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MOD Exam 1 > Ch. 2: Cellular Responses to Stress > Flashcards

Ch. 2: Cellular Responses to Stress Flashcards

1
Q

4 aspects of a disease process

A
  1. Etiology (Cause)
  2. Pathogenesis (development)
  3. Morphological changes (structural)
  4. Clinical Manifestations (functional)
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2
Q

What defines the function of a cell?

A

Structure and function determined by metabolism, differentiation, neighboring cells, & availability of metabolic substrates

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3
Q

Hypertrophy

A

an increase in size of cells in response to increased demand/workload

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4
Q

Define the major triggers for physiologic hypertrophy

A

Mechanical sensors triggered by workload

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5
Q

Define the major triggers for pathologic hypertrophy

A 
agonists
growth factors (TGF-B, IGF-1, FGF)
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6
Q

2 pathways involved in muscular hypertrophy

A
  1. PI3K/AKT (physiologic)

2. GPCR (pathologic)

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7
Q

Hyperplasia

A

increase in number of cells in an organ or tissue in response to stimulus.
Can only take place if the tissue cells are capable of division

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8
Q

Physiologic Hyperplasia

A

hormone or growth factor induced.
Response to a need for increased functional capacity or compensatory damage/resection.
Examples: Nephrectomy, female breast growth

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9
Q

Pathologic Hyperplasia

A

excessive/inappropriate actions of hormones on target cells

Example: BPH, Endometrial hyperplasia

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10
Q

Atrophy

A

reduction in size of tissue/organ due to decreased size & number of cells.

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11
Q

Common causes of atrophy (6)

A
  1. Decreased Workload (atrophy of disuse)
  2. Loss of Innervation (denervation atrophy)
  3. Diminished blood supply
  4. Inadequate nutrition
  5. Loss of Endocrine Stimulation
  6. Pressure
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12
Q

Senile Atrophy

A

brain undergoes progressive atrophy due to reduced blood supply a result of atherosclerosis

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13
Q

4 Adaptations of Cellular Growth & Differentiation

A
  1. Hypertrophy
  2. Hyperplasia
  3. Atrophy
  4. Metaplasia
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14
Q

Autophagy

A

process in which starved cells eat their own components to reduce nutrient demand to match supply

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15
Q

Metaplasia

A

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

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16
Q

What is the most common epithelial metaplasia?

A

columnar to squamous as in the respiratory tract in response to smoking

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17
Q

7 Causes of Cell Injury

A
  1. O2 deprivation
  2. Physical Agents
  3. Chemical Agents
  4. Infectious Agents
  5. Immunological Rxns
  6. Genetic Derangments
  7. Nutritional Imbalance
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18
Q

4 causes of hypoxia

A
  1. Ischemia
  2. cardiorespiratory failure
  3. decreased O2 carrying capacity
  4. Blood loss
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19
Q

Physical Agents that can cause cell injury

A
  1. Mechanical Trauma
  2. Extreme Temperature
  3. Radiation
  4. Electric shock
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20
Q

Chemical Agents causing cell injury

A

Environmental/Air pollutants
insecticides
carbon monoxide

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21
Q

How can genetic derangements cause cell injury?

A

deficiency of PRO’s
accumulation of damaged DNA/misfolded proteins
Sequence variants

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22
Q

What are hallmark signs of reversible cell injury?

A

Cell Swelling

Fatty Change

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23
Q

Features associated with Necrosis

A

Swelling
Pyknosis, Karyorrhexis, karyolysis
adjacent inflammation
damaged cellular membranes

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24
Q

Morphology of necrosis

A
  1. Increased Eosinophilia (Pink)
  2. Myelin figures
  3. Nuclear changes (PKK)
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25
Q

Karyolysis

A

Fading of basophilic chromatin

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26
Q

Pyknosis

A

Nuclear shrinkage and increased basophilia

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27
Q

Karyorrhexis

A

Fragmentation of Pyknotic nucleus

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28
Q

Coagulative Necrosis

A

Architecture of dead tissues is preserved for some days.

  • Tissue exhibits firm texture
  • Most common cause is Ischemia (except for brain)
  • Causes Infarct of tissue
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29
Q

Liquefactive Necrosis

A

Digestion of the dead cells that results in a liquid viscous mass.

  • Focal bacterial, fungal infections.
  • Pus
  • Often seen in Hypoxic death of CNS cells
30
Q

Gangrenous Necrosis

A

NOT a specific pattern, but applied clinically to describe loss of blood supply in a limb that has undergone necrosis and has bacterial infection

31
Q

Caseous Necrosis

A

“Cheese-like”
Most often found in TB infection
Structureless collection of lysed cells
Granuloma formation

32
Q

Fat Necrosis

A

Focal areas of fat destruction typically from release of activated pancreatic lipase into pancreas or peritoneal cavity

  • Acute Pancreatitis
  • Produces chalky white areas due to FAT SAPONIFICATION (FA + Ca)
33
Q

Fibrinoid Necrosis

A

Usually seen in immune reactions with blood vessels.

  • Ag-Ab complexes are deposited in the vessel walls with fibrin
  • Bright pink and amorphous on H&E
34
Q

What happens if necrotic cells are not removed by phagocytosis and enzymatic digestion?

A

Dystrophic Calcification

35
Q

What is the fundamental cause of necrotic cell death?

