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NRS 232 Pathophysiological Processes - MHCC > CH 2 Cellular Injury, Adaptation, and Maladaptive Changes > Flashcards

CH 2 Cellular Injury, Adaptation, and Maladaptive Changes Flashcards

1
Q

etiology

A

the original cause of a cellular alteration or disease

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2
Q

Examples of different distinctive cellular changes from etiologic agents

A
  • Exposure to extreme cold temperatures will cause localized frostbite and tissue necrosis.
  • Exposure to electrical current can burn tissue and cause cardiac rhythm disturbances.
  • Alcohol abuse can cause the liver to take on characteristic fatty changes.
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3
Q

Cells can do one of two things

A
  1. Develop adaptive, compensatory changes in an attempt to maintain homeostasis
  2. Develop maladaptive changes, which are derangements of structure or function

In overwhelming insult cell death or injury can result

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4
Q

Histology

A

the microscopic study of tissues and cells

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5
Q

Biopsy

A

extracts a cell sample from an organ or mass of tissue for a histological examination

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6
Q

pathognomonic changes

A

unique histological findings that represent distinct disease processes
Example: an inflamed, craterlike breach in the gastrointestinal mucosa, as seen on an endoscopic examination of the stomach and duodenum, is pathognomonic for peptic ulcer disease

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7
Q

Atrophy

A

cellular adaption in which cells revert to a smaller size in response to changes in metabolic requirements or their environment

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8
Q

Causes of cellular atrophy

A
  • Disuse or diminished workload
  • Lack of nerve stimulation (paralysis)
  • Loss of hormonal stimulation
  • Inadequate nutrition
  • Decreased blood flow (ischemia)
  • Aging
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9
Q

Paralysis

A

lack of nerve stimulation

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10
Q

ischemia

A

decreased blood flow

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11
Q

Paralysis causes

A

lack of muscle contraction, loss of nerve stimulation, and decreased workload of the muscles

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12
Q

Hypertrophy

A

increase in individuals cell size resulting in enlargement of functioning tissue mass.

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13
Q

Angiogenesis

A

stimulated by exercise to the growth of new blood vessel branches

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14
Q

Physiological Hypertrophy

A

the enlarged muscle is adequately perfused and supplied with blood flow, oxygen, and nutrients because of angiogenesis

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15
Q

Pathological Hypertrophy

A

when there is an increase in cellular size but not an increase in supportive structures necessary for the enlarged cell’s increased metabolic needs

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16
Q

Stimulus for hypertrophy increases the muscle cell’s:

A
  • actin and myosin filaments
  • enzymes
  • mitochondria
  • blood vessel growth
  • ATP production
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17
Q

Hyperplasia

A

the increase of number of cells in a tissue or organ, occurs only in cells capable of mitotic division

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18
Q

Hyperplasia stimulated by:

A

hormonal or compensatory cellular mechanisms

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19
Q

Keloid

A

maladaptive hyperplastic accumulation of epithelial tissues and connective tissue occurring in wound healing that creates an elevated, disfigured scar

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20
Q

Stem Cells

A

self-renewing cells

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21
Q

Benign Prostatic Hyperplasia (BPH)

A

prostate gland cells increase in number in the aging male caused by testosterone stimulation

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22
Q

Metaplasia

A

Replacement of one type of cell by another type of cell, likely a result of the cell’s genetic programming to a change in environmental conditions, such as inflammation and the substitution of cells ensures the tissues survival

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23
Q

GERD and Metaplasia

A

lower esophageal sphincter is weakened and allows stomach acid into the lower esophagus. The irritated cells inflame, and with prolonged irritation and no treatment, the cells turn from squamous epithelium to columnar stomach-like cells that have a greater tolerance for the acid

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24
Q

Barret’s esophagus

A

the metaplastic change from squamous to columnar cells. It requires periodic examination and aggressive treatment because it can deteriorate into cancer of the esophagus

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25
Q

Dysplasia

A

deranged cellular growth within a specific tissue, often a result of chronic inflammation or a precancerous condition

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26
Q

Dysplasia Histologic View

A

Vary in size, shape, and architectural organization compared to the healthy cells

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27
Q

Neoplasia

A

“new growth”, usually refers to disorganized, uncoordinated, uncontrolled proliferative cell growth that is cancerous. Neoplasm and tumor are often used interchangeably

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28
Q

Neoplasm classifications

A

benign or malignant, depends on differentiation of cells

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29
Q

Differentiation

A

the process where newly growing cells acquire the specialized structure and function of the cells they replace

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30
Q

Malignant neoplasm

A

contain poorly-differentiated cells which have a tendency to break away, enter the lymphatic or circulatory systems, and metastasize to distant sites to form secondary neoplasms.

