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Pathology > Ch1: Cellular Responses to Stress and Toxic Insults > Flashcards

Ch1: Cellular Responses to Stress and Toxic Insults Flashcards

1
Q

What is pathology?

A

Study of structural, biochemical, and functional changes in cells, tissues, and organs that underlie disease

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2
Q

What does pathology bridge?

A

Basic science and clinical medicine

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3
Q

Two categories of pathology?

A

General

Systemic

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4
Q

4 aspects of a disease

A
  1. Cause
  2. Pathogenesis (how it developed)
  3. Molecular and morphologic changes
  4. Clinical manifestations
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5
Q

If physiological stimuli are altered what happens?

A

Cell adapts

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6
Q

If cell has increased demand and increased stimulation, what can happen? (2)

A

Hyperplasia

Hypertrophy

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7
Q

If there is decreased nutrients and decreased stimulation, what happens?

A

Atrophy

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8
Q

Chronic irritation results in what?

A

Metaplasia

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9
Q

3 ways a cell can be injured?

A
  1. Reduce O2 supply
  2. Chemical injury
  3. Microbial infection
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10
Q

Type of injury if stimulus is acute and transient?

A

Reversible

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11
Q

Type of injury is stimulus is progressive and severe?

A

Irreversible –> Cell death

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12
Q

Cumulative sublethal injury over long time results in what?

A

Cellular aging

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13
Q

What is an adaptation?

A

Reversible functional AND structural response to physiologic and pathologic stresses

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14
Q

Cellular injury occurs if what happens?

A
  1. Limit of adaptations reached
  2. Injurious agents
  3. Nutrition deprivation
  4. Bad mutations
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15
Q

Is cell injury reversible?

A

Yes up to a certain point

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16
Q

Two types of cell death?

A

Necrosis

Apoptosis

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17
Q

When is cell death normal? 3

A
  1. Embryogenesis
  2. Development of organs
  3. Maintenance of homeostasis
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18
Q

Draw the chart for what is necessary for a normal cell to go through injury.

A

-

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19
Q

Besides death, how else can the cell respond to injurious stimuli? 3

A
  1. Intracellular accumulations
  2. Pathologic calcification
  3. Aging
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20
Q

When are intracellular accumulations common?

A

Metabolic derangements in cells and sublethal/chronic injury

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21
Q

What is hypertrophy?

A

Increase in size of cells

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22
Q

What does hypertrophy result in?

A

Increase in size of organ

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23
Q

Increased size in hypertrophy is due to what?

A

Synthesis of more structural components of cells

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24
Q

How is hypertrophy caused? 3)

A
  1. Increased functional demand/workload
  2. Stimulation of hormones and growth factors
  3. Vasoactive agents
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25
Q

The most common stimulus for hypertrophy of muscle is what?

A

Increased workload

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26
Q

When you lift weights, do you undergo hypertrophy or hyperplasia?

A

Hypertrophy

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27
Q

Hypertrophy is the heart is due to what?

A

Chronic hemodynamic overload from hypertension or faulty valves.

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28
Q

An example of hormones causing hypertrophy is where?

A

Gravid Uterus by estrogen hormones

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29
Q

Examples of hypertrophic growth factors? (3)

A

TFG-beta
IGF-1
Fibroblast growth factor

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30
Q

Example of vasoactive hypertrophic agents? 3

A

alpha-adrenergic agonists
endothelin-1
angiotensin II

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31
Q

Which two causes of hypertrophy are more important for pathologic states?

A

Agonists and growth factors

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32
Q

What is an example of a fetal/neonatal contractile protein taking over the adult form and causing hypertrophy?

A

Atrial-natriuretic factor

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33
Q

Where is ANF expressed?

When it’s high abnormally what does it cause?

A

Atrium and ventricle of embryonic heart

Cardiac hypertrophy

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34
Q

What is an example of subcellular organelles undergoing hypertrophy?

A

Smooth ER in hepatocytes hypertrophy due to alcohol and drugs such as barbituates

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35
Q

Hyperplasia is an increase in what?

A

Number of cells thus increasing the mass of organ or tissue

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36
Q

Two categories of physiologic hyperplasia?

A

Hormonal

Compensatory

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37
Q

Hormonal hyperplasia is seen where?

A

Female breast at puberty and pregnancy

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38
Q

Compensatory hyperplasia is seen when? (3)

A
  1. Increase tissue mass after damage
  2. Wound healing
  3. repair of liver
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39
Q

Pathologic hyperplasia is due to what?

