 Question 1

Needs Grading
A 52-year-old obese Caucasian male presents to the clinic with a 2-day history of fever, chills,
and right great toe pain that has gotten worse. Patient states this is the first time that this
has happened, and nothing has made it better and walking on his right foot makes it worse. He
has tried acetaminophen, but it did not help. He took several ibuprofen tablets last night which did
give him a bit of relief. Past medical history positive or hypertension treated with
hydrochlorothiazide and kidney stones. Social history negative for tobacco use but admits to drinking
“a fair amount of red wine” every week. General appearance: Ill appearing male who sits
with his right foot elevated. Physical exam remarkable for a temp of 101.2, pulse 108, respirations 18
and BP 160/88. Right great toe (first metatarsal phalangeal [MTP]) noticeably swollen and red.
Unable to palpate to assess range of motion due to extreme pain. CBC and Complete metabolic profile
revealed WBC 14,000 mm3 and uric acid 8.9 mg/dl. The APRN diagnoses the patient with acute gout.

Question 1 of 2:

Describe the pathophysiology of gout.

Correct
Answer:  
Gout is an inflammatory response to excessive quantities of uric acid in the blood and
other body fluids including synovial fluid. The elevated level of uric acid lea to the
formation of monosodium urate crystals in and around joints. When the uric acid levels
exceed approximately 6.8 mg/dl, it crystalizes and forms an insoluble precipitate that are
deposited into connective tissue through the body. When crystallization occurs in
synovial fluid, it triggers Tumor Necrosis Factor (TNF)-α, which causes the release of
inflammatory cytokines and interleukins. The result is an acute inflammatory response
within the joint.
Gout is caused by a defect in purine metabolism and kidney function. Uric acid is a
byproduct of purine nucleotides. People with gout may have an elevated level of purine
synthesis accompanied by a rise in uric acid level.

 Question 2
Needs Grading
A 52-year-old obese Caucasian male presents to the clinic with a 2-day history of fever, chills,
and right great toe pain that has gotten worse. Patient states this is the first time that this
has happened, and nothing has made it better and walking on his right foot makes it worse. He
has tried acetaminophen, but it did not help. He took several ibuprofen tablets last night which did
give him a bit of relief. Past medical history positive or hypertension treated with
hydrochlorothiazide and kidney stones. Social history negative for tobacco use but admits to drinking
“a fair amount of red wine” every week. General appearance: Ill appearing male who sits
with his right foot elevated. Physical exam remarkable for a temp of 101.2, pulse 108, respirations 18
and BP 160/88. Right great toe (first metatarsal phalangeal [MTP]) noticeably swollen and red.
Unable to palpate to assess range of motion due to extreme pain. CBC and Complete metabolic profile
revealed WBC 14,000 mm3 and uric acid 8.9 mg/dl. The APRN diagnoses the patient with acute gout.
Question 2 of 2:

Explain why a patient with gout is more likely to develop renal calculi. 
 Correct
Answer:  
Most uric acid is eliminated from the body through the kidneys. Urate is filtered at the
glomerulus and undergoes reabsorption and excretion within the proximal renal tubules.
In primary gout, urate excretion by the kidneys is sluggish. This may be caused by a
decrease in glomerular filtration of urate or acceleration in urate reabsorption. This
allows for urate crystals to be deposited in the renal tubules.

 Question 3
Needs Grading
Stan is a 45-year-old man who presents to the clinic complaining of intermittent fevers, joint pain,
myalgias, and generalized fatigue. He noticed a rash several days ago that seemed to appear and
disappear on different parts of his abdomen. He noticed the lesion below this morning and decided to
come in for evaluation. He denies recent international travel and the only difference in his usual
routine was clearing some underbrush from his back yard about a week ago. Past medical history non-
contributory with exception of severe allergy to penicillin resulting in hives and difficulty breathing.
Physical exam: Temp 101.1 ˚F, BP 128/72, pulse 102 and regular, respirations 18. Skin
inspection revealed a 4-inch diameter bull’s eye type red rash over the left flank area. The APRN,
based on history and physical exam, diagnoses the patient with Lyme Disease. She ordered
appropriate labs to confirm diagnosis but felt it urgent to begin antibiotic therapy to
prevent secondary complications.  

Question:

What is Lyme disease and what patient factors may have increased his risk developing Lyme
disease? 

Correct
Answer:  
Lyme disease is a multisystem inflammatory disease caused by a spirochete that is
transmitted by Ixodes tick bites. It is the most frequently reported vector-born illness in
the United States. The microorganism is difficult to culture, escapes immune defenses
through antigenic variation, blocks complement mediated killing, impedes release of
antimicrobial peptides, leukocyte chemotaxis, and antimicrobial killing. It hides in tissue
and is spread to other tissues by entering the capillary beds.
The disease is characterized by flu-like symptoms in the early stages and many patients
present with the classic “target or bull’s eye” lesion on the skin. If not treated early, there
is disseminated infection with secondary rash with myalgias, arthralgias, fever and
malaise. If left untreated, patients develop post Lyme disease syndrome or chronic Lyme
disease which can cause carditis, encephalitis, arthritis, polyneuropathy, and heart failure.
Stan was likely bitten by an infected tick when he was clearing brush from his property.

