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Endocrine system > Hyperthrodisum > Flashcards

Hyperthrodisum Flashcards

1
Q
  1. What do the paraventricular nuclei inside the hypothalamus secrete?
A

Thyrotropin-releasing hormone (TRH).

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2
Q
  1. Where does TRH go after secretion, and what cells does it stimulate?
A

TRH goes into the hypophyseal portal system and stimulates thyrotropes in the adenohypophysis.

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3
Q
  1. What is the role of TSH in the thyroid gland?
A

TSH binds to receptors (TSH-R) on the follicles, stimulating the production of thyroglobulin and iodine incorporation.

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4
Q

How is iodinated thyroglobulin produced?

A

TSH-R stimulates thyroid peroxidase,
converting iodide to iodine and
combining it with thyroglobulin.

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5
Q

What happens after iodinated thyroglobulin is endocytosed back into the follicular cell?

A

Proteases cleave thyroid hormone (T3 and T4) from iodinated thyroglobulin, releasing it into the blood.

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6
Q
  1. How does thyroid hormone enter cells, and what is the fate of T4 inside cells?
A

Thyroid hormone diffuses across cell membranes. The majority of T4 is converted to T3 by deiodinases.

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7
Q
  1. What are the general effects of thyroid hormone on all cells?

2 a-d

A

Increases sodium-potassium ATPases, stimulates glycogenolysis, glycolysis, lipolysis, and modifies cellular activity.

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8
Q

What cellular activities are stimulated by thyroid hormone in all cells?

number2a-d

A

Increases sodium-potassium ATPases, stimulates glycogenolysis, glycolysis, and lipolysis.

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9
Q

(3) What effects does thyroid hormone have on the liver?

A

Stimulates LDL uptake and regulates the production of steroid hormone binding globulins, e.g., thyroxine binding globulin.

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10
Q

(4) How does thyroid hormone influence the heart?

A

Increases beta-receptor sensitivity, leading to an increase in heart rate and contractility. Maintains vasomotor tone.

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11
Q

(5) What role does thyroid hormone play in bones?

A

Maintains the balance between bone resorption via osteoclasts and bone deposition via osteoblasts.

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12
Q

(6) How does thyroid hormone affect the brain?

A

Increases sympathetic nervous system activity.

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13
Q

(7) What changes does thyroid hormone induce in the GI tract?

6

A

Increases GI motility and GI secretions.

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14
Q
  1. What effects does thyroid hormone have on skeletal muscles?
A

Maintains normal muscle contraction, stimulates muscle development and regeneration, and maintains calcium ATPases on the sarcoplasmic reticulum.

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15
Q
  1. How does thyroid hormone affect the integumentary system?
A

Maintains good blood flow to skin, hair, and nails,
stimulates growth, and

maintains blood flow to sebaceous glands and eccrine sweat glands,
stimulating secretions.

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16
Q
  1. What role does thyroid hormone play in fibroblasts?
A

Maintains the production of glycosaminoglycan and
other extracellular proteins.

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17
Q

What are the effects of thyroid hormone on skeletal muscles?

A

Maintains
normal muscle contraction,
stimulates muscle development and regeneration, and maintains calcium ATPases on the sarcoplasmic reticulum.

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18
Q

How does thyroid hormone influence the integumentary system?

A

Maintains good blood flow to skin, hair, and nails, stimulates growth, and maintains blood flow to sebaceous glands and eccrine sweat glands, stimulating secretions.

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19
Q

What is the role of thyroid hormone in fibroblasts?

A

Maintains the production of glycosaminoglycan and other extracellular proteins.

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20
Q
  1. What happens when thyroid hormone leaks out of injured cells?
A

Causes transient hyperthyroidism, often followed by hypothyroidism.

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21
Q
  1. What are the causes of destruction of the thyroid gland?
A

(i) Hashimoto thyroiditis, (ii) Postpartum thyroiditis, (iii) Subacute granulomatous thyroiditis, (iv) Drug-induced thyroiditis, (v) Iodine-induced thyroiditis.

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22
Q

What are the causes of primary secondary hyperfunction of the thyroid gland?

A

(i) Graves’ disease, (ii) Toxic adenoma or toxic multinodular goiter (TMG),
2nd
(iii) Pituitary adenoma, (iv) Increased beta-hCG production.

