Knowledge Check: Module 5
1 of 1 Questions: Describe the pathophysiology of gout.
Gout is an inflammatory response to excessive quantities of uric acid in the blood (hyperuricemia
above 6.8mg/dL) and in other body fluids, including synovial fluid. These elevated levels lead to the
formation of monosodium urate (MSU) crystals in and around joints. Gout is closely linked to purine
metabolism and kidney function. At the cellular level, purines are synthesized to purine nucleotides,
which are used in the synthesis of nucleic acids, adenosine triphosphate, cyclic adenosine
monophosphate (cAMP), and cyclic guanosine monophosphate (cGMP).
1 of 2 Questions: Explain why a patient with gout is more likely to develop renal calculi.
Renal calculi are caused by too much uric acid in urine and elevated uric acid is the root cause of gout.
Renal calculi are more prevalent in people with primary gout than in the general population. Renal
calculi comprised of purse monosodium urate, but also may consist of calcium oxalate or calcium
phosphate. It can form in the collecting tubules, pelvis, or ureters, causing obstruction, dilation, and
atrophy of the more proximal tubules and leading eventually to acute renal failure.
2: What is Lyme disease and what patient factors may have increased his risk developing Lyme
disease?
Lyme disease is a multisystem inflammatory disease caused by the spirochete Borrelia burgdorferi
transmitted by Ixodes tick bites and is the most frequently reported vector-borne illness. Clearing some
underbrush from his back yard approximately a week ago is a contributing factor to developing the
disease condition. The symptoms of Lyme disease occur soon after the bite by tick-borne obligate
parasite within 3 to 32 days with erythema migrans and a bull'seye rash.
3: What is osteoporosis and how does it develop?
Osteoporosis is a complex, multifactorial chronic disease that often progresses silently for decades until
fractures occur. It is a disease in which bone weakening increases the risk of a broken bone. Osteoporosis
develops when the remodeling cycle, the process of bone resorption and bone formation, is disrupted,
leading to an imbalance in the coupling process.
4: Explain why patients with rheumatoid arthritis exhibit these symptoms and how does it differ
from osteoarthritis?
Rheumatoid arthritis results from a combination of genetic and environmental factors, many of which
are unknown. Rheumatoid arthritis (RA) is a chronic, systemic inflammatory autoimmune disease that
may involve many tissues and organs but particularly affects the joints. The pain is caused by pressure
from swelling, it also can be caused by sclerosis of subchondral bone and new bone formation. Stiffness
usually lasts for about 1 hour after arising in the morning and is caused by synovitis. Osteoarthritis is
not a common outcome in younger people with predisposing events, such as injury e.g., dislocations,
, fractures long-term mechanical stress. The incidence of OA increases with age and is more common in
women than in men older than age 50. It is caused by continued wear and tear on specific joints in the
patient’s body.
5: Why did the APRN order an HLA-B27 lab? How would that lab result assist in understanding what
ankylosing spondylitis?
Ankylosing spondylitis is a chronic inflammatory joint disease which is characterized by stiffening and
fusion of the spine and sacroiliac joints. Certain variations in the HLA-B27 gene are associated with
development of Ankylosing spondylitis. The Laboratory tests, including serum analysis for the presence
of the histocompatibility antigen HLA-B27 can be used to help monitor the course of Ankylosing
spondylitis. A misfolding of HLA-B27 occurs in the endoplasmic reticulum (ER) and, as a result, the
misfolded proteins accumulate. This results in a stress response of the ER and increased production of
interleukin-23 (IL-23), a potent cytokine that may also act on T-helper 17 cells.
6: Why did the APRN feel a wrist splint would be helpful? What patient characteristics lead to this
diagnosis.
The APRN purpose for using wrist splint is to reduce pain and inflammation and decrease the effort
required to perform hand‐related activities by providing rest, support, and stabilization of the wrist.
Epicondylitis is related to work activities that involves repetitive cyclic flexion and extension of the
elbow, or cyclic pronation, supination, extension, and flexion of the wrist that generates loads to the
elbow and forearm region. The sharp pain especially with pronation and supination as well as being
active with tennis lessons led the APRN to diagnose the patient’s condition lateral epicondylitis.
7: What is a seizure and why is status epilepticus so dangerous for patients?
Seizure is an abnormal autonomous discharge of electrical activities within the brain. If seizures develop,
the specific physical activity that occurs depends on the origin of the electrical activities and its extent
within the brain. Status epilepticus (SE) is a medical emergency associated with significant morbidity and
mortality. It is a continuous seizure lasting more than 30 min, or two or more seizures without full
recovery of consciousness between any of them. Status epilepticus can result to permanent brain
damage, abnormal heart rhythms and aspiration into the lungs.
8: What is multiple sclerosis and how did it cause the above patient’s symptoms?
Multiple sclerosis is a chronic inflammatory disease involving degeneration of CNS myelin, scarring
(sclerosis or plaque formation), and loss of axons. It is caused by an autoimmune response to self or
microbial antigens in genetically susceptible patients.
The loss of myelin disrupts nerve conduction thereby leading to symptom presentation. The optic
neuritis is a common presentation in one eye with progressive blurring of vision and pain with eye
movement. Brainstem syndromes results to facial sensory loss, weakness, or double vision while the
cerebellar syndromes cause lack of coordination and tremor.
9: What is the underlying pathophysiology of MG?
Myasthenia gravis results from a defect in nerve impulse transmission at the neuromuscular junction.
The primary defect is T-cell–dependent formation of autoantibodies (an IgG antibody) against nicotinic