Gout

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Gout

NMSK 2022

NMSK 2022

Anatomical terminology
Introduction to the central and peripheral nervous systems
Introduction to the somatic and autonomic nervous systems
Development of the axial skeleton
Bones of the vertebral column
Joints of the vertebral column
Muscles of the back
Vessels and nerves of the vertebral column
Anatomy clinical correlates: Bones, joints and muscles of the back
Superficial structures of the neck: Posterior triangle
Deep structures of the neck: Root of the neck
Anatomy clinical correlates: Vessels, nerves and lymphatics of the neck
Bones of the upper limb
Development of the limbs
Fascia, vessels and nerves of the upper limb
Muscles of the hand
Anatomy of the arm
Anatomy of the brachial plexus
Brachial plexus
Bones of the lower limb
Fascia, vessels and nerves of the lower limb
Muscles of the gluteal region and posterior thigh
Compartment syndrome
Sciatica
Bone remodeling and repair
Ectoderm
Skin histology
Skin anatomy and physiology
Skin and soft tissue infections: Clinical
Papulosquamous and inflammatory skin disorders: Pathology review
Eczematous rashes: Clinical
Skin cancer: Pathology review
Skin cancer: Clinical
Bone histology
Skeletal system anatomy and physiology
Bone disorders: Pathology review
Bone tumors: Pathology review
Paget disease of bone
Pediatric bone and joint infections: Clinical
Joint pain: Clinical
Gout
Rheumatoid arthritis
Nervous system anatomy and physiology
Neuromuscular junction and motor unit
Neuromuscular blockers
Skeletal muscle histology
Muscular system anatomy and physiology
Muscle contraction
Sliding filament model of muscle contraction
Muscle spindles and golgi tendon organs
Neuromuscular junction disorders: Pathology review
Muscle weakness: Clinical
Sympathetic nervous system
Parasympathetic nervous system
Adrenergic receptors
Cholinergic receptors
Opioid agonists, mixed agonist-antagonists and partial agonists
Cholinomimetics: Direct agonists
Substance misuse and addiction: Clinical
Pharmacodynamics: Desensitization and tolerance
Bones of the cranium
Anatomy of the cranial base
Anatomy of the orbit
Anatomy of the eye
Photoreception
Fascia and spaces of the neck
Superficial structures of the neck: Anterior triangle
Eye conditions: Inflammation, infections and trauma: Pathology review
Eye conditions: Refractive errors, lens disorders and glaucoma: Pathology review
Eye conditions: Retinal disorders: Pathology review
Pharyngeal arches, pouches, and clefts
Development of the face and palate
Development of the nervous system
Anatomy of the brainstem
Broca aphasia
Wernicke aphasia
Memory
Cerebrospinal fluid
Normal pressure hydrocephalus
Anatomy of the blood supply to the brain
Introduction to the cranial nerves
Cranial nerves
Cranial nerve pathways
Spina bifida
Congenital neurological disorders: Pathology review
Meningitis, encephalitis and brain abscesses: Clinical
Meningitis
Brain abscess
Encephalitis
Spinal cord disorders: Pathology review
Sensory receptor function
Somatosensory receptors
Anatomy of the ascending spinal cord pathways
Anatomy of the descending spinal cord pathways
Anatomy clinical correlates: Spinal cord pathways
Somatosensory pathways
Vitamin B12 deficiency
Motor cortex
Pyramidal and extrapyramidal tracts
Brown-Sequard Syndrome
Syringomyelia
Cauda equina syndrome
Myasthenia gravis
Lambert-Eaton myasthenic syndrome
Amyotrophic lateral sclerosis
Olfactory transduction and pathways
Trigeminal neuralgia
Bell palsy
Optic pathways and visual fields
Pituitary adenoma
Anatomy of the oculomotor (CN III), trochlear (CN IV) and abducens (CN VI) nerves
Anatomy clinical correlates: Oculomotor (CN III), trochlear (CN IV) and abducens (CN VI) nerves
Vestibulo-ocular reflex and nystagmus
Vestibular transduction
Cerebellum
Dizziness and vertigo: Clinical
Basal ganglia: Direct and indirect pathway of movement
Essential tremor
Huntington disease
Parkinson disease
Movement disorders: Pathology review
Anti-parkinson medications
Medications for neurodegenerative diseases
Hypokinetic movement disorders: Clinical
Multiple sclerosis
Leukodystrophy
Sleep
Toxidromes: Clinical
Cerebral vascular disease: Pathology review
Saccular aneurysm
Intracerebral hemorrhage
Arteriovenous malformation
Ischemic stroke
Transient ischemic attack
Anatomy clinical correlates: Posterior blood supply to the brain
Stroke: Clinical
Epidural hematoma
Brain herniation
Traumatic brain injury: Clinical
Traumatic brain injury: Pathology review
Concussion and traumatic brain injury
Adult brain tumors
Brain tumors: Clinical
Cluster headache
Tension headache
Migraine
Cavernous sinus thrombosis
Idiopathic intracranial hypertension
Migraine medications
Antidiuretic hormone
Hypoprolactinemia
Growth hormone and somatostatin
Oxytocin and prolactin
Anatomy of the limbic system
Frontotemporal dementia
Dementia with Lewy bodies
Vascular dementia
Creutzfeldt-Jakob disease
Syncope: Clinical
Amnesia

