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Pathology > Cell Adaptation and Injury > Flashcards

Cell Adaptation and Injury Flashcards

1
Q

What 3 things confine the normal cell to a narrow range of function and structure?

A
  • genetic programs of metabolism, differentiation, and specialization
  • constraints of neighboring cells
  • availability of metabolic substrates
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2
Q

Physiologic and morphologic cellular adaptations

A
  • achieve new (altered) steady state
  • preserve the viability of the cell
  • modulate function as cell responds to stimuli
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3
Q

When does cellular injury occur?

A

If the limits of the adaptive response to a stimulus are exceeded, or if a cell is exposed to an injurious agent or stress

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4
Q

The point of no return

A

If the stimulus persists or is severe enough from the beginning, the cell reaches the point of no return and suffers irreversible cell injury and cell death

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5
Q

Common sign of cell injury is _______

A

Cell swelling

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6
Q

Standard organelles

A
  • synthesis of lipids, proteins, CHO
  • energy production
  • transport of ions and other molecules
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7
Q

Homeostasis

A

Tight control of pH, electrolyte concentration, etc

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8
Q

Departure from homeostasis leads to _______

A

Cell damage

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9
Q

How do cells respond to homeostatic challenges?

A

Adaptation

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10
Q

What happens if a new level of homeostasis can not be achieved?

A

Cell death

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11
Q

Stages in the cellular response to stress and injurious stimuli

A

Normal cell –> (injurious stimulus) –> cell injury and cell death
OR
Normal cell –> (stress, increased demand) –> adaptation –> (inability to adapt) –> cell injury/death

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12
Q

Examples of cellular adaptations

A
  • increase in muscle mass with exercise
  • increase in cytochrome p450 mixed function oxidation expression in hepatocytes
  • cells respond by either increasing or decreasing content of organelles
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13
Q

Atrophy

A

Reduction in mass of a tissue or organ

  • loss of cells
  • reduction in size of cells within an organ
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14
Q

Hypertrophy

A

Increase in the size of cells, resulting in enlargement of organs

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15
Q

Hyperplasia

A

Increased number of cells in an organ or tissue

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16
Q

Metaplasia

A

Transformation or replacement of one adult cell type with another

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17
Q

Adaptive response to altered demands

A
  • decreased workload
  • decreased nutrition
  • loss of hormonal stimulation
  • decreased blood supply
  • loss of innervation
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18
Q

In what scenario is atrophy a good thing?

A

After a cow gives birth, the uterus will shrink back to normal size
- due to loss of cells

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19
Q

Cellular atrophy

A
  • reversible cellular change
  • reduced functional capacity
  • continue to control internal environment and produce sufficient energy for metabolic state
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20
Q

What happens during adrenal cortical atrophy?

A

Corticosteroid treatment inhibits ACTH –> low ACTH –> atrophy of adrenal cortex –> sudden withdrawal of CS tx = Addisonian crisis
- gradual withdrawal allows cells to return to normal function

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21
Q

Prolonged cellular atrophy may lead to _______

A

Death of some of the cells

- atrophy at the organ level may become irreversible at this point (muscle) or may be reversible by hyperplasia (liver)

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22
Q

At the organ level, ______ increases organ size without cellular proliferation

A

Hypertrophy

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23
Q

Changes in hypertrophic cells

A
  • increased protein content

- increased organelle number (myofibrils, mitochondria, ER)

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24
Q

____ process > ______ processes

A

Anabolic; catabolic

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25
Q

What happens in the liver with induction of hypertrophy?

A
  • response to certain drug administrations (phenobarb, alcohol)
  • mixed function oxidases (metabolize compounds, increase water solubility to allow excretion)
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26
Q

When is cellular hypertrophy detrimental to an animal?

A

Heart

  • inability to provide adequate energy/contraction, despite hypertrophy
  • conformational changes associated (decreased ejection volume)
  • may end up with organ failure
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27
Q

Induction of the liver

A
  • tolerance to certain drugs/toxins
  • more rapid removal of certain drugs/toxins
  • may increase susceptibility to some toxins (metabolites may be more toxic than precursors)
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28
Q

Do toxins become toxic when they are eaten?

A

No, they become toxic when the liver metabolizes them

- addition of charged particle or side group creates a free radical that can damage other molecules

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29
Q

Cell injury

A

Any change that results in loss of the ability to maintain the normal or adapted homeostatic state

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30
Q

How does the extent of cell injury vary?