A

Excess of hormones or GF’s

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40
Q

Two examples of pathologic hyperplasia?

A
  1. Warts (HPV)

2. Endometrial hyperplasia (BPH)

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41
Q

Hyperplasia results from what? (2)

A
  1. Growth factor driven proliferation of mature cells

2. Increased output of new cells from tissue stem cells

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42
Q

What is atrophy?

A

Reduced size of an organ or tissue resulting from a decrease in cell size and number

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43
Q

Two causes of physiologic atrophy?

A
  1. Atrophy of embryonic structures during normal development

2. Uterus decrease in size after parturition

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44
Q

6 causes of pathologic atrophy?

A
  1. Decreased workload (atrophy of disuse)
  2. Loss of innervation (denervation atrophy)
  3. Ischemia
  4. Inadequate nutrition
  5. Loss of endocrine stimulation
  6. Pressure
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45
Q

The specific change that occurs in atrophy? (2)

A
  1. Decreased protein synthesis in cells

2. Increased protein degradation in cells

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46
Q

Degradation of cellular proteins mainly through what pathway?

A

Ubiquitin-proteasome pathway

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47
Q

Nutrient deficiency and disuse activate what enzymes?
What do these do?
For what purpose?

A

Ubiquitin lipases

Attach ubiquitin to proteins

Once combined, these are targeted for degradation

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48
Q

What might the Ub-Pro pathway contribute to in cancer?

A

Cancer cachexia which is increased erosion of host body cell mass in response to a malignant growth

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49
Q

What is autophagy?

A

Process in which starved cell eats its own components in an attempt to find nutrients and survive

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50
Q

What is metaplasia?

A

Reversible change in which one differentiated cell type is replaced by another cell type

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51
Q

3 types of metaplasia

Which is most common?

A
  1. Columnar to squamous (most common)
  2. Squamous to columnar
  3. CT metaplasia
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52
Q

Where is columnar to squamous metaplasia seen? (2)

A
  1. Respiratory tract with Vitamin A deficiency or smoking

2. Stones in excretory ducts of salivary glands, pancreas, of bile ducts

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53
Q

Why does columnar to squamous metaplasia occur?

A

Sqamous epithelium can survive tougher conditions than fragile columnar epithelium can

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54
Q

What cells change in metaplasia, the actual cells or stem cells?

A

Stem cells

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55
Q

Where is squamous to columnar metaplasia seen?

A

Barrett esophagus which can lead to adenocarcinoma

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56
Q

What is the hallmark sign of barrett esophagus metaplasia?

A

Goblet cells

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57
Q

What is CT metaplasia?

A

Formation of cartilage, bone or adipose tissue in tissues that don’t normally have these

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58
Q

What is bone formation in muscle called?

A

Myositis ossificans

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59
Q

What is CT metaplasia more likely the result of?

A

Cell or tissue injury

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60
Q

Signals that cause stem cells to become metaplasic? 3

A

Cytokines, GF’s, and ECM environments

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61
Q

3 reversible causes of cell injury?

A
  1. Decreased oxidative phosphorylation
  2. Cellular swelling
  3. Alterations in intracellular organelles
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62
Q

What are usually the two components of necrosis?

A
  1. Damage to membranes allows lysosomal enzymes to enter cytoplasm and digest cell with cellular constituents leaking out.
  2. Severe mitochondrial damage with depletion of ATP
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63
Q

What cell type is involved in Necrosis?

A

Neutrophils

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64
Q

What is apoptosis?

A

DNA or protein damaged beyond repair

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65
Q

What is involved in apoptosis? (3)

A
  1. Nuclear dissolution
  2. Fragmentation of cells with complete loss of membrane integrity
  3. Rapid removal of cellular debris
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66
Q

Causes of cell injury and death? (7)

A
  1. oxygen deprivation
  2. physical agents
  3. chemical agents
  4. Infectious agents
  5. Immune reaction
  6. Genetic derangements
  7. Nutritional imbalances
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67
Q

What is hypoxia?

A

Deficiency of oxygen?

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68
Q

Hypoxia results in what?

