![10 At my last part, I have left upto the factor; Hyperprolactinaemia & Amenorrhoea, some points are left,so today i'm going to start from that, Hyperprolactinaemia causes secondary amenorrhoea in about 30% of women. There is anovulation & hypogonadotrophic hypogonadism. (I)Pituitary Adenoma (Prolactinoma):- Hyperprolactinaemia is commonly due to pituitary adenomas (microadenoma or macroadenoma). There are other various causes of hyperprolactinaemia. Causes of Hyperprolactinaemia; [A] Physiological:-(1) Stress & exercise(raised endogenous opioids) (2)Pregnancy(3)Stimulation of nipples (4) Sleep (5) Idiopathic.[B] Hypothalamus & pituitary:-(1) Craniopharyngioma (2) Tuberculosis (3) Hypothyroidism (4) Multiple endocrine disorder (Cushing's syndrome, Acromegaly) (5)Pituitary adenomas (Prolactinomas) (6) Resection of pituitary stalk. [C]Drugs:-Some drugs, like antidepressants [D] Others:- (1) Renal failure (2) Cirrhosis of liver (3) PCOS (4) Idiopathic. (J) SHEEHAN'S Syndrome:-There is history of severe postpartum haemorrhage, shock or severe infection. Depending upon the degree of anterior pituitary necrosis, the features vary. The common manifestations are failing lactation, loss of pubic & axillary hair, lethargy, hypotension, secondary amenorrhoea and atrophy of the breasts & genitalia. Gonadotrophin level is low, so also T3,T4 and cortisol. The hormones affected in order of frequency are, growth hormone (GH), prolactin, Gonadotrophins(FSH and LH),TSH and ACTH(Adrenocorticotrophic hormone). Hyponatremia may be present (30%). The syndrome may develop slowly over 8-10 years time. (K)Adrenal Tumour or Hyperplasia:-There is secondary amenorrhoea, infertility, acne and features of defeminisation followed by virilisation(hoarness of voice, hirsutism and enlargement of clitoris). In both the conditions there is excess production of androgens. Serum level of DHEA-S (dehydroepiandrosterone sulphate) correlates well with daily urinary 17KS excretion. (L) Cushing syndrome:- Cushing first described the syndrome in 1932. Androgens are formed as intermediate products in the synthesis of cortisol. The elevated cortisol level found in Cushing syndrome encompasses two distinct pathologic entities- (1) Cushing disease(ACTH dependent) (2) Adrenal tumour(ACTH independent). (Next part will upload at part 13 @Dr Priyanka Baishya) 13 Amenorrhoea(Part 13):-at my last part i have written upto the beginning of 'Cushing syndrome', so today i am going to discuss elaborately about this syndrome; In Cushing disease, there is excess production of ACTH from the anterior pituitary or from ectopic sites. The increased ACTH causes hyperstimulation of adrenal cortex leading to its hyperplasia which in turn leads to excess production of cortisol & androgens. ACTH independent causes(adrenal adenoma or cancer) may be iatrogenic(high dose corticosteroid therapy)or adrenal tumour. The cause of adrenal mischief is cortisol secreting adenoma which produces excess cortisol. The androgen production is usually less but may be markedly elevated in presence of adrenal carcinoma. Symptoms include:-weakness, oligomenorrhoea, amenorrhoea, acne and hirsutism. Virilism is rare. The syndrome is often associated with hypertension, osteoporosis and insulin dependent diabetes. (M) Thyroid Dysfunction:- Both hypo & hyperthyroid states may produce secondary amenorrhoea & anovulation, the former is common. Serum TSH is raised, while T3 and T4 values are lowered in hypothyroid state. In subclinical hypothyroid state,serum TSH is elevated but T4 is normal. Serum prolactin may be raised even beyond 20ng/ml in hypothyroid state. This is due to increased sensitivity of prolactin secreting cells of anterior pituitary to TRH (Thyroid Releasing Hormone). (N) Postpill Amenorrhoea:-It is observed in less than 1% of the women following the use of COC pills (Combined Oral Contraceptive) pills. The association is more coincidental rather than causal. Fertility rate is normal following discontinuation of the drug. Spontaneous resumption of menstruation occurs in majority of cases after a varying period. Otherwise such amenorrhoea should be investigated as in other cases of secondary amenorrhoea. (O) General disease:- Malnutrition, tuberculosis- both pulmonary & pelvic, diabetes & chronic nephritis are all implicated. Their diagnostic criteria vary accordingly. Straight X-ray chest in pulmonary tuberculosis, blood sugar in diabetes, urine analysis & blood urea in chronic nephritis are helpful to substantiate the diagnosis. [INVESTIGATIONS]:-Investigations aims at:- (1)To diagnose or confirm the offending factor. (2)To guide the management protocol either to restore menstruation and/or fertility.