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NUR1142 > Module 1 - Altered Cellular and Tissue Biology > Flashcards

Module 1 - Altered Cellular and Tissue Biology Flashcards

1
Q

Describe cellular adaptation

A
  • This is when cells adapt to their environment to escape and protect themselves from injury
  • An adapted cell is neither normal nor injured - condition lies between these 2 states
  • It is reversible changes in size, number, phenotype, metabolic activity or functions of cells
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2
Q

Give examples of adaptive changes in cells

A
  1. Atrophy - decrease in cells size
  2. Hypertrophy - increase in cell size
  3. Hyperplasia - increase in cell number
  4. Metaplasia - reversible replacement of one mature cell type by another less mature cell type or a change in the phenotype
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3
Q

What is Dysplasia?

A
  • This is deranged cellular growth, not a true adaptation
  • It is atypical hyperplasia
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4
Q

Atrophy

A

Decrease or shrinkage in cellular size

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5
Q

Where is atrophy most common?

A

Skeletal muscle, heart, secondary sex organs, brain

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6
Q

True or False: Atrophy can be physiological or pathological.

A

True

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7
Q

True or False: Atrophy is only physiological.

A

False

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8
Q

What does an atrophic muscle cell contains less of?

A

ER, mitochondria and myofilaments.

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9
Q

What causes immediate reduction of O2 consumption and amino acid uptake in muscular atrophy

A

Nerve loss.

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10
Q

What are the mechanisms of atrophy?

A
  1. Decreased protein synthesis
  2. Increased protein catabolism
  3. Ribosome biogenesis may also play a role
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11
Q

What is the primary pathway of protein catabolism?

A

UPS - ubiquitin-proteasome pathway.

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12
Q

An increase in proteasome activity is characteristic of what changes?

A

Atrophic muscle changes

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13
Q

Deregulation of UPS leads to what?

A

Abnormal cell growth and is associated with cancer and other diseases.

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14
Q

What accompanies atrophy due to chronic malnutrition?

A

It is accompanied by self eating process called autophagy that creates autophagic vacuoles.

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15
Q

What are autophagic vacuoles?

A
  • membrane bound vesicles within the cells
  • it contains cellular debris and hydrolytic enzymes which function to breakdown substances to the simplest unit of fat, carbs, or protein.
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16
Q

What happens to the levels of hydrolytic enzymes during atrophy?

A

It rises rapidly

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17
Q

What do these autophagic vacuoles do?

A

This is where hydrolytic enzymes are isolated to prevent uncontrolled cellular destruction. This process protects uninjured organelles from injured organelles. Theyare eventually engulfed and destroyed by lysosomes.

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18
Q

Give an example of granules that can persist and resist breakdown.

A

Examples are granules that contains lipofuscin - yellow brown pigment - usually accumulates in liver cells, myocardial cells, and atrophic cells.

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19
Q

Give examples of Atrophy

A
  1. Physiological - occurs in early development e.g. thymus gland undergoes physiological atrophy during childhood.
  2. Pathological -
    • decreases in workload, pressure, use, blood supply, nutrition, hormonal stimulation, and nervous system stimulation. e.g. individuals immobilized in bed for a prolonged period of time, aging causes brain cells to become atrophic, endocrine-dependent organs can shrink as hormonal stimulation decreases.
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20
Q

Hypertrophy

A

-Compensatory increase in the size of the cell in response to mechanical stimuli (also mechanical load or stress).
-Examples are from repetitive stretching, chronic pressure or volume overload.
-This can lead to increases in size of organ.

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21
Q

Which are the 2 organs most prone to hypertrophy/enlargement?

A

Heart and kidneys

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22
Q

What is involved in cardiac hypertrophy?

A

It involves changes in signaling and transcription factor pathways which leads to increased protein synthesis - this leads to LVH.

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23
Q

What remains intact with physical hypertrophy?

A

Myocardial structure and function despite increased workload of the heart.

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24
Q

Give examples of physical hypertrophy.

A
  1. Normal growth and development
  2. moderate endurance exercise training
  3. pregnancy
  4. early phases of increased pressure and volume loading on the adult human heart
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25
Q

What is associated with pathological hypertrophy in the heart?

