Chapter 2: Altered Cellular And Tissue Biology

Front 1

What can altered cellular and tissue biology result from?

Back 1

(1) adaptation
(2) injury
(3) neoplasia
(4) aging
(5) death

Front 2

What does adaptation occur in response to?

Back 2

both normal, or physiologic, conditions and adverse, or pathologic, conditions

Front 3

What is injury classified as?

Back 3

(1) chemical
(2) hypoxic (lack of sufficient oxygen)
(3) free radical
(4) intentional
(5) unintentional
(6) immunologic
(7) infection
(8) inflammatory

Front 4

How is cellular death confirmed?

Back 4

by structural changes seen when cells are stained and examined under a microscope

Front 5

What does cellular aging cause?

Back 5

structural and functional changes that eventually may lead to cellular death or a decreased capacity to recover from injury.

Front 6

Why do cells adapt to their environment?

Back 6

to escape and protect themselves from injury

Front 7

What are the most significant adaptive changes in cells?

Back 7

(1) atrophy (decrease in cell size)
(2) hypertrophy (increase in cell size)
(3) hyperplasia (increase in cell number)
(4) metaplasia (reversible replacement of one mature cell type by another less mature cell type)

Front 8

Is dysplasia (deranged cellular growth) considered a true cellular adaptation?

Back 8

no, it is considered an atypical hyperplasia

Front 9

What is atrophy?

Back 9

a decrease or shrinkage in cellular size

Front 10

What happens if atrophy occurs in a sufficient number of an organ's cells?

Back 10

the entire organ shrinks and becomes atrophic

Front 11

Atrophy can affect any organ but where is it most commonly seen?

Back 11

(1) skeletal muscle
(2) the heart
(3) secondary sex organs
(4) the brain

Front 12

When does physiologic atrophy occur?

Back 12

during early development

for example, the thymus gland undergoes physiologic atrophy during childhood

Front 13

Why does pathologic atrophy occur?

Back 13

it occurs as a result of decreases in workload, pressure, use, blood supply, nutrition, hormonal stimulation, and nervous stimulation

Front 14

What is disuse atrophy?

Back 14

a type of skeletal muscle atrophy exhibited by individuals who are immobilized in bed for a prolonged time

Front 15

What does aging cause in reference to atrophy?

Back 15

causes brain cells to become atrophic and endocrine-dependent organs, such as the gonads, to shrink as hormonal stimulation decreases

Front 16

How does an atrophic muscle cell differ from a regular muscle cell?

Back 16

it has less endoplasmic reticulum and fewer mitochondria and myofilaments (part of the muscle fiber that controls contraction) than does the normal cell

Front 17

What happens in muscular atrophy caused by nerve loss?

Back 17

oxygen consumption and amino acid uptake are immediately reduced

Front 18

List the possible mechanisms of atrophy.

Back 18

(1) decreased protein synthesis
(2) increased protein catabolism
(3) or both

Front 19

Where does lipofuscin accumulate in the body?

Back 19

(1) liver cells
(2) myocardial cells
(3) atrophic cells

Front 20

What cells of the body are particularly prone to enlargement by hypertrophy?

Back 20

(1) cells of the heart
(2) cells of the kidney

Front 21

What is the increase in cell size associated with? What is it not associated with?

Back 21

an increased accumulation of protein in the cellular components (plasma membrane, endoplasmic reticulum, myofilaments, mitochondria) and NOT with an increase in cellular fluid

Front 22

What is hypertrophy caused by?

Back 22

specific hormone stimulation or by increased functional demand

Front 23

List the triggers for hypertrophy.

Back 23

two types of signals:
(1) mechanical signals, such as stretch
(2) trophic signals, such as growth factors, hormones, and vasoactive agents

Front 24

Give examples of normal (physiologic) hypertrophy.

Back 24

(1) increase in skeletal muscle size due to increased workload
(2) increase in growth of uterus and mammary glands in response to pregnancy

Front 25

Give a pathologic example of hypertrophy.

Back 25

pathophysiologic hypertrophy in the heart secondary to hypertension or problem valves

Front 26

What is hyperplasia?

Back 26

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

Front 27

When does hyperplasia occur in response to injury?

Back 27

when the injury has been severe and prolonged enough to have caused cell death

Front 28

What often occurs along with hyperplasia?

Back 28

hypertrophy

Front 29

When do hyperplasia and hypertrophy occur together?

