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Hypothyroidism
Moderator- Dr MANZOOR WANI
Department of Gastroenterology
BY DR DEVARJUN PANNU
1ST YEAR DNB MEDICINE, JLNM SRINAGAR
Case of Hypothyroidism
• History – Rafeequa 34 year old unmarried female complains of fatigue,
blurring of vision , vertigo, cold intolerance, menorrhagia , and constipation .
• Physical examination- Vital signs includes a temperature of 97 F , pulse of
64/ min and regular , BP – 90/60 mm of Hg . She is thin weighing 41.5 kg ,
small 4’7 inches speaks slowly with pale with pale , cool , dry skin . The
thyroid gland is not palpable . The deep tendon reflux is delayed .
• Laboratory studies - WBC - 5,500/ml , Hg – 11.3 g/dl ( Microcytic
Hypochromic ), Platelets-=1,14,000/ml . Serum TSH- 432 uIU/ ml , T3 -0.35
ng/ml , T4 - 5.66 ug/dl . ESR - 15 mm/ hour , serum cholesterol 201mg/dl.
Radiological Investigation
 USG Abdomen- Liver Hypertrophied left caudate lobe with
atrophied Right lobe heterogeneous echo pattern with modular
margins. Gall bladder
showing multiple calculi (largest12mm) . Kidney Bilateral
medullary nephrocalcinosis
 USG thyroid- Chronic thyroiditis with heterogeneous parenchyma
echo pattern with increased vascularity in Doppler . Left lobe
shows well encapsulated nodule 26*17*26 mm with volume 6.3 ml
with central cystic area 8*8mm . ? Follicular neoplasm ,
?Adenomatous nodule TIRADS Grade 3
X- ray
HYPOTHYROIDISM
•2nd MC endocrine disorder after Diabetes Mellitus
•MC cause of hypothyroidism worldwide - iodine
Deficiency
•MCC in iodine sufficient areas- Hashimoto's
Thyroiditis
•99% cases- Primary Hypothyroidism
•<1% cases- Secondary Hypothyroidism
•Easy to diagnose & gratifying to treat
Introduction
 Condition where there is a reduced production of thyroid
hormone. Categorized as primary and secondary on the basis
of its cause
 Primary Hypothyroidism occurs due to improper functioning
of the thyroid gland.
May be further classified as overt and subclinical
hypothyroidism. Affects approximately 5% of individuals with
elderly women being most commonly affected.
 Secondary Hypothyroidism occurs due to inadequate
stimulation of thyroid gland by thyroid stimulating hormone
(TSH). May be due to
congenital or acquired defects in the pituitary or hypothalamus.
Primary Hypothyroidism Etiology
 Thyroid dysfunction -
 Autoimmune thyroiditis (Hashimoto's thvroiditis)
 Congenital absence or defect in the thyroid tissue
 Thyroid removal by surgery
 Radio ablation by radio active iodine or irradiation
 Destruction of thyroid tissue caused by infiltrative
 disorders(amyloidosis,sarcoidosis)
 Impaired synthesis of thyroid hormone -
 lodine deficiency---MOST COMMON CAUSE
 Congenital enzymatic defects
 Drug-mediated: thionamides , amiodarone , lithium, aminoglutethimide, carbemazole
Secondary Hypothyroidism Etiology
Reduced secretion of TRH or TSH
• Hypothalamic disorders
1. Tumor (lymphoma, germinoma , glioma)
2. Infiltrative disorders (sarcoidosis, hemochromatosis, and histiocytosis)
• Hypopituitarism
1. Mass lesions
2. Pituitary surgery
3. Pituitary irradiation
4. Hemorrhagic apoplexy (Sheehan's syndrome)
5. Lymphocytic hypophysitis
Clinical Manifestations Symptoms
 Tiredness/weakness -
 Weight gain with poor appetite
 Dry skin
 Cold sensation
 Hair loss(diffuse alopecia)
 Nail growth is retarded
 Poor concentration/memory loss
 Constipation
 Dyspnea
 Hoarseness of voice
 Hearing Impairment
 Carpal tunnel syndrome
 Menorrhaqia(miscarriage)
 Paresthesia
Clinical Manifestations Signs
 Cold peripheral extremities
 Dry, coarse and yellow skin
 Puffiness of face, hands and feet
 Pre tibial non pitting edema
 Hair loss and brittle nails
 Bradycardia/ diastolic hypertension
 Slow relaxation of tendon reflex (woltmans sign)
 Serous cavity effusions
 Normal/enlarged/atrophied thyroid gland
 Hypothyroidism in children
 Delayed growth in children and delayed appearance of permanent teeth
 Delayed or precocious puberty
 Pseudohypertrophy of muscles
Maternal Hypothyroidism
 One of the most common endocrine disorders in pregnancy .
