OSTEOARTHRITIS

Osteoarthritis (wear and tear disease of the cartilage) is defined as chronic, progressive
disorder affecting primarily the weight bearing diarthrodial joints, it’s characteristics
are progressive deterioration and loss of cartilage, osteophyte formation, pain limitation
of motion, deformity and disability.

RISK FACTORS
Non-modifiable factors:
- Gender: effect of menopause and decreasing estrogen levels.
- Age: 80% of patients older than 75 years have OA, due to chondrocyte apoptosis
- Genetics: Increased IL-1 levels → destruction of articular cartilage.
Modifiable Factors
- Obesity
- Joint trauma

ETIOLOGY
Primary causes: Idiopathic
Secondary causes:
- Metabolic conditions: Hemochromatosis, acromegaly, and deposition of
crystalline calcium.
- Inflammatory diseases: Septic, RA, ankylosing spondylitis.
- Structural anomalies: Leg length discrepancies, joint or. Hip dislocation
Diminished ability of chondrocytes to maintain and repair articular cartilage -> cartilage
degradation.

PATHOGENESIS
- Repetitive traumatic injury – release of inflammatory cytokines such as TNF-alpha, NO,
IL-1 and enzymes that breakdown extracellular matrix → less elastic cartilage →
stiffening of subchondral bone.
- Cartilage is avascular, but it contains chondrocytes which is responsible for cartilage
breakdown and repair in normal conditions.
- in early OA chondrocytes will try to repair the joints by producing osteophytes -- bony
outgrowths. – Pain and limited mobility.
- Early disease: Water content of the cartilage is increases → weakened collagen
network.
- Progression: Proteoglycan concentrations are less, with shorter glycosaminoglycan
side chains → decreased - net aggregate proteins, Type 1 collagen and keratin sulfate in
extracellular matrix.
- Chondrocytes are unable to produce macromolecules for maintainance of cartilage but
produce enzymes that break down the matrix.
Enzymes that degrade proteoglycans and collagen are aggrecanases and collagenases.
Collagen is cleaved by matrix metalloproteinases – MMP-1, MMP-8, MMP-13
- Imbalance between cartilage maintenance and degradation – erosion and
cartilage destruction

CLINICAL PRESENTATION
- deep, aching pain in affected joints. Pain accompanies joint activity and
decreases with rest.
- Limitation of motion, stiffness, crepitus, and deformities may occur. Patients
with lower extremity involvement may report weakness or instability.
- Upon arising, joint stiffness typically lasts less than 30 minutes and resolves with
motion.
- Presence of warm, red, and tender joints suggests inflammatory synovitis.
- Early hypertrophy of cartilage is followed by notable bone, ligament, tendon,
capsules, and synovial reaction, along with varying amounts of noninflammatory
joint effusion, ultimately resulting in the joint enlargement characteristic of
osteoarthritis.
- Mechanical block by intra-articular loose bodies or abnormally placed menisci
can occur and cause locking or catching. Deformity and subluxations can also
develop.
- Heberden and Bouchard nodes are bony enlargements (osteophytes) of the DIP
and PIP joints, respectively.
- Joints commonly affected - the distal interphalangeal (DIP) and proximal
interphalangeal (PIP) joints of the hand, first carpometacarpal joint, knees, hips,
cervical and lumbar spine, and first metatarsophalangeal (MTP) joint of the toe.

DIAGNOSIS
o X-rays - reveal marginal osteophytes, narrowing of the joint space, increased
density of the subchondral bone, subchondral cyst formation, bony remodeling,
and joint effusions.
o Laboratory studies are normal in osteoarthritis
- ESR may be slightly elevated if inflammation is present. Rheumatoid factor is
negative. Analysis of synovial fluid reveals high viscosity and mild leukocytosis
(<2000 white blood cells/mm3 ) with predominantly mononuclear cells

2
 o For hip OA, patient must have hip pain and two of the following: (1) ESR less
than 20 mm/h, (2) radiographic femoral or acetabular osteophytes, and/or (3)
radiographic joint space narrowing.
o For knee OA, patient must have knee pain and radiographic osteophytes in
addition to one or more of the following: (1) age more than 50 years, (2)
morning stiffness lasting 30 minutes or less, (3) crepitus on motion, (4) bony
enlargement, (6) bony tenderness, and/or (7) palpable joint warmth.

NONPHARMACOLOGIC THERAPY

• Educate patient about disease process and extent, prognosis, and treatment. Promote dietary counseling,
exercise, and weight loss program for overweight patients.
• Physical therapy—with heat or cold treatments and an exercise program—helps maintain range of motion and
reduce pain and need for analgesics.
• Assistive and orthotic devices (canes, walkers, braces, heel cups, insoles) can be used during exercise or daily
activities.
• Surgical procedures (eg, osteotomy, arthroplasty, joint fusion) are indicated for func- tional disability and/or
severe pain unresponsive to conservative therapy.

PHARMACOLOGIC THERAPY
Celecoxin + PPI or
misoprostal

Risk of GIT ulceration and Nonselective NSAID + PPI

bleeding or misoprostal

Alternative first-line
agents
Naproxen + PPI or
Tramadol Intra-articular
corticosteroids
Cardiovascular risk

Symptomatic pain and Tramadol or intraarticular

NSAIDS or COX2 inhibitors CKD
inflamayion injections

Tramadol, Intra-articular
hyaluron

Subtherapeutic response to
Duloxetine (Knee only)
NSAIDs or celecoxib

Surgery

Drug Starting Dose Usual Range

Oral Analgesics
Acetaminophen 325 – 500mg TDS 1g – Q6HRLY
Tramadol 25mg 1-0-0 Titrate by 25mg
increments to 50
-100mg TDS
Hydrocodone/acetaminophen 5mg/325mg TDS 2.5-10mg/650 3-
5 times a day
Oxycodone/acetaminophen 5mg/325mg TDS 2.5-10mg/650 3-
5 times a day
3
- Do not administer IA corticosteroids more frequently than once 3 months to
avoid systemic ADR After aseptic aspiration of the effusion and corticosteroid
injection, initial pain relief may occur within 24 to 72 hours, with peak relief
occurring after 7 to 10 days and lasting for 4 to 8 weeks. Local adverse effects
can include infection, osteonecrosis, tendon rupture, and skin atrophy at the
injection site
- NSAIDs cause minor GI complaints such as nausea, dyspepsia, anorexia,
abdominal pain, flatulence, and diarrhea in 10% to 60% of patients. They may
cause gastric and duodenal ulcers and bleeding through direct (topical) or
indirect (systemic) mechanisms.

