The patient is showing signs of confusion and restlessness. Upon examination, it is found that the patient has high blood pressure, a rapid pulse rate, increased respiration rate, and a high temperature. An ECG reveals rapid atrial fibrillation. Additionally, the patient exhibits crackling sounds in the lower parts of the lungs, pitting edema in both legs below the knee, and a mild yellowish tint in the sclera. The patient’s medical history is obtained from their GP office, which reveals that they have not renewed their prescription for carbimazole and bisoprolol on time. Based on these findings, the most probable diagnosis is a thyroid storm.

Further Reading:

The thyroid gland is an endocrine organ located in the anterior neck. It consists of two lobes connected by an isthmus. The gland produces hormones called thyroxine (T4) and triiodothyronine (T3), which regulate energy use, protein synthesis, and the body’s sensitivity to other hormones. The production of T4 and T3 is stimulated by thyroid-stimulating hormone (TSH) secreted by the pituitary gland, which is in turn stimulated by thyrotropin-releasing hormone (TRH) from the hypothalamus.

Thyroid disorders can occur when there is an imbalance in the production or regulation of thyroid hormones. Hypothyroidism is characterized by a deficiency of thyroid hormones, while hyperthyroidism is characterized by an excess. The most common cause of hypothyroidism is autoimmune thyroiditis, also known as Hashimoto’s thyroiditis. It is more common in women and is often associated with goiter. Other causes include subacute thyroiditis, atrophic thyroiditis, and iodine deficiency. On the other hand, the most common cause of hyperthyroidism is Graves’ disease, which is also an autoimmune disorder. Other causes include toxic multinodular goiter and subacute thyroiditis.

The symptoms and signs of thyroid disorders can vary depending on whether the thyroid gland is underactive or overactive. In hypothyroidism, common symptoms include weight gain, lethargy, cold intolerance, and dry skin. In hyperthyroidism, common symptoms include weight loss, restlessness, heat intolerance, and increased sweating. Both hypothyroidism and hyperthyroidism can also affect other systems in the body, such as the cardiovascular, gastrointestinal, and neurological systems.

Complications of thyroid disorders can include dyslipidemia, metabolic syndrome, coronary heart disease, heart failure, subfertility and infertility, impaired special senses, and myxedema coma in severe cases of hypothyroidism. In hyperthyroidism, complications can include Graves’ orbitopathy, compression of the esophagus or trachea by goiter, thyrotoxic periodic paralysis, arrhythmias, osteoporosis, mood disorders, and increased obstetric complications.

Myxedema coma is a rare and life-threatening complication of severe hypothyroidism. It can be triggered by factors such as infection or physiological insult and presents with lethargy, bradycardia, hypothermia, hypotension, hypoventilation, altered mental state, seizures and/or coma.

Hyperglycemia is a common occurrence in patients with phaeochromocytoma. This is primarily due to the excessive release of catecholamines, which suppress insulin secretion from the pancreas and promote glycogenolysis. Calcium levels in phaeochromocytoma patients can vary, with hypercalcemia being most frequently observed in cases where hyperparathyroidism coexists, particularly in MEN II. However, some phaeochromocytomas may secrete calcitonin and/or adrenomedullin, which can lower plasma calcium levels and lead to hypocalcemia. While not typical, potassium disturbances may occur in patients experiencing severe vomiting or acute kidney injury. On the other hand, anemia is not commonly associated with phaeochromocytoma, although there are rare cases where the tumor secretes erythropoietin, resulting in elevated hemoglobin levels and hematocrit.

Further Reading:

Phaeochromocytoma is a rare neuroendocrine tumor that secretes catecholamines. It typically arises from chromaffin tissue in the adrenal medulla, but can also occur in extra-adrenal chromaffin tissue. The majority of cases are spontaneous and occur in individuals aged 40-50 years. However, up to 30% of cases are hereditary and associated with genetic mutations. About 10% of phaeochromocytomas are metastatic, with extra-adrenal tumors more likely to be metastatic.