Back 29

both take place if the cells can synthesize DNA

Front 30

Which cells of the body cannot regenerate?

Back 30

(1) nerve cells
(2) skeletal muscle
(3) myocardial cells
(4) lens cells of the eye

Front 31

How are additional skeletal muscle cells made if they cannot regenerate?

Back 31

by the fusion of myoblasts

Front 32

In what parts of the body can significant hyperplasia occur?

Back 32

(1) epidermal and intestinal epithelia
(2) hepatocytes
(3) bone marrow cells
(4) fibroblasts

some hyperplasia is noted in:
(1) bone
(2) cartilage
(3) smooth muscle cells

Front 33

Give an example of compensatory hyperplasia involving epidermal cells.

Back 33

callus, or thickening, of the skin as a result of hyperplasia of epidermal cells in response to a mechanical stimulus

Front 34

What is dysplasia?

Back 34

abnormal changes in the size, shape, and organization of mature cells

Front 35

What is dysplasia often called?

Back 35

atypical hyperplasia

Front 36

Where are dysplastic changes often encountered?

Back 36

in epithelial tissue of the cervix and respiratory tract, where they are strongly associated with common neoplastic growths and often are found adjacent to cancerous cells.

Front 37

Why is dysplasia a worrisome change in cells?

Back 37

because it is most often found near cancer cells and data indicate that it appears to be involved with breast cancer development

Front 38

Can dysplastic changes be reversible?

Back 38

It can often be reversible if the inciting stimulus is removed

Front 39

What is metaplasia?

Back 39

the reversible replacement of one mature cell type by another, sometimes less differentiated, cell type.

Front 40

Give an example of metaplasia.

Back 40

replacement of normal columnar ciliated epithelial cells on the bronchial (airway) lining by stratified squamous epithelial cells.

the newly formed cells do not secrete mucus or have cilia, causing loss of a vital protective mechanism

bronchial metaplasia can be reversed if the inducing stimulus,usually cigarette smoking, is removed.

with prolonged exposure to the inducing stimulus, however, dysplasia and cancerous transformation can occur

Front 41

What do most disease begin with?

Back 41

cell injury

Front 42

When does cell injury occur?

Back 42

when the cell is unable to maintain homeostasis--a normal or adaptive steady state--in the face of injurious stimuli

Front 43

List some injurious stimuli of cells.

Back 43

(1) chemical agents
(2) lack of sufficient oxygen (hypoxia)
(3) free radicals
(4) infectious agents
(5) physical and mechanical factors
(6) immunologic reactions
(7) genetic factors
(8) nutritional imbalances

Front 44

What does the extent of cellular injury depend on?

Back 44

the type, state (including level of cell differentiation and increased susceptibility to fully differentiated cells), and adaptive processes of the cell, as well as the type, severity, and duration of the injurious stimulus

Front 45

Do two people exposed to an identical stimulus incur the same extent of cell injury?

Back 45

No, thay may incur varying degrees of of cellular injury

Front 46

Why may two individuals exposed to an identical stimulus have varying degrees of cellular injury?

Back 46

because modifying factors, such as nutritional status, can profoundly influence the extent of injury

Front 47

Can the precise "point of no return" that leads to cellular death be pinpointed to occur at a specific point?

Back 47

no

Front 48

Types of progressive cell injury: Adaptation

Give the response.

Back 48

atrophy, hypertrophy, hyperplasia, metaplasia

Front 49

Type of progressive cell injury: reversible

Give the response.

Back 49

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

Front 50

Type of progressive cell injury: irreversible

Give the response.

Back 50

"point of no return" structurally when severe vacuolization of the mitochondria occurs and Ca2+ moves into the cell

Front 51

Type of progressive cell injury: necrosis

Give the response.

Back 51

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

Front 52

Type of progressive cell injury: apoptosis, or programmed cell death

Give the response.

Back 52

cellular self-destruction for elimination of unwanted cell populations

Front 53

Type of progressive cell injury: chronic cell injury (subcellular alterations)

Give the response.

Back 53

persistent stimuli response may involve only specific organelles or cytoskeleton (e.g., phagocytosis of bacteria)

Front 54

Type of progressive cell injury: accumulations or infiltrations

Give the response.

Back 54

water, pigment, lipids, glycogen, proteins

Front 55

Type of progressive cell injury: pathologic calcification

Give the response.

