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Patho Exam 1 > Cell Injury and Adaptation > Flashcards

Cell Injury and Adaptation Flashcards

1
Q

___ is an increase in cell numbers

A

hyperplasia

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2
Q

___ is a decrease in cell numbers

A

hypoplasia

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3
Q

___ is an increase in cell size, and thus, tissue size

A

hypertrophy

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4
Q

___ is a decrease in cell size

A

atrophy

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5
Q

cellular adaptations may lead to a change in cell type, called ___

A

metaplasia

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6
Q

Hypertrophy is the result of increased production of cellular proteins–this is due to what 3 things?

A

1-hormones (mediated by growth factors and cytokines)
2-increased stress/workload
3-increased neurologic stimulus

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7
Q

What are the two physiologic causes of hyperplasia?

A

1-hormonal

2-compensatory (after loss or injury)

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8
Q

What are the two pathologic causes of hyperplasia?

A

1-excess hormone or growth factor

2-response to some viral infections

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9
Q

The liver, and potentially the kidney, respond to ____ produced by mesenchymal cells throughout the body to promote regeneration

A

scatter factors

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10
Q

What are the 6 causes of atrophy?

A 
1-decreased workload
2-loss of innervation
3-diminished blood supply/ischemia
4-inadequate nutrition
5-loss of endocrine stimulation
6-pressure from external compression or duct obstruction, and sometimes from autoimmune destruction
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11
Q

____ is a reversible change in which one adult cell type is replaced by another adult cell type; it is often adaptive, like due to chronic inflammation to protect the body, but it can lead to malignant transformation

A

metaplasia

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12
Q

What are the 7 causes of cell injury?

A

1-oxygen deprivation (hypoxia, anoxia, ischemia)
2-physical agents (heat, trauma, radiation, electric shock)
3-chemical (drugs, environment, alcohol–either the chemical itself or a toxic metabolite)
4-infectious agents (viruses, bacteria, parasites, prions)
5-immunologic reactions from autoimmunity or anaphylaxis
6-genetic derangements like sickle cell or CF
7-nutritional imbalances

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13
Q

____ is the most common cause of acute liver failure in the US

A

acetominophen toxicity

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14
Q

Acetaminophen toxicity is treated with ____, which reduces the death rate, but it must be given within 10 hours

A

antidote N-acetylcysteine

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15
Q

Acetaminophen is usually a safe drug but there are 4 problems that can occur:

A

1-too much acetaminophen, not enough glutathione to bind
2-increased activity of CYP system (more than normal 5% is pulled into CYP system so more hepatotoxic compounds are created)
3-there is a decreased amount of glutathione present to bind the hepatotoxic compounds
4-there is decreased conjugation to sulfate and glucuronide

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16
Q

How does N-acetylcysteine treat Acetaminophen overdose?

A

it helps to increase hepatocyte glutathione levels

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17
Q

A decreased amount of stored glutathione is usually due to what 2 things?

A

malnutrition and alcoholism

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18
Q

Alcohol, anticonvulsants, and antituberculous drugs can increase acetaminophen toxicity–how?

A

these cause excessive activity of cytochrome P450 system

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19
Q

The ____ correlates plasma levels of acetaminophen with time to assess acute toxicity; it can’t be used for chronic use or toxicity assessment

A

Rumach Matthew Nomogram

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20
Q

What is often the initial finding of cell injury?

A

ATP depletion

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21
Q

Which is worse for cells, ischemia or hypoxia? why?

A

ischemia–not only losing oxygen supply but also glucose and have accumulation of waste products

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22
Q

What is the reflow phenomenon?

A

It is when a previously ischemic area has blood re-introduced to it

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23
Q

What are the 6 effects of ATP depletion?

A

1-decreased function of energy dependent sodium pump–leads to cell swelling
2-change energy metabolism to glycolysis, increasing lactic acid levels and lowering cell pH
3-failure of calcium pump
4-reduction in protein synthesis
5-abnormal folding of proteins
6-membrane damage–mitochondrial, ER, lysosomal, cell…

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24
Q

What are the repercussions of ATP depletion and calcium influx?

A

-membrane damage, nuclear damage, and further ATP depletion

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25
Q

Production of free radicals is increased in the presence of what three metals?

A

iron, copper, and zinc

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26
Q

What 4 things protect the cell from free radicals?

A

1-rapid spontaneous decay of the unstable compounds
2-antioxidants Vit E, A, C, and glutathione
3-iron and copper binding proteins
4-enzymes such as catalase, superoxide dismutase, and peroxidases

27
Q

How do free radicals damage cells? Three ways

A

1-damage the cell membrane through lipid peroxidation
2-oxidative modification of proteins, causing them to lose enzymatic activity and fold abnormally
3-reacts with DNA to produce single and double stranded breaks and mutations

28
Q

Glucose 6 phosphate dehydrogenase deficiency, which is a decreased ability of cells to protect themselves and presents clinically with “coke” colored urine is a disease caused by what?

A

free radicals

29
Q

When a cell has ____, it is an irreversible damage and cell death is inevitable

A

mitochondrial damage

30
Q

What are the two factors that make cell injury irreversible?

A

1-mitochondrial function can’t recover

2-profound disturbances in membrane function

31
Q

How can reperfusion cause worsening of injury?