A

Cell injury by reducing aerobic oxidative respiration

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69
Q

Hypoxia is seen in what instances? (5)

A
  1. ischemia
  2. Cardiorespiratory failure
  3. anemia
  4. CO poisoning
  5. Severe blood loss
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70
Q

Physical agents capable of cell injury and death? (5)

A
  1. Mechanical trauma
  2. Extreme temperatures
  3. pressure changes
  4. Radiation
  5. Electric shock
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71
Q

Examples of chemical agents whose appearance will cause problems? 3

A
  1. Arsenic
  2. Cyanide
  3. Mercuric salts
  4. pollutants
  5. insecticides
  6. herbicides
  7. CO
  8. Asbestos
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72
Q

Example of chemical agents whose high concentrations will cause problems? (3)

A
  1. Glucose
  2. Salt
  3. Therapeutic drugs
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73
Q

Infectious agents that cause cell injury and death include? (5)

A
  1. prions
  2. viruses
  3. bacteria
  4. fungi
  5. parasites
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74
Q

2 immune reactions that will cause cell injury and death?

A
  1. Autoimmunity

2. hypersensitivity reactions

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75
Q

What is down syndrome’s genetic problem?

A

Trisomy 21

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76
Q

Consequences of down syndrome? (3)

A
  1. mental retardation
  2. congenital heart defects
  3. Increased risk of acute leukemia
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77
Q

What is sickle cell anemia’s genetic problem?

A

Single amino acid substition

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78
Q

What are some enzymatic deficiencies that can cause cell injury/death

A
  1. Phenylketonuria
  2. SCID
  3. Tay-sachs
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79
Q

What are 4 nutritional imbalances that will cause cell injury and death?

A
  1. Kwashiorkor
  2. Marasmus
  3. Vitamin deficiency
  4. Obestiy
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80
Q

What is Kwashiorkor?

A

Protein malnourishment

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81
Q

What is Marasmus?

A

Total calorie malnourishment

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82
Q

What is B12 vitamin deficiency called?

One prominent symptom?

A

Pernicious anemia

Peripheral neuropathy

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83
Q

Will folate fix B12 anemia?

A

No.

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84
Q

What is a vitamin C deficiency called?

A

Scurvy

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85
Q

Main consequence of Vitamin C deficiency?

A

Bad collagen

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86
Q

Obesity can result in what disease?

A

Type II diabetes mellitus

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87
Q

How long can it take to see gross changes between the stressor and the morphological reaction to stress?

A

Hours or days

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88
Q

So all in all, what are 9 reversible cell injuries?

A
  1. Depletion of ATP
  2. Swelling of cell and organelles
  3. Blebbing of PM
  4. Detachment of ribosomes from ER
  5. Clumping of chromosomes
  6. Loss of PM integrity
  7. Defects in protein synthesis
  8. Cytoskeletal defects
  9. DNA damage
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89
Q

What causes cell to pass through point of no return from reversible injury to irreversible?

A

Persistent or excessive injury

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90
Q

Two main things you can see under LM of reversible injury?

A
  1. Cellular swelling

2. Fatty change

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91
Q

When does cell swelling occur?

A

When cells are incapable of maintaining ionic and fluid homeostasis

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92
Q

What is fatty change in reversible cell injury?

A

Appearance of lipid vacuoles in cytoplasm

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93
Q

What are ultrastructural changes in reversible cell injury?

A
  1. Plasma membrane alterations (blebbing, blunting, loss of microvilli)
  2. Mitochondrial changes
  3. Dilation of ER
  4. Nuclear alterations
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94
Q

Compare necrosis and apoptosis in terms of cell size?

A

Necrosis: Enlarged (swelling)
Apoptosis: Reduced (shrinkage)

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95
Q

Compare necrosis and apoptosis in terms of nucleus?

A

Necrosis: Pynknosis –> Karyorrhexis –> Karyolysis
Apoptosis: Fragmentation into small fragments

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96
Q

Compare necrosis and apoptosis in terms of PM

A

Necrosis: Disrupted
Apoptosis: Intact; altered structure

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97
Q

Compare necrosis and apoptosis in terms of cellular contents?

A

Necrosis: Enzymatic digestion and may leak
Apoptosis: Intact: may be released in apoptotic bodies

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98
Q

Compare necrosis and apoptosis in terms of adjacent inflammation?

A

Necrosis: Frequent
Apoptosis: None

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99
Q

Compare necrosis and apoptosis in terms of physiologic or pathologic role?

A

Necrosis: Pathologic (result of injury)
Apoptosis: Physiologic usually (unwanted cells)

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100
Q

The morphologic appearance of necrosis is what?

A

Denaturation of intracellular proteins and enzymatic digestion of lethally injured cells

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101
Q

How long does it take for myocardial necrosis to become apparent?

