Hypothyroidism is a common endocrine disease in dogs that results from a deficiency of thyroid hormones. It is primarily caused by lymphocytic thyroiditis or idiopathic thyroid atrophy in 95% of cases. Clinical signs vary but commonly include dermatological abnormalities like hair loss and skin infections, obesity, lethargy, mental dullness, and cold intolerance. Untreated hypothyroidism can also impact the nervous, cardiovascular, ocular, and reproductive systems. Diagnosis is based on abnormal thyroid hormone levels and is typically treated with lifelong thyroid hormone supplementation.
Hypothyroidism is a common endocrinopathy in dogs resulting from a deficiency of thyroid hormones. It can be primary, secondary, or tertiary in origin. Primary hypothyroidism accounts for over 95% of cases and is usually caused by lymphocytic thyroiditis or idiopathic thyroid atrophy. Clinical signs vary but commonly include dermatological abnormalities such as hair loss and skin infections, obesity, lethargy, neurologic issues like peripheral neuropathy, and cardiovascular effects like bradycardia. Untreated hypothyroidism can impact multiple body systems and result in long-term health problems.
The document discusses the thyroid gland and hypothyroidism. It notes that the thyroid gland produces two important hormones, T4 and T3, and is located in the neck. Hypothyroidism is a common condition where the thyroid gland does not produce enough hormones. It has various causes including autoimmune disease and can cause symptoms like tiredness, dry skin, constipation, and weight gain. Long-term treatment involves daily levothyroxine replacement therapy.
This document discusses various thyroid disorders including goiter, cretinism, myxedema, Hashimoto's disease, Graves' disease, and thyroid nodules. It provides information on the causes, symptoms, diagnosis, and treatment of each condition. Goiter is commonly caused by iodine deficiency and can lead to hyperthyroidism or hypothyroidism. Cretinism causes physical and mental stunting and is treated with thyroid supplements. Myxedema is caused by diminished thyroid hormone production and causes edema of the skin. Hashimoto's disease is an autoimmune condition where the thyroid is gradually destroyed, while Graves' disease leads to thyroid overactivity from abnormal antibodies. Thyroid nodules can
Hypothyroidism is a condition caused by reduced production of thyroid hormones. The main types are primary hypothyroidism due to permanent thyroid damage or failure, and central/secondary hypothyroidism due to pituitary or hypothalamic issues. Hashimoto's disease is the most common cause of primary hypothyroidism. Symptoms include fatigue, dry skin, constipation, weight gain and slowed heart rate. Treatment involves thyroid hormone replacement via levothyroxine. Subclinical hypothyroidism may also be treated depending on risk factors. Hypothyroidism in pregnancy requires careful management to prevent complications. In severe cases, myxedema coma can develop with risk of high mortality and requires urgent
The document provides an overview of the thyroid gland including its embryology, histology, physiology, hormone synthesis, functions, and common disorders. It discusses that the thyroid originates from the pharynx and contains follicles composed of epithelial cells and colloid. The thyroid's primary function is to produce the hormones T3, T4, and calcitonin. Common disorders mentioned include hyperthyroidism, hypothyroidism, thyroiditis (such as Hashimoto's), goiter, and tumors. Graves' disease is highlighted as a cause of diffuse toxic goiter characterized by the triad of hyperthyroidism, diffuse thyroid enlargement, and ophthalmopathy.
lecture class for 4th year MBBS students. this lecture is based on the book 'Robbins' Pathologic basis of disease'. This is delivered by Dr. Umme Kulsum Munmun, Assistant professor (pathology) to the 4th year MBBS students of Chandpur Meducal College, Bangladesh
The document discusses various endocrine glands and hormones, including the thyroid gland which produces hormones that regulate metabolism, and the adrenal glands which produce cortisol to help the body cope with stress and aldosterone to regulate sodium levels. It also covers conditions that can arise from too much or too little of these hormones, such as hypothyroidism, hyperthyroidism, Cushing's syndrome, and adrenal insufficiency.
The document discusses disorders of the thyroid gland, including hypothyroidism and hyperthyroidism. It begins by reviewing the anatomy and physiology of the thyroid gland and hypothalamic-pituitary-thyroid feedback system. Hypothyroidism can be congenital or acquired, and if during childhood causes cretinism. Acquired hypothyroidism in adults is called myxedema. Hyperthyroidism results from increased thyroid hormone secretion and can be caused by Graves' disease. Thyroid storm is a life-threatening exacerbation of hyperthyroidism.
Hypothyroidism is a common endocrinopathy in dogs resulting from a deficiency of thyroid hormones. It can be primary, secondary, or tertiary in origin. Primary hypothyroidism accounts for over 95% of cases and is usually caused by lymphocytic thyroiditis or idiopathic thyroid atrophy. Clinical signs vary but commonly include dermatological abnormalities such as hair loss and skin infections, obesity, lethargy, neurologic issues like peripheral neuropathy, and cardiovascular effects like bradycardia. Untreated hypothyroidism can impact multiple body systems and result in long-term health problems.
The document discusses the thyroid gland and hypothyroidism. It notes that the thyroid gland produces two important hormones, T4 and T3, and is located in the neck. Hypothyroidism is a common condition where the thyroid gland does not produce enough hormones. It has various causes including autoimmune disease and can cause symptoms like tiredness, dry skin, constipation, and weight gain. Long-term treatment involves daily levothyroxine replacement therapy.
This document discusses various thyroid disorders including goiter, cretinism, myxedema, Hashimoto's disease, Graves' disease, and thyroid nodules. It provides information on the causes, symptoms, diagnosis, and treatment of each condition. Goiter is commonly caused by iodine deficiency and can lead to hyperthyroidism or hypothyroidism. Cretinism causes physical and mental stunting and is treated with thyroid supplements. Myxedema is caused by diminished thyroid hormone production and causes edema of the skin. Hashimoto's disease is an autoimmune condition where the thyroid is gradually destroyed, while Graves' disease leads to thyroid overactivity from abnormal antibodies. Thyroid nodules can
Hypothyroidism is a condition caused by reduced production of thyroid hormones. The main types are primary hypothyroidism due to permanent thyroid damage or failure, and central/secondary hypothyroidism due to pituitary or hypothalamic issues. Hashimoto's disease is the most common cause of primary hypothyroidism. Symptoms include fatigue, dry skin, constipation, weight gain and slowed heart rate. Treatment involves thyroid hormone replacement via levothyroxine. Subclinical hypothyroidism may also be treated depending on risk factors. Hypothyroidism in pregnancy requires careful management to prevent complications. In severe cases, myxedema coma can develop with risk of high mortality and requires urgent
The document provides an overview of the thyroid gland including its embryology, histology, physiology, hormone synthesis, functions, and common disorders. It discusses that the thyroid originates from the pharynx and contains follicles composed of epithelial cells and colloid. The thyroid's primary function is to produce the hormones T3, T4, and calcitonin. Common disorders mentioned include hyperthyroidism, hypothyroidism, thyroiditis (such as Hashimoto's), goiter, and tumors. Graves' disease is highlighted as a cause of diffuse toxic goiter characterized by the triad of hyperthyroidism, diffuse thyroid enlargement, and ophthalmopathy.
lecture class for 4th year MBBS students. this lecture is based on the book 'Robbins' Pathologic basis of disease'. This is delivered by Dr. Umme Kulsum Munmun, Assistant professor (pathology) to the 4th year MBBS students of Chandpur Meducal College, Bangladesh
The document discusses various endocrine glands and hormones, including the thyroid gland which produces hormones that regulate metabolism, and the adrenal glands which produce cortisol to help the body cope with stress and aldosterone to regulate sodium levels. It also covers conditions that can arise from too much or too little of these hormones, such as hypothyroidism, hyperthyroidism, Cushing's syndrome, and adrenal insufficiency.
The document discusses disorders of the thyroid gland, including hypothyroidism and hyperthyroidism. It begins by reviewing the anatomy and physiology of the thyroid gland and hypothalamic-pituitary-thyroid feedback system. Hypothyroidism can be congenital or acquired, and if during childhood causes cretinism. Acquired hypothyroidism in adults is called myxedema. Hyperthyroidism results from increased thyroid hormone secretion and can be caused by Graves' disease. Thyroid storm is a life-threatening exacerbation of hyperthyroidism.
Hypothyroidism affects up to 0.5% of the US population and is most commonly caused by Hashimoto's thyroiditis. Treatment focuses on thyroid hormone replacement therapy using levothyroxine. Replacement should begin at a low dose, especially in the elderly and those with cardiac risks, and the dose should be gradually increased while monitoring laboratory values. Annual monitoring of thyroid-stimulating hormone levels is usually unnecessary once a stable replacement dose is found, except possibly in older patients. Some patients may benefit from adding a low dose of triiodothyronine to levothyroxine therapy.
This document discusses thyroid disorders in children. It covers objectives related to hypothyroidism and hyperthyroidism. For hypothyroidism, it discusses the anatomy and physiology of the thyroid gland, hypothalamic-pituitary regulation, causes of primary, secondary and tertiary hypothyroidism including congenital and acquired forms. For hyperthyroidism, it discusses causes including neonatal forms and the clinical presentation and investigations of thyrotoxicosis. It also provides details on the thyroid gland, hormone synthesis and effects. Causes, clinical features and management of hypothyroidism and hyperthyroidism in children are outlined.
