The term comes from the Greek words Autos (meaning "self") and Akos (meaning "medicinal agent" or "remedy"). Therefore, an autacoid is literally a "self-remedy."
By definition, Autacoids are endogenous substances (made naturally inside the body) that act as biological factors or "local hormones".
A classic hormone (like insulin or thyroid hormone) is produced in a specific, centralized gland, dumped into the systemic bloodstream, and travels a long distance to reach its target organ.
Autacoids are DIFFERENT:
Note: However, if produced in massive, pathological amounts (like during severe anaphylactic shock), they can overcome local destruction, enter the systemic circulation, and have life-threatening systemic effects.
You must know the chemical classification of the different autacoids. Exam questions frequently mix these up:
| Chemical Class | Examples |
|---|---|
| Amines | Histamine, Serotonin (5-HT) |
| Polypeptides (Proteins) | Kinins (Bradykinin), Oxytocin, Angiotensin, Vasopressin, Endothelins |
| Fatty Acids (Eicosanoids) | Prostaglandins, Leukotrienes, Thromboxanes, Platelet Activating Factor (PAF) |
| Others | Nitric Oxide (NO - Endothelium-derived relaxing factor), Cytokines |
Histamine is a ubiquitous molecule. It is present everywhere: in bacteria, plants, animals, and notably in venoms and stinging fluids (like bee stings, wasp venom, or stinging nettle plants).
Because histamine is so incredibly potent, it must be deactivated rapidly if it isn't safely stored away. There are two major metabolic pathways the body uses to break it down and excrete it in the urine:
Where is histamine kept? In humans, it is mostly stored inside Mast Cells (found abundantly in tissues interfacing with the outside world like Skin, Lungs, and GI tract) and Basophils (circulating in the blood). Inside these cells, histamine is locked up in granules, tightly bound to a heparin-protein complex so it doesn't leak out.
Histamine can be released in two distinct ways: Immunologic (Antigen-mediated) and Non-Immunologic.
This is the classic Type I Hypersensitivity (Immediate Allergic Reaction).
In skin mast cells and blood basophils, the released histamine eventually binds back onto its own H2 receptors located on the mast cell's own surface. This acts as a biological "brakes" system, inhibiting further histamine release (Negative Feedback).
EXAM EXCEPTION: This feedback inhibition does NOT occur in lung mast cells! This is exactly why allergic asthma attacks in the lungs can spiral out of control so rapidly and become fatal; there are no built-in brakes to stop the continuous histamine release in the bronchioles.
This release mechanism does not require the immune system to be sensitized with IgE. It happens through direct physical or chemical interaction.
The Event: If a nurse pushes an intravenous dose of Morphine too fast, the patient may suddenly flush bright red, feel intensely hot, become incredibly itchy, and their blood pressure might drop precipitously.
The Mechanism: This is frequently mistaken for an allergy. It is not a true allergy (no IgE is involved). The rapid bolus of morphine chemically displaced histamine from the patient's mast cells all at once, causing sudden, massive vasodilation. This is a classic example of Non-Antigen Mediated Chemical Release.
The Fix: Stop the infusion, administer an antihistamine (like Diphenhydramine), and when restarting, push the morphine much slower.
Histamine regulates multiple physiological systems beyond just making you sneeze:
Histamine acts on four distinct receptors (H1, H2, H3, H4). ALL of them are G-Protein Coupled Receptors (GPCRs). Currently, clinical pharmacology heavily targets H1 and H2.