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23
Q

(1) What are the metabolic effects of excess thyroid hormone?

A

Increased metabolism, weight loss, increased appetite, elevated body temperature.

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24
Q

How does excess thyroid hormone affect sodium-potassium ATPase activity?

A

Increases ATP demand.

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25
Q

What are the effects of excess thyroid hormone on glycogenolysis and glycolysis?

A

Increases glycogenolysis (breakdown of glycogen into glucose) and glycolysis (breakdown of glucose into pyruvate).

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26
Q

What is the impact of excess thyroid hormone on lipolysis?

A

Increases lipolysis (breakdown of lipids into fatty acids and glycerol).

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27
Q

(2) How does excess thyroid hormone affect the heart?

A

Increases beta-receptor sensitivity, ->
heart rate, and
contractility, leading to tachycardia,
increased stroke volume, and hypertension.

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28
Q

(3) What effects does excess thyroid hormone have on bones?

A

Increases osteoclast activity,

leading to increased bone resorption and an

elevated risk of osteoporosis and fractures.
https://veritas.widen.net/content/xz1pbdqmve/png/osteoporosis-41878270.png?use=idsla&color=&retina=false&u=at8tiu&w=780&h=449&crop=yes&k=c

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29
Q

(4) How does excess thyroid hormone influence the brain?

A

Increases sympathetic nervous system activity, causing anxiety, restlessness, agitation, and features like lid lag and retraction.

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30
Q

(5) What changes occur in the GI tract due to excess thyroid hormone?

A

Increases GI motilityand secretions, leading to diarrhea.

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31
Q

(6) What effects does excess thyroid hormone have on skeletal muscles?

A

Increases muscle contractions and growth, potentially causing myopathy (muscle pain without damagethus NORMAL CK ).

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32
Q

(7) How does excess thyroid hormone affect the integumentary system?

A

Increases blood flow to skin, hair, and nails, resulting in thick and coarse hair, flushed skin, thicker nails with onycholysis, and increased sweating and sebum production.

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33
Q

(8) What changes occur in the liver due to excess thyroid hormone?

A

Increases the number of LDL receptors,leading to increased LDL uptake, and

enhances the production of steroid hormone binding globulins, including thyroxine binding globulin and sex hormone binding globulins.

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34
Q

(9) What clinical features are associated with fibroblasts in Graves’ disease?

A

TSH receptor antibodies can activate fibroblasts in the dermis, causing glycosaminoglycan accumulationalong with water , known as

pretibial myxedema. TSH receptor antibodies can also activate T-cells, leading to

exophthalmos.

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35
Q
  • How does Graves’ disease affect fibroblasts in the dermis?
A

TSH receptor antibodies in Graves’ disease can directly activate fibroblasts in the dermis, leading to glycosaminoglycan accumulation and pretibial myxedema.

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36
Q

(1) How is primary and secondary hyperthyroidism differentiated?

A

Both show increased free T4 levels, but the key is TSH levels vary. Increased TSH suggests pituitary adenoma, while

decreased TSH may indicate excess ß-hCG, requiring further investigation.

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37
Q

When is a ß-hCG check necessary in the diagnosis of hyperthyroidism?

A

If the patient is pregnant or excess ß-hCG is suspected.

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38
Q

(2) How is the cause of primary hyperthyroidism differentiated?

A

Thyroid exam with palpation for nodules is performed. Nodules may require further testing, such as a radioactive iodine uptake scan (first line) or ultrasound with doppler (second line). The uptake scan helps determine if the nodule is hot (benign), cold (likely malignant), or associated with Graves’ disease, toxic adenoma, or toxic multinodular goiter. No uptake or low uptake may indicate thyroiditis or exogenous use.

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39
Q

What further evaluation is needed for no uptake or low uptake hyperthyroidism?

A

Anti-thyroid antibodies, including TSH receptor antibodies (indicative of Graves’ disease) and anti-TPO antibodies (suggestive of Hashimoto thyroiditis or postpartum thyroiditis). Serum thyroglobulin levels can also help differentiate causes, with elevated levels indicating follicular cell injury and potential causes including thyroiditis, struma ovarii (confirmed with ultrasound and biopsy), and decreased levels suggesting exogenous thyroid use.

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40
Q

(1) What is the symptomatic treatment for hyperthyroidism?