The clinical features of phaeochromocytoma are a result of excessive catecholamine production. Symptoms are typically paroxysmal and include hypertension, headaches, palpitations, sweating, anxiety, tremor, abdominal and flank pain, and nausea. Catecholamines have various metabolic effects, including glycogenolysis, mobilization of free fatty acids, increased serum lactate, increased metabolic rate, increased myocardial force and rate of contraction, and decreased systemic vascular resistance.

Diagnosis of phaeochromocytoma involves measuring plasma and urine levels of metanephrines, catecholamines, and urine vanillylmandelic acid. Imaging studies such as abdominal CT or MRI are used to determine the location of the tumor. If these fail to find the site, a scan with metaiodobenzylguanidine (MIBG) labeled with radioactive iodine is performed. The highest sensitivity and specificity for diagnosis is achieved with plasma metanephrine assay.

The definitive treatment for phaeochromocytoma is surgery. However, before surgery, the patient must be stabilized with medical management. This typically involves alpha-blockade with medications such as phenoxybenzamine or phentolamine, followed by beta-blockade with medications like propranolol. Alpha blockade is started before beta blockade to allow for expansion of blood volume and to prevent a hypertensive crisis.

In an elderly patient with a history of gradual decline accompanied by high blood sugar levels, excessive thirst, and recent infection, the most likely diagnosis is hyperosmolar hyperglycemic state (HHS). This condition can be life-threatening, with a mortality rate of approximately 50%. Common symptoms include dehydration, elevated blood sugar levels, altered mental status, and electrolyte imbalances. About half of the patients with HHS also experience hypernatremia.

To calculate the serum osmolality, the formula is 2(K+ + Na+) + urea + glucose. In this case, the serum osmolality is 364 mmol/l, indicating a high level. It is important to discontinue the use of metformin in this patient due to the risk of metformin-associated lactic acidosis (MALA). Additionally, an intravenous infusion of insulin should be initiated.

The treatment goals for HHS are to address the underlying cause and gradually and safely:
– Normalize the osmolality
– Replace fluid and electrolyte losses
– Normalize blood glucose levels

If significant ketonaemia is present (3β-hydroxybutyrate is more than 1 mmol/L), it indicates a relative lack of insulin, and insulin should be administered immediately. However, if significant ketonaemia is not present, insulin should not be started.

Patients with HHS are at a high risk of thromboembolism, and it is recommended to routinely administer low molecular weight heparin. In cases where the serum osmolality exceeds 350 mmol/l, full heparinization should be considered.

Primary hyperaldosteronism is the leading endocrine cause of secondary hypertension, commonly affecting individuals between the ages of 30 and 50. It is characterized by metabolic alkalosis and often presents with hypernatraemia, although normal sodium levels can also be observed. When compared to pheochromocytoma, primary hyperaldosteronism is more frequently encountered. The diagnostic test of choice is the plasma aldosterone-to-renin ratio.

Further Reading:

Hyperaldosteronism is a condition characterized by excessive production of aldosterone by the adrenal glands. It can be classified into primary and secondary hyperaldosteronism. Primary hyperaldosteronism, also known as Conn’s syndrome, is typically caused by adrenal hyperplasia or adrenal tumors. Secondary hyperaldosteronism, on the other hand, is a result of high renin levels in response to reduced blood flow across the juxtaglomerular apparatus.

Aldosterone is the main mineralocorticoid steroid hormone produced by the adrenal cortex. It acts on the distal renal tubule and collecting duct of the nephron, promoting the reabsorption of sodium ions and water while secreting potassium ions.

The causes of hyperaldosteronism vary depending on whether it is primary or secondary. Primary hyperaldosteronism can be caused by adrenal adenoma, adrenal hyperplasia, adrenal carcinoma, or familial hyperaldosteronism. Secondary hyperaldosteronism can be caused by renal artery stenosis, reninoma, renal tubular acidosis, nutcracker syndrome, ectopic tumors, massive ascites, left ventricular failure, or cor pulmonale.