A
  • reoxygenation causes generation of ROS
  • increases intracellular calcium overload
  • inflammation
  • activation of complement system
  • can also cause hemorrhage
32
Q

In this type of cell death, the cell membrane ruptures, the lysosomal membrane ruptures, and the internal cell contents leak out, inflammation ensues

A

necrosis

33
Q

What causes the cell swelling in tissue necrosis?

A

ATP deprivation and failure of sodium/potassium pumps

34
Q

What causes the pH drop associated with tissue necrosis?

A

the cell changes to anaerobic conditions and lactic acid levels increase

35
Q

This type of necrosis is typically caused by ischemia and denaturation predominates, it is characteristic of hypoxic death of all cells except brain

A

coagulative necrosis

36
Q

This type of necrosis occurs commonly in the brain after infarct–autolysis predominates and the dead cells are completely digested

A

liquefactive necrosis

37
Q

This type of necrosis can be both coagulative and liquefactive and is usually seen in the lower leg; it can be wet or dry

A

gangrene

38
Q

This type of necrosis is often seen in Tb, it forms granulomas, and is called “cheesy”

A

caseous

39
Q

This type of necrosis is unique to fat and it may occur after trauma, surgery, or spilling of pancreatic enzymes; the fat becomes an irritant–often seen in pancreatitis, breast trauma

A

fat necrosis

40
Q

This type of necrosis occurs in blood vessels after immune reactions

A

fibrinoid necrosis

41
Q

Cell death by necrosis releases molecules that can be toxic–like potassium, uric acid, and myoglobin. How is potassium toxic?

A

the potassium can cause EKG changes, and arrhythmias can occur

42
Q

____ is programmed cell death in which own enzymes are activated for cell death

A

apoptosis

43
Q

Apoptosis is useful in prevention of what two things?

A

autoimmunity and too much inflammation

44
Q

What are the pathological conditions that induce apoptosis? 7

A

1-chromosomal DNA damage can’t be fixed; loss of p53 gene
2-accumulation of misfolded proteins
3-cell death due to injurious stimuli
4-cell injury in certain viral diseases
5-pathologic atrophy after duct obstruction
6-cytotoxic T-cell apoptosis

45
Q

Which type of cell death (necrosis or apoptosis) is energy dependent?

A

apoptosis

46
Q

This type of cell death starts with a genetically programmed signal transduction, but it more resembles necrosis with cell swelling, loss of ATP, etc.; it as no caspases but it starts like extrinsic phase of apoptosis with TNF receptor activation

A

necroptosis

47
Q

____ occurs in cells infected by microbes–when the body can’t get rid of the microbe it kills the cell to kill the microbe

A

pyroptosis

48
Q

_____ is the uptake of particulate material

A

phagocytosis

49
Q

____ is the uptake of soluble material

A

pinocytosis

50
Q

____ is the digestion of cell’s own components

A

autophagy

51
Q

abnormal intracellular fat accumulation due to either normal amounts of lipids but decreased metabolism and removal or increased amount of lipids greater than cells ability to remove it

A

steatosis

52
Q

this type of intracellular accumulation is due to lipid peroxidation of polyunsaturated lipids in the cell, a sign of free radical injury

A

lipofuscin

53
Q

an alpha-1 anti-trypsin disease will result in what?

A

intracellular accumulation of proteins

54
Q

A gross excess of ____ intracellularly is associated with liver, heart, and pancreas damage

A

ferratin

55
Q

____ calcification is not dependent on increased serum levels of calcium or phosphate and it is seen in areas of necrosis or areas of previous tissue damage or necrotic tissue, like in heart valves or old scars

A

dystrophic

56
Q

___ calcification is due to high levels of calcium and phosphate, and occurs primarily in normal interstitial tissues of organs which have an alkaline environment like the stomach, lungs, kidneys, cornea, systemic arteries, and pulmonary veins

A

metastatic

57
Q

Chronic renal failure due to intracellular accumulations of calcification is often due to elevated phosphate resulting in what?

A

secondary hyperparathyroidism

58
Q

___ are short repeated sequences of DNA present at the ends of chromosomes that are important for ensuring the complete replication of chromosome ends and protecting chromosomes from fusion and degradation

A

telomeres

59
Q

___ maintains the length of telomeres, is required for replication, and is important in neoplasms

A

telomerase

60
Q

_____ is after a fixed number of divisions the cells become arrested in non-dividing state; it is determined by genetics; after arrest the cell no longer responds to normal growth signals

A

cellular senescence

61
Q

Telomerase plays a key role in cell aging, is normally present in only germ and stem cells but it is also present in what cells (bad!)?

A

cancer cells

62
Q

This syndrome begins at about 20yo, has growth retardation, muscle and connective tissue atrophy, skin aged appearance, and joint deformities, development of cataracts and death around age 40 due to atherosclerosis, diabetes, or cancer

A

Werner’s syndrome

63
Q

Werner’s syndrome is caused by a mutation in the ___ gene

A

DNA helicase

64
Q

This disease is rare and appear normal at birth except that bones of skull fail to fuse; by the end of the first year there is growth retardation, loss of all body hair, lack of proper calcification of bones, loss of subcutaneous fat, thinning of skill and distinctive facial features like receding chin, large head, eak like nose, and protruding eyes. Patients have normal mentality but never reach puberty and die from extensive atherosclerosis at 12-13yo; the cause is unknown

A

Hutchinson-Gilford Progeria

Patho Exam 1 (5 decks)

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