Back 55

dystrophic and metastatic calcification

Front 56

List the four common biochemical themes that are important for understanding cell injury and cell death regardless of the injuring agent.

Back 56

(1) ATP depletion
(2) oxygen and oxygen-derived free radicals
(3) calcium alterations
(4) defects in membrane permeability

Front 57

List the common forms of cell injury.

Back 57

(1) hypoxic injury
(2) free radicals and reactive oxygen species injury
(3) chemical injury

Front 58

What is hypoxic cellular injury?

Back 58

lack of sufficient oxygen

Front 59

What are the common causes of hypoxic injury?

Back 59

(1) decreased amount of oxygen in the air
(2) loss of hemoglobin or hemoglobin function
(3) decreased production of red blood cells
(4) diseases of the respiratory and cardiovascular systems
(5) poisoning of the oxidative enzymes (cytochromes) within cells

Front 60

What is the most common cause of hypoxia?

Back 60

ischemia (reduced blood supply)

Front 61

What is ischemic injury often caused by?

Back 61

the gradual narrowing of arteries (arteriosclerosis), and complete blockage by blood clots (thrombosis)

Front 62

Progressive hypoxia caused by gradual arterial obstruction is better tolerated than the sudden acute ___________ caused by a sudden obstruction, as with an ______________.

Back 62

(1) anoxia (total lack of oxygen)

(2) embolus (blood clot or other plug in the circulation)

Front 63

What can an acute obstruction in a coronary artery cause?

Back 63

myocardial cell death (infarction) within minutes if the blood supply is not restored

Front 64

What does the gradual onset of ischemia in the heart usually result in?

Back 64

myocardial adaptation

Front 65

What do myocardial infarction and stroke generally result from?

Back 65

atherosclerosis (a type of arteriosclerosis) and consequent ischemic injury

Front 66

What does a reduction in ATP levels cause?

Back 66

the plasma membrane's sodium-potassium pump and sodium-calcium exchange to fail, which leads to an intracellular accumulation of sodium and calcium and diffusion of potassium out of the cell.

Sodium and water then can enter the cell freely, and cellular swelling, as well as early dilation of the ER, results.

Dilation causes the ribosomes to detach from the rough ER, reducing protein synthesis.

With continued hypoxia, the entire cell becomes markedly swollen, with increased concentrations of sodium, water, and chloride and decreased concentrations of potassium.

Front 67

What happens if oxygen is not restored to tissues?

Back 67

vacuolation (formation of vacuoles) occurs within the cytoplasm and swelling of lysosomes and marked mitochondrial swelling result from damage to the outer membrane.

Front 68

What does continued hypoxic injury along with accumulation of calcium activate?

Back 68

mulitple enzyme systems resulting in membrane damage, cytoskeleton disruption, activation of inflammation, DNA degradation, and eventual cell death

Front 69

What is irreversible damage characterized by?

Back 69

(1) lack of ATP generation because of mitochondrial damage (by accumulation of intracellular calcium in the mitochondria)
(2) major disturbances and damage in membrane function

Front 70

Restoration of oxygen, however, can cause additional injury called ______________.

Back 70

reperfusion injury

Front 71

What does reperfusion injury result from?

Back 71

the generation of highly reactive oxygen intermediates, sometimes called oxidative stress, including hydroxyl radical (OH-), superoxide (O2-), and hydrogen peroxide (H2O2).

Front 72

What can these radicals cause?

Back 72

further membrane damage and mitochondrial calcium overload

Front 73

What cell is especially affected with reperfusion injury?

Back 73

neutrophils, including neutrophil adhesion to the endothelium

Front 74

What reverses both neutrophil adhesion and, for example, neutrophil-meidated heart injury?

Back 74

antioxidant treatment

other potential and current treatments may include blockage of inflammatory mediators and inhibition of certain cell death (for example, apoptotic) pathways

Front 75

What is oxidative stress?

Back 75

injury induced by free radicals, especially by reactive oxygen species (ROS)

Front 76

When does oxidative stress occur?

Back 76

when excess ROS overwhelms endogenous antioxidant systems

Front 77

What is a free radical?

Back 77

an electrically uncharged atom or group of atoms that has an unpaired electron.

Front 78

What makes the free radical unstable? How does it stabilize?

Back 78

the unpaired electron

to stabilize, it gives up an electron to another molecule or steals one.

