Pharm Arthritis And Gout Part 1

Hydroxychloroquine is an antimalarial drug that is also used in the treatment of rheumatoid arthritis. It is known to reduce inflammation and pain in patients with rheumatoid arthritis. Additionally, hydroxychloroquine has been found to have immunomodulatory effects, meaning it can help regulate the immune system, which is beneficial in treating rheumatoid arthritis. Therefore, hydroxychloroquine is a suitable choice for a drug that can be used in the treatment of both malaria and rheumatoid arthritis.

Aspirin is an irreversible inhibitor of cyclooxygenase, which means it permanently inactivates the enzyme. Cyclooxygenase is responsible for the production of prostaglandins, which are involved in inflammation, pain, and fever. By inhibiting cyclooxygenase, aspirin reduces the production of prostaglandins, thereby reducing inflammation, pain, and fever. Other drugs listed are not irreversible inhibitors of cyclooxygenase.

Allopurinol is the correct answer because it is a medication that reduces the production of uric acid in the body. It inhibits the enzyme xanthine oxidase, which is responsible for the conversion of hypoxanthine to xanthine and then to uric acid. By reducing uric acid levels in both the blood and urine, allopurinol helps prevent the formation of urate crystals, which can cause gout and kidney stones.

Colchicine is the correct answer because it is an inhibitor of cell mitosis, making it useful in treating gouty attacks. It works by preventing the division of cells, particularly in the inflammatory response associated with gout. This helps to reduce the inflammation and pain caused by the condition.

Celecoxib is a selective inhibitor of cyclooxygenase 2. This means that it specifically targets and inhibits the action of cyclooxygenase 2 enzymes, which are responsible for producing inflammatory substances called prostaglandins. By inhibiting cyclooxygenase 2, celecoxib helps to reduce inflammation and relieve pain. It is commonly used to treat conditions such as arthritis, as well as acute pain and menstrual cramps.

Auranofin is a gold compound that is used in the treatment of rheumatoid arthritis. It is classified as a disease-modifying antirheumatic drug (DMARD) and works by reducing inflammation and suppressing the immune system. Auranofin is often used when other treatments have not been effective in managing the symptoms of rheumatoid arthritis. It is taken orally and has been shown to improve joint pain, swelling, and stiffness in patients with this condition.

The symptoms and signs of the patient suggest that she was affected by aspirin
hypersensitivity, a syndrome that can occur in 20-25% of middle-aged patients with asthma,
chronic urticaria or nasal polyps, like in the present case. The reaction does not appear to be
immunological in nature (it seems a pseudoallergic reaction). The mechanism is not known but
is likely to be related to the formation of increased amount of leukotrienes and other products of
lipoxygenase pathway, due to inhibition of cyclooxygenase pathway. Patients with this
syndrome experience a high degree of cross-sensitivity to other NSAIDs, which support the
conclusion that this reaction represents an abnormal response to a common pharmacological
action.
A, B, D, E) (see explanation above)

The pain occurring during menses is thought to result from uterine contractions and ischemia,
likely mediated by prostaglandins produced in the secretory endometrium. Contributing factors
may include an extremely tight cervical os because of thermocautery or conization, like in the
present case. Pain occurs when the uterus attempt to expel tissue through the cervical os. The
analgesic effects of NSAIDs in case of dysmenorrhea is due to the inhibition of prostaglandin biosynthesis in the endometrium.
A) NSAIDs do not act on prostaglandin receptors.
C) Even if a central action (inhibition of prostaglandins biosynthesis in the hypothalamus) may
contribute to the analgesic effect of NSAIDs, the effect is mainly peripheral. Acetaminophen is
the only analgesic-antipyretic drug whose analgesic effect is thought to be mediated by the
inhibition of prostaglandins biosynthesis in the hypothalamus.
D) Pelvic inflammatory disease may cause diffuse, continuous, low abdominal pain. In the
present case however the pain is present only during menses, so a pelvic inflammatory disease
is unlikely.
E) Leukotrienes can increase nociceptive nerve ending sensitivity, but NSAIDs do not affect
leukotrienes synthesis.

Azathioprine is an immunosuppressant drug commonly used in the treatment of rheumatoid arthritis. It works by suppressing the immune system, reducing inflammation and preventing joint damage. This drug is often prescribed when other medications have not been effective in managing the symptoms of rheumatoid arthritis. Azathioprine can help to reduce pain, swelling, and stiffness in the joints, improving overall quality of life for individuals with this condition. It is important to note that this medication can have side effects and should be used under the guidance of a healthcare professional.

By blocking cyclooxygenase pathway, NSAIDs inhibit the biosynthesis of prostaglandins
(including prostacyclin which is PGI2) and thromboxanes. They have negligible effect on
lipoxygenase pathway or on bradykinin biosynthesis..
A, B, D, E) (see explanation above)

Aspirin is the only NSAID that is able to acetylate the enzyme cyclooxygenase (the acetyl
moiety is bound covalently to the enzyme) and therefore the inhibition of the enzyme is
irreversible.
B, C, D, E) Aspirin does not cause these effects.

