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Advanced Pathophysiology > Cell Injury, Death, and Adaptation > Flashcards

Cell Injury, Death, and Adaptation Flashcards

Exam I

1
Q

Etiology categories of injurious agents causing cell injury/death/adaption

A

ATP depletion
Oxygen and oxygen-derived free radicals
Intracellular calcium and loss of calcium steady state
defects in membrane permeability

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2
Q

Karyorrhexis

A

fragmentation of nuclear material

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3
Q

Pyknosis

A

clumping of nuclear material

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4
Q

Karyolysis

A

dissolution of nuclear material

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5
Q

Cellular outcome of Na/K pump failure

A

Sodium ions enter freely (accompanied by water), potassium ions leave freely, and calcium ions gain abnormal entry into the cell and the intracellular organelles

When the cell swells, all of the organelles within the cell (which are also membrane-bound) swell
When the rough ER swells (where protein synthesis occurs), the ribosomes fall off and protein synthesis stops

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6
Q

Cellular outcome of lactic acid buildup

A

Lactic acid buildup causes the intracellular pH to decline, incapacitating cells (which function within a very narrow range of pH)

Leads to: Pyknosis, karyorrhexis, and karyolysis and the rupture of already swollen lysosomes

Lysosomes release their proteolytic enzymes, which autodigest cell contents and the cell membrane
Disruption of the cell membrane increases calcium influx into the cell/organelles and causes release of cellular contents into the tissue spaces and blood (extracellular fluid)

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7
Q

Results of excessive free intracellular calcium

A

This excessive free calcium activates proteases, endonucleases, and phospholipases that proceed to destroy the cell and its contents

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8
Q

Reperfusion injuries

A

Occur when blood flow is restored to tissue that has been anoxic and functioning under anaerobic metabolism

Restoration of blood flow causes a burst of oxidative metabolism and accumulation of oxygen free radicals

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9
Q

Free radicals

A

Unstable compounds with an unpaired electron in their outer ring, making them anxious to react with other substances

Normal byproducts of cellular metabolism that are always present in the body

Have a particular affinity for lipid substances

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10
Q

Free radical effect on cell membranes

A

Free radicals combine avidly with cell or organelle membranes and “drill a hole”, or have a phosphokinase-like effect

This binding results in the dissolution of the membrane and chain reactions of toxic byproduct production, in an effect called lipid peroxidation

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11
Q

Reactive oxygen species (ROS)

A

A subset of free radicals that contain oxygen (oxygen-based free radicals)

Formed as natural oxidant species in cells during mitochondrial respiration and ATP generation

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12
Q

Free radical removal

A

antioxidants

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13
Q

Endogenous agents

A

Normally found in the body

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14
Q

Exogenous agents

A

Not normally found in the body

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15
Q

Chronic alcoholism and lipids

A

increases the conversion of FFA to triglycerides

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16
Q

Cause of liver fat accumulation

A

Increased mobilization and delivery of free fatty acids to liver cells can result in fat accumulation

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17
Q

Unconjugated bilirubin

A

Fat-soluble and cannot be eliminated through the kidneys (urine)

Gradually released from macrophages into the plasma and combines with plasma albumin to transport to the liver

Taken up by liver cells and conjugated

18
Q

Conjugated bilirubin

A

Water-soluble and can be eliminated through urine

As the concentration of conjugated bilirubin in liver cells increases, it begins to diffuse out of the cell and into the blood (down its concentration gradient)

In addition, some of the conjugated bilirubin becomes part bile, which exits liver cells through the hepatic duct –> common bile duct –> into the duodenum

Once in the intestines, half of the conjugated bilirubin is converted by bacterial action into urobilinogen, which is highly soluble

In the feces, it becomes altered and oxidized to form stercobilin (gives stool brown color)

About 5% is excreted by the kidneys into the urine and becomes oxidized to urobilin (gives urine yellow color)

19
Q

Hemolytic jaundice

A

Excessive hgb breakdown and delivery of unconjugated bilirubin to the liver

Unconjugated bilirubin accumulates in plasma
Bilirubin absent in urine
Urobilinogen increased in urine and feces

