Journal of leukocyte biology

Running head: INTEGRATED CASE STUDY
INTEGRATED CASE STUDY
Name of the student:
Name of the university:
Author note:

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INTEGRATED CASE STUDY
Table of Contents
Introduction:....................................................................................................................................2
Discussion:.......................................................................................................................................2
Etiology and pathophysiology:.................................................................................................2
Clinical signs and symptoms and diagnosis:...........................................................................4
Treatment and complication:...................................................................................................5
Conclusion:......................................................................................................................................6
References:......................................................................................................................................8

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INTEGRATED CASE STUDY
Introduction:
Gout is considered as joint inflammation, most frequently in the first metatarsophalangeal
joint. Counsell et al. (2018), suggested that the systematic disease caused by monosodium urate
crystals deposition in a joint space. According to the Australian Bureau of Statistics 2017–18
National Health Survey, approximately 187000 Australian are suffering from gout In Australia,
it distresses about 70,000 people each year (Ting et al., 2016). Gout is most common amongst
males compared to females. Obesity, Hyperuricemia, male and consumption of certain
medications are considered risk factors for developing gout. Individuals with acute onset joint
pains are at high risk of developing gout (Rogenmoser & Arnold, 2018). The case study involves
a patient who admitted to the hospital due to severe pain in his right big toe. The patient had a
history of hypertension and hyperlipidemia. The report aims to provide etiology and risk factors
of gout, pathophysiology of gout, diagnosis and recommendation for managing ground in the
following paragraphs.
Discussion:
Etiology and pathophysiology:
Risk factors:
Gout is defined as joint inflammation, most frequently in the first metatarsophalangeal
joint. Hyperuricemia is the leading cause of gout. People with higher serum urate levels are at
high risk of developing gout (Ahmed et al., 2020). While Hyperuricemia is not the leading cause
of gout, older age, male sex, obesity, a purine diet, metabolic syndrome, alcohol consumption,
comorbid disease, and genetics are considered as the risk factors for developing the disease. The
case study suggested that Steven is male , obese ( 88kg) and metabolic syndrome like diabetes
type two, indicating that these are the risk factors for developing gout. Moreover, Steven is meat

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INTEGRATED CASE STUDY
eater and drinks alcohol which might be the reason behind development of gout. On the other
hand, consuming medications such as low dose aspirin, ethambutol, pyrazinamide, and
cyclosporine can result in gout. Proudman et al. (2019), highlighted that family history and
presence of genetic factors such as SLC2A9, ABCG2, SLC22A12, GCKR, and PDZK1 is
contributed factors for gout. Individuals with dietary habits such as shrimp, lobster, and red meat
are more likely to develop gout as discussed (Vieira et al., 2017). Moreover, high blood pressure
is another risk factor for gout as observed in this case study. The vital signs of Steven suggested
that he has high blood pressure (140/80 whereas normal blood pressure must be 120/80) which
can contributed to development of gout as high blood pressure increase uric acid level (Johnson
et al., 2019).
Triggers:
Proudman et al. (2019), suggested that every conditional that causes an alteration in the
deposition of extracellular urate concentration has the ability to trigger symptoms of gout. The
conditions that can trigger develop gout include surgical procedure, recent trauma, dietary factors
such as fatty food and alcohol. Metabolic symptoms can trigger the development as observed in
this case study (Craft et al., 2019). The patient had a history of diabetes and hyperlipidemia
which are the metabolic diseases that might be the reason behind the development of gout.
Pathophysiology:
Due to the presence of risk factors mentioned above, dysfunction of the purine
metabolism observed which resulted in hyperuricemia. Uric acid of the blood usually deposited
from endogenous purine breakdown and exogenous sources. The overproduction of uric acid
leads to the rise of serum uric acid levels and it can promote monosodium urate crystal
nucleation. Inflammation experience amongst patients when macrophages phagocytize

