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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
Karyolysis
Fading of basophilic chromatin
26
Pyknosis
Nuclear shrinkage and increased basophilia
27
Karyorrhexis
Fragmentation of Pyknotic nucleus
28
Coagulative Necrosis
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
29
Liquefactive Necrosis
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
Gangrenous Necrosis
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
Caseous Necrosis
"Cheese-like" Most often found in TB infection Structureless collection of lysed cells Granuloma formation
32
Fat Necrosis
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
Fibrinoid Necrosis
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
What happens if necrotic cells are not removed by phagocytosis and enzymatic digestion?
Dystrophic Calcification
35
What is the fundamental cause of necrotic cell death?
ATP depletion due to hypoxia, malnutrition, and mitochondrial damage
36
Effects of ATP depletion
1. Decreased Na/K Pump 2. Anaerobic Glycolysis & increased LA 3. Influx of Ca 4. Reduced Protein synthesis 5. Unfolded protein response
37
Mitochondrial permeability transition pore
Influx of Ca leads to increased mitochondrial permeability and loss of membrane potential. Target for Cyclosporin to treat GVHD
38
Oxidative Stress
Abnormal production or scavenging of ROS that leads to accumulation within the cell
39
What is the most reactive ROS and what is it's effect?
OH | - Damages lipids, proteins, and DNA
40
Mechanisms to remove free radicals
1. Antioxidants (Vit E, A) 2. Prevention of formation (sequestering transition metals) 3. Catalase, SOD, Glutathione Peroxidase
41
Pathologic effects of free radicals
1. Lipid Peroxidation- breaking of DB's to form peroxides 2. Protein modification 3. DNA lesions
42
3 most important sites of membrane damage
1. Mitochondrial 2. Plasma Membrane 3. Lysosome
43
2 consistent markers of irreversible damage
1. Inability to reverse mitochondrial dysfunction | 2. Profound membrane disturbance
44
Examples of proteins that can be detected in blood that would indicate damaged cells
1. Heart- CK & Troponin 2. Liver Bile ducts- alkaline phosphatase 3. Liver hepatocytes- Transaminases (ALT AST)
45
Hypoxia-inducible factor-1
Promotes new blood vessel formation Stimulates survival pathways Enhances Anaerobic glycolysis
46
Ischemia-reperfusion injury
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
Examples of Physiological Apoptosis
1. Embryogenesis 2. Involution of hormone-dependent tissues 3. Proliferative cell loss 4. Self-reactive lymphocytes
48
Pathologic Apoptosis
1. DNA damage 2. Misfolded Proteins 3. Infection 4. Pathologic atrophy due to duct obstructions
49
Intrinsic Pathway of Apoptosis
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
BCL2 Family
family of proteins involved in regulation of intrinsic apoptosis. - Anti-apoptotic: BCL2, BCL-XL, MCL1 - Pro-apoptotic: BAX, BAK
51
Extrinsic Pathway of Apoptosis
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
Examples of cells that die by intrinsic pathway
Hormone-sensitive cells Lymphocytes Neurons
53
Role of p53
Arrests cell cycle at G1 phase for repair | If damage is too great then it activates apoptosis
54
Unfolded protein response
Accumulation of unfolded proteins in ER results in: - decreased synthesis - Increased chaperones - Increased proteosomal degradation
55
ER Stress
Accumulation of misfolded proteins above threshold results in apoptosis
56
Diseases caused by misfolded proteins
1. CF 2. FHC 3. a-1-antitrypsin deficiency 4. Creutzfeldt-Jacob 5. Alzheimers
57
Necroptosis
Mechanistically apoptosis, Morphologically Necrosis - Involves RIP1 and RIP3 - Caspase-independent
58
Autophagy
Process of cell eating itself to preserve nutrients - Chaperone-mediated - Microautophagy - Macroautophagy (most common)
59
LC3
Useful marker of identifying cells in autophagy | - Targets protein aggregates and organelles marked for death
60
Steatosis
abnormal accumulation of TAGs in parenchymal cells
61
Xanthomas
Aggregations of foam cells formed by atherosclerosis found in skin and tendons
62
Cholesterolosis
accumulation of cholesterol filled macrophages in LP of GB
63
Russell Bodies
Homogenous eosinophilic inclusions caused by accumulation of proteins in ER.
64
Most common exogenous pigment and name for its deposition in lung tissue
Carbon (Coal Dust) | Anthracosis
65
Endogenous Pigments
Lipofuscin (wear-and-tear pigment) Melanin Hemosiderin
66
Causes of Hemosiderosis
1. Hemochromatosis 2. Hemolytic Anemia 3. Blood transfusions
67
Dystrophic Calcification
Encountered in areas of necrosis Seen in aging of heart valves and atherosclerosis Formation of PSAMMOMA bodies
68
Metastatic Calcification
Occurs in normal tissue due to hypercalcemia
69
Werner Syndrome
Premature aging due to DNA Helicase deficiency
70
Blood Syndrome & AT
Increased rate of aging due to mutated DNA repair proteins
71
p16 (INK4A)
Tumor Suppressor involved in chronological aging by controlling G1/S phase of cell cycle

MOD Exam 1 (5 decks)

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