The Adrenal Glands

The adrenal glands are two small structures situated one at top each kidney. Both in anatomy and in function, they consist of two distinct regions:

an outer layer, the adrenal cortex, which surrounds
the adrenal medulla.

The Adrenal Cortex

cells of the adrenal cortex secrete a variety of steroid hormones.

glucocorticoids (e.g., cortisol)
mineralocorticoids (e.g., aldosterone)
androgens (e.g., testosterone)

Production of all three classes is triggered by the secretion of ACTH from the anterior lobe of the pituitary.

Glucocorticoids

They Effect by raising the level of blood sugar (glucose). One way they do this is by stimulating gluconeogenesis in the liver: the conversion of fat and protein into intermediate metabolites that are ultimately converted into glucose.

The most abundant glucocorticoid is cortisol (also called hydrocortisone).

Cortisol and the other glucocorticoids also have a potent anti-inflammatory effect on the body. They depress the immune response, especially cell-mediated immune responses.

Mineralocorticoids

The most important of them is the steroid aldosterone. Aldosterone acts on the kidney promoting the reabsorption of sodium ions (Na⁺) into the blood. Water follows the salt and this helps maintain normal blood pressure.

Aldosterone also

acts on sweat glands to reduce the loss of sodium in perspiration;
acts on taste cells to increase the sensitivity of the taste buds to sources of sodium.

The secretion of aldosterone is stimulated by:

a drop in the level of sodium ions in the blood;
a rise in the level of potassium ions in the blood;
angiotensin II
ACTH (as is that of cortisol)

Androgens

The adrenal cortex secretes precursors to androgens such as testosterone.

Excessive production of adrenal androgens can cause premature puberty in young boys.

In females, the adrenal cortex is a major source of androgens. Their hypersecretion may produce a masculine pattern of body hair and cessation of menstruation.

Addison's Disease: Hyposecretion of the adrenal cortices

Addison's disease has many causes, such as

destruction of the adrenal glands by infection;
their destruction by an autoimmune attack;
an inherited mutation in the ACTH receptor on adrenal cells.

Cushing's Syndrome: Excessive levels of glucocorticoids

In Cushing's syndrome, the level of adrenal hormones, especially of the glucocorticoids, is too high.It can be caused by:

excessive production of ACTH by the anterior lobe of the pituitary;
excessive production of adrenal hormones themselves (e.g., because of a tumor), or (quite commonly)
as a result of glucocorticoid therapy for some other disorder such as
- rheumatoid arthritis or
- preventing the rejection of an organ transplant.

The Adrenal Medulla

The adrenal medulla consists of masses of neurons that are part of the sympathetic branch of the autonomic nervous system. Instead of releasing their neurotransmitters at a synapse, these neurons release them into the blood. Thus, although part of the nervous system, the adrenal medulla functions as an endocrine gland.The adrenal medulla releases:

adrenaline (also called epinephrine) and
noradrenaline (also called norepinephrine)

Both are derived from the amino acid tyrosine.

Release of adrenaline and noradrenaline is triggered by nervous stimulation in response to physical or mental stress. The hormones bind to adrenergic receptors transmembrane proteins in the plasma membrane of many cell types.

Some of the effects are:

increase in the rate and strength of the heartbeat resulting in increased blood pressure;
blood shunted from the skin and viscera to the skeletal muscles, coronary arteries, liver, and brain;
rise in blood sugar;
increased metabolic rate;
bronchi dilate;
pupils dilate;
hair stands on end (gooseflesh in humans);
clotting time of the blood is reduced;
increased ACTH secretion from the anterior lobe of the pituitary.

All of these effects prepare the body to take immediate and vigorous action.

Functional Divisions of the Nervous System:

1) The Voluntary Nervous System - (ie. somatic division) control of willful control of effectors (skeletal muscles) and conscious perception. Mediates voluntary reflexes.

