Chapter 4: Altered Cellular And Tissue Biology Flashcards

1
Q

Two main types of cell death:

A

Necrosis and Apoptosis and nutrient deprivation can initiate autophagy which results in cell death

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2
Q

Atrophy

A

decrease or shrinkage in cell size. Can be classified as physiologic or pathological.
Physiologic atrophy occurs with early development: Ie. The thymus gland undergoes physiologic atrophy during childhood.
Pathological atrophy occurs as a result of decrease in workload, pressure, use, blood supply, nutrition.

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3
Q

Hypertrophy

A

Compensatory increase in the size of cells in response to mechanical stimuli and consequently increases the size of the affected organ. The cells of the heart and kidney are especially prone to enlargement

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4
Q

Hyperplasia

A

An increase in the number of cells, resulting from an increased rate of cellular division.

Compensatory hyperplasia is an adaptive mechanism that enables certain organs to regenerate Ie. Removal of part of the leads to hyperplasia of the remaining liver cells, even with70% removal in two weeks regeneration is complete. (Callus, epidermal and intestinal epithelial, hepatocytes, bone marrow cells, and fibroblasts)

Hormonal hyperplasia: occurs in estrogen dependent organs (breasts, uterus) After ovulation the estrogen stimulates the endometrium to grow and thicken in prep for receiving fertilized ovum.

Pathologic hyperplasia: abnormal proliferation of normal cells, usually in response to excessive hormonal stimulation or growth factors on target cells (endometrium caused by an imbalance of estrogen and progesterone secretion, with over secretion of estrogen

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5
Q

Dysplasia

A

Refers to abnormal changes in size, shape, and organization of mature cells. Not considered true adaptive process but is often called a typical hyperplasia.

Often encountered in epithelial tissue of the cervix and respiratory tract, where they are strongly associated with neoplasticism growths and are often found adjacent to cancer cells.

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6
Q

Metaplasia

A

Is the reversible replacement of one mature cell type (epithelial or mesenchymal) by another, sometimes less differentiated, cell type. It is thought to develop, as an adaptive response better suited to withstand the adverse environment from a reprogramming of stem cells that exist on most epithelial or of undifferentiated mesenchymal cells present in connective tissue.

Example: replacement of normal columnar ciliated epithelial cells of bronchial lining by stratified squamous epithelial cells.

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7
Q

Cellular adaptation is a reversible, structural, or functional, response both to normal or physiologic conditions and to adverse or pathologic conditions. Cells can adapt to physiologic demands or stress to maintain a steady state called homeostasis.

A

Did you know?

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8
Q

What are the most common significant adaptive changes?

A

Atrophy, hyperplasia, Hypertrophy, and metaplasia

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9
Q

Atrophy

A

Decrease in cell size due to disuse, aging, or reduced/absent blood supply, hormonal stimulation, or neural stimulation. The amounts of ER, mitochondria, and mircrofilaments decrease. The mechanisms of atrophy probably include decreased protein synthesis, increased protein catabolism, or both. A new hypothesis called ribosome biogenesis involves the role of mRNA and protein translation.

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10
Q

Hypertrophy

A

An increase in the size of cells in response to mechanical stimuli and consequently increases the size of the affected organ . The amounts of protein in the plasma membrane, ER, mircrofilaments, and mitochondria increase. Can be classified as physiologic or pathologic.

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11
Q

Hyperplasia

A

Increase in the number of cells caused by an increased rate of cellular division. Hyperplasia is classified as physiologic (compensatory and hormonal) and pathologic

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12
Q

Metaplasia

A

Reversible replacement of of one mature cell type by another less mature cell type.

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13
Q

Dysplasia

A

A typical hyperplasia, abnormal change in the size, shape and organization of mature tissue cells. Considered atypical rather than true adaptive change.

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14
Q

Cellular Injury

A

Injury to cells and to the extra cellular matrix leads to injury of tissues and organs, ultimately determining the structural patterns of disease.

Loss of function is derived from cell and ECM injury and cell death. Cellular injury occurs if the cell is unable to maintain homeostasis in the face of injurious stimuli or stress.

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15
Q

Reversible injury

A

Cells recover

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16
Q

Irriversible injury

A

Cells die

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17
Q

Injurious stimuli:

A

Chemical agents, lack of sufficient oxygen (hypoxia), free radicals, infectious agents, physical and mechanical factors, immunologic reactions, genetic factors, and nutritional imbalances.

