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Pathophysiology NP > Altered Cellular and Tissue Biology > Flashcards

Altered Cellular and Tissue Biology Flashcards

1
Q

What are the 4 most significant cellular adaptive changes

A
  1. atrophy
  2. hypertrophy
  3. hyperplasia
  4. metaplasia
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2
Q

Dysplasia

A

atypical hyperplasia (not an adaptive change) abnormal change in size, shape and organization of mature tissue cells.

NOT cancer and may not progress to cancer. Dysplastic tissues that do not involve the entire thickness of the epithelium may be completely reversible.

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3
Q

What are the causes of cellular injury (8)

A
  1. hypoxia
  2. free radicals
  3. chemicals
  4. Infection
  5. Inflammation
  6. Genetic factors
  7. Starvation
  8. Physical trauma
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4
Q

Pathologic Calcification

A

calcium accumulation within surrounding damaged tissue

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5
Q

Autophagy

A

occurs during times of cellular stress and is typically triggered by deficiency of nutrients or growth factors.

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6
Q

What 4 biochemical themes are important to cell inury

A
  1. Hypoxia
  2. Depletion of ATP
  3. Increased concentration of intracellular calcium and loss of calcium steady state
  4. Defects in membrane permeability
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7
Q

Effects Hypoxia on a cell

A

-Can induce inflammation and inflamed areas can become hypoxic
-Common in: bacterial infections, wounds, CV defects and cancer

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8
Q

Reperfusion Injury Cause and effect

A

Caused by the generation of highly reactive oxygen intermediates or radicals and

-promotes proinflammatory neutrophil adhesion to the endothelium

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9
Q

Oxidative Stress

A

-Can activate intracellular signaling pathways modulate enzymes, and transcription factors.
-Difficult to control and can initiate chain reactions

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10
Q

Effect of Free radicals

A
  1. Lipid peroxidation or the destruction of unsaturated fatty acids
  2. alterations of proteins, protein loss, and protein misfolding
  3. Mutations in DNA
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11
Q

Livor mortis

A

the purple discoloration caused by blood pooling in the most dependent, or lowest tissues.

Begins in 30 min to 1 hour after death and becomes fixed 6-8 hours after death

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12
Q

Coagulative necrosis

A

result of protein denaturization where albumin is transformed from gelatinous state to firm opaque substance (infarct)

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13
Q

Caseous necrosis

A

commonly results from pulmonary TB infection. curdled or cheese like gross appearance. combines elements of both coagulative and liquefactive necrosis.

Dead cells disintegrate but the debris is not completely hydrolyzed causing a granulomatous inflammatory response resulting in formation of soft granular tissues resembling clumped cheese.

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14
Q

Atrophy

A

decrease in cellular size

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15
Q

Hypertrophy

A

increase cellular size

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16
Q

Hyperplasia

A

increase in the number of cells

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17
Q

Metaplasia

A

reversible replacement of one mature cell type by another, sometimes less differentiated, cell type. Associated with tissue damage, repair, and regeneration.

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18
Q

what changes does a cell undergo due to ischemia

A

-Lack of oxygen leads to decreased ATP

-decreases the Na pump and increases anaerobic glycolysis

-Na & Ca increase in the cell, K increases OUTside the cell. At the same time lactic acid is increasing

-Intracellular water increases as swelling, pH is falling, protein synthesis falls.

IS REVERSIBLE IF O2 IS DELIVERED QUICKLY

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19
Q

Liquefactive necrosis

A

digestion of the dead cells transforming tissue into viscous liquid. Common in CNS hypoxic injury, also seen in bacterial and fungal infections. (creation of pus)

20
Q

Gangrene

A

Tissue necrosis caused by hypoxia and subsequent bacterial infection

21
Q

Suffocation vs strangulation

A

Suffocation: process of dying as a result of lack of oxygen. can be from an airway obstruction or environmental

Strangulation: compression of blood vessels and air passages externally on the neck.

22
Q

Penetrating vs perforating bullet wounds

A

Penetrating: bullet remains in the body

Perforating: bullet exited the body

23
Q

dystrophic calcification vs metastatic calcification

A

Dystrophic: accumulation of calcium salts. always a sign of pathologic change, as it only occurs in injured or dead cells. (ca in the cytosol can cause activation of protein kinases, activation of phospholipases and membrane damage)

Metastatic: can occur in uninjured cells in those with hypercalcemia.

