The Biologic Basis for Disease in Adults and Children
9th Edition
• Author(s)Julia Rogers
TEST BANK
Question 1
Chapter 1, Cellular Communication and Signal Transduction
A researcher is studying a hormone that binds to a
transmembrane receptor, activating a G-protein which then
stimulates the enzyme adenylate cyclase. This is a classic
example of which type of cellular signaling pathway?
A. Intracrine signaling
B. Endocrine signaling
C. Ion channel-linked receptor signaling
D. G-protein-linked receptor signaling
Correct Answer: D
Rationale for Correct Answer (D): G-protein-linked receptors
are a major class of transmembrane receptors. Their activation
by a first messenger (e.g., a hormone) triggers the exchange of
GDP for GTP on the associated G-protein subunit, which then
dissociates and activates effector proteins like adenylate cyclase
to generate second messengers (e.g., cAMP).
Rationale for Incorrect Answers:
,A. Intracrine signaling involves chemical mediators that act
intracellularly on the same cell that synthesized them, without
being released.
B. Endocrine signaling describes the mode of delivery of a
hormone (via the bloodstream to distant targets), not the
specific mechanism of receptor action at the target cell.
C. Ion channel-linked receptors open a channel for ions to flow
through upon ligand binding; they do not typically involve G-
proteins or enzymes like adenylate cyclase.
Teaching Point: G-protein-coupled receptors (GPCRs) translate
extracellular first messenger binding into intracellular second
messenger production.
Question 2
Chapter 1, Cellular Metabolism
A patient with a history of chronic alcohol use is diagnosed with
Wernicke-Korsakoff syndrome. This condition is primarily
caused by a deficiency in a coenzyme derived from which
vitamin, crucial for the decarboxylation reactions in aerobic
glucose metabolism?
A. Niacin (B3)
B. Riboflavin (B2)
C. Thiamine (B1)
D. Pantothenic Acid (B5)
Correct Answer: C
,Rationale for Correct Answer (C): Thiamine (Vitamin B1) is a
precursor for thiamine pyrophosphate (TPP), an essential
coenzyme for the pyruvate dehydrogenase complex. This
complex decarboxylates pyruvate to acetyl-CoA, a critical step
linking glycolysis to the citric acid cycle.
Rationale for Incorrect Answers:
A. Niacin is a precursor for NAD+, a coenzyme for
dehydrogenases.
B. Riboflavin is a precursor for FAD, another coenzyme for
dehydrogenases.
D. Pantothenic acid is a component of coenzyme A (CoA), which
carries acyl groups but is not directly involved in the
decarboxylation reaction itself.
Teaching Point: Thiamine deficiency impairs pyruvate
conversion to acetyl-CoA, disrupting aerobic ATP production
and damaging highly metabolic tissues like the brain.
Question 3
Chapter 1, Structure and Function of Cellular Components
During a lecture on cell structure, a professor describes an
organelle that is the primary site of ATP production, contains its
own DNA, and can trigger apoptosis by releasing cytochrome c.
This description refers to the:
A. Golgi apparatus
B. Rough endoplasmic reticulum
, C. Mitochondrion
D. Lysosome
Correct Answer: C
Rationale for Correct Answer (C): The mitochondrion is the
"powerhouse of the cell" where oxidative phosphorylation
occurs. It contains mitochondrial DNA (mtDNA) and plays a
central role in programmed cell death (apoptosis) by releasing
pro-apoptotic factors like cytochrome c into the cytosol.
Rationale for Incorrect Answers:
A. The Golgi apparatus modifies, sorts, and packages proteins
for secretion; it is not involved in ATP production or apoptosis.
B. The rough endoplasmic reticulum is involved in protein
synthesis; it does not contain its own DNA or release
cytochrome c.
D. Lysosomes are involved in intracellular digestion using
hydrolytic enzymes; their rupture can cause cell death
(necrosis), not the regulated release seen in apoptosis.
Teaching Point: Mitochondria are semi-autonomous organelles
central to energy production and are key regulators of the
intrinsic pathway of apoptosis.
Question 4
Chapter 1, Membrane Transport: Cellular Intake and Output
A patient with cystic fibrosis has a defective CFTR protein. This