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CMBM Exam 3: Immunology > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

Define cell death

A

End result of progressive cell injury with both physiologic and pathologic causes

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2
Q

Adaptations are reversible or irreversible?

A

Reversible

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3
Q

Define an adaptation.

A

Reversible change in size, number, phenotype, metabolic activity, or function in response to changes in the cell’s environment

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4
Q

What are 4 types of adaptations that we discuss? Give a brief description of each

A
  1. Hypertrophy: increase in cell size
  2. Hyperplasia: increase in number of cells
  3. Atrophy: shrinkage of cell
  4. Metaplasia: replacement of a differentiated cell type by another cell type
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5
Q

What are 6 causes of cellular adaptations?

A
  1. Changes in cells/tissues
  2. Prolonged stimulation (nervous or endocrine)
  3. Lack of stimulation (damaged nerve)
  4. Lack of oxygen
  5. Lack of nutrients
  6. Chronic injury
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6
Q

Do hypertrophy and hyperplasia occur together or separately?

A

Usually occur separately but can occasionally occur together

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7
Q

What is hypertrophy due to?

A

Synthesis of more structural components, not due to swelling. Specifically due to increased functional demand on cells or by hormonal stimulation

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8
Q

In what cell populations (broadly) do we see hypertrophy?

A

Non-dividing cells (permanent cells such as nerve, cardiac myocytes, and skeletal muscle)

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9
Q

By what three mechanisms does hypertrophy happen? (Not asking what external stimuli hypertrophy is caused by)

A
  1. Signal transduction pathway => synthesis of cellular proteins => enlargement of the cytoskeleton
  2. Increased production of transcription factors => induction of proteins and increased production of growth factors
  3. Induce genes that encode TFs, GFs, and vasoactive agents
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10
Q

Working out and strengthening muscles is a form of physiologic hypertrophy. At the molecular level what occurs to facilitate hypertrophy?

A

Alpha form of the myosin heavy chain is replaced by the beta form which has a slower/more economical contraction

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11
Q

Hypertrophy is not just confined to the entire cell or tissue, it can also occur in sub cellular structures. Name 2

A
  1. Smooth ER: may become hypertrophied in response to certain drugs (ie barbituates) which cause an increase in amount of cytochrome P450 (this is the idea of tolerance)
  2. Mitochondria
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12
Q

In what cell populations (broadly) do we see hyperplasia?

A

Arises from stem cells. Essentially it takes place in a population of cells capable of dividing

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13
Q

There are two types of physiologic hyperplasia, what are they? And in what situations do they occur?

A
  1. Hormonal: increases functional capacity of tissue when needed (ex. glandular epithelium of breast during pregnancy)
  2. Compensatory: increase in tissue mass after damage or partial resection
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14
Q

What are two main stimuli of pathologic hyperplasia? Give an example of each

A
  1. Excessive hormonal stimuli (excessive estrogen => uterine bleeding or BPH)
  2. Excessive growth factor (may be linked to viruses such as HPV)
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15
Q

What are 4 mechanisms by which hyperplasia occurs?

A
  1. Increased local production of growth factors
  2. Increased levels of growth factor receptors
  3. Activation of intracellular signaling pathways
  4. Production of transcription factors
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16
Q

Define atrophy

A

Shrinkage of the size of a cell due to loss of cell substance

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17
Q

What are the two mechanisms of atrophy?

A
  1. Autophagy: cell digests its own contents using lysosome
  2. Ubiquitin-proteasome pathway: ubiquitin conjugates to proteins of the cytoskeleton which cause the proteasome to degrade them
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18
Q

Define metaplasia

A

A reversible change in which one differentiated cell type is replaced by another cell type

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19
Q

Give an example of metaplasia

A

Barrett’s Esophagus is a condition caused by GERD in which squamous cells of the inferior esophagus are replaced by glandular epithelium. Can also occur in smokers as there is a transformation of columnar cells to squamous cells in the respiratory tract which don’t have cilia and cannot trap particulate matter. Both can be premalignant

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20
Q

What is the mechanism by which metaplasia occurs?

