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APPROACH TO
ENDOCRINE DISORDERS
ENDOCRINE HISTORY
PRESENTING SYMPTOMS:
1.Polyuria and Polydipsia
Seen in:
 Diabetes mellitus
 Diabetes insipidus: Both Cranial Diabetes
insipidus and Nephrogenic Diabetes insipidus
 Thyrotoxicosis
 Hypoparathyroidism
 Conn’s syndrome
2.Weight loss
 Hyperthyroidism
 Addison’s disease
 Anorexia nervosa
 Type 1 Diabetes mellitus
3.Weight gain
 Hypothyroidism
 Cushing’s syndrome
 Polycystic ovarian disease
4.Muscle weakness
 Hyperthyroidism
 Cushing syndrome
 Osteomalacia
5.Temperature intolerence
 Cold intolerance:Hypothyroidism
 Heat intolerance:Hyperthyroididsm
6.Excessive sweating
 Hyperthyroidism
 Hypoglycemia
 Pheochromacytoma:Paroxysmal sweating
 Acromegaly:Increased size of sweat gland
7.Tremor
 Hyperthyroidism
 Hypoglycemia
8.Ocular symptoms
 Exophthalmos:Grave’s disease
 Visual disturbance:Pituitary tumor
 Ptosis:Myasthenia with thyrotoxicosis
 Puffy eyelid:Myxoedema
 Periorbital oedema:Grave’s disease
9.Palpitation
 Thyrotoxicosis
 Pheochromacytoma
 Hypoglycemia
10.Gynecomastia
 Klinefelter’s syndrome
 Estrogen producing tumors of testes
11.Galactorrhea
 Idiopathic:increased sensitivity to normal prolactin-Prolactinoma
 Hypothyroidism
 Acromegaly
 Premature thelarche
12.Amenorrhoea
 Primary:Hypothyroidism,Turner’s syndrome,Autoimmune ovarian failure
 Secondary:Prolactinoma,Cushing’s syndrome,PCOD
Other symptoms:
 Impotence: Testosterone deficieny,Diabetes
mellitus
 Hirsuitism:PCOD,Congenital adrenal
hyperplasia, Androgen secreting ovarian and
adrenal tumours
 Paresthesia:Neuropathy of diabetes mellitus,
Entrapment neuropathy of hypothyroidism and
acromegaly
 Muscle cramps:Hypocalcemia,
hypoparathyroidism
1.Thyroid diseases
 The most common presentations are
Thyrotoxicosis,hypothyroidism and
enlargement of thyroid gland.
 Most common symptoms and signs of :
1.THYROTOXICOSIS
Symptoms:
 Weight loss despite normal or increased
appetite
 Heat intolerance
 Palpitations
 Dyspnoea
 Irritability, Emotional lability
 Fatigue
 Sweating
 Tremor
Signs:
 Palmar erythema
 Sinus tachycardia
 Lid retraction, Lid lag
 Tremor
 Weight loss
INVESTIGATIONS
 First line investigations are serum T3,T4 and
TSH
 In most patients T3 and T4 are elevated
 Serum TSH is undetectable in Primary
thyrotoxicosis
 When biochemical thyrotoxicosis is confirmed
further investigations are done to identify the
underlying cause, like measurement of TR Ab-
elevated in Grave’s disease and isotope
scanning
 An ECG may demonstrate Sinus tachycardia or
Atrial fibrillation
 Radio-iodine uptake tests
MANAGEMENT
 Definitive treatment depends upon underlying
cause
 Anti-thyroid drugs, Radioactive iodine or
surgery
 A non-selective beta-blocker like Propranalol or
Nadolol may alleviate but not abolish symptoms
in most patients within 24-48 hrs
 Beta blockers should not be used for long term
treatment in thyrotoxicosis
2.HYPOTHYROIDISM
Symptoms:
 Weight gain
 Cold intolerance
 Fatigue, Somnolence
 Dry skin
 Dry hair
 Hemorrhagia
Signs:
 Weight gain
INVESTIGATIONS
 Primary hypothyroidism: Serum T4 is low and
TSH elevated
 Serum T3 measurements are unhelpful since
they do not discriminate between Euthyroidism
and Hypothyroidism
 ECG:Sinus bradycardia with low voltage
complexes and ST segment and T wave
abnormalities
MANAGEMENT
 Thyroxine replacement
Autoimmune thyroid diseases
1.GRAVE’S DISEASE
 Most commonly seen in women of 30 -50 years
 Other than common symptoms and signs of
thyrotoxicosis other features are:
❑ Ophthalmopathy
❑ Periorbital oedema
❑ Conjuctival irritation
❑ Exophthalmos and diplopia
❑ Pretibial myxoedema
2.HASHIMOTO’S THYROIDITIS
 Characterized by destructive lymphoid infiltration of
thyroid, leading to a varying degree of fibrosis and
thyroid enlargement
 Presented with: small or moderately sized diffuse
goitre –which is firm or rubbery in consistency
 Around 25% are presented with hypothyroidism rest of
which having T4 normal and TSH elevated or normal
develops overt hypothyroidism in future years
 Antithyroid peroxidase Ab present in serum,in more
than 90% cases.<20yrs ANF may also +ve.
