Health Information

Adequate fluoride has been proven increase the resistance to dental caries. It has been shown that the local effect of fluoride on enamel and plaque is more important than the systemic effect.

If the amount of fluoride in the drinking water is less than 700 micrograms per litre (0.7 parts per million), daily administration of fluoride tablets or drops is a suitable means of supplementation. Systemic fluoride supplements should not be prescribed without reference to the fluoride content of the local water supply, since increase fluoride can be harmful. Infants should not receive fluoride supplements until the age of 6 months.

Dentifrices which incorporate sodium fluoride or monofluorfophosphate are also a convenient source of fluoride.

Individuals who are either particularly caries prone or medically compromised may be given additional protection by use of fluoride rinses or by application of fluoride gels. Rinses can be used daily or weekly; daily use of a less concentrated rinse is more effective than weekly use of a more concentrated one. High-strength gels must be applied on a regular basis under professional supervision; extreme caution is necessary to prevent the child from swallowing any excess. Less concentrated gels are available for home use. Varnishes are also available and are particularly valuable for young or disabled children since they adhere to the teeth and set in the presence of moisture.

Leading to virilization - the clitoris of girls is enlarged - Female pseudohermaphroditism.
Prepubertal male - rapid development male sexual organs.
Postpubertal male - difficult to diagnosis.

Protein bound fraction is low.
Aldosterone metabolized to glucuronide derivitatives.
Most in live and some in kidney.
These glucuronide can be converted back to aldosterone by acid pH.
Effects of Aldosterone
Na + reabsorption in urine, sweat, saliva and GIT.
Glucocorticoids can not act on minieralocoticoids receptor since the effect of enzyme 11ß-hydroxysteroid dehydrogenase type-2.
If the enzyme is inhibited/absent cortisol act as mineralocorticoid – apparent mineralocorticoid excess. (AME)

Hyperaldosteronism Can be
Primary Hyperaldosteronism –tumor in zona glomerulosa- conn’s syndrome.
Secondary Hyperaldosteronism - high renin activity in cirrhosis, heart failure, nephrosis.

Increase aldosterone secretion –
Na+ retention and K+ depletion
Hypertension, weakness, tetany, polyuria….

Destroy the adrenal cortex – primary adrenal insufficiency.
Can be autoimmune effect or after TB.
Hypotension, hypoglycemia with fasting, stress can make patient collapse.
Increase ACTH level make pigmentation due to MSH effect of ACTH.
Addisonian crisis can occur – dehydration, low blood pressure, loss of consciousness.

Cortisol deficiency and lead to increase ACTH secretion.
Several types.
‘Cholesterol desmolase’ deficiency is fatal in fetus due inability to make progesterone by placenta.
Congenital enzyme deficiencies

Mutation of gene for ‘steroidogenic acute regulatory protein’ makes adrenal hyperplasia in new born (Placental hormone normal).
Accumulation of lipids in the gland, called ‘congenital lipid adrenal hyperplasia’.
Female genitalia develop regard less of genetic sex since androgens are not form
17alpha-hydroxylase deficiency - sex hormone production affect so female genitalia will develop.
Adrenogenital syndrome
Adrenogenital syndrome - Deficiency of the enzyme 21-hydroxylase of 95% of affected patients.
Adrenal glands overproduce certain intermediary hormones which have testosterone-like effects on the fetus and child.
About 75% of affected infants have the “salt-losing” form of the disorder – mineralocorticoid deficient
Severe deficiency is fatal.

Condition/the clinical picture due to
excess of cortisol production.
excessive use of cortisol or other similar steroid (glucocorticoid).
It can be
ACTH independent – adrenal tumors, prolong use as a treatment.
ACTH dependent – ACTH secreting tumors –Anterior pituitary (Cushing’s disease), Lungs etc.

Fat redistribution
Upper-body obesity, rounded face, increased fat around the neck – ‘buffalo hump’.
Thinning arms and legs.
Excess protein catabolism
Skin becomes fragile, thin.
Poor wounds healing, bruises easily.
Hair is thing.
Bones are weakened – osteoporosis - backaches, rib and spinal column fractures.
weak muscles.
Precipitate insulin-resistant diabetes
Amino acid from protein catabolism convert to glucose.
Decrease peripheral utility of glucose.

Mineralocorticoid effect – cortisol has mineralocorticoid action as well.
Salt and water retention.
Hypertension
K+ depletion and weakness.

Can produce mental changes – increased appetite, insomnia, euphoria……. Psychoses.
Acne
Irregular or stopped menstrual periods in females.
Erectile dysfunction in males.

Major androgen is dehydroepiandrosterone.
The rest are adrostenedione and testosterone.
Estrogens & testosteron form in the circulation from Adrostenedione.

17-ketosteroid is formed and excreted with urine.
Two-third of urinary ketosteroids in man come from adrenal + liver. Only rest from testes.
Adrenal androgens are regulated by ACTH, not by gonadotropins.
Effect of androgen
Testosterone from testes is the most active androgen.
Adrenal androgens are 20% active as testicular androgen.
Adrenal androgens in normal concentrations has very little masculinizing effect.
In excessive amount make masculinizing effects.
Effect of androgen
Excessive secretion make masculinization.
Prepubertal boy – precocious pseudopuberty.
Adult male – accentuate existing characteristics.
Female – pseudohermaphroditism, adrenogenital syndrome.

Angiotensin II –
Act on synthesis of aldosterone.
No effect on cortisol.
In hemorrhage, standing, constriction of inferior vena cava, restriction of Na+ intake increase aldosterone secretion with renin-angiotensin pathway.

Plasma aldosterone is high when working in upright position due to
renin effect of postural.
decrease removal by the liver.
Those who confined to bed show circadian rhythm – high in early morning.
ANP – decrease responsiveness of Zona glomerulosa to angiotensin II.

In adrenal insufficiency - Na+ lost in urine and K+ retained.
In mineralocorticoids excess -
K+ and H+ loss with urine.
Water retention with Na+ and hypertension will develop.
After certain level – Na+ excretion increase due ANP effect –escape phenomenon.
Regulation of mineralocorticoids
Stmulated by
ACTH
Angiotensin II
Direct stimuli of rise plasma K+ concentration on adrenal cortex – conversion of cholesterol to pregnenolone and corticosterone to aldosterone.
ACTH –
Amount need is higher than need for glucocorticoid.
Effect is transient -
after 1-2 hr aldosterone level decrease.