2) The Autonomic Nervous System - control of autonomic effectors - smooth muscles, cardiac muscle, glands. Responsible for "visceral" reflexes

Hormones are carried by the blood throughout the entire body, yet they affect only certain cells. The specific cells that respond to a given hormone have receptor sites for that hormone.

This is sort of a lock and key mechanism. If the key fits the lock, then the door will open. If a hormone fits the receptor site, then there will be an effect. If a hormone and a receptor site do not match, then there is no reaction. All of the cells that have receptor sites for a given hormone make up the target tissue for that hormone. In some cases, the target tissue is localized in a single gland or organ. In other cases, the target tissue is diffuse and scattered throughout the body so that many areas are affected.

Hormones bring about their characteristic effects on target cells by modifying cellular activity. Cells in a target tissue have receptor sites for specific hormones. Receptor sites may be located on the surface of the cell membrane or in the interior of the cell.

In general those protein hormones are unable to diffuse through the cell membrane and react with receptor sites on the surface of the cell. The hormone receptor reaction on the cell membrane activates an enzyme within the membrane, called adenyl cyclase, which diffuses into the cytoplasm. Within the cell, adenyl cyclase catalyzes or starts the process of removal of phosphates from ATP to produce cyclic adenosine monophosphate or c AMP. This c AMP activates enzymes within the cytoplasm that alter or change the cellular activity. The protein hormone, which reacts at the cell membrane, is called the first messenger. c Amp that brings about the action attributed to the hormone is called the second messenger. This type of action is relatively rapid because the precursors are already present and they just needed to be activated in some way.

The Nervous System Has Peripheral and Central Units

The central nervous system (CNS) is the brain and spinal column
The peripheral nervous system (PNS) consists of nerves outside of the CNS
There are 31 pairs of spinal nerves (mixed motor & sensory)
There are 12 pairs of cranial nerves (some are pure sensory, but most are mixed)

The pattern of innervation plotted on the skin is called a dermatome

The Nervous System Has Peripheral and Central Units

The central nervous system (CNS) is the brain and spinal column
The peripheral nervous system (PNS) consists of nerves outside of the CNS
There are 31 pairs of spinal nerves (mixed motor & sensory)
There are 12 pairs of cranial nerves (some are pure sensory, but most are mixed)

The pattern of innervation plotted on the skin is called a dermatome

Hemostasis - the stopping of the blood. Triggered by a ruptured vessel wall it occurs in several steps:

1) vascular spasm - most vessels will constrict strongly when their walls are damaged. This accounts for individuals not bleeding to death even when limbs are crushed. It also can help to enhance blood clotting in less severe injuries.

2) platelet plug - platelets become sticky when they contact collagen, a protein in the basement membrane of the endothelium exposed when the vessel wall is ruptured. As they stick together they can form a plug which will stem the flow of blood in minor vessels.

3) Formation of the Blood Clot:

A) release of platelet factors - as platelets stick together and to the vascular wall some are ruptured releasing chemicals such as thromboxane, PF3, ADP and other substances. These become prothrombin activators. Thromboxane also makes the platelets even stickier, and increases the vascular constriction. These reactions are self perpetuating and become a cascade which represents a positive feedback mechanism.

B) prothrombin activators : prothrombin (already in the blood) is split into smaller products including thrombin, an active protease.

C) thrombin splits soluble fibrinogen, already present in the plasma, into monomers which then polymerize to produce insoluble fibrin threads. The fibrin threads weave the platelets and other cells together to form the actual clot. This occurs within four to six minutes when the injury is severe and up to 15 minutes when it is not. After 15 minutes the clot begins to retract as the fibrin threads contract, pulling the broken edges of the injury together and smoothing the surface of the clot causing the chemical processes to cease. Eventually the clot will dissolve due to enzymes such as plasmin also present in the blood.

The extrinsic pathway: when tissues are damaged the damaged cells release substances called tissue thromboplastin which also acts as a prothrombin activator. This enhances and speeds coagulation when tissue damage is involved.