Clinical features of hyperaldosteronism include hypertension, hypokalemia, metabolic alkalosis, hypernatremia, polyuria, polydipsia, headaches, lethargy, muscle weakness and spasms, and numbness. It is estimated that hyperaldosteronism is present in 5-10% of patients with hypertension, and hypertension in primary hyperaldosteronism is often resistant to drug treatment.

Diagnosis of hyperaldosteronism involves various investigations, including U&Es to assess electrolyte disturbances, aldosterone-to-renin plasma ratio (ARR) as the gold standard diagnostic test, ECG to detect arrhythmia, CT/MRI scans to locate adenoma, fludrocortisone suppression test or oral salt testing to confirm primary hyperaldosteronism, genetic testing to identify familial hyperaldosteronism, and adrenal venous sampling to determine lateralization prior to surgery.

Treatment of primary hyperaldosteronism typically involves surgical adrenalectomy for patients with unilateral primary aldosteronism. Diet modification with sodium restriction and potassium supplementation may also be recommended.

Myxoedema coma is a condition characterized by severe hypothyroidism, leading to a state of metabolic decompensation and changes in mental status. Patients with myxoedema coma often experience electrolyte disturbances such as hypoglycemia and hyponatremia. In addition, laboratory findings typically show elevated levels of TSH, as well as low levels of T4 and T3. Other expected findings include hypoxemia and hypercapnia.

Further Reading:

The thyroid gland is an endocrine organ located in the anterior neck. It consists of two lobes connected by an isthmus. The gland produces hormones called thyroxine (T4) and triiodothyronine (T3), which regulate energy use, protein synthesis, and the body’s sensitivity to other hormones. The production of T4 and T3 is stimulated by thyroid-stimulating hormone (TSH) secreted by the pituitary gland, which is in turn stimulated by thyrotropin-releasing hormone (TRH) from the hypothalamus.

Thyroid disorders can occur when there is an imbalance in the production or regulation of thyroid hormones. Hypothyroidism is characterized by a deficiency of thyroid hormones, while hyperthyroidism is characterized by an excess. The most common cause of hypothyroidism is autoimmune thyroiditis, also known as Hashimoto’s thyroiditis. It is more common in women and is often associated with goiter. Other causes include subacute thyroiditis, atrophic thyroiditis, and iodine deficiency. On the other hand, the most common cause of hyperthyroidism is Graves’ disease, which is also an autoimmune disorder. Other causes include toxic multinodular goiter and subacute thyroiditis.

The symptoms and signs of thyroid disorders can vary depending on whether the thyroid gland is underactive or overactive. In hypothyroidism, common symptoms include weight gain, lethargy, cold intolerance, and dry skin. In hyperthyroidism, common symptoms include weight loss, restlessness, heat intolerance, and increased sweating. Both hypothyroidism and hyperthyroidism can also affect other systems in the body, such as the cardiovascular, gastrointestinal, and neurological systems.

Complications of thyroid disorders can include dyslipidemia, metabolic syndrome, coronary heart disease, heart failure, subfertility and infertility, impaired special senses, and myxedema coma in severe cases of hypothyroidism. In hyperthyroidism, complications can include Graves’ orbitopathy, compression of the esophagus or trachea by goiter, thyrotoxic periodic paralysis, arrhythmias, osteoporosis, mood disorders, and increased obstetric complications.

Myxedema coma is a rare and life-threatening complication of severe hypothyroidism. It can be triggered by factors such as infection or physiological insult and presents with lethargy, bradycardia, hypothermia, hypotension, hypoventilation, altered mental state, seizures and/or coma.

The most probable diagnosis in this case is primary hyperaldosteronism, which is caused by either an adrenal adenoma (Conn’s syndrome) or bilateral idiopathic adrenal hyperplasia. Conn’s syndrome is likely in a patient who has difficult-to-control hypertension, low levels of potassium (hypokalaemia), and elevated or high normal levels of sodium. If the aldosterone:renin ratio is raised (>30), it further suggests primary hyperaldosteronism. CT scanning can be used to differentiate between an adrenal adenoma and adrenal hyperplasia. Treatment for hyperaldosteronism caused by an adenoma typically involves 4-6 weeks of spironolactone therapy followed by surgical removal of the adenoma. Adrenal hyperplasia usually responds well to potassium-sparing diuretics alone, such as spironolactone or amiloride.

