The thyroid gland is a gland shaped like a butterfly which lies at the base of the anterior neck. It controls metabolism using hormone secretion.

Iodine is extremely important for the synthesis of hormones within the thyroid. It is internalised into the thyroid follicular cells via the sodium/iodide symporter (NIS).

The parathyroid glands are found posterior to the thyroid gland, with the recurrent laryngeal nerves running posteromedially.

The expected weight of a normal thyroid gland is about 30 grams.

T3 is produced by peripheral de-iodination of T4. It is more active than T4.

TBG, like most binding proteins, is increased in pregnancy. Because of this, measurement of free thyroid hormone concentration is more important than total.

T4 and T3 concentrations are decreased in Illness and starvation.

L-T4 that is the active molecule while D-T4 is inactive.

When there is a fall in ionised plasma calcium levels, the chief cells of the parathyroid glands are stimulated to secrete parathyroid hormone (PTH).

50% of extracellular calcium occurs as non-ionised, protein- (albumin-)bound calcium.

The degree of ionisation increases with low ph and decreases with high pH.

There is increased renal calcium excretion with secretion of calcitonin.

Aldosterone is produced in the zona glomerulosa of the adrenal cortex and acts to increase sodium reabsorption via intracellular mineralocorticoid receptors in the distal tubules and collecting ducts of the nephron.

Its release is stimulated by hypovolaemia, blood loss ,and low plasma sodium and is inhibited by hypertension and increased sodium. It is regulated by the renin-angiotensin system.

Triiodothyronine (T3) is more potent than thyroxine (T4). It is able to bind to more receptors (90%) compared to T4 (10%), and the onset of action is more immediate (within 12 hours) than T4 (2 days).

Ninety-three percent of thyroid hormones synthesized is T4, and the remaining 7% is T3. The half-life of T3 is shorter (1 day), and its affinity for thyroxine-binding globulin is lower than T4.

A beta-1 adrenoreceptor agonist is most likely the ligand that causes increased automaticity, increased chronotropy, increased excitability, and increased inotropy on the sino-atrial node. However, alpha-1 adrenoreceptor effects may cause an increase in systemic vascular resistance. Noradrenaline, adrenaline, dopamine, and ephedrine are examples of drugs with mixed alpha and beta effects.

Adrenaline, noradrenaline, dopamine, dopexamine, dobutamine, ephedrine, and isoprenaline are examples of drugs that have some beta-1 activity. The beta-1 receptor is a G protein-coupled metabotropic receptor. When the beta-1 agonist binds to the cell surface membrane, it causes a conformational change in the Gs unit, which triggers a cAMP-dependent pathway and a calcium influx into the cell.

Catecholamines also help to relax the heart muscle (positive lusitropy). Dromotropy is the ability to increase the atrioventricular (AV) node’s conduction velocity.

Inodilators cause an increase in intracellular calcium as a result of phosphodiesterase III (PDIII) inhibition. Milrinone, enoximone, and amrinone are some examples. Positive inotropy is caused by increased calcium entry into the myocytes. Lusitropy is also increased by phosphodiesterase inhibitors. Increased cAMP inhibits myosin light chain kinase, resulting in reduced phosphorylation of vascular smooth muscle myosin, lowering systemic and pulmonary vascular resistance.

The mechanism of action of alpha-1 adrenoreceptor agonists is an increase in intracellular calcium caused by an increase in inositol triphosphate (IP3). IP3 is a second messenger that causes an increase in systemic vascular resistance by stimulating the influx of Ca2+ into smooth muscle cells. Reflex bradycardia can occur as a result of the subsequent increase in blood pressure. Phenylephrine and metaraminol are examples of pure alpha-1 agonists.

Levosimendin is a novel inotrope that makes myocytes more sensitive to intracellular Ca2+. It causes a positive inotropy without changing heart rate or oxygen consumption significantly.

The Na-K-ATPase membrane pump in the myocardium is inhibited by digoxin. This inhibition promotes sodium-calcium exchange, resulting in an increase in intracellular Ca2+ and increased contraction force. The parasympathetic effects of digoxin on the AV node result in bradycardia. Systemic vascular resistance will not be affected by it.

Pituitary tumours that compress the optic chiasma primarily affect the neurones that decussate at this location. Bitemporal hemianopia is caused by neurones that emerge from the nasal half of the retina and transmit the temporal half of the visual field.

The axons of ganglion cells in the retina form the optic nerve.

It exits the orbit through the optic foramen and projects to the thalamic lateral geniculate body. The optic chiasma forms above the sella turcica as the nasal fibres decussate along the way. The optic radiation travels from the lateral geniculate body to the occipital cortex.

Lesions at various points along this pathway cause the following visual field defects:

Scotoma implies partial retinal or optic nerve damage.
Monocular vision loss occurs when the optic nerve is completely damaged.
Pathology at the optic chiasma causes bitemporal hemianopia.
Cortical blindness with occipital cortex pathology and homonymous hemianopia with lesions compromising the optic radiation.

The patellar (knee jerk) reflex is a monosynaptic stretch reflex arising from L2-L4 nerve roots. It occurs after a tap on the patellar tendon which causes the spindles of the quadriceps muscles to stretch.

The afferent nerve pathway occurred through A gamma fibres.

Wesphal’s sign refers to a reduction, or absence of the patellar reflex. It is often indicated of a neurological disease affecting the PNS.

A transection of the spinal cord results in a degree of shock which causes all reflexes to be reduced or completely absent, and required a period of approximately 6 weeks to recover.

Iron is a necessary micronutrient for proper erythropoietic function, oxidative metabolism, and cellular immune responses. Although dietary iron absorption (1-2 mg/d) is tightly controlled, it is only just balanced by losses.

The adult body contains 35-45 mg/kg iron (about 4-5 g)

Iron can be found in a variety of forms, including haemoglobin, ferritin, haemosiderin, myoglobin, haem enzymes, and transferrin bound proteins.