NURS 5315 SHOCK ADVANCED PATHOPHYSIOLOGY
COMPLETE QUESTIONS WITH CORRECT WELL DETAILED
ANSWERS GRADED A+
Metaplasia examples - ✅✅Most common is change from columnar cells to
squamous cells (chronic smokers).
Less common is change from squamous to columnar cells, like in Barrett
Esophagus caused by heart burn.
Carcinoma in situ - ✅✅Pre-invasive epithelial malignant tumors of glandular or
squamous origin. Sites including cervix, skin, oral cavity, esophagus, and bronchus
Hypoxic injury - ✅✅1. Decrease in oxygen in the air (high altitudes,
asphyxiation, drowning)
2. Loss of hemoglobin function (hemorrhage or sickle cell anemia)
3. Decrease in production of red blood cells (anemia or leukemia)
4. Diseases of cardiopulmonary systems (ischemia, blood supply loss,
arteriosclerosis)
Hypoxic injury clinical manifestations - ✅✅1. Increased CK (muscle and heart)
,2. Increased LDH (muscle, liver, lung, heart, RBC, brain)
3. Increased ALT and AST (liver)
4. Increased troponin (heart)
Reperfusion injury - ✅✅Oxygen supply is restored to ischemic tissues. Triggers
oxygen intermediates which causes cell membrane damage and mitochondrial
calcium overload.
Xanthine dehydrogenase --> xanthine oxidate. This makes large amounts of free
radicals, superoxide, and hydrogen peroxide. Causes cell membrane damage and
*mitochondrial calcium overload*
Reperfusion injury clinical manifestations - ✅✅White blood cell count is
impaired. Seen in tissue transplantation, ischemic syndromes of the heart, liver,
intestines, kidneys, and cerebrum.
Free Radical - ✅✅Molecules that have an unpaired electron on its outer shell.
This makes the molecule unstable.
Cause cellular injury, aging, and disease to occur.
, Reactive Oxygen Species (ROS) - ✅✅Produced as a normal byproduct of ATP
production in mitochondria. ROS can overwhelm the mitochondria and exhaust
intracellular antioxidants. Also produced by absorption of high energy sources like
radiation or UV light.
Ethanol - ✅✅Acute affects in the liver include inflammation, fatty infiltration,
hepatomegaly, acute liver necrosis, suppressed fatty acid oxidation. Chronic
ethanol use is mainly seen in the stomach and liver, and is caused by free radicals.
*Elevated anion gap and osmolar gap >10 is diagnostic*
Infarct - ✅✅Form of necrosis that is a SUDDEN insufficiency of arterial blood
flow. (ie: heart attack, cold leg, MI)
Apoptosis - ✅✅Programmed cell death (normal). Needed to prevent cellular
proliferation that would result in a large body.
Clinical implications: neurodegenerative disease, ischemic injury, death of virus
infected cells
Autophagy - ✅✅Autodigestion of the cell. When cells lack nutrition, autophagy
is triggered. During times of metabolic stress, autophagy provides ATP and other
macromolecules for energy and cell survival. When stress progresses, it leads to
cell death
COMPLETE QUESTIONS WITH CORRECT WELL DETAILED
ANSWERS GRADED A+
Metaplasia examples - ✅✅Most common is change from columnar cells to
squamous cells (chronic smokers).
Less common is change from squamous to columnar cells, like in Barrett
Esophagus caused by heart burn.
Carcinoma in situ - ✅✅Pre-invasive epithelial malignant tumors of glandular or
squamous origin. Sites including cervix, skin, oral cavity, esophagus, and bronchus
Hypoxic injury - ✅✅1. Decrease in oxygen in the air (high altitudes,
asphyxiation, drowning)
2. Loss of hemoglobin function (hemorrhage or sickle cell anemia)
3. Decrease in production of red blood cells (anemia or leukemia)
4. Diseases of cardiopulmonary systems (ischemia, blood supply loss,
arteriosclerosis)
Hypoxic injury clinical manifestations - ✅✅1. Increased CK (muscle and heart)
,2. Increased LDH (muscle, liver, lung, heart, RBC, brain)
3. Increased ALT and AST (liver)
4. Increased troponin (heart)
Reperfusion injury - ✅✅Oxygen supply is restored to ischemic tissues. Triggers
oxygen intermediates which causes cell membrane damage and mitochondrial
calcium overload.
Xanthine dehydrogenase --> xanthine oxidate. This makes large amounts of free
radicals, superoxide, and hydrogen peroxide. Causes cell membrane damage and
*mitochondrial calcium overload*
Reperfusion injury clinical manifestations - ✅✅White blood cell count is
impaired. Seen in tissue transplantation, ischemic syndromes of the heart, liver,
intestines, kidneys, and cerebrum.
Free Radical - ✅✅Molecules that have an unpaired electron on its outer shell.
This makes the molecule unstable.
Cause cellular injury, aging, and disease to occur.
, Reactive Oxygen Species (ROS) - ✅✅Produced as a normal byproduct of ATP
production in mitochondria. ROS can overwhelm the mitochondria and exhaust
intracellular antioxidants. Also produced by absorption of high energy sources like
radiation or UV light.
Ethanol - ✅✅Acute affects in the liver include inflammation, fatty infiltration,
hepatomegaly, acute liver necrosis, suppressed fatty acid oxidation. Chronic
ethanol use is mainly seen in the stomach and liver, and is caused by free radicals.
*Elevated anion gap and osmolar gap >10 is diagnostic*
Infarct - ✅✅Form of necrosis that is a SUDDEN insufficiency of arterial blood
flow. (ie: heart attack, cold leg, MI)
Apoptosis - ✅✅Programmed cell death (normal). Needed to prevent cellular
proliferation that would result in a large body.
Clinical implications: neurodegenerative disease, ischemic injury, death of virus
infected cells
Autophagy - ✅✅Autodigestion of the cell. When cells lack nutrition, autophagy
is triggered. During times of metabolic stress, autophagy provides ATP and other
macromolecules for energy and cell survival. When stress progresses, it leads to
cell death
