BSC 2085 EXAM 2 | QUESTIONS AND
CORRECT ANSWERS | 2026/2027 UPDATED |
100% CORRECT - MIAMI DADE COLLEGE.
120 Questions with Answers and Detailed Rationales
100 PERCENT GUARANTEED PASS
INSTANT DOWNLOAD ANSWERS INCLUDED
IMPORTANCE OF THIS DOCUMENT
This comprehensive examination preparation guide has been meticulously developed to help you succeed in the
BSC 2085 EXAM 2 | QUESTIONS AND CORRECT ANSWERS | 2026/2027 UPDATED | 100% CORRECT -
MIAMI DADE COLLEGE.. It contains 120 carefully selected questions that reflect the most current exam content
and testing strategies. Each question is accompanied by a correct answer and a detailed rationale that explains
the underlying pathophysiology, pharmacology, or clinical reasoning.
Self-Assessment – Test your knowledge and Exam Preparation – Familiarize yourself with the
identify areas requiring further question format and content
study areas
Concept Reinforcement – Deepen your Confidence Building – Develop test-taking
understanding through strategies and reduce
evidence-based exam anxiety
rationales
Time Management – Practice answering
questions under simulated
exam conditions
Review Summary 120 Questions
Foundations - Application - BSC 2085 2 AND Correct 2026/2027 Updated 100 Correct - Miami DADE
College Human Anatomy AND Physiology II BSC 2085 Undergraduate YEAR 2 Anatomy & Physiology II
All answers with rationales
,Table of Contents
Content Area Questions Key Topics
Integumentary System 1-20 Effect, Mechanism, Receptor, Likely, Finding
Skeletal System AND Joints 21-40 Likely, Channels, Right, Blocks, Effect
Muscular System 41-60 Explains, Potential, Effect, Muscle, Directly
Nervous System 61-80 Researcher, Describes, Blood, Neuron, Consequence
Sensory Systems 81-100 Describes, Likely, Mechanism, Lesion, Explains
Endocrine System 101-120 Cardiac, Pressure, Channels, Muscle, Blood
TOTAL 120 All questions include answers and detailed rationales
,Section A - Integumentary System
Q1.
A researcher discovers a novel hormone that, when administered, causes a rapid increase
in cyclic AMP in target cells but also desensitizes the receptor within minutes. Which
receptor type is most likely mediating these effects?
A. G protein-coupled receptor B. Receptor tyrosine kinase
C. Nuclear receptor D. Ligand-gated ion channel
Correct: A - G protein-coupled receptor
Rationale:G protein-coupled receptors (GPCRs) often signal via cAMP and are rapidly
desensitized by phosphorylation (e.g., by GRKs) and -arrestin binding. Receptor tyrosine
kinases activate kinase cascades, not directly cAMP. Nuclear receptors act slowly on
transcription. Ligand-gated ion channels cause fast ion fluxes.
Why the other answers are wrong:
B. Receptor tyrosine kinases activate kinase cascades, not directly cAMP, and desensitization
is slower.
C. Nuclear receptors act via gene transcription with a slow onset, not rapid cAMP increases.
D. Ligand-gated ion channels mediate fast ion fluxes, not second messenger cascades like
cAMP.
Reference: Tortora, G.J. & Derrickson, B. (2026). Principles of Anatomy and Physiology, 16th Ed., Ch. 17
Q2.
A patient with chronic renal failure has a hematocrit of 25% and a plasma erythropoietin
level that is inappropriately low. Which physiological mechanism best explains this
finding?
A. Decreased renal production of B. Increased destruction of erythropoietin by
erythropoietin due to loss of peritubular the liver
interstitial fibroblasts
C. Suppression of erythropoietin secretion D. Downregulation of erythropoietin
by high levels of urea receptors in the bone marrow
Correct: A - Decreased renal production of erythropoietin due to loss of peritubular
interstitial fibroblasts
Rationale:Erythropoietin is produced by peritubular interstitial cells (fibroblasts) in the kidney.
Chronic renal failure destroys these cells, leading to deficient EPO production and anemia.
Liver destruction, urea suppression, or receptor downregulation are not primary causes.
