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Adv Pathophysiology > Chapter 3: Cellular Adaptation > Flashcards

Chapter 3: Cellular Adaptation Flashcards

1
Q

REVERSIBLE cell injury

A

cells responds to stressors appropriately and can repair itself

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2
Q

IRREVERSIBLE cell injury

A

occurs when the stressor is prolonged, outlasting the adaptation capabilities of the cell
the cell dies

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3
Q

Atrophy

A

(without nourishment)

decrease in size and number of cells

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4
Q

Hypertrophy

A

(over nourishment)

increase in the SIZE of cells

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5
Q

Hyperplasia

A

(over formation)
increase in the NUMBER of cells
not seen in muscles, neurons, or cardiac cells

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6
Q

Metaplasia

A

change in formation

reversible change in which one adult cell type is replaced by another

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7
Q

Dysplasia

A

abnormal formation

deranged cell growth of a specific tissue that results in cells that vary in size, shape, and organization

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8
Q

Autophagia

A

starved cells eat their own cell components for survival

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9
Q

Expected atrophy

A

thymus (before puberty as levels of sex hormones increase)
uterus atrophy after delivery
breast tissue atrophy after lactation

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10
Q

DISUSE atrophy

A

having extremity in a cast

prolonged bed rest

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11
Q

DENERVATION atrophy

A

occurs in the muscles of paralyzed limbs due to loss of neural signals

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12
Q

LOSS OF ENDOCRINE STIMULATION atrophy

A

Menopause (loss of estrogen = atrophy of reproductive organs)
Hypopituitarism = atrophy of thyroid, gonads, and adrenal glands
Overuse of testosterone = testicular atrophy
Overuse of steroids = atrophy of the adrenal glands

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13
Q

INADEQUATE NUTRITION atrophy

A

Body depletes glycogen stores then fats then proteins (muscles)

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14
Q

Muscle wasting

A

cells being “eating” their own myosin and actin to stay alive

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15
Q

ISCHEMIA atrophy

A

atherosclerosis of cerebral blood vessels leads to brain atrophy

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16
Q

Labile and stable cells

A

capable of division

can undergo hypertrophy AND hyperplasia

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17
Q

Permanent cells

A

cardiac and skeletal muscle cells

can ONLY undergo hypertrophy

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18
Q

PHYSIOLOGIC hypertrophy

A

Physiologic conditions = increase in workload not caused by disease
Lifting weights, exercising

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19
Q

ADAPTIVE PATHOLOGIC hypertrophy

A

Responses are aimed at maintaining function
Hypertrophy of the myocardium d/t HTN
Hypertrophy of the stomach r/t pyloric stenosis
Hypertrophy of the bladder d/t BPH

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20
Q

COMPENSATORY PATHOLOGIC hypertrophy

A

One kidney is removed, the other will enlarge to compensate for the loss of its pair

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21
Q

HORMONAL-PHYSIOLOGIC hyperplasia

A

increase in # of cells to increase the functional capacity of the organ
Example: uterus response to increase in estrogen after ovulation

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22
Q

COMPENSATORY-PHYSIOLOGIC hyperplasia

A

increase in # of cells to increase the tissue mass after damage or partial removal
Regeneration of liver cells
Callus (hyperplasia of epithelial cells over over-worked area)
People living in high altitudes (hyperplasia of RBCs)

23
Q

NONPHYSIOLOGIC (PATHOLOGIC) hyperplasia

A

response to either excessive hormonal stimulation or abnormal production of hormonal growth factors
Examples: BPH, acromegaly, endometrial hyperplasia, warts and cancers caused by HPV, psoriasis

24
Q

EPITHELIAL metaplasia

A

Barrett’s esophagus - change in esophageal cells to columnar cells (found in the GI tract) that are better suited to exposure to acid
Smoking

