Lo 1 Nsaid

Learning Objects 1
NONSTEROIDAL ANTI-
INFLAMMATORY DRUGS (NSAID)
By: Batara, Fera, Suharso dan Sri
A. UNDERSTANDING
Non-steroidal anti-inflammatory drugs (AINs) are pharmacologically active non-homogeneous agents that
primarily work to inhibit prostaglandin production and are used for the treatment of acute and chronic pain with the
properties of reducing pain, fever with inflammation, and accompanied by other pain inflammatory disorders . These drugs
mainly work by inhibiting cyclo-oxygenase enzymes but not for lipoxygenase enzymes. NSAIDs are the most widely
available prescription especially in cases of inflammatory pain due to their strong effect in treating mild to moderate
inflammatory pain. In the preparation of NSAIDs, the most important is the consideration of therapeutic effects and side
effects associated with the mechanism of action of this drug preparation, especially in children. Where NSAIDs can occur in
the most important body organ such as the gastrointestinal tract, heart and kidneys.
AINS effectively reduces pain with mild to moderate intensity as in dental pain. For more severe pain, non-
dependent analgesics are needed, such as tramadol. NSAIDs have an analgesic effect on pain originating from non-viscous
integitors, such as headaches, myalgia and abralgia. Some NSAIDs are generally anti-inflammatory, analgesic, and
antipyretic. For example, ketoprofen, ibuprofen, naproksen, indometason, diclofenac, and others. Its antipyretic effect is only
seen at larger doses than its analgesic effect, and NSAIDs are relatively more toxic than classical antipyretics, so they are
only used for the treatment of joint inflammatory diseases such as rheumatoid arthritis, osteoarthritis, ankylosing spondylitis
and gout. Individual responses to NSAIDs can be highly variable even though they belong to the same chemical derivatives.
So failure with drugs can be tried with similar drugs from the same chemical derivatives.
B. THE PAIN AND ITS MANAGEMENT
Pain is a complex, universal, and individual sensation. It is said to be individual because the individual response
to pain is different. Simply put, pain can be interpreted as an unpleasant sensation both sensorially and emotionally related to
the existence of tissue damage or other factors, so that the individual feel tortured, suffered and finally the daily activities and
psychic disturbed.
Five classifications and types of pain:
1. Acute pain (mild, moderate, severe)
2. Chronic pain
3. Superficial pain
4. Somatic pain (bone, skeletal muscle, and joints)
5. Visceral pain or internal pain
Medications used to treat mild pain to moderate pain using nonnarkotic analgesics. These
drugs are effective for dull pain in headache, dysmenorrhea (menstrual pain), pain in
inflammation, minor abrasion, muscle pain, and mild to moderate athritis.
No Type of pain Definition

1 Acute pain Pain occurs suddenly and there is a response
in treatment.
2 Chronic pain Pain lasts for 6 months and is difficult to treat

or control.
3 Superficial pain Pain in surface areas such as skin, and mucous

membranes.
4 Visceral pain (deep pain) Pain from smooth muscles and organs.
5 Somatic pain Pain from skeletal muscle, ligaments, and

joints.
C. WORK MECHANISM NSAIDs
NSAIDs are believed to work inhibiting prostaglandin synthesis and inhibiting cellular
responses during inflammation. Most NSAIDs work on peripheral nerve receptors to reduce
transmission and pain relief.
Much of the workings of NSAIDs are based on the constraints of prostaglandin
synthesis, where both types of cyclo-oxygenase are blocked. The cyclo-oxygenase enzyme is
present in 2 isoforms called COX-1 and COX-2. COX-1 is essential in the maintenance of
various functions under normal conditions in various tissues especially the kidneys,
gastrointestinal tract, and platelets. In the gastric mucosa, activation of COX-1 produces
cytoprotective prostacyclin. Cyclooxygenase-2 is induced by various inflammatory stimuli,
including cytokines, endotoxins, growth factors. Thromboaksan A2, which is synthesized
platelets by COX-1 causes platelet aggregation, vasoconstriction and smooth muscle
proliferation. In contrast prostacyclin (PGI2) synthesized by KOKS-2 in the macrovascular
endothelium counteracts these effects and causes inhibition of platelet aggregation, vasodilation,
and anti-proliferative effects.
Ideal NSAIDs should inhibit COX-2 (inflammation) and do not inhibit COX-1 (for
gastric mucosal protection), but in fact inhibit COX-1 and COX-2. NSAIDs also inhibit lypo-
oxygenase (leukotriene formation). Although it has been intensively pursued since the late 1980s,
until now the ideal drug has not been found. Ideal drugs Today there are only three drugs with
somewhat selective work, meaning they are stronger to inhibit COX-2 than COX-1, ie COX-2
inhibitors of nabumeton and meloxicam. The celecoxib drug (Celebrex, 1999) is claimed to not
inhibit COX-1 altogether at the usual dose, but its clinical effects on the safety of the gastric
mucosa have not been ascertained.
Aspirin is 166 times more potent inhibiting COX-1 than COX-2. COX-2 inhibitors
were developed in the search for COX inhibitors for the treatment of inflammation and less pain
causing gastrointestinal toxicity and bleeding. Non-selective non-selective non-steroidal
inflammation is called traditional AINS (AINSt).
Here's a chart of Prostaglandin Biosynthesis:
D. SIDE EFFECTS OF NSAIDs
a. Effects on Respiration: Salicylates stimulate breathing either directly or indirectly. In doses of