4
RHEUMATOID ARTHRITIS
RA is an auto immune, chronic systemic inflammatory disorder of unknown aetiology
characterised by potentially deforming polyarticular systemic joint involvement and a
wide spectrum of extra articular systemic manifestations.
- Onset occurs in the 3rd or 4th decades of life except in the case of JIA.
- RA is a systemic disorder that involves multiple organs – pleuropulmonary and
cardiac, ophthalmic, vasculitis, connective tissue.

1.ETIOLOGY – UNKNOWN
- A genetic predisposition has been identified and, in White populations, localized to a
shared epitope in the HLA-DRB1 locus of class II histocompatibility antigens.
- Unknown or unconfirmed environmental factors (eg, viral infections, cigarette
smoking) are thought to play a role in triggering and maintaining joint inflammation.
Risk factors for rheumatoid arthritis include the following:
- Smoking Obesity, Sex hormones. Drugs
- Changes in microbiome of the gut, mouth, and lung
- Periodontal disease (periodontitis)

2. PATHOPHYSIOLOGY
• RA results from dysregulation of humoral and cell-mediated immunity. Most
patients produce antibodies called rheumatoid factors;
• Immunoglobulins (Ig) activate the complement system →chemotaxis,
phagocytosis, and release of lymphokines by mononuclear cells that are then
presented to T lymphocytes.
• TNF-α, IL-1, and IL-6 are proinflammatory cytokines → inflammation.Macrophages
are stimulated to release prostaglandins and cytotoxins.
• T-cell activation requires both stimulation by proinflammatory cytokines as well as
interaction between cell surface receptors, called costimulation. One such
costimulation interaction is between CD28 and CD80/86.
• Activated B cells produce plasma cells, → accumulation of polymorphonuclear
leukocytes. These leukocytes release cytotoxins, oxygen-free radicals, and hydroxyl
radicals that promote damage to synovium and bone.
•Vasoactive substances (histamine, kinins, prostaglandins) are released at sites of
inflammation, increasing blood flow and vascular permeability. This causes edema,
warmth, erythema, and pain, and facilitates granulocyte passage from blood vessels
to sites of inflammation.

5
 i. Inflammation of the synovial lining that surrounds the joint space – thin membrane
proliferates and transforms → synovial pannus
ii. Pannus: highly erosive enzyme-laden inflammatory exudate
Invades
articular
cartilage
(narrowing
of joint
space)

Erodes
bone
Joint
deformities pannus (resulting in
osteoporosi
s)

Destroys
periarticula
r structures
(ligaments
and
tendons)

6
3. CLINICAL PRESENTATIONS
• Nonspecific prodromal symptoms developing over weeks to months include
fatigue, weakness, low-grade fever, anorexia, and joint pain. Stiffness and myalgias
may precede development of synovitis.
• Joint involvement tends to be symmetric and affect small joints of the hands,
wrists, and feet; elbows, shoulders, hips, knees, and ankles may also be affected.
• Joint stiffness typically is worse in the morning, usually exceeds 30 minutes, and
may persist all day.
• On examination, joint swelling may be visible or apparent only by palpation. Tissue
is soft, spongy, warm, and may be erythematous.
•Joint deformities may involve sub- luxation of wrists, metacarpophalangeal joints,
and proximal interphalangeal joints (swan neck deformity, boutonniè re deformity,
and ulnar deviation).
- Swan neck deformity is characterized by extension at proximal interphalangeal
joint and flexion at distal interphalangeal joint.
- Boutonnière deformity is characterized by flexion at the proximal
interphalangeal joint and hyperextension at the distal interphalangeal joint.
- Ulnar deviation synovitis of the metacarpophalangeal joints with an ulnar drift
of the digits.
- Rheumatoid nodule- small subcutaneous nodules present at the extensor
surfaces of hand, wrist, elbow and back in rheumatoid arthritis patients.
•Extra-articular involvement may include rheumatoid nodules, vasculitis, pleural
effusions, pulmonary fibrosis, ocular manifestations, pericarditis, cardiac conduction
abnormalities, bone marrow suppression, and lymphadenopathy, felty’s syndrome –
splenomegaly neutropenia
- Popliteal (Baker) cysts can develop, causing calf swelling and tenderness
suggestive of deep venous thrombosis.
- Cricoarytenoid joint arthritis can manifest as voice hoarseness and respiratory
stridor.

7
 DIAGNOSIS

The criteria use a scoring system with a combined score of 6 or more out of 10 indicating that the patient has
definite RA.

•Laboratory abnormalities

1. positive rheumatoid factor (60%–70% of patients)

RF: Antibodies that recognize Fc portion of IgG, Can be IgM , IgG , IgA. Disorders that give
positive RF: Sjogrens syndrome (dry eyes and a dry mouth), Vasculitis, Sarcoidosis (growth
of tiny collections of inflammatory cells (granulomas) in any part of body), Systemic lupus
erythematosus, Cryoglobulinemia, Chronic liver disease, Infections- tuberculosis , bacterial
endocarditis, infectious mononucleosis, leprosy, syphilis, leishmaniasis

2. anticyclic citrullinated peptide (anti-CCP), IgG against synovial membrane

peptides damaged via inflammation.
3. positive anticitrullinated protein antibody (ACPA) (50%–85% of patients);
4. anti- nuclear antibodies (25% of patients).
- A normochromic (or slightly hypochromic)-normocytic anemia occurs in 80%
- Neutropenia occurs in 1 to 2% of cases, often with splenomegaly (Felty syndrome).

• Aspirated synovial fluid

- Turbidity, leucocytosis, reduced viscosity, and normal or low glucose relative to serum
concentrations.
- white blood cell counts 10,000 to 50,000/mcL

Radiologic findings

- soft tissue swelling and osteoporosis near the joint (periarticular osteoporosis). Erosions
later in the disease course are usually seen first in the metacarpophalangeal and
proximal interphalangeal joints of the hands and metatarsophalangeal joints of the feet.

