WGU D236 PATHOPHYSIOLOGY MAIN EXAMINATION
SET 2026-2027 QUESTIONS AND ANSWERS RATED A+
✔✔what are the three mechanisms of apoptosis - ✔✔intrinsic or mitochondrial pathway
extrinsic or death receptor pathway
apoptosis inducing factor
✔✔Apoptosis - mitochondrial pathway - ✔✔-healthy cell - protein Bcl-2 on surface -
inhibits apoptosis
-internal damage to cell
-protein Bax migrates to the surface of the mitochondria where it inhibits protective
effect of Bcl-2
-inserts self into outer mitochondrial membrane punching holes in it
-cytochrome c leaks out
-cytochrome c binds to the protein Apaf-1
-complexes aggregate to form apoptosomes
-bind to and activate caspase-9
-cleaves and activates other caspases (executioner ones)
-digestion of structural proteins in the cytoplasm
-degradation of chromosomal DNA
-phagocytosis of the cell
✔✔Apoptosis death-receptor pathway - ✔✔-Fas and TNF receptor are integral
membrane proteins with their receptor domains exposed at the surface of the cell
-binding of the complementary death activator (FasL and TNF) transmits a signal to the
cytoplasm
-actiavation of caspase 8
-initiates cascade of caspase activation
-phagocytosis of cell
✔✔apoptosis-inducing - ✔✔-neurons have another way to self-destruct that does not
use caspases
-AIF is a protein that is normally located in the intermembrane space of mitochondria
-when cell receives death signal, AIF:
-released from mitochondria
-migrates to nucleus
-binds to DNA
-triggers destruction of the DNA and cell death
✔✔relationship of apoptosis to cancer - ✔✔some viruses associated with cancers use
tricks to prevent apoptosis of the cells that they have performed
-HPV produces protein E6 that binds and inactivates apoptosis promoter p53
Epstein-Barr Virus - produces protein similar to Bcl-2 as well as a protein that increases
the production of Bcl-2. Both inhibiting apoptosis
, ✔✔relationship of apoptosis to AIDS - ✔✔-immune response to a foreign invader -
proliferation of lymphocytes (T and B cells)
-when their job is done they are removed via apoptosis leaving a small population of
memory cells
✔✔define aging and its relationship to cellular function/structure and genetic and
environemental factors - ✔✔-aging is the progressive loss of tissues overtime
-senescence is a process of permanent proliferative arrest on cells in response to
various stressors
-senescent cells accumulate - tissue dysfunction
-cellular changes of aging include:
-atrophy
-decreased function
-loss of cells (maybe apoptosis)
-free radicals damage tissues during aging
-DNA is vulnerable to breaks, deletions, and additions
-movement of intracellular and Extracellular substances decreases with age
✔✔causes of hypovolemia - ✔✔- loss of fluids from anywhere (thoracentisis,
paracentisis, vomiting, diarrhea, hemorrhage, suction)
- Third spacing (burns, ascites)
- diseases with polyuria (polyuria > oliguria > anuria > renal failure)
✔✔clinical manifestations of hypovolemia - ✔✔-Thirst
-Dry mucous membranes
-Decreased skin turgor/delay return/tenting
-Hypotension, tachycardia
-Weight loss
-Decreased urine output, concentrated urine
-Restless, drowsy, confused, dizzy, weak
✔✔total body water - ✔✔-usually expressed as a percentage of body weight
-varies based on body type, sex, and age
-female normal build 50% water
-male normal build 60% water
✔✔causes of hypervolemia - ✔✔Heart failure
Kidney disease
Cirrhosis
Overdose of sodium concentrated fluids
Fluid shifts in burns
Prolonged use of corticosteroids
Severe stress
Hyperaldosteronism
weight gain
SET 2026-2027 QUESTIONS AND ANSWERS RATED A+
✔✔what are the three mechanisms of apoptosis - ✔✔intrinsic or mitochondrial pathway
extrinsic or death receptor pathway
apoptosis inducing factor
✔✔Apoptosis - mitochondrial pathway - ✔✔-healthy cell - protein Bcl-2 on surface -
inhibits apoptosis
-internal damage to cell
-protein Bax migrates to the surface of the mitochondria where it inhibits protective
effect of Bcl-2
-inserts self into outer mitochondrial membrane punching holes in it
-cytochrome c leaks out
-cytochrome c binds to the protein Apaf-1
-complexes aggregate to form apoptosomes
-bind to and activate caspase-9
-cleaves and activates other caspases (executioner ones)
-digestion of structural proteins in the cytoplasm
-degradation of chromosomal DNA
-phagocytosis of the cell
✔✔Apoptosis death-receptor pathway - ✔✔-Fas and TNF receptor are integral
membrane proteins with their receptor domains exposed at the surface of the cell
-binding of the complementary death activator (FasL and TNF) transmits a signal to the
cytoplasm
-actiavation of caspase 8
-initiates cascade of caspase activation
-phagocytosis of cell
✔✔apoptosis-inducing - ✔✔-neurons have another way to self-destruct that does not
use caspases
-AIF is a protein that is normally located in the intermembrane space of mitochondria
-when cell receives death signal, AIF:
-released from mitochondria
-migrates to nucleus
-binds to DNA
-triggers destruction of the DNA and cell death
✔✔relationship of apoptosis to cancer - ✔✔some viruses associated with cancers use
tricks to prevent apoptosis of the cells that they have performed
-HPV produces protein E6 that binds and inactivates apoptosis promoter p53
Epstein-Barr Virus - produces protein similar to Bcl-2 as well as a protein that increases
the production of Bcl-2. Both inhibiting apoptosis
, ✔✔relationship of apoptosis to AIDS - ✔✔-immune response to a foreign invader -
proliferation of lymphocytes (T and B cells)
-when their job is done they are removed via apoptosis leaving a small population of
memory cells
✔✔define aging and its relationship to cellular function/structure and genetic and
environemental factors - ✔✔-aging is the progressive loss of tissues overtime
-senescence is a process of permanent proliferative arrest on cells in response to
various stressors
-senescent cells accumulate - tissue dysfunction
-cellular changes of aging include:
-atrophy
-decreased function
-loss of cells (maybe apoptosis)
-free radicals damage tissues during aging
-DNA is vulnerable to breaks, deletions, and additions
-movement of intracellular and Extracellular substances decreases with age
✔✔causes of hypovolemia - ✔✔- loss of fluids from anywhere (thoracentisis,
paracentisis, vomiting, diarrhea, hemorrhage, suction)
- Third spacing (burns, ascites)
- diseases with polyuria (polyuria > oliguria > anuria > renal failure)
✔✔clinical manifestations of hypovolemia - ✔✔-Thirst
-Dry mucous membranes
-Decreased skin turgor/delay return/tenting
-Hypotension, tachycardia
-Weight loss
-Decreased urine output, concentrated urine
-Restless, drowsy, confused, dizzy, weak
✔✔total body water - ✔✔-usually expressed as a percentage of body weight
-varies based on body type, sex, and age
-female normal build 50% water
-male normal build 60% water
✔✔causes of hypervolemia - ✔✔Heart failure
Kidney disease
Cirrhosis
Overdose of sodium concentrated fluids
Fluid shifts in burns
Prolonged use of corticosteroids
Severe stress
Hyperaldosteronism
weight gain