A

Symptomatic treatment involves the use of beta blockers, such as propranolol, which decreases T4 →T3 conversion in target cells, rendering thyroid hormone ineffective.

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41
Q

How does propranolol contribute to the symptomatic treatment of hyperthyroidism?

A

Propranolol decreases T4 →T3 conversion in target cells, making thyroid hormone ineffective.

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42
Q

(2) What are the anti-thyroid medications used for hyperthyroidism?

A

Methimazole (first line) and propylthiouracil decrease T4 →T3 conversion in target cells, rendering thyroid hormone ineffective. Propylthiouracil also inhibits thyroid peroxidase from iodinating thyroglobulin, preventing the production of functional thyroid hormone. Radioactive iodine ablation is used when other measures fail and involves the destruction of hyperfunctioning thyroid follicles with iodine-131.

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43
Q

How does radioactive iodine ablation work in the treatment of hyperthyroidism?

A

Iodine-131 is taken up by hyperfunctioning thyroid follicles, generating gamma waves that destroy the follicles, rendering them ineffective at synthesizing and producing thyroid hormone.

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44
Q

(3) When is surgery indicated in the treatment of hyperthyroidism?

A

Surgery is indicated for large goiters with surrounding compression, severe Graves’ with ophthalmopathy, and refractory hyperthyroidism with associated complications. Lobectomy or total thyroidectomy may be performed, with contraindications including pregnancy.

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45
Q

What are the indications and contraindications for thyroid surgery?

A

Indications include large goiters with surrounding compression, severe Graves’ with ophthalmopathy, and refractory hyperthyroidism with associated complications. Contraindications include pregnancy.

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46
Q

(1) What are some causes of thyrotoxicosis (thyroid storm)?

A

Causes include infection (sepsis), DKA, myocardial infarction, surgery, and trauma.

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47
Q

(2) What are the main clinical features of thyroid storm?

A

Hypertension, tachycardia, delirium or altered mental status, coma, and fever.

48
Q

(3) What is the treatment for thyroid storm?

A

Treatment includes propranolol or esmolol, propylthiouracil, potassium iodine (Lugol solution), prednisolone (corticosteroids), plenty of fluids, and pyretic control. Once stable, treatment of underlying causes is initiated.

49
Q

How do propranolol and propylthiouracil contribute to the treatment of thyroid storm?

A

Propranolol and propylthiouracil decrease T4 →T3 conversion in target cells, rendering thyroid hormone ineffective. Propylthiouracil also inhibits thyroid peroxidase from iodinating thyroglobulin, preventing the production of functional thyroid hormone.

50
Q

What is hyperthyroidism?

A

It is the overproduction of thyroid hormones (T3 and T4) by the thyroid gland.

51
Q

What does thyrotoxicosis refer to?

A

It refers to the effects of an abnormal and excessive quantity of thyroid hormones in the body.

52
Q

What characterizes primary hyperthyroidism?

A

It is due to thyroid pathology, where the thyroid gland behaves abnormally and produces excessive thyroid hormone.

53
Q

What is the cause of secondary hyperthyroidism?

A

It is due to pathology in the hypothalamus or pituitary, leading to excessive production of thyroid-stimulating hormone (TSH).

54
Q

Define subclinical hyperthyroidism.

A

It is a condition where thyroid hormones (T3 and T4) are normal, but thyroid-stimulating hormone (TSH) is suppressed, with absent or mild symptoms.

55
Q

What is Graves’ disease, and what triggers it?

A

Graves’ disease is an autoimmune condition where TSH receptor antibodies cause primary hyperthyroidism. The immune system produces antibodies that stimulate TSH receptors on the thyroid.

56
Q

What characterizes toxic multinodular goitre?

A

It is a condition where nodules develop on the thyroid gland, unregulated by the thyroid axis, continuously producing excessive thyroid hormones. Common in patients over 50 years.

57
Q

What is exophthalmos, and what condition is it associated with?

A

Exophthalmos is the bulging of the eyes caused by Graves’ disease. Inflammation, swelling, and hypertrophy of tissue behind the eyeballs force them forward.

58
Q

Describe pretibial myxoedema and its specificity.

A

Pretibial myxoedema is a skin condition caused by deposits of glycosaminoglycans under the skin on the anterior aspect of the leg. It is specific to Graves’ disease and is a reaction to TSH receptor antibodies.