A

Structure and functional changes to the heart.

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26
Q

Pathological hypertrophy is secondary to what conditions/factors?

A
  • HTN, coronary heart disease, problem valves.
  • Aging, strenuous exercise, sustained workload, or stress
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27
Q

What is a key risk factor to heart failure?

A

Pathological hypertrophy

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28
Q

What are the results of the structural and functional manifestations of pathological hypertrophy?

A
  • Interstitial fibrosis
  • Cellular death
  • Cardiac cardiac function
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29
Q

What is hyperplasia?

A

This is the increased number of cells resulting from an increased rate of cellular division.

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30
Q

When does hyperplasia occur as a response to injury?

A

It occurs when the injury has been severe and prolonged enough to have caused cellular death.

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31
Q

Hyperplasia and a. ___________ often occur together. Both take place if the cells can b.______________ DNA.

A
  1. Hypertrophy
  2. Synthesize
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32
Q

What are to types physiological hyperplasia?

A
  1. Compensatory
  2. Hormonal
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33
Q

Compensatory Hyperplasia

A

Adaptive mechanism that enables certain organs to regenerate

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34
Q

Give an example of Compensatory hyperplasia.

A
  • Removal of part of the liver –> leads to hyperplasia of hepatocytes to compensate for the loss. Even removal of 70% of liver, regeneration is complete in about 2 weeks.
  • Callus or thickening of the skin - because of hyperplasia of epidermal cells in response to a mechanical stimulus
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35
Q

What are induced and play a critical role in liver regeneration?

A

Several growth factors and cytokines (chemical messengers).

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36
Q

What types of cells cannot divide again once differentiated?

A

neurons, skeletal muscle cells.

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37
Q

Significant hyperplasia occurs in what areas?

A
  1. epidermal and intestinal epithelial
  2. hepatocytes
  3. bone marrow cells
  4. fibroblasts

Some hyperplasia is noted in bone, cartilage, and smooth muscle cells

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38
Q

Hormonal hyperplasia

A

occurs chiefly in estrogen-dependent organs, such as the uterus and breast.

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39
Q

Give an example of hormonal hyperplasia

A

After ovulation, for example, estrogen stimulates the endometrium to grow and thicken in preparation for receiving the fertilized ovum. If pregnancy occurs, hormonal hyperplasia, as well as hypertrophy, enables the uterus to enlarge

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40
Q

Pathological hyperplasia

A

abnormal proliferation of normal cells, usually in response to excessive hormonal stimulation or growth factors on target cells

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41
Q

What is the most common pathological hyperplasia

A

Most common - Pathological hyperplasia of the endometrium caused by an imbalance between estrogen and progesterone secretion, with over secretion of estrogen

Benign prostatic hyperplasia is another example which results from changes in hormone balance.

If hormonal imbalance is corrected, then hyperplasia regresses.

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42
Q

Dysplasia

A
  • is not a true adaptive change
  • refers to abnormal changes in the size, shape, and organization of mature cells
  • atypical hyperplasia
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43
Q

Where does dysplastic changes often occur?

A

Epithelial tissue of the cervix and respiratory tract
- they are strongly associated with common neoplastic growth
- often adjacent to cancerous cells

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44
Q

Metaplasia

A

Reversible replacement of one mature cell type (epithelial, mesenchymal) by another, sometimes less differentiated cell type.

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45
Q

Give an example of metaplasia

A

The best example of metaplasia is replacement of normal columnar ciliated epithelial cells of the bronchial (airway) lining by stratified squamous epithelial cells - e.g. cigarette smoking. If stimulus is removed then can be reversed, if not, then dysplasia and cancerous transformation can occurs.

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46
Q

When does cellular injury occur?

A

When the cell is unable to maintain allostasis - a normal or adaptive steady state - in the face injurious stimuli or stress.
Injured cells may recover (reversible) or die (irreversible)

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47
Q

Give examples of injurious stimuli

A
  1. Hypoxia
  2. free radicals
  3. infectious agents
  4. physical and mechanical factors
  5. immunological reactions
  6. genetic factors
  7. nutritional imbalances
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48
Q

What are the types of injuries?

