The commonest symptoms are- (i) obesity, (ii) hypertension and (iii) hirsutism in the females.

ex, or (iv) latrogenic (I e , produced by a doctor) causes, when somewhat inadvertently excess cortisol or analogs of cohisol has been given for a long time, for therapeutic purposes. The commonest symptoms are- (i) obesity, (ii) hypertension and (iii) hirsutism in the females. There (iv) may be gross mental symptoms like frank psychosis or sirong emotional changes. Cohisol has salt retaining power which explains the hypertension Hirsutism (appearance of beard/moustache in females, from Tiirsuir. meaning 'dirly') Is due to associated excess secretion of adrenal andragens Recall, as has been shown in lable & 4 1 .17 hydroxy progesterone (in line B) can be routed into line C, that is. 17 hydronypiogesterone is a precursor of both cortisol as well as androstenedione Effects of cortisoi in CNS (which explains the euphoria or other menial changes) has already been discussed Obiesiiy is peculiar, often it is present in face or shoulder regions only, producing , what the clinicians call m their picturesque phrases. the 'moon face' or the "buffalo hump' respectively. The cause of This peculiar dislnbulion of fat is not known. These patients often have hyperglytemia Cortisol, it may be recalled, is a hyperglycemic agent. In Cushmg's syndrome,Ihe plasma cortisol leva! is very high 2 Hyperaldosleronism Two Forms of hyperaldosteronism will be described, (i) pimary try peral dost eronism or Conn's syndrome, and (n) secondary hyperaidosteronism. (i) In primary hyper aid oste nanism, as Conn in 1956 found, there is an adenoma (a tumor) in the zona giomerulosa. secreting uncontrolled amounts of aldosterone. Recently however cases have been reported, where instead of an adenoma, there is (for no apparent reason) bilateral hyperplasia of the zone glomerulosa. Primary hype raid osteromsm is very rare. Symptoms are due Io excess aIdosier one and characteristically include hypertension and hypokalemia (ii)Secondary hyperaldostoronism is very common In this condition there is excess secretion of aldosterone. this occurs m different types of edema, like congestive cardiac failure (CCF). renal edema and cirrhosis of live. But why there should be hyperaidost eronism in such cases of edema, is not clearly known. Presence of excess aldostarone m such cases (CCF, renal edema, portal cirrhosis) make it difficult To Ireal [he edema. 3 Adrenal virilism In this condition there is excess secretion of adrenal androgens The excess secretion may be due to - (i) a tumor in the zona raticulans region, or. (ri) congenital enzymatic deficiency As it gives an insight into the physiology, the congenial varfety alone will be discussed The congenital type is usually known as 'adreno genital hyperplasia' In greal majority of cases, there is deficiency of 21 hydroiylase (see table 6 4 1], which converts 17 hydroxy progesterone into 11 deoxycortisol. As a result, no cortisol is formed but 17 hydroxypiogesterone accumulates There are two effects of this - (i) there is deficiency of corlisol. leading to cortisol deficiency syndrome, and (n) there is excess of adrenal androgens as 17 hydroxyprogesterone can form androgens (lable 6.4. 1 line B and line C), this leads to development of such symptoms as growth of facial hairs in the female (hirsutism}. temporal baldness, enlargement of clitoris, atrophy of the breasi and so on. In short, there are signs and symptoms of mascutinization in a female. Further, deficiency of corlisolh in these cases, leads to excess ACTH secretion and this in turn causes adrenal hypertrophy plus further synthesis of adrenal androgens (a vicious cycle). A full blown picture of adrenal Virilism. therefore consists of- (i) masculine features in a female (in signs of cortisol deficiency (weakness, hypotension, poor tolerance to stress} and (in) signs of excess ACTH (pigmentation, see below, Addison's disease) 4 Addison's disease This disease, first described by Thomas Add i son in 1B55, is also called primary adrenocortical deficiency. In this disease, both the suprarenal cortices are slowly destroyed When the destruction reaches advanced phase, clinical features begin to appear. The destruction m the past, (when tuberculosis was common), was mostly due To chrome tube rculosis and raiely due la other causes like fungal infection or cancer of the adrenal glands With the practical elimination of Tuberculosis in the Western World, another cause, namely, 'idrapathic atrophy', (where no cause of destruction is apparent; however, autoimmune disease is a possibility], is gaming importance The disease is charactenzed by - (i) muscular weakness, 00 pigmentation, fin) hypotension and (iv) other symptoms Muscular weakness is largely due to lack of cortisol; hypotension is due to the Na+ Foss [resulting from aldoslerone and cohisol deficiency) pigmentation is due to excess ACTH. Obviously, when the plasma corlisol concentration is low, the ACTH secretion becomes high (see. feed back mechanism, above) ACTH has some features like MSH (melanin stimulating hormone) and it causes pigmentation of the skin and mucous membrane (for further delails, see anterior phuitary hormones, chapter 5, section VI) Patients of ArJdison's disease cannot tolerate stress well Administration of cortisol causes spectacular improvement of the tolerance to the stress. Of the laboratory findings, the most constant one is - (i) abnormally low values of plasma cortisol level of blood Another notable finding is (ii) abnormal serum electrolyte values, semm Na+ is lowwhereas serum K+ is high 5 Secondary adrenocomcal insufficiency In this condition. the AC