Cansicio Gout Presentation

 

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Gout

Presented by Christoffer Cansicio

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Introduction

One of the most common causes of chronic inflammatory arthritis in the United States is gout, formerly known as the "disease of kings and king of diseases" and characterized by the deposition of monosodium urate (MSU) monohydrate crystals in the tissues. Since gout was originally identified before the common era, it is the rheumatic condition that is the easiest to understand and treat (Fenando et al. (2022).

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Given that hyperuricemia frequently manifests in people, humans are the only known mammal species can spontaneously acquire gout. The most common factor causing gout is hyperuricemia. Higher serum urate levels increase the risk of gout attacks and make attacks more likely to occur over time. In a study of more than 2000 older persons with gout, those with levels higher than 9 mg/dl had a threefold higher risk of experiencing a flare within the following 12 months than those with levels lower than 6 mg/dl. (Fenando et al. (2022).

Primary a small percentage of these people go on to develop gout, and hyperuricemia is not the only risk factor for the disease. The impact of nutrition on the uric acid levels in other non-uricase-producing species can be evaluated using the lower physiological uric acid range. Consuming animal products like red meat, organ meats like the liver and kidney, and shellfish like shrimp and lobster are dietary sources that can cause hyperuricemia and gout (pork, beef). Alcohol, sweetened beverages, sodas, and high-fructose corn syrup are a few beverages that may also exacerbate this condition.

Gout disease burden has increased according to epidemiological research, which can be largely attributed to sedentary lifestyles and changes in protein diet.

Older age, male sex, obesity, a purine diet, alcohol, drugs, concomitant conditions, and heredity are additional risk factors for gout and/or hyperuricemia. Diuretics, low-dose aspirin, ethambutol, pyrazinamide, and cyclosporine are among the offending drugs. Numerous genes have been linked to gout, according to genome-wide association studies (GWAS). SLC2A9, ABCG2, SLC22A12, GCKR, and PDZK1 are a few of these. (Fenando et al. (2022).

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Anatomy & Physiology

When monosodium urate (MSU) crystals form in joints, bones, and soft tissues, gout develops as a result (Merriman, 2022). Acute arthritis (a gout flare), chronic arthritis (chronic gouty arthritis), and tophi (tophaceous gout) may all occur from it. Although a common and necessary pathogenic factor in the development of gout, hyperuricemia is insufficient to explain the clinical manifestation of self-limited gout flare-ups, chronic gouty arthritis, or tophaceous gout. Hyperuricemia is typically defined as serum urate concentration >6.8 mg/dL. Additionally, MSU crystal formation, deposition in tissues, and acute and/or persistent inflammatory reactions to the presence of such crystals are necessary for these clinical symptoms (Merriman, 2022).

As the gene encoding the enzyme uricase is silenced by mutation, uric acid is the end result of purine metabolism in higher primate species like humans (Fenando et al. (2022). Urate is primarily produced endogenously by the liver, with a minor amount coming from the small intestines. Nearly all urate is filtered by the glomerulus, therefore in steady-state settings, renal excretion controls the body's urate pool. A hyperuremic state results in an expansion of the urate pool. The typical range for urate in men is 800–1000 mg, and for women it is 500–1000 mg. Between 500 and 1000 mg of urate are turned over each day. Children have lower serum urate concentrations, which rise to adult levels during male puberty.

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Gout Flares

Intensely painful and incapacitating inflammatory arthritis, gout flares often affect one joint but can also affect two or more. In a gout flare, therapy aims to quickly and safely end pain and incapacity. Without treatment, the gout flare typically goes away completely in a matter of days to weeks, especially in cases of early illness. However, symptoms improve more quickly when any of a wide range of anti-inflammatory medications is administered (Gafflo, 2022).

 

A patient is said to have entered a symptom-free (interval, intercritical, or between flares) period once a gout flare has subsided. The majority of patients, however, have flares again and again; with more frequent episodes, flares may be more severe and protracted, shortening asymptomatic times. In order to avoid repeated episodes of gout flare and chronic tophaceous disease, patients with recurrent flares, those who acquire chronic arthritis, or those who develop tophi, can benefit from long-term prophylactic therapy with a urate-lowering drug (Gafflo, 2022).

