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Analgetik anti inflamasi

Perjalanan
Nyeri
Biological effects.
The individual PG (PGE, PGF, PGI = prostacyclin) possess different
biological effects.

1) Nociceptors.
PG increase sensitivity of sensory nerve fibers towards ordinarypain
stimuli (p. 194), i.e., at a given stimulus strength there is an increased
rate of evoked action potentials.

2)Thermoregulation.
PG raise the set point of hypothalamic (preoptic) thermoregulatory
neurons; body temperature increases (fever).

3)Vascular smooth muscle.


PGE2 and PGI2 produce arteriolar vasodilation; PGF2α,
venoconstriction.

4)Gastric secretion.
PG promote the production of gastric mucus and reduce the formation
of gastric acid.
5) Menstruation.
PGF2α is believed to be responsible for the ischemic necrosis of
the endometrium preceding menstruation. The relative proportions of
individual PG are said to be altered in dysmenorrhea and excessive
menstrual
bleeding.

6)Uterine muscle.
PG stimulate labor contractions.

7)Bronchial muscle.
PGE2 and PGI2 induce bronchodilation; PGF2α causes constriction.

8)Renal blood flow. When renal blood flow is lowered, vasodilating


PG are released that act to restore blood flow
INHIBITION OF PROSTAGLANDIN BIOSYNTHESIS BY
NSAIDS

• The first enzyme in the prostaglandin synthetic pathway is prostaglandin G/H


synthase, also known as COX. This enzyme converts arachidonic acid (AA) to the
unstable intermediates PGG2 and PGH2 and leads to he production of thromboxane
A2 (TXA2) and a variety of prostaglandins (see Chapter 25). Therapeutic doses of
aspirin and other NSAIDs reduce prostaglandin biosynthesis by blocking COX, and
there is a reasonably good correlation between potency as COX inhibitors and
antiinflammatory activity. There are two forms of COX, COX-1 and COX-2. COX-1 is
a primarily constitutive isoform found in most normal cells and tissues, while
cytokines and inflammatory mediators that accompany inflammation induce COX-2
production. However, COX-2 also is constitutively expressed in certain areas of
kidney and brain, and is induced in endothelial cells by laminar shear forces.
Importantly, COX-1, but not COX-2, is expressed as the dominant, constitutive
isoform in gastric epithelial cells and is the major source of cytoprotective
prostaglandin formation. Inhibition of COX-1 at this site is thought to account largely
for the gastric adverse events that complicate therapy with tNSAIDs, thus providing
the rationale for the development of NSAIDs specific for inhibition of COX-2.
Enzim COX
NSAID
Golongan Contoh
Salisilat Aspirin , diflunisal
Derivat para amino fenol Paracetamol
Derivat asam asetat Indometasin, sulindak,
etodolac,

Fenamat (N-antranilat) Asam mefenamat,


meclofenamat , ketorolac,
diklofenak

Derivat asam propionat Ibuprofen, naproxen,


fenoprofen, ketoprofen

Derivat asam enolic Piroxicam, meloxicam


COX2 selective Celecoxib, valdecoxib,
parecoxib, etoricoxib
OPIOT
• Bekerja pada reseptor opiat di SSP ---- reseptor yang memodulasi
transmisi nyeri----- << persepsi nyeri dg cara menghambat nyeri pada
berbagai tingkat, terutama di otak tengah dan medulla spinalis
Terikatnya opiot pada reseptor – pengurangan masuknya ion Ca2+ ke dalam
sel --- hiperpolarisasi-- << ion Ca sel--- penurunan dopamin, seotonin,
peptida penghantar nyeri (substance p)--- rangsang nyeri terhambat

• Reseptor opiat ada 3 :


A. Reseptor μ (mu) : Berperan dalam Analgesia supraspinal, Depresi
respirasi, Euforia, Ketergantungan
B. Reseptor κ (kappa) : Berperan dalam analgesia spinal, miosis, sedasi
C. Reseptor δ (delta) : disforia, halusinasi, stimulasi pusat vasomotor
GOLONGAN OPIOT
GOLONGAN OPIOT
Minikuis
• 1. sebutkan mekanisme NSAID
• 2. sebutkan mekanisme Steroid
• 3. penghambatan COx1 bertanggungjawab pada….
• 4. penghamabatan COX2 bertanggungjawab pada …
• 5. contoh NSAID non selektif (min 5)
• 6. contoh NSAID selektif COX 2 (min 2)
• 7. sebutkan Efek samping NSAID !
• 8. contoh obat steroid (min 3)
• 9. contoh obat turunan asam propionat
• 10. contoh obat turunan N-antranilat

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