A

4-12 hours

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102
Q

What color are cells in necrosis?

A

Eosinophilic (Red)

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103
Q

What are the three nuclear changes in necrosis?

A
  1. Karylysis
  2. Pyknosis
  3. Karyorrhexis
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104
Q

What is karyolysis

A

Basophilia of chromatin fades

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105
Q

What is pyknosis?

A

Nuclear shrinkage and increased basophilia

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106
Q

What is karyorrhexis?

A

Pyknotic nucleus undergoes fragmentation

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107
Q

What is coagulative necrosis?

A

Localized area in which dead cells have preserved architecture

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108
Q

What may cause coagulative necrosis?

A

Vessel obstruction causing ischemia

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109
Q

What type of necrosis is the wedge shaped infarct in kidneys?

A

Coagulative

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110
Q

What is liquefactive necrosis?

Where is it seen the most?

A

Digestion of dead cells resulting in a liquid viscous mass.

Brain

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111
Q

Liquefactive necrosis is the feature of what?

A
  1. infections

2. hypoxic death of cells in CNS

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112
Q

What is gangrenous necrosis?

A

When blood supply is lost resulting in coagulative necrosis across multiple tissue planes

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113
Q

When bacterial infection combines with gangrenous necrosis what develops?

A

Wet gangrene (more liquefactive)

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114
Q

Caseous necrosis is seen most commonly with what?

A

Tuberculous infections and fungal infections?

115
Q

Fat necrosis normally is caused by what?

A

Acute pancreatitis in which pancreatic enzymes liquefy fat cell membrane

116
Q

Fat necrosis appears in what special manner?

A

Fat saponification (fatty acids combine with calcium)

117
Q

Fibrinoid necrosis is seen in what?

A

Deposition of immune complexes of antigen and antibodies and fibrin into walls of arteries

118
Q

Appearance of fibrinoid necrosis?

A

Bright pink appearance

119
Q

Cellular response to injury depends on what 3 things?

A
  1. nature of injury
  2. duration
  3. severity
120
Q

Consequences of cell injury depend on what 3 things?

A
  1. Type of cells
  2. State of the cell
  3. Adaptability of the cell
121
Q

What can cause depletion of ATP? 3

A
  1. Reduced supply of O2 and nutrients
  2. Mitochondrial damage
  3. chemical injury
122
Q

What is the result of abnormal sodium/potassium ATPase?

A

Cells swelling due to net gain of Na+ and H2O

123
Q

What is result of cells switching to anaerobic glycolysis to make ATP?

A

Accumulation of lactic acid causes pH to drop which decreases some enzymes activity causing nuclear chromatin to clump

124
Q

What is result of cells’ calcium pump failing?

A

Influx of calcium that stimulates cell death

125
Q

What is result of cells’ ER’s detaching ribosomes and resulting protein synthesis failure?

A

Mitochondria and lysosomal membranes become damaged.

126
Q

How much does ATP have to decrease in order to have serious effects?

127
Q

The result of mitochondrial damage is what?

A

Formation of high conductance mitochondrial permeability transition pore

128
Q

The formation of the permeability pore in mitochondria has what effect?

A
  1. Lose normal gradient so decreased ATP

2. Lose sequester proteins in between membranes that will activate apoptosis

129
Q

Two molecules that mitochondria sequester in between their membranes for apoptosis activation upon their release?

A
  1. Cytochrome C

2. Caspases

130
Q

Cytosolic free calcium is maintained at high or low levels?

131
Q

Consequences of increased Calcium ions include?

A
  1. Activate enzymes with bad effects
  2. Opening of mitochondrial permeability transition pore
  3. Induce apoptosis
132
Q

What are some enzymes that calcium can cause the release of? (4)

A
  1. ATPases (ATP)
  2. Phospholipases (PM)
  3. Proteases (PM)
  4. Endonucleases (Nucleus)
133
Q

Free radicals are important in what 4 types of cell damage?

A
  1. Chemical/radiation injury
  2. Ischemia-reperfusion injury
  3. Cellular aging
  4. microbial killing by phagocytes
134
Q

What are free radicals?

A

Chemical species with single unpaired electron in outer orbit

135
Q

Free radicals react with what?

A

Proteins
Lipids
Carbohydrates
Nucleic acids

136
Q

Free radicals initiate what processes?

A

Autocatalytic processes

137
Q

Free radicals react with what types of molecules?