 Question 4
Needs Grading
A 72-year-old female was walking her dog when the dog suddenly tried to chase a squirrel and pulled
the woman down. She tried to break her fall by putting her hand out and she landed on her
outstretched hand. She immediately felt severe pain in her right wrist and noticed her wrist looked
deformed. Her neighbor saw the fall and brought the woman to the local Urgent Care Center for
 evaluation. Radiographs revealed a Colles' fracture (distal radius with dorsal displacement of
fragments) as well as radiographic evidence of osteoporosis. A closed reduction of the
fracture was successful, and she was placed in a posterior splint with ace bandage wrap and instructed
to see an orthopedist for follow up.  

Question:

What is osteoporosis and how does it develop? 

Correct
Answer:  
Osteoporosis is considered a metabolic bone disease. Osteoporosis, also called porous
bone, is the most common bone disease in humans. Its main features include low bone
mineral density, impaired structural integrity of bone, decreased bone strength and
increased risk of fractures. The two types of osteoporosis are primary and secondary.
Primary osteoporosis, the most common is hormone mediated where bone loss is
accelerated by declining levels of estrogen in women and testosterone in men. Secondary
osteoporosis is caused by other conditions including endocrine disorders
(hyperparathyroidism, hyperthyroidism, diabetes mellitus) and certain medications such
as heparin, corticosteroids, phenytoin, barbiturates, and lithium) as well as tobacco and
alcohol.
There are three major bone cells that are involved in the formation, maintenance, and
reabsorption of bone. Osteoblasts are immature bone cells that under ideal circumstances
allow bone to formed and laid down. Osteocytes are cells that are responsible for the
normal maintenance, or the cycle, of bone. Osteocytes removed old bone cells which
allows the osteoblasts to form new bone. Osteoclasts are responsible for reabsorption of
bone.
Hormonal influences remain important in maintaining bone health, but new research has
demonstrated that genetic factors and the role of oxidative stress also contributes to the
development of osteoporosis. Reactive oxygen species (ROS) serve as signaling
molecules for osteoblasts, osteocytes, and osteoclasts. An imbalance between osteoblast
formation and osteoclast reabsorption is the primary cause of osteoporosis.

 Question 5
Needs Grading
A 42-year-old woman presents to the clinic with a four-
month history of generalized joint pain, stiffness, and swelling, especially in her hands. She
states that these symptoms have made it difficult to grasp objects and has made caring for her 6 and 4-
year-old children problematic. She admits to increased fatigue, but she thought it was due to her
stressful job as well as being a single mother. No significant past medical history but recalls that one
of her grandmothers had “crippling” arthritis. Physical exam remarkable for bilateral ulnar
deviation of her hands as well as soft, boggy proximal interphalangeal joints. The metatarsals of both
of her feet also exhibited swelling and warmth. The diagnosis for this patient is rheumatoid arthritis.

Question:

Explain why patients with rheumatoid arthritis exhibit these symptoms and how does it differ from
osteoarthritis? 
 Correct
Answer:  
Rheumatoid arthritis is an inflammatory, systemic disease that is autoimmune in nature.
Symptoms are mediated by antibodies against self-antigens and inflammatory cytokines,
especially CD4+ T cells that promote inflammation. Multiple inflammatory cells are
involved, and TNF and Interleukin-1 stimulate the synovial cells to secrete protease that
damages the hyaline cartilage. The inflammatory cytokines convert the synovium into an
abnormally thick layer of granulation tissue called pannus. The pannus acts like a locally
invasive tumor. Pannus is the tissue responsible for destruction of the articular cartilage.
The other inflammatory mediators affect the soft tissue structures like the tendons,
ligaments, and even the valves of the heart, especially the aortic valve. Long standing
inflammation causes interstitial fibrosis of the lungs which reduces pulmonary function.
Osteoarthritis (OA) is localized destruction of articular cartilage which can either be
idiopathic or secondary. Secondary OA is due to a prior injury or infectious process that
may affect the normal cartilage. Primary OA is very common in people >65 years of age
and there is a strong correlation between obesity and the development of OA. OA in a
non-inflammatory disease process.

