Michael J. Neal

Medical Pharmacology at a Glance


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heart, usually overcoming the direct β1‐stimulant action on the heart rate.

      Epinephrine by injection has an important use in the treatment of anaphylactic shock (Chapter 11).

      β‐receptor‐selective drugs

      Isoprenaline stimulates all β‐receptors, increasing the rate and force of the heartbeat and causing vasodilatation. These effects result in a fall in diastolic and mean arterial pressure with little change in systolic pressure.

      β2‐adrenoceptor agonists are relatively selective drugs that produce bronchodilatation at doses that cause minimal effects on the heart. They are resistant to MAO and are probably not taken up into neurones. Their main use is in the treatment of asthma (Chapter 11).

      α‐blockers

      α‐blockers reduce arteriolar and venous tone, causing a fall in peripheral resistance and blood pressure (Chapter 15). α‐blockers cause a reflex tachycardia, which is greater with non‐selective drugs that also block α2‐presynaptic receptors on the heart, because the augmented release of norepinephrine stimulates further the cardiac β‐receptors. Prazosin, a selective α1‐antagonist, causes relatively little tachycardia. BPH is common in men over 50 years old. As the prostate gland increases in size, pressure on the urethra obstructs urine flow. α1‐blockers increase urine flow (at least partially) by relaxing smooth muscle in the gland. Tamsulosin is selective for α1A‐adrenoceptors and is better tolerated than other antagonists.

      β‐blockers

      β‐blockers vary in their lipid solubility and cardioselectivity. However, they all block β1‐receptors and are equally effective in reducing blood pressure and preventing angina. The more lipid‐soluble drugs are more rapidly absorbed from the gut, undergo more first‐pass hepatic metabolism and are more rapidly eliminated. They are also more likely to enter the brain and cause central effects (e.g. bad dreams). Cardioselectivity is only relative and diminishes with higher doses. Nevertheless, selective β1‐blockade seems to produce less peripheral vasoconstriction (cold hands and feet) and does not reduce the response to exercise‐induced hypoglycaemia (stimulation of gluconeogenesis in the liver is mediated by β2‐receptors). Cardioselective drugs may have sufficient β2‐activity to precipitate severe bronchospasm in patients with asthma and they should avoid β‐blockers. Some β‐blockers possess intrinsic sympathomimetic activity (i.e. are partial agonists, Chapter 2). The clinical importance of this is debatable, see Chapter 16.

Schematic diagram displaying boxes at the left panel for cornea, iris, and ciliary muscle and boxes at left panel for retina, ciliary body, and cataract formation, with arrows linking to a mechanism at the center, etc.

      The eye is an inflated spherical shell, its outer layer being the tough, collagen‐rich sclera. The normal intraocular pressure (IOP) is about 15 mmHg. It is maintained by a balance of aqueous humour formation by the ciliary body (A thick arrow representing ciliary body.) and outflow through the trabecular meshwork into the canal of Schlemm (A solid north west arrow representing the canal of Schlemm.) or the uveoscleral pathway (A dashed north west arrow representing the uveoscleral pathway.). In open‐angle glaucoma, pathological changes in the retina progressively cause the death of ganglion cells and loss of vision. This process is often, but not always, associated with elevated IOP. Irrespective of the initial IOP, a reduction of the IOP by 20–40% reduces the average rate of visual loss by 50%. The pressure is reduced, usually with topical drugs. This is usually achieved either by increasing aqueous outflow with a prostaglandin analogue (bottom centre) or by reducing aqueous formation with a β‐blocker (middle right).

      At the front of the eye, the sclera runs into the cornea (top left), whose transparency is obtained by alignment of the collagen fibres. Many superficial manipulations, such as tonometry (measurement of the IOP) and the removal of corneal foreign bodies, require the instillation of a local anaesthetic. Fluorescein is commonly instilled into the eye to reveal damaged areas of corneal epithelium, which are stained bright green by the dye. Inflammation of the cornea resulting from allergy or chemical burns is treated with topical anti‐inflammatory drugs (Chapter 33). Infections are not treated with anti‐inflammatory agents, except together with an effective chemotherapeutic agent, because anti‐inflammatory drugs reduce resistance to invading microorganisms.

      The iris (middle left) possesses a sphincter muscle, which receives parasympathetic nerves, and a dilator muscle, which is innervated by sympathetic fibres. Thus, muscarinic antagonists and α‐adrenoceptor agonists dilate the pupil (mydriasis), while muscarinic agonists and α‐adrenoceptor antagonists constrict the pupil (miosis).

      Contraction of the parasympathetically innervated ciliary muscle (bottom left) allows the lens to become thicker and accommodation for near vision occurs. Thus, muscarinic antagonists paralyse the ciliary muscle (cycloplegia) and prevent accommodation for near vision, while agonists cause accommodation and a loss of far vision.

      The lens (middle top) provides the adjustable part of the eye's refractive power. Opacity of the lens is called a cataract. Some drugs, notably corticosteroids, may cause cataracts.

      The retina may occasionally be damaged by drugs (e.g. bottom right) or by high oxygen tension in newborn babies.

      Ciliary body

      The processes of the ciliary body are highly vascularized and are the sites of aqueous humour formation. The ciliary epithelial cells, which contain adenosine triphosphatase (ATPase) and carbonic anhydrase, absorb Na+ selectively from the stroma and transport it into the intercellular clefts, which open only on the aqueous humour side. The hyperosmolality in the clefts causes water flow from the stroma, producing a continuous flow of aqueous.

      Trabecular meshwork

      The aqueous humour circulates through the pupil and is drained into the canal of Schlemm, which is a circular gutter within the surface of the sclera at the limbus. The sieve‐like trabecular meshwork is the roof of the gutter, through which the aqueous must pass before it is eventually drained away into the episcleral veins. Some aqueous drains pass through the uveoscleral pathway.

      Glaucoma