NRNP 6665-01, Week 11 Final Exam Solutions 2026/2027 Advanced
PMHNP Care Across the Lifespan | Complex & Evolving Case Studies|
Actual Questions & Verified Solutions | Advanced Psychiatric-Mental
Health Nurse Practitioner | Pass Guarantee
CASE BLOCK 1: The Martinez Family - Intergenerational Trauma and
Complex ADHD
Case Background: The Martinez family presents to your integrated behavioral health
clinic. Elena Martinez, 38, brings her two children: Sofia (16) and Mateo (9). Elena
reports her own lifelong struggles with "scattered thinking" and emotional dysregulation.
Sofia has been cutting herself and failing school despite previous ADHD diagnosis.
Mateo is "explosive" at home and school. Elena discloses her own childhood trauma
(domestic violence, parental substance use) and wonders if "this runs in families." She
takes sertraline 100mg for anxiety with partial benefit.
Question 1
Elena describes lifelong difficulties with organization, emotional intensity, and rejection
sensitivity that have persisted despite her anxiety treatment. She scores 18/24 on the
Adult ADHD Self-Report Scale (ASRS-v1.1). Her PHQ-9 is 8 (mild depression). Which
diagnostic formulation best captures her presentation?
A. Generalized Anxiety Disorder with executive dysfunction secondary to chronic stress
B. ADHD, Combined Presentation, with comorbid generalized anxiety and complex
trauma features
C. Complex PTSD with dissociative features masquerading as ADHD
,D. Borderline Personality Disorder with attentional deficits as part of emotional
dysregulation
Correct Answer: B
Rationale: Elena's presentation demonstrates classic ADHD features persisting from
childhood (lifelong difficulties), significant functional impairment, and the hallmark
emotional dysregulation and rejection sensitivity often missed in adult ADHD
assessments. While she has trauma history (CPTSD consideration) and anxiety, the
primary attentional deficits predate her anxiety disorder and represent a distinct
neurodevelopmental condition. The ASRS score of 18/24 is highly suggestive of ADHD.
Option A is incorrect because executive dysfunction in pure anxiety tends to be
state-dependent and improves with anxiety treatment—Elena's persists. Option C is
tempting given her trauma history, but CPTSD typically shows symptom fluctuation with
trauma triggers rather than consistent executive dysfunction. Option D is incorrect
because while emotional dysregulation overlaps, BPD requires pervasive interpersonal
instability and identity disturbance not described here. The biopsychosocial model
supports a primary ADHD diagnosis with secondary anxiety and trauma-related features
requiring integrated treatment addressing all domains.
Question 2
You decide to initiate pharmacotherapy for Elena's ADHD. Her pharmacogenomic
testing shows: CYP2D6 *1/*4 (intermediate metabolizer), CYP2C19 *1/*17 (ultrarapid
metabolizer), and she carries the ADRA2A C-1291G polymorphism associated with
increased alpha-2A receptor sensitivity. Given her current sertraline 100mg and anxiety
disorder, which medication strategy is most appropriate?
,A. Lisdexamfetamine 30mg daily, discontinuing sertraline due to potential serotonin
syndrome risk
B. Atomoxetine 80mg daily, monitoring for increased norepinephrine effects given her
ADRA2A variant
C. Methylphenidate extended-release 18mg daily, continuing sertraline with monitoring
D. Guanfacine extended-release 2mg daily as monotherapy given her ADRA2A
polymorphism
Correct Answer: C
Rationale: Methylphenidate represents the optimal choice given Elena's profile. As a
CYP2D6 intermediate metabolizer, she processes medications dependent on this
pathway more slowly, but methylphenidate is primarily metabolized via plasma
esterases with minimal CYP involvement, making it metabolically "clean." The sertraline
combination is safe—stimulants and SSRIs have extensive co-prescribing data with rare
serotonin syndrome risk (unlike MAOIs or tramadol). Option A is incorrect:
lisdexamfetamine would be effective but discontinuing sertraline is unnecessary and
potentially destabilizing for her anxiety. Option B is problematic: atomoxetine is a potent
CYP2D6 substrate, and as an intermediate metabolizer, she would have significantly
increased exposure (2-3x AUC). Additionally, her ADRA2A polymorphism suggests
enhanced norepinephrine sensitivity, making atomoxetine's pure noradrenergic
mechanism potentially poorly tolerated (anxiety, insomnia, hypertension). Option D
underestimates her ADHD severity—alpha-2 agonists are adjunctive or for mild cases;
her ASRS score and functional impairment warrant first-line stimulant treatment.