A
  1. Adaptation
  2. Active cellular injury
  3. reversible
  4. Irreversible
  5. Necrosis
  6. Apoptosis or programmed cellular death
  7. Autophagy
  8. Chronic cellular injury
  9. Accumulations or infiltrations
  10. pathological calcification
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49
Q

What are the responses Adaptation?

A

Atrophy, hypertrophy, hyperplasia, metaplasia

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50
Q

What are the responses to Active cellular injury

A

Immediate response of entire cell

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51
Q

What are the responses to Reversible?

A
  • loss of ATP
  • cellular swelling
  • detachment of ribosomes
  • autophagy of lysosomes
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52
Q

What are the responses to Irreversible?

A

“Point of no return” structurally when severe vacuolization of mitochondria occurs and Ca++ moves into cell

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53
Q

What are the responses to Necrosis

A

Common type of cellular death with severe cell swelling and breakdown of organelles

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54
Q

What are the responses to Apoptosis

A

Cellular self destruction for elimination of unwanted cell populations

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55
Q

What are the responses to autophaghy?

A

Eating of self, cytoplasmic vesicles engulf cytoplasm and organelles, recycling factory

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56
Q

What are the responses to chronic cellular injury (subcellular alterations)

A

Persistent stimuli response may involve only specific organelles or cytoskeleton (e.g. phagocytosis of bacteria)

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57
Q

What are the responses to pathological calcifications?

A

Dystrophic and metastatic calcifications

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58
Q

The extent of cellular injury depends on what factors?

A
  1. type
  2. state (including level of cell differentiation and increased susceptibility to fully differentiated cells.)
  3. adaptive processes of the cell
  4. as well as the type, severity, and duration of the harmful stimulus
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59
Q

Give an example of a modifying factor that can profoundly influence the extent of injury?

A

Nutritional Status

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60
Q

Yes or No: Would 2 individuals exposed to an identical stimulus incur the same degree of cellular injury?

A

No

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61
Q

What are the biochemical mechanisms involved with cellular injury and death?

A
  1. ATP depletion
  2. Mitochondrial damage
  3. Oxygen and oxygen free derived free radical membrane damage
  4. Protein folding defects
  5. DNA damage defects
  6. Calcium level alterations
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62
Q

Give examples of common forms of cellular injury?

A
  1. hypoxic injury - most common
  2. free radicals and reactive oxygen species injury
  3. chemical injury
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63
Q

Describe ATP depletion

A
  • Loss of mitochondrial ATP and decreased ATP synthesis
  • results include cellular swelling, decreased protein synthesis, decreased membrane transport, and lipogenesis –> all changes that contribute to loss if integrity of plasma membrane
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64
Q

Describe ROS - reactive oxygen species

A

Lack of oxygen is key in progression of cellular injury in ischemia (reduced blood supply); activated oxygen species (ROS, O2*–, H2O2, *OH) cause destruction of cell membranes and cell structure

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65
Q

Describe Ca++entry

A

Normally intracellular cytosolic calcium concentrations are very low; ischemia and certain chemicals cause an increase in cytosolic Ca++ concentrations; sustained levels of Ca++ continue to increase with damage to plasma membrane; Ca++ causes intracellular damage by activating a number of enzymes

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66
Q

Describe mitochondrial damage

A

Can be damaged by increases in cytosolic Ca++, ROS; two outcomes of mitochondrial damage are loss of membrane potential, which causes depletion of ATP and eventual death or necrosis of cell, and activation of another type of cellular death (apoptosis)

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67
Q

Describe Membrane damage

A

Early loss of selective membrane permeability found in all forms of cellular injury, lysosomal membrane damage with release of enzymes causing cellular digestion

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68
Q

Describe Protein misfolding, DNA damage

A

Proteins may misfold, triggering unfolded protein response that activates corrective responses; if overwhelmed, response activates cell suicide program or apoptosis; DNA damage (genotoxic stress) also can activate apoptosis

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69
Q

What is the single most common cause of cellular injury?