Positive acute phase reactants (↑) Negative acute phase reactants (↓)

Mild elevations : Ceruloplasmin, Complement C3 & C4 – Albumin

Moderate elevations – Haptoglobulin, Fibrinogen (ESR),α1 – acid glycoprotein, α1 – proteinase – Transferri

inhibitor

Marked elevations- C-reactive protein (CRP), Serum amyloid A protein

8
SPONDYLITIS
Ankylosing spondylitis is a chronic, multi-system inflammatory disorder characterised
inflammation of the sacroiliac joints and axial skeleton.
AS is one of the spondyloarthropathies (SpA) that refers to a diverse group of conditions
associated with the HLA-B27 gene. The condition causes inflammation of the sacroiliac
joints and axial skeleton that presents as chronic back pain, morning stiffness, and
eventually spinal deformity in long-standing cases.
CLASSIFICATION

• Axial ankylosing spondylitis: Has predominantly axial involvement and

findings typical of bilateral sacroiliitis on imaging
• Nonradio graphic ankylosing spondylitis: Clinically similar to axial
ankylosing spondylitis but without findings typical of sacroiliitis on imaging
• Peripheral ankylosing spondylitis: Ankylosing spondylitis with
predominantly peripheral involvement

9
SIGNS AND SYMPTOMS
- Back pain—often nocturnal and of varying intensity—eventually becomes
recurrent.
- Morning stiffness, typically relieved by activity, and paraspinal muscle spasm
develop.
- Accentuated kyphosis, loss of lumbar lordosis, and fixed bent-forward posturing,
with compromised pulmonary function and inability to lie flat.
- There may be peripheral potentially deforming joint involvement, sometimes
involving isolated digits diffusely (dactylitis).
- Achilles and patellar tendinitis can occur.
- Arthritis, fatigue
- Enthesitis (inflammation at the insertion of tendons and ligaments)
Schöber test

The L5 spinous process is identified and marked with the patient standing up.
Typically lies at the level of the sacral dimples. Another mark is made 10 cm above
this first line. The patient is then asked to bend forward in an attempt to touch their
toes. The distance between the two lines is remeasured with the patient fully flexed.
An increase of < 5 cm during flexion is considered a positive test.
EXTRA-ARTICULAR MANIFESTATIONS:
- Aortitis: can lead to aortic regurgitation
- Anterior uveitis: inflammation of the middle layer of the eye (i.e. the uvea).
Typically causes unilateral eye pain, redness, and photophobia. Seen in 25-35%
of individuals with SpA
- Atrioventricular block
- Atlanto-axial instability: increases risk of cord compression
- Apical lung fibrosis
- Amyloidosis: secondary to chronic inflammation
- IgA nephropathy

DIAGNOSIS
Lumbosacral spine and sacroiliac joint radiography, sacroiliitis may be graded according
to x-ray findings:
- Grade 0 (normal)
- Grade I (suspicious): blurring of joint margins
- Grade II (minimal): localised erosion/sclerosis. No change to joint width
- Grade III (abnormal): advanced erosions with evidence of
sclerosis/widening/narrowing/partial ankylosis
- Grade IV (severe): complete ankylosis
Dagger sign: ossification of the supraspinous and interspinous ligaments leading to a
central radio dense line running up the spine. Bamboo spine: -Gives the impression of a
continuous lateral spinal border on x-rays like a bamboo stem.
- Blood tests (ESR, CRP, HLA-B27), and complete blood count) , MRI
10
RENAL REPLACEMENT THERAPY (RRT)
replaces nonendocrine kidney function in patients with renal failure and is occasionally used for some
forms of poisoning. Dialysis is a process that facilitates the removal of excess water and toxins
from the body, both of which accumulate as a result of inadequate kidney function.

HEMODIALYSIS – PRINCIPLES

- During HD, a patient’s anticoagulated blood (circulated to the dialyzer from a vein in
the arm) and an electrolyte solution that simulates plasma (dialysate) are
simultaneously perfused through a dialyzer (artificial kidney) on opposite sides of a
semipermeable membrane.
- Solutes (e.g., metabolic waste products, toxins, potassium, and other electrolytes)
are removed from the patient’s blood by diffusing across concentration gradients
into the dialysate.
- Solutes from the blood are removed through diffusion and convection. Diffusion is
the process whereby the molecule moves across its concentration gradient by
passing through pores in the dialysis membrane.
- Accumulated water is removed by the process of ultrafiltration. A controlled
pressure difference across the semipermeable membrane permits water movement
through the membrane pores, which carries with it solute into the dialysate, thereby
further enhancing solute removal
- . Flux is the rate of water transfer across the dialyzer. Convection is the process
that removes toxins and other dissolved solutes during dialysis through the
ultrafiltration of plasma water from the blood compartment. The removal of solutes
by convection during ultrafiltration generally is small relative to their elimination
through diffusion.

Dialyzer Characteristics

Their primary component is the dialysis membrane, made of cellulose (e.g., cuprammonium
cellulose), substituted cellulose (e.g., cellulose acetate cellulose triacetate), cellulosynthetic, or
synthetic polymer (e.g., polysulfone, polyacrylonitrile, and polymethylmethacrylate).Membranes
differ not only by composition but also by surface area, thickness, and configuration within the
dialyzer.

- dialyzers are characterized as low-flux or high-flux based on pore size and ability to
remove small versus large molecules.

Blood and Dialysate Flow

- A typical blood flow rate for dialysis is 400 to 500 mL/minute but is dependent on
the vascular access site and the cardiovascular status of the patient.

- Dialysate flow rates generally are 500 mL/minute and can be increased to 800
mL/minute for high-flux dialysis, which will increase urea clearance by 10%.

Dialysate Composition

- Water - reverse osmosis→ ion exchange with activated charcoal to remove

contaminants, such as aluminum, copper, chloramines, bacteria and endotoxins.

- Before delivery, the dialysate is heated to 37◦C to maintain body temperature and
avoid hemolysis, which can occur with excessive heating.
- Metabolic acidosis, is controlled with the addition of bicarbonate buffer to the
dialysate solution. → ADR CaCO3 ppt.
- Acetate enters the blood compartment by diffusion from the dialysate and is
metabolized to bicarbonate in vivo. Acetate, hypotension and cardiac instability
11
Permanent Vascular Access

- Different types - arteriovenous (AV) fistula, AV graft composed of expanded

polytetrafluoroethylene, double-lumen or tunneled catheters, and catheters with
subcutaneously implanted access ports. AV fistulas and grafts are placed in the
nondominant arm .