 

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Principle of Treatment

Colchicine, nonsteroidal anti-inflammatory medications (NSAIDs), intraarticular and systemic glucocorticoids, nonsteroidal anti-inflammatory drugs (IL-1 beta inhibitors), and biologics are all useful in the treatment of gout flares. Regardless of the specific anti-inflammatory drug utilized, a set of general guidelines are crucial for the efficient management of a gout flare. They consist of the following:

 

 

 

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Early Treatment

As soon as the patient notices the start of a flare, ideally within a few hours after the commencement of symptoms, treatment should begin. The earlier treatment is started, especially if treatment is started at the maximum recommended dose of the selected antiinflammatory drug, the more quickly and completely symptoms are resolved. Once a noticeable reduction in symptoms is attained, patients should continue medication for the length of the flare, usually at reduced doses. (Gafflo, 2022).

Duration of Therapy

With oral glucocorticoids, we occasionally taper more slowly to reduce the chance of a recurrent ("rebound") flare. Complete discontinuation of treatment for a gout flare can typically be done safely within two to three days of complete resolution of the flare.

Treatment for a gout flare may last anywhere from a few days (for example, in a patient treated shortly after experiencing symptoms) to several weeks (eg, in a patient begun on treatment after four or five days of symptoms). If anti-inflammatory medicine is started within 12 to 36 hours of symptom onset, many patients only need it for five to seven days to manage a gout flare. (Gafflo, 2022).

Gout flare prophylaxis 

Early on in urate-lowering therapy, low-dose anti-inflammatory therapy should often be continued. Antiinflammatory gout flare prophylaxis, a form of treatment, aims to lessen the likelihood of further flares, which are frequent early in the course of urate-lowering therapy.

 

Continuing urate-lowering therapy during flares

If a patient is already on urate-lowering medicine (such as allopurinol, febuxostat, probenecid, lesinurad, benzbromarone, or pegloticase) and their gout flares up, they should keep taking it continuously. Temporary discontinuance is not advantageous, and reinitiating the medication after a break from it could trigger another flare.

 

Although urate-lowering medications don't directly help in treating a gout flare, starting one together with anti-inflammatory therapy is still a viable option because it doesn't prevent the flare from going away.

 

Tophaceous gout

Although the presence of tophi is an indication for the beginning of long-term urate-lowering pharmacotherapy either during or after resolution of a gout flare to prevent or reverse chronic gouty arthritis and joint damage, the treatment of a gout flare does not differ significantly in patients with or without clinically apparent tophi.

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Gout flare prophylaxis 

Continuing urate-lowering therapy during flares

Tophaceous gout

Comorbidities (Gafflo, 2022).

Important comorbidities that are common in gout patients may alter the safety or effectiveness of antiinflammatory drugs, especially in older patients, taking these factors into account is crucial when selecting an antiinflammatory medication for a gout flare. When choosing an agent, the following elements should be taken into consideration:

•Renal function

•Cardiovascular disease, including heart failure, poorly controlled hypertension, and coronary artery disease

•Gastrointestinal disease, including peptic ulcer disease

•Concurrent medication use

•Diabetes mellitus, especially if poorly controlled

•Drug allergy or intolerance

•Concurrent infection

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Initial Treatment

Initial treatment (Gafflo, 2022).

 

There is no one therapy that works best for all gout patients undergoing a flare; instead, a variety of medications, including systemic and intraarticular glucocorticoids, nonsteroidal anti-inflammatory medicines (NSAIDs), and colchicine, are all beneficial. The opportunity to select the therapy that is most likely to achieve benefit and minimize the risk of negative therapeutic consequences is made possible by the availability of multiple classes of agents and approaches likely to provide treatment benefit. This choice can be made based on an assessment of specific features of the individual patient and the flare history.

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Gout Education Society (2022).

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Non-pharmacological approach

To stop further episodes, gout patients are urged to change their lifestyles. Dietary suggestions include minimizing alcohol use, avoiding meals high in purines (such as meat, shellfish, high fructose corn syrup, and sweetened soft drinks), and choosing low-fat or non-fat dairy products in place of those with higher fat contents. Reduced gout flare-up frequency can also be achieved with weight loss and proper hydration (Fenando et al. (2022).

A good diet can, at most, help lose 1.0 mg/dL of uric acid, but it can also help lose weight, which reduces your risk of gout by three times. Making dietary modifications can also assist you in identifying and avoiding items that set off flares. So along with uric acid-lowering medication, maintaining a healthy weight and adhering to excellent eating habits should be goals (Gout Education Society, 2022). It is recommended to eat low-purine meals. When attempting to eat healthy, the DASH diet and the Mediterranean diet are both excellent guides.

