The document summarizes key topics in endocrinology, including disorders of the thyroid, parathyroid, and adrenal glands. It discusses hypothyroidism and its causes, signs, symptoms, and treatment with levothyroxine replacement. It also covers thyrotoxicosis, hyperparathyroidism, Cushing's syndrome, and disorders of the adrenal cortex that can cause hormone deficiencies or excesses. The quiz at the end reviews topics like Cushing's syndrome and autoimmune destruction of pancreatic beta cells in type 1 diabetes.

1. Endocrinology
Continued…

3. Outline of presentation
• Disorders of the thyroid gland
• Disorders of the parathyroid gland
• Disorders of the adrenal gland

4. Disorders of the thyroid gland,,,,,MNGoitre

5. Disorders of the thyroid gland
• The thyroid gland produces two related hormones, thyroxine (T4) and
triiodothyronine (T3) which are mainly controlled by the TSH
hormone secreted by the pituitary gland under the command of
hypothalamus.
• Acting through thyroid hormone receptors α and β, these hormones
play a critical role in cell differentiation during development and help
maintain thermogenic and metabolic homeostasis in the adult.
• The thyroid also produces the hormone calcitonin, which plays a role
in calcium homeostasis.

8. Hypothyroidism
• Causes of hypothyroidism
•Primary: characterized by a high serum thyrotropin (TSH)
concentration and a low serum free (T4) and low (T3)
Iodine deficiency: most common cause
Autoimmune hypothyroidism: Hashimoto’s thyroiditis
Iatrogenic: subtotal or total thyroidectomy, external irradiation of neck for
lymphoma or cancer
Drugs: lithium, antithyroid drugs
Congenital hypothyroidism
NB primary cause of hypothyroidism is mostly from thyroid itself

9. Cont’d
•Secondary: characterized by a low serum T4 concentration and
a serum TSH concentration that is not appropriately elevated.
Hypopituitarism: tumors, pituitary surgery or irradiation, infiltrative,
trauma,
Isolated TSH deficiency or inactivity
Hypothalamic disease: tumors, trauma, infiltrative disorders, idiopathic
• Subclinical hypothyroidism is defined biochemically as a normal free
T4 concentration in the presence of an elevated TSH concentration.

10. Clinical Manifestations
• Symptoms
• Tiredness, weakness
• Dry skin
• Feeling cold
• Hair loss
• Difficulty concentrating and poor memory
• Constipation
• Weight gain with poor appetite
• Dyspnea
• Hoarse voice
• Menorrhagia (later oligomenorrhea or
amenorrhea)
• Paresthesia
• Impaired hearing
• Signs
• Dry coarse skin; cool peripheral
extremities
• Puffy face, hands, and feet
(myxedema)
• Diffuse alopecia
• Bradycardia
• Peripheral edema
• Delayed tendon reflex relaxation
• Carpal tunnel syndrome
• Serous cavity effusions

12. Evaluation of hypothyroidism
• TSH: elevated
• T4: low
• T3: low
• TPO antibodies: autoimmune thyroiditis
• FNA biopsy: autoimmune thyroiditis

14. Treatment of hypothyroidism
• Daily replacement dose of levothyroxine
• Follow-up measurement of TSH
• It is important to ensure ongoing adherence

15. Thyrotoxicosis
• Thyrotoxicosis is defined as the state of thyroid hormone excess.
• Primary Hyperthyroidism
Graves’ disease: the commonest cause
Toxic multinodular goiter
Toxic adenoma
Functioning thyroid carcinoma metastases
Drugs: iodine excess (Jod-Basedow phenomenon)

16. Cont’d
•Secondary Hyperthyroidism
TSH-secreting pituitary adenoma
Chorionic gonadotropin-secreting tumors
Gestational thyrotoxicosis

17. Clinical manifestations
•Symptoms
• Hyperactivity, irritability, dysphoria
• Heat intolerance and sweating
• Palpitations
• Fatigue and weakness
• Weight loss with increased appetite
• Diarrhea
• Polyuria
• Oligomenorrhea, loss of libido
• Signs
Tachycardia; atrial fibrillation in the
elderly
Tremor or hand vibration
Goiter
Warm, moist skin
Muscle weakness, proximal
myopathy
Lid retraction or lag
Gynecomastia
Grave’s Opthalmopathy,
exopthalmus and dermopathy

18. Graves disease pre tibial myex edema
Nb acropachy mean clubbing in goiter exopthalmus

19. Laboratory evaluation
• TSH: low
• T4: elevated
• T3: elevated

20. Treatment
• antithyroid drugs: thionamides, such as propylthiouracil, carbimazole,
and methimazole
• radioiodine (131I) treatment or
• thyroidectomy.