 Question 6
Needs Grading
A 32-year-old Caucasian male presents to the office with complaints of back pain, stiffness, especially
in the morning, interrupted sleep due to pain, and difficulty in leaning over to tie his shoes. The
patient first noticed these symptoms about 6 months ago but attributed them
to his weekend basketball team’s games. He said he is exhausted due to sleep interruption. He has
taken acetaminophen with some relief but says the naproxen seems to be working better. Married with
2 small children and works as a bank manager. Physical exam: Lungs clear but decreased chest
excursion noted as well as decreased range of motion of hips and forward flexion, rotation, and lateral
flexion restricted. Spine radiographs in the office revealed a slight kyphosis along with ankylosis
at L5-S1. The APRN suspects the patient may have ankylosing spondylitis (AS). The APRN orders
laboratory tests including an HLA-B27. 

Question:

Why did the APRN order an HLA-B27 lab? How would that lab result assist in understanding what

ankylosing spondylitis?  

Correct
Answer:  
AS is a chronic inflammatory disease of the axial skeleton. The usual age of onset is
approximately 25-34 years of age and affects men 5 times > women. There is synovial
inflammation with fibroblast response which results in dense fibrous scars. The etiology
is unknown but the link to HLA-B27 has been known for years. A misfolding of the
HLA-B27 occurs in the endoplasmic reticulum (ER) where they continue to accumulate.
There is a stress response in the ER which causes an increased production of
interleukins. Increased inflammation occurs.
There is significant pleuritic chest pain with decreases chest excursion. Inflammation of
the intercostal tendons eventually leads to scar tissue formation which effects pulmonary
function.
 Question 7
Needs Grading
A 17-year-old male presents to the clinic with a chief complaint of pain in his right elbow. He says the
pain is sharp, especially with pronation and supination.  He noticed the pain several weeks ago after
his tennis team went to a regional competition. When he rests, the pain seems to go away. The pain is
alleviated when he takes Naprosyn. No history of trauma or infection in the elbow. Past
medical and social history non contributary. He is a junior at the local high school and just
started taking tennis lessons 2 months ago and his coach is working with him on his backhand serve.
Focused physical exam revealed point tenderness over the lateral epicondyle which increases with
pronation and supination. The APRN diagnoses him with lateral epicondylitis and orders a wrist splint
to prevent wrist flexion.  

Question:

Why did the APRN feel a wrist splint would be helpful? What patient characteristics lead to this
diagnosis.  

Correct
Answer:  
Lateral epicondylitis, also called tennis elbow, is an inflammation or irritation of the
elbow tendon (carpi radialis brevis) which leads to swelling of the tendon and tendon 
sheath. This limits movement and causes pain. There may be microtears which cause
bleeding and increased swelling. A wrist splint, usually called a cock-up splint, is helpful
in preventing wrist flexion that causes increased stressors along the tendon, elbow, and
forearm. Lateral epicondylitis is often caused by repetitive back hand strokes such as
seen in tennis players.

 Question 8
Needs Grading
A 24-year-old Caucasian male was brought to the Emergency Room (ER) by Emergency Medical
System (EMS) after suffering a “convulsion” episode at work that didn’t stop. Upon arrival to the ER,
the patient was noted to be actively seizing with tonic-clonic movements. The patient’s boss
accompanied him to the ER and gave a statement that the patient appeared in his usual good health
earlier in the morning when they started working at their jobs in an auto parts store. The boss didn’t
know of any past medical history. The boss brought along the patients next of kin information, and the
patients mother told the ER that the patient has a prior history of seizures but hadn’t had a seizure in
several years. The family thought he had “outgrown them.” Past medical history, other than previous
seizures, and social history non-contributory. No history of alcohol or drug abuse and had no history
of vaping. The ER APRN diagnoses the patient with status epilepticus and along with the ER staff,
initiated appropriate treatment.

Question:

What is a seizure and why is status epilepticus so dangerous for patients?  

 Correct
Answer:  
Seizures are sudden, transient disruptions in brain electrical function caused by an
abnormal excessive discharge of cortical neurons. There are many causes of seizures that
are not related to epilepsy such as metabolic disorders, congenital malformations, genetic
predisposition, perinatal injury, trauma, infections, drug or alcohol use or intracranial
lesions. In true epilepsy, there is an interaction between genetic mutations with
environmental effects that cause abnormalities in synaptic transmission, an imbalance in
the brain’s neurotransmitters, or abnormal nerve connections or loss of nerves after
trauma. Some neurons may exhibit a paroxysmal depolarization shift and function as an
elipeptogenic focus. These hyperexcitable neurons are easily activated by hyperthermia,
hypoxia, hypoglycemia, hyponatremia, repeated sensory stimulation and certain sleep
phases. When the intensity reaches a certain threshold, the cortical excitation spreads.
This starts the excitation of other areas of the brain and correspond to the tonic phase.
The clonic phase begins when inhibitory neurons in various parts of the brain react to the
cortical excitation. The seizure discharge is interrupted, and the seizure stops. 
Status epilepticus is a potentially fatal type of seizure that is usually caused by sudden
interruption of anti-seizure medications but can also occur in untreated or inadequately
treated persons with seizure disorders. The clinical effects of hypoxia, due to the
hypermetabolic state of the seizure, can cause intellectual disability, dementia, and places
the patient at a high risk for aspiration.