Hashimoto's thyroiditis is an autoimmune disease that results in the destruction of the thyroid gland and gradual hypothyroidism. It is the most common cause of hypothyroidism in iodine-sufficient areas and typically affects those aged 45-65, predominately women. The thyroid gland may be destroyed through CD8+ cytotoxic T cell killing or cytokine-mediated cell death. Congenital hypothyroidism can be caused by an ectopic thyroid gland, defects in thyroid hormone synthesis (dyshormonogenesis), or mutations in the TSH receptor. Hypothyroidism causes dry, thickened skin and obesity due to a lowered metabolic rate and basal metabolic rate.
This document summarizes several endocrine disorders including growth hormone disorders, thyroid hormone disorders, and adrenocortical hormone disorders. It describes the etiology, pathogenesis, clinical manifestations, and treatment for conditions such as growth hormone deficiency, acromegaly, hypothyroidism, hyperthyroidism (Graves' disease), and adrenocortical insufficiency. The pathophysiological changes that can occur in the endocrine system due to hyperfunction or hypofunction of hormones are explained.
The document discusses the thyroid gland and various thyroid conditions. It begins by describing the location of the thyroid gland and possible enlargements or nodules. It then discusses the main functions of the thyroid gland and the hormones it secretes. Various thyroid conditions are summarized such as hyperthyroidism, hypothyroidism, thyroiditis, thyroid cancer, and dental management considerations for patients with thyroid disease.
Hashimoto's thyroiditis is an autoimmune disease characterized by the body's immune system attacking the thyroid gland, causing inflammation. It is the leading cause of hypothyroidism in the United States, occurring more often in women than men, possibly due to hormonal factors. Symptoms are generally mild but include fatigue, weight gain, dry skin and hair, and constipation. The condition is diagnosed through blood tests showing low thyroid hormone and high thyroid stimulating hormone levels. While there is no cure, symptoms can be managed through lifelong thyroid hormone replacement medication.
1. Thyroid dysfunction can cause a variety of psychiatric manifestations including depression, mood instability, psychosis, anxiety, and impaired memory. Hypothyroidism in particular can mimic symptoms of mental illnesses.
2. Depression is a common symptom of hypothyroidism, and depressed patients may be more likely to have underlying thyroid problems. Treating thyroid dysfunction is important for alleviating associated psychiatric symptoms.
3. Hyperthyroidism can also cause psychiatric issues in a significant percentage of patients, with anxiety being very common. Between 1-20% of hyperthyroid patients experience psychosis.
The document provides information about thyroid gland disorders including hypothyroidism and hyperthyroidism. It discusses the anatomy and blood supply of the thyroid gland. It describes Hashimoto's thyroiditis as the most common cause of hypothyroidism due to an autoimmune reaction. Graves' disease is outlined as the most common cause of hyperthyroidism, also caused by an autoimmune process involving thyroid stimulating antibodies. The clinical features, investigations, and treatment approaches for hypothyroidism and hyperthyroidism are summarized.
Hashimoto's thyroiditis is an autoimmune disease where the body's immune system attacks the thyroid gland. It is the most common cause of hypothyroidism in the United States. A 48-year-old female presented with a painless, diffuse swelling of the neck along with symptoms of fatigue, depression, constipation, weight gain, cold intolerance, and dry skin and hair. Laboratory tests showed high thyroid stimulating hormone and antibodies against thyroid peroxidase, consistent with a diagnosis of Hashimoto's thyroiditis. Treatment involves thyroid hormone replacement medication like levothyroxine to manage hypothyroidism.
This document discusses various aspects of hyperthyroidism and thyrotoxicosis. It defines hypothyroidism and hyperthyroidism, listing their typical metabolic, skin, ocular, gastrointestinal, musculoskeletal, reproductive, neuropsychiatric, and cardiovascular findings. It then discusses Graves' disease, its autoimmune pathogenesis, clinical features including diffuse goiter, exophthalmos and pretibial myxedema. Diffuse toxic goiter and its etiology, physical exam findings, and pathophysiology are outlined. Multinodular goiter and its causes are also summarized. Thyrotoxicosis is defined and its origins from thyroid, extrathyroidal, or exogenous sources are listed.
This document discusses hyperthyroidism and thyrotoxicosis. It begins by defining the terms and describing the thyroid gland's normal function. It then discusses the various causes of hyperthyroidism including Graves' disease, toxic multinodular goiter, subacute thyroiditis, and toxic adenoma. The document outlines the anatomy and physiology of the thyroid gland. It describes the clinical manifestations, diagnostic tests including thyroid function tests, ultrasound, and thyroid scintigraphy. It provides algorithms for diagnosis and outlines treatment options for hyperthyroidism including anti-thyroid medications, radioactive iodine treatment, and thyroidectomy.
This document discusses hyperthyroidism and thyrotoxicosis. It defines the terms and describes the thyroid gland's normal function of producing thyroid hormones. The main causes of hyperthyroidism are Graves' disease, toxic multinodular goiter, subacute thyroiditis, and toxic adenoma. The clinical manifestations and signs of hyperthyroidism are then outlined, along with specific symptoms of Graves' disease. Diagnostic tests like thyroid function tests, ultrasound, and thyroid scintigraphy are also summarized. The document concludes with treatments options for hyperthyroidism including anti-thyroid medications, radioactive iodine, and surgery.
Benign thyroid diseases discusses thyroid abnormalities including hypothyroidism and hyperthyroidism. Graves' disease is described as the most common cause of hyperthyroidism, resulting from autoimmune stimulation of the thyroid by antibodies. Symptoms and signs of hyperthyroidism include rapid heartbeat, sweating, anxiety and eye changes. Treatment involves antithyroid drugs, radioactive iodine therapy which destroys thyroid tissue, or surgery. Radioactive iodine is often used as it avoids surgery risks and provides definitive treatment, though can cause hypothyroidism in some cases.
Hypothyroidism is a condition characterized by thyroid hormone deficiency. It ranges from subclinical to myxedema coma. Common causes include iodine deficiency, autoimmune disease like Hashimoto's thyroiditis, and treatment of hyperthyroidism. Symptoms vary but can include fatigue, dry skin, weight gain, constipation, joint pain, and cognitive impairment. Diagnosis is made through blood tests of thyroid hormones and TSH. Treatment involves lifelong levothyroxine replacement therapy to normalize TSH levels. The dosage needs monitoring and adjustment based on repeat testing.
MYXOEDEMA
Adult onset severe hypothyroidism
Non pitting edema due to accumulation of hydrophilic mucopolysaccharides
Decreased serum levels of T3 & T4, increased serum levels of TSH (thyroid stimulating hormone)
Etiopathogenesis:
Ablation (decreasing the function) of the thyroid gland by surgery or radiation
Autoimmune (lymphocytic) thyroiditis
Endemic or sporadic goitre
endemic goitre= occurs when thyroid enlargement (iodine deficiency) is seen in more than 10% population in an area.
sporadic goitre= enlargement of thyroid gland in iodine sufficient area due to genetic or environment factors.
Hypothalamic pituitary lesions
Prolonged administration of anti thyroid drugs
Dyshormonogenesis (abnormal hormone synthesis due to genetic defects)
Clinical features:
Having cold intolerance
Mental and physical lethargy
Constipation
Slowing of speech and intellectual fuction
Puffiness of face
Loss of hair
altered texture of skin
Treatment:
substitution of thyroid hormones by taking thyroxine (T4) tablets usully in the form of levothyroxine.
HYPERTHYROIDISM:
Characterised by excess production of thyroid hormones
More frequent in females
Increased serum levels of T3 & T4.
T3 levels increase more than T4
when hyperthyroidism results in toxic clinical features , it is called as thyrotoxicosis
Etiopathogenesis:
Caused by many diseases
1. Primary cause= graves disease, toxic adenoma (overproduction of thyroid hormones from one or more nodules in thyroid gland)
2. secondary causes= thyroiditis, tumours of thyroid gland
Congenital hyperthyroidism in the newborn of mother with graves disease
Clinical features:
Emotional instability
Nervousness
Palpitations
Fatigue
Weight loss inspite of good appetite
Heat intolerance
Perspiration (loss of fluid through skin pores / sweating)
Menstrual disturbances
Tremors of hands
Tachycardia and cardiomegaly
Skeletal muscle weakness and osteoporosis (decrease in bone mass, bones become weak and brittle)
Exophthalmos (bulging eyes)
Treatment:
anti thyroid drugs (carbimazole, methimazole)
Partial or total removal of thyroid gland
Radioactive iodine therapy (radioactive iodine kill any remaining thyroid cancer cells that remain after surgery)
THYROIDITIS
Inflammation of thyroid gland
Types:
Acute thyroiditis:
Bacterial infection= staphylococcus, streptococcus
Fungal infection= aspergillus
Radiation injury
Chronic thyroiditis:
Autoimmune thyroiditis (Hashimoto thyroiditis)
Invasive fibrous thyroiditis
Hashimoto thyroiditis
Characterised by 3 features
Goitrous enlargement of the thyroid gland
Lymphocytes infiltration in thyroid gland
Presence of thyroid autoantibodies
Etiopathogenesis:
it occurs in association with graves disease, pernicious anaemia, diabetes mellitus type 1
Immune destruction of thyroid cells.