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31
Q

Benign Neoplasms

A

contain well-differentiated cells, or cells that resemble the healthy cells of the tissue of origin. the cells do not metastasize or break loose from the tissue of origin.

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32
Q

Cell injury occurs when:

A

cells are exposed to stress that no longer allows them to maintain homeostasis, resulting in structural and functional changes

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33
Q

Basic changes of cell injury

A
  • dysfunction of sodium-potassium pump
  • loss of plasma membrane integrity
  • mitochondrial dysfunction
  • defects in protein synthesis
  • intracellular accumulations
  • cellular swelling
  • DNA damage
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34
Q

Dysfunction of the Sodium Potassium Pump, when it’s not working: these things can happen

A
  • intracellular sodium increased because it can’t be adequately pumped out of the cell, leading to cellular swelling
  • lack of ATP, energy-dependent calcium pump becomes dysfunctional, calcium accumulates in cell and disrupts numerous biochemical processes
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35
Q

Calcium issues from dysfunction of sodium-potassium pump

A

Buildup of calcium activates a number of enzymes that further deplete ATP, damage the plasma membrane, disrupt DNA, and induce cell degeneration.

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36
Q

Pathological Calcification

A

the deposition of calcium and other minerals within tissues, occurs in a variety of conditions. Calcifications often accumulate in areas of cell injury and cell death

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37
Q

Conditions that cause pathological calcification (Box 2-2)

A
  • In arteriosclerosis, calcifications accumulate within long-standing plaque. Calcified plaque is hardened, fragile, and likely to break apart into small pieces that can travel in the bloodstream.
  • Aortic sclerosis, a common disorder in elderly individuals, involves a calcified aortic heart valve. Calcification causes thickening and narrowing of the heart valve with consequent blood disruption.
  • On mammography, a breast lesion containing microcalcifications is often indicative of a malignancy. Calcium deposits are seen within the nutrient-deprived cells of a malignant tumor in the breast.
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38
Q

Loss of Plasma Membrane Integrity - Cellular injury

A
  • injurious agents can affect any of the organelles
  • water can enter the intracellular compartment causing intracellular swelling
  • mitochondria can be damaged, halting the cell’s ability to produce energy
  • organelles can swell and deteriorate
  • nucleus can be left vulnerable to injury and the cell would then be left without the ability to regenerate
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39
Q

Defects in Protein synthesis ability- cellular injury

A

With dwindling ATP availability, the critical cellular process of protein synthesis begins to fail. The cells cannot manufacture proteins, which are crucial constituents for their own regeneration and many different kinds of body processes. Lack of protein synthesis can begin the process of cell degeneration or cell death.

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40
Q

Intracellular Accumulations - Cellular Injury

A

Can accumulate excessive amounts of various substances:
-cellular constituents
-environmentally acquired substances
-cell breakdown products
Due to abnormal metabolic function, these may be harmless or toxic to the cell and may be transient or become permanently embedded in the cell

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41
Q

Intracellular accumulation example - excessive alcohol

A

hepatocytes, involved in lipid metabolism, can sustain toxic injury from alcohol and accumulate large quantities of fat causing fatty liver

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42
Q

Fatty Liver

A

a distinct histological change associated with alcoholism causing the liver to enlarge and be dysfunctional in part due to intracellular accumulation

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43
Q

Familial Hypercholesterolemia - Intracellular Accumulation

A

Condition that causes defective cholesterol metabolism

-causes yellow, raised skin lesions from intracellular accumulation of excess cholesterol in epithelial cells

44
Q

Xanthomas and xanthelasma

A

yellow, raised lesions from intracellular accumulation of cholesterol in epithelial cells

45
Q

Anthracosis

A

Coal Miner’s Lung Disease
-environmentally derived from chronically inhaling coal dust, leads to cellular accumulation in respiratory tract epithelial cells leading to blackened lung tissue

46
Q

Jaundice

A

the yellow hue of skin and sclera, from the cellular accumulation of bilirubin in the bloodstream. If excess RBC breakdown or liver dysfunction occurs, bilirubin accumulates in bloodstream.

47
Q

Bilirubin

A

A yellow, pigmented substance, a breakdown product of hemoglobin. Constitutes of bile, synthesized by the liver, with a high affinity for elastin, a component of skin and sclera of the eye.

48
Q

Genetic Damage - Cellular Injury

A

Injury to the DNA causes mutations, changing the cell’s structure and function. Mutated DNA makes mutated RNA, instructs ribosomes to make abnormal proteins and manufacture abnormal secretions.