 Overt hypothyroidism found in 1.3 per 1000 pregnant women and
subclinical hypothyroidism in 23 per 1000 pregnant women .
 Most common cause: endemic iodine deficiency .
 Women with hypothyroidism carry an increased risk of infertility,
miscarriage, and obstetric complications
 Foetal complications: premature birth, low-birth weight (LBW), fetal
distress in labor, fetal death, perinatal death, and congenital
hypothyroidism .
 Even an untreated subclinical hypothyroidism during pregnancy can
lead to cognitive impairment in the offspring.
CONGENITAL HYPOTHYROIDISM
 1 in 4000 newborns
 2: 1 incidence in males as compared to males
 Can be
• Transient - if the mother has TSH-R blocking antibodies
• Permanent- majority
 Causes
• 80-85% cases - Thyroid gland dysgenesis
• 10-15% cases- Inborn errors of Thyroid hormone synthesis
• 5% cases- TSH-R antibody mediated
 Gene Mutations include:
PROP-1, PIT-1, TSH-receptor, TSH beta, Thyroid Peroxidase,
Thyroglobulin, Pendrin
Clinical manifestations
 Majority- appear normal at birth
 Few cases are diagnosed on the basis of clinical features &
biochemical screening
• Clinical Features include:
 Prolonged jaundice
Feeding problems
Hyotonia
 Enlarged tongue, Umbilical hernia
 Delayed bone maturation
• Complications:
 4 times increased chances forCongenital malformations (Cardiac)
 Permanent neurological damage
Diagnosis and Treatment
 Neonatal Screening programs
 Measurement of TSH or T4
 Heel prick blood sample
 • Treatment dose:
 T3 = 10-15 ug/kg per day
 Regular TSH monitoring
Management
Treatment- Clinical Hypothyroidism
 Dose of Levothyroxine (T4)
 Ideal time of taking?
 Goal of treatment?
 TSH monitoring?
 Symptom relief?
 Risk of over-treatment?
 Issues with adherence?
 Do not feel any difference after missing few doses
 If misses single dose?
 Increased requirements?
Subclinical hypothyroidism
 Indications of treatment
 TSH > 10 mlU/L
 TSH < 10 mIU/L
1. Symptoms, Goitre
2. Family history of autoimmune thyroid disease
Planning pregnancy or pregnant
3. .TPO antibody positive
4. Evidence of heart disease, dyslipidemia
5. Infertilitv
6. Psychiatic disorders
 Dose
 Start with low dose- 25-50 ug/day
Pregnancy
 Thyroid function should be monitored
 Before conception- therapy to target TSH in normal range
 TFT
1. Every 4 weeks in first half of preghancy
2. every 6-8 weks after 20 weeks
 Levothyroxine dose is increased by 45%
 After delivery dose- Pre pregnancy levels
Elderly
 Require 20% less dose than younger specially cardiac
patients
Starting dose 12.5 to 20g/day
 Gradual increments in 2-3 months
Levothyroxine (T4) – Drug Interaction
 Increase LT4 dose with
1. Drugs that reduce thyroxine production: lithium, iodine-containing drugs, and
amiodarone
2. Drugs that/reduce thyroxine absorption: sucralfate, ferrous sulfate,
cholestyramine, colestipol, aluminum-containing antacids, and calcium
supplements
3. Drugs that increase thyroxine metabolism: rifampin, phenobarbital,
carbamazepine, warfarin, and oral hypoglycemic agents
 Decrease LT4 dose with
1. Drugs that displace thyroxine from binding proteins: furosemide, mefenamic
acid, salicylates, vitamin C
Myxedema Coma
 Myxedema coma is a rare life-threatening condition.It is the
decompensated state of severe hypothyroidism in which-the
patient is hypothermic and unconscious.
