NURS 5315 ADVANCED PATHOPHYSIOLOGY
EXAM 1 FINAL TEST PAPER 2026 FULL
QUESTIONS AND SOLUTIONS VERIFIED A+
◉ Free Radical and Pathophysiology. Answer: may by initated with
in cells by (1) absorption of extreme energy sources such as
radiation or UV light; (2) the occurrence of endogenous reactions,
such as redox reactions in which oxygen is reduced to water have
role in development of Alzheimer's, Parkinson's, Amyotrophic
Lateral Sclerosis. Antioxidants are our bodies' defense, reducing
agents that provide missing electron that can stabilize the ________
◉ Reactive Oxygen Species (ROS) Pathophysiology. Answer: cause
lipid peroxidation, damage proteins which maintain ion pumps and
cellular transport, fragment DNA and causes less protein synthesis,
cause chromatin destruction, and damage mitochondria.
◉ Ethanol Etiology. Answer: ETOH is metabolized to acetaldehyde in
the cytoplasm of the cell, enzyme alcohol dehydrogenase (ADH)
helps with conversion
◉ Ethanol Clinical Manafestations. Answer: adverse effects on liver
and causes nutritional disorders. acute effects in the liver include
inflammation, fatty infiltration, hepatomegaly, acute liver necrosis
,and suppressed fatty acid oxidation. liver failure is irreversible effect
of chronic abuse
◉ Ethanol Pathophysiolody. Answer: Conversion oxidized niacin
(NAD+) is reduced to NADH. In the mitochondrial acetaldehyde is
further converted by ADH to acetate and further oxidized niacin
(NAD+) is reduced to NADH. the increased NADH/NAD+ ratio in the
liver causes the following
1.Pyruvate change to lactic acid causing lactic acidosis
2. Oxaloacetate converted to malate, preventing gluconeogenesis
leading to fasting hypoglycemia
3. Glyceraldehyde to glycerol which combines with fatty acids and
forms triglycerides, leads to triglycerides in the liver, aka
hepatosteatosis
4. decreases citric acid cycle production of NADH which leads to
utilization of Acetyl-CoA for ketogenesis (causing ketoacidosis) and
lipogenesis (causing hepatosteatosis)
◉ Oncosis Effects and Clinical Implications. Answer: cellular
swelling, cellular injury because with most injuries there is some
amount of O2 deprivation causing hypoxic injury
◉ Fatty infiltration Effects and Clinical Implications. Answer: E-
intracellular accumulation of lipids
,CI- most common site is liver, but can occur in heart and kidneys.
Caused by ethanol abuse or high fat diet, fatty infiltration of liver d/t
fail to metabolize lipids
◉ Dystrophic Calcification Effects and Clinical Implications. Answer:
E- accumulation of calcium that occurs in dying and dead tissues
CI- pulmonary TB, atherosclerosis and heart valve injury
◉ Metastatic Calcification Effects and Clinical Implications. Answer:
E-deposition of calcium in undamaged, normal tissues
CI- Result of hypercalcemia secondary to hyperparathyroidism,
hyperthyroidism, or toxic levels of vitamin D
◉ Urate accumulation Effects and Clinical Implications. Answer: E-
byproduct of purine degradation
CI-accumulation gets deposited into the tissues of the kidney, heart,
earlobes, joints
-liver can produce more uric acid than can be eliminated
-diuretics can trigger kidneys to increase absorption of uric acid
-over accumulation or under secretion of uric acid can result in gout
◉ Necrosis. Answer: spectrum of cell changes after the cell dies
, ◉ Infarct. Answer: necrosis which results from sudden insufficiency
of arterial blood flow
◉ 5 Types of Necrosis. Answer: coagulative, liquefactive, caseous, fat,
gangrenous
◉ Coagulative. Answer: occurs in the kidneys, heart, and adrenal
glands most commonly secondary to hypoxia (caused by protein
denaturation, tissue firm and slightly swollen)
◉ Liquefactive. Answer: nerve cell necrosis
◉ Caseous. Answer: necrosis specific to lung tissue and occurs in TB.