A

Hypoxia

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70
Q

What are the main consumers of Oxygen?

A

Mitochondria

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71
Q

________ are also possible hypoxia signalling molecules.

A

ROS

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72
Q

What is the most common cause of hypoxia?

A

Ischemia

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73
Q

What is somatic death?

A

Somatic death is the death of the whole person

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74
Q

How long after death does post mortem changes appear?

A

Within minutes, is diffuse and does not involve components of the inflammatory response.

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75
Q

What are the most notable manifestations of somatic death?

A

cessation of respiration and circulation

76
Q

What happens to the body temp after death?

A

falls gradually immediately then more rapidly (around 1 degree celsius/hour). After 24 hours, body temp = environment. If death caused by infective disease, body temp may continue to rise for a short time.

77
Q

Algor Mortis

A

Postmortem reduction of body temp.

78
Q

Livor mortis

A

Purple discoloration after death. Happens when gravity causes blood to settle in the most dependent, or lowest tissues.

79
Q

Rigor Mortis

A

Muscle stiffening - happens when acidic compounds accumulate within the muscles because of breakdown of carbs and depletion of ATP.

80
Q

What muscles are initially affected with rigor mortis?

A

Smaller muscles , particularly the muscles of the jaw.

81
Q

When does rigor mortis affect the whole body?

A

Within 12-14 hours

82
Q

When does rigor mortis diminishes and body becomes flaccid?

A

at 36-62 hours.

83
Q

When are signs of putrefaction generally obvious?

A

24-48 hours after death.

84
Q

Postmortem autolysis

A

Release of enzymes and lytic dissolution

85
Q

Describe Autophagy

A
  • eating of self
  • as a “recycling factory”, it’s a self-destructive process and a survival mechanism
  • involves delivery of cytoplasmic contents to the lysosomes for degradation
86
Q

What are the major forms of autophagy

A
  1. Macroautophagy
  2. Microautophagy
  3. Chaperone-mediated authophagy
87
Q

Describe macroautophagy?

A

involves with sequestration and transportation of parts of the cytosol in an autophagic vacuole (autophagosome)

88
Q

What is microautophagy?

A

inward invagination of the lysosomal membrane for cargo delivery

89
Q

Describe chaperone-mediated autophagy

A

chaperone-dependent proteins that direct cargo across the lysosomal membrane

90
Q

What is apoptosis?

A
  • An active process cellular destruction called program cellular death
  • happens in normal and pathological tissue change
91
Q

Give examples of pathological states that can involve death by apoptosis

A
  1. Severe cellular injury
  2. Accumulation of misfolded proteins
  3. Infections (particularly viral)
  4. Obstruction in tissue ducts
  5. Dysregulated apoptosis
92
Q

Describe apoptosis in relation to severe cellular injury?

A

When cellular injury exceeds repair mechanisms, the cell triggers apoptosis. DNA damage can result either directly or indirectly from production of free radicals.

93
Q

Discuss apoptosis in relation to misfolded proteins?

A

This state may result from genetic mutations or free radicals. Excessive accumulation of misfolded proteins in the ER leads to a condition known as ER stress (see Chapter 1). ER stress results in apoptotic cellular death. This mechanism explains several degenerative diseases of the CNS and other organs

94
Q

Discuss apoptosis in relation to infection

A

Apoptosis results directly from the infection or indirectly from the host immune response. Cytotoxic T lymphocytes respond to viral infections by inducing apoptosis and, therefore, eliminating the infectious cells. This process can cause tissue damage, and it is the same for cellular death in tumours and rejection of tissue transplants.

95
Q

Discuss apoptosis in relation to tissue duct

A

In organs with duct obstruction, including the pancreas, kidney, and parotid gland, apoptosis causes pathological atrophy.

96
Q

Discuss apoptosis in relation to Dysregulated Apoptosis

A

is either excessive or insufficient apoptosis and contributes further to disease. For instance, a low rate of apoptosis can permit the survival of abnormal cells, for example, mutated cells that can increase cancer risk. Defective apoptosis may not eliminate lymphocytes that react against host tissue (self-antigens), leading to autoimmune disorders. Excessive apoptosis is known to occur in several neuro-degenerative diseases, from ischemic injury (such as myocardial infarction and stroke), and from death of virus-infected cells (as seen in many viral infections).