59
Q

What does the term “goitre” refer to?

A

Goitre refers to the neck lump caused by the swelling of the thyroid gland.

60
Q

What does the mnemonic “GIST” represent in the context of hyperthyroidism causes?

A

GIST stands for Graves’ disease, Inflammation (thyroiditis), Solitary toxic thyroid nodule, and Toxic multinodular goitre.

61
Q

Name the causes of thyroiditis that can lead to hyperthyroidism.

A

De Quervain’s thyroiditis, Hashimoto’s thyroiditis, Postpartum thyroiditis, and Drug-induced thyroiditis.

62
Q

List the universal features associated with hyperthyroidism.

A

Anxiety and irritability, Sweating and heat intolerance, Tachycardia, Weight loss, Fatigue, Insomnia, Frequent loose stools, Sexual dysfunction, Brisk reflexes on examination.

63
Q

What are the specific features of Graves’ disease?

A

Diffuse goitre (without nodules), Graves’ eye disease including exophthalmos, Pretibial myxoedema, Thyroid acropachy (hand swelling and finger clubbing).

64
Q

What characterizes a solitary toxic thyroid nodule?

A

A single abnormal thyroid nodule acting alone to release excessive thyroid hormone, usually benign adenomas. Surgical removal is the treatment.

65
Q

Describe the three phases of De Quervain’s thyroiditis.

A

The three phases are Thyrotoxicosis, Hypothyroidism, and Return to normal.

66
Q

What are the symptoms of the thyrotoxic phase in De Quervain’s thyroiditis?

A

Excessive thyroid hormones, thyroid swelling and tenderness, flu-like illness (fever, aches, and fatigue), raised inflammatory markers (CRP and ESR).

67
Q

How is De Quervain’s thyroiditis treated during the thyrotoxic phase?

A

Supportive treatment, including NSAIDs for pain and inflammation, Beta blockers for hyperthyroidism symptoms, and Levothyroxine for hypothyroidism symptoms.

68
Q

What percentage of individuals with De Quervain’s thyroiditis remain hypothyroid long-term?

A

Under 10% remain hypothyroid long-term.

69
Q

What is another name for thyroid storm?

A

Thyrotoxic crisis

70
Q

What are the symptoms of thyroid storm?

A

Fever, tachycardia, delirium

71
Q

How is thyroid storm managed?

A

Treated similarly to other presentations of thyrotoxicosis, additional supportive care with fluid resuscitation, anti-arrhythmic medication, and beta-blockers may be required.

72
Q

Who guides the treatment of hyperthyroidism?

A

A specialist endocrinologist.

73
Q

What is the first-line anti-thyroid drug, and how long is it typically taken?

A

Carbimazole, usually taken for 12 to 18 months.

74
Q

What are the two approaches to continuing treatment after normalization of thyroid hormone levels with carbimazole?

A

Titration-block, where the carbimazole dose is titrated to maintain normal levels, and block and replace, where a higher dose blocks all production, and levothyroxine is added and titrated to effect.

75
Q

What is the second-line anti-thyroid drug?

A

Propylthiouracil

76
Q

Why is carbimazole preferred over propylthiouracil?

A

Carbimazole is preferred due to a lower risk of severe liver reactions, including death.

77
Q

What is the potential risk associated with carbimazole, and what symptoms should be monitored for?

A

There is a risk of acute pancreatitis. Symptoms of pancreatitis, such as severe epigastric pain radiating to the back, should be monitored.

78
Q

What serious side effect can both carbimazole and propylthiouracil cause, and what is a key presenting feature?

A

Both can cause agranulocytosis, presenting with a sore throat. Urgent full blood count and aggressive treatment of any infections are necessary.

79
Q

What does radioactive iodine treatment involve, and what precautions must be taken?

A

It involves drinking a single dose of radioactive iodine. Precautions include not being pregnant or breastfeeding (and avoiding pregnancy within 6 months of treatment for women), not fathering children within 4 months of treatment for men, and limiting contact with people, especially children and pregnant women, after the dose.

80
Q

Which beta blocker is commonly used to block adrenergic symptoms of hyperthyroidism, and why?

A

Propranolol is commonly used as it non-selectively blocks adrenergic activity.