Toxic doses of salicylates cause a direct depression of the respiratory center in the medulla.
Nausea and vomiting are common symptoms of salicylate toxicity. These symptoms are due in
part to gastric irritation, but mainly to the stimulation of the chemoreceptor trigger zone.

Renal elimination of methotrexate involves active tubular secretion of the drug by the system
that handles organic acids. Weak organic acids like salicylates can compete with methotrexate for
secretion so delaying the elimination of the drug, which can result in severe myelosuppression.
B, C, D, E) All these disorders are in fact indication, not contraindication, to salicylate therapy.

The antiinflammatory effect of NSAIDs is mediated by the inhibition of cyclooxygenase, the
enzyme that catalyzes the synthesis of prostaglandins which are known inflammatory
mediators.
Two different isoforms of cyclooxygenase have been found, cyclooxygenase 1 (COX-1) and
cyclooxygenase 2 (COX-2). Whereas COX-1 is expressed in most tissue of the body,
inflammatory mediators like cytokines upregulate COX-2 expression, leading to high level of
COX-2 in inflamed tissues. Most NSAIDs inhibit both isoforms of the enzyme, but their
antiinflammatory activity is most likely mediated mainly by the inhibition of COX-2.
B) (see explanation above)
A, C, D, F) NSAIDs do not inhibit these enzymes.

Ibuprofen is a non-steroidal antiinflammatory drug (NSAID) of the propionic acid derivative
class. All NSAIDs inhibit prostaglandin biosynthesis by blocking cyclooxygenase both in the
peripheral tissues and In the CNS. The release of prostaglandins (PGE1, PGE2) in the
hypothalamus seems the ultimate factor which adjusts the hypothalamic thermoregulatory
mechanism to maintain body temperature at higher than normal level. By inhibiting
prostaglandin synthesis NSAIDs promote the return of the hypothalamic thermostat to the
normal set point.
A, B, C) All these action can lead to an antipyretic effect but NSAIDs do not have these
actions.
E) The inhibition of cyclooxygenase in peripheral tissues can lead to an antiinflammatory effect
which can reduce fever. However the main mechanism of the antipyretic effect of NSAIDs is
central rather than peripheral.

The lab values indicate that the acid-base disturbance was respiratory alkalosis, which is an
effect of high therapeutic doses of salicylates. These drugs stimulate the respiration both
directly (by a direct effect on the respiratory center in the medulla) and indirectly (by increased
production of CO2 due to increased oxygen consumption). Compensation is achieved by
increased renal excretion of
bicarbonate. Unless toxic doses are given this stage seldom proceed further.
A, C, D, E) (see explanation above)

Salicylic acid is one of the few drugs (other examples include phenytoin and ethanol) that follow
a zero order elimination kinetics. Because of this the clearance and the half life of the drug are
not constant but depend upon the dose.

Mesalamine is a salicylate derivative that is primarily used in the treatment of inflammatory bowel disease. It works by reducing inflammation in the digestive tract, which helps to relieve symptoms such as abdominal pain, diarrhea, and rectal bleeding. This medication is commonly prescribed for conditions such as ulcerative colitis and Crohn's disease.

Gold compounds like auranofin concentrate in synovial membranes, kidney, liver, spleen and
bone marrow. Therefore the total body half life of these compounds is exceedingly long. The
epithelial cells of the renal tubule, which have a particular affinity for gold, show its presence
many year after therapy has ceased. Because of this there is no correlation between gold
plasma levels and either therapeutic effect or toxicity.
A, B, C, E, F) (see explanation above)

Potency refers to the dose needed to obtain a given effect. The lower the dose needed the
higher the potency of the drug. NSAIDs differ widely in their potency. For example, about the
same antiinflammatory effect can be obtained with 10 mg of piroxicam or 500 mg of aspirin.
NSAIDs can counteract the vasodilation, increased vascular permeability and oedema that
characterize the early phase of the inflammatory reaction. They have only limited effects on
cellular accumulation either in acute or chronic inflammation, an have negligible effects on the B) By inhibiting prostaglandin biosynthesis NSAIDs promote the return of the hypothalamic
thermostat to the normal set point. Therefore they can reduce fever due to an excessive
stimulation of the hypothalamic thermostat, but they cannot reduce hyperthermia due to
hypothalamic damage or malfunction (e.g. heat stroke).
C) NSAIDs can reduce pain due to inflamed tissues (arthritis, etc.), surgery, dysmenorrhea,
bone metastases, toothache, headache, but their analgesic effect is low (or even absent) in
severe ischemic and visceral pain.
D) NSAIDS are indicated, not contraindicated, in case of thromboembolic disorders, since they
decrease platelet aggregation.
F) NSAIDs block prostaglandin biosynthesis, but have no effect on prostaglandin receptors