24
Q

Rigor mortis

A

muscle stiffening or rigidity that begins within a few hours of death.
Starts in smaller muscles and increases over time, maintains for about 12 hrs, then diminishes in the same order as it started over the next 12-14 hrs.

25
Q

Apoptosis vs necrosis

A

Apoptosis: regulated or programmed cell process by the “dropping off” of cellular fragments called apoptotic bodies.

Necrosis: rapid loss of the plasma membrane structure, organelle swelling, mitochondrial dysfunction, and the lack of typical features of apoptosis

26
Q

Effect of excess hormonal stimulation on cells

A

hypertrophy

27
Q

Effect of reduced hormonal stimulation on cells

A

Atrophy

28
Q

Heavy metal poisoning, what metals and what is the physiology

A

Metals: lead, mercury, arsenic, and cadmium

Physiology: alteration to:
1. DNA repair mechanisms
2. tumor suppressor functions
3. signal transduction pathways

29
Q

Effect of deprivation of essential nutrients

A

cellular injury altering:
1. cellular structure
2. Function particularly of transport mechanisms
3. chromosomes, the nucleus and DNA

30
Q

What is cellular swelling and what causes it

A

the accumulation of excessive water in the cell, caused by the failure of transport mechanisms.
Is a sign of many types of cellular injury

31
Q

Mechanism of gout

A

disturbance of urate metabolism, resulting in hyperuricemia and deposition of sodium urate crystals in tissue

32
Q

Autophagy

A

a recycling factory, a self destructive process and survival mechanism where it degrades cytoplasmic components and organelles in lysosomes and and salvages key metabolites to promote metabolic and nutrient homeostasis.

Important in development, cell proliferation, remodeling, aging, cancer, heart disease, neurodegenerative disease, inflammation, infection, metabolic diseases and cell death.

33
Q

Fatty necrosis

A

cellular dissolution caused by lipases, that break down triglycerides, releasing free fatty acids that combine with calcium, magnesium and sodium ions creating soaps (saponification). Necrotic tissue appears opaque and chalky white.

34
Q

Fibrinoid necrosis

A

Unique vascular damage typically seen immune reactions involving blood vessels. Occurs from injury, and complexes of antigens and antibodies are deposited in the walls of arteries.
Also called immunologically mediated vasculitis syndromes.

35
Q

Senescence

A

Growing OLD

Results in loss of tissue repair capacity and produces proinflammatory and matrix degrading molecules known as the senescence associated secretory phenotype (SASP)

process of permanent proliferative arrest or nondividing state called replicative senescence.

36
Q

Inflammaging

A

increased levels of circulating cytokines and proinflammatory markers associated with aging.

37
Q

Somatic Death

A

Death of the organism. Does not involve the inflammatory response

38
Q

What are the 7 stages of death and possible 8th

A
  1. pallor mortis
  2. algor mortis
  3. rigor mortis
  4. livor mortis
  5. putrefaction
  6. decomposition
  7. skeletonization
  8. fossilization
39
Q

Chemical Asphixiants

A

Carbon monoxide
cyanide
hydrogen sulfide
methane

all displace or interfere with O2 delivery or use.

40
Q

Pallor mortis

A

First change after death where the skin becomes pale and yellowish.

41
Q

Algor mortis

A

Post mortem decrease in body temperature. Immediately after death the body temp gradually falls and then decreases more rapidly (1-1.5F/hr) until body temp is equal to environmental temp

42
Q

Liopfuscion

A

Yellow brown age pigment

43
Q

Karyolysis

A

Nuclear dissolution and lysis of chromatin

44
Q

Sarcopenia

A

loss of skeletal muscle and strength

45
Q

Pyknosis

A

shrunken nucleus, appearing as a small dense mass

46
Q

Steatosis

A

fatty changes in the liver

47
Q

Caspase

A

aspartic acid specific enzymes that trigger proteolytic activity in response to signals inducing apoptosis.

Pathophysiology NP (3 decks)

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