 Treatment:Thyroxine therapy and also shrink an
associated goitre
Transient thyroiditis
 Subacute thyroiditis
 Postpartum thyroiditis
Simple and multi nodular goitres
Thyroid neoplasia
 Toxic adenoma
 Differentiated carcinoma
 Medullary carcinoma
Congenital thyroid disease
 Dyshormonogenesis
 Thyroid hormone resistance
Reproductive diseases
Presenting problems:
 Delayed puberty
 Amenorrhoea
 Male hypogonadism
 Infertility
 Gynaecomastia
 Hirsuitism
POLYCYSTIC OVARIAN SYNDROME
Features:
MECHANISMS MANIFESTATIONS
Pituitary dysfunction High serum LH
High serum Prolactin
Anovulatory menstrual
cycles
Oligomenorrhoea
Secondary amenorrhoea
Cystic ovaries
Infertility
Androgen excess Hirsuitism
Acne
Obesity Hyperglycemia
Elevated estrogens
Insulin resistance Dyslipidemia
Hypertension
Management
 Reduce weight
 For menstrual irregularity and infertility:
❑ Metformin by reducing insulin resistance, may
restore regular ovulatory cycles in obese
women though less effective than clomifene at
restoring fertility
❑ Thiazolidinediones also increase insulin
sensitivity and restore menstrual regularity but
C/I in pregnancy
❑ Progestogens or Progestogen-impregnated
intrauterine coil
TURNER’S SYNDROME
DIAGNOSIS AND TREATMENT
 Confirmed by karyotype analysis
 Short stature: Responds to high doses of Growth
hormone
 Prophylactic gonadectomy for 45X0/46XY
mosaicism due to increased risk of
gonadoblastoma
 Pubertal development induced by estrogen
therapy-but may result in fusion of epiphysis
and cessation of growth
 Long term estrogen therapy should be
monitored periodically for aortic root
dilatation, hearing loss and other somatic
complications
KLINEFELTER’S SYNDROME
PARATHYROID DISEASES
Presenting problems:
 Hypercalemia
 Hypocalcemia
PRIMARY HYPERPARATHYROIDISM
 Caused by autonomous secretion of PTH leading to hypercalcemia
Clinical features:
❑ Symptoms and signs of hypercalcemia include
polyuria,polydipsia,renal colic, lethargy, anorexia, nausea,
dyspepsia and peptic
ulceration,constipation,depression,drowsiness and impaired
cognition
❑ Classical symptoms are described by adage
bones, stones and abdominal groans.
❑ 50% are asymptomatic and many have non-
specific symptoms
❑ In others symptoms are unrecognised till
presented with renal calculi
❑ Hypertension is common
INVESTIGATIONS:
▪ Raised PTH and hypercalcemia
▪ Ultrasound examination can be performed prior
to surgery to localise adenoma
MANAGEMENT:
 Surgery with excision of a solitary parathyroid
adenoma or hyperplastic glands
 Patients with vague symptoms are only to be
reviewed every 6-12 months to assess
symptoms, serum calcium levels and renal
function, and undergo DEXA scans periodically
 They are encouraged to maintain high oral fluid
intake to avoid renal stones
 When presented with severe life threatening
hypercalcemia managed with IV fluids and
bisphosphonates,if not effective urgent
parathyroidectomy.