(Next part details about investigations will upload at part 14, 14 Amenorrhoea (Part 14); Investigations aims at:-In secondary amenorrhoea, there is altered coordinated function of the hypothalamopituitary ovarian axis are to some pathology. As such, it is not easy in most cases to pinpoint the diagnosis only by clinical examination. However, meticulous history taking & clinical examinations are mandatory. Laboratory investigations either to diagnose or to confirm the clinical diagnosis are mostly needed. These are especially helpful for formulation of management protocols either to restore menstruation or fertility. It should be emphasised that pregnancy must be excluded prior hand irrespective of the status of the women -married, unmarried, widow, divorced or separated. With the aetiological factors in mind, one should proceed for investigations. Detailed history :- Enquiry should be made about (1)Mode of onset:-whether sudden or gradual preceded by hypomenorrhoea or oligomenorrhoea. (2) Sudden change in environment,emotional stress, psychogenic shock, or eating disorder(anorexia nervosa) (3)Sudden change in weight-loss or gain. (4) Intake of psychotrophic or antihypertensive drugs. Intake of oral 'pills' or its recent withdrawal. History of radiotherapy & chemotherapy or surgery. (5) Appearance of abnormal manifestations either coinciding or preceding the amenorrhoea such as:- (a) Acne, hirsutism (excessive growth of hair in normal & abnormal sites in female)or change in voice. (b) Inappropriate lactation (galactorrhoea)- abnormal secretion of milk unrelated to pregnancy & lactation.(c)Headache or visual disturbances. (d)Hot flushes & vaginal dryness (6) Obstetric history:-overzealous curettage leading to synechiae. (a) Caesarean section may be extended to hysterectomy of which the patient may be unaware. (b) Severe postpartum haemorrhage, or shock or infection. (c) Postpartum or postabortal uterine curettage (d) Prolonged lactation:-The patient may be amenorrhoeic since childbirth or she may have one or two periods, followed by amenorrhoea. (7) Medical history of tuberculosis (pulmonary or extra-pulmonary), diabetes, and chronic nephritis or over hypothyroid state should be enquired. (8) Family history-Premature menopause often runs in the family(mother or sisters) General examination:-The following features are to be noted-(1)Nutritional status(2)Extreme emaciation or marked obesity(3)Presence of acne or hirsutism (4)Discharge of milk from breast. (Next part will be upload at part 15,Homoeopathic Treatment will come, @Dr Priyanka Baishya) 15 Amenorrhoea(Part 15):-at part(14)few points of investigations have been left; today i am going to end up the investigations part & will going to begin the 'Homoeopathic way of treatment'; Investigations:-Abdominal examination:-(1)Presence of striate associated with obesity may be related to Cushing disease.(2)A mass in the lower abdomen. Pelvic examination:- (1) Enlargement of clitoris.(2) Adnexal mass suggestive of tubercular tubo-ovarian mass or ovarian tumour. With these methods, either a probable diagnosis is made or no abnormality is detected to account for amenorrhoea. Even though there is no inappropriate galactorrhoea, serum prolactin, TSH estimations & X-ray sella turica are mandatory. If these are normal, the following protocols are followed:- Step-1:- Progesterone challenge test is employed; Step-2:- Oestrogen - progesterone challenge test; Step-3:- Estimation of serum gonadotrophins is to be done; Step-4:-GnRH(Gonadotropin releasing hormone) dynamic test. Homoeopathic Way of Treating Amenorrhoea:-'Homoeopathy treats the patient not only the disease'- is a commonly used epigram in Homoeopathy. The Homoeopathic Physician cures the sick man by reversing the diseased condition to healthy state as a whole. We the Homoeopathic Physicians treats the patient in a 'Holistic way' I. e; Patient as a whole; by complete case taking; physical, mental, general symptoms with past history, family history. Through totality of symptoms; we should give a constitutional remedy. Yes there are lots of therapeutic medicines; but Holistic approach should be maintained. Through therapeutic way here I am going to mention few medicines, with red line symptoms but always prefer constitutional similimum in Holistic approach to attain complete cure. Few therapeutic way medications:- (1) Pulsatilla:- Derangements at puberty; menses, suppressed from getting the feet wet, too scanty, too late, slimy, painful, irregular, intermittent flow, with intense pain & great restlessness & tossing about. Delayed first