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
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
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
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).