Urinsyregikt - Amboss

Question 1

Hvilken epidemiologi har urinsyregikt?

Answer 1

Question 2

Hvilke etiologi har uremi?

Answer 2

Question 3

Hva gir primær uremi?

Answer 3

Question 4

Hvilke årsaker gir sekundær uremi

Answer 4

Nedsatt urinsyre ekskresjon

Økt urinsyreproduksjon

Blandet tilstand med nedsatt urinsyre ekskresjon og økt produksjon

Question 5

Hva kan gi nedsatt urinsyreekskresjon?

Answer 5

Estrogen promotes renal uric acid excretion. Postmenopausal women have decreased estrogen levels and are therefore more likely to develop gout.

Question 6

Hva kan gi økt urinsyreproduksjon?

Answer 6

Hemolysis of RBCs does not increase uric acid levels, as RBCs do not have nuclei (which means they have no purines). However, hemolysis also causes destruction of nucleated red blood cell precursor cells (reticulocytes), which results in hyperuricemia. Calcium-poor diets may also contribute to hyperuricemia. Higher BMI correlates with higher uric acid levels, regardless of dietary habits. Hyperuricemia occurs as a result of respiratory acidosis and hypoxia secondary to sleep apnea.

Question 7

Hva er som regel årsaken til blandet tilstand som gir økt produksjon og nedsatt ekskresjon av urinsyre?

Answer 7

Question 8

Hvilke medikamenter er det som regel gir uremi?

Answer 8

Question 9

Hva er patofysiologien bak “gikten” ved urinsyregikt?

Answer 9

Question 10

Hvilke triggere kan føre til dannelse av uratkrystaller?

Answer 10

Question 11

Hva er patofysiologien bak krystallartritter?

Answer 11

Question 12

Hva er den kroniske effekten av krystallartritt?

Answer 12

Question 13

Hvilke “stadier” kan man dele urinsyregikt inn i?

Answer 13

Asymptomatisk fase

Akutt giktartritt

“Intercritical stage”

Kronisk giktartritt

Question 14

Hva kjennetegner den asymptomatiske fasen ved urinsyregikt?

Answer 14

Question 15

Hva trigger den akutte giktartritten ved urinsyregikt?

Answer 15

Question 16

Hvilke manifestasjoner er vanligst ved den akutte giktartritten?

Urinsyregikt

Answer 16

Question 17

Ved hvilke lokalisasjoner oppstår manifestasjonen av den akutte giktartritten?

Answer 17

Risk factors include hospitalization, age > 65 years, female sex, renal insufficiency, and/or thiazide treatment. Polyarthritis more commonly occurs, however, as a flare-up in untreated cases. The tissue temperature within peripheral, small joints is physiologically lower, which promotes uric acid deposition.

Question 18

Hva viser bildet?

Answer 18

Question 19

Hva viser bildet?

Answer 19

Question 20

Hva viser bildet?

Answer 20

Question 21

Hva viser bildet?

Urinsyregikt

Answer 21

Question 22

Hva kjennetegner “intercritical stage” ved urinsyregikt?

Answer 22

Question 23

Hva kjennetegner kronisk urinsyregikt?

Answer 23

Chronic gouty arthritis appears in cases of inadequate treatment over a long period of time (i.e. after several years of attacks). Destruction due to recurring gout attacks and deposition of urate crystals next to joints. They typically develop several years after the onset of disease. Tophi formation due to urate crystal deposition in and around the joints.

Question 24

Hva viser bildet?

Answer 24

Question 25

Hva viser bildet?

Answer 25

Question 26

Hva viser bildet?

Answer 26

Question 27

Hva viser bildet?

Answer 27

Question 28

Hva viser bildet?

Answer 28

Question 29

Hva viser bildet?

Answer 29

Question 30

Hva er gullstandarden for å diagnostisere urinsyregikt?

Answer 30

Question 31

Ved hvilke indikasjoner tar man synovial væskeanalyse?

Answer 31

E.g., atypical presentation, lack of response to empiric treatment.

Question 32

Hva finner man i den synovialvæsken ved urinsyregikt?

Answer 32

In contrast to calcium pyrophosphate crystals in calcium pyrophosphate deposition disease, which are weakly positively birefringent.

Question 33

Hva viser bildet?

Answer 33

Question 34

Hvordan kan man klinisk diagnostisere urinsyregikt?

Answer 34

Typical clinical presentation can be podagra in a patient with risk factors for gout. The diagnostic rule for acute gout has not been validated for patients with oligoarthritis or polyarthritis. Although other clinical decision rules have been developed, this one is the most widely accepted.

Question 35

Hva inngår i “Diagnostic rule for acute gout”?

Answer 35

With a score ≤ 4; In the original study, performed in a primary care setting, the prevalence of gout was 2.2% among patients in this score range. In a validation study, performed in a rheumatology clinic, a score in this range had a positive predictive value of 87% for gout. In-between 4 and 8; In the original study, performed in a primary care setting, the prevalence of gout was 31.2% among patients in this score range. With a score ≥ 8; In the original study, performed in a primary care setting, there was an 82.5% prevalence of gout among patients in this score range. In a validation study, performed in a rheumatology clinic, a score in this range had a negative predictive value of 95% for gout.

Question 36

Hvilke lab.prøver er akt. ved urinsyregikt?

Answer 36

The normal range of serum uric acid levels varies according to age and sex. The normal range of serum uric acid levels for an adult male is 3.7–8.0 mg/dL and for an adult female is 2.7–6.1 mg/dL. There is no universally accepted serum uric acid level for diagnosing hyperuricemia. Hyperuricemia is typically diagnosed when serum uric acid levels are > 8.0 mg/dL in men or > 6.1 mg/dL in women. Consider Calcium pyrophosphate deposition disease (CPPD) as a differential diagnosis in patients with normal serum uric acid levels. The 2020 American College of Rheumatology (ACR) guidelines no longer endorse urinary acid measurement due to a lack of supportive evidence. Urinary uric acid measurement may be considered in patients who have a personal or family history of early-onset gout (< 25 years old), or a history of urolithiasis.