Arthritis And Gout

Question 1

Acetaminophen

Answer 1

May be used CAUTIOUSLY in pregnant women.

It is an antipyretic and analgesics WITHOUT anti inflammatory effects.

May be used for arthritis PAIN.

Actions:
Acetaminophen acts directly on the thermoregulatory cells in the hypothalamus to cause sweating and vasodilation; this in turn causes the release of heat and lowers fever. The mechanism of action related to the analgesic effects of acetaminophen has not been identified.

Question 2

Biological response modifiers. used for RA only!

Answer 2

Tumor necrosis factor is a locally released cytokine that can cause the death of tumor cells and stimulate a wide range of proinflammatory activities. This destroys tissues. Biological response modifiers block the action of TNF, and slow down swelling and joint damage. They are used for RA (NOT OA).

Medications: (mostly end in -mab)

1. Etanercept (enbrel)
2. Infiximab (remicade)
3. Adalimumab (humira)

Question 3

NSAIDs

Answer 3

Nonsteroidal antiinflammatory drugs (NSAIDs) provide strong antiinflammatory and analgesic effects without the adverse effects associated with the corticosteroids.

NSAIDs can cause pernicious anemia (low B12)

Action:
The antiinflammatory, analgesic, and antipyretic effects of the NSAIDs are largely related to inhibition of prostaglandin synthesis. The NSAIDs block two enzymes, known as COX-1 and COX-2. COX-1 is present in all tissues and seems to be involved in many body functions, including blood clotting, protecting the stomach lining, and maintaining sodium and water balance in the kidney. COX-1 turns arachidonic acid into prostaglandins as needed in a variety of tissues. COX-2 is active at sites of trauma or injury when more prostaglandins are needed, but it does not seem to be involved in the other tissue functions. By interfering with this part of the inflammatory reaction, NSAIDs block inflammation before all of the signs and symptoms can develop. Most NSAIDs, which block both COX-1 and COX-2, also block various other functions of the prostaglandins, including protection of the stomach lining, regulation of blood clotting, and water and salt balance in the kidney. The COX-2 inhibitors are thought to act only at sites of trauma and injury to more specifically block the inflammatory reaction.

Question 4

Osteoarthritis

Answer 4

Increasing age = degenerative joints, like your knees, hips, fingers, etc

When OA is found in a joint, there is usually a history of injury or unusual stress in that joint.

Symptoms:
1.Stiffness with pain starts after awakening and lasts less than 30 minutes, and pain decreases when movement is increased.

patient may have decreased range of motion

you may be able to palpate bony nodes in joints, and joints become tender and enlarged.

MEDICATION:

1. Non-opioid analgesics-
   - Acetylsalicylic acid (an NSAID)
   - Ibuprofen (an NSAID)

!!!It makes sense that NSAIDs are used… they reduce swelling!!!!

Question 5

DMARDs

Answer 5

Disease-modifying antirheumatic drugs:
They reduce joint destruction, and retards disease progression. Many rheumatologists are selecting DMARDs early in the diagnosis, before damage to the joints has occurred, because they alter the course of the inflammatory process. These drugs alter the disease process by altering the patient’s immune response to slow or block inflammation and damage that occurs with chronic inflammatory states.

Medication:

1. Methotrexate. In this case, folic acid/leucovorin is NOT needed to replace folic acid.
2. Hydroxychloroquine (which is very damaging to your liver)

Question 6

Glucocorticoids (for arthritis)

Answer 6

Glucocorticoids are hormones produced by the adrenal gland… the major one being cortisol. They have powerful anti-inflammatory properties. They increase protein breakdown and decrease protein formation, as well as cause lipogenesis (fat storage). These are important effects! They also can cause fungal infections of the fat pads.

Action:
Glucocorticoids enter target cells and bind to cytoplasmic receptors, initiating many complex reactions that are responsible for antiinflammatory and immunosuppressive effects.