Question 3
, Elena tolerates methylphenidate ER 18mg well initially, but at week 4 reports improved
focus but persistent emotional dysregulation, especially premenstrually. She describes
"rage outbursts" and feeling "out of control" during the luteal phase. Her blood pressure
is 128/82. Which intervention best addresses her residual symptoms?
A. Increase methylphenidate to 36mg daily with luteal phase dosing increase to 54mg
B. Add guanfacine ER 2mg daily to address emotional dysregulation and premenstrual
symptomatology
C. Switch to mixed amphetamine salts XR 20mg daily for better emotional symptom
coverage
D. Add oral contraceptive with drospirenone to stabilize hormonal fluctuations
Correct Answer: B
Rationale: Guanfacine ER augmentation targets Elena's specific residual symptom
cluster through multiple mechanisms. As an alpha-2A agonist, it enhances prefrontal
cortical regulation of emotional responses and reduces sympathetic reactivity—directly
addressing her "rage outbursts." Research supports guanfacine for ADHD-related
emotional dysregulation and premenstrual exacerbation of ADHD symptoms. Her mildly
elevated BP (128/82) is manageable and may actually improve with guanfacine's
antihypertensive effects. Option A is incorrect: increasing methylphenidate may worsen
emotional lability and cardiovascular parameters without specifically targeting affective
symptoms. Option C is incorrect: while amphetamines have some mood effects,
switching class without addressing the specific emotional dysregulation mechanism is
less targeted than augmentation. Option D addresses hormonal fluctuations but ignores
the neurobiological basis of her emotional dysregulation (prefrontal-limbic
dysconnectivity) and introduces potential mood side effects; hormonal interventions
PMHNP Care Across the Lifespan | Complex & Evolving Case Studies|
Actual Questions & Verified Solutions | Advanced Psychiatric-Mental
Health Nurse Practitioner | Pass Guarantee
CASE BLOCK 1: The Martinez Family - Intergenerational Trauma and
Complex ADHD
Case Background: The Martinez family presents to your integrated behavioral health
clinic. Elena Martinez, 38, brings her two children: Sofia (16) and Mateo (9). Elena
reports her own lifelong struggles with "scattered thinking" and emotional dysregulation.
Sofia has been cutting herself and failing school despite previous ADHD diagnosis.
Mateo is "explosive" at home and school. Elena discloses her own childhood trauma
(domestic violence, parental substance use) and wonders if "this runs in families." She
takes sertraline 100mg for anxiety with partial benefit.
Question 1
Elena describes lifelong difficulties with organization, emotional intensity, and rejection
sensitivity that have persisted despite her anxiety treatment. She scores 18/24 on the
Adult ADHD Self-Report Scale (ASRS-v1.1). Her PHQ-9 is 8 (mild depression). Which
diagnostic formulation best captures her presentation?
A. Generalized Anxiety Disorder with executive dysfunction secondary to chronic stress
B. ADHD, Combined Presentation, with comorbid generalized anxiety and complex
trauma features
C. Complex PTSD with dissociative features masquerading as ADHD
,D. Borderline Personality Disorder with attentional deficits as part of emotional
dysregulation
Correct Answer: B
Rationale: Elena's presentation demonstrates classic ADHD features persisting from
childhood (lifelong difficulties), significant functional impairment, and the hallmark
emotional dysregulation and rejection sensitivity often missed in adult ADHD
assessments. While she has trauma history (CPTSD consideration) and anxiety, the
primary attentional deficits predate her anxiety disorder and represent a distinct
neurodevelopmental condition. The ASRS score of 18/24 is highly suggestive of ADHD.