A
  1. Proteins
  2. Lipids
  3. Carbohydrates
  4. Nucleic acids
138
Q

Free radicals initiate what reactions?

A

Autocatalytic processes (what comes in contact with free radicals will turn into free radicals)

139
Q

When are ROS’s produced? 6

A
  1. Mitochondrial respiration and energy generation
  2. Absorption of radiant energy (UV, x rays)
  3. Production of ROS during inflammation
  4. enzymatic metabolism of exogenous chemicals
  5. Transition metals
  6. Nitric oxide
140
Q

ROS are dealt with how?

A

Degraded and removed by cellular defense systems

141
Q

What is it called when ROS overwhelm cell’s scavenging systems?

A

Oxidative stress

142
Q

Oxidative stress is involved in what 4 processes?

A
  1. cell injury
  2. cancer
  3. aging
  4. degenerative disease
143
Q

ROS is produced by what?

A

Leukocytes (neutrophils and macrophages)

144
Q

ROS are used by leukocytes to do what?

A

Destroying microbes, dead tissue, and other unwanted substances

145
Q

Free radicals are inherently stable or unstable?

146
Q

Are free radicals removed enzymatically or nonenzymatically?

147
Q

What are the five ways that free radicals are removed or dealt with?

A
  1. Antioxidants (vitamin a and vitamin E)
  2. Storage and transport proteins for iron and copper
  3. Glutathione peroxidase
  4. Catalase
  5. Superoxide dismutases
148
Q

Free radical damage is seen in what 3 main ways?

A
  1. Lipid peroxidation in membranes
  2. Lesions in DNA
  3. Oxidative modification of proteins
149
Q

Lipid peroxidation results in what?

A

Extensive membrane damage

150
Q

Lesions in DNA due to ROS can cause what? (4)

A
  1. Single or double stranded break
  2. Cross-linking of DNA and formation of adducts
  3. Cell aging
  4. Malignant transformation/cell death
151
Q

Oxidative modification of proteins can result in what? (3)

A
  1. Damage active sites of enzymes
  2. Disrupt conformation of structural proteins
  3. Enhance proteasomal degradation of unfolded or misfolded proteins.
152
Q

What is the main cell injury type that doesn’t have membrane damage?

153
Q

Mechanism of membrane damage include? (5)

A
  1. ROS
  2. Decreased phospholipid synthesis
  3. Increased phospholipid breakdown
  4. Cytoskeletal abnormalities
  5. Bacterial toxins, viral proteins, lytic complement components, and physical/chemical agents
154
Q

Consequence of mitochondrial membrane damage? 2

A
  1. loss of ATP

2. release of proteins that trigger apoptotic death

155
Q

Consequences of PM damage? 2

A
  1. Loss of osmotic balance and influx of fluids/ions

2. Loss of cellular contents

156
Q

Consequence of lysosomal membrane damage?

A

Enzymatic destruction of cell contents

157
Q

Damage to DNA and proteins results in what? 2

A
  1. Accumulation of improperly folded proteins that can trigger apoptosis.
  2. Severe damage can trigger apoptosis
158
Q

Cellular damage becomes irreversible when? 2

A
  1. Inability to reverse mitochondrial dysfunction

2. Profound disturbances in membrane function

159
Q

What is the most common type of cell injury in clinical medicine?

A

Hypoxia/Ischemia

160
Q

What is hypoxia?

A

Reduced oxygen availability

161
Q

What is ischemia?

A

Supply of oxygen and nutrients is decreased

162
Q

Ischemia most often occurs because of what?

A

Reduced blood flow as a result of mechanical obstruction

163
Q

Which damages faster and more severely, hypoxia or ischemia?

164
Q

What IC enzymes and proteins are leaked during ischemic/hypoxic injury? (2)

A

CK-MB

Troponin

165
Q

What is the mammalian adaptation to ischemic/hypoxic injury?

A

Hypoxia-Inducible Factor-1

166
Q

What does HIF-1 do? (3)

A

Promotes angiogenesis
Stimulates cell survival pathways
Enhances anaerobic glycolysis

167
Q

What is the therapeutic approach to reduce hypoxic/ischemic injury in brain and spinal cord injury?

A

Transient hypothermia

168
Q

Results of transient hypothermia? 2

A
  1. Decreases metabolic demands, cell swelling, and free radicals
  2. Inhibits host inflammation
169
Q

What is iscehmia-reperfusion injury?