A

Reprogramming of stem cells in normal tissue or undifferentiated mesenchymal cells in connective tissue differentiate along a different line in response to signals generated by cytokines, GFs, and ECM components.

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21
Q

What are 4 features of necrosis?

A
  1. Cellular swelling
  2. Protein denaturation
  3. Organelle breakdown
  4. Lysosomal enzymes leak into cytoplasm and digest cell => spilling of contents into environment
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22
Q

What are features of apoptosis?

A
  1. Programmed cell death
  2. Noxious stimuli damage DNA
  3. No loss of membrane integrity
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23
Q

Define necroptosis

A

Hybrid of necrosis and apoptosis that morphologically resembles necrosis and mechanistically resembles apoptosis

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24
Q

What is reversible cell injury? What does it ultimately cause?

A

Injury that leaves the cell with functional and morphologic features that are reversible. But causes decreased oxidative phosphorylation and decreased ATP concentration

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25
Q

What is irreversible cell injury characterized by?

A

Cell exhibits morphologic changes that are recognized as cell death with prominent functional changes

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26
Q

What are 8 major causes of cell injury?

A
  1. Hypoxia: decreased aerobic respiration, cell will either adapt or die
  2. Physical agents: mechanical trauma, temperature extremes, radiation, electrical shock
  3. Chemicals and Drugs: legal and illicit drugs, poisons, alcohol
  4. Microbiologic agents: virus, bacteria, parasites, protozoans
  5. Immunologic reactions: anaphylactic reaction, autoimmune diseases
  6. Genetic defects: chromosomal abnormalities, inborn errors of metabolism
  7. Nutritional Imbalances: malnutrition, obesity, hyperlipidemia
  8. Aging: cellular senescence
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27
Q

Mechanisms of Cell Injury

  1. Cellular responses to injurious stimuli depend on ___________ (3 things)
  2. Consequences of cell injury depend of _____________ (2 things)
  3. Cell injury results from ___________ (2 things)
A
  1. Type of injury, duration, and severity
  2. State and adaptability of the cell
  3. Functional and biochemical abnormalities of cellular components
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28
Q

What are 5 targets of injurious stimuli?

A
  1. Mitochondrial aerobic respiration
  2. Integrity of genetic apparatus
  3. Integrity of cell membrane
  4. Protein synthesis
  5. The cytoskeleton
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29
Q

What are 5 mechanisms of cell injury?

A
  1. Depletion of ATP
  2. Mitochondrial damage
  3. Influx of intracellular calcium
  4. Accumulation of oxygen derived free radicals
  5. Defects in membrane permeability
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30
Q

What are the 5 major effects of ATP depletion and what do each of them lead to?

A
  1. Decreased activity of the sodium/potassium pump: cell swelling and dilation of the ER
  2. Cellular energy metabolism is altered: increased glycolysis, decreased glycogen, decreased pH
  3. Failure of calcium pump: influx of calcium damages cellular components, even in small amounts it’s toxic
  4. Reduction in protein synthesis
  5. Unfolded protein response: decrease in oxygen or glucose => unfolded/misfolded proteins => cell injury or death
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31
Q

What are the 2 major effects of mitochondrial damage and what do each of them lead to?

A
  1. Formation of pores: inhibits oxidative phosphorylation => decreased ATP production
  2. Increased membrane permeability: leakage of cytochrome C => altered electron transport chain
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32
Q

What are the 4 major effects of calcium influx?

A
  1. Decreased phospholipid caused by inappropriate activation of phospholipases which in turn cause membrane damage
  2. Decreased ATP caused by inappropriate activation of ATPase
  3. Disruption of membrane and cytosolic proteins
  4. Chromatin damage caused by endonucleases
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33
Q

What are the 3 places calcium can influx from to the the cytosol?

A
  1. Extracellularly: the extracellular concentration is higher, this is maintained by the calcium pump
  2. Mitochondria
  3. Endoplasmic reticulum
34
Q

What are 4 causes of accumulation of oxygen derived free radicals?

A
  1. Radiant energy: uv light or x-rays
  2. Chemicals/Drugs: carbon tetrachloride (CCl4)
  3. Transition metals: Fe or Cu may donate/accept free electrons to generate radicals
  4. Nitric oxide: generated by endothelial cells/macrophages can act as a free radical
35
Q

What are 3 major effects of free radicals?