ADRENAL DISEASES
CUSHING’S SYNDROME:
INVESTIGATIONS
MANAGEMENT
 Untreated Cushing’s syndrome has a
50% 5-year mortality
 Most patients are treated surgically
with medical therapy given for a
few weeks prior to operation.
 Metyrapone and Ketoconazole are
used to inhibit corticosteroid
biosynthesis.
ENDOCRINE PANCREAS DISEASE
DIABETES MELLITUS
Type 1 diabetes
 Immune mediated
 Idiopathic
 T cell mediated autoimmune disease involving
destruction of the insulin secreting beta cells in the
pancreatic islets which takes place over many years.
 Hyperglycaemia accompanied by classical symptoms of
diabetes occurs only when 70-90% of beta cells have
been destroyed.
Type 2 diabetes
 There is combination of resistance to the
actions of insulin in the liver and muscle
together with impaired pancreatic beta cell
function leading to relative insulin deficiency
Symptoms of Hyperglycaemia:
❑ Thirst, Dry mouth
❑ Polyuria
❑ Nocturia
❑ Tiredness,Fatigue,Lethargy
❑ Noticeable change in weight(usually weight
loss)
❑ Blurring of vision
❑ Nausea, Head ache
❑ Hyperphagia,Predilection of sweet foods
❑ Mood change,irritability,difficulty in
concentrating, apathy
INVESTIGATIONS
Urine testing for
• Glucose
• Ketones
• Protein
Blood testing for:
▪ Glucose
▪ Glycated haemoglobin
MANAGEMENT:
▪ Dietary/life style modification
▪ Oral anti-diabetic drug
▪ Injected therapies - Insulin
HYPOTHALAMIC AND PITUITARY DISEASES
CLINIAL FEATURES OF PITUITARY DISEASE
ACROMEGALY
INVESTIGATIONS:
 Clinical diagnosis confirmed by measuring GH levels
during an oral glucose tolerance test.
 In 50% of patients there is paradoxical rise in GH
 Prolactin secretions are elevated in 30% cases.
MANAGEMENT:
 Trans-sphenoidal surgery is usually the first line of
treatment.
 External radiotherapy is usually second line treatment
if acromegaly persists even after surgery.
 Medical therapy is the next choice if acromegaly
persists even after surgery(Somatostatin analogues like
octreotide and lanreotide).
THANK YOU

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Approach to endocrine disorders

  • 2. ENDOCRINE HISTORY PRESENTING SYMPTOMS: 1.Polyuria and Polydipsia Seen in:  Diabetes mellitus  Diabetes insipidus: Both Cranial Diabetes insipidus and Nephrogenic Diabetes insipidus  Thyrotoxicosis  Hypoparathyroidism  Conn’s syndrome
  • 3. 2.Weight loss  Hyperthyroidism  Addison’s disease  Anorexia nervosa  Type 1 Diabetes mellitus 3.Weight gain  Hypothyroidism  Cushing’s syndrome  Polycystic ovarian disease
  • 4. 4.Muscle weakness  Hyperthyroidism  Cushing syndrome  Osteomalacia 5.Temperature intolerence  Cold intolerance:Hypothyroidism  Heat intolerance:Hyperthyroididsm 6.Excessive sweating  Hyperthyroidism  Hypoglycemia  Pheochromacytoma:Paroxysmal sweating  Acromegaly:Increased size of sweat gland
  • 5. 7.Tremor  Hyperthyroidism  Hypoglycemia 8.Ocular symptoms  Exophthalmos:Grave’s disease  Visual disturbance:Pituitary tumor  Ptosis:Myasthenia with thyrotoxicosis  Puffy eyelid:Myxoedema  Periorbital oedema:Grave’s disease 9.Palpitation  Thyrotoxicosis  Pheochromacytoma  Hypoglycemia
  • 6. 10.Gynecomastia  Klinefelter’s syndrome  Estrogen producing tumors of testes 11.Galactorrhea  Idiopathic:increased sensitivity to normal prolactin-Prolactinoma  Hypothyroidism  Acromegaly  Premature thelarche 12.Amenorrhoea  Primary:Hypothyroidism,Turner’s syndrome,Autoimmune ovarian failure  Secondary:Prolactinoma,Cushing’s syndrome,PCOD
  • 7. Other symptoms:  Impotence: Testosterone deficieny,Diabetes mellitus  Hirsuitism:PCOD,Congenital adrenal hyperplasia, Androgen secreting ovarian and adrenal tumours  Paresthesia:Neuropathy of diabetes mellitus, Entrapment neuropathy of hypothyroidism and acromegaly  Muscle cramps:Hypocalcemia, hypoparathyroidism
  • 8.
