NURS 5315 Advanced Pathophysiology Exam 1 | UTA | Questions and Answers
Atrophy E. Cells decrease in size
P. Still functional; imbalance between protein synthesis and degradation. Essentially
there is an increase in the catabolism of intracellular organelles, reducing structural
components of cell
Physiologic: thymus gland in early childhood
Pathological: disuse (muscle atrophy d/ decrease workload, pressure, use, blood
supply, nutrition, hormonal stimulation, or nervous stimulation)
Hyperplasia E: cells increase in number, mitosis (cell division) must occur, size of cell does not
change
Phys: increased rate of division, increase in tissue mass after damage or partial
resection; may be compensatory, hormonal, or pathologic
Patho: abnormal proliferation of normal cells usually caused by increased hormonal
stimulation (endometrial). increase of production of local growth factors
Ex: removal of part of the liver lead to hyperplasia of hepatocytes. uterine or
mammary gland enlargement during pregnancy
Dysplasia E. Not true adaptation; Cells abnormal change in size, shape, organization
(classified as mild, moderate, severe)
P. caused by cell injury/irritation, characterized by disordered cell growth. aka
atypical hyperplasia or pre-cancer, a disorderly proliferation
Physiologic: N/A
Pathologic: squamous dysplasia of cervix from HPV shows up on pap smear, breast
cancer development; pap smears often show dysplastic cells of the cervix that must
undergo laser/surgical tx
Metaplasia E: reversible change, one type of cell changes to another type for survival
P: reversible; results from exposure of the cells to chronic stressors, injury, or
irritation; Cancer can arise from this area, stimulus induces a reprogramming of
stem cells under the influence of cytokines and growth factors
Ex: Patho: Columnar cells change to squamous cells in lungs of smoker or normal
ciliated epithelial cells of the bronchial linings are replaced by stratified squamous
epithelial cells.; Phys: Barrett Esophagus- normal squamous cells change to
columnar epithelial cells in response to reflux, aka intestinal metaplasia
Hypoxia injury E. inadequate oxygenation of tissues
P. decrease in mitochondrial function, decreased production of ATP increases
anaerobic metabolism. eventual cell death.
C.M. hypoxia, cyanosis, cognitive impairment, lethargy
Free radical and ROS E. normal byproduct of ATP production, will overwhelm the mitochondria- exhaust
intracellular antioxidants
P. lipid peroxidation, damage proteins, fragment DNA
C.M. development in Alzheimer's, heart disease, Parkinson's disease, Amyotrophic
Lateral Sclerosis
Ethanol E. mood altering drug, long term effects on liver and nutritional status
P. metabolized by liver, generates free radicals
C.M. CNS depression, nutrient deficiencies-Mag, Vit B6, thiamine, PO4,
inflammation and fatty infiltration of liver, hepatomegaly, leads to liver failure
irreversible
Oncosis Na and H2O enter cell and cause swelling. Organ increases in weight, becomes
distended and pale. Associated with high fever, hypocalcemia, certain infections
Fatty Infiltration intracellular accumulation of lipids in the liver
liver fails to metabolize lipids. usually from ETOH or high fat diet. can lead to
cirrhosis
dystrophic calcification accumulation of Ca in dead or dying tissues
calcium salt clump and harden- interfere with cellular structure and function
r/t pulmonary TB, atherosclerosis, injured heart valves, chronic pancreatitis
, NURS 5315 Advanced Pathophysiology Exam 1 | UTA | Questions and Answers
metastatic calcification accumulation of Ca in normal tissue
result of hypercalcemia r/t hyperparathyroidism, hyperthyroidism, toxic levels of Vit
D. Can also r/t hyperphosphatemia in renal failure
urate accumulation sodium urate crystals are deposited in tissues- group of disorders collectively called
gout- acute arthritis, chronic gouty arthritis, tophus, nephritis
Coagulative Necrosis kidneys, heart, adrenals- secondary to hypoxia
Liquefactive Necrosis nerve cells- brain- accumulation of pus
Caseous Necrosis lung disease- usually TB- tissue looks like clumped cheese
Fat Necrosis breast, pancreas, abdominal structures- creates soaps
Gangrenous Necrosis Dry- dark shriveled skin
Wet- internal organs- can lead to death
Gas- from clostridium- antitoxins and hyperbaric therapy
Gout E. disturbances in serum urate levels. uncommon for < 30 years old.