 The condition occurs most often among elderly women in the
winter months and appears to be precipitated by cold.
 Myxedema coma, occasionally called myxedema crisis, is a rare
life- threatening clinical condition that represents severe
hypothyroidism with physiological decompensation.
 The condition usually occurs in patients with long-standing,
undiagnosed hypothyroidism.
Why term Myxedema ?
 Myxedema is also used to describe
the dermatologic changes that occur in
hypothyroidism which refers to
deposition of mucopolysaccharides in
the dermis, which results in swelling of
the affected area.
Factors precipitating
 Infection, Exposure to cold temperatures,
 Trauma
 Burns
 Cerebrovascular accident , Myocardial infarction
 Congestive heart failure
 Respiratory acidosis
 Medications - sedatives, narcotics, amiodarone , rifampin, beta blockers.
 Decreased drug metabolism leading to overdosing of medications particularly
sedatives, hypnotics, and anaesthetic agents; this can precipitate myxedema coma.
 Metabolic disturbances - hypoglycemia, hyponatremia, acidosis and hypercapnia.
Myxedema Coma
 20-40% mortality
 Almost always - Elderly patient
 Precipitating conditions- That impair respiration
1. Drugs, Pneumonia, CHF, MI
2. CVA, GI bleed
 Levothyroxine
• (Initial-200-400 ug IV bolus or through Nasogastric tube f/b
• Daily oral dose 1.6 ug/kg
 Liothyronine (T3)
• Since T4->T3 conversion is impaired
• 5-20 ug followed by 2.5-10 ug 8 hrly
 Supportive therapy
1. External warming
2. Parenteral Hydrocortisone (50 mg every 6 hrly)
3. Treat precipitating factor
4. Ventilatory support, ABG
5. Hypertonic saline or IV detrose
Thank you
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Presentation (1)-2.pptx

  • 1. Hypothyroidism Moderator- Dr MANZOOR WANI Department of Gastroenterology BY DR DEVARJUN PANNU 1ST YEAR DNB MEDICINE, JLNM SRINAGAR
  • 2. Case of Hypothyroidism • History – Rafeequa 34 year old unmarried female complains of fatigue, blurring of vision , vertigo, cold intolerance, menorrhagia , and constipation . • Physical examination- Vital signs includes a temperature of 97 F , pulse of 64/ min and regular , BP – 90/60 mm of Hg . She is thin weighing 41.5 kg , small 4’7 inches speaks slowly with pale with pale , cool , dry skin . The thyroid gland is not palpable . The deep tendon reflux is delayed . • Laboratory studies - WBC - 5,500/ml , Hg – 11.3 g/dl ( Microcytic Hypochromic ), Platelets-=1,14,000/ml . Serum TSH- 432 uIU/ ml , T3 -0.35 ng/ml , T4 - 5.66 ug/dl . ESR - 15 mm/ hour , serum cholesterol 201mg/dl.
  • 3. Radiological Investigation  USG Abdomen- Liver Hypertrophied left caudate lobe with atrophied Right lobe heterogeneous echo pattern with modular margins. Gall bladder showing multiple calculi (largest12mm) . Kidney Bilateral medullary nephrocalcinosis  USG thyroid- Chronic thyroiditis with heterogeneous parenchyma echo pattern with increased vascularity in Doppler . Left lobe shows well encapsulated nodule 26*17*26 mm with volume 6.3 ml with central cystic area 8*8mm . ? Follicular neoplasm , ?Adenomatous nodule TIRADS Grade 3
  • 5. HYPOTHYROIDISM •2nd MC endocrine disorder after Diabetes Mellitus •MC cause of hypothyroidism worldwide - iodine Deficiency •MCC in iodine sufficient areas- Hashimoto's Thyroiditis •99% cases- Primary Hypothyroidism •<1% cases- Secondary Hypothyroidism •Easy to diagnose & gratifying to treat
  • 6. Introduction  Condition where there is a reduced production of thyroid hormone. Categorized as primary and secondary on the basis of its cause  Primary Hypothyroidism occurs due to improper functioning of the thyroid gland. May be further classified as overt and subclinical hypothyroidism. Affects approximately 5% of individuals with elderly women being most commonly affected.  Secondary Hypothyroidism occurs due to inadequate stimulation of thyroid gland by thyroid stimulating hormone (TSH). May be due to congenital or acquired defects in the pituitary or hypothalamus.