25
Example of dysplasia
bronchopulmonary dysplasia (BPD) in preterm infants associated with prolonged supplemental oxygen concentration
26
Intracellular accumulations
represents to buildup of substances that cells cannot immediately use or eliminate
27
intracellular accumulation: NORMAL BODY SUBSTANCES
occurs when substances are produced at a rate that is higher than the body's metabolism for removal Examples: lipids, proteins, carbohydrates, melanin, bilirubin, fatty acids
28
intracellular accumulation: EXOGENOUS PRODUCTS
environmental agents (lead, mercury, coal dust) or ink (tattoos) that cannot be broken down by cells so they accumulate
29
intracellular accumulation: ENDOGENOUS PRODUCTS
can be related to inborn errors in metabolism and genetic disorders that can disrupt the metabolism of certain drugs Example: Tay Sachs disease
30
Pathologic calcifications
involves abnormal tissue deposition of calcium salts along with smaller amounts of other minerals
31
DYSTROPHIC calcification
macroscopic deposition that occurs in dead/dying tissue - frequent cause of organ dysfunction serum calcium levels will be NORMAL Causes: infarcts, thrombi, tumors, and cysts
32
METASTATIC calcification
occurs in normal tissues in response to increased serum calcium levels (hypercalcemia) Causes: hyperparathyroidism, prolonged immobilization, renal failure
33
Cell injury from MECHANICAL FORCES | physical agents
occurs as a result of body impact with another object | direct damage to cells - tears tissues, fractures bones, disrupts blood flow
34
Cell injury from EXTREMES OF TEMPERATURE | physical agents
Intense heat = coagulation of blood and tissue proteins | Extreme cold = increases blood viscosity, causes vasoconstriction (capillary stasis, thrombosis, edema)
35
Cell injury from ELECTRICAL INJURY | physical agents
causes extensive tissue injury and disruption of neural and cardiac impulses effect on the body is affected by VOLTAGE, TYPE OF CURRENT, PATHWAY of the current, RESISTANCE of the tissue, and DURATION of exposure
36
VOLTAGE
lightning and high voltage wires produce the most severe damage
37
ELECTRICAL CURRENT
AC (alternating current) is more dangerous than DC (direct current) due to violent muscle contractions, causing the person to be unable to release the electrical source
38
PATHWAY and RESISTANCE of electrical current
tissues with higher electrical resistance will suffer more damage Thick, dry skin will have higher resistance = localized injury (skin burns) Wet, thin skin has less resistance = deeper, systemic effects
39
Cell injury from CHEMICAL INJURY
chemicals can injure cells when they come into contact with the body or injure cells in the process of metabolism or elimination (excretion) Examples: pollution, tobacco smoke, processed/preserved foods, carbon monoxide, insecticides, drugs (alcohol, antineoplastics, acetaminophen), and lead (esp in infants and children)
40
Lead toxicity
absorbed through GI tract or lungs and stored in bone and excreted by kidneys Effects: inactivates enzymes competes with calcium interferes with nerve transmission and brain development
41
Major targets of lead toxicity
RBCs GI tract Kidneys Nervous system
42
Cell injury from BIOLOGIC AGENTS
Viruses - incorporate into DNA of cell and use up its resources Bacteria - damage cells through exotoxins or endotoxins Parasites
43
Cell injury from NUTRITIONAL IMBALANCES
nutritional excesses and nutritional deficiencies predispose cells to injury Obesity and high-fat diets = atherosclerosis Starvation = protein and calorie deficiencies = widespread tissue damage Selective deficiencies: iron, vitamin C, thiamine, niacin, folic acid, vitamin B12
44
HYPOXIC Cell Injury | mechanism of cell injury
Hypoxia deprives the cell of oxygen and interrupts oxidative metabolism and the generation of ATP = "power failure" Leads to anaerobic metabolism = lactic acid production = cell damage Brain is the first to deteriorate in hypoxic injury d/t high oxygen demand
45
IMPAIRED CALCIUM HOMEOSTASIS | mechanism of cell injury
calcium functions as a messenger for the release of many intracellular enzymes normally, extracellular Ca > intracellular Ca certain toxins can lead to the increase in intracellular metabolism
46
Patterns of REVERSIBLE cell injury
``` impairs cell function but does not result in cell death Cellular swelling (impairment of the Na/K-ATPase pump) Fatty change (intracellular accumulation of fat) ```
47
APOPTOSIS (programmed cell death)
highly selective, controlled autodigestion of cell components normal physiologic process in the body once apoptosis begins, it cannot be stopped - energy dependent
48
NECROTIC cell death
unregulated death caused by injuries to cells cells swell and rupture - inflammation results damage to one cell can have a snowball effect on other/surrounding cells not energy dependent
49
LIQUEFACTIVE necrosis
liquefies necrotic cells - softened center of an abscess common in brain (rich supply of enzymes) wet gangrene
50
COAGULATIVE necrosis
looks like a firm gray mass related to hypoxia and seen in infarcted areas (cardiac and muscle tissue) dry gangrene
51
CASEOUS necrosis
soft, cheesy appearance | mainly found in center of tuberculous granulomas (pulmonary tuberculosis)
52
DRY Gangrene
form of coagulative necrosis spreads very slowly line of demarcation exists interference of arterial blood supply
53
WET Gangrene
``` form of liquefactive necrosis area is cold, swollen, pulseless, moist, often with a foul odor spreads rapidly (can have severe systemic symptoms) interferes with venous return ```
54
GAS Gangrene
severe trauma introduces bacteria that release toxins affected muscle cells release gas bubble (hydrogen sulfide gas) spreads rapidly - can cause widespread edema can be fatal

Adv Pathophysiology (22 decks)

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