P. uric acid is deposited in the tissues of kidney, heart, earlobes, and joints.
C.M. inflammation, painful joints. result of diuretic use or diet high in cream sauces,
red wine, or red meat
Rhabdomyolysis E. cell hypoxia caused by severe muscle trauma, hyperthermia, crush injuries, or
severe dehydration
P. hypoxia to cell causes failure of the Na-K pump, causing accumulation of
intracellular sodium, oncosis, and eventual cell death. Cell death releases enzymes
such as CK, uric acid, LDH, AST, etc.
C.M. Causes: trauma, hyperthermia, crush injuries, severe dehydration; s/s: CK is
5x upper normal limit, muscle pain, weakness, dark, reddish-brown urine,
hypercalcemia, renal failure
Alpha Fetoprotein Origin Liver and germ cell tumors
Carcinoembryonic Antigen GI, pancreas, lung, breast tumors
Prostate Specific Antigen prostate tumors
Carcino- from epithelial tissue- renal cell carcinoma
Sarco- from connective tissue- chondrosarcoma
, NURS 5315 Advanced Pathophysiology Exam 1 | UTA | Questions and Answers
Carcinoma in situ preinvasive epithelial malignant tumors of glandular or squamous cells- cervix
Lung ca metastasis Multiple organs including brain
Colorectal ca metastasis Liver, lungs
Testicular ca metastasis Liver, lungs, brain
Prostate ca metastasis Bones (especially lumbar spine), liver
Head and neck ca metastasis Liver, bones, lymphatics
Ovarian ca metastasis Peritoneal surfaces, diaphragm, omentum, liver
Sarcoma metastasis Lungs
Melanoma metastasis In transit lymphatics, lung, liver, brain, GI tract
Mechanisms of ca metastasis Local invasion, followed by invasion of surrounding tissues. Cells then may invade
blood and lymphatic vessels. They must survive in circulation, then enter and
survive in a new location. Then the cells can multiply and form a new tumor.
TNM staging system T= tumor size >/= correlates with metastatic ability
N= whether lymph nodes are involved
M= extra nodal involvement (liver, lungs)
Intravascular fluid compartment In venous system- 20%
Osmolality The measure of solute concentration in a fluid.
280-295 mOsm
Interstitial fluid compartment Surrounds the cells and bathes them in nutrients- 20%
Intracellular fluid compartment Within the cells- 40% uk
, NURS 5315 Advanced Pathophysiology Exam 1 | UTA | Questions and Answers
Osmosis Passive- the movement of water from an area of low concentration of solute to one
of higher concentration
Osmotic pressure Pulling- the amount of pressure or force that is exerted by solute molecules of a
given compartment
Hydrostatic pressure Blood pressure- pushes fluid outside of the vessels, the force of fluid against the
walls of a compartment- venous obstruction, Na and water retention
Oncotic pressure Colloid pressure keeps water inside the compartment, attracts water from interstitial
space back into the capillary- losses or diminished albumin
Effective arterial blood volume The amount of blood within the arterial space- ECF changes will cause changes in
the EABV in the same direction
Renin Angiotensin Aldosterone System Activated by low blood volume, triggers release of renin which converts
angiotensinogen to angiotensin 1. ACE converts angiotensin 1 to angiotensin which
causes arterial vasoconstriction and stimulates release of aldosterone. Aldosterone
stimulates renal Na reabsorption and K+ excretion. Water is retained, less urine is
produced, blood volume increases.