A

ATP depletion due to hypoxia, malnutrition, and mitochondrial damage

36
Q

Effects of ATP depletion

A
  1. Decreased Na/K Pump
  2. Anaerobic Glycolysis & increased LA
  3. Influx of Ca
  4. Reduced Protein synthesis
  5. Unfolded protein response
37
Q

Mitochondrial permeability transition pore

A

Influx of Ca leads to increased mitochondrial permeability and loss of membrane potential.
Target for Cyclosporin to treat GVHD

38
Q

Oxidative Stress

A

Abnormal production or scavenging of ROS that leads to accumulation within the cell

39
Q

What is the most reactive ROS and what is it’s effect?

A

OH

- Damages lipids, proteins, and DNA

40
Q

Mechanisms to remove free radicals

A
  1. Antioxidants (Vit E, A)
  2. Prevention of formation (sequestering transition metals)
  3. Catalase, SOD, Glutathione Peroxidase
41
Q

Pathologic effects of free radicals

A
  1. Lipid Peroxidation- breaking of DB’s to form peroxides
  2. Protein modification
  3. DNA lesions
42
Q

3 most important sites of membrane damage

A
  1. Mitochondrial
  2. Plasma Membrane
  3. Lysosome
43
Q

2 consistent markers of irreversible damage

A
  1. Inability to reverse mitochondrial dysfunction

2. Profound membrane disturbance

44
Q

Examples of proteins that can be detected in blood that would indicate damaged cells

A
  1. Heart- CK & Troponin
  2. Liver Bile ducts- alkaline phosphatase
  3. Liver hepatocytes- Transaminases (ALT AST)
45
Q

Hypoxia-inducible factor-1

A

Promotes new blood vessel formation
Stimulates survival pathways
Enhances Anaerobic glycolysis

46
Q

Ischemia-reperfusion injury

A

Restoration of blood flow to ischemic tissues can exacerbate injury and cell death due to:

  • Oxidative stress (ROS)
  • Ca overload
  • Inflammation
  • Compliment activation (IgM)
47
Q

Examples of Physiological Apoptosis

A
  1. Embryogenesis
  2. Involution of hormone-dependent tissues
  3. Proliferative cell loss
  4. Self-reactive lymphocytes
48
Q

Pathologic Apoptosis

A
  1. DNA damage
  2. Misfolded Proteins
  3. Infection
  4. Pathologic atrophy due to duct obstructions
49
Q

Intrinsic Pathway of Apoptosis

A

Increased permeability of the OMM releases cytochrome C which binds with APAF-1 to form Apoptosome.
Apoptosome binds Cas-9 which activates Cas-3

50
Q

BCL2 Family

A

family of proteins involved in regulation of intrinsic apoptosis.

  • Anti-apoptotic: BCL2, BCL-XL, MCL1
  • Pro-apoptotic: BAX, BAK
51
Q

Extrinsic Pathway of Apoptosis

A

TNFR1 & Fas (CD95)

  • Binds to ligand expressed on CTLs which converge and bind FADD.
  • FADD binds Cas-8 which activates executioner caspases.
  • Inhibited by FLIP
52
Q

Examples of cells that die by intrinsic pathway

A

Hormone-sensitive cells
Lymphocytes
Neurons

53
Q

Role of p53

A

Arrests cell cycle at G1 phase for repair

If damage is too great then it activates apoptosis

54
Q

Unfolded protein response

A

Accumulation of unfolded proteins in ER results in:

  • decreased synthesis
  • Increased chaperones
  • Increased proteosomal degradation
55
Q

ER Stress

A

Accumulation of misfolded proteins above threshold results in apoptosis

56
Q

Diseases caused by misfolded proteins

A
  1. CF
  2. FHC
  3. a-1-antitrypsin deficiency
  4. Creutzfeldt-Jacob
  5. Alzheimers
57
Q

Necroptosis

A

Mechanistically apoptosis, Morphologically Necrosis

  • Involves RIP1 and RIP3
  • Caspase-independent
58
Q

Autophagy

A

Process of cell eating itself to preserve nutrients

  • Chaperone-mediated
  • Microautophagy
  • Macroautophagy (most common)
59
Q

LC3

A

Useful marker of identifying cells in autophagy

- Targets protein aggregates and organelles marked for death

60
Q

Steatosis

A

abnormal accumulation of TAGs in parenchymal cells

61
Q

Xanthomas

A

Aggregations of foam cells formed by atherosclerosis found in skin and tendons

62
Q

Cholesterolosis

A

accumulation of cholesterol filled macrophages in LP of GB

63
Q

Russell Bodies

A

Homogenous eosinophilic inclusions caused by accumulation of proteins in ER.

64
Q

Most common exogenous pigment and name for its deposition in lung tissue

A

Carbon (Coal Dust)

Anthracosis

65
Q

Endogenous Pigments

A

Lipofuscin (wear-and-tear pigment)
Melanin
Hemosiderin

66
Q

Causes of Hemosiderosis

A
  1. Hemochromatosis
  2. Hemolytic Anemia
  3. Blood transfusions
67
Q

Dystrophic Calcification

A

Encountered in areas of necrosis
Seen in aging of heart valves and atherosclerosis
Formation of PSAMMOMA bodies

68
Q

Metastatic Calcification

A

Occurs in normal tissue due to hypercalcemia

69
Q

Werner Syndrome

A

Premature aging due to DNA Helicase deficiency

70
Q

Blood Syndrome & AT

A

Increased rate of aging due to mutated DNA repair proteins

71
Q

p16 (INK4A)

A

Tumor Suppressor involved in chronological aging by controlling G1/S phase of cell cycle

MOD Exam 1 (5 decks)

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