Why the other answers are wrong:
Page 3
, Section A - Integumentary System
B. The liver is not a major site of erythropoietin degradation; this is not a primary mechanism.
C. Urea does not directly suppress erythropoietin secretion.
D. Receptor downregulation is not the cause of anemia in renal failure; the issue is hormone production.
Reference: Porth, C.M. (2025). Pathophysiology: Concepts of Altered Health States, 11th Ed., Ch. 8
Q3.
During exercise, sympathetic stimulation causes vasoconstriction in the renal and
splanchnic beds but vasodilation in skeletal muscle. This differential response is best
explained by which mechanism?
A. Differences in adrenergic receptor B. Higher density of sympathetic innervation
subtypes and local metabolic autoregulation in skeletal muscle
C. Parasympathetic withdrawal in skeletal D. Release of nitric oxide from renal and
muscle only splanchnic endothelium
Correct: A - Differences in adrenergic receptor subtypes and local metabolic
autoregulation
Rationale:Sympathetic activation releases norepinephrine, which binds ±1-adrenergic
receptors causing vasoconstriction in renal/splanchnic beds. In skeletal muscle, 2-adrenergic
receptors mediate vasodilation, and local metabolites (e.g., adenosine, CO2) override
sympathetic tone. Innervation density and parasympathetic withdrawal are not primary.
Why the other answers are wrong:
B. Skeletal muscle has similar or less innervation; the effect is receptor-mediated, not
innervation density.
C. Parasympathetic innervation to skeletal muscle is minimal; it does not mediate vasodilation.
D. Nitric oxide is released in skeletal muscle, not in renal/splanchnic beds, and is not the
primary cause of constriction.
Reference: Klabunde, R.E. (2025). Cardiovascular Physiology Concepts, 3rd Ed., Ch. 5
Q4.
A patient presents with massive splenomegaly and pancytopenia. Peripheral blood smear
shows teardrop cells and nucleated red blood cells. Which condition is most consistent
with these findings?
A. Myelophthisic anemia due to bone B. Autoimmune hemolytic anemia
marrow infiltration
C. Iron deficiency anemia D. Pernicious anemia
Correct: A - Myelophthisic anemia due to bone marrow infiltration
Page 4
CORRECT ANSWERS | 2026/2027 UPDATED |
100% CORRECT - MIAMI DADE COLLEGE.
120 Questions with Answers and Detailed Rationales
100 PERCENT GUARANTEED PASS
INSTANT DOWNLOAD ANSWERS INCLUDED
IMPORTANCE OF THIS DOCUMENT
This comprehensive examination preparation guide has been meticulously developed to help you succeed in the
BSC 2085 EXAM 2 | QUESTIONS AND CORRECT ANSWERS | 2026/2027 UPDATED | 100% CORRECT -
MIAMI DADE COLLEGE.. It contains 120 carefully selected questions that reflect the most current exam content
and testing strategies. Each question is accompanied by a correct answer and a detailed rationale that explains
the underlying pathophysiology, pharmacology, or clinical reasoning.
Self-Assessment – Test your knowledge and Exam Preparation – Familiarize yourself with the
identify areas requiring further question format and content
study areas
Concept Reinforcement – Deepen your Confidence Building – Develop test-taking
understanding through strategies and reduce
evidence-based exam anxiety
rationales
Time Management – Practice answering
questions under simulated
exam conditions
Review Summary 120 Questions
Foundations - Application - BSC 2085 2 AND Correct 2026/2027 Updated 100 Correct - Miami DADE
College Human Anatomy AND Physiology II BSC 2085 Undergraduate YEAR 2 Anatomy & Physiology II
All answers with rationales
,Table of Contents
Content Area Questions Key Topics
Integumentary System 1-20 Effect, Mechanism, Receptor, Likely, Finding
Skeletal System AND Joints 21-40 Likely, Channels, Right, Blocks, Effect
Muscular System 41-60 Explains, Potential, Effect, Muscle, Directly
Nervous System 61-80 Researcher, Describes, Blood, Neuron, Consequence
Sensory Systems 81-100 Describes, Likely, Mechanism, Lesion, Explains
Endocrine System 101-120 Cardiac, Pressure, Channels, Muscle, Blood
TOTAL 120 All questions include answers and detailed rationales
,Section A - Integumentary System
Q1.
