NURS 6501 Knowledge Check: Module 5 Student Response: Scenario 1: Gout
NURS 6501 Knowledge Check: Module 5 Student Response: Scenario 1: Gout
NURS 6501 Knowledge Check: Module 5 Student Response: Scenario 1: Gout
Student Response
This Knowledge Check reviews the topics in Module 5 and is formative in nature. It is
worth 20 points where each question is worth 1 point. You are required to submit a
sufficient response of at least 2-4 sentences in length for each question.
Scenario 1: Gout
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.
1 of 2 Questions:
Describe the pathophysiology of gout?
Gout is an inflammatory condition caused by excessive uric acid production in the blood
and other body fluids like a synovial fluid. Its pathophysiology is closely related to purine
metabolism and kidney function. Uric acid is a breakdown product of purine nucleotides
synthesized by purines at the cellular level that assist in synthesizing nucleic acids, adenosine
Elevated uric acid (hyperuricemia) results in the formation of monosodium urate (MSU) crystals
in and around joints; with a uric acid higher concentration greater than 6.8mg/dl, it starts to
crystallize and form insoluble precipitates of MSU that deposited in connective tissues. MSU
crystals triggers the acute inflammatory response that activates cytokines and interleukins, which
attract neutrophils out of the circulation and starts phagocytizing the crystals.Causing acute
2 of 2 Questions:
Explain why a patient with gout is more likely to develop renal calculi.
Individuals with gout have a higher risk of uric acid stone formation or renal calculi when
the uric acid levels in the urine are too high and urine pH is too low—leading to an environment
favorable for uric acid precipitation and crystallization. It is more prevalent in individuals with
primary gout than in the general population. Renal calculi may comprise of purse monosodium
Lyme disease is a common vector-borne illness transmitted by Ixodes tick bites resulting in a
multisystem inflammatory disease caused by the spirochete Borrelia burgdorferi. The patient
contributory factor in causing the disease is a tick bite coming from the underbrush of the patient
backyard after clearing a week ago. 50% of infected individuals are asymptomatic, aside from
localized infection that occurs right after the bite with erythemas migrans and a bulls-eye rash
Scenario 3: Osteoporosis
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?
Osteoporosis is the most common complex, multifactorial, chronic disease that affects the bone
—highly characterized by low bone mineral density, the bone's impaired structural integrity, and
decreased bone strength that often progresses silently for decades until fractures occur.
Osteoporosis developed when the process of bone resorption and bone formation called the
remodeling cycle is interrupted, leading to an imbalance in the coupling process. The field of
bone biology has a new understanding of the significant roles of hormones, growth, signaling
genetics and environmental factors. That affects nearly all joints of the body, particularly the
hands and feet. RA occurs when your immune system starts to attack the synovium, which is the
lining of the membranes surrounding your joints, leading to synovial inflammation or synovitis.
Causing fever, chills, sweat, increase fatigue, generalized pain, and stiffness. The inflammation
may spread to the articular cartilage, fibrous joint capsule, surrounding ligaments, and tendons
On the contrary, Osteoarthritis (OA), noninflammatory joint disease, is a wear and tear arthritis
as the smooth cushion between bones (cartilage) breaks down, the new bone formation of joint
margins and subchondral bone changes. Pain and stiffness associated with one or more weight-
bearing or load-bearing joints are the predominant symptoms of OA. It also includes swelling,
enlargement, or deformity of joints commonly starts in the 50s and affects women more than
and fusion of the spine and sacroiliac joints. The histocompatibility antigen human leukocyte
antigen (HLA-B27) is positively associated with the development of AS; the laboratory test
including serum analysis for histocompatibility antigen human presence leukocyte antigen
(HLA-B27) may help to assist and monitor the progress course of the disease. A misfolding of
HLA-B27 occurs in the endoplasmic reticulum, and, as a result, the misfolded proteins
accumulate. Resulting in the ER's stress response and increased production of interleukin-23 (IL-
that involve forceful and repetitive cyclic flexion and extension of the elbow and the wrist that
generates loads to the forearm region, promoting less pain and inflammation. Patient history is
active with tennis lessons working on his backhand serve induced forceful and repetitive cyclic
pronation, supination, extension, and elbow flexion and findings of point tenderness over the
lateral epicondyle that increases with pronation and supination due to tissue degeneration or
irritation of the extensor carpi radialis brevis tendon lead the APRN to a diagnosis of lateral
epicondylitis.
seizures lasting more than 5 minutes or rapidly recurring seizure attacks from preceding seizure.
It requires prompt medical emergencies due to its high morbidity and mortality rate resulting to
cerebral hypoxia, causing brain damage, aspiration to the lungs and death.
