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140 Cards in this Set

  • Front
  • Back

Decrease or shrinkage in cell & organ size.



(ex. skeletal muscle deprived of innervation)

Atrophy

Increase in the size of cells & organ.



(ex. skeletal & cardiac muscle)

Hypertrophy

Increase in number of cells.



(ex. liver enlarges to compensate if parts is removed & breasts enlarge due to hormonal signals during pregnancy)

Hyperplasia

Reversible replacement of one mature cell type by another cell type. It can progress to dysplasia & neoplasia (cancer).



(ex. in the bronchi smoking can cause pseudostratified ciliated columnar ep. to change stratified squamous ep.)

Metaplasia

Abnormal changes in size, shape & organization of mature cells. Not a true adaptive change. Due to persistent severe irritation. Often reversible if stimulus is removed. Can progress to neoplasia.



(ex. cervical dysplasia due to human papillomavirus)

Dysplasia

Cells can recover if injurious stimuli ceases

Reversible

Cells die due to injury

Irreversible

Due to lack of sufficient oxygen, usually from ischemia.

Hypoxic Injury

Reduced blood supply; if gradual, then adaptation can occur. (ex. a growing thrombus which gradually blocks a vessel)

Ischemia

Total lack of oxygen. This is not well tolerated by most tissues. (ex. an embolus which lodges in a vessel)

Anoxia

Cellular Response:



Lack of oxygen impairs cellular respiration. Results in failure of sodium-potassium pump & sodium-calcium exchange. Decreased protein synthesis & decreased membrane transport.

Decreased ATP levels

Sodium & Calcium accumulate _____

Inside cells

Potassium accumulates _____

Outside cells

Due to movement of sodium into cells

Cellular Swelling

If oxygen is not restored, _____ accumulates in the cytoplasm

Vacuoles

Membrane-bound spheres that may contain fluid, lipids or other materials.

Vacuoles

Cellular Response:



Organelles swell causing ribosomes to detach from the endoplasmic reticulum. Swelling may lead to rupture of lysosomes.

Vacuolation

Cellular Response:



Due to swelling which damages mitochondrial membrane. Changes in membrane permeability. Loss of membrane potential. Decreased ATP production.

Mitochondrial damage

Between the outer & inner membranes of the mitochondria are proteins that can activate the cell's suicide pathways, called _____


Apoptosis

Cellular Response:



Normally intracellular cytosolic calcium concentrations are very low. Ischemia & certain chemicals cause an increase in cytosolic Calcium concentrations. Calcium causes intracellular damage by activating a number of enzymes that further deplete ATP levels & cause membrane & DNA damage.

Accumulation of Calcium

Damage is irreversible when there is:

Severe swelling of the mitochondria


Severe damage to plasma membranes


Rupture of lysosomes & release of lysosomal enzymes


Cells may undergo either necrosis or apoptosis, depending on the cause

Electrically uncharged atom or group of atoms having an unpaired electron.

Free radicals & reactive oxygen species.

Damages membranes of cell & organelles, increases permeability

Lipid peroxidation

Especially those for ion pumps & transport proteins

Alteration of proteins

Fragmenting of DNA reduces protein synthesis

Alteration of DNA

Allows liberation of calcium into cytosol

Mitochondrial damage

Ionizing radiation can knock electrons out or orbit. This produces free radicals.

Radiation

CHEMICAL INJURY



Liver converts this to a toxic free radical. Causes lipid peroxidation. These result in fatty liver, cellular autodigestion & decreased ATP production.

Carbon tetrachloride (CCl4)

CHEMICAL INJURY



Neurological problems (interferes with neurotransmitter release). Causes anemia & renal problems.

Lead

CHEMICAL INJURY



Prevents oxygen from binding to hemoglobin. Causes cherry red coloring of skin.

Carbon monoxide

CHEMICAL INJURY



Acetaldehyde & free radicals in liver. Causes inflammation, fatty liver, membrane damage. Depresses CNS by acting on reticular formation which normally inhibits unacceptable behaviours.

Ethanol

CHEMICAL INJURY



Causes birth defects & brain damage in fetuses & small children.

Mercury

A term which defines a development of cancer or pre-cancerous

Dysplasia

TIA

Transient Ischemic Attack

Tends to accumulate endogenous materials of the cell

Complex substrate

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

Blunt force injuries

BLUNT FORCE INJURIES



"Bruise", release of blood into tissues from damaged vessels without break in skin

Contusion

BLUNT FORCE INJURIES



A collection of blood in soft tissues or an enclosed space, subdural space, etc.

Hematoma

BLUNT FORCE INJURIES



"Scrape", removal of the superficial layers of skin due to friction

Abrasion

BLUNT FORCE INJURIES



A rip or tear of the skin; irregular edges

Laceration

BLUNT FORCE INJURIES



An extreme laceration

Avulsion

BLUNT FORCE INJURIES



Breakage of bone tissue

Fractures

SHARP INJURIES



A cut that is longer than it is deep

Incised wounds

SHARP INJURIES




A penetrating sharp-force injury that is deeper than that is long

Stab wounds

SHARP INJURIES



Caused by pointed objects without sharp edges

Puncture wounds

SHARP INJURIES



Caused by axes, hatches, propeller blades, etc.

