Advanced Pathophysiology Exam 1 – 2026/2027
Academic Year | 230 Essential Practice Questions and
Confirmed Answers | Updated Study Guide | Key Exam
Topics | Your Guide to Excellent Grades
describe the effect of free cytosolic calcium (McCance & Huether, figure 2-24) - ANSWER
Calcium is normally removed from the cytosol by ATP dependent calcium pumps. In normal
cells, calcium is bound to buffering proteins, such as calbindin or paralbumin, and is contained
in the ER and the mitochondria.
If there is abnormal permeability of calcium ion channels, direct damage to membranes, or
depletion of ATP (i.e., hypoxic injury), calcium level increases in the cytosol.
If the free calcium cannot be buffered or pumped out of cells, uncontrolled enzyme activation
takes place, causing further damage.
Uncontrolled entry of calcium into the cytosol is an important final pathway in many causes of
cell death.
Free Ca= activation of enzymes causes: chromatin fragmentation, membrane damage,
cytoskeletal damage
Hypercalcemia d/t: hyperparathyroidism, toxic levels of Vit D, hyperthyroidism, Addison's
disease, sarcoidosis, leukemia/cancer, renal failure
compare and contrast: karyolysis, pyknosis, karyorrhexis - ANSWER necrosis in the nucleus:
karyolysis: Nuclear fading, DNA deteriorates
,pyknosis: nucleus condenses and shrinks
karyorrhexis: nuclear fragmentation "rupture"
differentiate among and give examples of necrosis - ANSWER Cellular death eventually leads to
cellular dissolution, or necrosis.
Necrosis is the sum of cellular changes after local cell death and the process of cellular self-
digestion, known as autodigestion or autolysis.
Types of necrosis:
o liquefactive necrosis: d/t ischemia or bacterial infection of neurons and glial cells in the brain-
forms cysts/pus
o coagulative necrosis: kidneys, heart, adrenal glands d/t hypoxia from ischemia/chemical injury
(ingestion toxins) causing coagulation by denatured proteins that cause albumin to change form
(gelatinous to firm-egg white cooked)--MI
o caseous necrosis: TB infection combo coagulative and liquefactive necrosis "clumped cheese"
o fat necrosis: breast, pancreas caused by lipases (enzymes) that break down triglycerides
releasing fatty acids that combine with ions creating soaps "chalk white"
o gangrenous necrosis: d/t hypoxic injury and bacterial invasion often arteriosclerosis or
blockage of major arteries (lower legs)
• dry gangrene: d/t coagulative necrosis, skin dry and shrinks, turns black
• wet gangrene: neutrophils invade causing liquefactive necrosis- usually internal organs, site
cold, swollen black with foul odor, pus
• gas gangrene: d/t clostridium infection "gas bubbles" form in muscle cells- need hyperbaric
chamber
, discuss systemic manifestations of cellular injury (McCance & Huether, table 2-9) - ANSWER o
fever: interleukin 1 released causing acute inflammatory response
o increased heart rate: metabolic processes resulting from fever
o increased leukocytes: d/t infection
o pain: d/t release of bradykinins
o presence of cellular enzymes in extracellular fluid: released enzymes from cells of tissue
• ie lactate: released from RBC, liver, kidney, skeletal muscle
• creatine kinase-CK: released from skeletal muscle, brain, heart
• ALT/AST: released from heart, liver, muscle, kidney, pancreas
differentiate between the cellular processes involved in cell necrosis and apoptosis - ANSWER
necrosis: cell swelling, nucleus: pyknosiskaryorrhexiskaryolysis, disrupted plasma membrane,
cellular contents leak enzymes, inflammation present, pathologic d/t irreversible cell injury= d/t
external factors
apoptosis: cell shrinkage, nucleus: fragmentation, altered plasma membrane "blebs", cellular
contents intact, no inflammation, often physiologic, can be pathologic with DNA damage=
natural
describe the three mechanisms involved in the process of apoptosis: - ANSWER 1. generated
by signals arising within the cell;
2. triggered by death activators binding to receptors at the cell surface: TNF-α, Lymphotoxin, Fas
ligand
3. triggered by dangerous reactive oxygen species.