 

Alterations to your way of life can help lessen the effects of gout on your body. Exercise on a regular basis is a fantastic way to maintain your body in shape. The CDC advises individuals to engage in moderate-intensity physical activity most days of the week for at least 30 minutes. Maintaining a healthy body weight is essential because crash diets and other quick weight loss methods raise the body's uric acid levels. Additionally, it's important to stay hydrated because, according to research, doing so may help prevent kidney stones and constipation, two diseases that can be influenced by gout (Gout Education Society, 2022).

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Abraham John United States University FNP592: Common Illnesses Across the Lifespan – Clinical Practicum Dr. Irene Benliro December 1, 2022 Diagnosis Presentation: Kawasaki disease

Kawasaki disease (KD): Overview

KD is a disorder that results in inflammation of the blood vessel walls in some of our body parts.

It most frequently affects babies and young children.

Fever and a rash are signs in the early stages. High temperature and skin peeling are symptoms.

In advanced stages, inflammation of medium-sized blood vessels is possible (vasculitis). Lymph nodes, skin, and mucous membranes, including those in the mouth, are also affected.

Usually, Kawasaki disease is curable. Aspirin and intravenous immunoglobulin therapy are two initial treatments that are administered in a medical setting.

Kawasaki Disease

The risk that a patient would experience mucocutaneous signs of KD is most strongly influenced by variations in age.

About 90% of patients with KD have oral mucous membrane abnormalities,

Followed by polymorphous rash in 70% to 90% of cases.

Expect to see limb changes in 50% to 85% of cases,

Lastly, eye changes in >75% of cases, and cervical lymphadenopathy in 25% to 70% of cases.

So watch out for these signs for KD!!

The most frequent sign of KD is an elevated body temperature.

Bilateral nonexudative conjunctivitis is seen in more than 90% of patients with conjunctivitis.

As KD worsens, mucositis frequently becomes visible. A "strawberry tongue" and cracked, red lips are traits.

Rash – The cutaneous symptoms of KD can take many different forms. The perineal erythema and desquamation that commonly precede the rash's onset during the first few days of illness are followed by macular, morbilliform, or targetoid skin lesions on the trunk and limbs.

Changes to the extremities — Changes to the extremities typically manifest last. Children experience generalized erythema on their palms and soles as well as indurated edema on the dorsum of their hands and feet.

Tachycardia that is out of proportion to fever and gallop noises are two cardiac symptoms that might appear within the first week to 10 days of an illness.

Anatomy & physiology

Most reported in Japan, the incidence has been reported to be 250/100,000 children under the age of 5, compared to the United States, where it is roughly 25/100,000 children under the age of 5.

85% of individuals affected are younger than 5 years old, with the disease typically manifesting in infancy and early childhood.

In the US, KD is the main contributor to childhood heart disease.

Coronary artery aneurysm incidence in untreated KD patients ranges from 15 to 25%.

The primary cause of death is myocardial infarction brought on by thrombotic blockage of the coronary arteries.

Patients of Asian heritage seem to have KD more frequently. The amount of the heart involvement and the promptness of medical care determine the prognosis.

A&P continued

KD's etiology is a mystery. Small to medium sized vessels, particularly the coronary arteries, are affected by the inflammation in KD.

When the immune system accidentally damages the blood vessels, Kawasaki disease results.

The crucial element that determines morbidity and mortality is the degree of coronary artery involvement.

According to researchers, vascular damage is promoted by mediators including tumor necrosis factor (TNF), interleukin (IL)-1B, interferon (INF), and IL-6 generated by activated T-cells and macrophages. The subendothelial buildup of T cells, mononuclear cells, macrophages, and monocytes is the earliest pathogenic change in the vessel wall that has been documented.

What diagnostic do we do!?

There are three phases in KD.

The acute phase starts with a high temperature without a clear cause that may linger for one to two weeks. Vasculitis and perivasculitis may cause acute myocardial infarction during the acute phase.

The fever decreases during the subacute period, which could last 2-4 weeks. In this stage, the skin may desquamate and coronary artery aneurysms may develop. The number of platelets increases and may exceed 106 per millimeter three. ESR and CRP are typically increased as well as other acute phase reactants.

Within 6 to 8 weeks of the illness's beginning, the symptoms of the convalescent phase end and the platelet count and ESR return to normal.

Diagnostic!?

Since KD is considered as a systemic inflammation both C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) must be checked.

Leukocytosis and a rise in immature neutrophils in the white blood cell count should be assessed, as thrombocytosis typically manifests after the seventh day of sickness.

Another acute-phase reactant that is increased in inflammatory circumstances in KD is ferritin.

Lymphocyte generally decrease during the acute stage of KD, then drastically increase during recovery.

By the second week of the illness, platelet counts typically increase and may approach 1,000,000/mm3.