Renal artery stenosis could also be suspected in a case of resistant hypertension, but it would be expected to cause a decline in renal function when taking a full dose of an ACE inhibitor like ramipril. However, in this case, the patient’s renal function is completely normal.

Phaeochromocytoma is associated with symptoms such as headaches, palpitations, tremors, and excessive sweating. The hypertension in phaeochromocytoma tends to occur in episodes. Since these symptoms are absent in this patient, a diagnosis of phaeochromocytoma is unlikely.

Cushing’s syndrome is characterized by various other clinical features, including weight gain, central obesity, a hump-like accumulation of fat on the back (buffalo hump), muscle wasting in the limbs, excessive hair growth (hirsutism), thinning of the skin, easy bruising, acne, and depression. Since this patient does not exhibit any of these features, Cushing’s syndrome is unlikely.

White coat syndrome is an unlikely diagnosis in this case because the initial diagnosis of hypertension was made based on ambulatory blood pressure monitoring.

Addison’s disease, also known as adrenal insufficiency, is characterized by a gradual onset of symptoms over several weeks, although it can sometimes occur suddenly. The diagnosis of Addison’s disease can be challenging as its symptoms, such as fatigue, muscle pain, weight loss, and nausea, are non-specific. However, a key feature is low blood pressure. The disease is associated with changes in pigmentation, ranging from increased pigmentation due to elevated ACTH levels to the development of vitiligo caused by the autoimmune destruction of melanocytes.

Patients with Addison’s disease often exhibit hyponatremia (low sodium levels) and hyperkalemia (high potassium levels). If the patient is dehydrated, this may be reflected in elevated urea and creatinine levels. While hypercalcemia (high calcium levels) and hypoglycemia (low blood sugar levels) can occur in Addison’s disease, they are less common than hyponatremia and hyperkalemia.

In contrast, diabetes insipidus, characterized by normal or elevated sodium levels, does not cause pigmentation changes. Cushing’s syndrome, which results from excess steroid production, is almost the opposite of Addison’s disease, with hypertension (high blood pressure) and hypokalemia (low potassium levels) being typical symptoms. Phaeochromocytoma, on the other hand, is associated with episodes of high blood pressure and hyperglycemia (high blood sugar levels).

Further Reading:

Addison’s disease, also known as primary adrenal insufficiency or hypoadrenalism, is a rare disorder caused by the destruction of the adrenal cortex. This leads to reduced production of glucocorticoids, mineralocorticoids, and adrenal androgens. The deficiency of cortisol results in increased production of adrenocorticotropic hormone (ACTH) due to reduced negative feedback to the pituitary gland. This condition can cause metabolic disturbances such as hyperkalemia, hyponatremia, hypercalcemia, and hypoglycemia.

The symptoms of Addison’s disease can vary but commonly include fatigue, weight loss, muscle weakness, and low blood pressure. It is more common in women and typically affects individuals between the ages of 30-50. The most common cause of primary hypoadrenalism in developed countries is autoimmune destruction of the adrenal glands. Other causes include tuberculosis, adrenal metastases, meningococcal septicaemia, HIV, and genetic disorders.

The diagnosis of Addison’s disease is often suspected based on low cortisol levels and electrolyte abnormalities. The adrenocorticotropic hormone stimulation test is commonly used for confirmation. Other investigations may include adrenal autoantibodies, imaging scans, and genetic screening.

Addisonian crisis is a potentially life-threatening condition that occurs when there is an acute deficiency of cortisol and aldosterone. It can be the first presentation of undiagnosed Addison’s disease. Precipitating factors of an Addisonian crisis include infection, dehydration, surgery, trauma, physiological stress, pregnancy, hypoglycemia, and acute withdrawal of long-term steroids. Symptoms of an Addisonian crisis include malaise, fatigue, nausea or vomiting, abdominal pain, fever, muscle pains, dehydration, confusion, and loss of consciousness.