  • 7. Primary Hypothyroidism Etiology  Thyroid dysfunction -  Autoimmune thyroiditis (Hashimoto's thvroiditis)  Congenital absence or defect in the thyroid tissue  Thyroid removal by surgery  Radio ablation by radio active iodine or irradiation  Destruction of thyroid tissue caused by infiltrative  disorders(amyloidosis,sarcoidosis)  Impaired synthesis of thyroid hormone -  lodine deficiency---MOST COMMON CAUSE  Congenital enzymatic defects  Drug-mediated: thionamides , amiodarone , lithium, aminoglutethimide, carbemazole
  • 8. Secondary Hypothyroidism Etiology Reduced secretion of TRH or TSH • Hypothalamic disorders 1. Tumor (lymphoma, germinoma , glioma) 2. Infiltrative disorders (sarcoidosis, hemochromatosis, and histiocytosis) • Hypopituitarism 1. Mass lesions 2. Pituitary surgery 3. Pituitary irradiation 4. Hemorrhagic apoplexy (Sheehan's syndrome) 5. Lymphocytic hypophysitis
  • 9. Clinical Manifestations Symptoms  Tiredness/weakness -  Weight gain with poor appetite  Dry skin  Cold sensation  Hair loss(diffuse alopecia)  Nail growth is retarded  Poor concentration/memory loss  Constipation  Dyspnea  Hoarseness of voice  Hearing Impairment  Carpal tunnel syndrome  Menorrhaqia(miscarriage)  Paresthesia
  • 10. Clinical Manifestations Signs  Cold peripheral extremities  Dry, coarse and yellow skin  Puffiness of face, hands and feet  Pre tibial non pitting edema  Hair loss and brittle nails  Bradycardia/ diastolic hypertension  Slow relaxation of tendon reflex (woltmans sign)  Serous cavity effusions  Normal/enlarged/atrophied thyroid gland  Hypothyroidism in children  Delayed growth in children and delayed appearance of permanent teeth  Delayed or precocious puberty  Pseudohypertrophy of muscles
  • 11. Maternal Hypothyroidism  One of the most common endocrine disorders in pregnancy .  Overt hypothyroidism found in 1.3 per 1000 pregnant women and subclinical hypothyroidism in 23 per 1000 pregnant women .  Most common cause: endemic iodine deficiency .  Women with hypothyroidism carry an increased risk of infertility, miscarriage, and obstetric complications  Foetal complications: premature birth, low-birth weight (LBW), fetal distress in labor, fetal death, perinatal death, and congenital hypothyroidism .  Even an untreated subclinical hypothyroidism during pregnancy can lead to cognitive impairment in the offspring.
  • 12. CONGENITAL HYPOTHYROIDISM  1 in 4000 newborns  2: 1 incidence in males as compared to males  Can be • Transient - if the mother has TSH-R blocking antibodies • Permanent- majority  Causes • 80-85% cases - Thyroid gland dysgenesis • 10-15% cases- Inborn errors of Thyroid hormone synthesis • 5% cases- TSH-R antibody mediated  Gene Mutations include: PROP-1, PIT-1, TSH-receptor, TSH beta, Thyroid Peroxidase, Thyroglobulin, Pendrin
  • 13. Clinical manifestations  Majority- appear normal at birth  Few cases are diagnosed on the basis of clinical features & biochemical screening • Clinical Features include:  Prolonged jaundice Feeding problems Hyotonia  Enlarged tongue, Umbilical hernia  Delayed bone maturation • Complications:  4 times increased chances forCongenital malformations (Cardiac)  Permanent neurological damage
  • 14. Diagnosis and Treatment  Neonatal Screening programs  Measurement of TSH or T4  Heel prick blood sample  • Treatment dose:  T3 = 10-15 ug/kg per day  Regular TSH monitoring
  • 16. Treatment- Clinical Hypothyroidism  Dose of Levothyroxine (T4)  Ideal time of taking?  Goal of treatment?  TSH monitoring?  Symptom relief?  Risk of over-treatment?  Issues with adherence?  Do not feel any difference after missing few doses  If misses single dose?  Increased requirements?
