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

Key points

Gland

Disorder

Case Study

Thyroid Gland

• Front part of the neck

• Two lobes

• Small Bridge- Isthmus

Parathyroid Gland

• Four pea sized glands

• Just behind thyroid gland

DisordersThyroid G

land

• Hypothyroidism

• Hyperthyroidism

Parathyroid G

land

• Hypoparathyroidism

• Hyperparathyroidism

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/ThyrotoxicosisAetiology

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

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

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

Failure of parathyroid glands to secrete parathyroid hormone.

Failure of parathyroid hormonesaction 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 manifestationo Numbness and tingling around

the mouth

o Muscle spasm

o Epilepsy

o Irritability

oCataracts

oPositive Trousseau’s sign

oPositive Chvostek’s sign

Hypoparathyroidism

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

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.

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.

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.

Mrs HP is a 49-year-old professional singer with Graves’ disease.She was initially treated with Carbimazole but developed a severegeneralised rash, which necessitated withdrawal of the drug. Asimilar rash occurred within 2 weeks of starting PTU. She is overtlythyrotoxic with a blood pressure of 160/50 mmHg, a pulse of 110beats/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?

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 ofdepression over many years and has recently beencomplaining of increased tiredness, lethargy and weightgain.

Thyroid function tests have shown a TSH elevated at 12mU/L (normal range, 0.3–5 U/L), but her free T4 is normalat 12.7 pmol/L (normal range, 10.5–25 pmol/L).

Case Study

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

• 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