  • 9. 1.Thyroid diseases  The most common presentations are Thyrotoxicosis,hypothyroidism and enlargement of thyroid gland.  Most common symptoms and signs of : 1.THYROTOXICOSIS Symptoms:  Weight loss despite normal or increased appetite  Heat intolerance  Palpitations
  • 10.  Dyspnoea  Irritability, Emotional lability  Fatigue  Sweating  Tremor Signs:  Palmar erythema  Sinus tachycardia  Lid retraction, Lid lag  Tremor  Weight loss
  • 11. INVESTIGATIONS  First line investigations are serum T3,T4 and TSH  In most patients T3 and T4 are elevated  Serum TSH is undetectable in Primary thyrotoxicosis  When biochemical thyrotoxicosis is confirmed further investigations are done to identify the underlying cause, like measurement of TR Ab- elevated in Grave’s disease and isotope scanning  An ECG may demonstrate Sinus tachycardia or Atrial fibrillation  Radio-iodine uptake tests
  • 12. MANAGEMENT  Definitive treatment depends upon underlying cause  Anti-thyroid drugs, Radioactive iodine or surgery  A non-selective beta-blocker like Propranalol or Nadolol may alleviate but not abolish symptoms in most patients within 24-48 hrs  Beta blockers should not be used for long term treatment in thyrotoxicosis
  • 13. 2.HYPOTHYROIDISM Symptoms:  Weight gain  Cold intolerance  Fatigue, Somnolence  Dry skin  Dry hair  Hemorrhagia Signs:  Weight gain
  • 14. INVESTIGATIONS  Primary hypothyroidism: Serum T4 is low and TSH elevated  Serum T3 measurements are unhelpful since they do not discriminate between Euthyroidism and Hypothyroidism  ECG:Sinus bradycardia with low voltage complexes and ST segment and T wave abnormalities MANAGEMENT  Thyroxine replacement
  • 15. Autoimmune thyroid diseases 1.GRAVE’S DISEASE  Most commonly seen in women of 30 -50 years  Other than common symptoms and signs of thyrotoxicosis other features are: ❑ Ophthalmopathy ❑ Periorbital oedema ❑ Conjuctival irritation ❑ Exophthalmos and diplopia ❑ Pretibial myxoedema
  • 16.
  • 17. 2.HASHIMOTO’S THYROIDITIS  Characterized by destructive lymphoid infiltration of thyroid, leading to a varying degree of fibrosis and thyroid enlargement  Presented with: small or moderately sized diffuse goitre –which is firm or rubbery in consistency  Around 25% are presented with hypothyroidism rest of which having T4 normal and TSH elevated or normal develops overt hypothyroidism in future years  Antithyroid peroxidase Ab present in serum,in more than 90% cases.<20yrs ANF may also +ve.  Treatment:Thyroxine therapy and also shrink an associated goitre
  • 18. Transient thyroiditis  Subacute thyroiditis  Postpartum thyroiditis Simple and multi nodular goitres Thyroid neoplasia  Toxic adenoma  Differentiated carcinoma  Medullary carcinoma Congenital thyroid disease  Dyshormonogenesis  Thyroid hormone resistance
  • 19. Reproductive diseases Presenting problems:  Delayed puberty  Amenorrhoea  Male hypogonadism  Infertility  Gynaecomastia  Hirsuitism
  • 20. POLYCYSTIC OVARIAN SYNDROME Features: MECHANISMS MANIFESTATIONS Pituitary dysfunction High serum LH High serum Prolactin Anovulatory menstrual cycles Oligomenorrhoea Secondary amenorrhoea Cystic ovaries Infertility Androgen excess Hirsuitism Acne Obesity Hyperglycemia Elevated estrogens Insulin resistance Dyslipidemia Hypertension
  • 21. Management  Reduce weight  For menstrual irregularity and infertility: ❑ Metformin by reducing insulin resistance, may restore regular ovulatory cycles in obese women though less effective than clomifene at restoring fertility ❑ Thiazolidinediones also increase insulin sensitivity and restore menstrual regularity but C/I in pregnancy ❑ Progestogens or Progestogen-impregnated intrauterine coil