A
  • severity of stimulus
  • type of cell involved
  • metabolic state at the time of injury
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31
Q

Reversible cell injury

A

Degeneration

- ex: swelling of endoplasmic reticulum and mitochondria

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32
Q

_______ changes lag behind ______ changes

A

Morphologic; functional

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33
Q

Irreversible cell injury

A

Necrosis

  • lysosome rupture
  • membrane blebs
  • nuclear condensation
  • fragmentation of cell membrane and nucleus
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34
Q

What are the 11 hallmarks of cell degeneration?

A
  • cell swelling
  • fatty change
  • glycogen accumulation
  • lipofuscin and ceroid
  • hyaline changes
  • amyloid
  • mucinous changes
  • calcification
  • gout
  • cholesterol crystals
  • inclusions
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35
Q

Lipofuscin and ceroid

A

Oxidized product from membrane lipids

- yellow to brown

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36
Q

Hyaline changes

A

Dense, homogenous, glossy, translucent

- protein leakage most common cause

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37
Q

Amyloid

A

Complex protein that accumulates within cells

- homogenous, pink material

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38
Q

Mucinous changes

A

Gelatinous, semi-solid, shiny, clear, stringy

- serous atrophy of fat

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39
Q

Calcification

A

Abnormal accumulation of calcium salts in soft tissue

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40
Q

Gout

A

Occurs in birds and reptiles

- associated with renal disease due to decreased excretion of urates

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41
Q

Cholesterol crystals

A

Areas of previous hemorrhage or inflammation

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42
Q

Inclusions

A

Viral disease

- intranuclear or intracytoplasmic

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43
Q

What is an early, universal sign of cell injury?

A

Cell swelling

  • loss of control of ions/water with net uptake of water
  • compresses adjacent structures
  • loss of energy control
  • often mild, reversible, but also occurs in lethal injury
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44
Q

Loss of sinusoids in liver is due to _______

A

Cell swelling

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45
Q

Staining characteristics of cell swelling

A

Pale, cloudy appearance (cloudy swelling, hydropic degeneration)
- cytoplasmic vacoules –> distended organelles, lipid droplets

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46
Q

Gross appearance of cell swelling

A

Organ is pale, enlarged, swollen

  • rounded margins
  • heavy
  • wet
  • bulges on cut surface
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47
Q

Cell swelling - effect on organ

A
  • brain: severe due to pressure necrosis
  • liver: decreased blood flow, decreased function
  • pharynx: airway obstruction
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48
Q

Fatty change

A

Accumulation of neutral fats (TG) in a cell

  • common change in cells that metabolize lots of lipids
  • sick cells accumulate TG
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49
Q

Does fatty change have anything to do with adipose tissue?

A

No

- commonly occurs in: hepatocytes, myocardial cells, renal tubular epithelial cells, diabetes melitus

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50
Q

Gross appearance of fatty change

A

Yellow discoloration (kidney, liver), enlargement (liver)

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51
Q

Microscopic appearance of fatty change

A
  • small to large
  • clear
  • non-membrane bound
  • intracytoplasmic vacuoles
  • nuclei pushed to cell periphery
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52
Q

Pathogenesis of fatty change

A 
Overload 
- increased mobilization of fats (anorexia), diabetes mellitus 
Injury to cells
- toxins, anoxia
Deficiencies
- methionine, choline
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53
Q

Lipidosis

A

Normal in young animals (milk diet), normal following fatty meals

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54
Q

Pathogenesis of glycogen accumulation

A
  • severe, prolonged hyperglycemia (diabetes mellitus)
  • presence of high levels of glucocorticoids (Cushing’s)
  • lysosomal storage disease , defects in a step of glycogen breakdown
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55
Q

Where is the nucleus located during glycogen accumulation?

A

Center of cells!!

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56
Q

Gross appearance of glycogen accumulation

A
  • swollen organ
  • rounded margins (liver)
  • increased pallor
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57
Q

Microscopic appearance of glycogen accumulation

A
  • enlarged cells
  • increased pallor
  • no nuclear displacement
58
Q

What is the number one cause of increased corticosteroids in animals?

A

Iatragenic - doctor induced

59
Q

Lipofuscin

A

Pigment that collects in cells

  • gross: brown discoloration of affected organs
  • micro: membrane bound, brown pigment, myelin figures
60
Q

What is a phrase for solid, glossy, semi-transparent material?