menstruation. (2)Cimicifuga:- Menses; irregular, exhausting, delayed or suppressed by mental emotions, from cold, from fever, with chorea, hysteria or mania, increase of mental symptoms during menstruation. (3)Ferrum Metallicum:-When amenorrhoea is relate with 'Iron deficiency anaemia'. Menses, too early, too profuse, too long lasting, with fiery red face, ringing in the ears, intermit two or three days & then return, flow pale, watery, debilitating. [Next part will upload at part 16 Amenorrhoea(Part 16); Homoeopathic Way of Treatment:- at my last part i have started about the 'Homoeopathic Way of Treatment', so today i am going to complete the topic; (4)Conium:-Menses; feeble, suppressed, too late, scanty of short duration with rash of small red pimples over body which ceases with the flow. (5)Calcarea Carb:- Menstruation too early, too profuse, too long lasting, with subsequent amenorrhoea & chlorosis with menses scanty or suppressed. (6)Sepia:-Irregular menses of nearly every form early, late, scanty, profuse, amenorrhoea Or menorrhagia. There are lots of medicines through therapeutic & constitutional way. I have mentioned few medicines with few red line symptoms; there should also count generalities, modalities, Past history, family history & then a similimum medicine will give. We Homoeopathic Physician select a medicine after proper case taking & miasmatic background of a case should be considered (Miasm:- Miasm denotes the dynamic disease producing power which pollutes the human organism & become the producer of every possible diseased condition). Never do any self medication; always consult with a Registered Homoeopathic Physician & take consultation. As Homoeopathic Medical Science treat a case through individualistic approach, so there are always different medicines to different individual. A same medicine which will come to an individual will never be the same with an another individual; So take medicines with a complete consultation with registered Homoeopathic Physician & be with a good health. So the vast series of 'Amenorrhoea' has completed today. Thanks to al](https://3.bp.blogspot.com/-xBeS4r7auQQ/W3PVsbTLsLI/AAAAAAAACew/KB3HmrwLhok2m--cNIjP0bhdLP6KeBpDgCLcBGAs/s1600/Untitled-26.jpg "web")
At my last article I have discussed about one of the important ovarian factor, PCOS (Poly cystic Ovarian Syndrome),so today i am going to discuss about the investigations part and risk factors; Investigations :-(1) Sonography:-Trans vaginal Sonography is specially useful in obese patient. Ovaries are enlarged in volume (>10cm3). Increased number (>12) of peripherally arranged cysts (2-9mm) are seen.
(2)Serum values- LH (Luteinizing Hormone) level is elevated and/or the ratio LH: FSH is > 2:1.
(3) Raised level of oestradiol & o estrogen- The oestrone level is markedly elevated.
(4) SHBG (Sex Hormone Binding Globulin)level is reduced.
(5) Hyperparathyroidism -mainly from the ovary, less from the adrenals.
(6)Raised serum testosterone & DHEA-S (dehydrogenate sulfate) may be marginally elevated. (7)Insulin Resistance (IR):- Raised fasting insulin levels.
(8)Laparoscopy:-Bilateral Poly cystic ovaries are characteristic of PCOS. Possible Rate Squealer of PCOS:- (1) Obese women(BMI>30) are at increased risk of developing diabetes Mellitus (15%) due to insulin resistance. (2) Risk of developing endometrial carcinoma due to persistently elevated level of oestrogens. Oestrogens effects are not opposed by progesterone because of chronic anovulatory state. (3)Risk of hypertension and cardiovascular disease as dyslipidaemia (lower level of HDL; high density lipoprotein, increase level of triglycerides & low density lipoprotein) is the most common metabolic abnormality in women with PCOS.
(4) Obstructive sleep apnoea. Premature Ovarian Insufficiency:-Premature ovarian insufficiency (failure)is defined when ovarian failure occurs before the age of forty. It occurs in about 1% of the female population. During intrauterine life either there is failure of germ cell migration or there may be normal germ cell migration but an accelerated rate of germ cell depletion (apoptosis)due to various reasons. This results in either no follicle or only few follicles left behind in the ovary by the time they reach puberty.
Causes of premature ovarian failure:-
(A)Genetic:- (1)Turner’s syndrome(45XO), (45X/46XX) (2) Gonadal dysgenesis 46XX;46XY. (3) Trisomy 18 & 13 (4) X-chromosome deletion, translocation.
(B) Autoimmune:– (1) Auto antibodies:- anti nuclear antibodies(ANA), Lupus anticoagulant (2) Polyglandular autoimmune syndrome(antibodies against thyroid; parathyroid; adrenal; islet cells of pancreas).