A
  1. Lipid peroxidation of membranes
  2. Oxidative modification of proteins: possibly cross-linking of proteins which => increased degradation or loss of enzymatic activity
  3. Lesions in DNA: free radicals react with thymine causing single stranded breaks in the DNA
36
Q

What are 3 ways in which we can deal with free radicals?

A
  1. Antioxidants: block initiation of free radicals (vit A, B, and glutathione)
  2. Binding of metals to storage and transport proteins
  3. Enzymes: catalase, superoxide dismutase (SOD), and glutathione peroxidase
37
Q

Defects in membrane permeability leads to what 5 things?

A
  1. Mitochondrial dysfunction
  2. Loss of membrane phospholipids
  3. Cytoskeletal abnormalities
  4. Reactive oxygen species
  5. Lipid breakdown products
38
Q

What are 4 characteristics of reversible cell injury?

A
  1. Acute cellular swelling
  2. Depleted glycogen
  3. Reduced intracellular pH
  4. Reduction in protein synthesis
39
Q

What are 8 characteristics of irreversible cell injury?

A
  1. Increased calcium in mitochondria
  2. Damage to plasma membrane
  3. Swelling of lysosomes
  4. Leakage of intracellular proteins
  5. Loss of membrane phospholipids
  6. Cytoskeletal abnormalities
  7. Toxic oxygen radicals
  8. Lipid breakdown products
40
Q

Free radicals have an unpaired electron which makes the molecule unstable causing it to react with both organic and inorganic chemicals. Name 3 things it damages in the cell.

A
  1. Lipid peroxidation of membranes
  2. DNA lesions
  3. Cross linking of proteins
41
Q

What 5 factors cause the conversion of molecular oxygen to a reactive oxygen species?

A
  1. Radiation
  2. Inflammation
  3. Oxygen toxicity
  4. Chemicals
  5. Reperfusion injury
42
Q

How does superoxide anion behave intracellularly?

A
  1. Stimulates degradative enzymes in leukocytes

2. Directly damages lipids, proteins, and DNA

43
Q

What is the most reactive of the reactive oxygen species and how is it made?

A

Hydroxyl free radical is most reactive is it made via the breakdown of hydrogen peroxide

44
Q

What is worse carbon tetrachloride (CCl4) or CCl3?

A

CCl3 is much worse because it is a free radical, it comes from the breakdown of CCl4

45
Q

Chemical injury occurs by two different means, what are they?

A
  1. Direct cytotoxic effects

2. Conversion to toxic metabolites

46
Q

What are the two factors associated with reversible cell injury?

A
  1. Cellular swelling

2. Fatty change (prominent in the liver)

47
Q

Necrosis is characterized at the cellular/molecular level by 4 characteristics, what are they?

A
  1. Loss of membrane integrity
  2. Elicit inflammation
  3. Denaturation of intracellular proteins
  4. Enzymatic digestion of the cell
48
Q

Morphologically necrosis is characterized by 3 main things, what are they?

A
  1. Increased eosinophilia (pinkish appearance)
  2. Myelin figures (phospholipid masses)
  3. Nuclear changes (karyolysis, pyknosis, and karyorrhexis)
49
Q

Describe karyolysis, pyknosis, and karyorrhexis.

A

Karyolysis: nuclei is fragmented and dispersed in fine/little fragments
Pyknosis: the nucleus is shrunken
Karyorrhexis: nucleus is fragmented but with larger fragments compared to karyolysis

50
Q

Name the 6 types of necrosis as well as conditions they may be associated with.

A
  1. Coagulative (myocardial infarct)
  2. Liquefactive (bacterial or fungal infections of soft tissue such as CNS or kidney)
  3. Caseous (Tuberculosis)
  4. Fat (Pancreatitis and trauma to the breast)
  5. Fibrinoid (Blood vessels have bright pink amorphous deposit due to an immune reaction)
  6. Gangrenous (Diabetes)
51
Q

What are 2 features of coagulation necrosis?