A researcher discovers a novel hormone that, when administered, causes a rapid increase
in cyclic AMP in target cells but also desensitizes the receptor within minutes. Which
receptor type is most likely mediating these effects?
A. G protein-coupled receptor B. Receptor tyrosine kinase
C. Nuclear receptor D. Ligand-gated ion channel
Correct: A - G protein-coupled receptor
Rationale:G protein-coupled receptors (GPCRs) often signal via cAMP and are rapidly
desensitized by phosphorylation (e.g., by GRKs) and -arrestin binding. Receptor tyrosine
kinases activate kinase cascades, not directly cAMP. Nuclear receptors act slowly on
transcription. Ligand-gated ion channels cause fast ion fluxes.
Why the other answers are wrong:
B. Receptor tyrosine kinases activate kinase cascades, not directly cAMP, and desensitization
is slower.
C. Nuclear receptors act via gene transcription with a slow onset, not rapid cAMP increases.
D. Ligand-gated ion channels mediate fast ion fluxes, not second messenger cascades like
cAMP.
Reference: Tortora, G.J. & Derrickson, B. (2026). Principles of Anatomy and Physiology, 16th Ed., Ch. 17
Q2.
A patient with chronic renal failure has a hematocrit of 25% and a plasma erythropoietin
level that is inappropriately low. Which physiological mechanism best explains this
finding?
A. Decreased renal production of B. Increased destruction of erythropoietin by
erythropoietin due to loss of peritubular the liver
interstitial fibroblasts
C. Suppression of erythropoietin secretion D. Downregulation of erythropoietin
by high levels of urea receptors in the bone marrow
Correct: A - Decreased renal production of erythropoietin due to loss of peritubular
interstitial fibroblasts
Rationale:Erythropoietin is produced by peritubular interstitial cells (fibroblasts) in the kidney.
Chronic renal failure destroys these cells, leading to deficient EPO production and anemia.
Liver destruction, urea suppression, or receptor downregulation are not primary causes.
Why the other answers are wrong:
Page 3
, Section A - Integumentary System
B. The liver is not a major site of erythropoietin degradation; this is not a primary mechanism.
C. Urea does not directly suppress erythropoietin secretion.
D. Receptor downregulation is not the cause of anemia in renal failure; the issue is hormone production.
Reference: Porth, C.M. (2025). Pathophysiology: Concepts of Altered Health States, 11th Ed., Ch. 8
Q3.
During exercise, sympathetic stimulation causes vasoconstriction in the renal and
splanchnic beds but vasodilation in skeletal muscle. This differential response is best
explained by which mechanism?
A. Differences in adrenergic receptor B. Higher density of sympathetic innervation
subtypes and local metabolic autoregulation in skeletal muscle
C. Parasympathetic withdrawal in skeletal D. Release of nitric oxide from renal and
muscle only splanchnic endothelium
Correct: A - Differences in adrenergic receptor subtypes and local metabolic
autoregulation
Rationale:Sympathetic activation releases norepinephrine, which binds ±1-adrenergic
receptors causing vasoconstriction in renal/splanchnic beds. In skeletal muscle, 2-adrenergic
receptors mediate vasodilation, and local metabolites (e.g., adenosine, CO2) override
sympathetic tone. Innervation density and parasympathetic withdrawal are not primary.
Why the other answers are wrong:
B. Skeletal muscle has similar or less innervation; the effect is receptor-mediated, not
innervation density.
C. Parasympathetic innervation to skeletal muscle is minimal; it does not mediate vasodilation.
D. Nitric oxide is released in skeletal muscle, not in renal/splanchnic beds, and is not the
primary cause of constriction.
Reference: Klabunde, R.E. (2025). Cardiovascular Physiology Concepts, 3rd Ed., Ch. 5
Q4.
A patient presents with massive splenomegaly and pancytopenia. Peripheral blood smear
shows teardrop cells and nucleated red blood cells. Which condition is most consistent
with these findings?
A. Myelophthisic anemia due to bone B. Autoimmune hemolytic anemia
marrow infiltration
C. Iron deficiency anemia D. Pernicious anemia
Correct: A - Myelophthisic anemia due to bone marrow infiltration
Page 4
