This presentation covers different thyroid and parathyroid disorder, their aetiology, clinical manifestation, signs, symptoms, treatments and case studies.

1. Disorders of Thyroid and
Parathyroid Gland
Presented By:
Nahid Akter
Frazana Islam
Kanzil Moula
Shaikat Marcel Gomes
Tasnova Nowrin
Azamu Shahiullah Prottoy
Shimu Akter
East West University
Program : M. Pharm in Clinical pharmacy and Molecular Pharmacology

2. Key points
Gland
Disorder
Case Study

3. Thyroid Gland
• Front part of the neck
• Two lobes
• Small Bridge- Isthmus
Parathyroid Gland
• Four pea sized glands
• Just behind thyroid gland

4. DisordersThyroidGland
• Hypothyroidism
• Hyperthyroidism
ParathyroidGland
• Hypoparathyroidism
• Hyperparathyroidism

5. Decreased production of thyroid
hormone or very rarely, form
tissues resistance
Epidemiology
 Primary hypothyroidism in UK
is common, hypothyroidism
being 3 per 1000 women.
 Total prevalence is of the order
of 14 per 1000 women whereas
<1 per 1000 men.
 10-20 times more frequently in
women than in men.
 30-60 years of age.
Classification
 Primary hypothyroidism
 Congenital hypothyroidism
 Immune
 Latrogenic
 Iodine deficiency
 Secondary hypothyroidism
 Hypopituitarism
 Hypothalmic
 Peripheral hypothyroidism
 Insensitivity to thyroid hormone
Hypothyroidism/Thyrotoxicosis
Aetiology

6. Signs and symptoms
of Hypothyroidism
• Skin and appendages : dry, cool,
flaking, thickened skin reduced
sweating, yellowish complexion, dry
hair, brittle nails .
• Neuromuscular system: slow
speech, poor memory and cognitive
function, carpal tunnel syndrome,
depression, hearing loss, muscle
pain and weakness
• Metabolic abnormalities: LDL
cholesterol, macrocytic anemia
• Cardiovascular: reduced cardiac
output , cardiac enlargement
• Gastrointestinal disturbance
Prevalence of hypothyroidism after
treatment of thyrotoxicosis
Treatment Options
 Thyroidectomy
6-75% hypothyroidism
Risk highest during first year after
surgery
 Antithyroid drugs [ >6 months ]
43% relapse in the first year
13-21% relapse in the next 4 years
 I therapy
24-90 % develop

7. Hyperthyroidism/Thyrotoxicosis
 Production of excessive amounts of
thyroid hormones
 Clinical syndrome associated with
prolonged exposure to elevated
levels of thyroid hormones
Epidemiology:
• 4.7/1000 women with active
disease
• The population prevalence
rose to 20/1000 in women
(for previously treated cases)
Aetiology
Graves disease
Thyroiditis
Nodular disease
Clinical Manifestations

8. Hyperthyroidism/Thyrotoxicosis
Exam & Tests:
Physical exam include:
High systolic blood pressure,
Increases heart rate, Enlarged
thyroid gland, Swelling or
inflammation around eyes, skin, hair
and nail changes
Blood tests:
1. Measuring TSH, T3 and T4,
2. Checking blood cholesterol levels
and glucose level
Imaging tests:
1. Radioactive iodine uptake and scan
2. Thyroid ultrasound
Investigation:
 Plasma free T3 or T4 levels are elevated
 TSH level is suppressed to subnormal
levels
Treatments:
1. Antithyroid medicines
- Propylthiouracil (PTU)
- Methimazole
- Thionamides
2. Thyroid ablative therapy
- Radioactive iodine
- Surgery

9.  Failure of parathyroid glands to
secrete parathyroid hormone.
 Failure of parathyroid hormones
action at the tissue level.
Aetiology
 Postsurgical
Medical
1. Autoimmune disease
2. Genetic disease
3. Infiltration of parathyroid glands
Epidemiology
In the united states, the surgical-
based incidence approach yielded
117,342 relevant surgeries resulting in
8901 cases in the year 2007 among
which almost 7.6% of surgeries
resulted in hypoparathyroidism (75%
transient, 25% chronic).
Clinical manifestation
o Numbness and tingling around
the mouth
o Muscle spasm
o Epilepsy
o Irritability
oCataracts
oPositive Trousseau’s sign
oPositive Chvostek’s sign
Hypoparathyroidism

