Cellular Adaptation and Injury Flashcards

1
Q

What is the difference between physiological and pathological adaptation patterns?

A

Physiological: Normal and expected process. (ex: uterine enlargement during pregnancy)

Pathological: Cellular response that is not considered normal but is necessary because of the harsh environment in which the cell resides (ex: left ventricular hypertrophy occurs due to chronically elevated BP)

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2
Q

What are the 5 main types of cellular adaptation?

A

Atrophy, Hypertrophy, Hyperplasia, Dysplasia, Metaplasia

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3
Q

What is atrophy?

A

Atrophy is a decrease or shrinkage in the size of the cell.

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4
Q

What is an example of physiological atrophy?

A

Shrinkage of the thymus gland during childhood is a physiological atrophy

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5
Q

What is disuse atrophy?

A

Disuse atrophy is skeletal muscle atrophy that occurs from a person being immobilized for a prolonged period of time.

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6
Q

What causes atrophy (pathology behind atrophy)?

A

There is an increase in the catabolism of intracellular organelles. The end result is a reduction of the structural components of the cell. This process of atrophy also includes a self eating process known as autophagy.

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7
Q

What is hypertrophy? What causes it?

A

Increase in the size of cells which ultimately increases the size of the organ. It is caused by hormonal stimulation or increased functional demand which increases the cellular protein in the cell which leads to increased cell size.

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8
Q

What are examples of physiological hypertrophy?

A

Skeletal muscle hypertrophy is a physiological adaptation pattern in those who do heavy lifting or weight lifting. This will decrease when workload decreases. Another example is that when one kidney is removed, the other will increase in size to accommodate for the increased work load.

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9
Q

What are examples of pathological hypertrophy?

A

Cardiomegaly is an example of a pathological cellular adaptation pattern which results from an increase workload in a hypertensive patient or one that has heart valve problems. Cardiac hypertrophy eventually leads to decreased systolic function and heart failure.

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10
Q

What is hyperplasia?

A

Hyperplasia is an increase in the number of cells, not the size of the cell which occurs from an increased rate of cell division. The cells only increase in NUMBER, not size.

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11
Q

How does hyperplasia occur?

A

Hyperplasia only occurs in cells that are capable of mitosis. It results from the production of growth factors which stimulate cells to produce new cellular contents and divide.

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12
Q

What are examples of physiological hyperplasia?

A
  1. This occurs when there is an increase in tissue mass after damage or partial resection. This allows the organ to regenerate. The removal of part of the liver leads to hyperplasia of the remaining hepatocytes. Even with 70% of the liver removed, regeneration is complete in just 2 weeks.
  2. Uterine and mammary gland enlargement occur during pregnancy to meet the demands of increased work load.
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13
Q

What is an example of pathological hyperplasia?

A

Endometrial lining of the uterus normally undergoes hyperplasia in response to estrogen secretion; however, the normal process is halted by the release of progesterone. This causes pathological hyperplasia and increases risk of endometrial cancer.

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14
Q

What is metaplasia?

A

Metaplasia is a reversible change in which one adult cell is replaced by another adult cell. This can occur due to chronic stressors, injury or irritation. The new cell is better adept to handle the chronic stressor.

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15
Q

What are examples of metaplasia?

A
  1. The change from columnar cells to squamous cells. This occurs in chronic smokers. The normal cilated epithelial cells of the bronchial linings are replaces by stratified squamous epithelial cells.
  2. The change from squamous cells to columnar epithelial cells (less common). This change causes what is known as Barrett Esophagus. This change occurs due to refluxed gastric acid (heart burn). Also called intestinal metaplasia.
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16
Q

What is dysplasia?

A

Dysplasia is the abnormal changes in the size, shape, and organization of mature cells due to severe cell injury or irritation. It is characterized by disordered cell growth and is found in epithelial tissue. When these cells move to the basement membrane (area between the epithelial tissue and connective tissue) it is considered carcinoma in situ. Often known as precancer.

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17
Q

What are free radicals?

A

They are molecules that have an unpaired electron in its outer shell. This makes the molecule unstable ad highly reactive.

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18
Q

What do free radicals do in the body?

A

In an attempt to stabilize itself, it will steal an electron from another molecule and when this is done, the molecule from which it stole becomes a free radical as well. This can cause cellular injury and eventual death.

19
Q

What are reactive oxygen species?

A

ROS are produced as a normal byproduct of ATP production in the mitochondria. Elevated ROS overwhelms the mitochondria and exhausts intracellular antioxidants. This is referred to as oxidative stress. This can lead to cellular injury.

20
Q

What can increased levels of ROS lead to?

A

Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis.

21
Q

What is the body’s defense against ROS? Examples?

A

Antioxidants. They are reducing agents that stabilize free radicals by providing the missing electron. Antioxidants include vitamin E, C, cysteine, glutathione, albumin, ceruloplasmin, and transferrin.

22
Q

How are free radicals produced?