97
Q

What are the 2 different pathways that converge on caspase in relation to apoptosis?

A
  1. Mitochondrial (intrinsic) pathway
  2. Death receptor (extrinsic pathway)
98
Q

What does cellular death eventually lead to?

A

Necrosis or cellular dissolution.

99
Q

What is necrosis?

A

The sum of cellular changes after local cellular deathand the process of cellular digestion (autodigestion or autloysis)

100
Q

What are the structural signs that indicate irreversible injury and progression to necrosis?

A

Dense clumping and progressive disruption both of genetic material and of plasma and organelle membranes.

101
Q

What happens when membrane integrity is lost during necrosis?

A

Necrotic cell contents leak out and may cause the signaling of inflammation in surrounding tissue.

102
Q

What happens in the alter stages of necrosis?

A
  • Disruption of organelles occur
  • karyolysis is underway (nuclear dissolution and lysis of chromatin from the action of hydrolytic enzymes)
  • in some cells, nucleus shrinks and becomes small, dense mass of genetic material.
103
Q

What is karyorrhexis

A

Fragmentation of the nucleus into smaller particles or nuclear dust.

104
Q

Give examples of the type of Necrosis.

A
  1. Coagulative Necrosis
  2. Liquefative necrosis
  3. Caseous necrosis
  4. Fatty Necrosis
  5. Gangrenous Necrosis
  6. Gas Gangrene
105
Q

Where does coagulative necrosis occur primarily?

A

Kidneys, heart, and adrenal glands.

106
Q

What does coagulative necrosis result from ?

A

Hypoxia by severe ischemia or hypoxia caused by chemical injury, especially ingestion of mercuric chloride.

107
Q

What do you call the area of coagulative necrosis?

A

Infarct

108
Q

What causes coagulation in relation to coagulative necrosis?

A

It is a result of protein denaturation, which causes the protein albumin to change from a gelatinous, transparent state to a firm opaque state.

109
Q

What commonly cause liquefactive necrosis?

A

It commonly results from ischemic injury to neurons and glial cells in the brain.

110
Q

List some bacterial infection that can cause liquefactive necrosis?

A

Staphylococci, Streptococci, e. coli

111
Q

What commonly causes caseous necrosis?

A

It usually results from tuberculous pulmonary infection especially by Mycobacterium tuberculosis.

112
Q

Caseous necrosis is a combination of what types of necroses?

A

Coagulative and liquefactive.

113
Q

Why does liquefactive necrosis readily affect dead brain tissue?

A

Because brain cells are rich in digestive hydrolytic enzymes and lipids and the brain contains little connective tissue.

114
Q

Explain the process of liquefactive necrosis?

A

Cells initiate autodigestion by their own hydrolases, so the tissue becomes soft, liquefies, and segregates from healthy tissue, forming cysts.

115
Q

Explain what happens in caseous necrosis.

A

The dead cells disintegrate, but the hydrolases do not completely remove all the debris. Tissues resemble clumped cheese in that they are soft and granular. A granulomatous inflammatory wall encloses areas of caseous necrosis.

116
Q

What is fatty necrosis?

A

Fat necrosis is cellular dissolution caused by powerful enzymes, called lipases that occur in the breast, pancreas, and other abdominal structures

117
Q

Where does fatty necrosis usually occur?

A

breast, pancreas, and other abdominal structures

118
Q

Explain the process of fatty necrosis.

A

Lipases break down triglycerides, releasing free fatty acids that then combine with calcium, magnesium, and sodium ions, creating soaps (saponification). The necrotic tissue appears opaque and chalk-white.

119
Q

What is the appearance of the necrotic tissue from fatty necrosis?

A

opaque and chalk-white.

120
Q

What causes gangrenous necrosis?

A

It results from severe hypoxic injury, which commonly occurs because of arteriosclerosis, or blockage, of major arteries, particularly those in the lower leg

121
Q

What type of gangrene is the result of coagulative necrosis?