A
  1. Structural outline of the cell is preserved

2. Intracellular components such as structural and enzymatic proteins dissolve/denature and become clumped

52
Q

What is liquefactive necrosis marked by?

A

Complete digestion of dead cells

53
Q

What is caseous necrosis marked by?

A

“Cheesy” appearance of a central necrotic area

54
Q

What is fat necrosis marked by? How does pancreatitis cause this?

A

Focal area of fat destruction

Pancreatitis causes lipases made by the pancreas to be released to inappropriate areas and digest fat

55
Q

What is the process by which fibrinoid necrosis occurs?

A

Complexes of antigen/antibodies are deposited to the walls of arteries where they bind to fibrin that has leaked out of the vessels. This results in a bright pink amorphous deposit

56
Q

Gangrenous necrosis may have two different appearances because it occurs via two other types of necrosis. What are they types of gangrene called, what necrotic processes are they a result of, and what is the general appearance of each? Also what area of the body do both types usually affect?

A

Dry gangrene occurs via coagulative necrosis causing the limb to appear dry and mummified
Wet gangrene occurs via liquefactive necrosis causing the limb to appear moist
Generally they affect the lower limbs, this is especially prominent in diabetics

57
Q

What are 5 subcellular responses to injury?

A
  1. Cytoskeletal abnormalities
  2. Lysosomal catabolism
  3. Mitochondrial alterations
  4. S.E.R. induction
  5. Activation of heat shock proteins
58
Q

Lysosomal catabolism can occur via two different pathways. Name and describe them

A
  1. Heterophagy (phagocytosis or pinocytosis): engulfing something that is outside of the cell
  2. Autophagy: engulfing something that is an intracellular component
59
Q

Both pathways of lysosomal catabolism generate what intracellular components?

A

Residual bodies which eventually form a lipofuscin pigment granule which may accumulate and be visible under the microscope

60
Q

Induction of S.E.R. as a response to injury generally leads to an increase in what? How does this increase occur? Clinically what is this called?

A

Increase in the metabolism of chemicals due to the modification of P450. Clinically this results in the idea of tolerance

61
Q

What are 3 mitochondrial alterations due to cell injury?

A
  1. Hypertrophy
  2. Atrophy
  3. Abnormalities (which can be either genetic or acquired)
62
Q

Cytoskeletal abnormalities due to injury result in what cellular process being defective?

A

Locomotion

63
Q

What is the disease called in which cytoskeletal abnormalities due to cell injury directly affect the microtubules? What cellular structure does this affect and clinically what is it’s significance?

A

Kartagener’s Syndrome: causes problems with the cilia which leads to upper respiratory tract problems and increased risk of pneumonia

64
Q

What are 2 microscopically observable effects of cytoskeletal abnormalities where the intermediate filaments are directly involved? What conditions are they associated with?

A

Mallory bodies: alcoholic hepatitis (caused by accumulation/precipitation of intermediate filaments)
Neurofibrillary tangles: Alzheimer’s disease

65
Q

Apoptosis occurs under both physiological and pathological conditions. What are 6 stimuli which cause apoptosis under a physiological state?

A
  1. Embryogenesis (remember hands initially form like flippers)
  2. Hormone dependent involution (menstrual cycle causes endometrium to disintegrate)
  3. Cell deletion in proliferating populations (suppression of an immune response)
  4. Acute inflammatory response
  5. Elimination of self reactive lymphocytes (during maturation)
  6. Induced by cytotoxic T cells (survey the health of cells)
66
Q

Apoptosis occurs under both physiological and pathological conditions. What are 4 stimuli which cause apoptosis under a pathological state?

A
  1. Injurious stimuli
  2. Viruses
  3. Atrophy from duct obstruction
  4. Tumors (even in the most aggressive cancers; chemotherapies can induce apoptosis)
67
Q

What are 4 morphological characteristics of apoptosis?

A
  1. Cell shrinkage
  2. Chromatin condensation
  3. Cytoplasmic blebs/apoptotic bodies
  4. Phagocytosis of apoptotic cells
    * Important to note that the membrane stays intact unlike in necrosis
68
Q

What are 3 biochemical features of apoptosis?

