Nf Iii Week 2

Front 1

Cellular Adaptations

Back 1

Allows stressed tissue to survive or maintain function

- Atrophy

- Hypertrophy

- Hyperplasia

- Metaplasia

- Dysplasia

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Atrophy

Back 2

Decreaseor shrinkage in cellular size. If sufficient in number, entire organ becomesatrophic (shrinks). Can happen with any organ, but commonly in skeletal muscle,heart, secondary sex organs, and brain

Front 3

Physiologic Atrophy

Back 3

Occurswith early development. E.g. thymus gland undergoes atrophy during childhood

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Pathologic Atrophy

Back 4

Occurs as result of decreases in workload, pressure use, blood supply, nutrition, hormonal stimulation, and nervous stimulation. Aging brain cells atrophy and endocrine-dependent organs, such as gonads, shrink as hormonal stimulation decreases

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Five Causes of Pathologic Atrophy

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1) Disuse

2) Denervation (paralyzed limbs)

3) Loss of endocrine stimulation (postmenopausal women)

4) Inadequate nutrition

5) Ischemia (decreased blood flow)

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Hypertrophy

Back 6

Increase in the size of cells and consequently in the size of the affected organ. The cells of the heart and kidney are prone to enlargement. Can be physiologic (skeletal muscle) or pathologic (heart enlarges secondary to HTN). Two triggers: mechanical signals and trophic signals

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Hyperplasia

Back 7

Increase in the number of cells resulting from an increased rate of cellular division. Can be physiologic or pathologic. Often occurs with hypertrophy in cells that can synthesize DNA, otherwise only hypertrophy can occur. Epidermis, intestinal epthelium, glandular tissue

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Physiologic Hyperplasia

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1) Compensatory Hyperplasia: adaptive mechanism enabling certain organs to regenerate

2) Hormonal Hyperplasia: occurs chiefly in estrogen-dependent organs such as uterus and breast

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Pathologic Hyperplasia

Back 9

Abnormal proliferation of normal cells, usually in response to excessive hormonal stimulation or growth factors on target cells. E.g. of endometrium from imbalance between over-secretion of estrogen resulting in excessive menstrual bleeding

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Metaplasia

Back 10

Reversible replacement of one mature cell type by another, sometimes less differentiated, cell type. May develop by reprogramming of stem cells that exist on most epithelia or of undifferentiated mesenchymal cells present in connective tissue. They mature along a new pathway because of signals generated by growth factors in cell's environment. E.g. Damage of cells lining bronchi

Front 11

Dysplasia

Back 11

Abnormal changes in the size, shape, uniformity, arrangement, growth, and structure of mature cells. Not true adaptive process, but r/t hyperplasia. Occurs in presence of chronic stressor. Is potentially reversible if stressor is removed. It can sometimes lead to cancer

Front 12

Cell Injury

Back 12

Occurs if the cell is unable to maintain homeostasis in the face of injurious stimuli; modifying factors such as nutritional status

Front 13

Mechanisms of Cell Injury

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1) Hypoxia

2) Impaired Calcium Homeostasis

3) Free Radical Injury

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Hypoxia

Back 14

Lack of sufficient oxygen. Most common cause of cellular injury. Can result from reduced oxygen in air, loss or decreased efficiency of hemoglobin, decreased RBC production, respiratory and CV diseases, and poisoning of oxidative enzymes within cells. Usually caused by ischemia (gradual is tolerated better than acute)

Front 15

Free Radical

Back 15

Electrically uncharged atom or group of atoms that has an unpaired electron making the molecule unstable - restabilizes by accepting or donating an electron. When attacked, electron is lost and molecule becomes a free radical

Front 16

Free Radicals and Reactive Oxygen Species

Back 16

Induce cellular injury known as oxidative stress which occurs when excess ROS overwhelm endogenous antioxidant systems. Highly reactive r/t low chemical specificity

Front 17

Mechanisms of Initiation of Free Radicals

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1) Absorption of extreme energy sources (UV, radiation)

2) Activation of endogenous reactions by systems of electron & oxygen transport

3) Enzymatic metabolism of exogenous chemicals or drugs

Front 18

Free Radical Damage

Back 18

1) Lipid peroxidation (destruction of polyunsaturated fats - steals an electron)

2) Protein alterations (leads to fragmentation of polypeptide chains)

3) DNA fragmentation (decreased protein synthesis)

4) Mitochondrial damage (liberation of Ca++ into cytosol)

Front 19

Causes of Cell Injury

Back 19

1) Physical Agents

2) Radiation Injury

3) Chemical Injury

4) Biologic Agents

5) Nutritional Imbalance

*others

Front 20

Physical Agents: Mechanical Forces (Blunt Force Trauma)

Back 20

Application of mechanical energy to the body resulting in the tearing, shearing or crushing of tissues: abrasion, laceration, fractures, stab wounds, incisions, punctures, gun shot entrance and exit wounds.