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monosodium urate crystals which resulted in the activation of cytosolic protein complexes
(NLRP2 inflammasome) (Craft et al., 2019). This protein subsequently recruits caspase-1 which
triggers pro-IL-1beta and IL-1beta. Ao, Gold blatt and Casson (2017), suggested that IL-1beta is
played a critical role in inducing inflammatory response to gout. The inflammation promotes
vasodilation and monocyte recruitment followed by inflammation cascade. IL-1beta secretion
leads to bone and cartilage break down (Hall et al., 2018). Other factors such as IL-6 and COX-2
also involved in the inflammatory response. It might be the case that the patient experienced
similar conditions which resulted in pain and severe inflammation which resulted in admission in
the hospital.
Clinical signs and symptoms and diagnosis:
The case study suggested that the patient admitted to the hospital due to severe pain in his
right toe. The patient had a history of hypertension and hyperlipidemia. The common clinical
signs and symptoms observed amongst patients include intense joint pain in the joints, ankle,
elbow, wrists, and fingers (Li et al., 2019). Other signs and symptoms include swollen, tender,
warm and red, limited mobility of the patients as observed in this case. The patient experienced
warms, swelling of the right metatarsophalangeal joint, painful and incapable of bearing
weight. Moreover, the respiratory rate of the patient is higher which might be a clinical
condition since uric acid crystals in the lungs; this complication is rare.
Diagnosis:
 X-ray imaging: it is helpful to assess other causes of joints inflammation
 Ultrasound: musculoskeletal ultrasound is effective in detecting urate crystal in a joint as
observed for this case.

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INTEGRATED CASE STUDY
 Patient history is required to consider in this case since patients with diabetes are more
likely to develop gout due to high uric acid in the blood (Craft et al., 2019).
 Blood test: the blood test is effective in detecting the level of uric acid and creatinine in
the blood. Since the patient had a history of hypertension as well as hyperlipidemia and
Type 2 Diabetes, the blood test can be a suitable means of detecting uric acid and
creatinine levels in the blood (González-Chica et al., 2019).
 Joint fluid test: Ao, Gold blatt and Casson (2017), suggested that in order to conduct a
joint fluid test, the fluid from the affected joints was assessed under the microscope since
urate crystals are visible under a microscope.
Apart from these diagnoses, assessment can be done forseptic arthritis, osteoarthritis or
Rheumatoid arthritis in order to confirm the health condition of Steven (Bryant and Knight,
2019).
Treatment and complication:
Pharmacological management:
 Xanthine oxidase inhibitors can be provided to the patients to reduce gout. It works by
inhibiting the synthesis of uric acid. Allopurinol is a Xanthine oxidase inhibitor that can
inhibit the growth of the uric acid and it is recommended first-line pharmacologic ULT in
gout (Kannangara et al., 2016).
 On the other hand, the patient can be provided with Uricosuric. Robinson and Stamp,
(2016).suggested that Uricosuric agents increase renal urate clearance. However, it is not
effective for patients with low creatinine levels.

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INTEGRATED CASE STUDY
 Additionally, for reducing the inflammation in patients, and Interleukin-1 inhibitor can be
provided to the patients which work by binding to the Il-1 inhibitor. The common
interleukin -1 inhibitors include anakinra and canakinumab.
Non-pharmacological therapy:
 The case study highlighted that the patient is a meat eater and drinks alcohol. He had a
habit of smoking 10 cigarettes per day. Since meat and alcohol can increase the risk of
gout, dietary management can be done (Robinson & Stamp, 2016). The dietary
recommendation, in this case, include limitation of alcohol consumption, meat, and high
fructose corn syrup and substituting it with low-fat dietary products along with adequate
hydration (Bryant and Knight, 2019). Moreover, Nuts, peanut butter, and grains, Eggs are
required to add. Since the patient belongs to Italian descent, the nutrition is required to
incorporate according to Italian descent.
 Physiotherapy is required to consider in this context for reducing the risk of
complications associated with physiotherapy (Bryant and Knight, 2019). Physiotherapy
increases the flow of blood as well as relaxes the muscles in the area of gout that is
responsible for pain. It can also help maintain a healthy body weight.
A complication for gout:
 The common and potential complication for gout is Joint deformity which can reduce the
mobility of the patients (Bryant and Knight, 2019). Since the patient is experiencing
intense pain, it can limit the ability to go chuck and involve in daily activities.

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INTEGRATED CASE STUDY
Conclusion:
On a concluding note, it can be said gout painful joint inflammation, most commonly in
the first metatarsophalangeal joint. People with higher serum urate levels are at high risk of
developing gout. While Hyperuricemia is not the leading cause of gout, older age, male sex,
obesity, a purine diet, alcohol consumption, comorbid disease, and genetics are considered as the
risk factors for developing the disease. Dysfunction of the purine metabolism observed which
resulted in hyperuricemia and increase inflammation. The common signs and symptoms
include joint pain in the joints, ankle, elbow, wrists, and fingers. Blood tests and joint fluid tests
are two common tests used for the patient. The pharamacological treatment can be Uricosuric,
Xanthine oxidase inhibitors. On the other hand, non-pharmacological treatment can dietary
intervention with physiotherapy.