81
Q

What is a definitive option for hyperthyroidism, and what are the two types of surgery?

A

Surgery is a definitive option. Thyroidectomy involves removing the whole thyroid gland, and removing toxic nodules is also an option. After thyroidectomy, patients will be hypothyroid and require lifelong levothyroxine

82
Q

What is thyrotoxicosis?Noti

A

The clinical, physiological, and biochemical state arising when the tissues are exposed to excess thyroid hormone.

83
Q

Define hyperthyroidism.

A

It refers specifically to conditions in which overactivity of the thyroid gland leads to thyrotoxicosis.

84
Q

What is the most common cause of hyperthyroidism?

A

Graves disease.

85
Q

What percentage of hyperthyroidism cases does Graves disease account for?

A

85%.

86
Q

In which gender is Graves disease more commonly observed, and what is the ratio?

A

Higher incidence in females, with a ratio of 10:1 (female to male).

87
Q

At what age range does Graves disease usually present?

A

Between 20-40 years.

88
Q

What are the genetic factors associated with Graves disease?

A

Increased incidence in family members, with sisters and children of affected women having a 5-8% risk of developing autoimmune thyroid disease. Susceptibility is associated with certain HLA haplotypes, and polymorphisms in immune regulation-associated genes such as CTLA-4 and PTPN-22 are linked to Graves’ disease. There is also an association with other autoimmune diseases.

89
Q

Name some other causes of thyrotoxicosis associated with hyperthyroidism.

A

Excessive thyroid stimulation, including Hashitoxicosis (transient hyperthyroidism caused by inflammation associated with Hashimoto’s thyroiditis, followed by hypothyroidism), Thyrotropinoma (TSH-secreting pituitary adenoma - very rare), Thyroid cancer (very rare), and Choriocarcinoma (trophoblast tumor secreting hCG). Thyroid nodules, including Toxic solitary nodule and Toxic multinodular goitre.

90
Q

What are some causes of thyrotoxicosis that are not associated with hyperthyroidism?

A

Thyroid inflammation, including Subacute (de Quervain’s) thyroiditis, Post-partum thyroiditis, and Drug-induced thyroiditis (e.g., amiodarone). Exogenous thyroid hormones, such as Over-treatment with levothyroxine and Thyrotoxicosis factitia. Ectopic thyroid tissue, involving Metastatic thyroid carcinoma and Struma ovarii (teratoma containing thyroid tissue).

91
Q

What is the pathophysiology of Graves disease?

A

It involves auto-antibodies to TSH receptor, thyroid peroxisomes, and thyroglobulin. The anti-TSH receptor antibodies stimulate the thyroid, resulting in increased function. Some antibodies can inhibit function, which may explain paradoxical episodes of hypofunction that can occur.

92
Q

Name some general symptoms of thyrotoxicosis.

A

Weight loss despite increased appetite, frequent loose bowel movements, sweating and heat intolerance, and goitre - diffuse in Graves, goitre with firm nodules if toxic multinodular goitre.

93
Q

What is the thyroid bruit associated with in thyrotoxicosis?

A

It is associated only with large goitres and reflects the hypervascularity of the thyroid. Auscultation is done over the thyroid.

94
Q

What are some symptoms related to the eyes in thyrotoxicosis?

A

Double vision and Graves ophthalmopathy.

95
Q

List some cardiovascular symptoms associated with thyrotoxicosis.

A

Increased pulse rate, palpitations, atrial fibrillation, and rarely cardiac failure.

96
Q

What musculoskeletal signs might be present in thyrotoxicosis?

A

Fine tremor of the outstretched fingers and muscle weakness, especially in thighs and upper arms.

97
Q

Name some neuropsychiatric symptoms associated with thyrotoxicosis.

A

Increased nervousness and excessive emotional response, sleep disturbance, depression, and insomnia.

98
Q

What changes might be observed in hair and skin in thyrotoxicosis?

A

Thin, brittle hair, and rapid fingernail growth.

99
Q

How does thyrotoxicosis affect the menstrual cycle?

A

It can cause menstrual cycle changes, including lighter bleeding and less frequent periods.

100
Q

What are specific signs of Graves’ disease?