A

Hyaline change

61
Q

Hyaline droplets

A

Cyotplasm contains rounded, eosinophilic droplets, vacuoles, or aggregates

62
Q

Hyaline casts

A

Protein casts within renal tubules

- unabsorbed protein: morphologic expression of proteinuria

63
Q

Connective tissue hyaline

A

Compacted collagen, scar tissue

64
Q

Amyloid

A

Homogenous, amorphic, eosinophilic matrix/substance deposited along basement membranes and between cells

65
Q

Gross description of amyloid

A

Enlarged, pale, waxy, translucent organ

66
Q

Serum amyloid A

A

Acute phase protein that increases during inflammation

- forms beta pleated sheets that stick together, so proteins are unable to break them apart

67
Q

Calcification

A

Abnormal deposition of calcium salts (calcium phosphate, calcium carbonate) in soft tissues

68
Q

Gross appearance of calcification

A

Chalky, white tissue

- hard, gritty on cut surface

69
Q

Microscopic appearance of calcification

A
  • dark blue staining material
  • along basement membrane
  • stippled throughout cell
  • large clumps
70
Q

Calcinosis

A

Widespread, excessive calcification

  • calcinosis circumscripta: big lumps of calcium
  • calcinosis cutis: non lumpy calcification of the skin and dermal connective tissue
71
Q

Calcium in the cavities or lumina

A

Calculi/calculus

- ex: urinary calculus, renal calculi

72
Q

Accumulation of urate crystals

A

Gout

  • tophus/topi
  • typically seen in birds, reptiles
73
Q

Gross appearance of gout

A

White, firm, crystal deposites

74
Q

Micro appearance of gout

A

Granulomas with radiating crystalline material (radiating spicules)

75
Q

Pathogenesis of gout

A
  • disturbance of purine metabolism
  • vitamin A deficiency
  • kidney failure
76
Q

What are the 2 forms of gout?

A
  • visceral

- articular

77
Q

Nuclear change

A
  • chromatin clumping
  • condensation (pyknosis)
  • dramatic nuclear change is usually indicative of necrosis
78
Q

Plasma membrane changes

A
  • loss of surface features (microvilli, cilia)
  • desmosome breakdown
  • bleb formation
79
Q

Mitochondria changes

A
  • swelling (may rupture)
  • loss of dense granules
  • calcium deposits
80
Q

ER changes

A
  • dilatation: contributes to vacuolar microscopic appearance
  • dissociation of ribosomes
81
Q

Other ultrastructural changes

A
  • phospholipids from damaged organelle membranes accumulate to form myelin figures
  • lysosomes: dilation and rupture (late event, terminal cell injury)
82
Q

What are 3 cellular histologic features of necrosis?

A
  • increased eosinophilia: altered protiens, loss of ribosomes, decreased cytoplasmic RNA
  • loss of cellular detail
  • nuclear changes
83
Q

What are 3 forms of nuclear changes?

A
  • pynkosis
  • karyorrhexis
  • karyolysis
84
Q

Oxygen depraivation

A

Hypoxia
- decreased blood oxygen (pulmonary/nonpulmonary)
- decreased blood flow (hypovolemia, vasoconstriction, cardiogenic, shock)
Ischemia
- infarction
- complete/almost complete loss of blood flow

85
Q

Physical agents of cell injury

A
  • trauma
  • radiation
  • burns
86
Q

Chemical agents of cell injury

A
  • huge variety
  • concentration, dose, length of exposure
  • variety of actions (injure membranes, interfere with metabolism)
87
Q

Infectious agents

A
  • viruses, bacteria, protozoa, fungi
  • elaborate toxins
  • host inflammatory responses
88
Q

Nutritional imbalances

A
  • deficiencies

- excesses

89
Q

Cellular response depends on

A
  • type of injury
  • duration of injury
  • cell state at the time of injury
  • adaptability of the injured cell
90
Q

What 4 intracellular systems are primarily vulnerable to injury?

A
  • cell membrane
  • aerobic respiration (mitochondria)
  • protein synthesis (rough ER, ribosomes)
  • preservation of genetic integrity (nucleus)
91
Q

What are the 2 mechanisms of cell injury?

A
  • interfere with substrates or enzymes

- produce enzymes or molecules that degrade cell components

92
Q

Most vulnerable systems are _____ production

A

Energy

  • glycolysis
  • citric acid cycle
  • oxidative phosphorylation
93
Q

What are the 5 components of the common pathway?