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INTEGRATED CASE STUDY
References:
Ahmed, F., Tscharke, B., O'Brien, J., Thompson, J., Samanipour, S., Choi, P., ... & Thomas, K.
(2020). Wastewater-based estimation of the prevalence of gout in Australia. Science of
The Total Environment, 715, 136925. https://doi.org/10.1016/j.scitotenv.2020.136925
Ao, J., Goldblatt, F., & Casson, R. J. (2017). Review of the ophthalmic manifestations of gout
and uric acid crystal deposition. Clinical & experimental ophthalmology, 45(1), 73-80.
doi: 10.1111/ceo.12749
Bryant, B &Knight, K.(2019) pharmacology for heath professionals (5th ed). chatwood NSW.
Elsevier Mosby
Counsell, A. B., Nguyen, A. D., Baysari, M. T., Kannangara, D. R., McLachlan, A. J., & Day, R.
O. (2018). Exploring current and potential roles of Australian community pharmacists in
gout management: a qualitative study. BMC family practice, 19(1), 54.
https://doi.org/10.1186/s12875-018-0744-3
Craft,J. Gordon,C. Huether,S.McCance,K.Brashers,V.&Rote ,N.(2019).Understanding
Pathophyiology (3rd ed). Chatwood NSW Elsevier Austrlia
González-Chica, D. A., Vanlint, S., Hoon, E., & Stocks, N. (2018). Epidemiology of arthritis,
chronic back pain, gout, osteoporosis, spondyloarthropathies and rheumatoid arthritis
among 1.5 million patients in Australian general practice: NPS MedicineWise
MedicineInsight dataset. BMC musculoskeletal disorders, 19(1), 20.
https://doi.org/10.1186/s12891-018-1941-x
Hall, C. J., Sanderson, L. E., Lawrence, L. M., Pool, B., Van Der Kroef, M., Ashimbayeva, E., ...
& Crosier, K. E. (2018). Blocking fatty acid–fueled mROS production within

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macrophages alleviates acute gouty inflammation. The Journal of clinical
investigation, 128(5), 1752-1771.doi 10.1172/JCI94584
Johnson, R. J., Choi, H. K., Yeo, A. E., & Lipsky, P. E. (2019). Pegloticase treatment
significantly decreases blood pressure in patients with chronic gout. Hypertension, 74(1),
95-101. https://doi.org/10.1161/HYPERTENSIONAHA.119.12727
Kannangara, D. R., Graham, G. G., Williams, K. M., & Day, R. O. (2016). Effect of xanthine
oxidase inhibitors on the renal clearance of uric acid and creatinine. Clinical
rheumatology, 35(9), 2375-2376. https://doi.org/10.1007/s10067-015-3165-x
Li, Q., Li, X., Wang, J., Liu, H., Kwong, J. S. W., Chen, H., ... & An, Z. (2019). Diagnosis and
treatment for hyperuricemia and gout: a systematic review of clinical practice guidelines
and consensus statements. BMJ open, 9(8), e026677. http://dx.doi.org/10.1136/bmjopen-
2018-026677
Proudman, C., Lester, S. E., Gonzalez-Chica, D. A., Gill, T. K., Dalbeth, N., & Hill, C. L.
(2019). Gout, flares, and allopurinol use: a population-based study. Arthritis research &
therapy, 21(1), 132. https://doi.org/10.1186/s13075-019-1918-7
Robinson, P. C., & Stamp, L. K. (2016). The management of gout: much has
changed. Australian
familyphysician,45(5),299.https://www.researchgate.net/profile/Philip_Robinson7/
publication/304349705_The_management_of_gout_Much_has_changed/links/
577cdcde08ae355e74f2c60f/The-management-of-gout-Much-has-changed.pdf
Rogenmoser, S., & Arnold, M. H. (2018). Chronic gout: Barriers to effective
management. Australian journal of general practice, 47(6), 351.
https://www1.racgp.org.au/RACGP/files/e5/e573c75f-93ed-47a9-917f-911a5ce68a1b.pdf

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Ting, K., Gill, T. K., Keen, H., Tucker, G. R., & Hill, C. L. (2016). Prevalence and associations
of gout and hyperuricaemia: results from an Australian population‐based study. Internal
medicine journal, 46(5), 566-573. https://doi.org/10.1111/imj.13006
Vieira, A. T., Galvão, I., Macia, L. M., Sernaglia, E. M., Vinolo, M. A. R., Garcia, C. C., ... &
Mackay, C. R. (2017). Dietary fiber and the short‐chain fatty acid acetate promote
resolution of neutrophilic inflammation in a model of gout in mice. Journal of leukocyte
biology, 101(1), 275-284. 6. DOI: 10.1189/jlb.3A1015-453RRR