NURS 5315
ADVANCED PATHOPHYSIOLOGY EXAM
QUESTIONS AND DETAILED ANSWERS
Atrophy - ANSWER-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 - ANSWER-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 - ANSWER-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 - ANSWER-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 - ANSWER-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 - ANSWER-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 - ANSWER-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 - ANSWER-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 - ANSWER-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 - ANSWER-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
metastatic calcification - ANSWER-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 - ANSWER-sodium urate crystals are deposited in tissues- group of disorders
collectively called gout- acute arthritis, chronic gouty arthritis, tophus, nephritis
Coagulative Necrosis - ANSWER-kidneys, heart, adrenals- secondary to hypoxia
,Liquefactive Necrosis - ANSWER-nerve cells- brain- accumulation of pus
Caseous Necrosis - ANSWER-lung disease- usually TB- tissue looks like clumped cheese
Fat Necrosis - ANSWER-breast, pancreas, abdominal structures- creates soaps
Gangrenous Necrosis - ANSWER-Dry- dark shriveled skin
Wet- internal organs- can lead to death
Gas- from clostridium- antitoxins and hyperbaric therapy
Gout - ANSWER-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 - ANSWER-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 - ANSWER-Liver and germ cell tumors
Carcinoembryonic Antigen - ANSWER-GI, pancreas, lung, breast tumors
Prostate Specific Antigen - ANSWER-prostate tumors
Carcino- - ANSWER-from epithelial tissue- renal cell carcinoma
Sarco- - ANSWER-from connective tissue- chondrosarcoma
Carcinoma in situ - ANSWER-preinvasive epithelial malignant tumors of glandular or squamous
cells- cervix
Lung ca metastasis - ANSWER-Multiple organs including brain
Colorectal ca metastasis - ANSWER-Liver, lungs
Testicular ca metastasis - ANSWER-Liver, lungs, brain
Prostate ca metastasis - ANSWER-Bones (especially lumbar spine), liver
Head and neck ca metastasis - ANSWER-Liver, bones, lymphatics
, Ovarian ca metastasis - ANSWER-Peritoneal surfaces, diaphragm, omentum, liver
Sarcoma metastasis - ANSWER-Lungs
Melanoma metastasis - ANSWER-In transit lymphatics, lung, liver, brain, GI tract
Mechanisms of ca metastasis - ANSWER-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 - ANSWER-T= tumor size >/= correlates with metastatic ability
N= whether lymph nodes are involved
M= extra nodal involvement (liver, lungs)
Intravascular fluid compartment - ANSWER-In venous system- 20%
Osmolality - ANSWER-The measure of solute concentration in a fluid.
280-295 mOsm
Interstitial fluid compartment - ANSWER-Surrounds the cells and bathes them in nutrients- 20%
Intracellular fluid compartment - ANSWER-Within the cells- 40% uk
Osmosis - ANSWER-Passive- the movement of water from an area of low concentration of
solute to one of higher concentration
Osmotic pressure - ANSWER-Pulling- the amount of pressure or force that is exerted by solute
molecules of a given compartment
Hydrostatic pressure - ANSWER-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 - ANSWER-Colloid pressure keeps water inside the compartment, attracts
water from interstitial space back into the capillary- losses or diminished albumin
Effective arterial blood volume - ANSWER-The amount of blood within the arterial space- ECF
changes will cause changes in the EABV in the same direction
Renin Angiotensin Aldosterone System - ANSWER-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 - ANSWER-ANP and BNP- released by heart- works opposite RAAS to
decrease blood volume, promotes urinary excretion of Na and water
ADVANCED PATHOPHYSIOLOGY EXAM
QUESTIONS AND DETAILED ANSWERS
Atrophy - ANSWER-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 - ANSWER-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 - ANSWER-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 - ANSWER-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 - ANSWER-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 - ANSWER-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 - ANSWER-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 - ANSWER-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 - ANSWER-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 - ANSWER-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
metastatic calcification - ANSWER-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 - ANSWER-sodium urate crystals are deposited in tissues- group of disorders
collectively called gout- acute arthritis, chronic gouty arthritis, tophus, nephritis
Coagulative Necrosis - ANSWER-kidneys, heart, adrenals- secondary to hypoxia
,Liquefactive Necrosis - ANSWER-nerve cells- brain- accumulation of pus
Caseous Necrosis - ANSWER-lung disease- usually TB- tissue looks like clumped cheese
Fat Necrosis - ANSWER-breast, pancreas, abdominal structures- creates soaps
Gangrenous Necrosis - ANSWER-Dry- dark shriveled skin
Wet- internal organs- can lead to death
Gas- from clostridium- antitoxins and hyperbaric therapy
Gout - ANSWER-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 - ANSWER-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 - ANSWER-Liver and germ cell tumors
Carcinoembryonic Antigen - ANSWER-GI, pancreas, lung, breast tumors
Prostate Specific Antigen - ANSWER-prostate tumors
Carcino- - ANSWER-from epithelial tissue- renal cell carcinoma
Sarco- - ANSWER-from connective tissue- chondrosarcoma
Carcinoma in situ - ANSWER-preinvasive epithelial malignant tumors of glandular or squamous
cells- cervix
Lung ca metastasis - ANSWER-Multiple organs including brain
Colorectal ca metastasis - ANSWER-Liver, lungs
Testicular ca metastasis - ANSWER-Liver, lungs, brain
Prostate ca metastasis - ANSWER-Bones (especially lumbar spine), liver
Head and neck ca metastasis - ANSWER-Liver, bones, lymphatics
, Ovarian ca metastasis - ANSWER-Peritoneal surfaces, diaphragm, omentum, liver
Sarcoma metastasis - ANSWER-Lungs
Melanoma metastasis - ANSWER-In transit lymphatics, lung, liver, brain, GI tract
Mechanisms of ca metastasis - ANSWER-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 - ANSWER-T= tumor size >/= correlates with metastatic ability
N= whether lymph nodes are involved
M= extra nodal involvement (liver, lungs)
Intravascular fluid compartment - ANSWER-In venous system- 20%
Osmolality - ANSWER-The measure of solute concentration in a fluid.
280-295 mOsm
Interstitial fluid compartment - ANSWER-Surrounds the cells and bathes them in nutrients- 20%
Intracellular fluid compartment - ANSWER-Within the cells- 40% uk
Osmosis - ANSWER-Passive- the movement of water from an area of low concentration of
solute to one of higher concentration
Osmotic pressure - ANSWER-Pulling- the amount of pressure or force that is exerted by solute
molecules of a given compartment
Hydrostatic pressure - ANSWER-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 - ANSWER-Colloid pressure keeps water inside the compartment, attracts
water from interstitial space back into the capillary- losses or diminished albumin
Effective arterial blood volume - ANSWER-The amount of blood within the arterial space- ECF
changes will cause changes in the EABV in the same direction
Renin Angiotensin Aldosterone System - ANSWER-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 - ANSWER-ANP and BNP- released by heart- works opposite RAAS to
decrease blood volume, promotes urinary excretion of Na and water