  • 17. Subclinical hypothyroidism  Indications of treatment  TSH > 10 mlU/L  TSH < 10 mIU/L 1. Symptoms, Goitre 2. Family history of autoimmune thyroid disease Planning pregnancy or pregnant 3. .TPO antibody positive 4. Evidence of heart disease, dyslipidemia 5. Infertilitv 6. Psychiatic disorders  Dose  Start with low dose- 25-50 ug/day
  • 18. Pregnancy  Thyroid function should be monitored  Before conception- therapy to target TSH in normal range  TFT 1. Every 4 weeks in first half of preghancy 2. every 6-8 weks after 20 weeks  Levothyroxine dose is increased by 45%  After delivery dose- Pre pregnancy levels
  • 19. Elderly  Require 20% less dose than younger specially cardiac patients Starting dose 12.5 to 20g/day  Gradual increments in 2-3 months
  • 20. Levothyroxine (T4) – Drug Interaction  Increase LT4 dose with 1. Drugs that reduce thyroxine production: lithium, iodine-containing drugs, and amiodarone 2. Drugs that/reduce thyroxine absorption: sucralfate, ferrous sulfate, cholestyramine, colestipol, aluminum-containing antacids, and calcium supplements 3. Drugs that increase thyroxine metabolism: rifampin, phenobarbital, carbamazepine, warfarin, and oral hypoglycemic agents  Decrease LT4 dose with 1. Drugs that displace thyroxine from binding proteins: furosemide, mefenamic acid, salicylates, vitamin C
  • 21. Myxedema Coma  Myxedema coma is a rare life-threatening condition.It is the decompensated state of severe hypothyroidism in which-the patient is hypothermic and unconscious.  The condition occurs most often among elderly women in the winter months and appears to be precipitated by cold.  Myxedema coma, occasionally called myxedema crisis, is a rare life- threatening clinical condition that represents severe hypothyroidism with physiological decompensation.  The condition usually occurs in patients with long-standing, undiagnosed hypothyroidism.
  • 22. Why term Myxedema ?  Myxedema is also used to describe the dermatologic changes that occur in hypothyroidism which refers to deposition of mucopolysaccharides in the dermis, which results in swelling of the affected area.
  • 23. Factors precipitating  Infection, Exposure to cold temperatures,  Trauma  Burns  Cerebrovascular accident , Myocardial infarction  Congestive heart failure  Respiratory acidosis  Medications - sedatives, narcotics, amiodarone , rifampin, beta blockers.  Decreased drug metabolism leading to overdosing of medications particularly sedatives, hypnotics, and anaesthetic agents; this can precipitate myxedema coma.  Metabolic disturbances - hypoglycemia, hyponatremia, acidosis and hypercapnia.
  • 24. Myxedema Coma  20-40% mortality  Almost always - Elderly patient  Precipitating conditions- That impair respiration 1. Drugs, Pneumonia, CHF, MI 2. CVA, GI bleed  Levothyroxine • (Initial-200-400 ug IV bolus or through Nasogastric tube f/b • Daily oral dose 1.6 ug/kg  Liothyronine (T3) • Since T4->T3 conversion is impaired • 5-20 ug followed by 2.5-10 ug 8 hrly
  • 25.  Supportive therapy 1. External warming 2. Parenteral Hydrocortisone (50 mg every 6 hrly) 3. Treat precipitating factor 4. Ventilatory support, ABG 5. Hypertonic saline or IV detrose