Often incompatible with life and will initiate change to bring about apoptosis (cell death)

49
Q

Apoptosis

A

programmed cell degeneration - death

50
Q

Oncoproteins

A

cancerous proteins manufactured by cancerous cells

51
Q

DNA mutations - Radiation

A

With exposure to high doses of radiation, it can damage the DNA in the genes and mutate them to oncogenes, triggering cancerous cell changes

52
Q

Causes of cell injury:

A
  • Hypoxic cell injury
  • Free radical injury (oxidative stress)
  • Physical agents of injury
  • Chemical injury
  • Infectious agent injury
  • Injurious immunological reactions
  • Genetic defects
  • Nutritional imbalances
53
Q

Hypoxia

A

oxygen deprivation, most common cause of cell injury

54
Q

Most common cause of cellular hypoxia

A

ischemia: diminished circulation

55
Q

Ischemia occurs most often from:

A

obstruction of arterial blood flow

56
Q

Most common arterial obstruction:

A

atherosclerotic plaque and clot formation blocking downstream circulation from the clot

57
Q

Xanthelasma

A

intracellular accumulation of cholesterol in skin cells around the eyelids

58
Q

Anemia and Hypoxia

A

in anemia blood lacks sufficient hemoglobin resulting in insufficient transport of oxygen by hemoglobin, cells not receiving fully oxygenated blood leads to cellular hypoxia

59
Q

Hypoxia and Anaerobic Metabolism

A

enter anaerobic conditions, creating only 2 ATP and pyruvic acid. Pyruvic acid turns to lactic acid which alters cellular biochemical activity. Anaerobic metabolism cannot sustained life for a prolonged time

60
Q

Causes of cellular hypoxia

A
  • Anemia
  • Ischemia
  • exposure to low concentrations of oxygen in the environment, such as occurs at high altitudes;
  • inadequate oxygen diffusion at the alveoli, as in pneumonia;
  • suffocation injury;
  • airway obstruction caused by a foreign body
  • inflammation of oropharyngeal tissues.
61
Q

Oxidative Phosphorylation

A

the process of cells generating energy in the mitochondria.

62
Q

Free Radicals are made by:

A

during oxidative phosphorylation, described as a respiratory burst, small amounts of reactive oxygen molecules are produced as by-products. The reactive oxygen molecules are free radicals

63
Q

Free Radical Make-Up

A

have a single unpaired electron in an outer orbit creating instability and reactivity with adjacent molecules

64
Q

Free Radicals are:

A

oxidizing agents with the ability to penetrate the cell’s plasma membrane, disrupt internal organelles, and damage the nucleus and its DNA.

65
Q

Free Radicals react with:

A

constituents of cell’s plasma membrane and organelle membranes causing causing oxidative degradation

66
Q

Oxidative Stress

A

when free radical generation overwhelms the mechanism s of removal causing cell injury

67
Q

superoxide dismutases

A

a series of enzymes, a cell’s multiple mechanisms to remove free radicals and minimize injury

68
Q

Individuals can counteract free radical injury by:

A

consumption of antioxidants such as vitamins A, E, C, and beta-carotene

69
Q

Ischemic-reperfusion injury

A

transient ischemia with subsequent resumption of circulation. Depending on the ischemic insult intensity and duration, variable numbers of cells die after blood flow is restored.

70
Q

Cells die from ischemic-reperfusion because

A

new damaging forces are activated by free-radicals during reperfusion casing cell death in cells that may have recovered

71
Q

A disease that commonly involves ischemic-reperfusion injury

A

heart disease. IR occurs when a blood clot obstructs coronary artery and causes cardiac muscle ischemia. Reperfusion happens with blood clot dissolution. by-products from mitochondria’s oxidative phosphorylation from temporary hypoxia, is free radicals. Those free radicals cause injury to surrounding tissue.

72
Q

Physical Agents of Injury

A
  • Mechanical trauma (laceration, gunshot, fall, etc.)
  • Temperature extremes
  • Electric shock
  • radiation
  • extreme changes in environmental pressure
  • excessive noise
73
Q

Physiological responses to physical trauma

A

often include initiation of the inflammatory response, leading to healing or further cell damage.

