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MOD > Chapter 2 Part 2 > Flashcards

Chapter 2 Part 2 Flashcards

1
Q

What are the morphologic features of necrosis?

A

Increased eosinophilia (due to loss of cytoplasmic RNA and denatured proteins), more glassy than normal cells due to loss of glycogen, may appear moth eaten, will eventually become myelin figures that are degraded, DNA changes will also appear

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2
Q

Define karyolysis

A

basophilia of chromatin fades, reflects loss of DNA because of enzymatic degradation

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3
Q

Define pyknosis

A

Nuclear shrinkage and increased basophilia

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4
Q

Define karyorrhexis

A

pyknotic nucleus undergoes fragmentation

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5
Q

What is the morphology of coagulative necrosis?

A

Necrosis in which the architecture of the tissue is preserved, eosinophilic cells may persist but will be phagocytosed by leukocytes

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6
Q

What is the morphology of liquefactive necrosis?

A

Digestion of dead cells resulting in the transformation of tissue to liquid, often presents in CNS

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7
Q

What is the morphology of gangrenous necrosis?

A

limb that has lost its blood supply and has undergone necrosis

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8
Q

What is the morphology of caseous necrosis?

A

Structureless collection of lysed cells and amorphous granular debris enclosed by a border

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9
Q

What is the morphology of fat necrosis?

A

Focal area of fat destruction due to activated pancreatic lipases in peritoneal cavity, fatty acids combine with calcium to produce fat saponification

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10
Q

What is the morphology of fibrinoid necrosis?

A

Necrosis seen in immune reactions involving blood vessels, complexes of antigens and antibodies deposited in walls of arteries and produces a bright pink and amorphous fibrinoid

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11
Q

The cellular response to injury depend on what three things?

A

Nature of the injury, duration, and severity

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12
Q

The consequences of cell injury depend on what three things?

A

The type of cell, state, and adaptability

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13
Q

What are the two main pathways of ATP production?

A

Oxidative phosphorylation and glycolytic pathway

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14
Q

What are the major causes of ATP depletion?

A

reduced oxygen and nutrients, damage to mitochondria and the actions of toxins

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15
Q

How is the activity of the plasma membrane energy-dependent sodium pump effected by ATP depletion?

A

Causes an accumulation of sodium and water inside the cell, and diffusion of potassium out of the cell

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16
Q

How is cellular energy metabolism altered by ATP depletion?

A

Increase in anaerobic glycolysis by rapidly using glycogen stores and causing the build up of lactic acid and reducing the intracellular pH

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17
Q

How does a decrease in ATP alter protein production?

A

The loss of ATP causes a disruption of proteins involved in synthesis, a detachment of ribosomes from the ER, overall reducing protein synthesis

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18
Q

What are the three major consequences of mitochondrial damage?

A

Opening of mitochondrial permeability transition pore, abnormal oxidative phosphorylation and activation of caspases

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19
Q

What are the consequences of the opening of the mitochondrial permeability transition pore?

A

Loss of mitochondrial membrane potential resulting in an overall depletion of ATP

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20
Q

What is the main consequence of abnormal oxidative phosphorylation as it relates to mitochondrial damage?

A

The production of ROS

21
Q

What is the main consequence of caspase activation as a result of mitochondrial damage?

A

apoptosis

22
Q

What are the main mechanisms of cellular injury due to Ca influx?

A

The opening of mitochondrial membrane permeability pores, activation of enzymes such as phospholipases, proteases, endonucleases, and ATPases, and ultimately the activation of apoptosis (caspases)

23
Q

What is a reactive oxygen species? Examples?

A

Oxygen-derived free radical; superoxide anion, hydrogen peroxide, hydroxyl anions

24
Q

How are free radical generated?

A

ReDox reactions in normal metabolic processes, absorption of radiation, leukocytes in inflammation, metabolism of exogenous chemicals, presence of transition metals

25
Q

How are free radicals removed?

A

Antioxidants, free iron or copper, and enzymes

26
Q

How is superoxide anion produced?

A

Incomplete reduction of oxygen during oxidative phosphorylation and by leukocytes

27
Q

How is superoxide anion inactivated?

A

Converted to hydrogen peroxide and oxygen by superoxide dismutases

28
Q

What are the pathological effects of superoxide anion?

A

Stimulates the production of enzymes that cause degradation, and may directly damage cell structures

29
Q

How is hydrogen peroxide produced?

A

Generated by superoxide dismutase from superoxide anion and by oxidases in peroxisomes

30
Q

How is hydrogen peroxide inactivated?

A

By conversion to water and oxygen by catalase in peroxisomes or by glutathione peroxidase in the cytosol or mitochondria

31
Q

What are the pathological effects of hydrogen peroxide?

A

Can be converted to hydroxyl radical or hypochlorite, destroying microbes and cells

32
Q

How is the hydroxyl radical produced?

A

Generated from water by hydrolysis

33
Q

How is the hydroxyl radical inactivated?

A

Conversion to water by glutathione peroxidase

34
Q

What are the pathologic effects of hydroxyl radical?

A

Damages lipids, proteins, and DNA

35
Q

How is peroxynitrite produced?

A

interaction of superoxide anion with nitric oxide

36
Q

How is peroxynitrite inactivated?

A

converted to nitrite (HNO2) by peroxiredoxins

37
Q

What are the pathological effects of peroxynitrite?

A

Damages lipids, proteins, DNA

38
Q

What are the main mechanisms of membrane damage?

A

ROS, decreased phospholipid synthesis, increased phospholipid breakdown, and cytoskeletal abnormalities

39
Q

What are the consequences of plasma membrane damage?

A

Loss of osmotic balance and influx of fluids and ions

40
Q

What are the consequences of injury to lysosomal membranes?

A

Leakage of enzymes into cytoplasm and activation of hydrolases, resulting in enzymatic damage to cells

41
Q

What are the two characteristics of irreversible cell damage?

A

Inability to reverse mitochondrial dysfunction, profound disturbances in membrane function

42
Q

Why can tissue specific cell injury be detected?

A

Damaged cell membranes cause the leakage of intracellular proteins into systemic circulation

43
Q

Describe lipid peroxidation in membranes

A

Oxidative damage is initiated when double bonds in unsaturated fatty acids of lipids are attacked by ROS, resulting in peroxides

44
Q

Describe oxidative modification of proteins

A

Free radicals cause the oxidation of amino acid side chains and protein backbone, resulting in the changes of their bonds and interactions, leading to misfolding

45
Q

Describe the pathological effects of free radicals as it relates to lesions in DNA

A

Free radicals are capable of causing breaks and cross-linking in DNA

46
Q

What is the mechanism of cell injury due to mild ischemia?

A

Reduced oxidative phosphorylation results due to decreased oxygen and nutrient availability. This decreased the amount of ATP and causes the failure of the Na pump and an influx of sodium and water. This leads to cell and organelle swelling.

47
Q

What is the mechanism of cell injury due to prolonged ischemia?

A

Severe mitochondrial swelling and calcium influx, lysosomal rupture, death by necrosis due to the release of cytochrome C

48
Q

What is the mechanism of cell injury due to reperfusion?

A

Blood brings calcium that overloads injured cells and causes mitochondrial injury, free radicals and cytokines induced by leukocytes, local activation of complement results

MOD (34 decks)

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