Dead cells disintegrate, but the debris is not digested completely by
hydrolyses, appearance resembles clumped cheese
◉ Fat. Answer: necrosis breast, pancreas and other abdominal
structures
◉ wet gangrene. Answer: develops when neutrophils invade the site,
causing liquefactive necrosis
◉ Gangrenous. Answer: tissue death resulting from severe tissue
hypoxia
EXAM 1 FINAL TEST PAPER 2026 FULL
QUESTIONS AND SOLUTIONS VERIFIED A+
◉ Free Radical and Pathophysiology. Answer: may by initated with
in cells by (1) absorption of extreme energy sources such as
radiation or UV light; (2) the occurrence of endogenous reactions,
such as redox reactions in which oxygen is reduced to water have
role in development of Alzheimer's, Parkinson's, Amyotrophic
Lateral Sclerosis. Antioxidants are our bodies' defense, reducing
agents that provide missing electron that can stabilize the ________
◉ Reactive Oxygen Species (ROS) Pathophysiology. Answer: cause
lipid peroxidation, damage proteins which maintain ion pumps and
cellular transport, fragment DNA and causes less protein synthesis,
cause chromatin destruction, and damage mitochondria.
◉ Ethanol Etiology. Answer: ETOH is metabolized to acetaldehyde in
the cytoplasm of the cell, enzyme alcohol dehydrogenase (ADH)
helps with conversion
◉ Ethanol Clinical Manafestations. Answer: adverse effects on liver
and causes nutritional disorders. acute effects in the liver include
inflammation, fatty infiltration, hepatomegaly, acute liver necrosis
,and suppressed fatty acid oxidation. liver failure is irreversible effect
of chronic abuse
◉ Ethanol Pathophysiolody. Answer: Conversion oxidized niacin
(NAD+) is reduced to NADH. In the mitochondrial acetaldehyde is
further converted by ADH to acetate and further oxidized niacin
(NAD+) is reduced to NADH. the increased NADH/NAD+ ratio in the
liver causes the following
1.Pyruvate change to lactic acid causing lactic acidosis
2. Oxaloacetate converted to malate, preventing gluconeogenesis
leading to fasting hypoglycemia
3. Glyceraldehyde to glycerol which combines with fatty acids and
forms triglycerides, leads to triglycerides in the liver, aka
hepatosteatosis
4. decreases citric acid cycle production of NADH which leads to
utilization of Acetyl-CoA for ketogenesis (causing ketoacidosis) and
lipogenesis (causing hepatosteatosis)
◉ Oncosis Effects and Clinical Implications. Answer: cellular
swelling, cellular injury because with most injuries there is some
amount of O2 deprivation causing hypoxic injury
◉ Fatty infiltration Effects and Clinical Implications. Answer: E-
intracellular accumulation of lipids
,CI- most common site is liver, but can occur in heart and kidneys.
Caused by ethanol abuse or high fat diet, fatty infiltration of liver d/t
fail to metabolize lipids
◉ Dystrophic Calcification Effects and Clinical Implications. Answer:
E- accumulation of calcium that occurs in dying and dead tissues
CI- pulmonary TB, atherosclerosis and heart valve injury
◉ Metastatic Calcification Effects and Clinical Implications. Answer:
E-deposition of calcium in undamaged, normal tissues
CI- Result of hypercalcemia secondary to hyperparathyroidism,
hyperthyroidism, or toxic levels of vitamin D
◉ Urate accumulation Effects and Clinical Implications. Answer: E-
byproduct of purine degradation
CI-accumulation gets deposited into the tissues of the kidney, heart,
earlobes, joints
-liver can produce more uric acid than can be eliminated
-diuretics can trigger kidneys to increase absorption of uric acid
-over accumulation or under secretion of uric acid can result in gout
◉ Necrosis. Answer: spectrum of cell changes after the cell dies
, ◉ Infarct. Answer: necrosis which results from sudden insufficiency
of arterial blood flow
◉ 5 Types of Necrosis. Answer: coagulative, liquefactive, caseous, fat,
gangrenous
◉ Coagulative. Answer: occurs in the kidneys, heart, and adrenal
glands most commonly secondary to hypoxia (caused by protein
denaturation, tissue firm and slightly swollen)
◉ Liquefactive. Answer: nerve cell necrosis
◉ Caseous. Answer: necrosis specific to lung tissue and occurs in TB.
Dead cells disintegrate, but the debris is not digested completely by
hydrolyses, appearance resembles clumped cheese
◉ Fat. Answer: necrosis breast, pancreas and other abdominal
structures
◉ wet gangrene. Answer: develops when neutrophils invade the site,
causing liquefactive necrosis
◉ Gangrenous. Answer: tissue death resulting from severe tissue
hypoxia