A

Dry Gangrene

122
Q

What does dry gangrene look like?

A

skin becomes very dry and shrinks, resulting in wrinkles, and its colour changes to dark brown or black.

123
Q

How does wet gangrene develop?

A

It develops when neutrophils invade the site, causing liquefactive necrosis.

124
Q

Where does wet gangrene usually occur?

A

Internal organs

125
Q

Describe some of the manifestations of wet gangrene?

A

Area becomes cold, swollen, and black. A foul odor is present, and death is a possibility if systemic symptoms become severe.

126
Q

What does gas gangrene result from?

A

This type of gangrene is the result of infection of injured tissue by one of many species of Clostridium.

127
Q

Describe the process of Gas gangrene

A

These anaerobic bacteria produce hydrolytic enzymes and toxins that destroy connective tissue and cellular membranes and cause bubbles of gas to form in muscle cells. Gas gangrene can be fatal if enzymes lyse the membranes of red blood cells, destroying their oxygen-carrying capacity. Shock is the main cause of death.

128
Q

What is the main cause of death with gas gangrene?

A

Shock

129
Q

What is an important manifestation of cellular injury?

A

Intracellular accumulation of abnormal amounts of various substances and the resultant metabolic disturbances

130
Q

What does cellular accumulations or infiltration results from ?

A

from sublethal, sustained injury of cells but also from normal (but inefficient) cell function.

131
Q

What are the 2 categories of substances than can produce accumulations?

A

(1) normal cellular substances (such as excess water, proteins, lipids, and carbohydrates) and (2) abnormal substances, either endogenous (such as a product of abnormal metabolism or synthesis) or exogenous (such as infectious agents or a mineral).

132
Q

Abnormal accumulations of substances can occur in what parts of the cell?

A

It can occur in the cytoplasm (often in the lysosomes) or in the nucleus

133
Q

What are some of the reasons why abnormal accumulations occur?

A

(1)There is insufficient removal of the normal substance because of altered packaging and transport, such as what happens with fatty change in the liver, (e.g., steatosis).
(2)An abnormal substance, often the result of a mutated gene, accumulates because of defects in protein folding, transport, or abnormal degradation.
(3)There is inadequate metabolism of an endogenous substance (normal or abnormal), usually because of lack of a vital lysosomal enzyme, and these are called storage diseases.
(4)Harmful exogenous materials, such as heavy metals, mineral dusts, or microorganisms, accumulate because of inhalation, ingestion, or infection.

134
Q

What is the most common degenerative change with cells?

A

Cellular swelling

135
Q

In hypoxic injury, what does movement of fluids and ions into the cell associated with?

A

it is associated with failure of metabolism and loss of ATP production.

136
Q

What happens during metabolic failure caused by hypoxia?

A

reduced levels of ATP and ATPase permit sodium to accumulate in the cell while potassium (K+) diffuses outward.

137
Q

What happens when intracellular Na+ concentration increases?

A

increases osmotic pressure, drawing more water into the cell. The cisternae of the ER swell, rupture, and then unite to form large vacuoles that isolate the water from the cytoplasm, a process called vacuolation.

138
Q

What is the process of vacuolation?

A

This is when the ER swell, rupture, and then unite to form large vacuoles that isolate the water from the cytoplasm

139
Q

What is cytoplasmic swelling?

A

Oncosis

140
Q

What happens with progressive vacuolation?

A

cytoplasmic swelling called oncosis

141
Q

What happens when cellular swelling affects all the cells in an organ ?

A

the organ increases in weight and becomes distended and pale.

142
Q

True of False: Cellular swelling is non-reversible and lethal

A

False - cellular swelling is reversible and sub-lethal. It is an earlier manifestation of almost all types of cellular injury.

143
Q

What clinical manifestations are associated with cellular swelling?

A

high fever, hypokalemia, and certain infections

144
Q

Where does lipids and carbs usually accumulate?

A

Spleen, liver, and CNS

145
Q

What happens when lipids and carbohydrates accumulate in the CNS?