Anticoagulation

- Anticoagulation is necessary to prevent blood from clotting in the extracorporeal

circuit. – IV Heparin

- Initiation: 2,000-unit bolus of IV heparin 3 to 5 minutes before initiation of dialysis,

followed by an infusion of 1,200 units/ hour.
- the direct thrombin inhibitors, argatroban and lepirudin. Their use is especially
attractive in individuals who experience heparin-induced thrombocytopenia (HIT)
- antithrombin product, lepirudin, is produced through recombinant DNA technology.
It is biologically simi- lar to hirudin, which is isolated from the saliva of leeches.
- Two heparinoids, danaparoid and fondaparinux. Danaparoid has a prolonged half-
life in renal failure, therefore monitoring with anti-Xa assays is recommended.
- The regional administration of trisodium citrate through the arterial line is an
alternative to systemic anticoagulation. It binds free calcium, which is necessary for
the coagulation process. → Pt. with high risk of bleeding

Complications

- Intradialytic hypotension (IDH) can produce a variety of clinical signs and

symptoms, including nausea and vomiting, dizziness, muscle cramps, and headache

Management: Patient in Trendelenburg position (leg raised and head lowered),

administer small bolus of normal saline (100ml), reduce ultrafilteration rate

- Muscle cramps: reduced ultrafilteration and infusion of hypertonic saline or glucose

to improve circulation. Long term tc Vit E 400 IU HS

- Hypersensitivity reactions

- Dialysis disequilibrium syndrome -Rapid removal of urea from the extracellular

space lowers plasma osmolality, thereby leading to a shift of free water into the
brain
- Thrombosis due to venous stenosis

- Infections: Cefazolin 20mg/kg 3 times weekly, Gentamicin 2mg/KG

- Amyloidosis: deposition of β2-microglobulin– containing amyloid in joints and soft

tissues over prolonged periods
- Malnutrition

12
PERITONEAL DIALYSIS – CAPD
PD uses the patient’s peritoneal mem- brane for the clearance of water and solutes.
Variations of PD include continuous ambulatory peritoneal dialysis (CAPD) and
automated peritoneal dialysis (APD)

Principles

13
 - Continuous ambulatory peritoneal dialysis is performed by the instillation of
2 to 3 L of sterile dialysate solution into the peri- toneal cavity through a
surgically placed resident catheter.
- The solution dwells within the cavity for 4 to 8 hours, and then is drained
and replaced with a fresh solution. This process of fill, dwell, and drain is
performed three to four times during the day, with an overnight dwell by the
patient in his or her normal home or work environment
- The peritoneal membrane covering the abdominal contents serves as an
endogenous dialysis membrane, and the vasculature embedded in the
peritoneum serves as the blood supply to equilibrate with the dialysate

Access - Delivery of dialysate into the peritoneal cavity is accomplished through an

indwelling catheter inserted through the abdominal wall. Tenckhoff catheter, made of silicone
rubber or polyurethane; it consists of a tube, straight or curled, with many holes in the distal
end for fluid inflow and outflow.

Dialysis Prescription
- The initial CAPD prescription for most patients consists of three exchanges
during the day with 1.5% dextrose and a fourth, overnight, exchange with
4.25% dextrose.
- This would be expected to achieve fluid removal of approximately 1,300 mL,
based on 200 mL from each daytime exchange and 700 mL overnight.
Complications: Infection, peritonitis, Weight gain

14
GOUT -
Gout involves hyperuricemia, (serum urate > 6.8mg/dL), manifests as recurrent attacks
of acute arthritis inflammation secondary to mono sodium urate (MSU) crystals in
synovial fluid. leukocytes, deposits of MSU crystals in tissues in and around joints
(tophi-hard nodules of MSU deposited in soft tissues most common in toes, fingers,
elbows), interstitial renal disease, and uric acid nephrolithiasis.
Gout – crystal induced arthropathy.

TYPES OF GOUT
1.. ASYMPTOMATIC HYPERURICEMIA
- abnormally high serum urate level, without gouty arthritis or nephrolithiasis.
Hyperuricemia is defined as a serum urate concentration greater than 7 mg/dL, the
approximate level at which urate is supersaturated in plasma.
2. ACUTE GOUT
Acute gout is characterized by the sudden onset of pain, erythema, limited range of
motion and swelling of the involved joint.

3. INTERCRITICAL GOUT
Following recovery from acute gouty arthritis, the patient reenters an asymptomatic
phase of the disease. This phase is referred to as “intercritical gout.” Medications
should be assessed to identify those that may aggravate the patient's condition (e.g.,
diuretics) and dietary education regarding purine-rich foods (which contribute to
higher serum uric acid levels) should be provided to the patient at this time
4.. RECURRENT GOUTY ARTHRITIS
Gouty arthritis has polyarticular involment, symmetric small-joint involvement and
tophaceous deposits on extensor tendon surfaces that resemble rheumatoid
nodules.
5..CHRONIC TOPHACEOUS GOUT
Tophi are chalky deposits of sodium urate that are large enough to be seen on radiographs and may
occur at virtually any site. The most common sites include the joints of the hands or feet. The helix of
the ear, the olecranon bursa and the Achilles tendon are classic,

6..PSEUDOUT
pseudogout is caused by calcium pyrophosphate crystals and is more accurately
termed calcium pyrophosphate disease

15
ETIOLOGY
Genetic Disorders: Hypoxanthine-guanine phosphoribosyltransferase deficiency
( Lesch-Nyhan syndrome); Glucose-6-phosphatase deficiency (von Gierke disease);
Fructose 1-phosphate aldolase deficiency; Superactivity of phosphoribosyl
pyrophosphate synthetase (PRPP)
Overproduction: Cell lysis from chemotherapy for malignancies, especially those of
the hematopoietic or lymphatic systems, can raise uric acid levels, as can excessive
exercise and obesity.
Myeloproliferative and lymphoproliferative disorders, psoriasis, and hemolytic
anemias
Underexcretion of uric acid include kidney insufficiency, lead nephropathy
(saturnine gout), starvation or dehydration, certain drugs, and chronic abuse of
ethanol (especially beer and hard liquor).
Medications Loop and thiazide diuretics; Niacin; Low-dose aspirin; Cyclosporine;
Pembrolizumab

Signs and symptoms

- Podagra – Inflammation of single joint, classicaly big toe
- Arthritis -- ankle, wrist, finger joints, and knee
- Monoarticular and polyarticular involvement
- Attacks that begin abruptly and typically reach maximum intensity within
8-12 hours;
- overlying skin may become tense, warm, shiny, and red or purplish.
- Tophi-- firm yellow or white papules or nodules, single or multiple. They
can develop in various locations, commonly the fingers, hands, feet, and
around the olecranon or Achilles tendon. Tophi can also develop in the
kidneys and other organs and under the skin on the ears.