There is no fixed consensus on diagnostic criteria for an Addisonian crisis, as symptoms are non-specific. Investigations may include blood tests, blood gas analysis, and septic screens if infection is suspected. Management involves administering hydrocortisone and fluids. Hydrocortisone is given parenterally, and the dosage varies depending on the age of the patient. Fluid resuscitation with saline is necessary to correct any electrolyte disturbances and maintain blood pressure. The underlying cause of the crisis should also be identified and treated. Close monitoring of sodium levels is important to prevent complications such as osmotic demyelination syndrome.

Thyroid storm is a rare condition that affects only 1-2% of patients with hyperthyroidism. However, it is crucial to diagnose it promptly because it has a high mortality rate of approximately 10%. Thyroid storm is often triggered by a physiological stressor, such as stopping antithyroid therapy prematurely, recent surgery or radio-iodine treatment, infections (especially chest infections), trauma, diabetic ketoacidosis or hyperosmolar diabetic crisis, thyroid hormone overdose, pre-eclampsia. It typically occurs in patients with Graves’ disease or toxic multinodular goitre and presents with sudden and severe hyperthyroidism. Symptoms include high fever (over 41°C), dehydration, rapid heart rate (greater than 140 beats per minute) with or without irregular heart rhythms, low blood pressure, congestive heart failure, nausea, jaundice, vomiting, diarrhea, abdominal pain, confusion, agitation, delirium, psychosis, seizures, or coma.

To diagnose thyroid storm, various blood tests should be conducted, including a full blood count, urea and electrolytes, blood glucose, coagulation screen, CRP, and thyroid profile (T4/T3 and TSH). A bone profile/calcium test should also be done as 10% of patients develop hypocalcemia. Blood cultures should be taken as well. Other important investigations include a urine dipstick/MC&S, chest X-ray, and ECG.

The management of thyroid storm involves several steps. Intravenous fluids, such as 1-2 liters of 0.9% saline, should be administered. Airway support and management should be provided as necessary. A nasogastric tube should be inserted if the patient is vomiting. Urgent referral for inpatient management is essential. Paracetamol (1 g PO/IV) can be given to reduce fever. Benzodiazepines, such as diazepam (5-20 mg PO/IV), can be used for sedation. Steroids, like hydrocortisone (100 mg IV), may be necessary if there is co-existing adrenal suppression. Antibiotics should be prescribed if there is an intercurrent infection. Beta-blockers, such as propranolol (80 mg PO), can help control heart rate. High-dose carbimazole (45-60 mg/day) is recommended.

Hypothyroidism often presents with various clinical features. These include weight gain, lethargy, intolerance to cold temperatures, non-pitting edema (such as swelling in the hands and face), dry skin, hair thinning and loss, loss of the outer part of the eyebrows, decreased appetite, constipation, decreased deep tendon reflexes, carpal tunnel syndrome, and menorrhagia.

Further Reading:

The thyroid gland is an endocrine organ located in the anterior neck. It consists of two lobes connected by an isthmus. The gland produces hormones called thyroxine (T4) and triiodothyronine (T3), which regulate energy use, protein synthesis, and the body’s sensitivity to other hormones. The production of T4 and T3 is stimulated by thyroid-stimulating hormone (TSH) secreted by the pituitary gland, which is in turn stimulated by thyrotropin-releasing hormone (TRH) from the hypothalamus.

Thyroid disorders can occur when there is an imbalance in the production or regulation of thyroid hormones. Hypothyroidism is characterized by a deficiency of thyroid hormones, while hyperthyroidism is characterized by an excess. The most common cause of hypothyroidism is autoimmune thyroiditis, also known as Hashimoto’s thyroiditis. It is more common in women and is often associated with goiter. Other causes include subacute thyroiditis, atrophic thyroiditis, and iodine deficiency. On the other hand, the most common cause of hyperthyroidism is Graves’ disease, which is also an autoimmune disorder. Other causes include toxic multinodular goiter and subacute thyroiditis.