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Gout is an inflammatory disease in which monosodium urate crystals deposit into a joint, making it red, hot, tender and swollen within hours.

When this happens, it’s called a gouty attack.

The underlying cause is hyperuricemia—too much uric acid in the blood, which results in the formation of sharp, needle-like crystals, in areas with slow blood flow like the joints and the kidney tubules.

Over time, repeated gouty attacks can cause destruction of the joint tissue which results in arthritis.

To understand where the uric acid comes from, let’s start with purines, which, together with pyrimidines, are nature’s most common nitrogen-containing heterocycles.

A heterocycle being any molecular ring or cycle with different types of atoms.

Purines, as well as pyrimidines, are key components of nucleic acids like DNA and RNA, and when cells, along with the nucleic acids in those cells, are broken down throughout the body, those purines are converted into uric acid—a molecule that can be filtered out of the blood and excreted in the urine.

Uric acid has limited solubility in body fluids, though. Hyperuricemia occurs when levels of uric acid exceed the rate of its solubility, which is about 6.8mg/dL.

At a physiologic pH of about 7.4, uric acid loses a proton and becomes a urate ion, which then binds sodium and forms monosodium urate crystals.

These crystals can form as a result of increased consumption of purines, like from consuming purine-rich foods like shellfish, anchovies, red meat or organ meat.

Also, though, they can result from increased production of purines, for example high-fructose corn syrup containing beverages could contribute to the formation of uric acid by increasing purine synthesis.

Another way crystals could form is from decreased clearance of uric acid, which can result from dehydration from not drinking enough water or from consumption of alcoholic beverages, both of allowing uric acid to precipitate out.

Regularly eating these kinds of foods can also lead to obesity and diabetes, both of which are risk-factors for gout.

Hyperuricemia can also develop as a result of chemotherapy or radiation treatment, since cells die at a faster-than-normal rate.

Also, some individuals have a genetic predisposition to overproduction of uric acid while others with chronic kidney disease may be unable to excrete the uric acid.

Finally, there are some medications like thiazide diuretics and aspirin which can also increase the levels of uric acid and therefore the risk of gout.

Sources

  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  3. "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
  4. "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
  5. "Gout" The Lancet (2016)
  6. "Update on gout: new therapeutic strategies and options" Nature Reviews Rheumatology (2010)
  7. "Diagnosis of Acute Gout: A Clinical Practice Guideline From the American College of Physicians" Annals of Internal Medicine (2016)