16
DIAGNOSIS
•
Joint aspiration and synovial fluid analysis
•
Serum uric acid measurement (though hyperuricemia is not diagnostic
of gout)
• 24-hour urinary uric acid evaluation
• Blood studies (including white blood cells [WBCs, triglyceride, high-
density lipoprotein, glucose, and kidney and liver function tests)
Radiography, ct; MRI; characteristics of erosions are:
• Maintenance of the joint space
• Absence of periarticular osteopenia
• Location outside the joint capsule
• Sclerotic (cookie-cutter, punched-out) borders
Ultrasonography
A “double-contour” sign -irregular line of MSU crystals on the surface of articular
cartilage
“Wet clumps of sugar,” representing tophaceous material
Bony erosions adjacent to tophaceous deposits

Management
Gout is managed in the following 3 stages:
I..Treating the acute attack – NSAIDs, Colchicine, corticosteroids, IL-1 Antagonist

Fenoprofen 400 mg three times daily 400–600 mg three to four times daily
Ibuprofen 400 mg three times daily 400–800 mg three to four times daily
50 mg three times daily initially until pain is tolerable then
Indomethacin 50 mg three times daily
rapidly reduce to complete cessation
75 mg three times daily or 50 mg four times
Ketoprofen 50–75 mg three to four times daily
daily
750 mg followed by 250 mg every 8 h until
Naproxen —
the attack has subsided

Colchicine
MOA: Inhibition of microtubule polymerization; Decreases the action of inflammayory
mediators such as cytokines and chemokines.
Dose: 1.2 mg can be followed with 0.6 mg 1 hour later; joint pain tends to
decrease after 12 to 24 hours and sometimes ceases within 3 to 7 days
ADR: Renal insufficiency, GI Upset, diarrhea.
drug interactions especially with clarithromycin, erythromycin (CYP3A4 Inhibitors)
and statins,fibrates may warrant reduction of dosage

Corticosteroids are used to treat acute flares.

- Aspiration of affected joints, followed by instillation of corticosteroid
ester crystal suspension, is very effective.
- Prednisone acetate 5 to 25 mg can be used, with dose depending on the
size of the affected joint. Oral prednisone (about 0.5 mg/kg once a day),
IM or IV corticosteroids,
- single-dose adrenocorticotropic hormone (ACTH) 80 U IM Providing
prophylaxis to prevent acute flare.
IL-1 Antagonist – Anakinra (100mg SC OD) – until symptoms resolve

Nonpharmacologic Therapy -Local ice application is the most effective adjunctive

treatment. Dietary supplements (eg, flaxseed, celery root) are not recommended.

17
Management of Hyperuricemia

Blocking urate production with xanthine oxidase inhibitors (XOI) MOA:

Xanthine oxidase inhibitors reduce uric acid by impairing conversion of
hypoxanthine to xanthine and xanthine to uric acid.

Allopurinol starting dose no greater than 100 mg daily and then gradually
titrating every 2 to 5 weeks up to a maximum dose of 800 mg/day until the
serum urate target is achieved.

adverse effects -- skin rash, leukopenia, GI problems, headache, and

urticaria. toxic epidermal necrolysis, erythema multiforme, or exfoliative
dermatitis

Febuxostat The recommended starting dose is 40 mg once daily. Increase

the dose to 80 mg once daily for patients who do not achieve target serum
uric acid concentrations after 2 weeks of therapy.
Increasing urate excretion with a uricosuric drug –
Probenecid increases renal clearance of uric acid by inhibiting the
postsecretory renal proximal tubular reabsorption of uric acid.
Dose: Initial probenecid dose is 250 mg twice daily for 1 to 2 weeks, then 500
mg twice daily for 2 weeks. Increase the daily dose thereafter by 500mg
increments every 1 to 2 weeks
ADR: GI irritation, rash and hypersensitivity, precipitation of acute gouty
arthritis, and stone formation.

Recombinant Urate Oxidase Drugs (URICASE)

Pegloticase is a pegylated recombinant uricase that reduces serum uric acid

by converting uric acid to allantoin, which is water soluble.

Dose: 8 mg by IV infusion over at least 2 hours every 2 weeks. Ascorbic

acid 500mg daily

18
SYSTEMIC LUPUS ERYTHROMATOUS
Systemic lupus erythematosus (SLE) is a multi-system, inflammatory, autoimmune
disorder characterized by antibodies to nuclear and cytoplasmic
antigens, multisystem inflammation, protean clinical manifestations, and a relapsing
and remitting course.
Multisystem involvement: Cardiac, GIT, Musculoskeletal, renal, pulmonary, vascular
and hematologic systems
Etiopathogenesis

Genetics

Genes previously associated with other autoimmune diseases have been associated
with SLE (eg, PTPN22 and diabetes; STAT4 and rheumatoid arthritis).

Infections and Microbes as Triggers

- Epstein-Barr virus (EBV

- Chronic infections may induce anti-DNA antibodies or even lupus like
symptoms, and acute lupus flares often follow bacterial infections.

Other Risk Factors and Environmental Triggers

- Pregnancy
- Vitamin D deficiency
- Silica dust exposure and cigarette smoking
- Estrogen use in postmenopausal women
- Ultraviolet light stimulates keratinocytes, leads to overexpression of nuclear
ribonucleoproteins (snRNPs) on their cell surfaces
Possible early-life risk factors include the following :
- Low birthweight (< 2500 g)
- Preterm birth (≥1 month early)
- Childhood exposure to agricultural pesticides
Clinical Presentation

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Diagnosis

• Clinical criteria
• Cytopenias
• Autoantibodies
According to ACR, The disgnosis of SLE is made when 4 of the 11 criteria are met

Antiphospholipid antibodies:
• Anticardiolipin antibodies or
• Anti-beta2 glycoprotein 1 antibodies or
• Lupus anticoagulant

Complement proteins:
• Low C3 or low C4
• Low C3 and low C4

SLE-specific antibodies:
• Anti-dsDNA antibody or
• Anti-Smith antibody

Imaging studies
• Joint radiography
• Chest radiography and chest CT scanning
• Echocardiography
• Brain MRI/MRA
• Cardiac MRI

