NSG 533 PATHOPHYSIOLOGY FINAL EXAM NEWEST
2025 ACTUAL EXAM COMPLETE ACCURATE
QUESTIONS WITH DETAILED VERIFIED ANSWERS
||ALREADY GRADED A+
what are the 5 essentials of pathophysiology
etiology, epidemiology, pathogenesis, clinical manifestations, outcomes
etiology
the cause, the why of the disease
epidemiology
the relationship between the characteristics of a population and the incidence and
prevalence of a disease
prevalence
existing cases (new and old) in a population during a given time period
incidence
new cases
pathogenesis
the sequence of events for a disease from the stimulus to manifestations
clinical manifestations
signs: objective, what we assess
symptoms: subjective, what the pt reports
diagnostic factor
outcomes
cure, remission, chronicity, or death
ATP
body's main energy source and we need a constant supply of ATP to perform cellular
functions (transmembrane pumps, protein synthesis, protein function, and cellular
division)
what is the most common cause of ATP depletion
hypoxia (respiratory problems, blood flow problems (ischemia), lack of effective
hemoglobin to carry oxygen (anemia))
how ATP depletion leads to cell death
leads to the Na/K pump not working and leads to anaerobic glycolysis
issues when the Na/K pump doesn't work
hyperkalemia, hyponatremia, increase in intracellular calcium, increase in intracellular
H2O causing cell swelling and cell lysis
issues with anaerobic glycolysis
decrease in glycogen, increase in lactate, decrease in pH leading to nuclear clumping,
fragmentation and dissolution
pyknosis
clumping of nuclear material
,karyorrhexis
fragmentation of nuclear material
karyolysis
dissolution of the nuclear material
decrease in pH causes
pyknosis, karyorrhexis, and karyolysis
rupture of lysosomes and release of proteolytic enzymes, autodigestion of cell
membrane causing cell damage and release of intracellular components including cell-
type specific enzymes (troponin, CK, AST/ALT, amylase)
cellular metabolism steps
digestion, glycolysis, citric acid cycle, oxidative phosphorylation
extracellular digestion (step 1 of cellular metabolism )
food digested into polysaccharides and then into simple sugars
glycolysis (step 2 of cellular metabolism)
breaks down the sugars into pyruvate and then into acetyl coA(goes to citric acid cycle)
accompanied by small amount of ATP and NADH produced
citric acid cycle (step 3 of cellular metabolism)
production of NADH yielding ATP via electron transport waste products
oxidative phosphorlyation (step 4 of cellular metabolism)
O2 goes to H2O and H2O is excreted with CO2, NH3, and urea and 30 ATP molecules
are produced
causes of cell injury/death
ATP depletion
defects in membrane permeability - lysis by enzymes, lysis by viruses, free radicals,
physical/chemical stressors)
lysis by enzymes
breakdown the cell membrane (usually done by bacteria bc they're trying to dissolve
surrounding tissues to gain access to body)
lysis by viruses
cause membrane rupture from virions leaving the host cell (HIV and hep B)
physical and chemical stressors causing defects in membrane permeability
air pollution, chemicals, street drugs, alcohol, aphysixation, trauma
what does ischemia do the mitochondria
decreased mitochondrial oxygenation
why is intracellular calcium accumulation bad?
causes an increase in cellular enzyme activities including activating ATPase (depletes
ATP), phospholipases, proteases, and endonuclease enzymes all leading to cell
membrane and nuclear damage
also increases mitochondrial permeability changes
free radicals/ROS
unstable molecules with an unpaired electron on the outer ring (that wants to bind to
lipid molecules aka cell membrane and cell organelles)
, normal byproduct of metabolism and comes from the mitochondria
oxidative stress
when there are too many free radicals and the antioxidants can't keep up with them
antioxidants
fight against the free radicals and help them mate or pair off so that it doesn't cause too
much damage
conditions associated with excess free radicals
aging, atherosclerosis, inflammatory diseases, diabetes, cancer, reperfusion injury,
cardiac myopathy, oxygen toxicity
what is a reperfusion injury
blood flow is restored so a lot of O2 comes in (to a cell that was living without it) causing
a release in increased free radicals and damage/necrosis to the cell
fat accumulation in the cell occurs where
liver or myocardial cells (liver more common)
mechanisms of fat accumulation
increase in FFAs, increase in triglycerides, decrease in apoproteins, failure of lipids to
bind to apoproteins and make lipoproteins, failure to move lipoproteins out of the cell,
damage to liver ER from alcohol
acute fatty change can lead to
acute heart or liver failure
bilirubin
pigment released when RBCs are destroyed or broken down
unconjugated bilirubin
fat soluble, cannot be excreted
what turns unconjugated bili to conjugated bili
glucoronic acid and occurs in the liver
conjugated bilirubin
water soluble and can be eliminated through the kidney
conjugated bilirubin leaves the liver in what 2 ways
-in the blood down its concentration gradient
-through the bile and eliminated in urine or stool
why is hyperbilirubinemia more severe in infants
the BBB is immature so bilirubin can cross it and it is extremely toxic to nerve tissues
and exposure can lead to severe neurological deficits or death (kernicterus)
jaundice occurs when bilirubin levels are
greater than 2 mg/dL
causes of hyperbilirubinemia
immature liver, hemolysis (incompatible blood with mom in pregnancy), dehydration/not
feeding well, breastfeeding
types of jaundice
hemolytic, obstructive, hepatocellular
hemolytic jaundice
excessive destruction of RBCs so unconjugated bilirubin builds up in the blood
obstructive jaundice
obstruction of the flow of bile so bilirubin cannot be excreted