salicylate therapy increases oxygen consumption and CO2 production. Salicylates reach the medulla,
stimulating the direct respiratory center resulting in deep and rapid breathing hyperventilation.
b. Effects Against Acid-Base Balance. : In high therapeutic doses, salicylates lead to increased
oxygen consumption and CO2 production especially in skeletal muscle due to stimulation of oxidative
phosphorylation. Bicarbonate excretion accompanied by Na + and K + through the kidney increases, so the
bicarbonate in plasma decreases and the blood pH returns to normal. This condition is called a respiratory
alkalosis that is compensated, and is found in adults. The worse usually occurs in children and infants who
receive toxic doses.
c. Uricosuric Effect: This effect is determined by the amount of dose. Small doses (1g or 2g daily)
inhibit uric acid excretion, so uric acid levels in the blood increase. A dose of 2 or 3 g daily usually does not
alter the excretion of uric acid. Dosage of more than 5 g per day increased urinary acid excretion through
urine, so the acid level in the blood decreased. Uricosuric effects increase when urine is alkaline.
d. Effects on Blood: In healthy people aspirin causes an extension of the bleeding period. A single
dose of 650 mg of aspirin may extend the bleeding period by approximately 2-fold. Small doses of aspirin are
used for the prophylaxis of coronary and cerebral thrombosis. Aspirin should not be given to patients with
severe liver damage, hypoprothrombinema, vitamin K deficiency and hemophilia, because it can cause
bleeding.
e. Effects on the Heart and Kidney: Salicylates are hepatotoxic. Growings that are often seen only
increase in SGOT and SGPT, indicate hepatomegaly, anorexia, nausea and jaundice. If aspirin jaundice
occurs, it should be discontinued because of fatal liver necrosis. Salicylates may decrease renal function in
patients with hypovolemia or heart failure.
f. Farmokokinetik: On oral administration, some salicylates are absorbed rapidly in intact form in
the stomach, but mostly in the upper intestine. The rate of absorption depends on the speed of disintegration
and dissolution of the tablet, the pH of the mucosal surface and the time of gastric emptying. While rectal
administration is slower and imperfect. Salicylic acid is absorbed rapidly from healthy skin, but toxicity can
occur on a large spread of skin. The aspirin is absorbed intact, hydrolyzed to salicylic acid primarily in the
liver, so only about 30 minutes is present in the plasma. Salicylated biotranformation occurs in microsomes
and mitochondrial liver. Salicylates are secreted in the form of their metabolites through the kidneys, sweat,
and bile.
g. Antipyretic Indications. : Salicylic dose for adult is 325 mg - 650 mg every 3 or 4 hours.
Children 15-20 mg / kgBW given every 4-6 hours with a total dose not exceeding 3.6 g per day.
h. Analgesics: Salicylates are useful for treating non-specific pain such as headache, joint pain,
menstrual pain, neuralgia and myalgia.
i. Acute Rheumatic Fever: Dose for adult 5-8 g per day, given 1 g per time. For children 100-125
mg / kgBW / day, given every 4-6 hours, after which it is reduced to 60 mg / kgBW / day.
j. Rheumatoid arthritis: Salicylates are still considered standard drugs in comparative studies with
other antireumatic drugs. Rheumatoid arthritis can be controlled with salicylate alone. The dose is 4-6 g / day,
but a dose of 3 g daily is sometimes quite satisfactory.
k. Other Uses: Aspirin is used to prevent coronary thrombus and deep-vein thrombus based on the
inhibitory effect of platelet aggregation.
l. Intoxication: Salicylates are often used to treat all mild and insignificant complaints so that
many are misused. Salicylic poisoning causes death, generally salicylate disorder is mild.

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Learning Objects 1

No Type of pain Definition

2 Chronic pain Pain lasts for 6 months and is difficult to treat

3 Superficial pain Pain in surface areas such as skin, and mucous

5 Somatic pain Pain from skeletal muscle, ligaments, and

a. Effects on Respiration: Salicylates stimulate breathing either directly or indirectly. In doses of

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