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Autocoids and Autocoid Antagonists
Autocoids and Autocoid Antagonist

Additional Pharmacology Flashcards




What are autacoids?

Autacoids are a group of compounds such as prostaglandins, histamine, and serotonin that are heterogeneous substances which have widely differing structures and pharmacologic activities. They are called autacoids meaning they are formed by the tissues on which they act, from Greek autos (self) and akos (remedy). Autacoids differ from other circulating hormones because they are produced by many tissues rather than specific endocrine glands.

Briefly describe the use of prostaglandins (PG) in the treatment of pulmonary hypertension, peptic ulcer disease and as abortifacients.

Prostaglandins are unsaturated fatty acid derivatives that act on the tissues in which they are synthesized and are rapidly metabolized to inactive products at the site of action.

Pulmonary HTN: Iloprost and Epoprostenol are examples of prostaglandins used to treat pulmonary HTN. They can both be given IV, resulting in systemic effects, or Iloprost can be given via inhalation, resulting in a more focused effect on the lungs. They both cause Beta-2 receptor stimulation, causing broncho and vasodilation by increasing cAMP.

PUD: Misoprostol can be used to treat peptic ulcer disease by inhibiting secretion of HCL and pepsin, and enhancing mucosal resistance. Useful for patients with gastric ulcers who chronically take NSAIDs

Abortifacients: Mifepristone (RU-486) is a synthetic steroid given orally with antiprogestational effects, followed within 24 hours by Misoprostol, a synthetic prostaglandin, administered vaginally. The combination of these two drugs causes first trimester abortions with over 95% success rate.

Summarize the pharmacology of histamine. Include mechanism of action and role in allergy and anaphylaxis.

Histamine, an amine, is a chemical messenger located in all tissues, which is usually released in response to various stimuli. Histamine can bind to any of the 4 histamine receptors, H1, H2, H3, and H4. H1 and H2 are widely expressed and are the targets of clinically useful drugs, while H3 and H4 receptors are in only a few cell types and are clinically unclear.


Stimulation of H1 receptors promote vasodilation and increase capillary permeability, cause an increased production of nasal and bronchial mucus, constrict bronchioles decreasing lung capacity, constrict intestinal smooth muscle causing cramps and diarrhea, and can cause itching and pain at sensory nerve endings.


Stimulation of H2 receptors increases gastric HCL secretion, and also has an effect on vasodilation and increased capillary permeability. In response to an allergic reaction, histamine is released and can either cause a local response, producing reactions on the skin or respiratory system, or a full-blown anaphylactic response systemically. It is thought that the major determinant on type of reaction, local or anaphylactic, is dependent on the rate of release of histamine. For example, if it is released slow enough to permit inactivation before entering the bloodstream, only a local response will occur. Antihistamines are aimed at blocking the receptor sites.

H1 receptor stimulation causes vascular endothelium to release nitric oxide (NO) which in turn causes vasodilation.

True or False: H-2 receptors are located in the stomach and skin?

Note: If you want to block a systemic histamine reaction (eg, allergic reaction), you would administer an H1 blocker (eg, diphenhydramine) plus an H2 blocker (eg, famotidine, ranitidine or cimetidine). The H2 blocker works in the stomach and to prevent skin flushing, the H1 blocker works everywhere else. The other histamine receptors (H3 and H4) are clinically unimportant. If on the other hand you wanted to block histamine receptors in the stomach to reduce acid production, then you would just administer and H2 blocker. If you are treating cold symptoms or chronic sinusitis, you would use an H1 blocker.
Outline the pathophysiology and medical management of Migraine Headaches. Make sure to include the role of the triptans.

There are two types of migraines;

1. Migraine without aura- a severe, unilateral pulsating headache that can last from 2-72 hours and is usually associated with nausea, vomiting, photophobia, and phonophobia.

2. Migraine with aura- is when the headache is preceded by neurologic symptoms called auras, which can be visual, sensory, or cause speech or motor disturbances that begin before onset of pain. These auras are caused by hypoperfused regions of the brain prior to hyperperfusion.

In both types of migraines, the pain is caused by extracranial and intracranial arterial dilation, which in response to the stretching, leads to release of neuroactive molecules.

Treatment of migraines can occur several ways. Some meds, such as Beta-blockers, TCAs Anticonvulsants and Calcium-channel blockers, have been successful in reducing the frequency and severity of migraines prophylactically if the patient suffers from multiple monthly attacks. During an attack, symptomatic treatment may be used to reduce severity of symptoms. The triptans (sumatriptan, naratriptan, rizatriptan, eletriptan, almotriptan, frovatriptan, and zolmitriptan) have been shown to rapidly and effectively abort or markedly reduce the severity of migraine headaches. These drugs are serotonin agonists and act at 5-HT1D receptors.

Note: sumatriptan = Imitrex. Know which classes of drugs can prevent migraine and which class can treat an active migraine.

It is easy to confuse whether drugs like ondansetron, sumatriptan and many other drugs acting on 5HT are agonists or antagonists. Here is how I remember the triptans: 5HT = 5-hydroxytryptamine which was named "serotonin" because it was found in serum = "sero" + "tonin" = it increases vascular tone (in other words, serotonin is a vasoconstrictor). Migraines are caused by arterial dilation, serotonin is a vasoconstrictor, so if a drug acting on serotonin receptors is useful in treating migraines then it must be a 5HT agonist. I find that if I just try to memorize this type of info I soon get confused about which drugs are agonists and which are antagonists.

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