74
Q

Hypertension - cell injury

A

Constant high pressure on endothelial lining of arteries and vasculature causes shearing injury on endothelial lining. Also creates weakened integrity of smooth muscle in artery walls.
Endothelial injury initiates development of atherosclerosis in arterial system and developments of aneurysm

75
Q

Chemical injury caused by:

A

caused by endogenous biological substances like

  • hypernatremia
  • hyperglycemia

or exogenous synthetic substances like
-drugs

76
Q

Hypernatremia

A

high sodium levels in blood stream

77
Q

Advanced Glycation End Products

A

produced when high levels of blood glucose react with endothelial membrane consituents. These damage coronary and kidney arteries, and vessels of lower extremity, and retina of the eyes

78
Q

Infectious Agents of Injury

A
  • bacteria
  • fungi
  • viruses
  • parasites
  • other varieties of microorganisms
79
Q

Allergies

A

adverse immune reactions in response to environmental substances called antigens

80
Q

Rheumatoid Arthritis

A

immune cells are triggered by an unknown antigen to attack own body’s joints

81
Q

Genetic Defects - Cell Injury

A

genetic disorders damage and mutate DNA, initiating disease

82
Q

Malnutrition

A

inadequate daily intake of carbs, fats, proteins, vitamins, and minerals. Adversely affects cell function

83
Q

Fat soluble vitamins

A

A, D, E, K

84
Q

Endothelium Secretes:

A
  • vascular endothelial growth factor (VEGF)
  • nitric oxide (NO)
  • endothelin
85
Q

Vascular Endothelial Growth Factor (VEGF)

A

also called angiogenesis growth factor

-stimulates synthesis of collateral blood vessel branches

86
Q

Nitric Oxide from endothelium does what

A

vasodilates

87
Q

Endothelin secreted by endothelium does what?

A

Vasoconstricts

88
Q

Blood constituents that acts on endothelium are:

A
  • glucose
  • lipids
  • platelets
  • norepinephrine
  • epinephrine
  • acetylcholine
  • vasopressin
  • natriuretic peptides
  • angiotensin II
89
Q

Considered the body’s largest organ

A

endothelium

90
Q

Endothelial Injury acts as an initiate of ________ and is the fundamental cell change that causes
______ ______

A

arteriosclerosis, cardiovascular disease

91
Q

Most significant injurious agents of endothelial cells

A
  • hypertension
  • diabetic hyperglycemia
  • free radicals
  • persistent angiotensin II secretion
  • LDL - C
92
Q

Aneurysm

A

weakened area in an arterial wall

93
Q

circle of willis

A

arterial network within the brain, where a berry aneurysm takes place.

94
Q

Angiotensin II

A

product of renin-angiotensin-aldosterone cacade. Vasoconstrictor, raises BP.

95
Q

Atherogenesis Definition

A

gradual and progressive development of atherosclerotic plaque in arteries initiated by endothelial injury

96
Q

Steps of atherogenesis

A
  1. Areas of endothelial injury undergo inflammation, attracting WBCs and platelets to the region.
  2. Inflammatory changes cause diminished vasodilatory capacity, setting up conditions for LDL-C deposits and clot formation
  3. LDL-C accumulates in macrophages to form foam cells, the foundation for large spans of atherosclerotic plaque along artery walls
  4. During atherosclerotic formation, endothelial nitric oxide (NO) is depleted, inhibiting vasodilatory capacity of arteries.
  5. Depletion of NO and changes of endothelium and LDL deposition cause arterial vasoconstriction and atherosclerosis, detrimental combination for coronary arteries: atherogenesis
97
Q

Types of cell death

A

Apoptosis

Necrosis

98
Q

Apoptosis

A

Programmed cell death. Cells degenerate at a specific time with no adverse effects on the body

99
Q

Necrosis

A

Cell death caused by injury. Cell is overcome by insult, cannot maintain homeostasis, before severely dysfunctional, and may adversely affect neighboring tissues or the organ as a whole.

100
Q

Examples of Physiological Apoptosis

A
  • hand’s embryonic development in the womb

- female ovaries in menopause

101
Q

What happens when cells fail to undergo apoptosis

A

cells survive for an abnormally long amount of time and give rise to certain cancers, tumors, and detrimental hyperplastic cell changes

102
Q

Increased cellular apoptosis, what is it and what diseases are linked to it

A

excessive cell rate death, spinal muscular atrophy and hashimotos thyroiditis

103
Q

Infarction

A

ischemic necrosis, the death of tissue as a consequence of prolonged ischemia

104
Q

Elevated levels of _____ and ____ confirm death of myocardial tissue

A

CPKmb (lysosmal enzyme), troponin (cardiac protein)

105
Q

Gangrene occurs when

A

tissues endure prolonged ischemia, undergo infarction, and necrosis, then are exposed to bacteria that thrive on decaying tissue

106
Q

Bacteria associated with Gangrene

A

Clostridium perfringens

107
Q

Gangrene is most often seen in:

A

Patients with peripheral arterial disease of the lower extremities

NRS 232 Pathophysiological Processes - MHCC (11 decks)

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