A

It can cause neurological dysfunction and severe intellectual disability. Lipids accumulate in Tay-Sachs disease, Niemann-Pick disease, and Gaucher’s disease

146
Q

What is the most common site of intracellular lipid accumulation or fatty change (steatosis)?

A

liver cells

146
Q

What is the most common cause of fatty change in the liver in developed countries?

A

alcohol abuse

147
Q

What are other causes of fatty change?

A

diabetes mellitus, protein malnutrition, toxins, anoxia, and obesity.

148
Q

What happens once lipid fill the cells?

A

vacuolation pushes the nucleus and other organelles aside. The liver’s outward appearance is yellow and greasy.

149
Q

What are some of the mechanisms instigated by cellular injury that leads to lipid accumulation?

A

1.Increased movement of free fatty acids into the liver (starvation, e.g., increases the metabolism of triglycerides in adipose tissue, releasing fatty acids that subsequently enter liver cells)
2.Failure of the metabolic process that converts fatty acids to phospholipids, resulting in the preferential conversion of fatty acids to triglycerides
3.Increased synthesis of triglycerides from fatty acids (increased levels of the enzyme α-glycerophosphatase can accelerate triglyceride synthesis)
4.Decreased synthesis of apoproteins (lipid-acceptor proteins)
5.Failure of lipids to bind with apoproteins and form lipoproteins
6.Failure of mechanisms that transport lipoproteins out of the cell
7.Direct damage to the ER by free radicals released by alcohol’s toxic effects

150
Q

When does intracellular accumulations of glycogen occur?

A

It occur in genetic disorders called glycogen storage diseases and in disorders of glucose and glycogen metabolism.

151
Q

What is the results of glycogen accumulation?

A

excessive vacuolation of the cytoplasm.

152
Q

What is the most common cause of glycogen accumulation?

A

the disorder of glucose metabolism (i.e., diabetes mellitus)

153
Q

What does protein provide to the cells?

A

It provides cellular structure and constitute most of the cell’s dry weight.

154
Q

How does accumulation of protein damage the cell?

A
  1. Cellular organelle damage may occur when metabolites (enzymes produced when the cell attempts to digest some proteins) are released from lysosomes.
  2. Additionally, when excessive amounts of protein are present in the cytoplasm, they may push against cellular organelles, disrupting organelle function and intracellular communication.
155
Q

Where does excess of protein primarily accumulate?

A
  1. pithelial cells of the renal convoluted tubules of the nephron unit
  2. in the antibody-forming plasma cells (B lymphocytes) of the immune system
156
Q

Where does endogenous pigments come from?

A

Endogenous pigments come from amino acids, for example (e.g., tyrosine, tryptophan). They include melanin and the blood proteins porphyrins, hemoglobin, and hemosiderin.

157
Q

What is the most common exogenous pigment?

A

carbon (coal dust), a pervasive air pollutant in urban areas. Inhaled carbon interacts with lung macrophages and travels by lymphatic vessels to regional lymph nodes. This accumulation blackens lung tissues and involved lymph nodes.

Other exogenous pigments include mineral dusts containing silica and iron particles, lead, silver salts, and dyes for tattoos.

158
Q

Where does melanin accumulate?

A

accumulates in epithelial cells (keratinocytes) of the skin and retina.

159
Q

What is the function of melanin?

A

it protects the skin against long exposure to sunlight and is an essential factor in the prevention of skin cancer

160
Q

What stimulates syntheses of melanin?

A

Ultraviolet light (e.g., sunlight)

161
Q

What does melanin look like?

A

brown-black pigment

162
Q

Where is melanin derived from?

A

derived from the amino acid tyrosine. Melanocytes synthesize this pigment and melanosomes, membrane-bound cytoplasmic vesicles store it.

163
Q

What is the most essential of the normal endogenous pigment?

A

Hemoproteins

164
Q

What’s included as hemoproteins?

A

hemoglobin and the oxidative enzymes or cytochromes.

165
Q

What can cause hemoprotein accumulation in cells?

A

Excessive storage of iron that transfers from bloodstream to cells

166
Q

How does iron enter blood?

A

(1) tissue stores, (2) the intestinal mucosa (mainly the stomach), and (3) macrophages that remove and destroy dead or defective red blood cells.