 Question 9
Needs Grading
A 32-year-old while female presents to the Urgent Care with complaints of blurry vision and “fuzzy
thinking” which has been present for the last several weeks or so. She works as an executive for an
insurance company and put her symptoms down to the stress of preparing the quarterly report. Today,
she noticed that her symptoms were worse and were accompanied by some fine tremors in her hands.
She has been having difficulty concentrating and has difficulty voiding. She remembers her eyes were
bothering her a few months ago and she went to the optometrist who recommended reading glasses
with small prism to correct double vision. She admits to some weakness as well. No other complaints
of fevers, chills, upper respiratory tract infections, or urinary tract infections. Past medical and social
history noncontributory. Physical exam significant for 4th cranial nerve palsy. The fundoscopic exam
reveals edema of right optic nerve causing optic neuritis. Positive nystagmus on positional
maneuvers. There are left visual field deficits. There was short term memory loss with listing of
familiar objects. The APRN tells the patient that she will be referred to a neurologist due to the high
index of suspicion for multiple sclerosis (MS).  

Question:

What is multiple sclerosis and how did it cause the above patient’s symptoms? 

Correct
Answer:  
MS is a chronic inflammatory disease involving degeneration of CNS myelin, scarring
(or sclerosis or plaque formation) and loss of axons. It is caused by an autoimmune
response to self or microbial antigens in genetically susceptible people. The usual age of
onset is between 20 and 40 years of age and is more common in women.
When reviewing the demyelinating lesions in the spinal cord and brain of patients with
MS shows myelin loss, destruction of oligodendrocytes, and reactive astrogliosis, often
 with relative sparing of the axon cylinder. In some MS patients, however, the axon is
also aggressively destroyed. One of the earliest steps in lesion formation is the
breakdown of the blood-brain barrier. Enhanced expression of adhesion molecules on the
surface of lymphocytes and macrophages seems to underlie the ability of these
inflammatory cells to penetrate the blood-brain barrier. The elevated immunoglobulin G
(IgG) level in the cerebrospinal fluid, which can be shown by an oligoclonal band pattern
on electrophoresis, suggests an important humoral (i.e., B-cell activation) component to 
MS. Variable degrees of antibody-producing plasma cell infiltration have been
demonstrated in MS lesions. The patient’s symptoms are directly related to the
inflammation and demyelination of the nerve sheath. The short- term memory loss
indicates that there may be demyelinating lesions in the brain as well.

 Question 10
Needs Grading
61-year-old male complains of intermittent weakness and muscle fatigue that has progressively
worsened over the past month. He was an internationally known extreme mountain climber but now
he says he has difficulty in getting his morning paper. Initially he thought his symptoms of profound
leg weakness and fatigue were due to his age and history of injuries from mountain climbing. Over the
past few months, he also reports having noticed “blurriness” when working on his antique train
collection or reading for long periods of time. He has developed intermittent double vision that seems
to be worse when reading at bedtime. He also reports an occasional “droopy” eye lid. Past medical
and social history noncontributory. Physical exam reveals weakness of right extra ocular muscle
(EOM) with repetition. There is positive nystagmus and symmetrical upper extremity weakness
with fasciculations. Lower extremities within normal limits (WNL).   The APRN suspects the patient
has myasthenia gravis (MG).  

Question:

What is the underlying pathophysiology of MG?  

Correct
Answer:  
MG is an autoimmune disease of the neuromuscular junction and is mediated by
acetylcholine receptor (AChR) antibodies. It is often associated with other autoimmune
diseases. There is a defect in nerve impulse transmission as the neuromuscular junction.
IgG antibodies attack AChR. Antibody-antigen complex and inflammation inhibit
neuromuscular transmissions. There is a breakdown of immune tolerance that involves
the thymus. It affects 20,000 to 70,000 Americans. Women have MG more than men
before age 50. Peak onset 20-40 years of age. Men are more commonly diagnosed at the
ages of 60-80. There is painless, striated muscle weakness that worsens with activity and
improves with rest. Exacerbating factors include emotional stress, rapid changes in body
temperature, infection, trauma, and multiple medications. Ocular manifestations such as
diplopia and ptosis are common. Upper extremity weakness is more common than lower
extremity weakness.

 Question 11
Needs Grading
A 67-year-old male presents to the clinic along with his family with a chief complaint of having
problems with his short-term memory. His family had dismissed these problems and
attributed them to the aging process. Over time they have noticed changes in his behavior, along with
increased confusion and difficulty completing basic tasks. He got lost driving home from the bowling
 alley and had to be brought home by the police department. He is worried that he may have
Alzheimer’s Disease (AD). Past medical and social history positive for a minor cerebral vascular
accident when he was 50 years old but without any residual motor or sensory defects. No history of
alcohol or tobacco use. Current medication is clopidogrel 75 mg po qd.  Neurological testing confirms
the diagnosis of AD. 