A

Pretibial myxoedema, thyroid acropachy (thickening of the extremities manifested by digital clubbing, soft tissue swelling of the hands and feet, and periosteal new bone formation), Graves eye disease (autoimmune inflammatory disorder of the orbit and periorbital tissues), and diffuse goitre.

101
Q

What is thyroid acropachy, and how is it manifested?

A

Thyroid acropachy is thickening of the extremities and is manifested by digital clubbing, soft tissue swelling of the hands and feet, and periosteal new bone formation.

102
Q

What characterizes Graves eye disease?

A

Graves eye disease is an autoimmune inflammatory disorder of the orbit and periorbital tissues, characterized by upper eyelid retraction, lid lag, swelling, erythema, conjunctivitis, and bulging eyes (exophthalmos). It occurs in ~20% of Graves’ patients and results from autoimmune inflammation of the extra-ocular muscles as orbital fat and connective tissue TSH receptors.

103
Q

What are the associations and characteristics of Graves eye disease?

A

Graves eye disease is associated with smoking (smoking cessation is very important), can precede the diagnosis of Graves’, can be unilateral, and most cases are mild but can be severe and sight-threatening.

104
Q

What investigations are conducted for Graves’ disease?

A

Thyroid hormones are assessed, and in primary hyperthyroidism, TSH is low, and free T3/T4 are high. In secondary hyperthyroidism, TSH is high, and free T4 and T3 are high (or ‘normal’). Thyroid autoantibodies are checked, including Anti-TPO antibody (70-80%), Anti-thyroglobulin antibody (30-50%), and TSH receptor antibody (stimulating, 70-100%). Scintiscan is used in antibody-negative patients to look for toxic nodular disease.

105
Q

What are the first-line antithyroid drugs for Graves’ disease?

A

Carbimazole is the first-line antithyroid drug for Graves’ disease. PTU (Propylthiouracil) is used in the 1st trimester of pregnancy.

106
Q

How long does the gradual dose regimen of antithyroid drugs last for Graves’ disease?

A

The gradual dose regimen of antithyroid drugs for Graves’ disease lasts 12-18 months.

107
Q

What is the block and replace regimen for Graves’ disease, and how long does it take?

A

The block and replace regimen for Graves’ disease takes 6 months. In this regimen, a higher dose of antithyroid drugs is used to block all production, and levothyroxine is added and titrated to effect.

108
Q

What is the approximate relapse rate for Graves’ disease management with antithyroid drugs?

A

The relapse rate for Graves’ disease management with antithyroid drugs is approximately 50%.

109
Q

How is mild Graves’ eye disease treated?

A

Mild Graves’ eye disease is treated topically, for example, with lubricants.

110
Q

What are the treatment options for more severe Graves’ eye disease?

A

More severe Graves’ eye disease can be treated with steroids, radiotherapy, or surgery.

111
Q

Which medications are useful for immediate symptomatic relief of thyrotoxic symptoms?

A

β-blockers are useful for immediate symptomatic relief of thyrotoxic symptoms. If β-blockers are contraindicated (e.g., in asthma), calcium channel blockers (CCBs) can be used.

112
Q

What is the first-choice treatment for relapsed Graves’ disease and nodular thyroid disease?

A

Radioiodine is the first-choice treatment for relapsed Graves’ disease and nodular thyroid disease. However, it has a high risk of hypothyroidism when used in Graves’ disease (1:2).

113
Q

In what situations is thyroidectomy useful in the management of hyperthyroidism?

A

Thyroidectomy is useful when radioiodine is contraindicated, for example, during pregnancy. However, it comes with the risk of leaving a scar and various surgical/anaesthetic risks, including recurrent laryngeal nerve palsy, hypothyroidism, and hypoparathyroidism.

114
Q

What characterizes thyroid storm, and when is it typically seen?

A

Thyroid storm is characterized by the rapid deterioration of hyperthyroidism with hyperpyrexia, severe tachycardia, extreme restlessness, cardiac failure, and liver dysfunction. It is typically seen in hyperthyroid patients with an acute infection/illness or recent thyroid surgery.

115
Q

What is the management approach for thyroid storm?

A

The management of thyroid storm includes high-dose carbimazole, β-blockers (propranolol), potassium iodide, hydrocortisone, IV fluids +/- inotropes, and treating the precipitating cause (e.g., MI, infection, PE).

Endocrine system (12 decks)

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