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Pathology > Test 1: 02-03 Cell Injury and Death version 2 > Flashcards

Test 1: 02-03 Cell Injury and Death version 2 Flashcards

1
Q
  1. Give 7 causes of cellular injury
A

i. Hypoxia<br></br>
ii. Chemical injury<br></br>
iii. Physical injury <br></br>
iv. Infections <br></br>
v. Immunological reactions<br></br>
vi. Genetic disorders<br></br>
vii. Nutritional/vitamin disorders <br></br>

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2
Q
  1. What is hypoxia and what does it lead to? <br></br>What are 4 consequences?
A

Reduced/lack of oxygen.
<br></br>
Leads to inability of cell to maintain energy in ATP form
<br></br>
Consequences include:
<br></br>
i. No E for NaK pump -> cell swelling (osmotic gradient)
<br></br>
ii. No energy for Ca++ -> intracellular Ca -> activate enzymes (Mb damage)
<br></br>
iii. Chromatin clumping (DNA damage)
<br></br>
iv. Detached Ribosomes – monosomes -> decreased protein Synthesis (housekeeping proteins)

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3
Q
  1. Oxidative stress is? <br></br>Caused by? <br></br>What do these alter?
A

Oxidative stress is the accumulation of damage caused by oxygen-derived free radicals<br></br>
Free radicals are highly reactive and form bonds that alter the structure of proteins, nucleic acids, and lipids

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4
Q
  1. Major mechanisms of free radical damage in cells is lipid peroxidation of membranes<br></br>
    What is attacked?<br></br>
    What is formed?<br></br>
    What does this formed thing react with?<br></br>
A

Double bonds of unsaturated fatty acids are attacked by <br></br>oxygen-derived free radicals.<br></br>
Peroxides are formed
<br></br> The peroxides are unstable and they react with membrane lipids to both damage them and to form more peroxides.

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5
Q
  1. Give 4 free radical scavengers/antioxidants
A

i. Vitamin E<br></br>
ii. Vitamine A <br></br>
iii. Vitamin C <br></br>
iv. β carotene<br></br>

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6
Q
  1. What are the 3 major mechanisms of free radical damage in cells: Oxidation of Proteins?
A

Oxidation of side chains changes function/structure of proteins<br></br>
Oxidation of some enzymes will inactivate them<br></br>
Formation of disulfide bonds leads to cross-linking

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7
Q
  1. What 3 Major mechanisms of free radical damage in cells: DNA damage?
A

Free radical interaction with thymine causes single-stranded breaks in DNA<br></br>
Single-stranded breaks in DNA and free radicals causing mutations have also shown been implicated in carcinogenesis.<br></br>
Also has been implicated as one cause of cellular aging

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8
Q
  1. What does the Mechanisms of Cell Injury: Defects in membrane permeability do? (2)
A

Damage to membrane permeability causes activation of phospholipases in cytosol <br></br>
Lack of ATP prevents reacylation of phospholipids and diminishes synthesis so that the cell membrane can’t repair itself

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9
Q
  1. Compare necrosis and apoptosis
A

Necrosis – cell death resulting form either exogenous or endogenous damage. Eventual damage to membrane results in leaking cellular contents.<br></br><br></br>
Apoptosis – programmed cell death can be result of external or internal cell damage, physiologic, or developmental. Results in cell fragmentation and phagocytosis.

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10
Q
  1. In necrosis what is not required? <br></br>Cytoplasmic changes are? <br></br>Nuclear changes include?
A

a. Necrosis refers to cell death that is not controlled by the cell and does not require the signals or activation of genes<br></br>
b. Cytoplasmic changes - eosinophilia, glassy appearance, vacuolation<br></br>
c. Nuclear changes – pyknosis, karyorrhexis, karyolysis<br></br>

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11
Q
  1. What are 6 types of necrosis?
A

i. Coagulative<br></br>
ii. Liquefactive<br></br>
iii. Caseous<br></br>
iv. Enzymatic Fat<br></br>
v. Fibrinoid <br></br>
vi. Gangrenous<br></br>

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12
Q
  1. Give three instances where coagulative necrosis is seen?<br></br>
    Exception?<br></br>
    Appearance?<br></br>
A

a. Usually seen in death due to ischemia, hypoxia, reperfusion injury<br></br>
b. Brain<br></br>
c. Basic outline of cell preserved but with no nuclei (ghost like)<br></br>

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13
Q
  1. What leads to liquefactive necrosis and why?<br></br>
    Seen in?<br></br>
    Microscopically appears?<br></br>
A

a. Death of brain tissue usually leads to liquefactive necrosis because of lack of supporting connective tissue<br></br>
b. Seen in abscess where the center is made up of enzymatic digested neutrophils (pus)<br></br>
c. Amorphous, granular under the microscope. Loss of cells and tissue structure

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14
Q
  1. What happens in caseous necrosis

<br></br> Caseous necrosis appears?