Question:

What is Alzheimer’s Disease and how does amyloid beta factor into the development and progression
of the disease? 

Correct
Answer:  
AD, also called Dementia of Alzheimer’s Disease type (DAT) senile disease complex is
the leading cause of cognitive dysfunction in older adults. There are 3 recognized types:
late onset, early onset familial AD, and early onset. Other risk factors include age and
family history, along with diabetes, midlife hypertension, hyperlipidemia, midlife
obesity, smoking, depression, cognitive inactivity, female gender and lack of estrogen,
and head trauma. The major genetic risk factor is related to apolipoprotein E which
interferes with amyloid beta clearance from the brain. Pathologic alterations in the brain
include collection of neuritic plaques containing a core of abnormally folded amyloid
beta and tau proteins that eventually cause lack of acetylcholine. This accumulation of
abnormal proteins cause disruption of nerve impulses. Amyloid also is deposited in the
smooth muscle of cerebral arteries, causing an amyloid angiopathy and disturbances in
cerebral blood flow. Loss of synapses, acetylcholine, and other neurotransmitters
contribute to the decline of memory and attention and the loss of other cognitive
functions associated with AD.

 Question 12
Needs Grading
A 22-year-old male was an unrestrained front seat passenger of a car traveling at 50 miles per hour.
The driver swerved to avoid hitting a deer that darted in front of the car and hit a tree. The
patient was ejected from the vehicle. He was awake and alert at the scene when the paramedics
arrived, and his pupils were equal and reactive to light. He was placed in a hard-cervical collar per
protocol and log rolled onto a long backboard. He was breathing spontaneously at the scene, but pulse
oximetry in the EMS unit revealed a SaO2 of 88% on room air. He was placed on 100% oxygen via
non-rebreather mask and was taken to a Level I trauma center with the following vital signs: 

Vital signs: BP 90/50, Pulse 48 and regular, Respirations 24 and shallow with some use of accessory
muscles, temp 95.2 F rectally. He was awake and answering questions appropriately but says he
cannot feel his arms or legs. Glasgow Coma Scale 14. His skin was warm and dry with minor
abrasions noted on his arms. According to family members, past medical history noncontributory and
social history reveals only occasional alcohol use and no tobacco or vaping history. Full work up in
the ED revealed a fracture-dislocation
of C4 with assumed complete tetraplegia (formerly called quadriplegia). No other injuries noted He
was given several liters of IV fluid, but his blood pressure remained low.  

Question 1 of 2:
 Explain the differences between primary and secondary spinal cord injury (SCI)? 

Correct
Answer:  
Primary SCIs occur with the initial mechanical trauma and immediate tissue destruction
from shearing, compression, or penetration. These injuries can also occur as a result of
inadequate immobilization immediately following an injury. SCIs can occur without
spinal column fractures due to longitudinal stretching of the cord. The stretching causes
altered axon transport, edema, myelin degeneration and Wallerian degeneration.
Secondary spinal cord injury results from microscopic hemorrhages into the central gray
matter and pia-arachnoid, increasing in size until the entire gray matter is hemorrhagic
and necrotic. Edema in the white matter occurs, impairing the microcirculation of the
cord. Hemorrhages and edema are followed by loss of autoregulation and reduced
vascular perfusion and development of ischemic areas which are maximal at the injury as
well as 2 levels above and below the injury. This is critically important, especially in the
cervical region, where swelling of the cord could compromise innervation to the phrenic
nerve exits between C3 and C5. Cardiorespiratory functions mediated by the medulla
oblongata may be lost.

 Question 13
Needs Grading
A 22-year-old male was an unrestrained front seat passenger of a car traveling at 50 miles per hour.
The driver swerved to avoid hitting a deer that darted in front of the car and hit a tree. The
patient was ejected from the vehicle. He was awake and alert at the scene when the paramedics
arrived, and his pupils were equal and reactive to light. He was placed in a hard-cervical collar per
protocol and log rolled onto a long backboard. He was breathing spontaneously at the scene, but pulse
oximetry in the EMS unit revealed a SaO2 of 88% on room air. He was placed on 100% oxygen via
non-rebreather mask and was taken to a Level I trauma center with the following vital signs: 

Vital signs: BP 90/50, Pulse 48 and regular, Respirations 24 and shallow with some use of accessory
muscles, temp 95.2 F rectally. He was awake and answering questions appropriately but says he
cannot feel his arms or legs. Glasgow Coma Scale 14. His skin was warm and dry with minor
abrasions noted on his arms. According to family members, past medical history noncontributory and
social history reveals only occasional alcohol use and no tobacco or vaping history. Full work up in
the ED revealed a fracture-dislocation
of C4 with assumed complete tetraplegia (formerly called quadriplegia). No other injuries noted He
was given several liters of IV fluid, but his blood pressure remained low.  