Natriuretic hormones ANP and BNP- released by heart- works opposite RAAS to decrease blood volume,
promotes urinary excretion of Na and water
Fluid volume deficit Dehydration- intake is not enough for body's needs
C.M. Poor skin turgor, dry mucous membranes, sunken eyes, sunken fontanelles,
decreased urine output, fatigue
Fluid volume excess Fluid intake exceeds body's needs
C.M. Edema, rales, HTN, weight gain, bounding pulses, intake> output, JVD,
restlessness or anxiety
Edema Accumulation of fluid within the interstitial space- venous obstruction, Na and water
retention
C.M. can be localized or dependent, tightness of skin, facial swelling, rales,
decreased wound healing, increased risk of pressure sores, weight gain
Euvolemic Hypernatremia total body water loss, usually from DI
C.M. severe polyuria and mild hypernatremia, weight loss, weak pulses,
tachycardia, postural hypotension, fever, restless
hypovolemic hypernatremia from GI losses or diuretics
C.M. Volume depletion, orthostatic hypotension, tachycardia, lack of organ
perfusion
hypervolemic hypernatremia administration of hypertonic saline
C.M. volume overload, edema, chf, htn, pulmonary edema
mild hyponatremia Na 125-135
C.M. anorexia, apathy, restless, nausea, lethargy, muscle cramps
Atrophy E. Cells decrease in size
P. Still functional; imbalance between protein synthesis and degradation. Essentially
there is an increase in the catabolism of intracellular organelles, reducing structural
components of cell
Physiologic: thymus gland in early childhood
Pathological: disuse (muscle atrophy d/ decrease workload, pressure, use, blood
supply, nutrition, hormonal stimulation, or nervous stimulation)
Hyperplasia E: cells increase in number, mitosis (cell division) must occur, size of cell does not
change
Phys: increased rate of division, increase in tissue mass after damage or partial
resection; may be compensatory, hormonal, or pathologic
Patho: abnormal proliferation of normal cells usually caused by increased hormonal
stimulation (endometrial). increase of production of local growth factors
Ex: removal of part of the liver lead to hyperplasia of hepatocytes. uterine or
mammary gland enlargement during pregnancy
Dysplasia E. Not true adaptation; Cells abnormal change in size, shape, organization
(classified as mild, moderate, severe)
P. caused by cell injury/irritation, characterized by disordered cell growth. aka
atypical hyperplasia or pre-cancer, a disorderly proliferation
Physiologic: N/A
Pathologic: squamous dysplasia of cervix from HPV shows up on pap smear, breast
cancer development; pap smears often show dysplastic cells of the cervix that must
undergo laser/surgical tx
Metaplasia E: reversible change, one type of cell changes to another type for survival
P: reversible; results from exposure of the cells to chronic stressors, injury, or
irritation; Cancer can arise from this area, stimulus induces a reprogramming of
stem cells under the influence of cytokines and growth factors
Ex: Patho: Columnar cells change to squamous cells in lungs of smoker or normal
ciliated epithelial cells of the bronchial linings are replaced by stratified squamous
epithelial cells.; Phys: Barrett Esophagus- normal squamous cells change to
columnar epithelial cells in response to reflux, aka intestinal metaplasia
Hypoxia injury E. inadequate oxygenation of tissues
P. decrease in mitochondrial function, decreased production of ATP increases
anaerobic metabolism. eventual cell death.
C.M. hypoxia, cyanosis, cognitive impairment, lethargy
Free radical and ROS E. normal byproduct of ATP production, will overwhelm the mitochondria- exhaust
intracellular antioxidants
P. lipid peroxidation, damage proteins, fragment DNA
C.M. development in Alzheimer's, heart disease, Parkinson's disease, Amyotrophic
Lateral Sclerosis
Ethanol E. mood altering drug, long term effects on liver and nutritional status
P. metabolized by liver, generates free radicals
C.M. CNS depression, nutrient deficiencies-Mag, Vit B6, thiamine, PO4,
inflammation and fatty infiltration of liver, hepatomegaly, leads to liver failure
irreversible
Oncosis Na and H2O enter cell and cause swelling. Organ increases in weight, becomes
distended and pale. Associated with high fever, hypocalcemia, certain infections
Fatty Infiltration intracellular accumulation of lipids in the liver
liver fails to metabolize lipids. usually from ETOH or high fat diet. can lead to
cirrhosis
dystrophic calcification accumulation of Ca in dead or dying tissues
calcium salt clump and harden- interfere with cellular structure and function
r/t pulmonary TB, atherosclerosis, injured heart valves, chronic pancreatitis
, NURS 5315 Advanced Pathophysiology Exam 1 | UTA | Questions and Answers
metastatic calcification accumulation of Ca in normal tissue
result of hypercalcemia r/t hyperparathyroidism, hyperthyroidism, toxic levels of Vit
D. Can also r/t hyperphosphatemia in renal failure
urate accumulation sodium urate crystals are deposited in tissues- group of disorders collectively called
gout- acute arthritis, chronic gouty arthritis, tophus, nephritis
Coagulative Necrosis kidneys, heart, adrenals- secondary to hypoxia
Liquefactive Necrosis nerve cells- brain- accumulation of pus
Caseous Necrosis lung disease- usually TB- tissue looks like clumped cheese
Fat Necrosis breast, pancreas, abdominal structures- creates soaps
Gangrenous Necrosis Dry- dark shriveled skin
Wet- internal organs- can lead to death
Gas- from clostridium- antitoxins and hyperbaric therapy
Gout E. disturbances in serum urate levels. uncommon for < 30 years old.