A

Accumulation of mononuclear cells that mediate the chronic inflammatory reaction and granuloma formation to the offending organism. The lipid in the wall of the organism can’t be fully broken down. The dead cells persist indefinitely as amorphous, coarsely granular, eosinophilic debris<br></br>
Grossly is grayish, whitish or yellowish, soft, friable and cheesy in appearance
<br></br>

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15
Q
  1. What happens in Enzymatic Fat Necrosis? <br></br>
    Appearance?<br></br>
    Microscopically appears? <br></br>
    What would it appear histologically and why?<br></br>
A

a. Fat is changed due to action of lipases. The fatty acids that are released react with calcium to form soap-like substance<br></br>
b. Grossly looks white, chalky<br></br>
c. Microscopic appearance shows material in fat cells rather than the normal clear appearance. <br></br>
d. If there is enough calcium, the deposits will be basophilic<br></br>

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16
Q
  1. What happens in Fibrinoid necrosis? <br></br>Stains?<br></br>
A

Injury in blood vessels with accumulation of plasma proteins causing the wall to stain intensely eosinophilic

17
Q
  1. When/where does Gangrenous Necrosis (gangrene) occur? <br></br>
    What is wet gangrene?
A

a. Usually applied to a limb that has died because of loss of circulation; also applied to bowel<br></br>
b. Combination of gangrene with superimposed bacterial infection is called wet gangrene<br></br>

18
Q
  1. Ischemia/Reperfusion injury is caused by?
A

Ischemia is caused by the reduction of available oxygen, and when it leads to tissue death, you end up with heart attack, stroke, etc.

19
Q
  1. Reperfusion is and provides?
A

Reperfusion is when blood flow/oxygenation of the tissue is restored – Giving clot breaking therapy (TPA) during heart attack and stroke or in transplantation.

20
Q
  1. What are the compounds that lead to a large amount of ROS damage?
A

O2-, •OH, ONOO•, and lipid peroxide radicals

21
Q
  1. In cellular mechanisms, the ROS reacts with:
A

Lipid peroxide radicals – disruption of plasma membranes and organelles<br></br>
Oxidation of proteins – abnormal folding of proteins and affects Enzyme activity<br></br>
Oxidation of DNA – mutations, breaks

22
Q
  1. What do cytokines and cell adhesion molecules do? <br></br> What does ischemia/reperfusion injury activate?
A

a. Expression of cytokines and cell adhesion molecules cause accumulation of neutrophils which in turn cause further injury<br></br>
b. Activation of complement pathway

23
Q
  1. What are 2 characteristics of apoptosis?
A

i. enzymatic degradation of proteins and DNA (initiated by caspases)<br></br>
ii. removal of dead cells by phagocytes.

24
Q
  1. In apoptosis what do the cells destined to die activate? <br></br>
    How does the plasma membrane change here? <br></br>
    How is necrosis different? Cause type?
A

a. Cells destined to die activate enzymes capable of degrading the cells’ own nuclear DNA and proteins<br></br>
<br></br> b. The dead cell is rapidly cleared before its contents have leaked out, and therefore cell death by this pathway does not elicit an inflammatory reaction in the host
<br></br> c. This differs from necrosis, which is characterized by loss of membrane integrity, enzymatic digestion of cells, leakage of cellular contents.
Can be physiologic or pathologic

25
Q
  1. What are 6 Physiological Roles of Apoptosis?
A

<br></br> i. Embryogenesis
<br></br> ii. Hormone-dependent involution
<br></br> iii. Cell deletion in proliferating cell population
<br></br> iv. Normal immune defense against viral infected or neoplastic transformed cells as cytotoxic T cells clearance
<br></br> v. Removal of self-reactive lymphocyte clones
<br></br> vi. Removal of cells that have served their purpose (inflammatory cells)

26
Q
  1. How is apoptosis seen in cancer? <br></br> DNA damage from low doses will? <br></br> <br></br>Surgery? <br></br>Muscle size? <br></br> Diseases?
A

<br></br> i. Cell death in tumors - cytotoxic anticancer drugs
<br></br> ii. DNA damage from low doses of some agents (radiation, extreme temperatures, drugs) that would cause necrosis in larger doses
<br></br> iii. Transplant rejection
<br></br> iv. Atrophy after duct obstruction
<br></br> v. Some viral diseases

27
Q
  1. What are four stages of apoptosis?
A

<br></br> i. Signaling pathways initiate apoptosis
<br></br> ii. Intracellular signals further commit the cell to the apoptotic pathway
<br></br> iii. Execution phase: execution caspases catabolize the cytoskeleton and activate endonucleases which cause DNA breakdown
<br></br> iv. Removal of dead cells

28
Q
  1. In apoptosis what receptor initiated? <br></br>What do these 2 activate?
A

Extrinsic pathway - death receptor initiated<br></br>

Fas (CD95), TNF (tumor necrosis factor) activate adaptor proteins which bind caspases

29
Q
  1. In apoptosis intrinsic pathway, what happens and leads to?
A

Intrinsic pathway – Bax and Bak dimerize and form channels in the mitochondrial membrane leading to permeability of Cytochrome c leakage and activation of caspases

Pathology (6 decks)

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