, 20. discuss the relationship of apoptosis to: cancer, HIV, organ transplant - ANSWER cancer:
Some cancer cells, especially lung and colon cancer cells, secrete elevated levels of a soluble
"decoy" molecule that binds to FasL, plugging it up so it cannot bind Fas. Thus, cytotoxic T cells
(CTL) cannot kill the cancer cell. Other cancer cells express high levels of FasL, and can kill any
cytotoxic T cells
AIDS: All T cells, both infected and uninfected, express Fas. Expression of a HIV gene (called Nef)
in a HIV-infected cell causes the cell to express high levels of FasL at its surface while preventing
an interaction with its own Fas from causing it to self-destruct. However, when the infected T
cell encounters an uninfected one (e.g. in a lymph node), the interaction of FasL with Fas on the
uninfected cell kills it by apoptosis
organ transplantation: Graft rejection: The patient's immune system "sees" an allograft as
foreign (antigenic) and mounts an immune response against it.
define aging and its relationship to cellular function/structure and genetic and environmental
factors - ANSWER aging: a normal physiologic process that is universal and inevitable
Cellular changes characteristic of aging include atrophy, decreased function, and loss of cells,
possibly by apoptosis. Loss of cellular function from any of these causes initiates the
compensatory mechanisms of hypertrophy and hyperplasia of remaining cells, which can lead to
metaplasia, dysplasia, and neoplasia. All these changes can alter receptor placement and
function, nutrient pathways, secretion of cellular products, and neuroendocrine control
mechanisms.
If a normal individual began to take thyroid hormone 100 mcgs. every day as a medication,
which of the following would result?
a. hypertrophy of the thyroid gland
b. hyperplasia of the thyroid gland
c. atrophy of the thyroid gland
d. hypertrophy and hyperplasia of the thyroid gland - ANSWER B
Academic Year | 230 Essential Practice Questions and
Confirmed Answers | Updated Study Guide | Key Exam
Topics | Your Guide to Excellent Grades
describe the effect of free cytosolic calcium (McCance & Huether, figure 2-24) - ANSWER
Calcium is normally removed from the cytosol by ATP dependent calcium pumps. In normal
cells, calcium is bound to buffering proteins, such as calbindin or paralbumin, and is contained
in the ER and the mitochondria.
If there is abnormal permeability of calcium ion channels, direct damage to membranes, or
depletion of ATP (i.e., hypoxic injury), calcium level increases in the cytosol.
If the free calcium cannot be buffered or pumped out of cells, uncontrolled enzyme activation
takes place, causing further damage.
Uncontrolled entry of calcium into the cytosol is an important final pathway in many causes of
cell death.
Free Ca= activation of enzymes causes: chromatin fragmentation, membrane damage,
cytoskeletal damage
Hypercalcemia d/t: hyperparathyroidism, toxic levels of Vit D, hyperthyroidism, Addison's
disease, sarcoidosis, leukemia/cancer, renal failure
compare and contrast: karyolysis, pyknosis, karyorrhexis - ANSWER necrosis in the nucleus:
karyolysis: Nuclear fading, DNA deteriorates
,pyknosis: nucleus condenses and shrinks
karyorrhexis: nuclear fragmentation "rupture"
differentiate among and give examples of necrosis - ANSWER Cellular death eventually leads to
cellular dissolution, or necrosis.
Necrosis is the sum of cellular changes after local cell death and the process of cellular self-
digestion, known as autodigestion or autolysis.