Procedures
• Arthrocentesis
• Lumbar puncture
• Kidney biopsy

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TREATMENT
Antimalarials – Joint and skin manifestations
Useful in preventing and treating lupus skin rashes, constitutional symptoms,
arthralgias, and arthritis; antimalarials also help to prevent lupus flares
Hydroxychloroquine sulfate 200-400mg P/O BID
Hydroxychloroquine inhibits chemotaxis of eosinophils and locomotion of
neutrophils and impairs complement -dependent antigen-antibody reactions.
ADR: Chronic use leads to maculopathy – ophthalmic examinations necessary,
cardiac or skeletal muscle toxicity
Alternatives: Chloroquine 250 mg P/O OD; Quinacrine 50 to 100 mg OD
NSAIDs
symptomatic relief for arthralgias, fever, headache, and mild serositis. ADR: elevated
creatinine or LF risk of gastrointestinal ulceration. – Ibuprofen, Diclofenac, Naproxen
DMARDS, Immunomodulators
Disease-modifying antirheumatic drugs (DMARDS) are immunomodulatory agents that
act as immunosuppressives and cytotoxic and anti-inflammatory medications.
Cyclophosphamide IV 0.5-1g/m2 monthly, then 6 monthly then quarterly
Methotrexate 5–15 mg P/O as a single weekly
Methotrexate is used for managing arthritis, serositis, cutaneous, and constitutional
symptoms. It blocks purine synthesis and 5-aminoimidazole-4-carboxamide
ribonucleotide (AICAR), thus increasing anti-inflammatory adenosine concentration at
sites of inflammation.
Azathioprine 1-3mg P/O OD or BID
Azathioprine antagonizes purine metabolism and inhibits synthesis of DNA, RNA, and
proteins.
Mycophenolate 1-3g P/O BID
This agent inhibits inosine monophosphate dehydrogenase (IMPDH) and suppresses de
novo purine synthesis by lymphocytes, thereby inhibiting their proliferation.
Mycophenolate also inhibits antibody production.
Immune globulin IV (IGIV)
It neutralizes circulating myelin antibodies through anti-idiotypic antibodies. This agent
downregulates proinflammatory cytokines, including interferon-gamma; blocks Fc
receptors on macrophages; suppresses inducer T and B cells; and augments suppressor
T cells. Immune globulin also blocks complement cascade, promotes remyelination, and
may increase cerebrospinal fluid IgG (10%).

Rheumatologic agents
Belimumab 10mg/kg IV Q2weekly for fist 3 doses --> monthly
Belimumab inhibits the biologic activity of B-lymphocyte stimulator (BLyS); BLyS is a
protein required for survival and for development of B-lymphocyte cells into mature
plasma B cells that produce antibodies.

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 Corticosteroids
Preparations include oral, intravenous, topical, and intra-articular
injections.
Methylprednisolone Prednisone(0.125 – 2mg/kg orally OD)
It decreases inflammation by suppressing migration of polymorphonuclear leukocytes
and reversing increased capillary permeability

Rituximab - monoclonal antibody and an immunosuppressant that eliminates

mature circulating B-cells.

Interferon Antagonists
Anifrolumab - a human monoclonal antibody to type I interferon receptor subunit 1
that suppresses interferon gene signatures and substantially reduced SLE disease
activity

Calcineurin Inhibitors
Tacrolimus and Voclosporin
Calcineurin is an enzyme that activates T-cells of the immune system. volcosporin 23.7
mg twice daily is given.
Pregnancy
- Should remain on hydroxychloroquine throughout pregnancy + low dose aspirin
- When APS – Antiphospholipid Syndrome (+) – LMWH advised
- `Mycophenolate Mofetil → teratogenic, thus switch to azathioprine before
conceiving

PATIENT EDUCATION
- Use of sunscreen, protective clothing, avoid uv lights and sunlights
- Stress management strategies and exercise
- Ice therapy to relieve pain and swelling of joints
- Smoking cessation, weight loss
- Chronic use of corticosteroids need vitamin D supplements and calcium

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LEUKEMIA
Leukemia is a hematologic malignancy that is derived from cytogenic alterations of
hematopoietic cells – pluripotent stem cells. It involves the excess production of
immature or abnormal leukocytes.
Abnormal proliferation, aberrant differentiation, clonal expansion and diminished
apoptosis leads to malignant cells.

CLASSIFICATION OF LEUKEMIA
Acute or Chronic – based on percentage of leukemia cells in marrow or blood
Myeloid or Lymphoid – predominant lineage of malignant cells
A. Acute Myeloid Leukemia (33%) - AML
Clonal proliferation of myeloid precursors with reduced capacity to differentiate into
mature cellular elements. Leukemic blasts are formed in bone marrow, peripheral blood
and other tissues.
Signs and Symptoms
Anemia: Fatigue, malaise, pallor, weakness, dyspnea on exertion, tachycardia
Thrombocytopenia: mucosal or gingival bleeding, ecchymoses, purpura, menorrhagia
Granulocytopenia (neutropenia) Increased risk of infections.
Leukemia Cutis: papules or nodules and plaques – erythematous, brown, hemorrhagic,
violaceous greyish/blue.
B. Acute Lymphoblastic Leukemia (11%) - all
Similar to AML, due to genetic aberrations. Malignant transformation usually occurs at
pluripotent stem cell level, although sometimes involves a committed stem cell with
limited capacity for self-renewal. Most common pediatric leukemia
They are of two types B-ALL (B-lymphoblastic Leukemia) or T-ALL
Signs and symptoms same as AML
Organ infiltration: Enlargement of liver, spleen and lymph nodes. Bone marrow
infiltration – bone and joint pain.
CNS and meningeal penetration: Cranial nerve palsies, headache, visual or auditory
symptoms, stroke, altered mental status.
C. Chronic Lymphocytic Leukemia
Characterized by progressive accumulation of phenotypically mature malignant B
lymphocytes in – Peripheral blood, none marrow, lymph nodes and spleen. Or
overproduction of functionally incompetent B-cells from single stem cell clone in bone.
Signs and symptoms
- Lymphadenopathy, splenomegaly, hepatomegaly, Fatigue, fever, night
sweats, weight loss
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 D. Chronic Myeloid Leukemia
Myeloproliferative disorder characterized by unregulated stem cell proliferation in
bone marrow leading to overproduction of mature and immature granulocytes in
blood.
Signs and symptoms – 3 stages:
Chronic or benign: Indolent period (5 to 6 years) – malaise, anorexia, weight loss
Accelerated: Tx failure, worsening anemia, thrombocytopenia, persisting
splenomegaly, clonal evolution, increased basophils and increasing marrow blasts.
Blast phase: accumulation in extra medullary sites – bone, CNS, lymph nodes, skin,
blasts in bone marrow is > 20% survival is less than 3 months. qqq

DIAGNOSIS OF COMMON LEUKEMIAS

Feature

ALL AML CLL CML

Age of Childhood Any age Middle ad old age Adulthood
incidence
WBC count High in 50% High in 60% High in 98% High in 100%
Differential Many Many Small lymphocytes Entire myeloid
Count Lymphoblasts myeloblasts series
Anemia Severe >90% Severe>90% Mild in 50% Mild in 80%
Other CNS Aur nodes in Hemolytic anemia, Low ALP level,
Features commonly myeloblasts hypogammaglobulinemia Philadelphia
involved chromosome
positive >90%

PA TH O PH YSIO LO GY OF CLL

- CD5+ B cells undergo malignant transformation.