10. Investigation
 Hypocalcaemia is primary
biochemical abnormality.
 Hyperphosphataemia.
 Pseudohypoparathyroidism can
be distinguished if there excessive
PTH secretion and reduced target
organ responsiveness.
 Drugs (calcitonin, plicamycin,
phosphates, bisphosphates,
cisplatin, 5-fluoro uracil)
Treatment
 PTH therapy
 Oral
– Vitamin D preparation
(ergocalciferon, colecalciferol,
calcitriol, dihydrotachysterol)
– Calcuim supplementation
 Intravenous (10% calcium
gluconate, alfacalcidol, calcitriol)
Hypoparathyroidism

11. Hyperparathyroidism
Occurs due to increased production of PTH.
 Two types of hyperparathyroidism:
1. Primary hyperparathyriodism
2.Secondary Hyperparathyroidism
 Epidemiology
25/100000 of the population per year.
Incidence is 2 to 3 times higher in
women.
 Aetiology
• Primary hyperparathyroidism
occurs due to single parathyroid
adenomas or rarely hyperplasia
of all four glands.
• Secondary hyperparathyroidism
occurs due to chronic renal
failure and vitamin D deficiency.

12.  Clinical manifestation
 Bone disease and renal stone are relatively
uncommon. Radiology evidence is rare in
these patients.
 Measurement of bone mineral content by
densitometry scanning indicates bone loss
and risk is increased.
Hyperparathyroidism
 Signs and symptoms
 Anorexia
 Weight loss
 Polyuria
 Mental changes (poor
concentration and memory)
 Fatigue
 Nausea
 Vomiting
 Constipation
 Hypertension
 Renal stone
 Bone pain and deformity.

13.  Investigation
Hypercalcaemia is the primary biochemical
abnormality in primary hyperparathyroidism.
 Phosphate level decreased.
 PTH level elevated.
 Other causes of hypercalcaemia include
 Malignancy
 Drugs (thiazides, excess vitamin D)
 Thyrotoxicosis
 Sarcoidosis.
 For neck exploration surgeons require neck
ultrasound.
 Isotope scanning, CT, MRI and selective
venous sampling is also done.
Hyperparathyroidism
 Treatment
 Surgical removal of gland
 Bisphosphonates for osteoporosis,
anti-hypertensives, acid-lowering
therapy and laxatives.
 Approximately 10% patient
develop permanent
hyperparathyroidism.

14. Mrs HP is a 49-year-old professional singer with Graves’ disease.
She was initially treated with Carbimazole but developed a severe
generalised rash, which necessitated withdrawal of the drug. A
similar rash occurred within 2 weeks of starting PTU. She is overtly
thyrotoxic with a blood pressure of 160/50 mmHg, a pulse of 110
beats/min and a large thyroid gland with a vascular bruit.
Laboratory results show an elevated free T4 and an undetectable
TSH.
Case Study
1. What are the options for treatment and what factors could influence her
choice of treatment modality?
2. If Mrs HP elects to have an ablative dose of radioactive iodine,
what adjunctive therapy would you now consider?

15. 1. What is Mrs MG's thyroid state?
2. Should T4 therapy be instituted, and if so, how should it be
monitored?
Mrs Smith is a 66-year-old woman. She has a history of
depression over many years and has recently been
complaining of increased tiredness, lethargy and weight
gain.
Thyroid function tests have shown a TSH elevated at 12
mU/L (normal range, 0.3–5 U/L), but her free T4 is normal
at 12.7 pmol/L (normal range, 10.5–25 pmol/L).
Case Study

16. Conclusion
• The parathyroid glands make parathyroid hormone (PTH),
• Keep the right balance of calcium and phosphorous.
• Disruption in this balance cause diseases .
• Treatment is aimed at restoring the balance of calcium and
phosphorous.
Hyperparathyroidism Hypoparathyroidism
Extra/elevated PTH Less PTH
Blood calcium rises Low blood calcium level.
Nausea, vomiting, constipation, or passing large
amounts of urine
These may include 'pins and needles' in the face, hands or feet,
or muscle spasms known as tetany in the hands
For most patients the best treatment is surgery to
remove the affected gland. This cures the
condition.
Calcium infusions may be needed for the immediate treatment
of a patient with severe symptoms. long term the most widely
used treatment is with an analogue of vitamin D
Two types primary and secondary

17. • The thyroid regulates your metabolism.
• The two main thyroid hormones are T3 and T4.
• Thyroid disorders are common, and they include goiters,
hyperthyroidism, and hypothyroidism.
• They can develop at any age
Conclusion