It Gives Information about Thyroid disease(its type), Thyroid Gland & Thyroid System. The Presentation also Give information on Hyperthyroidism ( like its Etiology, Symptoms, Diagnostic Evaluation and Treatment.

1. THYROID DISEASE
Prepared By:- Rohitkumar S.
Rathi
Student:- Final year B-pharm

2. THYROID GLAND
• Two lobes
• Situated in the lower neck
• Synthesise, stores, release T3 & T4
(triiodothyronine & thyroxine)
BIOSYNTHESIS
• Dietary iodine Inorganic iodide
• Iodide + Tyrosine Monoiodotyrosine
• Monoiodotyrosine + Iodide Diiodotyrosine
• A coupling reaction binds MIT & DIT T3 & T4

4. • Hypothalamus
• TRH
• Pituitary gland
•
• TSH
• inhibit Thyroid gland stimulate
•
• increased decreased
• level TH level
•

5. • HORMONE TRANSPORT
• TSH Stimulation T3 & T4 Cleaved from thyroglobulin
Released to circulation
• In circulation , TH Bound to plasma proteins
Advantages
 Protect from premature metabolism and excretion.
 Prolongs half life in circulation.
 Reach its site of action.
 Hormone is metabolized by deiodination.

6. HORMONE FUNCTION
 Growth and development
 Increasing rate of metabolism
 Increase metabolic rate in CVS increases blood flow,
cardiac output, heart rate.
 Regulating cerebral conduction in CNS
 Sleep
 Lipid metabolism

7. THYROID FUNCTIONS TEST
 Serum total thyroxine (TT4)
 Serum total triiodothyronine (TT3)
 Resin triiodothyronine uptake (RT3U)
 Serum thyrotropin assays
 Free thyroxine index

8. Serum total thyroxine (TT4)
 Test indicating hormone availability to tissues
 Total (free & bound) T4 is determined by radioimmunoassay.
 Disease & condition interactions are possible
 Normal range : 5-12 mcg/dL

9. Serum total triiodothyronine (TT3)
 Measures total (free & bound) T3
 Useful for early detection or to rule out hyperthyroidism
 Not diagnostically significant for hypothyroidism
 Normal range : 80 -180 ng/dL

10. Resin triiodothyronine uptake (RT3U)
 Test clarifies whether abnormal T4 levels are the result of a thyroid
disorder or abnormalities in the binding proteins.
 Evaluate binding capacity of thyroxine binding globulin (TBG).
 If abnormalities in binding proteins underlie the abnormal levels of
TH , TH level decreases with TBG level increases.
 Normal range – 35 % to 45 %

11.  Several drugs can cause changes in the resin triiodothyronine
uptake
 Asparaginase
 Contraceptives
 Oral corticosteroids
 Estrogens
 Fluorouracil

12. Serum thyrotropin (TSH) assays
 Most sensitive test for detecting the hypothyroid state
 Slight decrease in TH level release more TSH
 Done by immunoradiometric or immunometric (using monoclonal
antibody) method.
 Used for diagnostic and monitoring purpose.

13.  Control over treatment (TSH < 0.4mlU/L)
 Over treatment may cause
 reduced bone density
 ECG changes
 Atrial fibrillation
 LFT elevation

14. Free thyroxine index
 Estimation of the free T4 level through a mathematical
interpretation of the relationship between resin triiodothyronine
uptake and T4 levels.
FTI = TT4×RT3U/mean serum RT3U.
 Normal range – 5.5 to 10.5
 Elevated in hyperthyroidism.

15. THYROID DISEASE
HYPOTHYROIDISM
HYPERTHYROIDISM

17. HYPOTHYROIDISM
 Inability of thyroid gland to supply sufficient thyroid hormone.
PRIMARY SECONDARY
TERTIARY SUBCLINICAL
TYPES

18. PRIMARY HYPOTHYROIDISM
 Result of gland destruction or dysfunction caused by disease or
medical therapies (e.g. Radiation or surgical procedure)
 Or failure of the gland to develop or congenital incompetence
(cretinism)
SECONDARY HYPOTHYROIDISM
 Result of pituitary disorder that inhibits TSH secretion. So lack of
appropriate stimulation.
TERTIARY HYPOTHYROIDISM
 Due to defect of hypothalamus to secrete TRH , to stimulate
pituitary.

