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Disease and Defense > Cell and Tissue Injury > Flashcards

Cell and Tissue Injury Flashcards

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
Q

what happens when there is mitochondrial damage / dysfunction?

A

failure of oxphos –> ATP depletion and increased formation of ROS - loss of membrane potential - release of proteins that activate apoptosis

26
Q

What leads to influx of calcium?

A

ischemia and toxins –> release of calcium from intracellular stores and increased influx across PM

27
Q

Accumulation of ROS - cell injury involved damage by free radicals - two major pathways

A
  1. all cells during redox reactions

2. phagocytic leukocytes (neutrophils and macrophages)

28
Q

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?

A

fibrinoid necrosis

29
Q

When do we usually see fibrinoid necrosis?

A

Vasculitis

30
Q

Fat necrosis?

A

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
Q

Caseous necrosis?

A

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
Q

Which necrosis is characteristic of tuberculosis infection

A

Caseous

33
Q

Liquefactive Necrosis

A

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
Q

Coagulative necrosis

A

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
Q

What is gangrenous necrosis?

A

subset of coagulative necrosis in which multiple tissue layers are involved

36
Q

Cytoplasmic changes seen in irreversible injury ?

A

increased eosinophelia - inceased binding of eosin to denatured cytoplasmic proteins - and loss of RNA basophilia in cytoplasm

37
Q

Nuclear changes in irreversible injury

A

Pyknosis
Karyorrhexis
Karyolysis

38
Q

Pyknosis

A

nuclear shrinkage and increased basophilia (DNA condenses)

39
Q

Karyorrhexis

A

pyknotic nucleus fragments

40
Q

Karyolysis

A

dissoluation of nucleus (basophilia of chromatin fades secondary to deoxyribonuclease activity - breakdown of denatured chromatin)

41
Q

Irreversible cell injury (2)

A

necrosis

apoptosis

42
Q

Intracellular changes associated with reversible injury (4)

A

Plasma membrane blebing
mitochondrial changes (swelling)
dilation of ER with ribosomal detachment
nuclear alterations (chromatin clumping)

43
Q

Fatty changes?

A

accumulation of lipid in hepatocytes (or other cells)
Reversible
Due to increased entry and synthesis of FFAs and decreased FA oxidation

44
Q

Cell swelling?

A

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
Q

What are some common causes of cell injury and death?

A 
oxygen deprivation 
chemical agents
infectious agents 
immune reactions
genetics
nutrition
46
Q

Reversible cell injury

A

Recoverable if damaging stimulus is removed

Injury has not progressed to severe membrane damage and nuclear dissolution

47
Q

Irreversible injury (cell death) (2)

A

necrosis

apoptosis

48
Q

What is it called when there is reversible change in which one adult/differentiated cell type is replaced by another adult / differentiated cell type?

A

metaplasia

- cell type sensitive to a particular stress is replaced by another cell type better able to withstand particular stress

49
Q

Barrett esophagus is an example of?

A

metaplasia

50
Q

What is it called when there is a decrease in size and functional capacity of a cell

A

atrophy

51
Q

example of physiologic atrophy

A

loss of hormone stimulation in menopause - decreased workload - aging

52
Q

pathologic atrophy e.g.

A

denervation or diminished blood supply

53
Q

mechanism of atrophy

A

decreased protein syntehsis and increased protein degradation (ubquitin proteasome pathway)

54
Q

what is it called when there is an increase in teh number of cells in response to stimulus or injury?

A

hyperplasia

55
Q

physiologic hyperplasia, e.g.

A

hormonal (female breast)

compensatory (liver)

56
Q

pathologic hyperplasia e.g.

A

excessive hormonal or GF stimulation (e.g. endometrial hyperplasia, BPH)

If stimulation removed, hyperplasia should abate (contrast with cancer)

57
Q

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)

A

Hypertrophy

58
Q

what is an example of physiologic hypertrophy

A

gravid uterus

59
Q

what is an example of pathologic hypertrophy

A

left ventricular hyperplasia in HTN

60
Q

Can hypertrophy and hyperplasia occur together?

A

yes

61
Q

what characterizes cellular adaptations to stress?

A

reversible changes in number, size, phenotype, metabolic activity, or functions of cells in response to changes in their environment - physiologic / pathologic

62
Q

4 cellular adaptations to stress

A

hypertrophy
hyperplasia
atrophy
metaplasia

Disease and Defense (12 decks)

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