Multiple sclerosis (MS) is a chronic illness involving degeneration of central nervous system
(CNS) myelin, scarring, and loss of axons. It is caused by an autoimmune response when an
immune system attacks myelin, the protective layer around nerve fibers that causes
inflammation, scar tissue, or lesions. The loss of myelin sheath disrupts nerve conduction,
making it difficult for your brain to send signals to the rest of your body that causes the patient
symptoms. The symptom can be multifocal, including brainstem syndrome, vision disturbances,
coordination, tremor, gait instability, and ataxia. The spinal cord syndrome can involve sensory
and motor tracks starting from one side and progressing to the other, indicating diffuse CNS
involvement. As MS progresses, cognitive deficits like memory and attention problems are
common.
defective against the nicotinic acetylcholine receptor (AChR), muscle-specific kinase ((MuSK),
acetylcholine from binding to them and thus preventing the muscle from responding to the nerve
signal, resulting in incomplete muscle depolarization that usually affects the muscle of the eyes,
face, mouth, throat, and neck. That may lead to the manifestation of diplopia, ptosis, ocular
palsies, facial droop, and expressionless face. Difficulty chewing, swallowing can lead to
choking and aspiration, while affected respiratory muscle can cause ineffective deep breathing,
disease that gradually worsens over time. It is the most common cause of dementia that alters
mild short-term memory deficits to the total loss of cognition and executive functions as AD
4 (apoE4) on chromosome 19, which interferes with amyloid-beta clearance from the brain and
also is processed into neurotoxic fragments found in the plaques and tangles in the brain of
people with AD. Amyloid is also deposited in the smooth muscle of cerebral arteries, leading to
amyloid angiopathy and blood flow disturbance. Process failure to clear amyloid precursor
protein results in the build-up of amyloid-beta protein's toxic fragments, resulting in diffuse
mechanical trauma, immediate tissue destruction from shearing, compression, or penetration can
also occur if an injured spine is not adequately immobilized immediately following injury. In
secondary SCI is a pathologic cascade of vascular, cellular, and biochemical events that begins
within a few minutes after injury and continue for weeks. Microscopic hemorrhages appear in
the central gray matter and pia-arachnoid, increasing in size until the entire gray matter is
hemorrhagic and necrosis. Hemorrhages and edema followed by loss of autoregulation and
Question 2 of 2:
What is spinal shock and how it is different from neurogenic shock?
Spinal shock occurs immediately after injury due to loss of continuous tonic discharge from the
edema, or anatomic transection. While neurogenic shock occurs with cervical or upper thoracic
cord injury above T6 and may see in addition to spinal shock. The absence of sympathetic
activity is caused by loss of supraspinal control and unopposed parasympathetic tone mediated
compression, deformation, displacement, stretching, shearing, tearing, and crushing of brain and
blood vessels. It can be focal, affecting one area of the brain, or diffuse, involving more than one
area of the brain. Secondary TBI is caused by the indirect consequence of the primary injury,
including trauma and stroke syndromes, and includes systemic responses and a cascade of
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?
Cerebral autoregulation is a homeostatic process that regulates and maintains cerebral blood flow (CBF)
constant during cerebral perfusion pressure changes that progressively lost in an increased intracranial
pressure. When cerebral vasodilatation occurs, the increase in the vessels' radius decreases the CVR and
augments cerebral perfusion pressure. Without autoregulation, vasodilatation causes the hydrostatic
blood pressure in the vessels to drop and blood volume increases, which may obstruct venous outflow,
increasing ICP. Other factors that may contribute to a rise in intracranial content include tumor growth,
within minutes. In about one-third of people who have a TIA, however, the blocked artery does
not open up fast enough, leading to a tiny region of damage in the brain. In such cases, uninjured
parts of the brain rapidly take over the damaged tissue's function, and the symptoms resolve
Atrial fibrillation occurs when the heart's electrical impulses become disorganized, leading to
rapid and irregular heart rhythm. Ineffective blood pumping raises the likelihood of the
development of coagulation and thrombosis. These blood clots forming in the heart may circulate
to other organs such as the brain, leading to blocked blood flow (ischemia) to an artery in the
bone due to an active response of chondrocytes in the articular cartilage and the inflammatory
cells in the surrounding tissues. The release of enzymes from these cells breaks down collagen
bone results in sclerosis, followed by reactive remodeling changes that lead to the formation
of osteophytes and subchondral bone cysts. The joint space lost progressively over time. Primary
OA is more common in older people occurs without a known precipitating cause (insidious). By
using your joints over and over damages the cartilage, leading to pain and swelling. Water builds up
in the cartilage, and its proteins break down. It may start to flake or get tiny tears. Secondary
osteoarthritis happens when another disease or medical condition damages your cartilage. Things that
can cause it or make it more likely include: Injury or surgery to the joint, obesity, Body mechanics,
widespread pain in her joints and muscles. She states that her skin seems sensitive and
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
for her divorce from her husband 14 months ago. She is the mother of 2 small children
exam remarkable for tender points over her posterior supraspinatus muscles, occiput,
trapezius, gluteal area, and sacroiliac joints bilaterally. The APRN tells the patient that
Question 1 of 2:
What are the underlying causes of fibromyalgia?
Fibromyalgia (FM) has unclear pathophysiology, but several factors likely contribute to the
condition. Research has suggested genetics may play an essential part in the development of
fibromyalgia. It can also often triggered by a stressful event, including physical stress or
emotional (psychological) stress, as indicated with the patient's recent divorce, two small
children, and work demands. Other main factors that may contribute to FM's development
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?
The American College of Rheumatology has identified new criteria for the diagnosis of
fibromyalgia. A tender point evaluation is no longer required; instead, the use of a widespread
pain index (WPI) and symptom severity inventory (SSI) is recommended. For the WPI
evaluation, the individual also is asked to identify body regions where pain has been experienced
during the last 1-week time period. For the SSI evaluation, the individual is asked to rank
specific symptoms of fatigue, waking unrefreshed, cognitive symptoms, and somatic symptoms
on a scale of 1 to 3. A diagnosis of FM is determined based on both the WPI score and SSI score.