Types of necrosis:
o liquefactive necrosis: d/t ischemia or bacterial infection of neurons and glial cells in the brain-
forms cysts/pus
o coagulative necrosis: kidneys, heart, adrenal glands d/t hypoxia from ischemia/chemical injury
(ingestion toxins) causing coagulation by denatured proteins that cause albumin to change form
(gelatinous to firm-egg white cooked)--MI
o caseous necrosis: TB infection combo coagulative and liquefactive necrosis "clumped cheese"
o fat necrosis: breast, pancreas caused by lipases (enzymes) that break down triglycerides
releasing fatty acids that combine with ions creating soaps "chalk white"
o gangrenous necrosis: d/t hypoxic injury and bacterial invasion often arteriosclerosis or
blockage of major arteries (lower legs)
• dry gangrene: d/t coagulative necrosis, skin dry and shrinks, turns black
• wet gangrene: neutrophils invade causing liquefactive necrosis- usually internal organs, site
cold, swollen black with foul odor, pus
• gas gangrene: d/t clostridium infection "gas bubbles" form in muscle cells- need hyperbaric
chamber
, discuss systemic manifestations of cellular injury (McCance & Huether, table 2-9) - ANSWER o
fever: interleukin 1 released causing acute inflammatory response
o increased heart rate: metabolic processes resulting from fever
o increased leukocytes: d/t infection
o pain: d/t release of bradykinins
o presence of cellular enzymes in extracellular fluid: released enzymes from cells of tissue
• ie lactate: released from RBC, liver, kidney, skeletal muscle
• creatine kinase-CK: released from skeletal muscle, brain, heart
• ALT/AST: released from heart, liver, muscle, kidney, pancreas
differentiate between the cellular processes involved in cell necrosis and apoptosis - ANSWER
necrosis: cell swelling, nucleus: pyknosiskaryorrhexiskaryolysis, disrupted plasma membrane,
cellular contents leak enzymes, inflammation present, pathologic d/t irreversible cell injury= d/t
external factors
apoptosis: cell shrinkage, nucleus: fragmentation, altered plasma membrane "blebs", cellular
contents intact, no inflammation, often physiologic, can be pathologic with DNA damage=
natural
describe the three mechanisms involved in the process of apoptosis: - ANSWER 1. generated
by signals arising within the cell;
2. triggered by death activators binding to receptors at the cell surface: TNF-α, Lymphotoxin, Fas
ligand
3. triggered by dangerous reactive oxygen species.
, 20. discuss the relationship of apoptosis to: cancer, HIV, organ transplant - ANSWER cancer:
Some cancer cells, especially lung and colon cancer cells, secrete elevated levels of a soluble
"decoy" molecule that binds to FasL, plugging it up so it cannot bind Fas. Thus, cytotoxic T cells
(CTL) cannot kill the cancer cell. Other cancer cells express high levels of FasL, and can kill any
cytotoxic T cells
AIDS: All T cells, both infected and uninfected, express Fas. Expression of a HIV gene (called Nef)
in a HIV-infected cell causes the cell to express high levels of FasL at its surface while preventing
an interaction with its own Fas from causing it to self-destruct. However, when the infected T
cell encounters an uninfected one (e.g. in a lymph node), the interaction of FasL with Fas on the
uninfected cell kills it by apoptosis
organ transplantation: Graft rejection: The patient's immune system "sees" an allograft as
foreign (antigenic) and mounts an immune response against it.
define aging and its relationship to cellular function/structure and genetic and environmental
factors - ANSWER aging: a normal physiologic process that is universal and inevitable
Cellular changes characteristic of aging include atrophy, decreased function, and loss of cells,
possibly by apoptosis. Loss of cellular function from any of these causes initiates the
compensatory mechanisms of hypertrophy and hyperplasia of remaining cells, which can lead to
metaplasia, dysplasia, and neoplasia. All these changes can alter receptor placement and
function, nutrient pathways, secretion of cellular products, and neuroendocrine control
mechanisms.
If a normal individual began to take thyroid hormone 100 mcgs. every day as a medication,
which of the following would result?
a. hypertrophy of the thyroid gland
b. hyperplasia of the thyroid gland
c. atrophy of the thyroid gland
d. hypertrophy and hyperplasia of the thyroid gland - ANSWER B