A

When blood flow is restored to cells that have been ischemic but not died, the injury is exacerbated because so much O2 overwhelms the cell and results in ROS forming that damage the cell

170
Q

What new damaging processes are started in reperfusion injury? (4)

A
  1. Increased ROS and nitrogen
  2. Calcium can enter
  3. Inflammation from cytokines and expression of adhesion molecules
  4. Activation of complement system
171
Q

Mercuric chloride attacks what organs? (2)

A

GI and kidney

172
Q

Toxic metabolites are formed by what enzymes?

A

Cytochrome p-450 oxidases

173
Q

Acetaminophen is converted into what toxic metabolite?

174
Q

What is added to NAPQI to make it nontoxic?

A

N-acetyl-cysteine (glutathione)

175
Q

Too much acetaminophen results in what?

A

Liver necrosis

176
Q

Apoptosis is defined how?

A

Pathway of cell death that is induced by tightly regulated suicide program

177
Q

What do cells break into during apoptosis?

A

Apoptotic bodies

178
Q

Forming apoptotic bodies limits what?

A

Inflammatory response

179
Q

Apoptosis is physiologic in what processes? 5

A
  1. Embryogenesis
  2. Involution of hormone-dependent tissue after hormone withdrawal
  3. Cell loss in proliferating cell populations (lymphocytes)
  4. Elimination of self-reactive lymphocytes
  5. Death of host cells that have run their course
180
Q

Minor DNA damage results in what?

181
Q

Large amounts of DNA damage will result in what?

182
Q

Excessiv eaccumulation of misfolded proteins leads to what?

A

ER stress and apoptosis

183
Q

What types of viruses can cause apoptosis? 3

A
  1. Adenovirus
  2. HIV
  3. viral hepatitis
184
Q

Apoptosis occurs in parenchymal organs (pancreas, parotid, kidney) following what?

A

Duct obstruction

185
Q

4 morphological changes in apoptosis?

A
  1. cell shrinkage
  2. chromatin condensation
  3. cytoplasmic blebs and apoptotic bodies
  4. phagocytosis of apoptotic bodies
186
Q

3 biochemical features of apoptosis?

A

Activation of caspases
DNA and protein breakdown
Membrane alterations and recognition by phagocytes

187
Q

What do caspases do?

A

Initiate or execute apoptosis

188
Q

What membrane alterations take place in apoptosis?

A

Movement of phosphatidylserine from inner leaflet to outer

189
Q

What are the two pathways of apoptosis?

A
  1. Intrinsic (mitochondrial) pathway

2. Extrinsic (death receptor-initiated)

190
Q

What is the major apoptotic pathway in mammals?

A

Intrinsic pathway

191
Q

Intrinsic pathway of apoptosis is the result of what? (2)

A
  1. Increased mitochondrial permeability

2. Release of pro-apoptotic molecules

192
Q

Release of mitochondrial proteins in apoptosis is controlled by what?

A

Balance between pro-and anti-apoptotic members of the Bcl family of protein

193
Q

What are the three anti-apoptotic Bcl proteins? (3)

A

Bcl-2
Bcl-X
Mcl-1

194
Q

Problems with Bcl-2 result in what?

A

Follicular lymphoma (lymph don’t die)

195
Q

Where are the anti-apoptotic proteins found?

A

Cytoplasm and mitochondrial membranes

196
Q

The anti-apoptotic proteins control what?

A

Membrane permeability so prevent leakage of mitochondrial proteins that trigger cell death.

197
Q

Pro-apoptotic proteins include what? 3

A
  1. Bim
  2. Bid
  3. Bad
198
Q

The pro-apoptotic proteins activate what?

A

Bax and Bak

199
Q

Bax and Bak proteins do what?

A

Form channels in mitochondrial membrane

200
Q

The net result of Bax-Bak activation and loss of antiapoptotic proteins is what?

A

Activation of the caspase cascade

201
Q

How is caspase-9 activated?

A

Cytochrome c is released and binds to Apoptosis-activating factor-1) forming apoptosome

202
Q

What is the function of Smac/DIABLO in apoptosis?

A

Enter cytoplasm and neutralize physiologic inhibitors of apoptosis (IAP’s)

203
Q

The extrinsic pathway of apoptosis involves what?

A

Engagement of plasma membrane death receptors (TNF receptor family)

204
Q

Examples of receptors in extrinsic apoptosis? (2)

A
  1. Type 1 TNF (TNFR1)

2. Fas (CD95)

205
Q

The fas ligand is expressed where?

