MALE HYPOGONADISM: Hira_Fj'23

Pathophysiology:

∴
Clinical Features:
∴Loss of Libido
∴Lethargy with Muscle Weakness
∴Decreased Frequency of Shaving
∴Gynecomastia
∴Infertility
∴Delayed Puberty
∴Osteoporosis
∴Anemia of Chronic Disease
Investigations:
∴Low Fasting 0900 hrs serum testosterone
∴LH and FSH to differentiate between hypogonadotrophic and hypergonadotrophic
hypogonadism
Management:
∴Testosterone replacement to prevent osteoporosis and restore muscle power and libido

*Do not consider patch as it’s not in 24 ed

*Testosterone therapy can aggravate prostatic carcinoma, so prostate specific antigen should be
measured before therapy
*Androgen replacement can cause polycythemia
*Testosterone replacement inhibits spermatogenesis

GYNECOMASTIA:
Pathophysiology:

Hira_Fj'23

∴Due to imbalance between androgen and estrogen activity

∴Androgen deficiency or Estrogen excess
∴Prolactin Excess alone does NOT cause gynecomastia
∴In older men due to decreasing testosterone

Investigations:
∴USG or Mammography to distinguish between gynecomastia and adipose tissue
∴Random Blood sample for testosterone
∴LH, FSH, Estradiol, Prolactin and hCG
∴Elevated estrogen is in testicular tumors and hcG producing neoplasm
Management:
∴Reassurance
∴Surgical excision
∴Androgen replavement
∴Anti estrogen tamoxifen

PRECOCIOUS PUBERTY:
∴ early development of any secondary sexual characteristics before the age of 9 years in a boy
and 6–8 years of age in a girl.

Pathophysiology:
1)Central PP is due to the early maturation of the hypothalamic–pituitary–gonadal axis and
thus is gonadotrophin-dependent. It is more common in girls than boys and often no structural
cause is identified, i.e. ‘the physiological clock is running fast’

2) Structural causes are found

more commonly in younger children and in boys and include:
• central nervous system (CNS) tumours such as astrocytomas, germ-cell tumours secreting
human chorionic gonadotrophin (hCG) and hypothalamic harmartomas
• CNS injury caused by infection, inflammation or trauma/ surgery
• congenital CNS structural abnormalities
3) Pseudo (or peripheral) PP is much less common, and is due to excess sex steroids in the absence of
pituitary gonadotrophins, with causes including congenital adrenal hyperplasia and McCune–Albright
syndrome

Investigations:
1)basal and GnRH-stimulated gonadotrophin levels

2) Imaging of the CNS is required in cases of central PP, while adrenal and ovarian imaging is
indicated in peripheral PP

Hira_Fj'23
Management:
Long acting GnRh analgoues

PCOS:
Criteria:
2 out of 3 features:
i)Menstrual Irregularity
ii)Androgen excess (clinical or biochemical)
iii)Multiple cysts in ovary
Clinical Features:
Management:
∴Wt Loss
∴Metformin (restore ovulatory cycle in obese women by reducing insulin resistance)
*High estrogen can cause endometrial hyperplasia
∴Progestogens administered cyclically to induce endomaterial shedding
∴For Hirsutism :Electrolysis and Laser Treatment
∴ Eflornithine cream inhibits ornithine decarboxylase in hair follicles
and may reduce hair growth when applied daily to affected
areas of the face

Hira_Fj'23
 ______________________________________________________________________________________________________________

PARATHYROID HORMONE:

Hira_Fj'23

HYPERCALCEMIA:
Pathophysiology:
Clinical Features: Hira_Fj'23
∴Polyuria
∴Polydipsia
∴Renal Colic
∴Lethargy
∴Anorexia, Nausea
∴Dyspepsia
∴Peptic Ulceration
∴Constipation
∴Depression
∴Drowsiness
∴Impaired Cognition
∴Bones, Stones and Abdominal Groans
∴HTN
Step up:
Hira_Fj'23
HYPOCALCEMIA:
Better in Step up:

Hira_Fj'23
MANAGEMENT OF HYPERPARATHYROIDISM:
∴Surgery with excision of solitary parathyroid adenoma or hyperplastic glands
∴Surgery indications : Symptomatic pt or with complications
∴Cincalcet is calcimimetic (enhances sensitivity of calcium sensing receptors)

FAMILIAL HYPOCALCIURIC HYPERCALCEMIA:

∴AD Disorder
∴Caused by Inactivating mutations in one of the alleles of calcium sensing receptor genes
∴So more Calcium is req to suppress PTH Secretion
∴ Mild Hypercalcemia and PTH at upper end
∴Increased tubular reabsorption of calcium
∴Hypocalciuria
___________________________________________________________________________________________________________

ADRENALS:
Hira_Fj'23
Hira_Fj'23
 Hira_Fj'23
CUSHING SYNDROME:
Pathophysiology:
∴Due to Excessive activation of glucocorticoid receptors
i)Excessive Intake of glucocorticoids
ii) Pituitary adenoma secreting ACTH
iii)Ectopic ACTH
iv)Tumor

Clinical Features:
Hira_Fj'23
Investigations:
∴Serum cortisol of <100nmol/l (3.6 micro gram /dL) at 0800-0900 hrs shows exogenous
glucocorticoid use
CRITERIA:
2/3 tests :
Hira_Fj'23
I) Failure to suppress serum cortisol with low doses of oral dexamethasone
ii) Loss of normal circadian rhythm of cortisol (elevated night serum)
iii)Increased 24 hr urine free cortisol
Hira_Fj'23
 Hira_Fj'23

∴ ONDST = Overnight dexamethasone suppression test:

administer 1mg dexamethasone at 2300 hrs and measure serum cortisol at 0900 hrs next day
∴LDDST = low dose dexamethasone suppression test
Administer 0.5 mg dexamethasone 4 times daily for 48 hrs and measure serum cortisol next day
ABNORMAL if Serum cortisol is >50nmol/L
*Stop estrogen beforehand
∴ACTH is measured at 0900 hrs in morning
∴HDDST= adminsiter 2mg dexa in 48 hrs 4 times
STEP UP:
 Hira_Fj'23

Management:
1. Iatrogenic Cushing syndrome: tapering of glucocorticoid
2. Pituitary Cushing syndrome: surgery (transsphenoidal ablation of pituitary adenoma)—
usually safe and effective
3. Adrenal adenoma or carcinoma: surgery (adrenalectomy )

____________________________________________________________________