P. uric acid is deposited in the tissues of kidney, heart, earlobes, and joints.
C.M. inflammation, painful joints. result of diuretic use or diet high in cream sauces,
red wine, or red meat
Rhabdomyolysis E. cell hypoxia caused by severe muscle trauma, hyperthermia, crush injuries, or
severe dehydration
P. hypoxia to cell causes failure of the Na-K pump, causing accumulation of
intracellular sodium, oncosis, and eventual cell death. Cell death releases enzymes
such as CK, uric acid, LDH, AST, etc.
C.M. Causes: trauma, hyperthermia, crush injuries, severe dehydration; s/s: CK is
5x upper normal limit, muscle pain, weakness, dark, reddish-brown urine,
hypercalcemia, renal failure
Alpha Fetoprotein Origin Liver and germ cell tumors
Carcinoembryonic Antigen GI, pancreas, lung, breast tumors
Prostate Specific Antigen prostate tumors
Carcino- from epithelial tissue- renal cell carcinoma
Sarco- from connective tissue- chondrosarcoma
, NURS 5315 Advanced Pathophysiology Exam 1 | UTA | Questions and Answers
Carcinoma in situ preinvasive epithelial malignant tumors of glandular or squamous cells- cervix
Lung ca metastasis Multiple organs including brain
Colorectal ca metastasis Liver, lungs
Testicular ca metastasis Liver, lungs, brain
Prostate ca metastasis Bones (especially lumbar spine), liver
Head and neck ca metastasis Liver, bones, lymphatics
Ovarian ca metastasis Peritoneal surfaces, diaphragm, omentum, liver
Sarcoma metastasis Lungs
Melanoma metastasis In transit lymphatics, lung, liver, brain, GI tract
Mechanisms of ca metastasis Local invasion, followed by invasion of surrounding tissues. Cells then may invade
blood and lymphatic vessels. They must survive in circulation, then enter and
survive in a new location. Then the cells can multiply and form a new tumor.
TNM staging system T= tumor size >/= correlates with metastatic ability
N= whether lymph nodes are involved
M= extra nodal involvement (liver, lungs)
Intravascular fluid compartment In venous system- 20%
Osmolality The measure of solute concentration in a fluid.
280-295 mOsm
Interstitial fluid compartment Surrounds the cells and bathes them in nutrients- 20%
Intracellular fluid compartment Within the cells- 40% uk
, NURS 5315 Advanced Pathophysiology Exam 1 | UTA | Questions and Answers
Osmosis Passive- the movement of water from an area of low concentration of solute to one
of higher concentration
Osmotic pressure Pulling- the amount of pressure or force that is exerted by solute molecules of a
given compartment
Hydrostatic pressure Blood pressure- pushes fluid outside of the vessels, the force of fluid against the
walls of a compartment- venous obstruction, Na and water retention
Oncotic pressure Colloid pressure keeps water inside the compartment, attracts water from interstitial
space back into the capillary- losses or diminished albumin
Effective arterial blood volume The amount of blood within the arterial space- ECF changes will cause changes in
the EABV in the same direction
Renin Angiotensin Aldosterone System Activated by low blood volume, triggers release of renin which converts
angiotensinogen to angiotensin 1. ACE converts angiotensin 1 to angiotensin which
causes arterial vasoconstriction and stimulates release of aldosterone. Aldosterone
stimulates renal Na reabsorption and K+ excretion. Water is retained, less urine is
produced, blood volume increases.
Natriuretic hormones ANP and BNP- released by heart- works opposite RAAS to decrease blood volume,
promotes urinary excretion of Na and water
Fluid volume deficit Dehydration- intake is not enough for body's needs
C.M. Poor skin turgor, dry mucous membranes, sunken eyes, sunken fontanelles,
decreased urine output, fatigue
Fluid volume excess Fluid intake exceeds body's needs
C.M. Edema, rales, HTN, weight gain, bounding pulses, intake> output, JVD,
restlessness or anxiety
Edema Accumulation of fluid within the interstitial space- venous obstruction, Na and water
retention
C.M. can be localized or dependent, tightness of skin, facial swelling, rales,
decreased wound healing, increased risk of pressure sores, weight gain
Euvolemic Hypernatremia total body water loss, usually from DI
C.M. severe polyuria and mild hypernatremia, weight loss, weak pulses,
tachycardia, postural hypotension, fever, restless
hypovolemic hypernatremia from GI losses or diuretics
C.M. Volume depletion, orthostatic hypotension, tachycardia, lack of organ
perfusion
hypervolemic hypernatremia administration of hypertonic saline
C.M. volume overload, edema, chf, htn, pulmonary edema
mild hyponatremia Na 125-135
C.M. anorexia, apathy, restless, nausea, lethargy, muscle cramps