A

T-cells that recognize self-antigens and cytotoxic T-lymphocytes?

206
Q

How many Fas are required to form a Fas-associated death domain?

207
Q

The FADD will activate what?

208
Q

Extrinsic pathway of apoptosis can be inhibited how?

A

FLIP which binds to pro-caspase-8

209
Q

How do some viruses block extrinsic apoptosis of infected cell?

A

Produce FLIP

210
Q

Execution phase of apoptosis uses what enzymes?

Which act on what?

A

Caspase 3 and 6

Cellular components

211
Q

Execution phase involves what processes?

A
  1. Increased DNAase activity
  2. Fragmentation of nuclei
  3. FOrmation of membrane blebs/apoptotic bodies
212
Q

Dead cells signal their removal how? 2

A
  1. Release factors that recruit phagocytes

2. Coat with natural antibodies and complement

213
Q

DNA damage apoptosis involves what gene?

A

Tumor suppressor p53

214
Q

Protein misfolding is seen in what diseases? 4

A
  1. Alzheimer’s
  2. Huntington’s
  3. Parkinson’s
  4. Type II DM
215
Q

Apoptosis induced by TNF receptor family is seen in what instance?

A

ELimination of self-reactive lymphocytes

216
Q

Cytotoxic T-lymphocyte-mediated apoptosis is seen in what instance?

A

Cytotoxic-T lymphocytes recognizing foreign antigens presented on infected host cells

217
Q

If cell is injured, what does p53 do?

A

Directs repair or apoptosis

218
Q

What happens in cell with mutated/absent p53?

A

Even with damaged DNA, the cell will survive.

219
Q

The most common genetic abnormality in human cancers is what?

A

P53 mutation

220
Q

What do chaperones do?

A

Control proper protein folding

221
Q

What happens if chaperones get overwhelmed?

222
Q

Disorders associated with defective apoptosis are? (2)

A
  1. Cancer

2. autoimmune disorders

223
Q

Disorders associated with increased apoptosis and excessive cell death? (3)

A
  1. Neurodegenerative disease
  2. Ischemic injury
  3. Death of virus-infected cells
224
Q

Autophagy is done how?

A

Organelles and cytosol are sequestered in an autophagic vacuole and fused with lysosomes to form an autophagolysosome

225
Q

Intracellular accumulations are the manifestation of what?

A

Metabolic derangement

226
Q

4 types of intracellular acumulations?

Example of each

A
  1. Inadequate metabolism of normal substance (fatty liver)
  2. Production and accumulation of abnormal endogenous substance (alpha-1 anti-trypsin)
  3. Defective metabolism of endogenous substance (lysosomal storage disease)
  4. Abnormal exogenous substance accumulates (carbon in macrophage)
227
Q

What is steatosis?

A

Abnormal accumulations of triglycerides in parenchymal cells

228
Q

Where does steatosis occur the most?

229
Q

Causes of steatosis? (5)

A
  1. Toxins
  2. Protein malnutrition
  3. DM
  4. Obesity
  5. Anoxia
230
Q

Main cause of fatty liver disease in developed nations? 2

A

Alcohol abuse

Nonalcoholic fatty liver disease

231
Q

What are 3 causes of fatty liver?

A
  1. Excessive entry of lipids
  2. Defective metabolism of lipids
  3. Defective export of lipids
232
Q

Is fatty liver reversible?

233
Q

What is the Tigered effect?

A

Bands of yellow myocardium alternating with bands of darker uninvolved heart

234
Q

What are atherosclerotic plaques?

A

Smooth muscle cells and macrophages in intimal layer of aorta and large arteries are filled with lipid vacuoles from cholesterol to form atheromas

235
Q

What is a Xanthoma?

A

Intracellular accumulation of cholesterol within macrophages to form clusters of foamy cells in subepithelial CT tissue of skin and tendons

236
Q

Are xanthomas acquired or hereditary?

237
Q

What is Niemann-Pick disease, type C?

A

Lysosomal storage disease due to defective transport of cholesterol between cells

238
Q

Where is the genetic mutation for Niemann-Pick type C?

A

NPC-1 gene on chromosome 18.

239
Q

Niemann-Pick disease type C results in what?

A

Brain tissue damage

240
Q

What is proteinuria?

A

Reabsorption droplets in proximal renal tubule of protein

241
Q

Example of intracellular transport and secretion of critical proteins defect?

