General, Organic & Biological Chemistry with Lab | Review Questions
and Verified Answers | Grade A | 100% Correct - Chamberlain
Question 1
A 32-year-old patient presents with persistent low mood, anhedonia, poor
concentration, and insomnia for the past six weeks. The PMHNP considers
starting a selective serotonin reuptake inhibitor (SSRI).
Which of the following neurotransmitter systems is primarily targeted by
SSRIs to produce antidepressant effects?
A. Dopamine and acetylcholine
B. Serotonin reuptake inhibition
C. GABA receptor enhancement
D. Histamine blockade
Correct Answer: B – Serotonin reuptake inhibition
Rationale:
Selective serotonin reuptake inhibitors (SSRIs) act primarily by blocking the
serotonin transporter (SERT), which is responsible for the reuptake of
serotonin (5-hydroxytryptamine, or 5-HT) from the synaptic cleft back into
the presynaptic neuron. This inhibition leads to increased serotonin
availability in the synaptic space, allowing for enhanced stimulation of
postsynaptic serotonin receptors in key brain regions associated with mood
regulation, such as the prefrontal cortex and limbic system. The resulting
elevation in serotonergic neurotransmission contributes to the alleviation of
depressive and anxiety symptoms commonly seen in mood disorders. In
contrast, dopamine and acetylcholine systems (Option A) are more directly
influenced by agents like bupropion and anticholinergics, respectively.
GABA receptor enhancement (Option C) describes the mechanism of
benzodiazepines, which promote anxiolytic and sedative effects rather than
,antidepressant outcomes. Histamine blockade (Option D) is linked to the
sedative and weight gain effects of drugs such as tricyclic antidepressants or
mirtazapine, not the primary therapeutic mechanism of SSRIs. Therefore,
serotonin reuptake inhibition best explains how SSRIs exert their
antidepressant efficacy.
Question 2
A patient with type 1 diabetes presents with rapid breathing, fruity-smelling
breath, and confusion after missing insulin doses for 48 hours. The PMHNP
recalls this reflects a metabolic shift away from glucose utilization. Which
metabolic process predominates when cells are starved for insulin and
carbohydrates?
A. Increased glycolysis leading to lactic acidosis
B. Increased fatty acid β-oxidation and ketogenesis
C. Increased glycogen synthesis in the liver
D. Increased pentose phosphate pathway activity
Correct Answer: B – Increased fatty acid β-oxidation and ketogenesis
Rationale:
When insulin is absent or low, peripheral tissues cannot uptake glucose
efficiently, so adipose tissue releases free fatty acids that travel to the liver
where they undergo β-oxidation; excess acetyl-CoA from β-oxidation is
diverted into ketone body formation (ketogenesis). The resulting ketones
(acetoacetate, β-hydroxybutyrate) accumulate, causing ketoacidosis and
producing fruity breath. Glycolysis (A) is not the dominant pathway in
insulin deficiency; glycogen synthesis (C) requires insulin and is decreased,
and the pentose phosphate pathway (D) is a secondary pathway not
responsible for the systemic metabolic picture described.
Question 3
A patient on a monoamine oxidase inhibitor (MAOI) eats aged cheese and
rapidly develops severe headache, neck stiffness, and dangerously high
blood pressure. The clinician knows this reaction is due to excess of which
,vasoactive amine?
A. Serotonin (5-HT)
B. Norepinephrine (NE) / Epinephrine
C. Gamma-aminobutyric acid (GABA)
D. Acetylcholine (ACh)
Correct Answer: B – Norepinephrine (NE) / Epinephrine
Rationale:
Tyramine in aged cheese is normally metabolized by monoamine oxidase in
the gut and liver; when MAO is inhibited, tyramine is absorbed and causes
release of stored catecholamines (mainly norepinephrine and some
epinephrine) from sympathetic nerve endings, producing hypertensive crises
(severe headache, neck stiffness, autonomic signs). Serotonin (A) excess
causes serotonin syndrome in different settings, but the classic cheese
reaction is catecholaminergic. GABA (C) and acetylcholine (D) are not
implicated in the MAOI-tyramine hypertensive crisis.
Question 4
During an acid–base lab, a student is asked which conjugate acid–base pair
most effectively buffers a solution near pH 7.4. Which pair is most
appropriate for physiological buffering?
A. Acetic acid / acetate (pKa ≈ 4.8)
B. Carbonic acid / bicarbonate (pKa ≈ 6.1 for H₂CO₃ ⇌ HCO₃⁻ system in
water/CO₂ context)
C. Ammonium / ammonia (pKa ≈ 9.25)
D. Hydrofluoric acid / fluoride (pKa ≈ 3.2)
Correct Answer: B – Carbonic acid / bicarbonate
Rationale:
Buffering is most effective when the pKa of the conjugate acid is within ±1
pH unit of the target pH; physiological pH ≈ 7.4 is best matched by the
bicarbonate buffer system because of its role in blood: CO₂ (aqueous/
H₂CO₃) ⇌ HCO₃⁻ and the lung-kidney regulation maintains pH around 7.4.
, Although the pKa of dissolved CO₂/H₂CO₃ is often cited around 6.1, the
system’s capacity and physiological regulation (ventilation and renal
bicarbonate handling) make it ideal for physiological buffering. Acetate (A)
and fluoride (D) have pKa values far below 7.4; ammonium/ammonia (C)
buffers around alkaline pH, not near 7.4.
Question 5
A chemistry lab asks which molecular orbital interaction explains why
oxygen (O₂) is paramagnetic, showing attraction to a magnetic field, even
though simple Lewis structures predict all electrons paired. Which orbital
explanation is correct?
A. All bonding electrons are paired in sigma orbitals—oxygen is
diamagnetic.
B. Oxygen has two unpaired electrons in degenerate π* antibonding
molecular orbitals.
C. Unpaired electrons arise from lone pairs in nonbonding orbitals on
oxygen atoms.
D. Paramagnetism is due to ionic character producing free radicals in
oxygen.
Correct Answer: B – Oxygen has two unpaired electrons in degenerate π*
antibonding molecular orbitals
Rationale:
Molecular orbital theory for O₂ shows that after filling bonding π orbitals,
electrons occupy the degenerate π* antibonding orbitals, leaving two
electrons unpaired (one in each π* orbital). These two unpaired electrons
produce paramagnetism and are experimentally observed by O₂’s attraction
to a magnetic field. Simple Lewis structures fail to predict this because they
do not consider molecular orbital antibonding occupancy. Lone pairs (C) in
atomic orbitals do not explain O₂’s paramagnetism, and (D) is incorrect
since O₂’s paramagnetism is an intrinsic molecular orbital property, not due
to ionic dissociation or free radicals.