Front 79

What happens to the molecule that the free radical steals an electron from?

Back 79

it becomes a free radical and is capable of injurious chemical bond formation with proteins, lipids, and carbohydrates--key molecules in membranes and nucleic acids.

Front 80

Why are free radicals highly reactive?

Back 80

because they have low chemical specificity, meaning they can react with most molecules close by

Front 81

During normal metabolism, what organelle is the greatest source and target of ROS?

Back 81

mitochondria

Front 82

How do ROS affect mitochondria? What are they related to?

Back 82

cause mitochondria dysfunction and are related to many human diseases and aging

Front 83

Why is inefficiency of antioxidants more serious in mitochondria?

Back 83

mitochondria in most cells lack catalase

Front 84

What does excessive production of hydrogen peroxide and eventually hydroxyl radical in mitochondria do?

Back 84

damage lipid, proteins, and mitochondrial DNA (mDNA), which then causes cells to die of necrosis or apoptosis

Front 85

What has mitochondrial oxidative stress been implicated in?

Back 85

heart disease
alzheimer disease
Parkinson disease
prion diseases
amyotrophic lateral sclerosis (ALS)
as well as aging itself

Front 86

What are the 4 major ways that free radicals cause cellular injury?

Back 86

(1) lipid peroxidation, which is the destruction of polyunsaturated lipids (the same process by which fats become rancid) leading to membrane damage and increased permeability
(2) attacking critical proteins that affect ion pumps and transport mechanisms
(3) fragmenting DNA, causing decreased protein synthesis
(4) damaging mitochondria, causing the liberation of calcium into the cytosol

Front 87

What does chemical injury begin with?

Back 87

a biochemical interaction between a toxic substance and the cell's plasma membrane, which is ultimately damaged, leadin to increased permeability

Front 88

What are poisons?

Back 88

highly toxic substances

Front 89

What chemicals can cause cellular injury?

Back 89

air pollutants
insecticides
herbicides
carbon monoxide
carbon tetrachloride
social drugs, such as alcohol
recreational drugs
over-the-counter drugs
prescribed drugs

Front 90

What is lead?

Back 90

a heavy metal that persists in the environment

Front 91

What is the primary chemical hazard to children?

Back 91

lead toxicity

Front 92

Compared to adults, children absorb lead more readily through the ______________.

Back 92

intestines

Front 93

What dietary deficiencies enhance the toxic effects of lead?

Back 93

iron
calcium
zinc
vitamin D

Front 94

Why is lead exposure particularly worrisome during pregnancy?

Back 94

because the fetal nervous system is especially vulnerable and can result in learning disorders, hyperactivity, and attention problems

Front 95

What are the organ systems primarily affected by lead ingestion?

Back 95

(1) nervous system
(2) hematopoietic system (tissues that produce RBCs)
(3) the kidneys

Front 96

Lead affects many different biologic activities, many of which may be related to the function of ______________,

Back 96

calcium

Front 97

How are gaseous substances classified?

Back 97

according to their ability to asphyxiate (interrupt respiration) or irritate

Front 98

What do toxic asphyxiants do?

Back 98

directly interfere with cellular respiration

Front 99

What are some examples of toxic asphyxiants?

Back 99

carbon monoxide, hydrogen cyanide, and hydrogen sulfide

Front 100

How does carbon monoxide deprive the body of oxygen?

Back 100

Normally, oxygen molecules are carried to tissues bound to hemoglobin in RBCs.
Because CO's affinity for hemoglobin is 300 times greater than that of oxygen, it quickly binds with the hemoglobin, preventing oxygen molecules from doing so.

Front 101

What symptoms are related to carbon monoxide poisoning?

Back 101

headache
giddiness
tinnitus (ringing in the ears)
nausea
weakness
vomiting

Front 102

Cellular damage is increased by __________ and __________________.

Back 102

(1) reactive oxygen species (ROS)

(2) oxidative stress

Front 103

What is the most common source of human exposure to mercury?

Back 103

fish consumption
dental amalgams
vaccines

Front 104

What are blunt force injuries caused by?

Back 104

the application of mechanical energy to the body resulting in the tearing, shearing, or crushing of tissues

Front 105

What are the most common type of injuries seen in most health care settings?

Back 105

blunt force injuries

Front 106

Blunt force injury may be caused by __________, __________, or a combination of both.