21. Disorders of the parathyroid gland

22. Disorders of the parathyroid gland
• the four parathyroid glands are located posterior to the thyroid
gland.
• produce parathyroid hormone (PTH), which is the primary regulator
of calcium physiology
• Primary sites of actions are
Bone: induces calcium release
Kidney: enhances calcium reabsorption in the distal tubules
GI: through vit D which increases GI Ca+2 absorption

24. Hypoparathyroidism
• Most commonly seen following thyroidectomy, when it is usually
transient but may be permanent
• May also occur after surgical removal of a parathyroid adenoma for
primary hyperparathyroidism
• Other causes include: autoimmune, congenital
• Results in hypocalcemia and hyperphosphatemia

25. Clinical features
• In the acute state causes tetany, with muscle cramps, irritability,
carpopedal spasm, and convulsions; tingling of the circumoral area,
hands, and feet is almost always present
• Symptoms of the chronic disease are lethargy, personality changes,
anxiety state, blurring of vision due to cataracts, parkinsonism, and
mental retardation
• Chvostek's sign: facial muscle contraction on tapping the facial nerve
in front of the ear
• Trousseau's phenomenon: carpal spasm after application of a cuff

26. Carpopedal
spasm

27. Chvostek’s
sign
Trousseau's
phenomenon

28. Laboratory features
• Serum calcium-low
• Serum phosphate-high
• PTH-low
• Serum Magnesium- Hypomagnesemia frequently accompanies
hypocalcemia and may exacerbate symptoms and decrease
parathyroid function
• ECG shows prolonged QT intervals and T wave abnormalities

29. Treatment
• IV Calcium gluconate initially
• Oral calcium supplementation
• Vit D
• Monitoring of serum calcium at regular intervals (at least every 3
months) is mandatory

30. Hyperparathyroidism
• Primary hyperparathyroidism is caused by hypersecretion of PTH,
usually by a single parathyroid adenoma, and less commonly by
hyperplasia by two or more parathyroid glands, or carcinoma
• Results in hypercalcemia
• Chronic bone resorption induced by excessive PTH in the circulation
may produce
• Diffuse demineralization,
• Pathologic fractures, or
• Cystic bone lesions throughout the skeleton (osteitis fibrosa cystica).

32. Clinical features
• The most common clinical presentation of primary
hyperparathyroidism is asymptomatic hypercalcemia
• Symptoms and signs of hyperparathyroidism
Bone disease
Nephrolithiasis
Hypophosphatemia
Increased production of calcitriol
Proximal renal tubular acidosis
Hypomagnesemia
Hyperuricemia and gout
Anemia

33. • Clinical manifestations of hypercalcemia
Polyuria, polydipsia, Nephrolithiasis, Nephrogenic DI
Anorexia, N&V, PUD, Pancreatitis
Muscle weakness, bone pain, osteopenia
Decreased concentration, confusion, coma
Bradycardia, hypertension, shortening of the QT interval

34. Laboratory findings
• Serum Ca+2- elevated
• Serum PTH- high
• Serum phosphate- low

35. Treatment
• Parathyroidectomy: in symptomatic patients
• A number of measures should be recommended to patients who do
not undergo surgery, including the following:
Avoid factors that can aggravate hypercalcemia, including thiazide
diuretic, volume depletion, prolonged bed rest or inactivity, and a
high calcium diet
Encourage physical activity to minimize bone resorption.
Encourage adequate hydration
Maintain a moderate calcium intake
Maintain moderate vitamin D intake

36. Disorders of the adrenal gland
• The adrenal glands (also known as suprarenal glands) are endocrine
glands that produce a variety of hormones including adrenaline and
the steroids aldosterone and cortisol.
• They are found above the kidneys.
• Each gland has an outer cortex which produces steroid hormones
and an inner medulla.