Chopping wounds

GUNSHOT WOUNDS



Usually have an abrasion collar

Entrance wounds

GUNSHOT WOUNDS



Muzzle touching skin, blow-back & muzzle imprint

Contract range entrance wound

GUNSHOT WOUNDS



Muzzle not touching skin; less than 48 inches away.

Intermediate range entrance wound

GUNSHOT WOUNDS



Fragments of gunpowder driven into skin or cause abrasion

Tattooing & stippling

Caused by a failure of cells to receive or use oxygen

Asphyxial injuries

ASPHYXIAL INJURIES



Caused by lack of oxygen in environment or blockage of external airways

Suffocation

ASPHYXIAL INJURIES



Blockage of internal airways

Chocking asphyxiation

ASPHYXIAL INJURIES



Caused by compression & closure of blood vessels & air passageway by external pressure. Death due to lack of blood flow to brain.

Strangulation

ASPHYXIAL INJURIES



Caused by suspension

Hanging

ASPHYXIAL INJURIES



Caused by cord around neck

Ligature

ASPHYXIAL INJURIES



Caused by hands

Manual strangulation

ASPHYXIAL INJURIES



Prevent delivery or utilization of oxygen in tissues.

Chemical asphyxiants

ASPHYXIAL INJURIES



prevents oxygen binding to cytochrome oxidase in mitochondria, causing cherry red coloring like CO poisoning.

Cyanide

ASPHYXIAL INJURIES



Alteration of oxygen delivery due to breathing fluid into lungs.

Drowning

Pathogenicity of a microorganism

Infectious injury

INFECTIOUS INJURY



Disease-producing potential depends on organisms ability for:

Invasion & destruction


Toxin production


Production of hypersensitivity reactions

Pathologic accumulations can occur due to:

1. Excess production of normal substance


2. The substance not being broken down due to lack of an enzyme


3. Accumulation of harmful exogenous substances

CELLULAR ACCUMULATIONS:



Enters cells due to lack of ATP & failure of Sodium-Potassium pump, causing cellular swelling.

Water

CELLULAR ACCUMULATIONS:



(Hydropic degeneration) Water accumulates in endoplasmic reticulum forming vacuoles separate from cytoplasm. Visually the organs appear pale.

Oncosis

CELLULAR INJURY MECHANISMS



Reperfusion injury due to

Oxidative stress

CELLULAR INJURY MECHANISMS



When oxygen is restored, reactive oxygen intermediates damage organelles. Can be prevented using antioxidants.

Reperfusion injury

Involves phagocytic cells, immune & inflammatory substances, & membrane alterations

Immunologic & Inflammatory Injury

IMMUNOLOGIC & INFLAMMATORY INJURY



Cause leakage of potassium out of cell & influx of sodium & water

Membrane alterations

Can trigger immune attack & lysis

Antibodies

Stored form of glucose

Glycogen

Formation of glycogen

Glycogenesis

Breakdown of glycogen

Glycogenolysis

Organ that performs glycogenesis

Liver

It is a clinical disturbance defined by a pH less than 7.35 & a low HC03 level

Metabolic acidosis

Accumulate (usually in spleen, liver & CNS) due to metabolic disorders like Tay-Sachs & Niemann-Pick disease

Lipids & Carbohydrates

Can be caused by disruptions of normal lipid metabolism.

Fatty change

Occurs in disorders of glucose & glycogen metabolism. Includind diabetes mellitus.

Glycogen

Accumulate during pathological change in renal tubes & B lymphocytes

Proteins

During glomerular disorders that cause proteinuria

Renal tubes

Excess antibodies form in multiple myeloma cells

B lymphocytes

Accumulation may be normal or signal pathological changes

Pigments

A pigment where:



Normal - suntan


Pathologic - melanoma

Melanin

A pigment where:




Pathologic: Bruising & Jaundice

Hemoproteins, hemosiderin & bilirubin (from RBC breakdown)

Occurs due to hypoxia or excess levels of calcium

Calcium

Occurs in dying & dead tissues, advanced atherosclerosis, etc.

Dystrophic calcification

Mineral deposits that occur in undamaged normal tissues as the result of hypercalcemia

Metastatic calcification

Due to increased levels of uric acid from purine catabolism

Urate

CELLULAR DEATH



Cellular dissolution. Sum of cellular changes after local cell death & the process of cellular autodigestion.

Necrosis

CELLULAR DEATH PROCESSES

Karyolysis


Pyknosis


Karyorrhexis

CELLULAR DEATH PROCESS



Nuclear dissolution & chromatin lysis

Karyolysis

CELLULAR DEATH PROCESS



Clumping of the nucleus

Pyknosis

CELLULAR DEATH PROCESS



Fragmentation of the nucleus

Karyorrhexis

Substrate + Enzyme = ?

Products

Produces sodium

Osmotic pressure

Produces albumin

Oncotic pressure

Stiffening/hardening of artery; more general term that describes the hardened arteries; lessen elasticity

Arteriosclerosis

Lipid accumulation; narrowing of artery because of lack formation; under of arteriosclerosis

Atherosclerosis

Occurs in kidneys, heart & adrenal glands.

