Advanced Pathophysiology Exam 1 - Exam Prep, Questions & Answers
Hypertophy Increase in the size of cells resulting in an increase in size of the organ; no new
cells, just larger cells
• Due to synthesis and assembly of additional intracellular structural components;
result of increased cellular protein production
hyperplasia increase in
number of cells
what cells undergo hypertrophy only Permanent cells (striated muscle, nerve tissue, cardiac muscle)
Physiologic hypertrophy vs Pathological - growth of uterus during pregnancy (stimulated by
hormones) resulting mainly from hypertrophy of smooth muscle fibers: hormone
signaling leads to increased synthesis of smooth muscle proteins and increased cell
size
- "Working out": enlargement of individual skeletal
muscle fibers in response to increased demand
Versus: Pathological hypertrophy; Increase work load on heart muscle secondary to
hypertension or aortic stenosis
Physiologic hyperplasia vs Pathological Physiologic hyperplasia - example: proliferation of the
glandular epithelium of the female breast at puberty and during pregnancy, usually
accompanied by enlargement (hypertrophy) of the glandular epithelial cells
• Pathologic hyperplasia usually caused by excessive or
inappropriate actions of hormones or growth factors
acting on target cells (e.g., endometrial hyperplasia)
Atrophy Decrease in size of cells, secondary to:
•DECREASED WORKLOAD
•DENERVATION
•DECREASED BLOOD FLOW
•DECREASED NUTRITION
•AGING (involution)
•PRESSURE
Metaplasia •Replacement of one differentiated (mature, adult) cell by another cell type
•Reversible, but if persists can lead to dysplasia
•Most common is columnar to squamous
•Results from either reprogramming of local tissue stem cells, or, colonization by
differentiated cell populations from adjacent sites
•Stimulated by signals generated by cytokines, growth factors, and ECM
components in cells' environment
Cell death is it reversable reversable= cell injury. not reversable=death
Hypoxia deficiency of oxygen; causes cell injury by reducing aerobic oxidative respiration
What causes hypoxia?
• reduced blood flow (ischemia)
• inadequate oxygenation of the blood due to cardiorespiratory failure
• decreased oxygen-carrying capacity of the blood (anemia, carbon monoxide
poisoning and severe blood loss)
pathology of ischemia decrease in blood flow, oxygen decrease
•REDUCED oxidative phosphorylation
•ATP depletion/ loss or reduction of Na+/K+ pump.
•Na+ enters cell and water
•Cellular "SWELLING
ISCHEMIA is REVERSABLE
Stuvia 2026-2027 | Latest Version
, Advanced Pathophysiology Exam 1 - Exam Prep, Questions & Answers
necrosis - characterized by denaturation of cellular
proteins, leakage of cellular contents through damaged
membranes, local inflammation, and enzymatic digestion of the lethally injured cell
-IRREVERSIBLE MITOCHONDRIAL DYSFUNCTION
-PROFOUND MEMBRANE DISTURBANCES
-Nucleus becomes pyknotic, disintegrates
Coagulative necrosis Solid organs, cellular outline maintained, nucleus dissolves (kidney, heart, liver)-
localized area of coagulative necrosis = infarct
Architecture (cell outlines) preserved, nucleus disappears
Local area of coagulative necrosis - infarct
Liquefactive Necrosis in Brain
Digestion of dead cells resulting in
liquid, viscous mass
• Occurs in Brain
• Occurs in abscesses (bacteria)
Gangrenous necrosis (Extremities, Bowel, non-specific)
Not specific pattern of cell death - term commonly used in clinical practice
• Example: limb, generally lower leg,
that has lost its blood supply and has undergone necrosis (typically coagulative
necrosis) involving
multiple tissue planes
• When bacterial infection is superimposed, there is more liquefactive necrosis
because of the
actions of degradative enzymes in the bacteria and attracted leukocytes (wet
gangrene)
Fibrinoid necrosis Rheumatoid, vessels, non-specific
Special form of vascular damage usually seen in
immune reactions involving blood vessels
• Deposits of these immune complexes, along with plasma proteins that has leaked
out of vessels, result in a bright pink and amorphous appearance in H&E stains
called "fibrinoid" (fibrin-like) by pathologists
Caseous necrosis Tuberculosis, granulomas
- friable white appearance of area of necrosis
what is a granulomas Aggregation of macrophages - forms in response to chronic inflammation. This
occurs when the immune system attempts to isolate foreign substances that it is
otherwise unable to eliminate, which include infectious organisms including bacteria
(TB) and fungi, as well as foreign objects, keratin, and suture fragments
fatty necrosis breast or pancreas
Infections, viruses, trauma, ischemia and toxins may
damage pancreas causing enzymes to be released
• Breast tissues can also have fat necrosis triggered by
trauma
• Gross appearance: soft chalky-white area on the
pancreas.