Front 21

Contusion (bruise)

Back 21

Bleeding into skin or underlying tissues. Duration depends on extent, location, and degree of vascularization. Hematoma is collection of blood in soft tissue

Front 22

Lacertaion

Back 22

Tear or rip resulting when tensile strength of skin or tissue is exceeded. Ragged or irregular with abraded edges. Lacerations of internal organs are normal in blunt-force trauma

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Fracture

Back 23

Blunt-force blows or impacts can cause bone to break or shatter

Front 24

Gun Shot Wounds: Entrance and Exit

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Can be penetrating (stays in) or perforating (exits); can also fragment

Entrance: All wounds share common features, and overall appearance is most affected by range of fire

Exit: Same appearance no matter the range of fire. Speed and degree of deformation are most important. Usually as clean edges.

*Bullets usually stop just beneath skin

Front 25

Physical Agents: Electrical Forces

Back 25

Electricity travels along the least resistant pathway: bone - fat - tendons - skin- muscles - blood - nerves (highly resistant to least resistant)

Front 26

Physical Agents: Temperature Extremes - Hypothermic Injury

Back 26

Chilling or freezing of cells, creating high intracellular Na+ concentrations. Slows metabolic processes. Abrupt drop in temperature leads to vasoconstriction and increase in blood viscosity blood. Result is ischemia, infarction, and necrosis

Front 27

Physical Agents: Temperature Extremes - Hyperthermic Injury

Back 27

Caused by excessive heat and varies in severity according to nature, intensity, and extent of heat. Accelerates metabolic processes ^1degree = ^10% metabolic demand (increased risk of cellular hypoxia). E.g. burns, burn blisters, heat cramps from vigorous exercise w/o water and salt loss. Heat stroke is life-threatening

Front 28

Types of Radiation Injury

Back 28

Radiation is wave propagated energy

1) Ionizing

2) Ultraviolet

3) Non-ionizing

Front 29

Radiation Injury: Ionizing Radiation

Back 29

Any form of radiation that can remove orbital electrons from atoms and molecules (X-rays, gamma rays, alpha and beta particles).

Can: kill cells, interrupt replication, and cause genetic mutations (lethal & non-lethal)

Caused by: swelling, disruption of mitochondrion, damage to membrane and nucleus

Effects: blood vessel damage, necrosis, fibrosis and tissue scarring, dermatitis

Front 30

Radiation Injury: Ultraviolet

Back 30

Disrupts intracellular bonds

Can cause: Skin cancer and sunburn

Depends on: type of UV ray, exposure intensity, amount of melanin in skin

Causes: release of free radicals and damage to DNA

Front 31

Radiation Injury: Non-ionizing Radiation

Back 31

Can rotate and vibrate atoms and molecules resulting in thermal energy

Types: infrared light, microwaves, laser energy

Capable of: dermal and subcutaneous injury

Front 32

Injury from Nutritional Imbalances

Back 32

Pathophysiologic cellular effects develop from nutritional excess such as hyperglycemia, hyperlipidemia (cholesterol - HDL, LDL, VLDL), and nutritional deficiency such as albumin and vitamins

Front 33

Chemical Injury

Back 33

Mechanism: triggers a biochemical reaction between the toxic substance and the cell membrane (increase permeability). Site of injury is often the liver

Front 34

Chemical Injury: Drugs

Back 34

Street, prescription, OTC

Front 35

Chemical Injury: Lead Toxicity

Back 35

Inactivates enzymes, can demyelinate nervous tissue, and cause anemia

Sources: Cosmetics, mining, paint, soil, pipes

Absorption: GI, lungs, cuts in skin

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Chemical Injury: Mercury Toxicity

Back 36

Sources: tuna, swordfish, shark, compact fluorescent light bulbs

Absorption: GI, lungs

Front 37

Chemical Injury: Carbon Monozide

Back 37

Sources:

Front 38

Chemical Injury: Ethylene Glycol

Back 38

Sources:

Front 39

Biologic/Infectious Agents: Viruses and Bacteria

Back 39

Pathogenicity: ability to survive and proliferate in the human body

Virulence (disease-producing potential) depends on: ability to invade and destroy cells, produces toxins, and produce hypersensitivity reactions

Injury of cell membrane (K+ leakage and rapid H2O influx) triggers inflammatory response

Front 40

Other Factors Causing Cell Injury

Back 40

Medication errors in health care, asphyxia, genetic factors (sickle cell anemia and muscular dystrophy), atmospheric pressure changes (blast injury, decompression sickness), illumination injury (cataract formation), noise (hearing loss), immune and inflammatory substances (histamine, antibodies, etc)

Front 41

Manifestation of Cellular Injury: Oncosis (Hydropic Degeneration)

Back 41

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Front 42

Coagulative Necrosis

Back 42

Primarily in kidneys, heart, and adrenal glands. Usually from ischemia/hypoxia due to chemical injruy. Caused by protein denaturation, causing albumin to change from gelatinous & transparent to firm and opaque

Front 43

Liquefactive Necrosis

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Usually ischemic injury to neurons and glial cells in brain. Digested by their own enzymes, tissue becomes liquefied and segregates from healthy tissue, forming cysts

Front 44

Caseous Necrosis

Back 44

Usually results from Tb pulmonary infection. Combination of coagulative and liquefactive necroses. Dead cells disintegrate, but debris isn't completely digested. Tissue resembles clumps of cheese

Front 45

Fat Necrosis

Back 45

Cellular dissolution by lipases that occur in breast, pancreas, and other abdominal structures. Tissue appears opaque and chalk-white

Front 46

Somatic Death

Back 46

Death of entire person. Post-mortem change is diffuse and does not involve components of the inflammatory response. Changes appear within minutes after death (e.g. cessation of respiration and circulation)

Front 47

Algor Mortis

Back 47

Post-mortem reduction of body temperature, which falls gradually immediately after death and then more rapidly until after about 24 hours when body temperature equals that of the environment. Death by certain infective diseases may allot body temperature to continue to rise for a short time

Front 48

Livor Mortis

Back 48

Settling of blood by gravity in lowest tissues resulting in a purple discoloration. BP within retinal vessels decreases and causes muscle tension to decrease and pupils to dilate. Face, nose, and chin become sharp as blood and fluid drain from head. Incisions usually fail to cause bleeding. Skin loses elasticity and transparency

Front 49

Rigor Mortis

Back 49

Muscle stiffening. Within 6 hours after edath, acidic compounds accumulate within muscle because of breakdown of carbs and depletion of ATP. This interferes with ATP-dependent detachment of myosin from actin, and rigor mortis develops. Smaller muscles are usually affected first, particularly of the jaw. Within 12-14 hours, rigor mortis usually affects entire body

Front 50

Putrefaction

Back 50

Process of decay or rotting of the body. Signs are obvious within 24-48 hours. Rigor mortis gradually diminishes and body becomes flaccid 36-62 hours. Putrefaction changes vary depending on temperature of environment. Greenish discoloration of skin, slipage of skin from underlying tissues at same time, and then liquefactive changes occur

Front 51

Stress

Back 51

Nonspecific response of the body to forces or demands, capable of disturbing homeostasis. The body's response to a threat or demand

Front 52

Homeostasis

Back 52

Purposeful maintenance of a stable internal environment coordinated by physiological responses that resist internal and external disturbances to promote adaptation and healthy survival. Operates via negative feedback systems

Front 53

Negative Feedback Mechanisms

Back 53

A control system to regulate the body's internal conditions. An increase in a substance triggers an event/cascade to lower the substance

Front 54

Allostasis

Back 54

The process of achieving homeostasis in the presence of a challenge. Involves interactive physiologic changes in the neuroendocrine, autonomic, and immune systems in response to homeostatic threats

Front 55

Allostatic Load

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The persistence of allostatic mechanisms. Used to measure the cumulative effects of stress

Front 56

General Adaptation Syndrome

Back 56

Stressors from different sources produce a similar physical response. Three stages:

1) Alarm reaction

2) Stage of resistance

3) Stage of exhaustion

Stressor stimulates CNS, multiple responses occur because of HPA axis activation and the autonomic nervous system

Front 57

GAS: Alarm Stage

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