Presence of genes associated with this disease
Ex: DR3,DR4,DR5 genes
Activation of CD4 T cells, which induces CD8 T cell infiltration that destroys thyroid cells producing hormones.
Production of autoantibodies
This document discusses thyroid hormone function and physiology, as well as hypothyroidism. It covers:
1. The roles of thyroid hormones T3 and T4 in regulating metabolism, growth, and development across multiple organ systems.
2. The causes of congenital hypothyroidism, including thyroid dysgenesis, defects in hormone synthesis, transport, and other rare genetic disorders.
3. The rationale for newborn screening, which allows for early detection and treatment of asymptomatic congenital hypothyroidism to prevent intellectual and growth disabilities.
This document provides information about goiter (enlargement of the thyroid gland). It begins by defining goiter and discussing the causes, which can be inflammatory, toxic, autoimmune, or physiological. It then classifies thyroid swellings and discusses the pathophysiology, clinical presentation, investigations and treatment of simple goiter. It also discusses hypothyroidism, its causes, symptoms, diagnosis and treatment. Finally, it discusses hyperthyroidism/toxic goiter, the causes including Graves' disease, and discusses Graves' disease in more detail.
The thyroid gland develops from the fourth pharyngeal pouch and normally weighs around 20 grams. It is butterfly-shaped with two lobes connected by an isthmus. The gland produces the hormones thyroxine (T4) and triiodothyronine (T3) which regulate metabolism. Hyperthyroidism, or an overactive thyroid, can result from conditions like Graves' disease. It causes a variety of symptoms affecting many body systems. Diagnosis involves blood tests showing elevated T3 and T4 with low or undetectable TSH. Treatment options include antithyroid medications, surgery, or radioactive iodine.
Based on the lab results provided:
- T3/T4 are high
- TSH is low
This pattern is seen in primary hyperthyroidism.
The diagnosis would be A) Primary hyperthyroidism.
This document provides information about goiter (enlargement of the thyroid gland). It begins by defining goiter and discussing the causes, which can be inflammatory, toxic, autoimmune, or physiological. It then classifies thyroid swellings and discusses the pathophysiology, clinical presentation, investigations and treatment of simple goiter. It also discusses hypothyroidism, its causes, symptoms, diagnosis and treatment. Finally, it discusses hyperthyroidism/toxic goiter, the causes including Graves' disease, and discusses Graves' disease in more detail.
Haemorrhagic_Septicemia in Ruminant ,Gal ghotusKavitaJaidiya
Pasteruella multocida and Mannheimia haemolytica are bacteria that can cause pasteurellosis in cattle and other animals. P. multocida causes haemorrhagic septicemia in cattle, fowl cholera in fowl, and atropic rhinitis in pigs. M. haemolytica causes shipping fever in cattle. Haemorrhagic septicemia is an acute disease in cattle characterized by fever, respiratory distress, and diarrhea. The bacteria enter through ingestion or inhalation and spread systemically, causing hemorrhages on membranes. Johne's disease is a chronic wasting disease of ruminants caused by Mycobacterium paratuberculosis.
Canine hypoadrenocorticism, also known as Addison's disease, is a disorder caused by a lack of hormones produced by the adrenal glands. It results in electrolyte and blood pressure issues and can be fatal if not treated. Diagnosis involves ruling out other causes through tests of electrolyte and cortisol levels before and after administration of ACTH. Treatment focuses on rapid fluid therapy and steroid hormone replacement to correct electrolyte imbalances and restore blood volume and pressure. Long term management relies on mineralocorticoid and glucocorticoid supplementation through oral or injectable medications.
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Hypothyroidism affects up to 0.5% of the US population and is most commonly caused by Hashimoto's thyroiditis. Treatment focuses on thyroid hormone replacement therapy using levothyroxine. Replacement should begin at a low dose, especially in the elderly and those with cardiac risks, and the dose should be gradually increased while monitoring laboratory values. Annual monitoring of thyroid-stimulating hormone levels is usually unnecessary once a stable replacement dose is found, except possibly in older patients. Some patients may benefit from adding a low dose of triiodothyronine to levothyroxine therapy.
This document discusses thyroid disorders in children. It covers objectives related to hypothyroidism and hyperthyroidism. For hypothyroidism, it discusses the anatomy and physiology of the thyroid gland, hypothalamic-pituitary regulation, causes of primary, secondary and tertiary hypothyroidism including congenital and acquired forms. For hyperthyroidism, it discusses causes including neonatal forms and the clinical presentation and investigations of thyrotoxicosis. It also provides details on the thyroid gland, hormone synthesis and effects. Causes, clinical features and management of hypothyroidism and hyperthyroidism in children are outlined.
Hashimoto's thyroiditis is an autoimmune disease that results in the destruction of the thyroid gland and gradual hypothyroidism. It is the most common cause of hypothyroidism in iodine-sufficient areas and typically affects those aged 45-65, predominately women. The thyroid gland may be destroyed through CD8+ cytotoxic T cell killing or cytokine-mediated cell death. Congenital hypothyroidism can be caused by an ectopic thyroid gland, defects in thyroid hormone synthesis (dyshormonogenesis), or mutations in the TSH receptor. Hypothyroidism causes dry, thickened skin and obesity due to a lowered metabolic rate and basal metabolic rate.
This document summarizes several endocrine disorders including growth hormone disorders, thyroid hormone disorders, and adrenocortical hormone disorders. It describes the etiology, pathogenesis, clinical manifestations, and treatment for conditions such as growth hormone deficiency, acromegaly, hypothyroidism, hyperthyroidism (Graves' disease), and adrenocortical insufficiency. The pathophysiological changes that can occur in the endocrine system due to hyperfunction or hypofunction of hormones are explained.
The document discusses the thyroid gland and various thyroid conditions. It begins by describing the location of the thyroid gland and possible enlargements or nodules. It then discusses the main functions of the thyroid gland and the hormones it secretes. Various thyroid conditions are summarized such as hyperthyroidism, hypothyroidism, thyroiditis, thyroid cancer, and dental management considerations for patients with thyroid disease.
Hashimoto's thyroiditis is an autoimmune disease characterized by the body's immune system attacking the thyroid gland, causing inflammation. It is the leading cause of hypothyroidism in the United States, occurring more often in women than men, possibly due to hormonal factors. Symptoms are generally mild but include fatigue, weight gain, dry skin and hair, and constipation. The condition is diagnosed through blood tests showing low thyroid hormone and high thyroid stimulating hormone levels. While there is no cure, symptoms can be managed through lifelong thyroid hormone replacement medication.
1. Thyroid dysfunction can cause a variety of psychiatric manifestations including depression, mood instability, psychosis, anxiety, and impaired memory. Hypothyroidism in particular can mimic symptoms of mental illnesses.
2. Depression is a common symptom of hypothyroidism, and depressed patients may be more likely to have underlying thyroid problems. Treating thyroid dysfunction is important for alleviating associated psychiatric symptoms.
3. Hyperthyroidism can also cause psychiatric issues in a significant percentage of patients, with anxiety being very common. Between 1-20% of hyperthyroid patients experience psychosis.
The document provides information about thyroid gland disorders including hypothyroidism and hyperthyroidism. It discusses the anatomy and blood supply of the thyroid gland. It describes Hashimoto's thyroiditis as the most common cause of hypothyroidism due to an autoimmune reaction. Graves' disease is outlined as the most common cause of hyperthyroidism, also caused by an autoimmune process involving thyroid stimulating antibodies. The clinical features, investigations, and treatment approaches for hypothyroidism and hyperthyroidism are summarized.
Hashimoto's thyroiditis is an autoimmune disease where the body's immune system attacks the thyroid gland. It is the most common cause of hypothyroidism in the United States. A 48-year-old female presented with a painless, diffuse swelling of the neck along with symptoms of fatigue, depression, constipation, weight gain, cold intolerance, and dry skin and hair. Laboratory tests showed high thyroid stimulating hormone and antibodies against thyroid peroxidase, consistent with a diagnosis of Hashimoto's thyroiditis. Treatment involves thyroid hormone replacement medication like levothyroxine to manage hypothyroidism.
This document discusses various aspects of hyperthyroidism and thyrotoxicosis. It defines hypothyroidism and hyperthyroidism, listing their typical metabolic, skin, ocular, gastrointestinal, musculoskeletal, reproductive, neuropsychiatric, and cardiovascular findings. It then discusses Graves' disease, its autoimmune pathogenesis, clinical features including diffuse goiter, exophthalmos and pretibial myxedema. Diffuse toxic goiter and its etiology, physical exam findings, and pathophysiology are outlined. Multinodular goiter and its causes are also summarized. Thyrotoxicosis is defined and its origins from thyroid, extrathyroidal, or exogenous sources are listed.