• Microscopic. Anucleated adipocytes with pinker
cytoplasm containing amorphous mass of necrotic
material; may see inflammation
Stuvia 2026-2027 | Latest Version
, Advanced Pathophysiology Exam 1 - Exam Prep, Questions & Answers
Reperfusion injury Restored blood flow reintroduces oxygen within
cells which damages cellular proteins, DNA,
and the plasma membrane
• Formation of free radicals
Apoptosis Form of programmed cell death - nuclear dissolution, ATP needed
•• Protein Digestion
• DNA breakdown
• Phagocytic Recognition
• Cell contents don't leak out, DOES NOT elicit inflammation (v. necrosis)\
Reduced Cell cells with intact cell content and plasma membrane.
anthracosis lung accumulating pigments from industrial society/smoke
Lipofuscin finely granular yellow-brown pigment granules composed of lipid- containing
residues of lysosomal digestion.
"wear and tear" pigment
Acute Inflammation Neutrophil
Polymorphonuclear Leukocyte, PMN "Leukocyte"
Granulocyte, Neutrophilic granulocyte
What does acute inflammation feel like redness, heat, swelling, pain, loss of function
Vascular changes for inflammation changes in flow and caliber
increase vascular permeability
occurs before inflammatory cells arrive
Increased permeability dialation with endothelial gaps and leaking of exudative fluid
Margination the sticking of phagocytes to blood vessels in response to cytokines at the site of
inflammation
Vascular changes in inflammation results: stasis,
edema, and margination of neutrophils to mobilize cells to site if injury outside the
vessel lumen
Steps of inflammation overview starts with dialation
Step 1: margination
• Step 2: rolling
• Step 3: adhesion
• Step 4: transmigration
• Step 5: chemotaxis
1-3 is within lumen
3 and 4 is through the lumen and to the site of the injury
Adhesion molecules SECRETINS - rolling
INTEGRINS- adhesion of WBC to the cell
Chemotaxis Nuetrophils going to site of injury after transmigration
Phagocytosis RECOGNITION (opsonization)
ENGULFMENT: Ingestion - engulfed microbes form phagosomes which fuse with
lysosomes: phagolysosomes Dependent on polymerization of actin
KILLING: (DEGRADATION/DIGESTION)
Stuvia 2026-2027 | Latest Version
Hypertophy Increase in the size of cells resulting in an increase in size of the organ; no new
cells, just larger cells
• Due to synthesis and assembly of additional intracellular structural components;
result of increased cellular protein production
hyperplasia increase in
number of cells
what cells undergo hypertrophy only Permanent cells (striated muscle, nerve tissue, cardiac muscle)
Physiologic hypertrophy vs Pathological - growth of uterus during pregnancy (stimulated by
hormones) resulting mainly from hypertrophy of smooth muscle fibers: hormone
signaling leads to increased synthesis of smooth muscle proteins and increased cell
size
- "Working out": enlargement of individual skeletal
muscle fibers in response to increased demand
Versus: Pathological hypertrophy; Increase work load on heart muscle secondary to
hypertension or aortic stenosis
Physiologic hyperplasia vs Pathological Physiologic hyperplasia - example: proliferation of the
glandular epithelium of the female breast at puberty and during pregnancy, usually
accompanied by enlargement (hypertrophy) of the glandular epithelial cells
• Pathologic hyperplasia usually caused by excessive or
inappropriate actions of hormones or growth factors
acting on target cells (e.g., endometrial hyperplasia)
Atrophy Decrease in size of cells, secondary to:
•DECREASED WORKLOAD
•DENERVATION
•DECREASED BLOOD FLOW
•DECREASED NUTRITION
•AGING (involution)
•PRESSURE
Metaplasia •Replacement of one differentiated (mature, adult) cell by another cell type
•Reversible, but if persists can lead to dysplasia
•Most common is columnar to squamous
•Results from either reprogramming of local tissue stem cells, or, colonization by
differentiated cell populations from adjacent sites
•Stimulated by signals generated by cytokines, growth factors, and ECM
components in cells' environment
Cell death is it reversable reversable= cell injury. not reversable=death
Hypoxia deficiency of oxygen; causes cell injury by reducing aerobic oxidative respiration
What causes hypoxia?
• reduced blood flow (ischemia)
• inadequate oxygenation of the blood due to cardiorespiratory failure
• decreased oxygen-carrying capacity of the blood (anemia, carbon monoxide
poisoning and severe blood loss)
pathology of ischemia decrease in blood flow, oxygen decrease
•REDUCED oxidative phosphorylation
•ATP depletion/ loss or reduction of Na+/K+ pump.