Anti-thrombin III - this factor helps to prevent clotting when no trigger is present by removing any thrombin present. Its function is magnified many times when heparin is present. Therefore heparin is used clinically as a short-term anticoagulant.

Vitamin K - stimulates the production of clotting factors including prothrombin and fibrinogen in the liver. This vitamin is normally produced by bacteria in the colon. Coumarin (or coumadin) competes with Vitamin K in the liver and is used clinically for long-term suppression of clotting.

Several factors important to clotting are known to be absent in forms of hemophilia. These factors are produced by specific genes which are mutated in the deficient forms. The factors are VIII, IX, and XI.

Calcium is necessary for blood clotting and its removal from the blood by complexing with citrate will prevent the blood from clotting during storage

There Are 12 Pairs of Cranial Nerves
The 12 pairs of cranial nerves emerge mainly from the ventral surface of the brain
Most attach to the medulla, pons or midbrain
They leave the brain through various fissures and foramina of the skull

Nerve	Name	Sensory	Motor	Autonomic Parasympathetic
I	Olfactory	Smell
II	Optic	Vision
III	Oculomotor	Proprioception	4 Extrinsic eye muscles	Pupil constriction Accomodation Focusing
IV	Trochlear	Proprioception	1 Extrinsic eye muscle (Sup.oblique)
V	Trigeminal	Somatic senses (Face, tongue)	Chewing
VI	Abducens	Proprioception	1 Extrinsic eye muscle (Lat. rectus)
VII	Facial	Taste Proprioception	Muscles of facial expression	Salivary glands Tear glands
VIII	Auditory (Vestibulocochlear)	Hearing, Balance
IX	Glossopharyngeal	Taste Blood gases	Swallowing Gagging	Salivary glands
X	Vagus	Blood pressure Blood gases Taste	Speech Swallowing Gagging	Many visceral organs (heart, gut, lungs)
XI	Spinal acessory	Proprioception	Neck muscles: Sternocleidomastoid Trapezius
XII	Hypoglossal	Proprioception	Tongue muscles Speech

Many of the functions that make us distinctly human are controlled by cranial nerves: special senses, facial expression, speech.
Cranial Nerves Contain Sensory, Motor and Parasympathetic Fibers

A small fraction of cardiac muscle fibers have myogenicity and autorhythmicity.

Myogenicity is the property of spontaneous impulse generation. The slow sodium channels are leaky and cause the polarity to spontaneously rise to threshold for action potential generation. The fastest of these cells, those in the SA node, set the pace for the heartbeat.

Autorhythmicity - the natural rhythm of spontaneous depolarization. Those with the fastest autorhythmicity act as the 1. heart's pacemaker.

Contractility - like skeletal muscle, most cardiac muscle cells respond to stimuli by contracting. The autorhythmic cells have very little contractility however. Contractility in the other cells can be varied by the effect of neurotransmitters.

Inotropic effects - factors which affect the force or energy of muscular contractions. Digoxin, epinephrine, norepinephrine, and dopamine have positive inotropic effects. Betal blockers and calcium channel blockers have negative inotropic effects

Sequence of events in cardiac conduction: The electrical events in the cardiac cycle.

1) SA node depolarizes and the impulse spreads across the atrial myocardium and through the internodal fibers to the AV node. The atrial myocardium depolarizes resulting in atrial contraction, a physical event.

2) AV node picks up the impulse and transfers it to the AV Bundle (Bundle of His). This produces the major portion of the delay seen in the cardiac cycle. It takes approximately .03 sec from SA node depolarization to the impulse reaching the AV node, and .13 seconds for the impulse to get through the AV node and reach the Bundle of His. Also during this period the atria repolarize.

3) From the AV node the impulse travels through the bundle branches and through the Purkinje fibers to the ventricular myocardium, causing ventricular depolarization and ventricular contraction, a physical event.

4) Ventricular repolarization occurs.

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