The symptoms and signs of thyroid disorders can vary depending on whether the thyroid gland is underactive or overactive. In hypothyroidism, common symptoms include weight gain, lethargy, cold intolerance, and dry skin. In hyperthyroidism, common symptoms include weight loss, restlessness, heat intolerance, and increased sweating. Both hypothyroidism and hyperthyroidism can also affect other systems in the body, such as the cardiovascular, gastrointestinal, and neurological systems.

Complications of thyroid disorders can include dyslipidemia, metabolic syndrome, coronary heart disease, heart failure, subfertility and infertility, impaired special senses, and myxedema coma in severe cases of hypothyroidism. In hyperthyroidism, complications can include Graves’ orbitopathy, compression of the esophagus or trachea by goiter, thyrotoxic periodic paralysis, arrhythmias, osteoporosis, mood disorders, and increased obstetric complications.

Myxedema coma is a rare and life-threatening complication of severe hypothyroidism. It can be triggered by factors such as infection or physiological insult and presents with lethargy, bradycardia, hypothermia, hypotension, hypoventilation, altered mental state, seizures and/or coma.

When treating thyroid storm, it is important to administer certain drugs immediately. These include a beta blocker like propranolol or a calcium channel blocker if a beta blocker cannot be used. Corticosteroids like hydrocortisone or dexamethasone are also given. Additionally, antithyroid drugs like propylthiouracil are administered. However, it is crucial to wait at least one hour after giving the antithyroid drugs before administering iodine solution such as Lugol’s iodine. This is because iodine can worsen thyrotoxicosis by stimulating thyroid hormone synthesis. Propylthiouracil, on the other hand, inhibits the normal interactions of iodine and peroxidase with thyroglobulin, which is why it is given first and allowed time to take effect.

Further Reading:

The thyroid gland is an endocrine organ located in the anterior neck. It consists of two lobes connected by an isthmus. The gland produces hormones called thyroxine (T4) and triiodothyronine (T3), which regulate energy use, protein synthesis, and the body’s sensitivity to other hormones. The production of T4 and T3 is stimulated by thyroid-stimulating hormone (TSH) secreted by the pituitary gland, which is in turn stimulated by thyrotropin-releasing hormone (TRH) from the hypothalamus.

Thyroid disorders can occur when there is an imbalance in the production or regulation of thyroid hormones. Hypothyroidism is characterized by a deficiency of thyroid hormones, while hyperthyroidism is characterized by an excess. The most common cause of hypothyroidism is autoimmune thyroiditis, also known as Hashimoto’s thyroiditis. It is more common in women and is often associated with goiter. Other causes include subacute thyroiditis, atrophic thyroiditis, and iodine deficiency. On the other hand, the most common cause of hyperthyroidism is Graves’ disease, which is also an autoimmune disorder. Other causes include toxic multinodular goiter and subacute thyroiditis.

The symptoms and signs of thyroid disorders can vary depending on whether the thyroid gland is underactive or overactive. In hypothyroidism, common symptoms include weight gain, lethargy, cold intolerance, and dry skin. In hyperthyroidism, common symptoms include weight loss, restlessness, heat intolerance, and increased sweating. Both hypothyroidism and hyperthyroidism can also affect other systems in the body, such as the cardiovascular, gastrointestinal, and neurological systems.

Complications of thyroid disorders can include dyslipidemia, metabolic syndrome, coronary heart disease, heart failure, subfertility and infertility, impaired special senses, and myxedema coma in severe cases of hypothyroidism. In hyperthyroidism, complications can include Graves’ orbitopathy, compression of the esophagus or trachea by goiter, thyrotoxic periodic paralysis, arrhythmias, osteoporosis, mood disorders, and increased obstetric complications.

Myxedema coma is a rare and life-threatening complication of severe hypothyroidism. It can be triggered by factors such as infection or physiological insult and presents with lethargy, bradycardia, hypothermia, hypotension, hypoventilation, altered mental state, seizures and/or coma.