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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
Q

Example of dysplasia

A

bronchopulmonary dysplasia (BPD) in preterm infants associated with prolonged supplemental oxygen concentration

26
Q

Intracellular accumulations

A

represents to buildup of substances that cells cannot immediately use or eliminate

27
Q

intracellular accumulation: NORMAL BODY SUBSTANCES

A

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
Q

intracellular accumulation: EXOGENOUS PRODUCTS

A

environmental agents (lead, mercury, coal dust) or ink (tattoos) that cannot be broken down by cells so they accumulate

29
Q

intracellular accumulation: ENDOGENOUS PRODUCTS

A

can be related to inborn errors in metabolism and genetic disorders that can disrupt the metabolism of certain drugs
Example: Tay Sachs disease

30
Q

Pathologic calcifications

A

involves abnormal tissue deposition of calcium salts along with smaller amounts of other minerals

31
Q

DYSTROPHIC calcification

A

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
Q

METASTATIC calcification

A

occurs in normal tissues in response to increased serum calcium levels (hypercalcemia)
Causes: hyperparathyroidism, prolonged immobilization, renal failure

33
Q

Cell injury from MECHANICAL FORCES

physical agents

A

occurs as a result of body impact with another object

direct damage to cells - tears tissues, fractures bones, disrupts blood flow

34
Q

Cell injury from EXTREMES OF TEMPERATURE

physical agents

A

Intense heat = coagulation of blood and tissue proteins

Extreme cold = increases blood viscosity, causes vasoconstriction (capillary stasis, thrombosis, edema)

35
Q

Cell injury from ELECTRICAL INJURY

physical agents

A

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
Q

VOLTAGE

A

lightning and high voltage wires produce the most severe damage

37
Q

ELECTRICAL CURRENT

A

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
Q

PATHWAY and RESISTANCE of electrical current

A

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
Q

Cell injury from CHEMICAL INJURY

A

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
Q

Lead toxicity

A

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
Q

Major targets of lead toxicity

A

RBCs
GI tract
Kidneys
Nervous system

42
Q

Cell injury from BIOLOGIC AGENTS

A

Viruses - incorporate into DNA of cell and use up its resources
Bacteria - damage cells through exotoxins or endotoxins
Parasites

43
Q

Cell injury from NUTRITIONAL IMBALANCES

A

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
Q

HYPOXIC Cell Injury

mechanism of cell injury

A

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
Q

IMPAIRED CALCIUM HOMEOSTASIS

mechanism of cell injury

A

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
Q

Patterns of REVERSIBLE cell injury

A 
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
Q

APOPTOSIS (programmed cell death)

A

highly selective, controlled autodigestion of cell components
normal physiologic process in the body
once apoptosis begins, it cannot be stopped - energy dependent

48
Q

NECROTIC cell death

A

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
Q

LIQUEFACTIVE necrosis

A

liquefies necrotic cells - softened center of an abscess
common in brain (rich supply of enzymes)
wet gangrene

50
Q

COAGULATIVE necrosis

A

looks like a firm gray mass
related to hypoxia and seen in infarcted areas (cardiac and muscle tissue)
dry gangrene

51
Q

CASEOUS necrosis

A

soft, cheesy appearance

mainly found in center of tuberculous granulomas (pulmonary tuberculosis)

52
Q

DRY Gangrene

A

form of coagulative necrosis
spreads very slowly
line of demarcation exists
interference of arterial blood supply

53
Q

WET Gangrene

A 
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
Q

GAS Gangrene

A

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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