Musculoskeletal Gout / Lupus (Exam 4) Flashcards
Gout
An inflammatory disease resulting from deposits of uric acid crystals in tissues and fluids within the body
The disease of KINGS (From eating wealthy people food)
Gout: Pathogenesis
Uric acid Crystal deposits in tissues
Crystals form from breakdown of purines. Body makes purine
Purine Food (Gout)
Organ meats, shellfish, anchovies, herring, asparagus, mushrooms
Normal Uric acid is
Dissolved in the blood and excreted by the kidneys
Hyperuricemia is caused by
Overproduction of uric acid and under secretion of uric acid
Gout Risk Factors
Obesity
African American
Men
Pre Existing diseases
Consuming ETOH
Diet rich in meat and seafood
Use of diuretics
Phase of Gout
Phase: 1
Phase: 2
Phase: 3
Phase: 4
1: Asymptomatic but with elevated serum uric acid levels and deposits in tissues
-Crystals accumulate and tissues is damaged
-Acute inflammation occurs
2: Acute flares or attacks – Hyperuricemia
3: Clinically inactive until next flare – continued hyperuricemia
-May be months or years before the next flare. Later, recurring attacks get closer and closer together
4: Chronic arthritis- joint pain and symptoms present most of the time
Gout: Clinical Manifestations
PAIN
-May be mild or excruciating
-Usually the lower extremities (Feet and big toe)
Burning
Redness
Swelling and warmth
Fever
Symptoms present for days to weeks
Gout Complications
Tophi: Large HARD nodules composed of uric acid crystals deposited in soft tissues
-May form below the skin around the joints
-Can cause a local inflammatory response
-May drain CHALKY MATERIAL
Renal Calculi (Kidney Stones)
Gout Pharm Goal
Decrease symptoms of an acute attack and prevent recurrent attacks
First line treatment for GOUT
NSAIDS
allopurinol
colchicine
probenecid
Systemic Lupus Erythematosus
SLE Lupus
Lupus Pathogenesis
Autoimmune condition
B-lymphocytes are hyperactive and produce autoantibodies.
Autoanitbodies attack our DNA on any or all of our major organ systems
The inflammatory response destroys tissues
Most common antibody in lupus
ANA: Antinuclear Antibody
Most common area of SLE Immune complexes
Kidney
Lupus Risk Factors
Genetics
Females
20-40
Blacks
Environmental Triggers
Allergy to antibiotics
Hormonal Factors (Oral birth control)
Smoking
Lupus Manifestations
EXTREME fatigue
Photosensitivity
Butterfly Rash
Unusual Hair Loss
Edema
Raynaud’s
Lupus: more clinical manifestations
Brain (Seizures HA Stoke)
Lungs (Pleuritis / Effusions)
Heart (Myocarditis / Endocarditis)
Kidneys (Nephritis)
Blood vessels (Vasculitis)
Blood (Anemia)
Joint (Arthtitis)
(all infections or inflammation) (LUPUS infection all organ systems)
SLE: Clinical Course
Exacerbations and remissions.
A flare is an acute exacerbation of symptoms
Warning signs of a lupus flare
Fatigue
Pain
Headache
SLE Flares: Prevention
Recognize warning signs and avoid triggers
SLE: Triggers
Sunlight exposure
Infections
Abruptly stopping medications
Stress
SLE: Pharmacotherapy
Depends on what is involved
SLE Pharm: H/A - msk - pleuritis - pericarditis
NSAIDS
SLE Pharm: Kidney dz and CNS
High dose corticosteroids
SLE Pharm: Arthritis
Low dose corticosteroids
SLE Pharm: Severe Organ Involvement
Methotrexate
(immunosuppressive)