Question 2 of 2:

What is spinal shock and how it is different from neurogenic shock? 

Correct
Answer:  
 Spinal shock develops immediately with a spinal cord injury involving the lower thoracic
cord and must be considered hemorrhagic until proven otherwise. Spinal shock is defined
as the complete loss of all neurologic function, including reflexes and rectal tone, below
a specific level that is associated with autonomic dysfunction. Spinal shock is a state of
transient physiologic (rather than anatomic) reflex depression of cord function below the
level of injury, with associated loss of all sensorimotor functions.
An initial increase in blood pressure due to the release of catecholamines, followed by
hypotension, is noted. Flaccid paralysis, including of the bowel and bladder, is observed.
These symptoms tend to last several hours to days until the reflex arcs below the level of
the injury begin to function again where there is a return of the bulbocavernosus reflex
and muscle stretch reflex.
Neurogenic shock refers to the hemodynamic triad of hypotension, bradycardia, and
peripheral vasodilation resulting from severe autonomic dysfunction and the interruption
of sympathetic nervous system control in acute spinal cord injury. Hypothermia is also
characteristic. This condition does not usually occur with spinal cord injury below the
level of T6 but is more common in injuries above T6, secondary to the disruption of the
sympathetic outflow from T1-L2 and to unopposed vagal tone, leading to a decrease in
vascular resistance, with the associated vascular dilatation. Neurogenic shock needs to be
differentiated from spinal and hypovolemic shock. Hypovolemic shock tends to be
associated with tachycardia.

 Question 14
Needs Grading
A 22-year-old male was an unrestrained front seat passenger of a car traveling at 50 miles per hour.
The driver swerved to avoid hitting a deer that darted in front of the car and hit a tree. EMS on the
scene noted a stellate fracture of the windshield on the passenger side. The patient was non-
responsive at the at the scene when the paramedics arrived, and his pupils were unequal with the left
pupil larger and sluggish to react to light. He was placed in a hard-cervical collar per protocol and log
rolled onto a long backboard. He was breathing spontaneously at the scene, but pulse oximetry in the
EMS unit revealed a SaO2 of 78% on room air. He was intubated at the scene for airway protection
and transported to a Level 1 trauma center. Glasgow Coma Scale=3 

After a full trauma work up, the patient was diagnosed with an isolated traumatic brain injury with
acute subdural hematoma secondary to coup-contrecoup mechanism of injury. He was emergently
taken to the operating room for craniotomy after which he was taken to the Intensive Care Unit (ICU)
for close monitoring. He had an intracranial bolt for measurements of his intracranial pressure (ICP).
Question 1 of 2:

Explain the differences between primary and secondary traumatic brain injuries (TBIs)? 

Correct
Answer:  
The primary injury usually causes structural changes, such as epidural hematoma,
subdural hematoma, subarachnoid hemorrhage, intraventricular hemorrhage, or cerebral
contusion.
A diffuse injury results from an acceleration/deceleration mechanism often accompanied
by rotational component. This is often seen in patients who have coup-contrecoup
injuries. The coup injury is a result of direct contact of the head with an object (like a
windshield) and the contrecoup injury is a result of the brain rebounding and hitting the
opposite side of the skull. This causes widespread edema of the brain tissue which can
lead to diffuse axonal injury.
 A secondary injury results from hypotension, hypoxia, acidosis, edema, or other
subsequent factors that can secondarily damage brain tissue (see Secondary injuries).
Free radicals are thought to contribute to these secondary insults, especially during
ischemia.

 Question 15
Needs Grading
A 22-year-old male was an unrestrained front seat passenger of a car traveling at 50 miles per hour.
The driver swerved to avoid hitting a deer that darted in front of the car and hit a tree. EMS on the
scene noted a stellate fracture of the windshield on the passenger side. The patient was non-
responsive at the at the scene when the paramedics arrived, and his pupils were unequal with the left
pupil larger and sluggish to react to light. He was placed in a hard-cervical collar per protocol and log
rolled onto a long backboard. He was breathing spontaneously at the scene, but pulse oximetry in the
EMS unit revealed a SaO2 of 78% on room air. He was intubated at the scene for airway protection
and transported to a Level 1 trauma center. Glasgow Coma Scale=3 

After a full trauma work up, the patient was diagnosed with an isolated traumatic brain injury with
acute subdural hematoma secondary to coup-contrecoup mechanism of injury. He was emergently
taken to the operating room for craniotomy after which he was taken to the Intensive Care Unit (ICU)
for close monitoring. He had an intracranial bolt for measurements of his intracranial pressure (ICP).
Question 2 of 2:

The APRN is called by the ICU staff because the patient’s ICP has risen to 22 mmHg. The APRN
recognizes the urgent need to lower the ICP. The APRN institutes measures to decrease the ICP and
increase the cerebral perfusion pressure (CPP). What are the factors that determine CPP?