  • 23. DIAGNOSIS AND TREATMENT  Confirmed by karyotype analysis  Short stature: Responds to high doses of Growth hormone  Prophylactic gonadectomy for 45X0/46XY mosaicism due to increased risk of gonadoblastoma  Pubertal development induced by estrogen therapy-but may result in fusion of epiphysis and cessation of growth  Long term estrogen therapy should be monitored periodically for aortic root dilatation, hearing loss and other somatic complications
  • 25. PARATHYROID DISEASES Presenting problems:  Hypercalemia  Hypocalcemia PRIMARY HYPERPARATHYROIDISM  Caused by autonomous secretion of PTH leading to hypercalcemia Clinical features: ❑ Symptoms and signs of hypercalcemia include polyuria,polydipsia,renal colic, lethargy, anorexia, nausea, dyspepsia and peptic ulceration,constipation,depression,drowsiness and impaired cognition
  • 26. ❑ Classical symptoms are described by adage bones, stones and abdominal groans. ❑ 50% are asymptomatic and many have non- specific symptoms ❑ In others symptoms are unrecognised till presented with renal calculi ❑ Hypertension is common INVESTIGATIONS: ▪ Raised PTH and hypercalcemia ▪ Ultrasound examination can be performed prior to surgery to localise adenoma
  • 27. MANAGEMENT:  Surgery with excision of a solitary parathyroid adenoma or hyperplastic glands  Patients with vague symptoms are only to be reviewed every 6-12 months to assess symptoms, serum calcium levels and renal function, and undergo DEXA scans periodically  They are encouraged to maintain high oral fluid intake to avoid renal stones  When presented with severe life threatening hypercalcemia managed with IV fluids and bisphosphonates,if not effective urgent parathyroidectomy.
  • 30. MANAGEMENT  Untreated Cushing’s syndrome has a 50% 5-year mortality  Most patients are treated surgically with medical therapy given for a few weeks prior to operation.  Metyrapone and Ketoconazole are used to inhibit corticosteroid biosynthesis.
  • 31. ENDOCRINE PANCREAS DISEASE DIABETES MELLITUS Type 1 diabetes  Immune mediated  Idiopathic  T cell mediated autoimmune disease involving destruction of the insulin secreting beta cells in the pancreatic islets which takes place over many years.  Hyperglycaemia accompanied by classical symptoms of diabetes occurs only when 70-90% of beta cells have been destroyed.
  • 32. Type 2 diabetes  There is combination of resistance to the actions of insulin in the liver and muscle together with impaired pancreatic beta cell function leading to relative insulin deficiency Symptoms of Hyperglycaemia: ❑ Thirst, Dry mouth ❑ Polyuria ❑ Nocturia ❑ Tiredness,Fatigue,Lethargy
  • 33. ❑ Noticeable change in weight(usually weight loss) ❑ Blurring of vision ❑ Nausea, Head ache ❑ Hyperphagia,Predilection of sweet foods ❑ Mood change,irritability,difficulty in concentrating, apathy INVESTIGATIONS Urine testing for • Glucose • Ketones • Protein
  • 34. Blood testing for: ▪ Glucose ▪ Glycated haemoglobin MANAGEMENT: ▪ Dietary/life style modification ▪ Oral anti-diabetic drug ▪ Injected therapies - Insulin
  • 35. HYPOTHALAMIC AND PITUITARY DISEASES CLINIAL FEATURES OF PITUITARY DISEASE
  • 37. INVESTIGATIONS:  Clinical diagnosis confirmed by measuring GH levels during an oral glucose tolerance test.  In 50% of patients there is paradoxical rise in GH  Prolactin secretions are elevated in 30% cases. MANAGEMENT:  Trans-sphenoidal surgery is usually the first line of treatment.  External radiotherapy is usually second line treatment if acromegaly persists even after surgery.  Medical therapy is the next choice if acromegaly persists even after surgery(Somatostatin analogues like octreotide and lanreotide).