A
  • ATP depletion
  • oxygen and oxygen derived free radicals
  • intracellular calcium loss/loss of calcium homeostasis
  • defects in membrane permeability
  • irreversible mitochondrial damage
94
Q

ATP depletion

A
  • oxidative phosphorylation of ADP to ATP
  • glycolytic pathway –> ATP from glucose in the absence of oxygen
  • frequent pathway in ischemic and toxic injuries
95
Q

Organ variation in glycolysis

A
  • brain: no glycolysis, rapid anoxic injury and death (4 min)
  • muscle: abundant glycolysis
96
Q

Oxygen and oxygen derived free radicals

A

Partially reduced reactive oxygen species (damage proteins, lipids, nucleic acid)
- kept under control by scavenging systems –> dead end molecules that absorb free radical energy without passing it on

97
Q

Free radicals are ________

A

Auto-catalytic

- especially in membranes!!

98
Q

Normal cytosolic Ca is maintained at ______

A

Low concentrations

- Mg/Ca ATP pumps

99
Q

Increased calcium leads to

A

Increased:

  • membrane permeability
  • phospholipase activity
  • protease activity
  • ATPase activity
  • endonuclease activity
  • also causes self destruction via activation of apoptotic pathways
100
Q

Defects in membrane permeability

A
  • plasma membrane
  • mitochondrial membrane
  • direct damage: perforin, complement (MAC), inflammation
  • indirect damage –> calcium levels, ATP depletion
101
Q

Irreversible mitochondrial damage

A

Direct/indirect targets of all cell injury

- damaged by everything from toxin to hypoxia leading to increased Ca, oxygen stress, degradation of phospholipids

102
Q

High conductance channel formation

A

Mitochondrial permeability transition

- prevents maintenance of the proton motive force/membrane potential that runs the electron transport chain

103
Q

Hypoxic injury

A

Decrease in oxygen to affected tissues

  • respiratory efficiency
  • cardiac function
  • tissue demand
  • blood flow remains –> substrates for anaerobic metabolism delivered, or glycolytic pathway is used
104
Q

Ischemic injury

A

Loss of blow flow to affected tissues

  • hypovolemia
  • infarction
  • vasoconstriction
  • shock
  • loss of oxygen AND loss of substrates –> rapid depletion of ATP, and loss of cell function
  • reversible, to a point
105
Q

Reperfusion injury

A

Paradoxical increase in death of cells after blood flow is restored (shift back from anaerobic to aerobic creates free radicals)

  • GDV
  • stroke
  • myocardial infarction
106
Q

Decrease in oxidative phosphorylation in the mitochondria leads to

A

ATP depletion, and widespread cellular effects

  • Na/K ATPase –> Na accumulates in cell, water follows = cell swelling
  • ADP, phosphates, lactate cause further swelling
107
Q

How is energy metabolism altered with hypoxia/ischemia?

A

Decrease in ATP and ADP leads to glycolysis

  • decrease glycogen stores
  • increase lactic acid
  • increase organic phosphates
  • decrease pH
108
Q

Structural disruption of protein synthesis

A
  • detachment of ribosomes from RER

- dissociation of polysomes into monosomes

109
Q

Functional consequences of ischemia/hypoxia

A
  • heart muscle stops contracting within 60 seconds

- neurons stop firing or fire erratically leading to loss of consciousness

110
Q

Continuous ATP depletion causes

A
  • cytoskeleton dispersal –> loss of microvilli, formation of blebs
  • swelling of mitochondria
  • ER dilation
  • more cell swelling
111
Q

______ dysfunction leads to membrane damage

A

Mitochondrial
- decrease ATP –> increase Ca –> activation of mitochondrial phospholipases –> accumulation of FFAs –> change in membrane permeability –> short circuits oxidative phosphorylation, decreasing ATP

112
Q

Loss of membrane phospholipids leads to

A

Activation of phospholipases

  • decrease in membrane phospholipids
  • inccrease in Ca
113
Q

How does reaction oxygen species cause membrane damage?

A

Free radicals!