This document discusses hyperthyroidism and thyrotoxicosis. It begins by defining the terms and describing the thyroid gland's normal function. It then discusses the various causes of hyperthyroidism including Graves' disease, toxic multinodular goiter, subacute thyroiditis, and toxic adenoma. The document outlines the anatomy and physiology of the thyroid gland. It describes the clinical manifestations, diagnostic tests including thyroid function tests, ultrasound, and thyroid scintigraphy. It provides algorithms for diagnosis and outlines treatment options for hyperthyroidism including anti-thyroid medications, radioactive iodine treatment, and thyroidectomy.
This document discusses hyperthyroidism and thyrotoxicosis. It defines the terms and describes the thyroid gland's normal function of producing thyroid hormones. The main causes of hyperthyroidism are Graves' disease, toxic multinodular goiter, subacute thyroiditis, and toxic adenoma. The clinical manifestations and signs of hyperthyroidism are then outlined, along with specific symptoms of Graves' disease. Diagnostic tests like thyroid function tests, ultrasound, and thyroid scintigraphy are also summarized. The document concludes with treatments options for hyperthyroidism including anti-thyroid medications, radioactive iodine, and surgery.
Benign thyroid diseases discusses thyroid abnormalities including hypothyroidism and hyperthyroidism. Graves' disease is described as the most common cause of hyperthyroidism, resulting from autoimmune stimulation of the thyroid by antibodies. Symptoms and signs of hyperthyroidism include rapid heartbeat, sweating, anxiety and eye changes. Treatment involves antithyroid drugs, radioactive iodine therapy which destroys thyroid tissue, or surgery. Radioactive iodine is often used as it avoids surgery risks and provides definitive treatment, though can cause hypothyroidism in some cases.
Hypothyroidism is a condition characterized by thyroid hormone deficiency. It ranges from subclinical to myxedema coma. Common causes include iodine deficiency, autoimmune disease like Hashimoto's thyroiditis, and treatment of hyperthyroidism. Symptoms vary but can include fatigue, dry skin, weight gain, constipation, joint pain, and cognitive impairment. Diagnosis is made through blood tests of thyroid hormones and TSH. Treatment involves lifelong levothyroxine replacement therapy to normalize TSH levels. The dosage needs monitoring and adjustment based on repeat testing.
MYXOEDEMA
Adult onset severe hypothyroidism
Non pitting edema due to accumulation of hydrophilic mucopolysaccharides
Decreased serum levels of T3 & T4, increased serum levels of TSH (thyroid stimulating hormone)
Etiopathogenesis:
Ablation (decreasing the function) of the thyroid gland by surgery or radiation
Autoimmune (lymphocytic) thyroiditis
Endemic or sporadic goitre
endemic goitre= occurs when thyroid enlargement (iodine deficiency) is seen in more than 10% population in an area.
sporadic goitre= enlargement of thyroid gland in iodine sufficient area due to genetic or environment factors.
Hypothalamic pituitary lesions
Prolonged administration of anti thyroid drugs
Dyshormonogenesis (abnormal hormone synthesis due to genetic defects)
Clinical features:
Having cold intolerance
Mental and physical lethargy
Constipation
Slowing of speech and intellectual fuction
Puffiness of face
Loss of hair
altered texture of skin
Treatment:
substitution of thyroid hormones by taking thyroxine (T4) tablets usully in the form of levothyroxine.
HYPERTHYROIDISM:
Characterised by excess production of thyroid hormones
More frequent in females
Increased serum levels of T3 & T4.
T3 levels increase more than T4
when hyperthyroidism results in toxic clinical features , it is called as thyrotoxicosis
Etiopathogenesis:
Caused by many diseases
1. Primary cause= graves disease, toxic adenoma (overproduction of thyroid hormones from one or more nodules in thyroid gland)
2. secondary causes= thyroiditis, tumours of thyroid gland
Congenital hyperthyroidism in the newborn of mother with graves disease
Clinical features:
Emotional instability
Nervousness
Palpitations
Fatigue
Weight loss inspite of good appetite
Heat intolerance
Perspiration (loss of fluid through skin pores / sweating)
Menstrual disturbances
Tremors of hands
Tachycardia and cardiomegaly
Skeletal muscle weakness and osteoporosis (decrease in bone mass, bones become weak and brittle)
Exophthalmos (bulging eyes)
Treatment:
anti thyroid drugs (carbimazole, methimazole)
Partial or total removal of thyroid gland
Radioactive iodine therapy (radioactive iodine kill any remaining thyroid cancer cells that remain after surgery)
THYROIDITIS
Inflammation of thyroid gland
Types:
Acute thyroiditis:
Bacterial infection= staphylococcus, streptococcus
Fungal infection= aspergillus
Radiation injury
Chronic thyroiditis:
Autoimmune thyroiditis (Hashimoto thyroiditis)
Invasive fibrous thyroiditis
Hashimoto thyroiditis
Characterised by 3 features
Goitrous enlargement of the thyroid gland
Lymphocytes infiltration in thyroid gland
Presence of thyroid autoantibodies
Etiopathogenesis:
it occurs in association with graves disease, pernicious anaemia, diabetes mellitus type 1
Immune destruction of thyroid cells.
Presence of genes associated with this disease
Ex: DR3,DR4,DR5 genes
Activation of CD4 T cells, which induces CD8 T cell infiltration that destroys thyroid cells producing hormones.
Production of autoantibodies
This document discusses thyroid hormone function and physiology, as well as hypothyroidism. It covers:
1. The roles of thyroid hormones T3 and T4 in regulating metabolism, growth, and development across multiple organ systems.
2. The causes of congenital hypothyroidism, including thyroid dysgenesis, defects in hormone synthesis, transport, and other rare genetic disorders.
3. The rationale for newborn screening, which allows for early detection and treatment of asymptomatic congenital hypothyroidism to prevent intellectual and growth disabilities.
This document provides information about goiter (enlargement of the thyroid gland). It begins by defining goiter and discussing the causes, which can be inflammatory, toxic, autoimmune, or physiological. It then classifies thyroid swellings and discusses the pathophysiology, clinical presentation, investigations and treatment of simple goiter. It also discusses hypothyroidism, its causes, symptoms, diagnosis and treatment. Finally, it discusses hyperthyroidism/toxic goiter, the causes including Graves' disease, and discusses Graves' disease in more detail.
The thyroid gland develops from the fourth pharyngeal pouch and normally weighs around 20 grams. It is butterfly-shaped with two lobes connected by an isthmus. The gland produces the hormones thyroxine (T4) and triiodothyronine (T3) which regulate metabolism. Hyperthyroidism, or an overactive thyroid, can result from conditions like Graves' disease. It causes a variety of symptoms affecting many body systems. Diagnosis involves blood tests showing elevated T3 and T4 with low or undetectable TSH. Treatment options include antithyroid medications, surgery, or radioactive iodine.
Based on the lab results provided:
- T3/T4 are high
- TSH is low
This pattern is seen in primary hyperthyroidism.
The diagnosis would be A) Primary hyperthyroidism.
This document provides information about goiter (enlargement of the thyroid gland). It begins by defining goiter and discussing the causes, which can be inflammatory, toxic, autoimmune, or physiological. It then classifies thyroid swellings and discusses the pathophysiology, clinical presentation, investigations and treatment of simple goiter. It also discusses hypothyroidism, its causes, symptoms, diagnosis and treatment. Finally, it discusses hyperthyroidism/toxic goiter, the causes including Graves' disease, and discusses Graves' disease in more detail.
Similar to 1525488865092_presented_Credit_seminar_canine_hypothyroidism[1].pptx (20)
Haemorrhagic_Septicemia in Ruminant ,Gal ghotusKavitaJaidiya
Pasteruella multocida and Mannheimia haemolytica are bacteria that can cause pasteurellosis in cattle and other animals. P. multocida causes haemorrhagic septicemia in cattle, fowl cholera in fowl, and atropic rhinitis in pigs. M. haemolytica causes shipping fever in cattle. Haemorrhagic septicemia is an acute disease in cattle characterized by fever, respiratory distress, and diarrhea. The bacteria enter through ingestion or inhalation and spread systemically, causing hemorrhages on membranes. Johne's disease is a chronic wasting disease of ruminants caused by Mycobacterium paratuberculosis.
Canine hypoadrenocorticism, also known as Addison's disease, is a disorder caused by a lack of hormones produced by the adrenal glands. It results in electrolyte and blood pressure issues and can be fatal if not treated. Diagnosis involves ruling out other causes through tests of electrolyte and cortisol levels before and after administration of ACTH. Treatment focuses on rapid fluid therapy and steroid hormone replacement to correct electrolyte imbalances and restore blood volume and pressure. Long term management relies on mineralocorticoid and glucocorticoid supplementation through oral or injectable medications.
This document discusses the Trade-Related Aspects of Intellectual Property Rights (TRIPS) agreement. It notes that TRIPS sets minimum standards for intellectual property protection as part of the World Trade Organization agreements. It was signed by 153 parties and subjects intellectual property rights to enforcement mechanisms, national treatment principles, and the WTO dispute settlement process. The document outlines some of the key provisions of TRIPS regarding availability and scope of intellectual property rights, enforcement, procedures, transitional agreements, and dispute resolution.