Option A is incorrect because executive dysfunction in pure anxiety tends to be
state-dependent and improves with anxiety treatment—Elena's persists. Option C is
tempting given her trauma history, but CPTSD typically shows symptom fluctuation with
trauma triggers rather than consistent executive dysfunction. Option D is incorrect
because while emotional dysregulation overlaps, BPD requires pervasive interpersonal
instability and identity disturbance not described here. The biopsychosocial model
supports a primary ADHD diagnosis with secondary anxiety and trauma-related features
requiring integrated treatment addressing all domains.
Question 2
You decide to initiate pharmacotherapy for Elena's ADHD. Her pharmacogenomic
testing shows: CYP2D6 *1/*4 (intermediate metabolizer), CYP2C19 *1/*17 (ultrarapid
metabolizer), and she carries the ADRA2A C-1291G polymorphism associated with
increased alpha-2A receptor sensitivity. Given her current sertraline 100mg and anxiety
disorder, which medication strategy is most appropriate?
,A. Lisdexamfetamine 30mg daily, discontinuing sertraline due to potential serotonin
syndrome risk
B. Atomoxetine 80mg daily, monitoring for increased norepinephrine effects given her
ADRA2A variant
C. Methylphenidate extended-release 18mg daily, continuing sertraline with monitoring
D. Guanfacine extended-release 2mg daily as monotherapy given her ADRA2A
polymorphism
Correct Answer: C
Rationale: Methylphenidate represents the optimal choice given Elena's profile. As a
CYP2D6 intermediate metabolizer, she processes medications dependent on this
pathway more slowly, but methylphenidate is primarily metabolized via plasma
esterases with minimal CYP involvement, making it metabolically "clean." The sertraline
combination is safe—stimulants and SSRIs have extensive co-prescribing data with rare
serotonin syndrome risk (unlike MAOIs or tramadol). Option A is incorrect:
lisdexamfetamine would be effective but discontinuing sertraline is unnecessary and
potentially destabilizing for her anxiety. Option B is problematic: atomoxetine is a potent
CYP2D6 substrate, and as an intermediate metabolizer, she would have significantly
increased exposure (2-3x AUC). Additionally, her ADRA2A polymorphism suggests
enhanced norepinephrine sensitivity, making atomoxetine's pure noradrenergic
mechanism potentially poorly tolerated (anxiety, insomnia, hypertension). Option D
underestimates her ADHD severity—alpha-2 agonists are adjunctive or for mild cases;
her ASRS score and functional impairment warrant first-line stimulant treatment.
Question 3
, Elena tolerates methylphenidate ER 18mg well initially, but at week 4 reports improved
focus but persistent emotional dysregulation, especially premenstrually. She describes
"rage outbursts" and feeling "out of control" during the luteal phase. Her blood pressure
is 128/82. Which intervention best addresses her residual symptoms?
A. Increase methylphenidate to 36mg daily with luteal phase dosing increase to 54mg
B. Add guanfacine ER 2mg daily to address emotional dysregulation and premenstrual
symptomatology
C. Switch to mixed amphetamine salts XR 20mg daily for better emotional symptom
coverage
D. Add oral contraceptive with drospirenone to stabilize hormonal fluctuations
Correct Answer: B
Rationale: Guanfacine ER augmentation targets Elena's specific residual symptom
cluster through multiple mechanisms. As an alpha-2A agonist, it enhances prefrontal
cortical regulation of emotional responses and reduces sympathetic reactivity—directly
addressing her "rage outbursts." Research supports guanfacine for ADHD-related
emotional dysregulation and premenstrual exacerbation of ADHD symptoms. Her mildly
elevated BP (128/82) is manageable and may actually improve with guanfacine's
antihypertensive effects. Option A is incorrect: increasing methylphenidate may worsen
emotional lability and cardiovascular parameters without specifically targeting affective
symptoms. Option C is incorrect: while amphetamines have some mood effects,
switching class without addressing the specific emotional dysregulation mechanism is
less targeted than augmentation. Option D addresses hormonal fluctuations but ignores
the neurobiological basis of her emotional dysregulation (prefrontal-limbic
dysconnectivity) and introduces potential mood side effects; hormonal interventions
