Musculoskeletal Gout / Lupus (Exam 4) Flashcards

1
Q

Gout

A

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)

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2
Q

Gout: Pathogenesis

A

Uric acid Crystal deposits in tissues

Crystals form from breakdown of purines. Body makes purine

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3
Q

Purine Food (Gout)

A

Organ meats, shellfish, anchovies, herring, asparagus, mushrooms

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4
Q

Normal Uric acid is

A

Dissolved in the blood and excreted by the kidneys

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5
Q

Hyperuricemia is caused by

A

Overproduction of uric acid and under secretion of uric acid

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6
Q

Gout Risk Factors

A

Obesity
African American
Men
Pre Existing diseases
Consuming ETOH
Diet rich in meat and seafood
Use of diuretics

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7
Q

Phase of Gout

Phase: 1
Phase: 2
Phase: 3
Phase: 4

A

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

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8
Q

Gout: Clinical Manifestations

A

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

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9
Q

Gout Complications

A

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)

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10
Q

Gout Pharm Goal

A

Decrease symptoms of an acute attack and prevent recurrent attacks

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11
Q

First line treatment for GOUT

A

NSAIDS
allopurinol
colchicine
probenecid

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12
Q

Systemic Lupus Erythematosus

A

SLE Lupus

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13
Q

Lupus Pathogenesis

A

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

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14
Q

Most common antibody in lupus

A

ANA: Antinuclear Antibody

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15
Q

Most common area of SLE Immune complexes

A

Kidney

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16
Q

Lupus Risk Factors

A

Genetics

Females

20-40

Blacks

Environmental Triggers

Allergy to antibiotics

Hormonal Factors (Oral birth control)

Smoking

17
Q

Lupus Manifestations

A

EXTREME fatigue

Photosensitivity

Butterfly Rash

Unusual Hair Loss

Edema

Raynaud’s

18
Q

Lupus: more clinical manifestations

A

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)

19
Q

SLE: Clinical Course

A

Exacerbations and remissions.

A flare is an acute exacerbation of symptoms

20
Q

Warning signs of a lupus flare

A

Fatigue
Pain
Headache

21
Q

SLE Flares: Prevention

A

Recognize warning signs and avoid triggers

22
Q

SLE: Triggers

A

Sunlight exposure

Infections

Abruptly stopping medications

Stress

23
Q

SLE: Pharmacotherapy

A

Depends on what is involved

24
Q

SLE Pharm: H/A - msk - pleuritis - pericarditis

25
Q

SLE Pharm: Kidney dz and CNS

A

High dose corticosteroids

26
Q

SLE Pharm: Arthritis

A

Low dose corticosteroids

27
Q

SLE Pharm: Severe Organ Involvement

A

Methotrexate

(immunosuppressive)