Back 106

(1) blows (where a moving object strikes the body)
(2) impacts (where the moving body strikes a fixed object)

Front 107

What is a contusion?

Back 107

bleeding into the skin or underlying tissues as a consequence of a blow that squeezes or crushes the soft tissues and ruptures blood vessels without breaking the skin

(bruise)

Front 108

How long does it take for a contusion (bruise) to show up?

Back 108

it may take several hours after injury before any change in skin color is seen

Front 109

Describe the color changes a bruise (contusion) goes through.

Back 109

Initially it will be red-purple, eventually becoming blue-black, and then gradually changing to yellow-brown or green before fully disappearing

Front 110

What do the color changes of bruises reflect?

Back 110

the progression of tissue damage and healing that develops in the area of underlying injury.

Front 111

What does the length of time it takes for a bruise to resolve depend on?

Back 111

factors such as the extent and location of the injury and the degree of vascularization in the area.

small contusions may resolve in a matter of days, whereas larger ones can take weeks to completely heal

Front 112

What is a hematoma?

Back 112

a collection of blood in soft tissues or an enclosed space

Front 113

What is a subdural hematoma?

Back 113

a collection of blood between the inner surface of the dura mater and the surface of the brain, resulting in the shearing of small veins that bridge the subdural space.

Front 114

What can cause subdural hematomas?

Back 114

blows, falls, or sudden accleration/deceleration of the head, as occurs in shaken baby syndrome

Front 115

What is an epidural hematoma?

Back 115

a collection of blood between the inner surface of the skull and the dura.

Front 116

What is an epidural hematoma caused by?

Back 116

a torn artery and is almost always associated with a skull fracture

Front 117

What do contusions of the brain result from?

Back 117

(1) a blow or (2) a fall or impact

Front 118

What does an abrasion (scrape) result from?

Back 118

the removal of the superficial layers of the skin that was caused by friction between the skin and the injuring object.

Front 119

What is a laceration?

Back 119

a tear or rip resulting when the tensile strength of the skin or tissue is exceeded.

Front 120

How is a laceration different from an incision?

Back 120

a laceration is much more jagged and irregular, and the edges are abraded.

an incision is where the tissue is cleanly divided by a sharp edge

Front 121

What are lacerations of internal organs more common in?

Back 121

blunt force injuries

Front 122

What are fractures?

Back 122

the breakage or shattering of bones during blunt force blows or impacts

Front 123

What is an incised wound?

Back 123

a cut that is LONGER than it is DEEP.

Front 124

What are hesitation marks?

Back 124

multiple superficial incisions grouped in the same area as the deep, lethal cut in suicides

Front 125

What is a stab wound?

Back 125

a penetrating sharp-force injury that is DEEPER than it is LONG.

Front 126

Give an example of a puncture wound.

Back 126

a wound of the foot caused by stepping on a nail

Front 127

Gunshot wounds may be either ___________ or ______________.

Back 127

(1) penetrating (bullet retained in the body)
(2) perforating (bullet exits)

Front 128

What are the most important factors determining the appearance of a gunshot injury?

Back 128

(1) whether it is an entrance or exit wound
(2) the range of fire

Front 129

What are asphyxial injuries caused by?

Back 129

a failure of cells to receive or utilize oxygen

Front 130

Deprivation of oxygen may be __________ or ___________.

Back 130

(1) partial (hypoxia)
(2) total (anoxia)

Front 131

What are the 4 general categories that asphyxial injuries are grouped into?

Back 131

(1) suffocation
(2) strangulation
(3) chemical asphyxiants
(4) drowning

Front 132

What is suffocation?

Back 132

oxygen failing to reach the blood

Front 133

What is strangulation caused by?

Back 133

compression and closure of the blood vessels and air passages resulting from external pressure on the neck

Front 134

How do chemical asphyxiants work?

Back 134

by either preventing the delivery of oxygen to the tissues OR block its utilization

Front 135

What is the most common chemical asphyxiant?

Back 135

carbon monoxide

Front 136

What is drowning?

Back 136

an alteration of oxygen delivery to tissues resulting from the breathing in of fluid, usually water

Front 137

What is the most important pathologic abnormality in drownings?

Back 137

airway obstruction

Front 138

No matter what mechanism is involved, ______________ will lead to unconsciousness in minutes.