38. • The adrenal cortex produces three classes of corticosteroid
hormones:
glucocorticoids (e.g., cortisol),
mineralocorticoids (e.g., aldosterone),
adrenal androgen precursors (e.g., dehydroepiandrosterone [DHEA])
• The medulla produces catecholamines epinephrine and
norepinephrine
• Disorders of the adrenal cortex are characterized by deficiency or
excess of one or several of the three major corticosteroid classes.

40. • Hormone deficiency can be caused by inherited glandular or
enzymatic disorders or by destruction of the pituitary or adrenal
gland by autoimmune disorders, infection, infarction, or iatrogenic
events such as surgery or hormonal suppression.
• Hormone excess is usually the result of neoplasia, leading to
increased production of ACTH by the pituitary or neuroendocrine cells
(ectopic ACTH) or increased production of corticosteroids by adrenal
nodules.

41. Cushing’s syndrome
• A rare disease which reflects a constellation of clinical features that
result from chronic exposure to excess glucocorticoids of any etiology
• It can be
ACTH-dependent: eg. pituitary corticotrope adenoma, ectopic
secretion of ACTH by nonpituitary tumor
ACTH-independent: eg. adrenocortical adenoma, adrenocortical
carcinoma, nodular adrenal hyperplasia
Iatrogenic: eg. administration of exogenous glucocorticoids
• The term Cushing’s disease refers specifically to Cushing’s syndrome
caused by a pituitary corticotrope adenoma.

42. Clinical manifestations

43. Cushing
syndrome

44. Diagnosis
• 24-h urinary free cortisol excretion- high
• Dexamethasone suppression test- failure to appropriately suppress
morning cortisol after overnight exposure to dexamethasone
• Midnight cortisol-evidence of loss of diurnal cortisol secretion with
high levels at midnight
• Plasma ACTH

45. Treatment
• Surgery based on the underlying cause
• Medical therapy may have a place

46. References
• Harrison’s principles of internal medicine, 19th ed.
• Uptodate 21.6

47. Quiz

48. 1. Which one of the following is an example of disorder caused by
excess hormone production?
A. DM type I
B. DM type 2
C. Cushing syndrome
D. Addison’s disease
2. Of the endocrine glands in our body, one is considered as “master
gland”
A. Adrenal gland
B. Pituitary
C. Parathyroid gland
D. Testis/Ovary

49. 3. In type I diabetic patients, which one of the following is considered
as an underlying pathogenic mechanism?
A. Insulin resistance
B. Excessive production of glucagon
C. Autoimmune destruction of beta pancreatic cells
D. All
4. Which one of the following is not the clinical manifestation of
thyrotoxicosis?
A. Irritability
B. Sinus tachycardia/ AF
C. Hot intolerance
D. Hypoactivity

50. 5. Which one of the following is among acute complications of DM?
A. Diabetic foot ulcer
B. Hypoglycemia
C. Peripheral vascular disease
D. Peripheral neuropathy
6. In which of the following endocrine disease can we alter the natural
history by different intervention including exercise, nutrition,…?
A. Type I DM
B. Graves disease
C. Hyperparathyroidism
D. Type II DM

51. 7. Which of the following statement about DM is true?
A. DKA only occurs in type I DM
B. The prevalence of DM in Ethiopia is decreasing
C. Chronic complications of DM only occurs in type II DM
D. Older individuals >45 years of age should be screened for type II
DM
8. Which one of the following diseases can be prevented by utilization
of iodinized salts?
A. Thyrotoxicosis
B. Gestational DM
C. Hypothyroidism
D. Addison’s disease

52. 9. The commonest cause of primary hyperthyroidism is
A. Iodine deficiency
B. Toxic MNG
C. Hashimoto’s thyroiditis
D. Graves disease
10. Comprehensive diabetic care doesn’t include
A. Optimized and individualized glycemic control
B. Foot care
C. Diabetic education
D. Eye screening
E. All
F. None
11. Mention hormone produced by pineal gland and its use…..BONUS
Answer melatoninused for sleep awake cycle