167
Q

The amount of iron in the blood plasma depends of what other factor?

A

It depends also on the metabolism of the major iron transport protein, transferrin.

168
Q

What are the 2 forms of iron in tissue cells?

A
  1. Ferritin
  2. when increased levels of iron are present, as hemosiderin.
169
Q

What is hemosiderin?

A

a yellow-brown pigment derived from hemoglobin.

170
Q

What is hemosiderosis

A

is a condition in which excess iron is stored as hemosiderin in the cells of many organs and tissues.

171
Q

What is hemosiderosis common in?

A
  • is common in individuals who have received repeated blood transfusions or prolonged parenteral administration of iron.
  • is also associated with increased absorption of dietary iron, and conditions where iron storage and transport are impaired, as well as hemolytic anemia (when there is excessive breakdown of red blood cells).
  • Excessive alcohol (e.g., wine) ingestion also can lead to hemosiderosis.
172
Q

What is hemochromatosis?

A

(a genetic disorder of iron metabolism and the most severe example of iron overload), are associated with liver and pancreatic cell damage.

173
Q

What is bilirubin?

A

is a normal, yellow-to-green pigment of bile derived from the porphyrin structure of hemoglobin.

174
Q

3 circumstances that can lead to hyperbilirubinemia?

A

(1) mass destruction of red blood cells (erythrocytes), such as in hemolytic jaundice; (2) diseases affecting the metabolism and excretion of bilirubin in the liver; and
(3) diseases that cause obstruction of the common bile duct, such as gallstones or pancreatic tumours. Certain medications (specifically chlorpromazine [Largactil] and other phenothiazine derivatives), estrogenic hormones, and halothane (Fluothane) (an anaesthetic) can cause the obstruction of normal bile flow through the liver.

175
Q

What are the 2 causes that unconjugated bilirubin causes?

A
  1. uncoupling of oxidative phosphorylation and
  2. a loss of cellular proteins.

These two changes could cause structural injury to the various membranes of the cell.

176
Q

What is an important mechanism of cellular calcification?

A

influx of extracellular calcium in injured mitochondria.

177
Q

Pathological calcification can be _______ or ________

A

dystrophic or metastatic

178
Q

Where does dystrophic calcification occur

A

1.occurs in dying and dead tissues in areas of necrosis

179
Q

Where is dystrophic calcification present?

A

It is present in chronic tuberculosis of the lungs and lymph nodes, advanced atherosclerosis (narrowing of the arteries because of plaque accumulation), and heart valve injury, and centre of tumours.

180
Q

What does calcification of heart valve interfere with?

A

interferes with their opening and closing and causes heart murmurs

181
Q

What can predispose arteries to severe narrowing and thrombosis which can lead to MI?

A

Calcification of coronary artery

182
Q

Psammoma bodies

A

Several layers of calcium salts that clump together. They resemble grains of sand.

183
Q

What does metastatic calcification consist of?

A

mineral deposits that occur in undamaged normal tissues as the result of hypercalcemia

184
Q

What are the conditions that can cause hypercalcemia?

A

hyperparathyroidism, toxic levels of vitamin D, hyperthyroidism, idiopathic hypercalcemia of infancy, Addison’s disease (adrenocortical insufficiency), systemic sarcoidosis, milk-alkali syndrome, and the increased bone demineralization that results from bone tumours, leukemia, and disseminated cancers.

185
Q

What is urate?

A

major end product of purine catabolism because of the absence of the enzyme, urate oxidase.

186
Q

What are systemic manifestations of cellular injury?

A
  1. Fever
  2. Increased HR
  3. Leukocytosis
  4. Pain
  5. Presence of cellular enzyme
  6. Lactate dehydrogenase (LDH) (LDH isoenzymes)
  7. Creatine kinase (CK) (CK isoenzymes)
  8. Aspartate aminotransferase (AST/SGOT)
  9. Alanine aminotransferase (ALT/SGPT)
  10. Alkaline phosphatase (ALP)
  11. Amylase
  12. Aldolase

NUR1142 (112 decks)

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