Back 138

cerebral hypoxia

Front 139

What does the disease-causing ability of a microorganism depend on?

Back 139

its ability to (1) invade and destroy cells, (2) produce toxins, and (3) produce damaging hypersensitivity reactions

Front 140

List some mechanisms of cellular injury.

Back 140

(1) genetic factors
(2) nutritional imbalances
(3) physical agents

Front 141

What are some physical agents that can cause cellular injury?

Back 141

(1) temperature extremes
(2) atmospheric pressure
(3) ionizing radiation
(4) illumination
(5) mechanical stresses
(6) noise

Front 142

When do cellular accumulations occur?

Back 142

(also called infiltrations)

occur not only when injury is sublethal and sustained in injured cells but also in normal cells

Front 143

What is the most common degernative change in cells?

Back 143

cellular swelling

Front 144

What is cellular swelling caused by?

Back 144

the shift of extracellular water into the cells.

Front 145

In hypoxic injury, what is the movement of fluid and ions into the cell associated with?

Back 145

acute failure of metabolism and loss of ATP production

Front 146

How does hypoxic injury cause acute failure of metabolism and loss of ATP production?

Back 146

Normally, the pump that transports sodium ions out of the cell is maintained by the presence of ATP and ATPase, the active-transport enzyme.

In metabolic failure caused by hypoxia, reduced ATP and ATPase permit sodium to accumulate in the cell while potassium diffuses outward.

The inreased intracellular sodium increases osmotic pressure, drawing more water into the cell.
The cisternae of the ER become distended, rupture, and coalesce to form large vacuoles that isolate the water from the cytoplasm, a process called vacuolation.

Front 147

What does progressive vacuolation result in?

Back 147

in oncosis or vacuolar degeneration or swelling (degeneration by water).

if cellular swelling affects all the cells in an organ, the organ increases in weight and becomes distended and pale.

Front 148

What is oncosis?

Back 148

a form of cell death where the mechanism is failure of the sodium/potassium pumps of the plasma membrane.

Front 149

What is oncosis caused by?

Back 149

by ischemia and possibly by toxic agents that interfere with ATP generation

Front 150

How long does it take for oncosis to evolve into cellular death?

Back 150

about 24 hours

Front 151

What is cell death usually accompanied by?

Back 151

nuclear dissolution

Front 152

True or False. Cellular swelling is reversible.

Back 152

True

Front 153

What is the early manifestation of almost all types of cellular injury?

Back 153

cellular swelling

Front 154

What is cellular swelling associated with?

Back 154

high fever
hypokalemia (abnormally low concentration of potassium in the blood)
certain infections

Front 155

What is the most common cause of glucose accumulation?

Back 155

the disorder of glucose metabolism, diabetes mellitus

Front 156

What is the function of protein in the cell?

Back 156

cellular structure

Front 157

What consitutes most of the cell's dry weight?

Back 157

proteins

Front 158

Where are proteins synthesized?

Back 158

on ribosomes in the cytoplasm

Front 159

What does the presence of a significant amount of protein in the urine indicate?

Back 159

cellular injury and altered cellular function

Front 160

Where do calcium salts accumulate?

Back 160

in both injured and dead tissues

Front 161

List the mechanism of cellular calcification.

Back 161

(1) the influx of extracellular calcium in injured mitochondria
(2) excretion of acid in alveoli, gastric epithelium, and renal tubules leading to the local production of hydroxyl ions which cause calcium accumulation in these sites

Front 162

When does damage caused by calcium occur?

Back 162

when calcium salts clump and harden, interferring with normal cellular structure and function

Front 163

Pathologic calcification can be _________ or _________.

Back 163

(1) dystrophic
(2) metastatic

Front 164

What conditions cause hypercalcemia?

Back 164

hyperparathyroidism
toxic levels of vitamin D
hyperthyroidism
idiopathic hypercalcemia of infancy
Addison disease (adrenocortical insufficiency)
systemic sarcoidosis
milk-alkali syndrome
increased bone demineralization that results from bone tumors, leukemia, and disseminated cancers

may also occur in advanced renal failure with phosphate retention, resulting in hyperparathyroidism

Front 165

What does chronic hyperuricemia result in?

Back 165

the deposition of urate in tissues, cell injury, and inflammation

Front 166

What are the systemic manifestations of cellular injury?