East Coast Fever is caused by the parasite Theileria parva, which is transmitted between cattle via ticks. It causes high mortality in cattle and poses a major economic burden for farmers in sub-Saharan Africa. The study examined treating cattle naturally infected with ECF early through diagnosis and chemotherapy. It found a high recovery rate with this approach and that it can help cattle develop immunity against future infections, providing an alternative to vaccination.
The document provides information on hepatic (liver) diseases in canines and felines. It discusses the structure and functions of the liver. It describes infectious causes of hepatitis including viral, parasitic, and bacterial sources. Non-infectious causes such as drugs/toxins, autoimmunity, and endocrine disorders are also outlined. Clinical signs, diagnosis including liver enzymes and imaging, and treatment approaches including medications, fluid therapy, and nutrition are summarized.
The document summarizes autophagy and electron microscopy. It defines autophagy as the degradation of cells through lysosomes and discusses its importance in survival, cancer, and disease. Three forms of autophagy are identified: macroautophagy, microautophagy, and chaperone-mediated autophagy. Electron microscopes use electron beams for high magnification imaging of cells and materials. Transmission electron microscopes image thin samples while scanning electron microscopes image surface structure of bulk samples. Sample preparation for electron microscopy involves cleaning, coating, and thin film deposition depending on the analysis needs.
This document provides an overview of microbiology and principles of laboratory diagnosis of infectious diseases. It discusses the history of microbiology from the discovery era to the modern era. Key figures who contributed to early discoveries include Van Leeuwenhoek, Pasteur, Koch, Fleming and others. The document also summarizes different sample types used for diagnosis, specimen collection and transport, staining techniques including Gram staining and acid-fast staining, and isolation of bacteria through culture. The overall principles of laboratory diagnosis involve direct examination, culture, antigen detection and antibody detection.
Malassezia dermatitis is a common skin infection in dogs caused by the yeast Malassezia pachydermatis. It develops due to disorders that alter the skin environment or immune system. Clinically, it presents as erythematous, alopecic, and scaly skin with pruritus. Diagnosis is based on cytology and culture. Treatment involves systemic antifungals like ketoconazole for 3-4 weeks along with topical shampoos. Prognosis is good with prolonged therapy and follow up to prevent recurrence.
hematic appreciation test is a psychological assessment tool used to measure an individual's appreciation and understanding of specific themes or topics. This test helps to evaluate an individual's ability to connect different ideas and concepts within a given theme, as well as their overall comprehension and interpretation skills. The results of the test can provide valuable insights into an individual's cognitive abilities, creativity, and critical thinking skills
Or: Beyond linear.
Abstract: Equivariant neural networks are neural networks that incorporate symmetries. The nonlinear activation functions in these networks result in interesting nonlinear equivariant maps between simple representations, and motivate the key player of this talk: piecewise linear representation theory.
Disclaimer: No one is perfect, so please mind that there might be mistakes and typos.
dtubbenhauer@gmail.com
Corrected slides: dtubbenhauer.com/talks.html
Authoring a personal GPT for your research and practice: How we created the Q...Leonel Morgado
Thematic analysis in qualitative research is a time-consuming and systematic task, typically done using teams. Team members must ground their activities on common understandings of the major concepts underlying the thematic analysis, and define criteria for its development. However, conceptual misunderstandings, equivocations, and lack of adherence to criteria are challenges to the quality and speed of this process. Given the distributed and uncertain nature of this process, we wondered if the tasks in thematic analysis could be supported by readily available artificial intelligence chatbots. Our early efforts point to potential benefits: not just saving time in the coding process but better adherence to criteria and grounding, by increasing triangulation between humans and artificial intelligence. This tutorial will provide a description and demonstration of the process we followed, as two academic researchers, to develop a custom ChatGPT to assist with qualitative coding in the thematic data analysis process of immersive learning accounts in a survey of the academic literature: QUAL-E Immersive Learning Thematic Analysis Helper. In the hands-on time, participants will try out QUAL-E and develop their ideas for their own qualitative coding ChatGPT. Participants that have the paid ChatGPT Plus subscription can create a draft of their assistants. The organizers will provide course materials and slide deck that participants will be able to utilize to continue development of their custom GPT. The paid subscription to ChatGPT Plus is not required to participate in this workshop, just for trying out personal GPTs during it.
Unlocking the mysteries of reproduction: Exploring fecundity and gonadosomati...AbdullaAlAsif1
The pygmy halfbeak Dermogenys colletei, is known for its viviparous nature, this presents an intriguing case of relatively low fecundity, raising questions about potential compensatory reproductive strategies employed by this species. Our study delves into the examination of fecundity and the Gonadosomatic Index (GSI) in the Pygmy Halfbeak, D. colletei (Meisner, 2001), an intriguing viviparous fish indigenous to Sarawak, Borneo. We hypothesize that the Pygmy halfbeak, D. colletei, may exhibit unique reproductive adaptations to offset its low fecundity, thus enhancing its survival and fitness. To address this, we conducted a comprehensive study utilizing 28 mature female specimens of D. colletei, carefully measuring fecundity and GSI to shed light on the reproductive adaptations of this species. Our findings reveal that D. colletei indeed exhibits low fecundity, with a mean of 16.76 ± 2.01, and a mean GSI of 12.83 ± 1.27, providing crucial insights into the reproductive mechanisms at play in this species. These results underscore the existence of unique reproductive strategies in D. colletei, enabling its adaptation and persistence in Borneo's diverse aquatic ecosystems, and call for further ecological research to elucidate these mechanisms. This study lends to a better understanding of viviparous fish in Borneo and contributes to the broader field of aquatic ecology, enhancing our knowledge of species adaptations to unique ecological challenges.
The binding of cosmological structures by massless topological defectsSérgio Sacani
Assuming spherical symmetry and weak field, it is shown that if one solves the Poisson equation or the Einstein field
equations sourced by a topological defect, i.e. a singularity of a very specific form, the result is a localized gravitational
field capable of driving flat rotation (i.e. Keplerian circular orbits at a constant speed for all radii) of test masses on a thin
spherical shell without any underlying mass. Moreover, a large-scale structure which exploits this solution by assembling
concentrically a number of such topological defects can establish a flat stellar or galactic rotation curve, and can also deflect
light in the same manner as an equipotential (isothermal) sphere. Thus, the need for dark matter or modified gravity theory is
mitigated, at least in part.
The ability to recreate computational results with minimal effort and actionable metrics provides a solid foundation for scientific research and software development. When people can replicate an analysis at the touch of a button using open-source software, open data, and methods to assess and compare proposals, it significantly eases verification of results, engagement with a diverse range of contributors, and progress. However, we have yet to fully achieve this; there are still many sociotechnical frictions.
Inspired by David Donoho's vision, this talk aims to revisit the three crucial pillars of frictionless reproducibility (data sharing, code sharing, and competitive challenges) with the perspective of deep software variability.
Our observation is that multiple layers — hardware, operating systems, third-party libraries, software versions, input data, compile-time options, and parameters — are subject to variability that exacerbates frictions but is also essential for achieving robust, generalizable results and fostering innovation. I will first review the literature, providing evidence of how the complex variability interactions across these layers affect qualitative and quantitative software properties, thereby complicating the reproduction and replication of scientific studies in various fields.
I will then present some software engineering and AI techniques that can support the strategic exploration of variability spaces. These include the use of abstractions and models (e.g., feature models), sampling strategies (e.g., uniform, random), cost-effective measurements (e.g., incremental build of software configurations), and dimensionality reduction methods (e.g., transfer learning, feature selection, software debloating).
I will finally argue that deep variability is both the problem and solution of frictionless reproducibility, calling the software science community to develop new methods and tools to manage variability and foster reproducibility in software systems.
Exposé invité Journées Nationales du GDR GPL 2024
The use of Nauplii and metanauplii artemia in aquaculture (brine shrimp).pptxMAGOTI ERNEST
Although Artemia has been known to man for centuries, its use as a food for the culture of larval organisms apparently began only in the 1930s, when several investigators found that it made an excellent food for newly hatched fish larvae (Litvinenko et al., 2023). As aquaculture developed in the 1960s and ‘70s, the use of Artemia also became more widespread, due both to its convenience and to its nutritional value for larval organisms (Arenas-Pardo et al., 2024). The fact that Artemia dormant cysts can be stored for long periods in cans, and then used as an off-the-shelf food requiring only 24 h of incubation makes them the most convenient, least labor-intensive, live food available for aquaculture (Sorgeloos & Roubach, 2021). The nutritional value of Artemia, especially for marine organisms, is not constant, but varies both geographically and temporally. During the last decade, however, both the causes of Artemia nutritional variability and methods to improve poorquality Artemia have been identified (Loufi et al., 2024).