2025 ACTUAL EXAM COMPLETE ACCURATE
QUESTIONS WITH DETAILED VERIFIED ANSWERS
||ALREADY GRADED A+
what are the 5 essentials of pathophysiology
etiology, epidemiology, pathogenesis, clinical manifestations, outcomes
etiology
the cause, the why of the disease
epidemiology
the relationship between the characteristics of a population and the incidence and
prevalence of a disease
prevalence
existing cases (new and old) in a population during a given time period
incidence
new cases
pathogenesis
the sequence of events for a disease from the stimulus to manifestations
clinical manifestations
signs: objective, what we assess
symptoms: subjective, what the pt reports
diagnostic factor
outcomes
cure, remission, chronicity, or death
ATP
body's main energy source and we need a constant supply of ATP to perform cellular
functions (transmembrane pumps, protein synthesis, protein function, and cellular
division)
what is the most common cause of ATP depletion
hypoxia (respiratory problems, blood flow problems (ischemia), lack of effective
hemoglobin to carry oxygen (anemia))
how ATP depletion leads to cell death
leads to the Na/K pump not working and leads to anaerobic glycolysis
issues when the Na/K pump doesn't work
hyperkalemia, hyponatremia, increase in intracellular calcium, increase in intracellular
H2O causing cell swelling and cell lysis
issues with anaerobic glycolysis
decrease in glycogen, increase in lactate, decrease in pH leading to nuclear clumping,
fragmentation and dissolution
pyknosis
clumping of nuclear material
,karyorrhexis
fragmentation of nuclear material
karyolysis
dissolution of the nuclear material
decrease in pH causes
pyknosis, karyorrhexis, and karyolysis
rupture of lysosomes and release of proteolytic enzymes, autodigestion of cell
membrane causing cell damage and release of intracellular components including cell-
type specific enzymes (troponin, CK, AST/ALT, amylase)
cellular metabolism steps
digestion, glycolysis, citric acid cycle, oxidative phosphorylation
extracellular digestion (step 1 of cellular metabolism )
food digested into polysaccharides and then into simple sugars
glycolysis (step 2 of cellular metabolism)
breaks down the sugars into pyruvate and then into acetyl coA(goes to citric acid cycle)
accompanied by small amount of ATP and NADH produced
citric acid cycle (step 3 of cellular metabolism)
production of NADH yielding ATP via electron transport waste products
oxidative phosphorlyation (step 4 of cellular metabolism)
O2 goes to H2O and H2O is excreted with CO2, NH3, and urea and 30 ATP molecules
are produced
causes of cell injury/death
ATP depletion
defects in membrane permeability - lysis by enzymes, lysis by viruses, free radicals,
physical/chemical stressors)
lysis by enzymes
breakdown the cell membrane (usually done by bacteria bc they're trying to dissolve
surrounding tissues to gain access to body)
lysis by viruses
cause membrane rupture from virions leaving the host cell (HIV and hep B)
physical and chemical stressors causing defects in membrane permeability
air pollution, chemicals, street drugs, alcohol, aphysixation, trauma
what does ischemia do the mitochondria
decreased mitochondrial oxygenation
why is intracellular calcium accumulation bad?
causes an increase in cellular enzyme activities including activating ATPase (depletes
ATP), phospholipases, proteases, and endonuclease enzymes all leading to cell
membrane and nuclear damage
also increases mitochondrial permeability changes
free radicals/ROS
unstable molecules with an unpaired electron on the outer ring (that wants to bind to
lipid molecules aka cell membrane and cell organelles)
, normal byproduct of metabolism and comes from the mitochondria
oxidative stress
when there are too many free radicals and the antioxidants can't keep up with them
antioxidants
fight against the free radicals and help them mate or pair off so that it doesn't cause too
much damage
conditions associated with excess free radicals
aging, atherosclerosis, inflammatory diseases, diabetes, cancer, reperfusion injury,
cardiac myopathy, oxygen toxicity
what is a reperfusion injury
blood flow is restored so a lot of O2 comes in (to a cell that was living without it) causing
a release in increased free radicals and damage/necrosis to the cell
fat accumulation in the cell occurs where
liver or myocardial cells (liver more common)
mechanisms of fat accumulation
increase in FFAs, increase in triglycerides, decrease in apoproteins, failure of lipids to
bind to apoproteins and make lipoproteins, failure to move lipoproteins out of the cell,
damage to liver ER from alcohol
acute fatty change can lead to
acute heart or liver failure
bilirubin
pigment released when RBCs are destroyed or broken down
unconjugated bilirubin
fat soluble, cannot be excreted
what turns unconjugated bili to conjugated bili
glucoronic acid and occurs in the liver
conjugated bilirubin
water soluble and can be eliminated through the kidney
conjugated bilirubin leaves the liver in what 2 ways
-in the blood down its concentration gradient
-through the bile and eliminated in urine or stool
why is hyperbilirubinemia more severe in infants
the BBB is immature so bilirubin can cross it and it is extremely toxic to nerve tissues
and exposure can lead to severe neurological deficits or death (kernicterus)
jaundice occurs when bilirubin levels are
greater than 2 mg/dL
causes of hyperbilirubinemia
immature liver, hemolysis (incompatible blood with mom in pregnancy), dehydration/not
feeding well, breastfeeding
types of jaundice
hemolytic, obstructive, hepatocellular
hemolytic jaundice
excessive destruction of RBCs so unconjugated bilirubin builds up in the blood
obstructive jaundice
obstruction of the flow of bile so bilirubin cannot be excreted