  • return of blood flow –> increase in free radicals
  • deactivate/denature enzymes
  • deactivate/denature membrane components (self propagating)
114
Q

Lipid breakdown products

A

Unesterified fatty acids, acyl carnitine

  • detergent effect on membranes
  • increase permeability of membranes
115
Q

Intracellular amino acids have a ______ against free radical damage

A

Protective

- loss of intracellular AA leads to membrane damage

116
Q

Loss of membrane integrity causes ____ to enter mitochondria

A

Ca

117
Q

Hypoxia and ischemia affect ________, causing decreased ______

A

Oxidative phosphorylation; ATP

118
Q

What is a critical step in the movement of a cell from reversible to irreversible damage?

A

Membrane damage

119
Q

What is an important mediator of biochemical and morphologic alterations that leads to cell death?

A

Ca

120
Q

Chemical species with an unpaired electron in their outer orbit

A

Free radicals

121
Q

What are free radicals reactive to?

A

Adjacent molecules

  • proteins, lipids, carbs, nucleic acids
  • especially damaging to membranes
122
Q

Free radical induced membrane damage is _______

A

Autocatalytic

  • molecules that free radicals react with are converted into free radicals
  • self propagating!
123
Q

How are free radicals formed?

A
  • absorption of radiant energy
  • metabolism of chemicals (CCL4)
  • byproduct of normal metabolism
  • transition metals
  • nitric oxide
124
Q

Free radical formation as a byproduct of normal metabolism

A

Normal respiration molecular oxygen is reduced sequentially to form water

  • intermediates produced:
  • superoxide anion radical
  • hydrogen peroxide
  • hydroxyl ions
125
Q

Lipid peroxidation of membranes

A

Initiated when double bonds of unsaturated fatty acids are attacked (especially by OH)

  • yields peroxides (reactive, propagates)
  • reaction continues until termination event occurs –> free radical captured by a scavenger (vitamin E)
126
Q

Oxidative modification of proteins

A

Oxidation of amino acid side chains

  • protein-protein cross links
  • oxidation of protein backbone –> protein fragmentation
  • enhanced degradation/turnover of critical proteins
127
Q

DNA lesions

A

Reach with thymine to form cross links

  • single stranded breaks
  • implicated in cell aging
  • implicated in malignant transformation of cells
128
Q

Non enzymatic systems to inactivate free radicals

A

Anti-oxidants
- block formation or scavenge
- vitamin A, E, ascorbic acid, glutathione
Metal transport/storage proteins
- bind to Fe, Cu to prevent them from participating in Fenton rxn
- transferrin, ferritin, lactoferrin, ceruloplasmin

129
Q

Enzymatic systems to inactivate free radicals

A

Catalase
- peroxisomes
Superoxide dismutases
Glutathione peroxidase

130
Q

Directly toxic compounds

A

Capable of interacting with critical molecular components or cellular organelles
- ex: mercuric chloride, cyanide, chemotherapeutic agents

131
Q

What pathway does cyanide block?

A

Oxidative phosphorylation

132
Q

Indirectly toxic compounds

A

Converted to reactive toxic metabolites by mixed function oxidases (P450)

  • SER of liver, lung, etc
  • metabolites directly interact with cell membranes/proteins (less common)
  • metabolites are/form free radicals (more common)
133
Q

Are most toxins directly or indirectly toxic?

A

Indirectly

134
Q

Carbon tetrachloride

A

CCl4

- oxidation of fatty acids –> autocatalytic rxn

135
Q

Acetaminophen

A

Sulfonation/glucuronidation in liver

  • small amount converted to highly reactive metabolite –> normally scavenged by glutathion scavenger
  • GSH system overwhelmed –> massive cell necrosis
136
Q

What is the order of cell changes during prolonged injury?

A

Cell death –> ultrastructural changes –> light microscopic changes –> gross morphologic changes (takes longest to occur)

137
Q

Morphologic hallmarks of irreversible cell injury and death

A
  • severe mitochondrial swelling
  • large flocculent densities in mito matrix
  • increased loss of proteins, enzymes, coenzymes
  • increased membrane permeability –> leakage of enzymes, initiation of inflammation
138
Q

During irreversible cell injury you have massive influx of _____ into the cell

A

Ca

  • worsens during reperfusion
  • Ca functions as a 2nd messenger to activate/deactivate various enzymes
139
Q

Lysosomal membrane permeability

A
  • leakage of lysosomal enzymes
  • activation of acid hydrolases
  • digestion of cytosolic/membrane constituents
140
Q

1 - 2 punch

A

Mitochondrial dysfunction and membrane damage

141
Q

What is the central factor in irreversible cell injury?

A

Membrane damage

Pathology (19 decks)

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