A
  1. Protein cleavage by caspases (destruction of cytoskeleton allows for blebbing)
  2. DNA breakage (DNases can only cleave linking DNA between histones resulting in DNA fragments with 180bp multiples)
  3. Phagocytic recognition
69
Q

There are 2 pathways by which apoptosis can occur, what are they?

A

Extrinsic: includes the interaction of cell surface death receptors FAS and TNF receptor
Intrinsic: mediated by a balance of pro apoptotic and protective molecules as well as the release of death inducers

70
Q

What 4 things trigger apoptosis?

A
  1. Growth factor deprivation (think about circulating neutrophils)
  2. DNA damage
  3. TNF receptor activation
  4. Cytotoxic T lymphocytes (perforin and granzyme B)
71
Q

Misfolded proteins and heat shock proteins are implicated in what 3 diseases?

A
  1. Alzheimer’s
  2. Huntington’s
  3. Parkinson’s
72
Q

Misfolded proteins can be dealt with using what 2 pathways?

A
  1. Heat shock proteins trying to properly fold the protein

2. Ubiquitin proteasome pathway

73
Q

What are 3 ways in which substances can accumulate intracellularly?

A
  1. Endogenous substances that are synthesized to quickly or synthesized at normal rate but degraded to slowly
  2. Genetic or acquired defects in metabolism transport or secretion
  3. Deposition of an exogenous substance (think asbestos or silica)
74
Q

Give 3 examples of endogenous pigments that accumulate and the process by which they accumulate

A
  1. Melanin: due to melanomas
  2. Hemosiderin (is an iron storage complex made of ferritin/denatured ferratin): caused by RBC breakdown especially when RBCs have infiltrated certain spaces such as the lungs, as is seen in congestive heart failure
  3. Lipofuscin: occurs due to normal “wear and tear” of the cell but can also occur under pathological states
75
Q

Give 2 examples of exogenous pigments

A
  1. Carbon with anthracosis (which usually comes from smoking)
  2. Tattoos
76
Q

Genetic or acquired defects in metabolism transport or secretion cause intracellular accumulation of certain substances. Give examples of what conditions may occur and what the general cause of accumulation is.

A
  1. Abnormal metabolism: can result in fatty liver due to problems with fat transport
  2. Genetic mutations: result in an abnormally folded protein which may either aggregate or is unable to be properly secreted due to abnormal structure
  3. Lack of enzyme: causes accumulation of substrate which is what occurs in certain lysosomal and glycogen storage diseases
77
Q

In what 2 cell types does cholesterol pathologically accumulate? What conditions does this result in?

A

Cholesterol may accumulate in macrophages and smooth muscle cells.
Recall macrophages at sites of injury/inflammation will absorb lipids and turn into foam cells and will have a much longer life.
This can lead to atherosclerosis resulting in blockage of blood vessels

78
Q

Excessive amounts of secretory proteins form what cytoplasmic inclusion?

A

Russell bodies

79
Q

There are 2 types of pathological calcifications, what are they and how do they occur?

A
  1. Dystrophic: occurs in a setting of normal or elevated serum calcium levels; the calcium is deposited in an abnormal structure (ie cardiac valve)
  2. Metastatic: occurs only in a hypercalcemic state; calcium is deposited in normal structures (ie gastic mucosa, kidneys, lungs); generally do not cause any clinical dysfunction
80
Q

What are 4 features associated with cellular aging?

A
  1. Structural and biochemical changes due to oxidative damage and/or abnormally folded proteins
  2. Replicative senescence: limited dividing of cells
  3. Gene mutations
  4. Accumulation of damage (either genetic or physical)
81
Q

What are 4 patters of acute and chronic cell injury which can generally be observed at the macroscopic level? What are characteristics associated with each?

A
  1. Serous (blister from burning skin): generally protein poor
  2. Fibrinous (pericarditis): increased vascular permeability and accumulation of fibrin
  3. Suppurative (usually from bacterial infection): abscesses and pus present
  4. Ulceration (aka erosion): results from eroded epithelium

CMBM Exam 3: Immunology (21 decks)

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