- Mutation -> activation of B cells → Monoclonal B cell lymphocytosis (MBL)
→ genetic abnormality, oncogenic transformation → CLL

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BREAST CANCER
Breast cancer is malignancy originating from breast tissue. It often involves epithelial
tumors involving the ducts or lobules.
- Disease confines to a localized breast lesion: early, primary, localized or
curable.
- Disease detected clinically or radiographically in sites distant from the
breast is advanced or metastatic breast cancer.
Diagnosis
- Careful history, physical examination of the breast
- Mammography (3D and digital):
- Breast Tomosynthesis (3D Mammography): helpful in women with dense
breast tissue
- Breast Examination: Clinical Breast examination (CBE) and Breast Self
examination
- MRI: recommended for women with BRCA gene mutation
- Biopsy: Analysis of estrogen and progesterone receptors and for HER2
proteins
ANALYSIS OF METASTATIC DISEASE
- Chest X ray, CBC, liver tests and measurement of sr. Calcium
- Immunology: Carcinoembryonic antigen CEA, CA- 15-3, CA 27-29
- Bone scanning: Bone pain, elevated ALP, stage III or IV
- Abdominal CT: adnominal pain, elevated liver enzymes
- Chest Ct: Pulmonary symptoms
Staging:
Stage (anatomical extent of disease) is based on primary tumor extent and size (T 1–4),
presence and extent of lymph node involvement (N1–3), and presence or absence of
distant metastases (M0–1). The staging system determines prognosis and assists with
treatment decisions. Simplistically stated, these stages may be represented as
follows:

✓ Early Breast Cancer

•Stage 0: Carcinoma in situ or disease that has not invaded the basement membrane

• Stage I: Small primary invasive tumor without lymph node involvement

• Stage II: Involvement of regional lymph nodes

✓ Locally Advanced Breast Cancer

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• Stage III: Usually a large tumor with extensive nodal involvement in which the
node or tumor is fixed to the chest wall; also includes inflammatory breast cancer,
which is rapidly progressive

✓ Advanced or Metastatic Breast Cancer

• Stage IV: Metastases in organs distant from the primary tumor

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EARLY BREAST CANCER

Local-Regional Therapy

- Surgery alone can cure most patients with in situ cancers and approximately one
half of stage II cancers
- Breast-conserving therapy (BCT) is often primary therapy for stage I and II disease;
BCT includes removal of part of the breast, surgical evaluation of axillary lymph
nodes, and radiation therapy (RT) to prevent local recurrence.
- RT is administered to the entire breast over 4 to 6 weeks to eradicate residual
disease after BCT. Reddening and erythema of the breast tissue with subsequent
shrinkage of total breast mass are minor complications associated with RT.
- Simple or total mastectomy involves removal of the entire breast without dissection
of underlying muscle or axillary nodes.

Adjuvant Chemotherapy Therapy

Initiate chemotherapy within 12 weeks of surgical removal of the primary tumor.

Optimal duration of adjuvant treatment is unknown but appears to be 12 to 24 weeks
Examples :ACT – FOLLOW AC → Paclitaxel 80mg/m2 IV weekly repeat weekly for 12
cycles
Or Paclitaxel 80mg/m2 IV 12 weeks →FAC

Adjuvant Endocrine Therapy

Tamoxifen, toremifene, oophorectomy, ovarian irradiation, luteinizing hormone– releasing

hormone (LHRH) agonists, and aromatase inhibitors (AI) are hormonal therapies used in the
treatment of primary or early-stage breast cancer.

- Tamoxifen 20 mg daily, after chemotherapy for 5 years Estrogen receptor agonist.

- Aromatase inhibitors (Anastrozole, exemestane, letrozole – block peripheral
production of estrogen in post menopausal women.
ADR: Bone loss, osteoporosis, hot flashes, myalgia, arthralgia, vaginal dryness, mild
headaches
- Premenopausal women benefit from ovarian ablation with LHRH agonists (eg,
goserelin) in the adjuvant setting, either with or without concurrent tamoxifen

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METASTATIC DISEASE
Choice of therapy depends on the following:

- Hormone-receptor status of the tumor.

-Length of the disease-free interval (from remission to manifestation of
metastases)
- Number of metastatic sites and organs affected
-Patient’s menopausal status

Endocrine therapy
premenopausal women – SERM, LHRN Agonist

postmenopausal women, aromatase inhibitors - additional forms of

endocrine therapy (eg, progestins, the antioestrogen fulvestrant)

Single Agent Chemotherapy:

- Paclitaxel 80mg/m2 Qweekly

- Docetaxel 60–100 mg/m2 IV over 1 hour Repeat cycles every 21 days
- Capecitabine 2,000–2,500 mg/m2 per day orally, divided twice daily for 14
days - Repeat cycles every 21 days
-
Gemcitabine 600–1,000 mg/m2/week IV, days 1, 8, and 15
Repeat cycles every 28 days (may need to hold day 15 dose based on blood
counts)
- Liposomal doxorubicin 30–50 mg/m2 IV over variable duration Repeat cycles
every 28 days

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DRUG INDUCED RENAL DISORDERS

RADIOCONTRAST MEDIA INDUCED ACUTE TUBULAR NECROSIS

Signs:

- Contrast-induced nephropathy (CIN) usually presents as a nonoliguric ATN,

- It is also differentiated from other forms of ATN in that the FENa is usually less than
1% (vs. the typical >2%).
- Nephropathy is indicated by a progressive rise in creatinine 24 to 48 hours after
contrast administration, which usually peaks within 5 days.

Moa:

- the radiocontrast medium produces renal vasodilation and an osmotic diuresis. →

followed by intense vasoconstriction in the medullary portion of the kidney, which
has been demonstrated by significant decreases in medullary Po 2 after contrast
administration.
- The ischemia is compounded by the increased medullary oxygen consumption
because of the osmotic diuresis. Consequently, disequilibrium exists between
oxygen supply and demand, creating ischemic ATN.