Back 166

a general sense of fatigue and malaise, a loss of well-being, and altered appetite

fever is often present because of biochemicals produced during the inflammatory response

Front 167

What causes pain?

Back 167

various mechanisms, such as release of bradykinins, obstruction, pressure

Front 168

What does cellular death eventually lead to?

Back 168

cellular dissolution, or necrosis

Front 169

What is necrosis?

Back 169

the sum of cellular changes after local cell death and the process of cellular self-digestion known as autodigestion, or autolysis

Front 170

What are the structural signs that indicate irreversible injury and progression to necrosis?

Back 170

dense clumping and progressive disruption of genetic material and disruption of the plasma and organelle membranes

Front 171

What are the 4 major types of necroses?

Back 171

(1) coagulative
(2) liquefactive
(3) caseous
(4) fatty

Front 172

Where does coagulative necrosis primarily occur?

Back 172

(1) kidneys
(2) heart
(3) adrenal glands

Front 173

What does coagulative necrosis commonly result from?

Back 173

hypoxia caused by severe ischemia or hypoxia caused by chemical injury, especially ingestion of mercuric chloride

Front 174

What is coagulation caused by?

Back 174

protein denaturation, which causes the protein albumin to change from a gelatinous, transparent state to a firm, opaque state

Front 175

What does liquefactive necrosis commonly result from?

Back 175

ischemic injury to neurons and glial cells in the brain

Front 176

What can cause brain tissue to die and be walled off from healthy tissue by cyst formation?

Back 176

bacterial infection, esp. staphylococci, streptococci, and Escherichia coli

Front 177

What does caseous necrosis usually result from?

Back 177

tuberculous pulmonary infection, esp. by Mycobacterium tuberculosis.

Front 178

What is caseous necrosis a combination of?

Back 178

coagulative and liquefactive necroses

Front 179

Describe the process of caseous necrosis.

Back 179

dead cells disintegrate, but the debris is not completely digested by the hydrolases. Tissues resemble clumped cheese in that they are soft and granular. A granulomatous inflammatory wall encloses areas of caseous necrosis.

Front 180

What does gangrenous necrosis refer to?

Back 180

death of tissue

Front 181

What does gangrenous necrosis result from?

Back 181

severe hypoxic injury, commonly occurring because of arteriosclerosis, or blockage, of major arteries, particularly those in the lower leg

Front 182

What is dry gangrene usually the result of?

Back 182

coagulative necrosis
ie: dead, black toes from foot problems related to diabetes

Front 183

What are the characteristics of dry gangrene?

Back 183

the skin becomes very dry and shrinks, resulting in wrinkles, and its color changes to dark brown or black

Front 184

When does wet gangrene develop?

Back 184

when neutrophils invade the site, causing liquefactive necrosis.

Front 185

Where does wet gangrene usually develop?

Back 185

in internal organs

Front 186

What are the characteristics of wet gangrene?

Back 186

the site becomes cold, swollen, and black

a foul odor is present, and if systemic symptoms become severe, death can ensue

Front 187

What is gas gangrene?

Back 187

a special type of gangrene caused by infection of injured tissue by one of many species of Clostridium

Front 188

What do Clostridium bacteria produce?

Back 188

hydrolytic enzymes and toxins that destroy connective tissue and cellular membranes and cause bubbles of gas to form in muscle cells

Front 189

What causes gas gangrene to be fatal?

Back 189

if enzymes lyse the membranes of red blood cells, destroying their oxygen-carrying capacity.

Death is caused by shock.

Front 190

What is apoptosis?

Back 190

an active process of cellular self-destruction called programmed cell death--that is, cells need to die otherwise endless proliferation would lead to gigantic bodies

Front 191

How many new cells does the average human create in a day?

Back 191

about 10 billion new cells, and kill off the same number

Front 192

What are the activated genes that cause apoptosis called? Why?

Back 192

suicide cells

because their activation by the nucleus inactivates so-called life-sustaining genes and promotes pathways leading to killer genes

Front 193

What cells does apoptosis affect?

Back 193

scattered, single cells; although there are examples of it occurring in widespread areas

Front 194

Describe the process of apoptosis.

Back 194

nuclear and cytoplasmic shrinkage of a cell followed by fragmentation into membrane-bound fragments and subsequent phagocytosis by neutrophils from neighboring healthy cells

Front 195

What does apoptosis determine?

Back 195

the size, patterning, and function of many tissues

Front 196

How can apoptosis be activated exogenously?