| Receptor | Location / Distribution | Post-Receptor Mechanism | Selective Antagonists (Blockers) |
|---|---|---|---|
| H1 | Smooth muscle (bronchi, gut), Endothelium, Brain | Gq → ↑ IP3, DAG → ↑ Intracellular Ca2+ | Mepyramine, Cetirizine, Loratadine |
| H2 | Gastric mucosa (parietal cells), Cardiac muscle, Mast cells, Brain | Gs → ↑ cAMP | Ranitidine, Cimetidine, Famotidine |
| H3 | Presynaptic neurons (Brain, myenteric plexus) | Gi → ↓ cAMP, ↓ Ca2+ | Thioperamide |
When histamine hits H1 receptors, it causes severe, rapid inflammatory changes:
If you take a dull instrument and firmly scratch a person's skin, histamine is released locally. This causes three distinct, highly predictable visual phases to appear on the skin:
H3 receptors are mostly presynaptic (they sit on the nerve terminal that is releasing the chemical, acting as volume control knobs).
Because H3 receptors regulate brain chemistry so heavily, they are massive potential therapeutic targets for cognitive and psychiatric disorders such as Sleep disorders (Narcolepsy), Parkinson's disease, ADHD, and Schizophrenia.
Examples of H3 Agonists:
Doctors rarely give pure histamine as a treatment because it is highly uncomfortable and dangerous (it causes shock and asthma). However, it has one specific diagnostic use:
Diagnostic Positive Control: It is used as a positive control injection during allergy skin testing. If a doctor is trying to see what you are allergic to, they will prick your back with 20 different allergens. They will also prick you with pure histamine. If the pure histamine prick doesn't produce a Weal and Flare, it means either your immune system is completely unresponsive, or you cheated and took an antihistamine pill before the test, rendering the entire allergy test invalid.
These drugs competitively block histamine from binding to H1 receptors. They reliably relieve sneezing, itchy eyes, runny nose, and hives. They are also used for allergies, motion sickness, vertigo, and insomnia.
They are divided into two distinct generations based heavily on their ability to cross the Blood-Brain Barrier (BBB).
These are lipophilic, cross the BBB easily, block H1 in the brain (causing profound sleepiness), and often lack specificity (they also block muscarinic receptors, causing dry mouth, blurred vision, and urinary retention).
These are bulky or ionized molecules that do not cross the BBB well. They are mainly pure anti-allergics with little to no sleepiness and fewer muscarinic side effects.
The Truck Driver: If a commercial truck driver has bad seasonal allergies, you MUST NOT prescribe Diphenhydramine (1st gen), or he will fall asleep at the wheel and crash. You must prescribe Loratadine or Fexofenadine (2nd gen).
The Itchy Sleepless Patient: Conversely, if a patient cannot sleep because they are covered in an incredibly itchy poison ivy rash, Diphenhydramine is the absolutely perfect drug because it cures the itch *and* utilizes its sedative side effect to help them sleep.
For Vertigo/Migraines: Flunarizine and Cinnarizine are specifically noted for having excellent antivertigo and antimigraine properties by regulating inner ear fluid and blood flow.
H2 blockers profoundly reduce stomach acid production by competitively blocking histamine at the H2 receptors on the stomach's parietal lining. They are primarily used to treat heartburn, Gastroesophageal Reflux Disease (GERD), peptic ulcers, and indigestion.
You must know the relative potencies and dosing strategies of these drugs:
| Drug | Relative Potency | Typical Acute Ulcer Dose | GERD Dose |
|---|---|---|---|
| Cimetidine | 1 (Least Potent) | 800 mg HS (at bedtime) or 400 mg bid (twice daily) | 800 mg bid |
| Ranitidine | 4 - 10x stronger | 300 mg HS or 150 mg bid | 150 mg bid |
| Nizatidine | 4 - 10x stronger | 300 mg HS or 150 mg bid | 150 mg bid |
| Famotidine | 20 - 50x stronger (Most Potent) | 40 mg HS or 20 mg bid | 20 mg bid |
Although it is the historical prototype H2 blocker, Cimetidine is famous on pharmacology exams primarily for its negative side effects.
Because of these issues, Ranitidine or Famotidine are usually preferred clinically, as they lack these severe side effects while being much more potent.
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Pharmacology
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