Correct
Answer:  
Cerebral perfusion pressure (CPP) depends on the mean systemic arterial pressure
(MAP) and ICP, which is calculated by the following relationship: CPP = MAP – ICP
where MAP = (1/3 systolic BP) + (2/3 diastolic BP)
As a result, CPP can be reduced from an increase in ICP, a decrease in blood pressure, or
a combination of both factors. Through the normal regulatory process called pressure
autoregulation, the brain can maintain a normal cerebral blood flow (CBF) with a CPP
that ranges from 50-150 mm Hg. At CPP values less than 50 mm Hg, the brain may not
be able to compensate adequately, and CBF falls passively with CPP. 1700 cc is the
capacity of the normal adult skull – brain is 1400 cc, CSF 150 cc, blood 150 cc (75%
venous, 25% arterial). If there are it changes in one it will cause changes in all
intracranial contents.

 Question 16
Needs Grading
A 68-year-old man was brought to the emergency department by his family. During his routine
morning walk he noticed a sudden onset of left facial numbness associated with a dull headache on the
right posterior aspect of his head. He was staggering to the right side and feeling unsteady and
nauseated, with no vomiting. He telephoned his wife, who noticed his speech was slow and slurred,
but there was no word-finding difficulty. His family immediately took him to the hospital. There was
a history of hypertension, hypercholesterolemia, ischemic heart disease (MI and PCI with bare metal
stent in 2007) and probable transient ischemic attack (TIA) at the time of cardiac intervention. His
medication included atenolol, ramipril, simvastatin, aspirin and clopidogrel.
 Within one hour, the patient’s symptoms had totally resolved. The diagnosis of transient ischemic
attack was made, and the patient was discharged to home with instructions to contact his healthcare
provider (HCP) for follow-up.

Question:

Why did the patient’s symptoms totally resolve?

Correct
Answer:  
TIA is a sudden onset of transient focal neurological deficit, often lasting for only a few
minutes, although the definition is for all symptoms and signs to have completely
resolved within 24 hours. Patients will often present late and, therefore, the diagnosis
needs to be made on history rather than examination and investigation. Patients often
present with weakness, numbness, sudden confusion, loss of balance, loss of vision or
sudden severe headache resulting from focal cerebral ischemia.

 Question 17
Needs Grading
An 83-year-old man presents with a history of atrial fibrillation (AF), hypertension, and diabetes. His
daughter, who accompanied the patient, states that yesterday the patient had a period when he could
not speak or understand words, and that approximately 4 weeks prior he staggered against a wall and
was unable to stand unaided because of weakness in his legs. She states that both instances lasted
approximately a half-hour. She was unable to persuade her father to go to the emergency room either
time. Today he suffered another episode of right sided weakness, dysarthria, and difficulty with
speech. Past medical history: Hypertension for 15 years, well controlled; diabetes for the past 10
years, and hyperlipidemia. Medications: Diltiazem CD 300 mg daily; lisinopril 40 mg daily;
metformin 500 mg twice daily; aspirin 81 mg daily and atorvastatin 20 mg po qhs.  

Social history: reported former smoker with 40 pack year history. Alcohol -drinks one beer a day.
Denies any other substance abuse. Review of systems: Denies dyspnea, dizziness, or
syncope; complains that he cannot move or feel his right arm or leg. Difficulty with speech.  

Physical exam: Vitals: height = 70 inches; weight = 185 pounds; body mass index = 26.5; BP =
134/82 mm Hg; heart rate = 88 bpm at rest, irregularly irregular pattern.  

HEENT remarkable for expressive aphasia, eyes with contralateral homonymous hemianopsia. 

No loss of sensation but unable to voluntarily move right arm or leg. 

The patient was diagnosed with a right middle cerebral artery

 vascular accident (CVA) secondary to atrial fibrillation (AF)  

Question:

How does atrial fibrillation contribute to the development of a CVA? 

Correct
Answer:  
In AF, there is often pooling of blood in the left atria which leads to the development of a
thrombus that causes fragments of the embolic clot to enter the cerebral circulation and
lodge in a cerebral artery. The most common site of occlusion is in the middle cerebral
artery. That causes cerebral infarction as the area of the brain distal to the clot receives
no blood due to the vascular occlusion. Other risk factors for embolic strokes include left
ventricular aneurysm, left atrial thrombus, recent myocardial infarction (MI), rheumatic
valvular disease, mechanical prosthetic valve, and patent foramen ovale. When a patient
has AF, a piece of the atrial thrombus breaks off, becomes and embolus, and enters the
cerebral circulation causing the CVA.