Back 196

by exogenous factors such as a long-lasting viral infection

Front 197

How can apoptosis be activated endogenously?

Back 197

by the absence of certain growth factors

Front 198

What is physiologic apoptosis important in?

Back 198

in the development of body tissues

for example, it is responsible for local deletion of cells during tissue turnover and normal embryonic development. It has been shown to occur in endocrine-dependent tissues undergoing normal atrophic change

Front 199

What is pathologic apoptosis the result of?

Back 199

intracellular events or adverse exogenous stimuli.

for example, deficiencies of specific enzymes can lead to disease where cells have undergone apoptosis.

liver cells infected with viral hepatitis C, for example, can undergo apoptosis

Front 200

What has apoptosis in hemopoietic cells been linked to?

Back 200

the production of free radicals and can spontaneously occur in some malignant tumors and cells treated with ionizing radiation and chemotherapy.

Front 201

What can absence of apoptosis cause?

Back 201

pathologic change

a mutaton in a gene (bcl-2, for example) that promotes apoptosis may only give the signal to proliferate and not die. Thus, lymphocytes may accumulate, enlarging lymph nodes and eventually proliferating into the blood.

Front 202

What is aging usually defined as?

Back 202

a normal physiologic process that is both universal and inevitable

Front 203

What do the basic mechanisms of aging depend on?

Back 203

the irreversible and universal processes at the cellular and molecular level

Front 204

What happens to cells as they age?

Back 204

atrophy, decreased function, and loss of cells, possibly caused by apoptosis

Front 205

What is sarcopenia?

Back 205

loss of muscle mass

Front 206

What total body changes occur in aging?

Back 206

(1) decrease in height
(2) reduction in circumference of the neck, thighs, and arms
(3) widening of the pelvis
(4) lengthing of the nose and ears

Front 207

What are several of the total body changes the result of?

Back 207

tissue atrophy and decreased bone mass caused by osteoporosis and osteoarthritis

Front 208

What is somatic death?

Back 208

death of the entire person

Front 209

How is postmortem change different than the changes that follow cellular death in a live body?

Back 209

postmortem change is diffuse and does not involve components of the inflammatory response.

Front 210

What are the most notable manifestations that death of the person has occurred?

Back 210

complete cessation of respiration and circulation

the surface of the skin usually becomes pale and yellowish; however, the lifelike color of the cheeks and lips may persist after death that is caused by CO poisoning, drowning, or chloroform poisoning

Front 211

What happens to body temperature after death?

Back 211

it falls gradually immediately after death and then more rapidly (approx. 1.0* to 1.5* F/hr) until, after 24 hours, body temperature equals that of the environment

Front 212

What is postmortem reduction of body temperature called?

Back 212

algor mortis

Front 213

What happens to blood pressure in the retinal vessels after death?

Back 213

it decreases, causing muscle tension to decrease and the pupils to dilate. The face, nose, and chin become sharp or peaked-looking as blood and fluids drain away.

Front 214

What is gravity's effect on blood after death?

Back 214

it causes the blood to settle in the most dependent, or lowest, tissues, which develop a deep purple discoloration called livor mortis

Front 215

What is livor mortis?

Back 215

a deep purple discoloration in the tissues from settling blood

Front 216

What happens within 6 hours after death?

Back 216

acidic compounds accumulate within the muscles because of the breakdown of carbohydrate and depletion of ATP. This interferes with ATP-dependent detachment of myosin from actin (contractile proteins), and muscle stiffening, or rigor mortis, sets in.

Front 217

What is rigor mortis?

Back 217

muscle stiffening

Front 218

How long after death does rigor mortis affect the entire body?

Back 218

within 12 to 14 hours

Front 219

When are the signs of putrefaction obvious?

Back 219

about 24 to 48 hours after death

Front 220

When does rigor mortis diminish causing the body to become flaccid?

Back 220

at 36 to 62 hours

Front 221

Give sequence of events for the death of a cell

Back 221

* Decrease in ATP production
*Na+-K+ pump failure
* cellular swelling
* Ribosome detachment from endo. retic.
* Decrease in protein synthesis
* Intracellular Ca+ brings mitocondrial swelling
* Vacuolation (creates vacuoles)
* Lysozome leakage of digestive enzymes
*Autodigestion of intracellular structures
*Plasma membrane lysis