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1. Describe the surface anatomy of affected area

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1. Describe the surface anatomy of affected area

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Thickening of nail plate (onychauxis).

Nail surface appear rough & uneven with ridges or groove.

Nail become misshapen with curvatures or lifting (onycholysis).

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Yellowish or brownish discoloration due to subungual hyperkeratosis & accumulation of keratin debris.

Presence of tophi deposits under or near the nail.

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Thickened, callus-like tissue develops beneath the nail due to chronic inflammation.

Tophi deposition displace nail.

Periungual skin appears red, swollen and tender.

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Nail become brittleness & fragility.

Chronic inflammatory process disrupt nail matrix.

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Chronic tophaceous deposits in 1st metatarsophalangeal joint cause visible joint swelling.

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3. Discuss the pathophysiology of the joint inflammation

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3. Discuss the pathophysiology of the joint inflammation

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Autoimmune reactions

Crystal deposition

Trauma

Infection

Joint inflammation begins with a trigger that activate the immune system response in the synovial tissue.

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i. Synovial cell activation (type A & type B)

Synoviocytes Type A

Responsible for clearing debris & pathogens in the joint space through phagocytosis.

Synoviocytes Type B

Overproduction of hyaluronic acid leading to joint swelling, however the fluid becomes diluted & mixed with inflammatory exudates.

ii. Angiogenesis

Type B secrete vascular endothelial growth factor (VEGF) promote new blood vessel in synovial membrane & increase vascular permeability.

iii. Hyperplasia of synovial lining

Proliferating Type B form pannus, a thickened synovial membrane which contribute to enlargement of the joint capsule.

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i. Neutrophils

It migrate into the synovial fluid & release :

- Reactive oxygen species

(ROS)

- Proteolytic enzymes (matrix

metalloproteinase)

ii. Macrophages

Activated macrophage produce cytokines & enzymes that lead to tissue destruction.

iii. Lymphocytes

In autoimmune arthritis, Th1 & Th17 release IFN-γ to active macrophages & IL-17 to enhance neutrophil recruitment & tissue destruction.

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i. Cartilage damage

Inflammatory cytokines stimulate chondrocytes, leading to

Increased production of matrix degrading enzymes that breakdown proteoglycans & collagen in cartilage.

Loss of cartilage resilience & structure, impairing joint function.

ii. Bone erosion

Osteoclast activation by RANKL (receptor activator nuclear factor-κB ligand), lead to resorption of bone (bone erosion & deformities).

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i. Prostaglandins

Prostaglandin (E2) is a mediator of pain in inflammation which it sensitize the nociceptors in the joint which it cause pain & swelling.

ii. Bradykinin & histamine

PGE2 also enhance bradykinin & histamine, leading to :

Vasodilation of blood vessels at the site of inflammation, increase blood flow lead to redness (erythema) in inflamed tissue.

Increase vascular permeability which it allow plasma protein & immune cell to leak to tissue contributing to edema & swelling.

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i. Pannus formation

The pannus invades and destroys cartilage & bone leading to joint deformaties.

ii. Fibrosis

Fibrosis replaces the healthy synovial tissue causing joint stiffness & loss of mobility.

iii. Ankylosis

In severe cases, inflammatory and fibrotic changes which it characterized by the replacement of normal joint structures with fibrous connective tissue

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2. Discuss the pathogenesis of the joint inflammation

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2. Discuss the pathogenesis of the joint inflammation

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A stimulus (e.g., trauma, infection, autoantigens, or irritants like urate crystals) disrupts normal joint homeostasis.

The stimulus activates the innate immune system via pattern recognition receptors (PRRs) like Toll-like receptors (TLRs) on immune and synovial cells.

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The synovial membrane becomes activated, leading to :

Release of pro-inflammatory cytokines (TNF-α, IL-1, IL-6) and eicosanoids (prostaglandins, leukotrienes).

Recruitment of immune cells to the joint.

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Chemokines attract immune cells, such as neutrophils, macrophages, and T cells, which infiltrate the synovium.

The immune cells release inflammatory mediators (e.g., reactive oxygen species, proteolytic enzymes), causing tissue damage.

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Cartilage breakdown by matrix metalloproteinases (MMPs).

Bone erosion due to osteoclast activation driven by RANKL (receptor activator of nuclear factor kappa-Β ligand).