 Question 18
Needs Grading
A 57-year-old male construction worker comes to the clinic with a chief complaint of pain in his right
hip. The pain has progressively gotten worse over the last 2 months and he has been having trouble
sleeping. There is little pain in the morning, but he is a bit stiff. The pain increases as the day
wears on.  has taken acetaminophen without any relief but states that the ibuprofen does work a little
bit. He is anxious since the hip pain has limited his ability to work and he is afraid that his boss will
fire him if he cannot perform his usual duties. There is no history of past trauma or infection in the
joint. Past medical history noncontributory. Social history without history of alcohol, tobacco, or illicit
drug use. Physical exam remarkable for decreased range of motion of the right hip. BMI
34 kg/m2. Radiographs in the office demonstrated asymmetrical joint space narrowing of the right hip
with osteophyte formation. Several areas of the hip showed bone-on-bone contact with loss of the
articular cartilage. The APRN tells the patient he has osteoarthritis (OA) and refers the patient to
an orthopedist for evaluation of his need for a total hip replacement.  

Question:

Describe how osteoarthritis develops and forms and distinguish primary osteoarthritis from

secondary arthritis.   

Correct
Answer:  
Osteoarthritis is a slow, progressive, non-inflammatory disease of joints. There is loss
articular cartilage, thickening of the subchondral bone with osteophyte formation. In the
early stages, there is edema in the extracellular matrix ad the cartilage loses its smooth
appearance, and microcracks begin to form. In the later stages, the cracks deepen
resulting in fissuring, cartilage fragments may appear in the joint, and there is sclerosis of
subchondral bone. Osteophyte formation results from damage to the cartilage that
triggers a massive metabolic response at the level of the chondrocytes. Initial enzymatic
 tissue breakdown results in a decrease in proteoglycan content in the matrix, in turn
causing cartilage softening and loss of elasticity. The body compensates for these
changes by chondrocytes increasing their synthesis of collagen and proteoglycans.
However, this increase cannot keep pace with the progressive destruction by enzymes
digesting cartilage → increasing friction →á damage → Type I collagen scarring.
Primary OA is often called idiopathic because it forms without any precipitating event.
OA usually appears in few joints, especially the larger weight bearing one, but can
appear in any joint. Secondary OA is usually caused by a prior injury to the joint. It can
also be caused by certain medications such as corticosteroids, colchicine, and
indomethacin.

 Question 19
Needs Grading
A 34-year-old Caucasian female presents to the clinic with a chief complaint of widespread pain in
her joints and muscles. She states that her skin seems sensitive and sometimes it hurts to be touched.
She has had extreme fatigue for the past 4 months. She admits to being depressed and it unable to
sleep well. She has had to drop out of her gardening club due to pain. She says that bright lights and
loud noises really bother her. Past medical history noncontributory. Social history is significant for her
divorce from her husband 14 months ago. She is the mother of 2 small children and works as an
administrative assistant as the local insurance company. Physical exam remarkable for tender points
over her posterior supraspinatus muscles, occiput, trapezius, gluteal area, and sacroiliac joints
bilaterally. The APRN tells the patient that she most likely has fibromyalgia, based on her physical
exam.  

Question 1 of 2:

What are the underlying causes of fibromyalgia? 

Correct
Answer:  
The cause is unknown but there appears to be a strong genetic link. There may be an
interaction between genetic factors and environmental exposures that triggers alterations
in gene expression. There is an abnormal and exaggerated perception of pain. Cytokines
have recently been indicated as a possible pathogenesis of fibromyalgia.

 Question 20
Needs Grading
A 34-year-old Caucasian female presents to the clinic with a chief complaint of widespread pain in
her joints and muscles. She states that her skin seems sensitive and sometimes it hurts to be touched.
She has had extreme fatigue for the past 4 months. She admits to being depressed and it unable to
sleep well. She has had to drop out of her gardening club due to pain. She says that bright lights and
loud noises really bother her. Past medical history noncontributory. Social history is significant for her
divorce from her husband 14 months ago. She is the mother of 2 small children and works as an
administrative assistant as the local insurance company. Physical exam remarkable for tender points
over her posterior supraspinatus muscles, occiput, trapezius, gluteal area, and sacroiliac joints
bilaterally. The APRN tells the patient that she most likely has fibromyalgia, based on her physical
exam.  
Question 2 of 2:
The APRN tells the patient that the tender points are no longer used to diagnose FM. She suggests
that the patient takes the Widespread Pain Index (WPI) and the Symptom Severity Inventory (SSI).
The patient asks the APRN what these tests are for. What is the APRN’s best answer?
Correct
Answer:  
The American College of Rheumatology recently identified new criteria for diagnosing
FM. The WPI and SSI tests are used to quantify the symptoms of FM. For the WPI,
patients answer the questions about where the pain has been experienced during a one-
week period. For the SSI, the patient is asked to rank specific symptoms of fatigue,
cognitive symptoms, waking unrefreshed and other somatic symptoms. The numerical
scores are then totaled, and the diagnosis of FM is based on the results of the scores.