19. SUBCLINICAL HYPOTHYROIDISM
 Refers to patient without clinical symptoms
 Normal free thyroxine level and elevated TSH level.
 Treatment not recommended.

20. CAUSES
1) Hashimoto thyroiditis
 Autoimmune disorder
 In which the thyroid gland is gradually destroyed by a variety of
cell- and antibody-mediated immune processes.
2) Treatment of hyperthyroidism
 over usage of antithyroid drugs

21. 3)Goiter
ENDEMIC
•Due to inadequate
dietary intake of
iodine
SPORADIC
•Due to ingestion of
drugs and foods
containing
progoitrin.

22.  Progoitrin hydrolysis Goitrin (activated)
 Goitrins inhibit oxidation of iodine to iodide.
 So they decrease the TH production.
Food & drugs containing Progoitrin
• Cabbage, Spinach,
Mustard, Cauliflower,
Peanuts etc.
Food
•Propylthiouracil,
Phenylbutazone,
Cobalt, Lithium etc.
Drug

23. SIGNS AND SYMPTOMS
EARLY…………………….
 Lethargy
 Fatigue
 Forgetfulness
 Unexplained weight gain
 Sensitivity to cold
 Constipation
PROGRESSIVE……………..
 Dry, inelastic skin
 Slowed speech and thought
 Puffy face
 If untreated – MYXEDEMA COMA

24. THERAPEUTIC AGENTS
1) Desiccated thyroid preparations
 Prepared from beef and pork
 Now not much used due to lack of bio equivalency with new
agents.
2)Fixed-ratio liotrix preparations
 Synthetic thyroid agent
 Combination of T3 & T4
 Not considered drug of choice for replacement therapy because
offers no therapeutic advantage over levothyroxine sodium and may
result in excessive serum T3 concentrations.
 Adverse effects (T3) includes tremor, headache, palpitations etc

25. 3) Levothyroxine (levothroid, synthroid, levoxyl)
 Agent of choice.
 Predictable result & lack T3 induced side effects.
 Average adult maintenance dose is 75-150 µg/day
Precautions and monitoring
 Elderly patient and patient with cardiac disease – begin therapy
with low dose (25 µg/day)
 Gradually increase the dose – usually <100µg/day
 Possibility of cardiac complications (angina ,palpitations,
arrhythmias)
 Monitor sensitive TSH test , T4 levels.
 Long term therapy can cause thyrotoxicosis (T4).

26. • Accelerate bone loss
• Drug interactions
1) Cholestyramine & colestipol – 6hr gap is needed
2) Calcium carbonate
3) Estrogens & selective estrogen receptor modulators – reduce the
free T4 levels & TSH levels.
4) Raloxifene – malabsorption
5) Ciprofloxacin

27. HYPERTHYROIDISM

28.  DEFINITION
Hyperthyroidism is defined as increased
synthesis and release of thyroid hormones
by the thyroid gland.

29.  INCIDENCE
The incidence of hyperthyroidism is 4 to 10
times greater in women and the highest
frequency is in the 30-50 years age.

30. ETIOLOGY
 GRAVES DISEASE
 MULTINODULAR GOITER
 THYROID TUMOR
 TREATMENT OF HYPOTHYROIDISM
 RADIATION EXPOSURE
 HEREDITY

32. PATHOPHYSIOLOGY
 Excess TSH release from the pituitary
gland
overstimulation of thyroid gland
increased thyroid hormone level
increased metabolic rate

33. Increased number of beta adrenergic
receptors in the body
Enhance the activity of nor epinephrine
Fight or flight response
Symptoms of hyperthyroidism

34. SYMPTOMS
 CARDIOVASCULAR SYSTEM
Tachycardia
Palpitation
Increased cardiac output
Heart intolerance

35. NEUROLOGICAL
Fatigue
Restlessness
Insomnia
Emotional instability
Tremor

36. Pulmonary
Dyspnea
Intugmentary
Diaphoresis
Soft hair

37. Gastrointestinal system
Increased appetite
Weight loss
Diarrhoea

38. REPRODUCTIVE SYSTEM
Erectile dysfunction
Amenorrhea

39. DIAGNOSTIC EVALUATION
HISTORY COLLECTION
PHYSICAL EXAMINAION
SERUM T3 , T4 & TSH TEST
THYROID SCAN
TRH STIMULATION TEST