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Formation of kidney stones -> Kidney damage -> Renal disease

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Deposition of uric acid -> Macrophages stimulates production of pro-inflammatory & pro-resorptive cytokines -> Induction of RANKL expression -> Increased production of osteoclasts -> Bone erosion -> Joint damage

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1. Tophi deposition

2. Subconjunctival transparent vesicles and hemorrhage

3. Vascular changes

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Increased risk of atherosclerotic diseases

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Increased risk of atherosclerotic diseases

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1. Myocardial infarction

2. Heart failure

3. Stroke

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1. Osteoporosis

2. Nerve/Spinal cord impingement

3. Chronic renal failure

4. Decreased joint mobility

5. Joint deformity

6. Fractures

7. Severe degenerative arthritis

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6. Describe the management/treatment of gout

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6. Describe the management/treatment of gout

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1. Reducing inflammation

2. Accelerating renal excretion of uric acid

3. Reducing conversion of purines to uric acid

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Primary Causes: Genetic predisposition & Overproduction of uric acid

Secondary Causes: Dietary Intake, Alcohol Consumption, Metabolic Disorders, Kidney Dysfunction, Medications, Lead Poisoning, Hypertension, Postmenopausal State & Heart Failure

Pharmacological Treatment: Xanthine Oxidase Inhibitors, Uricosuric Agents, Uricase Enzyme Therapy & Anti-Inflammatory Agents

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1. NSAIDs -> indomethacin

-Reduction of PG formation

-Inhibition of crystal phagocytosis by macrophages

Toxicity

NSAIDs -> renal damage (indomethacin -> bone marrow suppression)

2. Anti-gout agent -> colchicine

Inhibition of microtubule assembly in leukocyte -> Reduce production of leukotriene B4 -> Decrease free radical formation

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Weak acids that compete with uric acid for reabsorption by the weak acid transport mechanism in the proximal tubules

At low doses, these agents may compete with uric acid for secretion by the tubule and occasionally can elevate serum uric acid con.

1. Probenecid

2. Sulfinpyrazone

Toxicity

May precipitate acute gout attacks during early phase of action -> administer with colchicine or indomethacin

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1. Allopurinol

Allopurinol -> Oxypurinol (Alloxanthine) -> Inhibition of xanthine oxidase

*Alloxanthine

Irreversible suicide inhibitor of XO Inhibits other enzymes involved in purine-metabolism as well

2. Febuxostat

-Non-purine selective inhibitor

-Highly specific

Toxicity & drug interactions

-GIT upset, rash, and rarely, peripheral nephritis, vasculitis, or bone marrow dysfunction

-Inhibits metabolism of mercaptopurine & azathioprine

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1. Health education

2. Lifestyle modification

3. Concomitant medications

4. Topical ice

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Caused by the deposition of monosodium urate crystals in joints.

Most commonly affects the first metatarsophalangeal joint.

Often caused by alcohol, red meat, shellfish or dehydration.

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Bacteria such as Staphylococcus aureus cause joint infections.

Symptoms include acute joint pain, swelling, redness and systemic symptoms (such as fever).

The absence of systemic symptoms and the strong evidence for gout make septic arthritis an unlikely cause in this case.

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1. List the causes of the sudden onset of localized pain and swelling big toe

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1. List the causes of the sudden onset of localized pain and swelling big toe

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Recent trauma or repeated microtrauma to the toe might produce regional discomfort and swelling.

Associated with bruising, deformity or history of recent injury.

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3. Describe the bones forming metatarsophalangeal joint, blood supply, & nerve supply.

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3. Describe the bones forming metatarsophalangeal joint, blood supply, & nerve supply.

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The bones forming metatarsophalangeal joints

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The bones forming metatarsophalangeal joints

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The metatarsophalangeal (MTP) joints are formed by the articulation of the metatarsal heads with the proximal phalanges of the toes:

Metatarsal bones: The long bones that connect the mid and rear foot to the toes.

Proximal phalanges: The toe bones.

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The dorsalis pedis and posterior tibial arteries supply the blood to the foot.

The dorsalis pedis artery supplies the dorsal aspect of the metatarsals and the tarsal bones.

The posterior tibial artery enters the sole of the foot through the tarsal tunnel and divides into the medial and lateral plantar arteries.

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The plantar digital nerves are the main nerve supply to the MTP joints.

The deep peroneal and medial dorsal cutaneous nerves supply the dorsal aspect of the first MTP joint. The deep peroneal nerve supplies the second MTP joint. The lateral dorsal cutaneous nerve supplies the fourth and fifth MTP joints.

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2. Describe the pathological changes of the joints and extra-articular tissue in gout

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2. Describe the pathological changes of the joints and extra-articular tissue in gout

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monosodium urate crystals are deposited in the synovial fluid and cartilage.

