabolic activity, or functions of cells in response to changes in their environment - physiologic / pathologic
62
4 cellular adaptations to stress
hypertrophy hyperplasia atrophy metaplasia

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