40. TREATMENT
I) BETA BLOCKERS
 Propranolol
 Reduce peripheral manifestations like tachycardia, sweating,
tremor, nervousness etc.
 Also inhibit peripheral conversion of T4 to T3
II) ANTITHYROID AGENTS
1) Propylthiouracil
2) Methimazole
 Direct interfere with thyroid hormone synthesis.
 Inhibit iodine oxidation and coupling

41. PROPYLTHIOURACIL
 For adults the initial dose is 300-450 µg/day as tid
 Adult with severe disease require 600-1200 µg/day initially.
 Initial dose is continued for about 2 months , then a
maintenance
 dose of 100-150 µg/day is given as od or bd up to 1 year.
 Then gradually discontinued over 1-2 months

42. METHIMAZOLE
 Initial dose range is 5-60 µg/day as tid
 After 2 month of therapy a maintenance dose of 5-30 µg/day is
initiated, continued up to 1 year and gradually discontinued
over 1-2 months
PRECAUTIONS & MONITORING
 Serum thyroid levels & free thyroxine index should be
monitored.
 Adverse effects includes…….
 Dermatologic reactions – rash, urticaria, pruritus, hair loss,
skin pigmentation
 Headache, drowsiness, nausea, vomiting, vertigo, loss of taste,
myalgia, joint pain etc.

43.  Serious adverse effects includes…….
 Hematological abnormalities
 Drug fever
 Hepatitis

44. RADIO ACTIVE IODINE(Destroy thyroid tissue)
 Thyroid gland picks up iodine-131
 This treatment takes advantage of the fact that thyroid cells are the
only cells in the body which have the ability to absorb iodine
 By giving a radioactive form of iodine, the thyroid cells which
absorb it will be damaged or killed.
ADVANTAGES
1. High cure rate
2. Avoid surgical risk
3. Less expensive

45. DISADVANTAGES
1. Risk of delayed hypothyroidism (excessive cell death).
2. Genetic damage
DOSAGE
 A dose of 80-100 mCi of iodine 131/estimated gram of thyroid
gland recommended.
PRECAUTIONS & MONITORING
 Generally reserved for patients past the child bearing years.
 Monitored for early recurrent of hyperthyroidism and later
for hypothyroidism.

46. SURGERY
 Subtotal thyroidectomy
 If drug therapy fails or radioactive iodine is undesirable
 Rapid cure
 Success rate is high
 Difficult procedure & complications

47. THYROID STORM
 Sudden exacerbation of hyperthyroidism
 Rapid release of thyroid hormone
 Fatal, if not treated
 Leads to dehydration, shock and death
 Precipitating factors includes
 Thyroid trauma
 Surgery
 Radio active iodine
 Infection and sudden stopping of antithyroid therapy
 TT4 level – 25-30 µg/dL (Normal 5-12 µg/dL)

48.  Fever, tachycardia, restlessness, tremor
TREATMENT
 Propylthiouracil – 150-250 µg orally Q6H
 Block peripheral T4 T3
 Methimazole – 15mg orally Q6H (if necessary)
 Propranolol – 20-200 mg orally Q6H or 1-3mg iv Q4-6H (unless
contraindicated)
 Potassium iodide – 50-100mg Q12H (minimize intrathyroidal
iodine uptake)
 Supportive therapy – rest, rehydration, cooling, sedation etc.

49. REFERENCES
 Textbook Of Therapeutics – Drug And Disease
management ; 8th edition – Eric T. Herfindal
 Pharmacotherapy- A Pathophysiologic Approach ;
7th edition - Joseph T. Dipiro
 Clinical Pharmacy and Therapeutics ; 4th edition -
Roger Walker and Cate whittlesea
 Comprehensive Pharmacy Review ; 7th edition -
Leon Shargel
 Essentials of medical Pharmacology ; 8th edition -
K DTripathi
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50. Thank you