WBCs are frequently detected by urinary microscopy.

Diagnotic continued

KD diagnosis in accordance with clinical recommendations:

The existence of a fever lasting 5 days along with at least four of the following five physical characteristics, without a compelling medical reason

Bilateral injections into the bulbar conjunctiva

Oral mucous membrane alterations, such as strawberry tongue, injected pharynx, or fissured or injected lips.

Peripheral extremity alterations, such as periungual desquamation, erythema of the palms or soles, or edema of the hands or feet.

Multifaceted rash

Cervical lymphadenopathy (at least one lymph node with a diameter of 1.5 cm or greater)

Treatment

The American Heart Association's (AHA's) and the American Academy of Pediatrics' (AAP's) recommendations for treating patients with KD are Intravenous immune globulin (IVIG; 2 g/kg), given as a single infusion over 8 to 12 hours, is the recommended initial therapy

Due to its anti-inflammatory actions (such as a shortening of the duration of a fever) and antiplatelet effects, aspirin was one of the first medications utilized for KD. But it's not obvious if using aspirin in addition to IVIG has more anti-inflammatory effects.

The recommended range for aspirin dosage to have an anti-inflammatory impact during the acute phase of disease is 30 to 100 mg/kg per day in four divided doses, this is considered a heavy dose for someone young.

Treatment

Glucocorticoids — Glucocorticoids have been shown to decrease the rate of CA abnormalities in Japanese patients with KD at high risk for IVIG resistance

Tumor necrosis factor inhibition — Some KD patients have been shown to have elevated levels of tumor necrosis factor (TNF) alpha. Anti-TNF-alpha medications like etanercept or infliximab have so been investigated as both a primary illness adjuvant therapy and a monotherapy for refractory KD.

Information relating to the needs of the patient

Although older children can sometimes be affected, children under the age of five are most frequently diagnosed with Kawasaki disease.

KD is more prevalent in the winter and spring, and it affects boys more frequently. Although the precise cause of KD is uncertain, it is thought that an infection may be the starting point. Children who are genetically predisposed to the condition may also experience it, moreover, there is no spread of Kawasaki disease.

Kawasaki disease cannot be diagnosed using a particular test.

Instead, a child's symptoms and a physical examination are used to make the diagnosis of Kawasaki disease.

A protracted fever (defined as one that lasts for more than five days) is frequently the first sign that prompts a clinician to think about Kawasaki disease.

Lab analyses could support a diagnosis. Blood and urine tests, an electrocardiogram (ECG) to examine the heart's electrical system, and an echocardiography (heart ultrasound) to assess the size of the blood arteries around the heart and the condition of the heart are possible.

Information cont…

Due to the concern over the association between aspirin use and Reye syndrome, parents are occasionally hesitant to provide aspirin to their children. Reye syndrome, an inflammatory condition that affects the brain and liver, has been seen in aspirin-taking individuals who have chicken pox or influenza.

Most medical professionals advise getting your child vaccinated against influenza if they are taking aspirin for an extended period of time for any reason. You should seek medical help right away if your child is taking aspirin and has chicken pox or has been exposed to it.

Information cont….

Because damage to the coronary arteries frequently does not manifest itself for several weeks, follow-up care is crucial. Fortunately, most kids with KD don't experience any long-term effects with the right care.

Children with coronary artery involvement require routine cardiology exams. The degree of coronary alterations may influence how frequently these visits are made. These individuals typically experience a positive outcome with the appropriate medical care.

Refereneces

Kawasaki Syndrome | CDC. (n.d.). https://www.cdc.gov/kawasaki/index.html

McCrindle, B. W., Rowley, A. H., Newburger, J. W., Burns, J. C., Bolger, A. F., Gewitz, M., Baker, A. L., Jackson, M. A., Takahashi, M., Shah, P. B., Kobayashi, T., Wu, M. H., Saji, T. T., & Pahl, E. (2017). Diagnosis, Treatment, and Long-Term Management of Kawasaki Disease: A Scientific Statement for Health Professionals From the American Heart Association. Circulation, 135(17). https://doi.org/10.1161/cir.0000000000000484

TePas, E. (2022). Kawasaki disease: Clinical features and diagnosis. UpToDate. https://www.uptodate.com/contents/kawasaki-disease-clinical-features-and-diagnosis?search=kawasaki%20disease%20children&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#

Sundel, R. (2022). Kawasaki disease: Initial treatment and prognosis. UpToDate. https://www.uptodate.com/contents/kawasaki-disease-initial-treatment-and-prognosis?search=kawasaki%20disease%20children%20treatment&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H4233359

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