Prevention
- Use IV hydration: 5%Dextrose in water with sodium carbonate 154 mEq/l or
0.9%NaCl
- Ascorbic Acid 3g before procedure and 2g BID X 2 doses after procedure
- Acetylcysteine 600 -1200mg BID 2 doses before and 2 doses after procedure

AMINOGLYCOSIDE INDUCED ACUTE TUBULAR NECROSIS

Presentations:
- The onset occurs after 5 to 7 days of treatment and presents as a hypo-osmolar, non-
oliguric renal failure with a slow rise in SCr.
- Because of the tubular necrosis that occurs, the urinalysis is often positive for low-
molecular-weight proteins, tubular cellular casts, epithelial cells, WBCs, and brush-
border cells

MOA
- Aminoglycosides are polycationic and bind to the negatively charged brush-border
cells within the tubule lumen. →pinocytosis and enter the intracellular space, →
formation of myeloid bodies. →the brush-border cells swell and burst, releasing
large concentrations of aminoglycoside and lysosomal enzymes into the tubule
lumen, thereby beginning a cascade of further tubular destruction.

- neomycin > gentamicin = tobramycin = amikacin = netilmicin > streptomycin

Prevention: Extended-interval regimen – dose every 24 hours or several days in RF

patients
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DRUG-INDUCED ACUTE INTERSTITIAL NEPHRITIS
Agents:
penicillin, cephalosporins, quinolones, sulfonamides, rifampin and NSAIDs

MOA:

- Humoral immune reactions occur within minutes to hours of drug exposure and
involve the drug or its metabolite acting as a hapten that binds to host proteins,
making them antigenic. The drug–protein antigens become lodged in the renal
tubules, which initiate the inflammatory cascade.
- Cell-mediated injury can occur days to weeks after drug exposure and is identified
by the presence of mononuclear inflammation and the lack of detectable immune
complexes. This suggests a delayed hypersensitivity rather than a direct cytotoxic
effect from a given drug.

Symptoms:

- fever, macular rash, and malaise

- azotemia, elevated SCr, proteinuria, cellular urinary sed- iment, eosinophilia, and
eosinophiluria.

Treatment: prednisone 1 mg/kg for 7 days, Dialysis for oliguric patients

DRUG INDUCED NEPHROLITHIASIS

MOA: many commonly prescribed drugs are insoluble in urine and crystallise in the
distal tubule.
- Drugs that are weak acids (e.g., methotrexate, sulfonamides) precip tate in acidic
urine; drugs that are weak bases (e.g., indinavir, other protease inhibitors)
precipitate in alkaline urine. Other eg: Acyclovir, Triamterene

POST-RENAL FAILURE
- usually results from a mechanical barrier to moving urine from the collecting
tubules into the bladder
- Mechanical obstruction : enlargement of the prostate, kidney stones, Drugs
that precipitate in the kidney (acyclovir, ganciclovir), Co-trimoxazole

NSAIDS
- COX-2 exists as a constitutive enzyme in the thick part of the ascending loop
of Henle and in the renal medulla
- COX-2 causes natriuresis and diuresis
- Inhibition of COX-2 by selective COX-2 inhibitors, such as celecoxib and
rofecoxib causes renal dysfunction

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PSORIASIS
Psoriasis is a complex, chronic, multifactorial, inflammatory disease that involves
hyperproliferation of the keratinocytes in the epidermis, with an increase in the
epidermal cell turnover rate.

Acrodermatitis Pustular psoriasis confined to distal fingers or toes,

continua of sometimes just one digit
Hallopeau Replaced by scale and crust when it resolves

Gradual or sudden onset of diffuse erythema, usually in

patients with plaque psoriasis (possibly the first
Erythrodermic manifestation of erythrodermic psoriasis); typical
psoriasis psoriatic plaques less prominent or absent
Most commonly triggered by inappropriate use of
topical or systemic corticosteroids or light therapy

Generalized Explosive onset of widespread erythema and sterile

pustular psoriasis pustules

Abrupt appearance of multiple plaques 0.5 to 1.5 cm in

Guttate psoriasis diameter, usually on the trunk in children and young
adults after streptococcal pharyngitis

Psoriasis of intertriginous areas (usually the inguinal,

gluteal, axillary, inframammary, and retroauricular folds
and the glans of the uncircumcised penis)
Inverse psoriasis
Possibly formation of cracks or fissures in the center or
edge of involved areas
Possibly absence of scales

Pitting, stippling, fraying, discoloration (oil spot sign),

and thickening of the nails, with or without separation
Nail psoriasis of the nail plate (onycholysis)
May resemble a fungal nail infection
Affects 30–50% of patients with other forms of psoriasis

Palmoplantar Hyperkeratotic, discrete plaques on palms and/or soles

psoriasis that tend to become confluent

Gradual appearance of discrete, erythematous papules

or plaques covered with thick, silvery, shiny scales
Plaque psoriasis
Lesions that remit and recur spontaneously or with
appearance and resolution of triggers

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ETIOLOGY
1.. Environmental Factors
- cold, trauma,
- infections (eg, streptococcal, staphylococcal, human immunodeficiency
virus),
- Alcohol, and drugs (eg, iodides, steroid withdrawal, aspirin, lithium, beta-
blockers, chloroquine, ACE inhibitors, indomethacin, terbinafine, and
interferon-alfa))

2.. Genetic Factors

- Psoriasis is associated with certain human leukocyte antigen (HLA) alleles,
the strongest being human leukocyte antigen Cw6 (HLA-Cw6).
- In some families, psoriasis is an autosomal dominant trait.

SIGNS AND SYMPTOMS

• Worsening of a long-term erythematous scaly area
• Sudden onset of many small areas of scaly redness
• Pain
• Pruritus (especially in eruptive, guttate psoriasis)
• Afebrile (except in pustular or erythrodermic psoriasis in which the patient
may have high fever)
• Long-term rash with recent presentation of joint pain

Diagnosis
Laboratory Studies
• Test result for rheumatoid factor (RF) is negative.
• Uric acid level may be elevated in psoriasis (especially in pustular
psoriasis), causing confusion with gout in psoriatic arthritis.
• Fluid from pustules is sterile with neutrophilic infiltrate.
• Perform fungal studies. – to choose topical steroids
Biopsy of the skin lesion may reveal basal cell hyperplasia, proliferation of
subepidermal vasculature, absence of normal cell maturation, and keratinization.
Radiographs of affected joints can be helpful in differentiating types of arthritis. Joint
x-rays can facilitate the diagnosis of psoriatic arthritis.
Auspitz sign-small droplets of blood appear within a few seconds from exposed
vessels in the dermal papillae; this is known as the

32