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PATHO 370 Midterm Review , Verified And Correct Answers, West Coast University
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Chapter 2 Homeostasis and Adaptive Responses to StressorsHomeostasis- state of equilibrium
Allostasis- Ability to successfully adapt to changes
Stress: a state manifested by a specific syndrome of the body developed in response to any
stimuli that made an intense demand on it. Influenced by genetics, socioeconomic status, prior
susceptibilities, pre-existing health status, allostatic state and ability to manage stress
General Adaptation Syndrome (GAS):
Involves 3 STAGES:
• Alarm stage: stimulation of the SNS, resulting in release of catecholamines & cortisol
• Resistance stage: body selects the most effective and economic channels of defense;
cortisol levels present in first stage drop b/c they are no longer needed
• Exhaustion stage: resources are depleted & signs of “wear & tear” or systemic damage
appear
Acute versus Chronic Stress:
• Acute stress: associated with the ANS, the fight or flight response; persons with
preexisting heart disease can have complications with acute stress response that can lead
to arrhythmias; in healthy individuals acute stress response can redirect attention from
behaviors that promote health and interrupt compliance with medication regiments &
exercise programs
• Chronic stress: it has been linked to health disorders including diseases of the
cardiovascular, gastrointestinal, immune, & neurological systems; sympathetic activity
& cortisol are elevated
Physiological stress & psychosocial stress:
• Physiological stress: stress-induced changes in body functions; detected by body’s
normal regulatory sensors; the body alters function to restore normal balance; when
normal balance is restored, negative feedback stops the reaction
• Psychosocial stress: Directly affects central nervous system; turns on the stress
responses, even when the body’s internal sensors have not detected an imbalance
,Adaptation & Coping Mechanisms:
Adaptation: the ability to respond to challenges of physical or psychological homeostasis & to
return to a balanced state.
• Influenced by previous learning, physiologic reserve, time, genetic endowment, age,
health status & nutrition, sleep-wake cycles, & psychosocial factors.
Coping Mechanisms:
• Guided Imagery: scene visualization
• Music therapy: listening to music to ease anxiety or stress
• Massage therapy: manipulation of soft tissues to promote relaxation & relief of muscle
tension
• Biofeedback: technique in which individual leans to control physiologic functioning
Catecholamines
Epinephrine: Released from the adrenal medulla.
• Increases heart rate, BP and cardiac output bronchodilation.
• Increases glycogenolysis and elevates blood glucose levels
• Supplementation and prolongation of fight or flight response, pupil dilation, dry mouth,
increased blood coagulability.
Norepinephrine: Released from postganglionic fibers.
• Constricts blood vessels and raises blood pressure.
• Reduces gastric secretions.
• Increases night and far vision
Adrenal Cortical hormones
Cortisol: Primary glucocorticoid, found in adrenal cortex
• Alteration in glucose, fat, and protein metabolism;
• Suppression of inflammatory & immune responses
Aldosterone: Primary mineralocorticoid
• reabsorption of sodium and water
• Increases blood pressure
Chapter 4 Cell Injury, Aging, and Death
,Cellular response to Stress/Adaptation to stress: cells may adapt by undergoing changes in
size, number, and type. These changes may lead to atrophy, hypertrophy, hyperplasia, metaplasia
and dysplasia. Cellular stresses also include intracellular accumulations & storage of products in
abnormal amounts.
Reversible Cell Injury:
Hydropic swelling: water accumulation. Malfunction of Na-K pump with accumulation of Na+
within the cell. Any injury that results in loss of energy (ATP) will also result in swelling.
Generalized swelling of cells in organs can lead to increase in size and weight; “megaly”
Intracellular Accumulations: Excess accumulations of substances in cells. Leads to cellular
injury due to: toxicity, immune response and taking up cellular space. Ex. Fatty liver
Cellular changes:
Atrophy: decrease in cell size (cell shrinks). Cells that are atrophied reduce oxygen consumption
and other cellular functions by decreasing the size and number of their organelles. ↓ functional
demand. General causes:
• Disuse: reduction in muscle use
• Denervation: atrophy in muscles of paralyzed limbs
• Loss of endocrine stimulation: in relationship with disuse atrophy
• Inadequate nutrition and ischemia: cells decrease size and energy requirements due to
inadequate nutrition and decreased oxygen.
Hypertrophy: increase in cell size and with it an increase in the amount of functioning tissue
mass. ↑ functional demand. Cause increased cell protein content
• Pathogenic Hypertrophy: thickening of urinary bladder and myocardial hypertrophy.
Hyperplasia: increase in the number of cells in an organ or tissue due to mitosis. Occurs in
tissues such as epidermis, intestinal epithelium, and glandular tissue. Causes: usually in response
to increased physiologic demands or hormonal stimulation, persistent cell injury, chronic
irritation of epithelial cells. ↑ functional demand. Ex:
• Breast and uterine enlargement during pregnancy
• regeneration of the liver that occurs after partial hepatectomy
• when removing a kidney, the other kidney with experience compensatory hyperplasia.
, Most forms on NONPHYSIOLOGICAL HYPERPLASIA are due to excessive hormonal or the
effects of growth factors on target tissues.
Metaplasia: a reversible change in which one adult cell type is replaced by another adult cell
type. Usually occurs in response to irritation and inflammation. Fully reversible when injurious
stimulation is removed.
Dysplasia: A deranged cell growth of a specific tissue that results in cells that varies in size,
shape, and organization. Strongly implicated as a precursor of cancer; reversible change.
Cellular Injury:
Reversible: Although impairing cell function, does not result in cell death. 2 patterns can be
observed under microscope:
• Cellular swelling: occurs with impairment of Na+/K+ pump, usually as a result of
hypoxic cell injury
• Fatty change: linked to intracellular accumulations of fat; reversible, usually indicates
severe injury.
Irreversible: Cell death or necrosis can occur in irreversibly damaged cells. Usually occurs as a
consequence of ischemia or toxic injury.
Necrosis: cell death and degradation; UNREGULATED death caused by injuries to cells; cell
swells and ruptures; INFLAMMATION results.
It occurs when the injury is too severe or prolonged to allow adaptation. Usually from a
disruption in blood supply
Cells may undergo liquefaction (brain), coagulation (heart), fat (pancreas), or caseous
(lungs)
Local and systemic indicators of cell death: Pain, elevated serum enzyme levels,
inflammation (fever, increased WBC, malaise), loss of function
Gangrene: Large area of necrotic tissue. Results from interruption of blood supply to a
particular part of the body. Types:
Dry gangrene: lack of arterial blood supply but venous flow can carry fluid OUT of tissue
Wet gangrene: lack of venous flow lets fluid ACCUMULATE in tissue
Gas gangrene: Clostridium infection produces toxins and bubbles.
Fournier’s gangrene: Affects perineal, perianal, genital areas
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