Brine shrimp (Artemia spp.) are used in marine aquaculture worldwide. Annually, more than 2,000 metric tons of dry cysts are used for cultivation of fish, crustacean, and shellfish larva. Brine shrimp are important to aquaculture because newly hatched brine shrimp nauplii (larvae) provide a food source for many fish fry (Mozanzadeh et al., 2021). Culture and harvesting of brine shrimp eggs represents another aspect of the aquaculture industry. Nauplii and metanauplii of Artemia, commonly known as brine shrimp, play a crucial role in aquaculture due to their nutritional value and suitability as live feed for many aquatic species, particularly in larval stages (Sorgeloos & Roubach, 2021).
EWOCS-I: The catalog of X-ray sources in Westerlund 1 from the Extended Weste...Sérgio Sacani
Context. With a mass exceeding several 104 M⊙ and a rich and dense population of massive stars, supermassive young star clusters
represent the most massive star-forming environment that is dominated by the feedback from massive stars and gravitational interactions
among stars.
Aims. In this paper we present the Extended Westerlund 1 and 2 Open Clusters Survey (EWOCS) project, which aims to investigate
the influence of the starburst environment on the formation of stars and planets, and on the evolution of both low and high mass stars.
The primary targets of this project are Westerlund 1 and 2, the closest supermassive star clusters to the Sun.
Methods. The project is based primarily on recent observations conducted with the Chandra and JWST observatories. Specifically,
the Chandra survey of Westerlund 1 consists of 36 new ACIS-I observations, nearly co-pointed, for a total exposure time of 1 Msec.
Additionally, we included 8 archival Chandra/ACIS-S observations. This paper presents the resulting catalog of X-ray sources within
and around Westerlund 1. Sources were detected by combining various existing methods, and photon extraction and source validation
were carried out using the ACIS-Extract software.
Results. The EWOCS X-ray catalog comprises 5963 validated sources out of the 9420 initially provided to ACIS-Extract, reaching a
photon flux threshold of approximately 2 × 10−8 photons cm−2
s
−1
. The X-ray sources exhibit a highly concentrated spatial distribution,
with 1075 sources located within the central 1 arcmin. We have successfully detected X-ray emissions from 126 out of the 166 known
massive stars of the cluster, and we have collected over 71 000 photons from the magnetar CXO J164710.20-455217.
The debris of the ‘last major merger’ is dynamically youngSérgio Sacani
The Milky Way’s (MW) inner stellar halo contains an [Fe/H]-rich component with highly eccentric orbits, often referred to as the
‘last major merger.’ Hypotheses for the origin of this component include Gaia-Sausage/Enceladus (GSE), where the progenitor
collided with the MW proto-disc 8–11 Gyr ago, and the Virgo Radial Merger (VRM), where the progenitor collided with the
MW disc within the last 3 Gyr. These two scenarios make different predictions about observable structure in local phase space,
because the morphology of debris depends on how long it has had to phase mix. The recently identified phase-space folds in Gaia
DR3 have positive caustic velocities, making them fundamentally different than the phase-mixed chevrons found in simulations
at late times. Roughly 20 per cent of the stars in the prograde local stellar halo are associated with the observed caustics. Based
on a simple phase-mixing model, the observed number of caustics are consistent with a merger that occurred 1–2 Gyr ago.
We also compare the observed phase-space distribution to FIRE-2 Latte simulations of GSE-like mergers, using a quantitative
measurement of phase mixing (2D causticality). The observed local phase-space distribution best matches the simulated data
1–2 Gyr after collision, and certainly not later than 3 Gyr. This is further evidence that the progenitor of the ‘last major merger’
did not collide with the MW proto-disc at early times, as is thought for the GSE, but instead collided with the MW disc within
the last few Gyr, consistent with the body of work surrounding the VRM.
1. Department of Veterinary Medicine
College of Veterinary & Animal science, Bikaner
Rajasthan University of Veterinary & Animal Science , Bikaner
Submtited By
Kavita Jaidiya
PHD Scholar
2. Introduction
Hypothyroidism (HpoT) is a multisystemic disease that results from
deficiency of thyroid hormones (TH), thyroxine (T4) and
triiodothyronine (T3)( Cooper and Ladenson 2013) .
Hypothyroidism is of primary origin in about 95% of cases,
affecting mainly middle-aged dogs ( Feldman and Nelson 2015) .
It is a single endocrinological disease suspected most commonly in
canine suffering from alopecia (Doering and Jensen, 1973).
3. Anatomy of Thyroid Gland
Located lateral to the trachea, in the region of the proximal
tracheal rings (evans et al , 2013).
Functional unit is the thyroid follicle, which comprises the
follicular cells (thyrocytes) and colloid, each gland containing
both large (resting) follicles and small (active) follicles.
1: Resting follicles (larger and with numerous
vacuoles)
2: Active follicles (smaller in size).
4. Thyroid Hormone
It is a Iodine-containing amino acids.
100 % of T4, but only 20% of T3 is derived from the thyroid gland. Rest of
T3 is derived from extrathyroidal enzymatic deiodination of T4 (Catharine,
2010).
In the dog T4 is bound to: TBG (thyroid hormone-binding globulin) 60 %,
TBPA (transthyretin)17%, Albumin 12% and HDL2 (apolipoprotiens)11%
(Victor, 2011).
Only 0.1% is free T4 fraction (FT4), which is the bioavailable hormone
(Wang et al., 2000) and determines the thyroid condition of the individual.
In contrast to the protein-bound T4 fraction, FT4 concentration remains
constant regardless of fluctuations in plasma transporter proteins (Morreale
et al.,2002).
5. Function of thyroid
hormone
Thyroid hormones increase the metabolic rate and oxygen
consumption of most tissues, (with the exception of the adult brain,
testes, uterus, lymph nodes, spleen, and anterior pituitary).
Thyroid hormones have positive inotropic and chronotropic effects
on the heart. They increase the number and affinity of beta-
adrenergic receptors and enhance the response to catecholamines.
Thyroid hormones have catabolic effects on muscle and adipose
tissue, stimulate erythropoiesis, and regulate both cholesterol
synthesis and degradation.
Thyroid hormones are also essential for the normal growth and
development of the neurologic and skeletal systems.
6. Classification based on etiology
Primary hypothyroidism accounts for more than 95 percent of the
cases and is usually caused by lymphocytic thyroiditis or idiopathic
thyroid atrophy (Carmel, 2003).
Secondary Hypothyroidism (thyroid stimulating hormone, TSH)
deficiency due to congenital malformation, pituitary destruction
(tumors, trauma, autoimmune hypophysitis) or even its
suppression, normally caused by hormones or drugs such as
glucocorticoids ( Feldman and Nelson 2015)
Tertiary hypothyroidism, caused by a thyrotropin releasing
hormone (TRH) deficiency due to pituitary adenoma. (Robert et al.,
2007)
Not reported in dogs.
7. Primary hypothyroidism
A- Lymphocytic thyroiditis
Lymphocytic thyroiditis is a common canine condition that
can lead to functional hypothyroidism. It is associated with
more than 50% of cases of canine hypothyroidism.(Peter A.
Graham et al., 2001)
heritable in beagles and borzois(Patty, 2012)
Characterized by infiltration of the thyroid gland by
lymphocytes, plasma cells, and macrophages.
Lastly fibrous connective tissue replaces parenchyma.
Clinical hypothyroidism develops only when greater than
75% of the functioning thyroid tissue has been destroyed by
the infiltrative process.
8. B. Idiopathic atrophy
45 -50 % of cases
Degenerative disorder ,no inflammatory infiltrate
although initially the disease is characterized by goiter (slight
to significant increase in gland volume) (Feldman and
Nelson, 1996), in last parenchyma replaced by adipose
tissue.
Fibrosis and inflammation are minimal.
Idiopathic thyroid atrophy may be the result of thyroiditis.
As with thyroiditis, hypothyroidism develops slowly over
time .
9. C- Thyroid neoplasia
Does not develop until at least 75% of the thyroid has been destroyed
(Patty, 2012).
Most are euthyroid , 7 % hyperthyroid , 40 % hypothyroid
D- Other congenital or acquired forms of primary hypothyroidism
(thyroid gland dysgenesis, dyshormonogenesis, iodine deficiency) are rare.
-Many affected puppies die early in life and are categorized as ‘fading puppy’
syndrome.
-Also due to deficient dietary iodine intake.
- Causes disproportionate dwarfism.
-Ruled out in dogs being evaluated for pituitary dwarfism.
10. Central Hypothyroidism (secondary and tertiary)
Naturally-occurring secondary hypothyroidism is rare and is
usually congenital but if acquired is most likely the result of a
pituitary tumour.
Central hypothyroidism is most commonly associated with
congenital disorders affecting the pituitary gland (Kooistra et
al., 2000) in association with neoplasia (Mooney and
Anderson , 1993).
11. Congenital hypothyroidism
Congenital hypothyroidism (CH) is one of the most common
neonatal endocrine disorders, presenting with abnormal growth
and intellectual impairment.(shiguo liu et al,2018)
Congenital hypothyroidism is caused by thyroid dysgenesis,
dyshormonogenesi, defects in the transport of thyroid hormones,
TSH receptor-blocking antibodies, maternal medications, or a
deficiency (endemic goitre) or excess of iodine (LaFranchi 2007).