(C)Infections:- Mumps, tuberculosis
(D)Iatrogenic:-Radiation therapy, chemotherapy, surgery.
(E)Metabolic:- Galactosaemia, 17alfa hydroxyls deficiency. In Galactosaemia, the enzyme gelatos -1-phosphate luridly transferees’ is absent. Follicles are destroyed by the toxic effects of galactose.
(F) Environmental:- Smoking
(G) FSH receptor absence or post receptor defect (Savage’s syndrome).
(H) Idiopathic: Diagnosis/Investigations :- (1) History of amenorrhoea is less than 35years of age. (2) Serum gonadotrophin level (FSH >40mIU/ml) is high. (3) Cerotype abnormality (4) Organ specific humeral antibody (ant thyroid commonest) (5) Ovarian biopsy (a follicular; follicular and autoimmune variety) is not essential to the diagnosis. In autoimmune variety, there is per follicular lymphocyte infiltration. In resistant ovarian syndrome, follicles are present. FSH receptor is either absent or defective. (6) Patient presents with amenorrhoea -primary (25%) or secondary (75%). Features of hypo estrogenic state like hot flushes, vaginal dryness, dyspareunia and psychological symptoms are there. (B) Masculinising Ovarian Tumour:-There are features of gradual defeminisation followed by appearance of masculinising features such as hoarseness of voice, hirsute and enlargement of clitoris. Abdominal and pelvic examination reveal an adnexal tumour, the exact nature is confirmed by biopsy. Serum testosterone level is elevated to >2ng per ml while DHEAS level (dehydrate epiandrosterone sulphate) is normal. (C) Hypothalamic (Factors) Amenorrhoea:- Hypothalamic dysfunction is one of the major causes of true secondary amenorrhoea. There is often history suggestive of stress, exercise, rapid gain or loss of weight. (D) Weight Related Amenorrhoea:- Female athletes, runners, ballet dancers are under constant stress and performing strenuous exercise. They have high level of corticotrophin releasing hormone (CRH). The levels of ACTH (adrenocorticotropic hormone) cortical & endogenous opioids are high. Leptin levels are low. CRH (corticotrophin releasing hormone) directly inhibits GnRH secretion via raised endogenous opioids. They are more likely to develop amenorrhoea due to decrease in GnRH (Gonadotropin – releasing hormone)pulse frequency.
According to body weight hypothesis, body weight should be above critical level to achieve menarche and regular menstruation. To achieve menarche, body fat should reach 17% of the body weight. And for regularity of menstruation body fat should be maintained at least at 22%. Reduction of body fat by about one – third will result in menstrual abnormality. Menstruation becomes irregular when the BMI is < 19 kg/m2. These subjects are hypo oestrogenic & have got elevated prolactin & cortisol level. (E) Anorexia Nervosa:- It is a state of self-imposed starvation. This is a psychosexual problem where the patient suffers from the illusion of excessive body fat & distorted body image. Patient denies food & is markedly under-weight. Amenorrhoea is the rule. Constipation is common. Release of GnRH is affected. FSH and LH levels are low, cortisol level is high. This may be a life-threatening disorder.
(F) Obesity:-Obese women so often suffer from irregular menstrual bleeding. Excess number of fat cells in obese women, convert peripheral androgens to oestrogen(aromatisation). There is also low level of sex-hormone binding globulin, which helps free androgens to be converted to oestrone. Obesity with polycystic ovarian disease can cause oligomenorrhoea or amenorrhoea.
(G) Kallmann syndrome:- Embryologically GnRH neurons develop in the ectodermal olfactory placode before they migrate finally to the hypothalamus, GnRH(Gonadotropin releasing hormone)neurones are absent due to partial or complete agenesis of olfactory bulb (Olfactogenital dysplasia).This disorder is characterised by hypogonadotrophic hypogonadism, anosmia and colour blindness. There may be associated cleft lip and palate. Patients present with primary amenorrhoea. Mode of inheritance is due to a variety of genetic mutations in the KAL gene(X linked) or as an autosomal dominant or recessive fashion. Menstruation can be induced with combined oestrogen and progestin therapy.
(H)Pituitary factors:- Adenoma:-In adenoma either micro or macro, there is usually associated inappropriate lactation, secondary amenorrhoea & infertility. There may be headache with disturbed vision. (I) Hyperprolactinaemia and Amenorrhoea:-Prolactin inhibits GnRH pulse secretion. Gonadotrophin levels are suppressed.
Writer- Dr Priyanka Baisya.
Writer- Dr Priyanka Baisya.