20
Q

Hepatocellular jaundice

A

Liver disease state
Unable to uptake, conjugate, &/or excrete bilirubin

Severe elevation of serum bilirubin
Conjugated and unconjugated bilirubin in plasma
LFTs abnormal

21
Q

Obstructive jaundice

A

Obstruction to the flow of bile

Conjugated bilirubin accumulates in the liver and diffuses into the blood

Clay-colored stools (no bilirubin through intestines) and dark urine (how most of the conjugated bilirubin is excreted)

22
Q

Hyperbilirubinemia outcomes

A

CNS toxicity

23
Q

Kernicterus

A

significant neurological deficits or death due to hyperbilirubinemia

24
Q

Cell necrosis

A

Uncontrolled, irreversible cell injury and eventual cell death due to pathological processes

A pathologic, disorganized sequence of events that results in swelling of cell organelles, plasma membrane rupture, and eventual lysis of cells and stimulates the inflammatory process

25
Q

Coagulative necrosis

A

Most common type

Cell architecture remains preserved and tissue is usually replaced by scar/fibrous tissue

Gangrene is a subset (results from interruption of arterial blood supply to a tissue)

26
Q

Dry gangrene

A

An area is free of infection and in which the line of demarcation between live and dead tissue is apparent

Tissue undergoing dry gangrene becomes dry and shrunken (mummified)

27
Q

Wet gangrene

A

A combination of coagulative AND liquefactive necrosis

Infection is present in the area between live and dead tissue

The presence of an acute inflammatory reaction and inflammatory exudate are responsible for the “wet” component

Often malodorous, and the line of demarcation between live and dead tissue is unclear until the infection is arrested

28
Q

Gas gangrene

A

Wet gangrene caused by Clostridium perfringens, an organism that produces gas within the destroyed tissue

29
Q

Liquefactive gangrene

A

Most commonly observed in the CNS, and can occur in bacterial infections (pus)

Dying cells are digested by hydrolytic enzymes and lose their structural integrity, turning into a viscous mass

Formation of cysts

30
Q

Fat gangrene

A

Occurs in acute pancreatitis when pancreatic enzyme release leads to liquefaction of the fat cells in the peritoneal cavity

Saponification

31
Q

Caseous gangrene

A

“Cheesy”

Takes place in tuberculosis infection

Necrotic area is referred to as a granulom

32
Q

Apoptosis

A

Type I programmed cell death

Genetically controlled, but can be physiologic or pathologic

Initiated by activation of caspase enzymes

	○ Apoptosis components:
		§ Promoter: p53
		§ Bcl-2
		§ Apaf-1
		§ Caspase 9
                    § Cytochrome c

Eliminates individual cells, which are normally phagocytized

Not associated with inflammation

33
Q

Autophagy

A

Type II programmed cell death

A survival mechanism that salvages key metabolites to promote homeostasis (garbage collecting and recycling)

34
Q

Atrophy

A

A reduction in cell size and reversion to a lower and more efficient level of functioning

Occurs in response to a decrease in work demands or adverse environmental condition

35
Q

Hypertrophy

A

An increase in cell size and functional components within the cell resulting in an increase in tissue size

Occurs in response to an increase in work demands

36
Q

Hyperplasia

A

An increase in the number of cells in an organ or tissue that is still capable of mitotic division

Occurs in response to an increase in work demands

37
Q

Metaplasia

A

The substitution of one type of normal cell with another type of normal cell, but one that is not normally found in that tissue

The replacement cells are better able to survive under stressful circumstances

Often occurs in response to chronic irritation

38
Q

Dysplasia

A

Characterized by deranged cell growth and differentiation within a specific tissue, resulting in disorderly cells that vary in size, shape, and appearance

Preneoplastic

39
Q

Causes of aging

A

Thought to be a result of an accumulation of DNA and metabolic (free radical) damage

Cells may age more quickly when DNA repair mechanisms are faulty and when metabolic damage is excessive because of reduced antioxidants

Possible genetic, epigenetic, inflammatory, oxidative stress, and metabolic origins

Diet is thought to play a major role in the development of age-related disease

Associated with inflammation, hypercoagulability, and immune changes

May involve an increase in autoantibodies and damage accumulation

40
Q

Cross-linking theory of aging

A

Decrease in cell permeability

Advanced Pathophysiology (6 decks)

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