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18
Q

Type of cell injury and response:

Adaptation

A

Adaptation: Atrophy, Hypertrophy, hyperplasia, metaplasia

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19
Q

Type of cell injury and response:

Active cell injury

A

Immediate response of the “entire” cell

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20
Q

Type of cell injury and response:

Reversible

A

Loss of ATP, cellular swelling, detachment of ribosomes, autophagy of lysosomes

21
Q

Type of cell injury and response:

Irreversible

A

“Point of no return” structurally when severe vacuolization of mitochondria occurs and CA++ moves into cell

22
Q

Type of cell injury and response:

Necrosis

A

Common type of cell death with severe cell swelling and breakdown of organelles

23
Q

Type of cell injury and response:

Apoptosis, or programmed cell death

A

Cellular self destruction for elimination of unwanted cell populations

24
Q

Type of cell injury and response:

Autophagy

A

Eating of self, cytoplasmic vesicles engulfs cytoplasm, and organelles, recycling factory

25
Q

Type of cell injury and response:

Chronic cell injury (sub cellular alterations)

A

Persistent stimuli response may involve only specific organelles or cytoskeleton (eg. Phagocytosis of bacteria)

26
Q

Type of cell injury and response:

Accumulations or infiltrations

A

Water, pigments, lipids, glycogen, proteins

27
Q

Pathologic Calcification

A

Dystrophic and metas tic calcification

28
Q

What is the “point of no return” when it comes to cell death?

A

a puzzle, but once changes to the nucleus occur and cell membranes are disrupted the cell moves to irreversible injury and death.

29
Q

Common forms of cell injury:

A
  1. Hypoxic injury (Not enough O2 in the blood)
  2. Free radicals and reactive oxygen species injury
  3. Chemical injury
30
Q

Common theme in cell injury and cell death:

ATP depletion

A

Loss of mitochondrial apt and decreased ATP synthesis: results incl. cellular swelling, decreased protein synthesis, decreased membrane transport, and lipogenesis, all changes that contribute to loss of integrity to plasma membrane

31
Q

Common theme in cell injury and cell death:

Reactive oxygen species

A

Lack of oxygen is key in progression of cell injury ischemia( reduced blood supply); activated oxygen species (ROS, O2, H2O2, OH) cause destructions of cell membranes and structures

32
Q

Common theme in cell injury and cell death:

Ca++ entry

A

Normally intracellular cytosolic calcium concentrations are very low; ischemia and certain chemicals cause an increase in cytosolic Ca++ concentrations; sustained levels of Ca++ continue to increase with damage to plasma membrane; ca++ causes intracellular damage by activating a number of enzymes

33
Q

Common theme in cell injury and cell death:

Mitochondrial damage

A

Can be damaged by increase in cytosolic Ca++, ROS; two outcomes of mitochondrial damage are loss of membrane potential, which causes depletion of ATP and eventual death or necrosis of cell, and activation of another type of cell death apoptosis

34
Q

What is necrosis?

A

Type of cell death with severe cell swelling and a breakdown of organelles

35
Q

Common theme in cell injury and cell death:

Membrane damage

A

Early loss of selective membrane permeability found in all forms of cell injury, lysosomal membrane damage with release of enzymes causing cellular digestion

36
Q

Common theme in cell injury and cell death:

Protein misfolding, DNA damage

A

Proteins May misfolding, triggering unfolded protein response that activates corrective responses; if overwhelmed, response activates cell suicide program or apoptosis; DNA damage (genotoxic stress) also can activate Apoptosis

37
Q

Hypoxia

A

Lack of sufficient oxygen within cells

Most common cause of cell injury

38
Q

Hypoxia can result from

A

A reduced amount of oxygen in the air, loss of hemoglobin, or decreased efficacy of hemoglobin, decreased production of red blood cells, diseases of the respiratory and cardiovascular systems, and poisoning of oxidative enzymes (cytochromes) witching the cells.

39
Q

What roles does hypoxia play in?

A

Hypoxia plays a roll in physiologic process including cell differentiation, angiogenesis, proliferation, erithropoiesis, and overall cell viability

40
Q

Cellular mechanisms involved in hypoxia and inflammation are emerging and include activation of immune r3esponses and oxygen-sensing compounds called

A

PHDs; prolly hydroxylases and HIFs: hypoxia-induced idle transcription factor

41
Q

HIF Hypoxia inducible factor

A

Is a family of transcription regulators that coordinate the expression of many genes in response to oxygen deprivation.

42
Q

Most common cause of hypoxia

A

Ischemia

43
Q

Ischemia

A

(Most common cause of hypoxia)
Reduced blood supply

Ischemic injury is often caused by gradual narrowing of arteries (arteriosclerosis) or complete blockage by blood clots (thrombosis), or both

44
Q

Progressive hypoxia caused by gradual arterial obstruction is better tolerated than the acute anoxia (total lack of oxygen), caused by a sudden obstruction, as with an embolus (a blood clot or other blockage in the circulation)

A

Anoxia- total lack of oxygen

45
Q

An acute obstruction in a coronary artery can cause myocardial death (infarction) within minutes if the blood supply is not restored, where as the gradual onset of ischemia usually results in myocardial adaptation

A

Myocardial infarction and strokes is most common death in US, generally result from atherosclerosis (type of arteriosclerosis) and consequent ischemic injury

46
Q

Vacuolation

A

Formation of vacuoles, occurs within the cytoplasm and swelling of lysosomes and marked mitochondrial swelling result from damage to the outer membrane

47
Q

Persistent ischemia is associated with

A

Irreversible injury and necrosis

Irreversible injury is associated with severe swelling of mitochondria and swelling of lysosomes. Overall death is usually by necrosis but apoptosis also contributes

48
Q

Ischemia repercussion injury

A

Associated with tissue damage during myocardial and cerebral infarction