A

Alpha1 antitrypsin deficiency

242
Q

Examples of accumulation of cytoskeletal proteins? (2)

A
  1. Alcoholic hyaline

2. Neurofibrillary tangles

243
Q

Example of aggregation of abnormal proteins?

A

Amyloidosis

244
Q

Intranuclear inclusions are known as what?

A

Dutcher bodies

245
Q

Russell bodies are what?

A

Excessive protein in plasma cells

246
Q

Alpha-1 antitrypsin cytoplasmic inclusions are described as how?

A

Panacinar emphysema

247
Q

An alcoholic hyaline liver has what inclusions?

A

Mallory bodies

248
Q

Mallory bodies are of what?

A

Intemediate filament accumulations

249
Q

Glycogen is stored where?

A

Cytoplasm of healthy cells

250
Q

Excessive intracellular deposits of glycogen are seen in what?

A

Patients with abnormality of glucose or glycogen such as Diabetes or glycogen storage diseases

251
Q

What is most common exogenous pigment?

A

Carbon (coal dust)

252
Q

What is the effect of carbon on the lung?

A

Anthracosis (blackens the tissue)

253
Q

What might happen to coal miners?

A

Aggregates of carbon dust induce fibroblastic reaction or emphysema

254
Q

For a tattoo, where do the pigments go?

A

Phagocytosed by dermal macrophages

255
Q

Color of lipofuscin?

A

Yellow-brown

256
Q

Release of lipofuscin indicates what?

A

Free Radical injury

257
Q

Melanin is formed when?

A

Tyrosinase catalyzes oxidation of tyrosine to dihydroxyphenylalanine in melanocytes

258
Q

Hemosiderin is derived from where?

Color?

A

Hemoglobin

Golden-brown

259
Q

Hemosiderin does what?

A

Stores iron

260
Q

Local excesses of hemosiderin result in what?

A

Hemorrhages in tissue

261
Q

WHat is hemosiderosis?

A

Hemosiderin being deposited in many organs

262
Q

What is hemochromatosis?

A

Excessive iron accumulation

263
Q

Hemochromatosis is what type of disease?

A

Autosomal recessive (HFE gene on chromosome 6)

264
Q

Hemochromatosis can lead to what?

A

Diabetes mellitus and skin pigmentation (Bronze diabetes)

265
Q

What are the heart failure cells?

A

Pulmonary alveolar macrophages with hemosiderin granules

266
Q

What is bilirubin derived from?

267
Q

Excess bilirubin results in what?

268
Q

What is dystrophic calcification?

A

Normal serum calcium but calcification that occurs in dead/dying tissues

269
Q

What is a metastatic calcification?

A

Hypercalcemia in normal tissues

270
Q

Which of the two types of calcification can cause dysfunction of organs?

A

Dystrophic (aortic stenosis)

271
Q

Metastatic calcification is the result of what?

A

Increased production of PTH

272
Q

Causes of metastatic calcification? (3)

A
  1. Destruction of bone
  2. Vitamin D-related disorders
  3. Renal failure with phosphate retention
273
Q

Metastatic calcification can be caused by destruction of bone. What are three examples of this?

A
  1. Paget disease
  2. Tumor
  3. Immobilization
274
Q

Which vitamin D-related disorder can result in metastatic calcification?

A

Sarcoidosis

275
Q

Cellular aging is the result of what?

A

Progressive decline in cellular function and viability caused by genetic abnormalities and the accumulation of cellular and molecular damage due to the effects of exposure to exogenous influences

276
Q

What is the nondividing state of cells called?

A

Senescence

277
Q

What enzyme is not see at all in senescent cells?

A

Telomerase

278
Q

Where is the cause of Werner syndrome?

What do these patients show?

A

DNA helicase mutation

Premature aging

279
Q

What happens in ataxia-telangiectasia?

A

Mutated gene encodes a protein involved in repairing double-strand breaks in DNA.

280
Q

What is Progeria caused by?

Result?

A

Mutation in LMNA gene

Accelerated aging

281
Q

What does LMNA gene produce?

Function of this?

A

Lamin A protein

Structural scaffolding that holds nucleus of cell together

282
Q

Do progeria patients have normal mental development?

When do they die?

A

Yes

Die before age 20 of strokes and heart attacks

283
Q

Most effective way of prolonging life span is what?

A

Calorie restriction

284
Q

What mediates the calorie-aging relatinoship?

A

Proteins called sirtuins

Pathology (36 decks)

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