•Na+ enters cell and water
•Cellular "SWELLING
ISCHEMIA is REVERSABLE
Stuvia 2026-2027 | Latest Version
, Advanced Pathophysiology Exam 1 - Exam Prep, Questions & Answers
necrosis - characterized by denaturation of cellular
proteins, leakage of cellular contents through damaged
membranes, local inflammation, and enzymatic digestion of the lethally injured cell
-IRREVERSIBLE MITOCHONDRIAL DYSFUNCTION
-PROFOUND MEMBRANE DISTURBANCES
-Nucleus becomes pyknotic, disintegrates
Coagulative necrosis Solid organs, cellular outline maintained, nucleus dissolves (kidney, heart, liver)-
localized area of coagulative necrosis = infarct
Architecture (cell outlines) preserved, nucleus disappears
Local area of coagulative necrosis - infarct
Liquefactive Necrosis in Brain
Digestion of dead cells resulting in
liquid, viscous mass
• Occurs in Brain
• Occurs in abscesses (bacteria)
Gangrenous necrosis (Extremities, Bowel, non-specific)
Not specific pattern of cell death - term commonly used in clinical practice
• Example: limb, generally lower leg,
that has lost its blood supply and has undergone necrosis (typically coagulative
necrosis) involving
multiple tissue planes
• When bacterial infection is superimposed, there is more liquefactive necrosis
because of the
actions of degradative enzymes in the bacteria and attracted leukocytes (wet
gangrene)
Fibrinoid necrosis Rheumatoid, vessels, non-specific
Special form of vascular damage usually seen in
immune reactions involving blood vessels
• Deposits of these immune complexes, along with plasma proteins that has leaked
out of vessels, result in a bright pink and amorphous appearance in H&E stains
called "fibrinoid" (fibrin-like) by pathologists
Caseous necrosis Tuberculosis, granulomas
- friable white appearance of area of necrosis
what is a granulomas Aggregation of macrophages - forms in response to chronic inflammation. This
occurs when the immune system attempts to isolate foreign substances that it is
otherwise unable to eliminate, which include infectious organisms including bacteria
(TB) and fungi, as well as foreign objects, keratin, and suture fragments
fatty necrosis breast or pancreas
Infections, viruses, trauma, ischemia and toxins may
damage pancreas causing enzymes to be released
• Breast tissues can also have fat necrosis triggered by
trauma
• Gross appearance: soft chalky-white area on the
pancreas.
• Microscopic. Anucleated adipocytes with pinker
cytoplasm containing amorphous mass of necrotic
material; may see inflammation
Stuvia 2026-2027 | Latest Version
, Advanced Pathophysiology Exam 1 - Exam Prep, Questions & Answers
Reperfusion injury Restored blood flow reintroduces oxygen within
cells which damages cellular proteins, DNA,
and the plasma membrane
• Formation of free radicals
Apoptosis Form of programmed cell death - nuclear dissolution, ATP needed
•• Protein Digestion
• DNA breakdown
• Phagocytic Recognition
• Cell contents don't leak out, DOES NOT elicit inflammation (v. necrosis)\
Reduced Cell cells with intact cell content and plasma membrane.
anthracosis lung accumulating pigments from industrial society/smoke
Lipofuscin finely granular yellow-brown pigment granules composed of lipid- containing
residues of lysosomal digestion.
"wear and tear" pigment
Acute Inflammation Neutrophil
Polymorphonuclear Leukocyte, PMN "Leukocyte"
Granulocyte, Neutrophilic granulocyte
What does acute inflammation feel like redness, heat, swelling, pain, loss of function
Vascular changes for inflammation changes in flow and caliber
increase vascular permeability
occurs before inflammatory cells arrive
Increased permeability dialation with endothelial gaps and leaking of exudative fluid
Margination the sticking of phagocytes to blood vessels in response to cytokines at the site of
inflammation
Vascular changes in inflammation results: stasis,
edema, and margination of neutrophils to mobilize cells to site if injury outside the
vessel lumen
Steps of inflammation overview starts with dialation
Step 1: margination
• Step 2: rolling
• Step 3: adhesion
• Step 4: transmigration
• Step 5: chemotaxis
1-3 is within lumen
3 and 4 is through the lumen and to the site of the injury
Adhesion molecules SECRETINS - rolling
INTEGRINS- adhesion of WBC to the cell
Chemotaxis Nuetrophils going to site of injury after transmigration
Phagocytosis RECOGNITION (opsonization)
ENGULFMENT: Ingestion - engulfed microbes form phagosomes which fuse with
lysosomes: phagolysosomes Dependent on polymerization of actin
KILLING: (DEGRADATION/DIGESTION)
Stuvia 2026-2027 | Latest Version
