Primary and secondary gout
Gout is a prominent manifestation of purine metabolism disorders. Primary gout has a congenital, familial character and is often combined with obesity, diabetes, and cholelithiasis. Sodium urate crystals are deposited in the cartilage of the auricles, joints, and tendons.
Tissue necrosis develops around the salt deposits, triggering perifocal inflammation with the formation of giant cells, followed by the proliferation of connective tissue. The outcome of this process is tophi (tophi urici) and joint deformation. In the kidneys, urates clog the tubules, causing secondary atrophic and inflammatory processes.
Secondary gout develops as a complication of other pathologies:
- Tumors of the hematopoietic tissue due to massive cell breakdown;
- Endocrine disorders;
- Kidney diseases leading to nephrocirrhosis and impaired uric acid excretion.
Uric acid infarct in newborns
This condition is not true necrosis, but a special metabolic phenomenon characteristic of full-term newborns who have lived for at least two days.
- Causes: Intensive metabolism in the first days of life and the natural adaptation of the kidneys to extrauterine conditions.
- Morphology: Amorphous masses of sodium and ammonium urate precipitate in the lumen of the tubules and collecting ducts.
- Macroscopic picture: On a kidney section, yellow-red stripes are visible, converging at the papillae of the medullary layer.
Etiology and pathogenesis of calculi formation
Calculi formation in the body is associated with general metabolic disorders (lipid, carbohydrate, mineral) and local factors, such as secretion stasis, inflammatory processes, and impaired secretion.
The process of calculus formation consists of two mandatory stages:
- Formation of the organic matrix (colloidal component consisting of mucus, leukocytes, desquamated cells, and protein substances).
- Crystallization of salts (crystalloid component).
Inflammation and calculi mutually support each other, creating a vicious circle. Calculi are most commonly localized in the biliary and urinary tracts, excretory ducts of the pancreas and salivary glands (sialolithiasis), and in the bronchi.
The chemical composition of calculi is diverse:
- Gallstones: cholesterol, pigment, calcareous, and mixed.
- Urinary calculi: urates, phosphates, oxalates (having a rough surface resembling a "mulberry"), cystine, and xanthine stones.
Significance and complications of calculi formation
The presence of calculi in organs can remain asymptomatic for a long time, but eventually, they cause severe complications:
- Obturation: impaired outflow of secretion leads to jaundice when the biliary tract is blocked or to hydronephrosis when the ureter is obstructed.
- Pressure sores and necrosis: constant pressure of the calculus on the organ wall causes its death and perforation.
- Inflammation: calculi constantly maintain a chronic infectious and inflammatory process.
Briefly: answers to topical questions
What changes develop in the kidneys in gout?
In gout, gouty nephropathy develops in the kidneys, caused by the deposition of urates in the interstitium and tubular epithelium. The following forms and changes are distinguished:
- Chronic interstitial process — a slowly developing abacterial pyelonephritis leading to nephrosclerosis.
- Acute renal blockade — obturation of the lumen of the tubules and collecting ducts by uric acid with their severe damage and the development of acute renal failure.
- Calculi formation — deposition of urate crystals in the collecting tubules and pelves.
The outcome of the pathology is the formation of a gouty shrunken kidney and the development of chronic renal failure.
What is the mechanism of pigment gallstone formation?
The mechanism of pigment gallstone formation is based on the crystallization of calcium bilirubinate in the organic matrix when its concentration increases. The pathogenesis depends on the calculus subtype:
- Black stones — form predominantly against the background of hemolysis (e.g., in sickle cell disease) and liver cirrhosis from unconjugated bilirubin salts.
- Brown stones — form against the background of chronic inflammation in the intra- and extrahepatic bile ducts, including mucins, cholesterol, and bacterial components in the core.
The general mechanism includes impaired secretion or bile stasis, which leads to the precipitation of substances into the colloidal matrix.
What consequences result from ureteral obturation by a calculus?
Ureteral obturation by a calculus leads to impaired urine excretion. Confirmed consequences include:
- Hydronephrosis and hydroureter — signs of obstruction by a calculus; renal atrophy is possible in hydronephrosis.
- Inflammation — calculi maintain chronic inflammation; pyelonephritis and renal abscesses are possible in urolithiasis.
- Pressure sores and necrosis — occur as a result of calculus pressure on the tissue, with possible death of the organ wall and perforation.
- Nephrosclerosis — listed among the complications of urolithiasis.
- Renal colic — also listed among the complications of urolithiasis.
Anuria is possible when the ureter is blocked by a calculus.
What is the microscopic structure of a gouty tophus?
The microscopic structure of a gouty tophus (tophi urici) is characterized by the development of productive granulomatous inflammation around the salt deposits. When stained with hematoxylin and eosin, the following elements are determined:
- Necrosis zone — the central area where sodium urate crystals (urates) are located.
- Inflammatory infiltrate — forms around the crystals and consists of lymphocytes, macrophages, neutrophils, fibroblasts, as well as epithelioid and multinucleated foreign body giant cells.
- Sclerosis zone — proliferation of connective tissue at the periphery of the lesion as an outcome of chronic inflammation.
Gout affects the joints and ears (tophi), while calculi grow where there is secretion stasis, inflammation, and a ready protein matrix.
Class and exam questions
Is uric acid infarction a true necrosis?
No, uric acid infarct is not true necrosis. It is a metabolic phenomenon occurring in newborns in the first days of life as a reflection of renal adaptation to extrauterine conditions.
What are the main components required for stone formation?
Calculus formation requires two components: the creation of an organic matrix (colloidal component consisting of mucus, proteins, and inflammatory cells) and subsequent salt crystallization (crystalloid component).
What is the tissue reaction surrounding salt deposits in gout?
Tissue necrosis develops around the deposits, perifocal inflammation with a granulomatous reaction and accumulation of giant cells, as well as the proliferation of connective tissue.
What else to study on this topic
- Morphological characteristics of various types of urinary calculi (urate, oxalate, phosphate)
- Microscopic structure of tophi and giant cell reaction
- Association of urolithiasis with gout and uric acid diathesis
- Macroscopic forms of calculi (faceted and staghorn stones)
- The role of inflammation in sustaining the vicious cycle of stone formation
Master the entire topic in the "Pathological Anatomy" course
This is a summary. The course covers everything tested in classes and exams.
- Complete study guide on "Nucleoprotein Metabolism Disorders and Stone Formation" and 4,414 more pages for this subject
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 153 video lessons on the subject
Other topics in the section "Morphology of Metabolic Disorders — Dystrophies"
Free video lessons: pathological anatomyShort lessons with study notes — no registration required.
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.