Adenocortical hormones control the metabolism of carbohydrate (CHO), protein, fat and water
/electrolytes
Adencortical hormones are classified into:
a) Glucocorticoid – Cortisone
- Hydrocortisone (Cortisol)
b) Mineralocorticoid – Aldosterone - Desoxycorticosterone
c) Sex Hormone – Estrogen - Androgen
Glucocorticoids
The important glucorticoid secreted in man is hydrocortisone. It posseses some
mineralocorticoid activity as well. Cortisone is less potent and is converted to hydrocortisone by
liver.
They are classified as
- Short acting e.g cortisone, hydrocortisone
- Intermediate acting e.g predinsolone, triamcinolone
- Long acting e.g dexamethasone, betamethasone)
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Dexamethasone and betamethasone have got a high glucorticoid activity while cortisone and
hydrocortisone have high mineralocorticoid action. Therapeutic activity in inflammatory disorder
is proportional to the glucocorticoid activity.
Actions on CHO metabolism:
- antinsulinic effect
- decreases Peripheral utilization of glucose,
- increases gluconeogenesis
- promote glycogen storage
Protein metabolism: - Inhibit protein synthesis,
- Increases catabolism
Fat metabolism: - Interferes with fat storage causing deposits with characteristic distribution (neck,
supraclavicular area, and face
Electrolyte and H2O metabolism - Sodium and water retention
- Hypokalmia
Suppression of pitutary adenocortical system
CNS: Euphoria and stimulation
CVS: Restore vascular reactivity
GIT: Increase gastric acid secretion
Blood: Increase number of RBC, Hypercoagulability
Uric acid: Increased excretion
Calcium metabolism: increased Ca++excretion, interfere with Ca++ absorption
Antinflammatory: Inhibit exudation, capillary dilatation, migration of phagocyte, fibroblast, inhibit
fibrous tissue formation
Antiallergic: through inhibition of antibody production suppress tissue inflammatory response.
Absorption and fate: It has fair absorption, bound to α -globuin (transcortin).And in the liver,
cortisone is converted into hydrocortisone.
Therapeutic use
1) Replacement therapy: In Addisons disease and Addisonian crisis
2) Antinflammatory: in conditions like Collagen disease (rheumatoid carditis, arthritis),
3) Hypersensitivity reactions: (Bronchial Asthma, status asthmatic), Blood disease due to
circulating antibodies (autoimmune disease), Skin disease (eczema), Eye disease (allergic
inflammation of the eye), Nephrotic syndrome, Acute gout.
4) Immunosuppression: In tissue / organ transplantation.
Precautions - Check weight for fluid retention
- Test urine for sugar
- Follow blood pressure through measurement and check bones by X-ray for osteoporosis
- Doses should be tapered slowly (Don’t stop abruptly)
- Increase dose in surgery, infection
- Encourage diet rich in K+
, protein and adequate calcium, low Nacl - Rule- out infection before initiation of treatment
Side effects: - Due to prolonged use: Weight gain and edema hypokalmia, hyperglycemia, osteoporosis,
psychiatric disturbance, susceptibility to infection (like TB), peptic ulceration, cushing
syndrome, retarded growth - Complication with rapid withdrawal results in adrenacortical insufficiency due to depression of
adrenocortical activity
Contraindication:
They are contraindicated in patients with peptic ulcer disease, acute infection like active
tuberculosis, diabetes mellitus, psychosis, pregnancy
Mineralocorticoid
Aldosterone
It is the main mineralocorticoid of adrenal cortex. It increases absorption of Na at distal tubule
and increases K+
excretion. They are not widely used in therapeutics rather its antagonists are
of value in cases of edema.
Thyroid and Antithyroid Drugs
They inhibit the function of the thyroid gland and used in hyperthyroidism.
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Antithyroid drugs include:
- Thiourea compounds, e.g. , propylthiouracil, methimazole, carbimazole
- Ionic inhibitors, e.g. , potassium percholate, potassium thiocyanate
- Iodide, e.g. , Lugol’s iodine, potassium iodide
- Radioactive iodine (131I)
Thiourea Compounds
Inhibit the formation of throid hormone through inhibiting the oxidation of iodide to iodine
by peroxidase enzyme and blocking the coupling of iodothryosines to form
iodothyronines.
They are contraindicated in pregnant and lactating women.
Toxicities include drug fever, skin rashes, increased size and vascularity of the thyroid
gland, and agranulocytosis.
Ionic Inhibitors
Potassium percholate prevents the synthesis of thyroid hormones through inhibition of
uptake and concentration of iodide by the gland. It has the risk of aplastic anemia,
therefore no longer used in the treatment of hyperthyroidism.
Iodides:
Improve manifestations of hyperthyroidism by decreasing the size and vascularity of the
gland so they are required for preoperative preparation of the patient for partial
thyroidectomy.
Iodides act through inhibition of the “protease” enzyme which releases T3 and T4 from
thyroglobulin, and organification.
Radioactive Iodine:
It is used in hyperthyroidism as sodium 131I orally. It is trapped and concentrated as
ordinary iodine, which emits beta rays that act on parenchymal cells of the gland.
It is contraindicated in pregnancy and lactation as it affects thyroid gland in the fetus and
the infant. Its important toxicity is hypothyroidism.
Propranolol
This is an important drug which controls the peripheral manifestations of hyperthyroidism
(tachycardia, tremor). In addition, it decreases the peripheral conversion of T4 to T3.
Thryoid Storm (Crisis)
This is a sudden acute exacerbation of all the symptoms of thyrotoxic which rarely occur
after thyroidectomy. Manifestations include hyperpyrexia, gastrointestinal symptoms,
dehydration, tachycardia, arrhythmia, restlessness, etc. which may progress to shock
and death.
Management: It consists of infusion of intravenous fluids, supportive management, and
also administration of propylthiouracil, sodium iodide, hydrocortisone, and propranolol.
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