Medications: (end in -one)

1. Dexamethasone
2. Prednisone
3. Methylprednisolone
4. Cortisone

The problems with taking drugs in this category:

1. CNS: vertigo, headaches, insomnia, paresthesia (pins and needles).
2. GI: nausea, vomiting, ulcers, weight gain (remember that cortisol stores FAT)
3. Cardiovascular: among many things, hypotension, arrhythmia, and fluid retention.
4. Loss of muscle mass, etc (remember cortisol breaks down protein and decreases protein formation aka muscle).
5. Immunosuppression, impaired wound healing.

There is much more in book!

Question 7

Rheumatoid arthritis

Answer 7

RA is an autoimmune connective tissue disease, and affects organs, blood, lungs, and heart.

Inflammation of the synovium/joint lining causes pain, stiffness, SWELLING, warmth, and erythema (superficial reddening of the skin).

Exacerbation of RA means it is active… remission of RA means there is little to no activity.

Pathophysiology: RA is a chronic, systemic autoimmune disease. Patients have a high level of rheumatoid factor (RF) and an antibody to immunoglobulin (IgG). Together they form an immune complex and deposits in the synovial fluid and causes swelling, then what happens is…

1. Phagocytosis producing enzymes are releases into the joint, destroying the tissues.
2. More swelling happens d/t the tissue damage. Edema, proliferation of the synovial membrane, and pannus (scar tissue) forms.
3. Cartilage destruction and erosion of bone.
4. This process results in the loss of articular surfaces, muscle fiber degeneration, and loss of muscle contraction and elasticity.

Signs and Symptoms:

1. Usually a symmetrical pattern of of inflammation (remember that osteoarthritis happens in specific joints… RA is a systematic disease).
2. Pain and stiffness last for longer than 30 min after waking up, or after a long rest.

Medication:

1. NSAIDs- block COX-1 (enzymes that protect the stomach lining) and COX-2 (enzymes involved in inflammatory response).
2. Acetylsalicylic acid (remember it is NSAID)
3. Celecoxib (this drug is a COX-2 inhibitor. COX-2 is an enzyme involved in inflammatory response…. so if COX-2 is being inhibited, there will not be an inflammatory response. Remember that all NSAIDs are anti-inflammatory).
4. DMARDs- Methotrexate
5. Biological response modifiers

Question 8

Gout

Answer 8

Gout is caused by monosodium crystal deposits. It is a defect of purine (compound found in meat, seafood, and organ meat) metabolism which results in hyperuricemia (high uric acid). This could be due to an OVERSECRETION of uric acid, or decreased EXCRETION of uric acid secondary to renal defects.

An acute attack may be triggered by trauma, alcohol, dieting, certain medications, surgical stress, or illness.

Gout is extremely painful, causing redness, swelling, and warmth of the affected joint. Over time with repeated attacks, the crystals form a Tophi (big lump on articular tissue, osseous soft tissue, and cartilage… ex big toe, hands, ears etc). Some other effects it can have is gouty neuropathy, renal impairment, and uric acid calculi (aka kidney stones).

Clinical Manifestations of gout:

1. Early attack’s subside in 3-10 days (even w/o treatment)
2. Symptom free until next attack.
3. Over time the frequency of attacks increase, last longer, and involve more joints.
4. The higher the serum uric acid, the more extensive the tophi.

Primary reasons:

1. Severe dieting or starvation.
2. Excessive intake of food high in purine (shellfish and organ meats).
3. Hereditary

Secondary reasons:

1. Leukemia
2. Multiple myeloma
3. Anemia
4. Psoriasis

Medications:

1. Colchicine- can PREVENT and treat ACUTE attacks by lowering deposition of uric acid and reduces inflammation, pain, and swelling. Prolonged use may decrease vitamin B12 absorption and cause GI upset. (side note, B12 is found in dairy products, Eggs, fortified cereals, meat, poultry, and seafood).
2. Allopurinol- for CHRONIC gout. Xanthine oxidase inhibitor decreases uric acid levels by interrupting breakdown of purines before uric acid is formed. May cause GI upset or bone marrow depression.
3. Probenecid- blocks renal uptake of uric acid, corrects hyperuricemia, and dissolves deposited urate. A side effect is kidney stones.

Vitamin b12 is also called cobolamin