Congenital hypothyroidism causes impaired development of the
central nervous system (CNS) and skeleton (Beaver and Haug ,
2003 ).
Congenital hypothyroidism is an inherited autosomal recessive
trait in rat terriers, toy fox terriers, and giant schnauzers
(Patty,2012).
12. Sings of Congenital hypothyroidism
Congenital hypothyroidism results in mental retardation and
stunted disproportionate growth due to epiphyseal dysgenesis and
delayed skeletal maturation (Cathrine, 2010).
Affected dogs are mentally dull and have large, broad heads, short
thick necks, short limbs, macroglossia, hypothermia, delayed
dental eruption, ataxia, and abdominal distention.
Dermatologic findings are similar to those seen in the adult
hypothyroid dog.
Other clinical signs may include gait abnormalities, stenotic ear
canals, sealed eyelids, and constipation.
Affected puppies are often the largest in the litter at birth but start
to lag behind their littermates within three to eight weeks of age.
13. Subclinical hypothyroidism
Subclinical hypothyroidism is the first phase of the disease, representing
approximately 25% of all cases (Snyder,2000).
Subclinical hypothyroidism is defined as an elevated serum TSH level associated
with normal total or free T4 and T3 values(Michael et al .,2001)
Subclinical hypothyroidism is associated with an increased risk of CHD events and
CHD mortality in those with higher TSH levels, particularly in those with a TSH
concentration of 10 mIU/L or greater.(rodondi et al.,2010)
The system responds with increased thyrotropic cell sensitivity to TRH
stimulation (Castillo et al., 2001).
The first changes are seen in lipid metabolism (increase in the LDL-cholesterol
fraction), the reproductive and immune systems, and the skin (with recurrent
infections) (Victor, 2011) .
14. Clinical hypothyroidism
At this stage the daily secretion of T4 is severely affected.
Clinical signs vary greatly because thyroid hormone impacts
myriad of systems .
Clinical are not always the typical obesity, lethargy and poor hair
cover as described in many textbooks (Victor, 2011) .
1- Dermatological sign
Dermatologic abnormalities are the most common presenting
complaints (Beale, 1993). But they appear in later stages of the
disease.
Dermatologic changes occur in 60-80 percent of hypothyroid
dogs (Catharine, 2010).
15. Dry scaly or greasy skin (Seborrhea sicca or oleosa), change in
coloration, strong smelling of skin , hyperkeratosis, hyperpigmentation.
Poor hair coat quality, fading of hair color, failure of hair re-growth.
The hair is often brittle and easily epilated, and loss of undercoat or
primary guard hairs may result in a coarse appearance or a puppy hair
coat (short, softer under coat).
Most dogs with hypothyroidism do not show generalized hair loss but
“rat tail” is common (Victor, 2011), which spares head and extremities.
Hypothyroid dogs are predisposed to recurrent bacterial infections of the
skin like Malassezia spp. infections and demodicosis.
Myxedema (cutaneous mucinosis) is a rare dermatologic manifestation
of hypothyroidism characterized by puffy but nonpitting thickening of
the skin, especially of the eyelids, cheeks, and forehead and is
classically referred to as ‘tragic face’ (Doering and Jensen, 1973).
Dermatological sign---
----
16. Appearance is due to drooping of the eyelids and thickening of the lips and
of the skin over the forehead, leading to more skin folds .
It is caused by deposition of hyaluronic acid and glycosaminoglycan in the
dermis.
Satish et al. (2007) found skin abnormality – 94%, Generalized hair loss -
88%, Typical rat tail - 83%, Skin lesions, pigmentation and pruritus - 27%,
Brittle, dry and lusterless coat - 83% . Puppy – like coat - 22% , Myxedema -
16%.
Other changes include ceruminous otitis, poor wound healing and increased
bruising.
A variety of other ‘atypical’ and secondary dermatological abnormalities are
also possible. The alopecia may be patchy and asymmetric or may only affect
one area (e.g., the bridge of the nose) (Carmel, 2003).
Retarded turnover of hair (carpet coat) or hypertrichosis can occur
particularly in Irish setters and boxers (Carmel,2003).
Dermatological sign---
----
18. BMR related Signs
Common clinical signs attributable to decreased metabolic rate
include lethargy, mental dullness, weight gain, unwillingness to
exercise, and cold intolerance.
Obesity occurs in approximately 40% of hypothyroid dogs, but most
obese dogs suffer from over-nutrition rather than hypothyroidism
(Catharine, 2010). Many dogs may present with normal body
weight or even weight loss. This is due to poor digestion and
nutrient assimilation, as a result of altered motility of the small
bowel and less bile secretion (Gebhard et al., 1992).
The decrease in glucose consumption leads to lethargy and
increased sleepiness, though some dogs may become aggressive
(Beaver and Haug , 2003).
Satish et al. (2007) recorded obesity - 88%, generalized weakness,
lethargic, dull and listless, exercise intolerance, dyspnoea, gasping,
bradycardia, cyanotic tongue - 55%
27. 3- Neurologic dysfunction
A-Peripheral neuropathy
About 2-4% dogs exhibit some behavioral changes and neurological signs such
as, head tilt, seizures, ataxia, circling and facial nerve paralysis (Nesbit et al.,1980
and Baker, 1997).
Peripheral neuropathy caused by hypothyroidism affects primarily middle-aged
and older individuals (Jaggy et al., 1994), especially of middle- to large-sized
breeds.
Neurological symptoms of hypothyroidism can originate from the central and
peripheral nervous systems (Rudas et al.,2005 and Nunez et al., 2008) as well as
from the muscles.
Specific presentations and their incidence that would be included under behavioral
signs include aggression, cold intolerance (15%), decreased libido, exercise
intolerance, lethargy or mental dullness (20% to 70%), prolonged anestrus (4% to
40%), and weight gain or obesity (41% to 60%).(Bonnie V. Beaver et al,2013)
28. In neurological manifestations of hypothyroidism, the dog may not show
any of the classical symptoms such as lethargy and dermatological
changes (Srivastava et al., 2013 and Budsberg et al.,1993).
However, (Indrieri et al., 1987) reported dermatological changes, weight
gain and hypercholesterolaemia (Cuddon, 2002) in dogs with peripheral
neuropathies.
Symptoms from the peripheral nervous system are exercise intolerance,
general weakness, ataxia, paraparesis, tetraparesis, deficits of conscious
proprioception, and decreased spinal reflexes (Catharine, 2010) and
symptoms of the cranial nerves such as facial paralysis (McKeown, 2002)
vestibular syndrome, trigeminal nerve (Fors, 2006), reduced spinal
reflexes and muscle atrophy (Bischel et al.,1988).
Proprioceptive positioning deficits and decreased spinal reflexes are
generally more evident in the hind limbs, however(jaggy et al., 1994).
The clinical signs of generalised peripheral neuropathy reduced spinal
reflexes in all four limbs can occur caused by hypothyroidism are usually
reversible after two to three months treatment using thyroid hormone
supplements (Cizinauskas et al.,2000). Intermittent, as well as constant,
forelimb lameness is described in dogs with hypothyroidism (Budsberg et
al.,1993).
29. Cardiovascular system:
Sinus bradycardia, weak apex beat, low QRS voltages, and
inverted T waves occur in hypothyroid dogs.
Reduced left ventricular pump function but rarely myocardial
failure in dogs.
Dilated cardiomyopathy and hypothyroidism may occur
concurrently with dramatic long-term improvement in cardiac
function after treatment with l-thyroxine.
Canine hypothyroidism may occur in association with other
immune-mediated endocrine disorders such as
hypoadrenocorticism and diabetes mellitus.
Hypothyroidism causes insulin resistance and may mask the
classic electrolyte changes of hypoadrenocorticism.
Polyendocrinopathies
30. Ocular changes:
Corneal lipidosis, corneal ulceration, uveitis, lipid effusion
into the aqueous humor, secondary glaucoma, lipemia retinalis,
retinal detachment, and keratoconjunctivitis sicca may occurs
in hypothyroidism.
Hemostasis
• Decreased plasma von Willebrand factor concentration has
been reported in hypothyroid dogs but canine hypothyroidism
is rarely associated with clinical bleeding, and platelet
function.
31. Epidemiology:
Hypothyroidism is the most common hormone imbalance of
dogs with the incidence rate at about 1: 150 to 1: 500 (Chastain
and Panaciera, 1995).
Dogs beyond 8 yrs are more susceptible (Panaciera, 1994).
Most cases are seen in dogs over one year of age middle-aged
dogs and is rarely diagnosed in dogs less than two years of age
(Carmel, 2003) although perhaps 10% may be in younger
animals.
A small number (approx. 3%) of cases are congenital, while the
rest relate to pathology acquired during growth (Victor, 2011).
Hypothyroidism can affect any age or breed of dog (Dixon et
al., 1999).
32. Hypothyroidism secondary to lymphocytic thyroiditis appears to
develop at a younger age than idiopathic thyroid atrophy (Patty,
2012).