A
  1. As a result of normal cellular respiration
  2. By the absorption of extreme energy sources such as radiation or UV light
  3. By the metabolism of exogenous chemicals, drugs, and pesticides
  4. By the transition of metals, which donate or accept free electrons during intracellular processes.
  5. By nitric oxide acting like a chemical mediator and as a free radical.
23
Q

What are examples of free radicals?

A
  1. Reactive oxygen species
  2. hydrogen peroxide
  3. hydroxyl radicals
  4. nitric oxide (has normal physiologic effects in the body but can also act as a free radical)
24
Q

How does ROS affect the body?

A

ROS causes endothelial injury which leads to atherosclerosis. This causes a decrease in vasodilation. This occurs because ROS causes inflammation, hypertrophy, etc to the endothelium which leads to its dysfunction. Oxidative stress induced by ROS can cause arrhythmias and lead to sudden death.

25
Q

How does hypoxia occur?

A
  1. Decreased amount of oxygen in the air which is common in high altitudes or occurs with asphyxiation or drowning.
  2. Loss of Hg which can occur with hemorrhage or sickle cell anemia
  3. Decreased production of RBC’s which happen with anemia and leukemia
  4. Ischemia where the the cells are deprived of oxygen and other nutrients.
26
Q

How does hypoxic cellular injury occur?

A

Begins with ischemia that progresses to hypoxia. Lack of oxygen to the cell causes a decrease in mitochondrial function. This causes a decreased production of ATP where eventually the cell will die.

27
Q

What does the reduction of ATP in the body cause?

A

Reduction of ATP levels impair the Na-K and Na-Ca pumps and they fail. This leads to a higher intracellular concentration of sodium and calcium and diffuses potassium out of the cell. Because of the high intracellular sodium, water follow into the cell which causes cellular swelling. This causes ribosomes and mitochondrial functions to malfunction. The intracellular calcium will activate enzymes that eventually kill the cell.

28
Q

What are the intracellular enzymes?

A
  1. Creatinine Kinase is an enzyme found in muscle cells including the heart.
  2. AST and ALT are found in liver cells.
  3. Troponin is found in cardiac cells
29
Q

When does re-perfusion injury occur?

A

This occurs when oxygen supply is restored to the ischemic tissues. This triggers production of free radicals that cause cell membrane damage and mitochondrial calcium overload.

30
Q

How does re-perfusion injury develop?

A

Begins with xanthine dehydrogenase. When oxygen is restored, xanthine dehydrogenase is converted to xanthine oxidate. During the period of ischemia prior to reperfusion, the lack of ATP leads to massive amounts of free radicals. These free radicals cause cell membrane damage and mitochondrial calcium overload.

31
Q

What is the legal definition of drunk?

A

a blood alcohol level of 80 mg/dL

32
Q

What can elevated alcohol levels cause?

A

Wernicke encephalopathy, peripheral neuropathy, and Korsakoff psychosis. Phosphorus deficiency can increase the risk for the development of rhabdomyolysis in a person who chronically abuses alcohol. Folic acid deficiency can also occur.

33
Q

What are the characteristics of fetal alcohol syndrome?

A
  1. smooth philtrum
  2. thing vermilon border
  3. small palpebral fissures
34
Q

How does a child develop fetal alcohol syndrome?

A

ETOH crosses the placenta and the fetus liver has less than 10% alcohol dehydrogenase and therefore is unable to metabolize the ETOH. Amniotic fluid acts as a reservoir for ETOH and prolongs the fetus exposure to ETOH. This adversely affects the brain.

35
Q

What does ethanol break down into?

A

Ethanol-> acetaldehyde-> acetate

36
Q

What is an infarct?

A

An area of necrosis which results from a sudden insufficiency of arterial blood flow.

37
Q

What is apoptosis?

A

Programmed cell death. This is a normal physiological process and is different from necrosis. Can also occur in pathological conditions as well.

38
Q

What are examples of aptopsis?

A
  1. severe cell injury where the cells cannot be repaired.
  2. cytotoxic T cells attach any invading virus by inducing apoptosis which eliminates the affected cell.
  3. accumulation of mis-folded proteins trigger apoptosis which leads to Alzheimer’s disease
39
Q

What is autophagy?

A

Autodigestion of a cell. This has a catabolic and anabolic side to it. The catabolic side degradation of cellular organelles. The anabolic side involves the preservation of significant metabolites

40
Q

What is ketogenesis and how does it occur?

A

It is the formation of ketone bodies and occurs mostly in the mitochondria of hepatocytes. It occurs as a result of unavailability of glucose.

41
Q

What is the process of ketogenesis?

A

In states of starvation of diabetes, the cells do not receive enough glucose to produce energy. The end of the b-oxidation cycle results in the formation of acetyl-CoA. This is then processed by hepatocytes and undergoes transformation to 3 ketone bodies. This causes diabetic ketoacidosis (DKA)

42
Q

What are the three ketone bodies?

A

acetoacetate, acetone, and b hydroxybutyrate.

43
Q

What maintained the body during the first 3 days of starvation? After?

A

Glucose levels are maintained by hepatic glycogenolysis and the release of free fatty acids. After, adipose stores are used as the main energy source. Once these stores are depleted, organ failure and death occur.