Coagulative Necrosis

Results from hypoxia caused by severe ischemia or chemical injury (ex. mercuric chloride intake)

Protein denaturation

Occurs in neurons & glial cells of the brain



Bacterial infection: Staphylococci, streptococci & E.coli

Liquefactive Necrosis

From lysozyme in dying cells

Hydrolytic enzymes

Occurs in tuberculosis pulmonary infection. Combination of coagulative & liquefactive necrosis. Cells disintegrate but are not completely digested.

Caseous Necrosis

Occurs in breast, pancreas, & other organs that have lipases enzyme

Fat Necrosis

Releases free fatty acids that react with calcium, magnesium & sodium

Action of lipases

Causing death of tissue from severe hypoxic injury & Gas gangrene

Gangrenous Necrosis

Often due to atherosclerosis or trauma

Death of tissue from severe hypoxic injury

Coagulative

Dry gangrene

Liquefactive necrosis (internal organs)

Wet gangrene

Bacteria produce hydrolytic enzymes & create gas bubbles in muscles

Gas gangrene

Anaerobic bacteria responsible for gas gangrene

Clostridium

Death of unnecessary cells due to action of enzymes produces within cell

Apoptosis

Prevents overgrowth of cells

Programmed cellular death

Can cause overgrowth of cells, resulting in cancer

Defects in apoptosis

Physiologic of Apoptosis include:

During embryonic development


As a result of hormonal changes


In nutrient deprived tissues

Pathologic of Apoptosis include:

Severe cell injury


Accumulation of misfolded proteins


Viral infections


Obstruction of tissue ducts

Remains bound in a membrane forming apoptotic bodies which are removed by neutrophils & macrophages

Cellular debris

Due to damage from exogenous injury. Usually involves many cells in area of injury. Cell membranes rupture, releasing cell contents into tissue. Triggers inflammatory response.

Necrosis

AGING & ALTERED CELLULAR & TISSUE BIOLOGY



Time-dependent loss of structure & function that proceeds slowly due to accumulated small injuries

Aging

AGING & ALTERED CELLULAR & TISSUE BIOLOGY



Abnormal dysfunction due to injury

Disease

AGING & ALTERED CELLULAR & TISSUE BIOLOGY



Across culture the maximal life span is 80-100 years.

Normal life span

AGING & ALTERED CELLULAR & TISSUE BIOLOGY



Females have a life expectancy about 5 years greater than males.

Gender differences

3 THEORIES & MECHANISMS OF AGING

1. Genetic & Environmental-Lifestyle Factors


2. Alterations of cellular control mechanisms


3. Degenerative extracellular & vascular changes

THEORIES & MECHANISMS OF AGING



Programmed aging, Somatic mutation hypothesis & Catastrophic or error-prone theory are under of?

Genetic & Environmental-Lifestyle Factors

THEORIES & MECHANISMS OF AGING



Cells have a finite lifespan with a finite number of possible divisions, after which the DNA loses the capacity for mitosis

Programmed aging

THEORIES & MECHANISMS OF AGING



Repetitive injury to the DNA causes progressive mutations that interfere with the ability of the cell to repair itself & maintain DNA & protein synthesis

Somatic mutation hypothesis

THEORIES & MECHANISMS OF AGING



The enzymes responsible for transcription & translation become increasingly abnormal, leading to increasing errors in protein synthesis

Catastrophic or error-prone theory

THEORIES & MECHANISMS OF AGING



Neuroendocrine theory & Immune theory are under of?

Alterations of cellular control mechanisms

THEORIES & MECHANISMS OF AGING



The genetic program for aging is encoded in the brain & is controlled & relayed to peripheral tissues through hormonal & neural signals

Neuroendocrine theory

THEORIES & MECHANISMS OF AGING



With aging, there is decreased immunity to invades & cancer & increased autoimmunity (immune system attacks self)

Immune theory

THEORIES & MECHANISMS OF AGING



Binding of collagen, free radical effects (oxidative stress) & alterations in peripheral blood vessels are under of?

Degenerative extracellular & vascular changes

THEORIES & MECHANISMS OF AGING



Crosslinking, decreased synthesis & increased breakdown of collagen

Binding of collagen

THEORIES & MECHANISMS OF AGING



Damage to DNA; malignancies & cell death

Free radical effects (oxidative stress)

THEORIES & MECHANISMS OF AGING



Decreased vessel integrity & atherosclerosis

Alterations in peripheral blood vessels

Consists of Cellular aging, tissue & systemic aging, & Frailty

Aging

Characterized by atrophy, decreased function, & loss of cells

Cellular aging

Every physiologic process declines in efficiency with age

Tissue & systemic aging

Arterial, pulmonary, & musculoskeletal systems

Progressive stiffness & rigidity

Loss of muscle mass & strength

Sarcopenia

Decreased mobility, balance, muscle strength, motor activity, cognition, nutrition, endurance & bone density result in increased falls 7 fractures. Accompanied by declining hormone levels & increased levels of proinflammatory cytokines

Frailty