Labrador, Doberman, Golden Retriever, German shepherd,
Spaniels, Great Dane, Dachshund have great risk (Patty, 2012
and Nesbitt et al., 1980).
More common in mid to large pure-bred dogs (Carmel, 2003).
33. In india Spitz was showing high incidence (56%) followed
by Labrador (28%) and German shepherd (17%) (Satish et
al., 2007).
This variation could probably be due to the habitation of
different breeds in different regions.
Spayed females and castrated males are at greater risk
(Panaciera, 1994).
Males and females, either neutered or entire, appear to be
affected equally (Carmel, 2003).
35. Total triiodothyronine (T3)
T3 is three to five times more potent than T4 (pro-hormone).
Measurement of T3 therefore reflects metabolic status more
accurately, but it plays no role in the diagnosis of hypothyroidism
(Carmel, 2003), as circulating concentrations are often maintained
in the reference range in hypothyroid dogs (Peterson et al., 1997).
This is because of compensatory mechanisms both within the
thyroid gland (increasing secretion of T3), and possibly in extra-
thyroidal tissue (up-regulating peripheral T4 conversion).
TT3 concentrations fluctuate out of reference ranges even more
than TT4 concentrations in euthyroid dogs (Catharine,2010).
36. Total Thyroxin (T4)
Circulating total T4 concentration is invariably low in hypothyroid
dogs (Peterson et al., 1997; Dixon and Mooney, 1999).
Extremely valuable screening test to rule out hypothyroidism unless
anti-T4 antibodies cause a spurious increase, which are produced in
2% of dogs with hypothyroidism (Graham et al., 2001).
Basal T4 has a 95% positive predictive value, the 5% lacking are
due to the presence of T4 antibodies (Cauzinille, 2005), but it is
poorly specific due to numerous nonthyroidal factors like non-
specific hormone fluctuation in healthy dogs, breed, any non-
thyroidal illness and numerous drug therapies including
glucocorticoids, potentiated sulphonamides and anticonvulsants
(Muller et al., 2000; Kantrowitz et al., 2001).
Thus, a low total T4 concentration alone does not confirm
hypothyroidism. Total T4 concentrations do not differ significantly
between males and females but are higher in small dogs than in
medium and large-breed dogs
38. Free thyroxin (FT4)
Free T4 is the active fraction of total T4 and is more closely reflect
metabolic status at the tissue level than total T4.
It is less affected by the myriad factors (drug therapies, non-
thyroidal illness, breed) and T4 autoantibodies etc. capable of
lowering total T4 and is thus a more specific diagnostic test for
hypothyroidism.
Overall, it is considered to be the best single diagnostic test for
hypothyroidism but it is not without problems (Peterson et al.,
1997; Dixon and Mooney, 1999), as free T4 is only accurately
measured by equilibrium dialysis or ultrafiltration techniques and
these are not widely available and are relatively expensive.
39. Certain drugs, particularly anticonvulsants and glucocorticoids,
are capable of lowering both total and free T4 concentrations
(Muller et al., 2000) and severe nonthyroidal illness has also been
associated with decreased free T4 concentration in a few cases
(Kantrowitz et al., 2001).
With regard to THs, FT4 is the fraction that best reflects the
peripheral thyroid condition and is the first to become affected
(Wang et al., 2000).
A decrease in FT4 is indicative of hypothyroidism in all dogs
diagnosed for clinical hypothyroidism, 30% presented with
protein-bound T4 levels close to the lower limit, with diminished
FT4 and increased TSH levels, together with morphological
alterations of the gland and clinical signs (Victor, 2011).
40. Endogenous thyroid-stimulating hormone
(TSH)
Decreased circulating thyroid hormone concentrations reduce the
negative feedback effect on the pituitary gland and consequently, in
primary hypothyroidism, TSH concentrations rise.
Approximately 20 to 30% (Kooistra et al., 2000), 13% to 38%
(Catharine,2010) of hypothyroid dogs have a TSH concentration
within the reference range, which might be due to suppressive
effects of concurrent non-thyroidal illnesses or from drug
therapies, non-specific fluctuation, existence of secondary
hypothyroidism or production of unrecognizable TSH isomers
41. TSH concentrations increase above the reference range in 7% to
18% of euthyroid dogs, however, limiting the specificity of
measuring TSH alone for diagnosis of hypothyroidism
(Catharine,2010).
TSH is the best estimator of the thyroid gland axis, and is the most
sensitive marker for evaluating thyroid function. TSH elevation is
diagnostic of hypothyroidism, independently of the T4 values
(Snyder, 2000).
Despite the low specificity of TSH alone for diagnosis of
hypothyroidism, in dogs with concurrent low TT4 or fT4
concentration, specificity of an increased TSH concentration for
diagnosis of hypothyroidism approaches 100%.
42. Effect of Drugs on Thyroid Hormone Concentrations
Glucocorticoids influence
peripheral metabolism of thyroid
hormones and inhibit TSH
secretion. The effect of
glucocorticoids is dependent on
the dose and specific preparation.
In most studies oral
administration of
glucocorticoids at
immunosuppressive doses (1 to 2
mg/kg q12h) resulted in rapid
decreases in TT4, fT4, and T3,
but little change in serum TSH.
43. Evaluation of the lipid
profile
30-40% of all dogs with hypothyroidism present with total
cholesterol elevation (Xenoulis and Steiner ,2010).
It is important to measure LDL-cholesterol, since an
increase in relation to HDL-cholesterol can indicate thyroid
deficiency (Xenoulis and Steiner , 2010).
45. Therapeutic response
Therapeutic response has also been suggested as a method of
confirming hypothyroidism in dogs with inconclusive total T4 and
cTSH concentrations. However, caution is advised. Thyroid
hormone supplementation suppresses TSH production and
endogenous thyroid function. Hypofunction invariably occurs once
supplementation is withdrawn and can lead to confusing clinical
signs for up to eight weeks later (Panciera et al., 1989).
Thyroid hormone supplementation is known to have several
physiological effects that can easily be misinterpreted as a
successful response to therapy in euthyroid dogs.
46. Thyroid Ultrasound
thyroid gland in many hypothyroid dogs has a smaller volume and
s-sectional area and tends to be less echogenic (Catharine, 2010).
Ultrasound is a useful imaging tool for assessment of thyroid glands
and measurement of thyroid size.(Lyshchik et al,2004)
Three-dimensional ultrasound is a useful and precise image method in
the measurement of thyroid volume as compared with 2D
ultrasonography, and this method enables to exactly detect the alteration
of the thyroid lobe volume in a relatively short time.(Alireza Vajhi et
al,2010)
47. How are hypothyroid dogs
treated?
Synthetic T4 products have greater standardization and potency
and a longer shelf life compared with crude preparations. T4 itself
is considered to be a physiological pro-hormone, serves to
normalize both circulating T4 and T3 concentrations and pituitary
cTSH production, and can effectively be administered once daily.
The recommended dose in clinical hypothyroidism is 11-22 μg/kg,
starting with the lower dose and gradually increasing the dosage
until the desired concentration has been reached. (Dixon et al.,
2002).
48. In adequately treated dogs, there is usually a dramatic improvement
in metabolic signs within days. Dermatological abnormalities can
take several months to improve and, frequently, there is worsening
of alopecia before new hair re-growth commences.
There is wide inter-individual variation in gastrointestinal
absorption and response to T4 replacement therapy. As a
consequence, it is important to monitor dogs after commencing
therapy.
49. Administration of lower doses (3-10 μg/kg) in subclinical
hypothyroidism.
Administration of lower doses in elderly animals.
Presence of heart failure or kidney disease: administration of
lower doses in order not to overburden the affected organs.
Gestation or proximity to mating: administration of higher doses
(between 25-50%) in order to secure good ovulation or
spermatogenesis and avoid embryonic and fetal
deaths/reabsorptions.
Dogs with oncological diseases or chronic infections, where
metabolic rest is indicated: administration of lower doses.
Recommendation for treatment
(Victor, 2011)
50. Dixon and Mooney (1999) advise initially administering
levothyroxine every 12h, progressing to once daily dosing).
Reassessment can then be performed every 6-12 months (Dixon
et al.,2002).
In the case of congenital hypothyroidism, treatment should start as
soon as possible in order to avoid irreparable damage to the
central nervous system. The dosage in puppies with congenital
hypothyroidism or juvenile hypothyroidism is 5-20 μg/kg.
Adequately treated animals have a normal life expectancy and
quality of life.
Regular monitoring is required and consideration needs to be
given to the development of other immune mediated
endocrinopathies (polyglandular syndromes). In such cases,
hypothyroidism most commonly occurs in association with
hypoadrenocorticism or diabetes mellitus.
51.
52.
53. Improvement in activity - first 1 to 2 weeks of treatment.
Weight loss - within 8 weeks.
Normal hair coat- several months and the coat may initially appear
worse as telogen hairs are shed.
Improvement in myocardial function - 8 weeks but may be delayed
for as long as 12 months.
Neurologic deficits - 8 to 12 weeks.
Vestibular symptoms - two to four months (Jaggy et al., 1994 and
Bischel et al., 1988 ).
Time of Clinical Improvement