Synovitis: Acute inflammation causes synovial membrane hyperemia, swelling, and infiltration by neutrophils and monocytes

Eccentric soft tissue swelling around the joints and extra-articular tissue

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urate crystals in the synovial membrane are released into the synovial fluid

penetrate the entire thickness of cartilage and collect in subchondral and deeper osseous areas

Tophaceous deposits also occur in periarticular tissues, such as the joint capsules, tendons, ligaments, and bursae, particularly in the olecranon and prepatellar regions

These deposits may appear as irregular, hard masses and produce ulceration of the overlying skin, with extrusion of chalky masses or urate crystals.

As they become larger, tophi may calcify or ossify, producing tendon rupture and nerve compression with paralysis.

Joint spaces and periarticular bone density are maintained until late disease.

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1. Describe the pathogenesis of gouty arthritis

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1. Describe the pathogenesis of gouty arthritis

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1. Hyperuricemia (High Uric Acid Levels):

Excess uric acid in the blood leads to the precipitation of urate crystals in joints.

2. Crystal Deposition:

The urate crystals trigger inflammation by activating the complement system and recruiting immune cells like monocytes and neutrophils.

3. Monocyte Activation:

Monocytes phagocytose (ingest) the urate crystals and release inflammatory cytokines such as:

IL-1 (Interleukin-1).

TNF (Tumor Necrosis Factor).

IL-6 (Interleukin-6).

4. Neutrophil Chemotaxis:

The complement system and cytokines attract neutrophils to the site of inflammation.

5. Neutrophil Activation and Phagocytosis:

Neutrophils attempt to phagocytose urate crystals. This process often fails, leading to neutrophil lysis (cell destruction) and release of:

Lysosomal enzymes.

Leukotriene B4 (LTB4), prostaglandins, and free radicals—all of which amplify inflammation.

6. Cartilage and Synovium Damage:

Inflammatory mediators (cytokines, proteases) damage the cartilage and synovium, leading to joint pain and swelling.

7. Tissue Injury and Inflammation:

The accumulation of inflammatory cells, enzymes, and mediators results in:

8. Tissue injury.

Acute inflammation, clinically presenting as red, swollen, and painful joints.

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3.  Differentiate gout and other acute or chronic articular disease

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3.  Differentiate gout and other acute or chronic articular disease

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Primary gout caused by manifestation of the disease by genetic or environment factors.

Secondary gout caused by increase urid acid due to known disease such as renal insufficiency, metabolic & hematological disorders .

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2. Describe the causes of hyperuricemia 

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2. Describe the causes of hyperuricemia 

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Primary Gout Gene Defect

Purine Recycling: The HPRT enzyme converts hypoxanthine and guanine back into usable forms.

Uric Acid Buildup: In individuals with HPRT deficiency, these purines are not recycled efficiently, leading to increased uric acid production.

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Secondary gout nucleic acid DNA

Purine Breakdown: Nucleic acids, including DNA and RNA, are composed of nucleotides, which contain purine bases (adenine and guanine).

Uric Acid Production: When nucleic acids are broken down, the purine bases are converted into uric acid, a waste product that is normally filtered out by the kidneys.

Increased Nucleic Acid Turnover and Gout:

When nucleic acid turnover is increased, more purines are released, leading to an increase in uric acid production. If the kidneys are unable to effectively eliminate this excess uric acid, it can build up in the blood, leading to hyperuricemia. This can eventually lead to the formation of uric acid crystals in the joints, causing the painful symptoms of gout.  Purine Breakdown: Nucleic acids, including DNA and RNA, are composed of nucleotides, which contain purine bases (adenine and guanine).

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5. Describe the adverse effect of medication to gout arthritis.

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5. Describe the adverse effect of medication to gout arthritis.

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Diclofenac (injections): blistering, peeling, loosening of the skin, red skin lesions, sores or ulcers on the skin and fever.

Diclofenac (oral): Upset stomach, nausea, heartburn, diarrhea, constipation, gas, headache, drowsiness, dizziness and blurred visions.

Colchicine: Diarrhea, nausea, vomiting, and abdominal pain.

Allopurinol: Skin rashes, nausea, and diarrhea.

Probenecid: Nausea, headache, and dizziness.

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2. Describe the anatomy of synovial joint & its type

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2. Describe the anatomy of synovial joint & its type

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1. Articular / Hyaline cartilage.

2. Capsule or capsular ligament.

3. Synovial membrane.

4. Synovial fluid.

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1. Plane

2. Hinge

3. Pivot

4. Ball and Songket

5. Saddle

6. Condyloid

7. Ellipsoid