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  • Question 1 - A 75-year-old gentleman is brought in by ambulance from his assisted living facility...

    Incorrect

    • A 75-year-old gentleman is brought in by ambulance from his assisted living facility with a decreased level of consciousness. He has a history of type II diabetes mellitus, which is managed with glibenclamide and metformin. He is unconscious but breathing on his own and has a strong pulse. You order a blood glucose test, and his result is 1.0 mmol/l. Intravenous access has been established.
      What is the MOST appropriate initial step in managing this patient?

      Your Answer: Administer 1 mg glucagon IM or SC

      Correct Answer: Administer 150 mL of 10% dextrose

      Explanation:

      This woman is experiencing hypoglycemia, most likely due to her treatment with glibenclamide. Hypoglycemia is defined as having a blood glucose level below 3.0 mmol/l, and it is crucial to promptly treat this condition to prevent further complications such as seizures, stroke, or heart problems.

      If the patient is conscious and able to swallow, a fast-acting carbohydrate like sugar or GlucoGel can be given orally. However, since this woman is unconscious, this option is not feasible.

      In cases where intravenous access is available, like in this situation, an intravenous bolus of dextrose should be administered. The recommended doses are either 75 mL of 20% dextrose or 150 mL of 10% dextrose.

      When a patient is at home and intravenous access is not possible, the preferred initial treatment is glucagon. Under these circumstances, 1 mg of glucagon can be given either intramuscularly (IM) or subcutaneously (SC).

      It is important to note that immediate action is necessary to address hypoglycemia and prevent any potential complications.

    • This question is part of the following fields:

      • Endocrinology
      20.1
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  • Question 2 - A 10 year old male is brought into the emergency department due to...

    Incorrect

    • A 10 year old male is brought into the emergency department due to worsening fatigue, vomiting, and frequent urination over the past 48 hours. You assess for potential underlying causes, including diabetic ketoacidosis (DKA). DKA is characterized by which of the following?

      Your Answer: Raised plasma osmolality, high anion gap and hypernatraemia

      Correct Answer: Hyperglycaemia, acidosis and ketonaemia

      Explanation:

      DKA is characterized by three main symptoms: high blood sugar levels (hyperglycemia), an acidic pH in the body (acidosis), and an increased presence of ketones in the blood (ketonaemia).

      Further Reading:

      Diabetic ketoacidosis (DKA) is a serious complication of diabetes that occurs due to a lack of insulin in the body. It is most commonly seen in individuals with type 1 diabetes but can also occur in type 2 diabetes. DKA is characterized by hyperglycemia, acidosis, and ketonaemia.

      The pathophysiology of DKA involves insulin deficiency, which leads to increased glucose production and decreased glucose uptake by cells. This results in hyperglycemia and osmotic diuresis, leading to dehydration. Insulin deficiency also leads to increased lipolysis and the production of ketone bodies, which are acidic. The body attempts to buffer the pH change through metabolic and respiratory compensation, resulting in metabolic acidosis.

      DKA can be precipitated by factors such as infection, physiological stress, non-compliance with insulin therapy, acute medical conditions, and certain medications. The clinical features of DKA include polydipsia, polyuria, signs of dehydration, ketotic breath smell, tachypnea, confusion, headache, nausea, vomiting, lethargy, and abdominal pain.

      The diagnosis of DKA is based on the presence of ketonaemia or ketonuria, blood glucose levels above 11 mmol/L or known diabetes mellitus, and a blood pH below 7.3 or bicarbonate levels below 15 mmol/L. Initial investigations include blood gas analysis, urine dipstick for glucose and ketones, blood glucose measurement, and electrolyte levels.

      Management of DKA involves fluid replacement, electrolyte correction, insulin therapy, and treatment of any underlying cause. Fluid replacement is typically done with isotonic saline, and potassium may need to be added depending on the patient’s levels. Insulin therapy is initiated with an intravenous infusion, and the rate is adjusted based on blood glucose levels. Monitoring of blood glucose, ketones, bicarbonate, and electrolytes is essential, and the insulin infusion is discontinued once ketones are below 0.3 mmol/L, pH is above 7.3, and bicarbonate is above 18 mmol/L.

      Complications of DKA and its treatment include gastric stasis, thromboembolism, electrolyte disturbances, cerebral edema, hypoglycemia, acute respiratory distress syndrome, and acute kidney injury. Prompt medical intervention is crucial in managing DKA to prevent potentially fatal outcomes.

    • This question is part of the following fields:

      • Endocrinology
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  • Question 3 - You are following up on a 62 year old patient who had been...

    Correct

    • You are following up on a 62 year old patient who had been referred to the medical team for investigation of electrolyte imbalances and unexplained symptoms. You observe that the patient has undergone a water deprivation test and the results are as follows:

      Serum osmolality after fluid deprivation: 348 mOSm/Kg
      Urine osmolality after fluid deprivation
      but before desmopressin: 188 mOSm/Kg
      Urine osmolality after desmopressin: 824 mOSm/Kg

      What is the probable diagnosis?

      Your Answer: Cranial diabetes insipidus

      Explanation:

      After the fluid restriction period, the urine is checked to determine if it remains relatively dilute (less than 600 mOsm/kg). If it does, desmopressin is administered and the urine is rechecked to see if it responds and becomes more concentrated.

      If the urine osmolality significantly increases after desmopressin, it indicates that the kidneys have responded appropriately to the medication and the urine has concentrated. This suggests that the patient is not producing ADH in response to water loss, indicating cranial DI.

      It is important to note that some units may use a lower cut-off of greater than 600 mOsm/kg instead of 800 mOsm/kg.

      Further Reading:

      Diabetes insipidus (DI) is a condition characterized by either a decrease in the secretion of antidiuretic hormone (cranial DI) or insensitivity to antidiuretic hormone (nephrogenic DI). Antidiuretic hormone, also known as arginine vasopressin, is produced in the hypothalamus and released from the posterior pituitary. The typical biochemical disturbances seen in DI include elevated plasma osmolality, low urine osmolality, polyuria, and hypernatraemia.

      Cranial DI can be caused by various factors such as head injury, CNS infections, pituitary tumors, and pituitary surgery. Nephrogenic DI, on the other hand, can be genetic or result from electrolyte disturbances or the use of certain drugs. Symptoms of DI include polyuria, polydipsia, nocturia, signs of dehydration, and in children, irritability, failure to thrive, and fatigue.

      To diagnose DI, a 24-hour urine collection is done to confirm polyuria, and U&Es will typically show hypernatraemia. High plasma osmolality with low urine osmolality is also observed. Imaging studies such as MRI of the pituitary, hypothalamus, and surrounding tissues may be done, as well as a fluid deprivation test to evaluate the response to desmopressin.

      Management of cranial DI involves supplementation with desmopressin, a synthetic form of arginine vasopressin. However, hyponatraemia is a common side effect that needs to be monitored. In nephrogenic DI, desmopressin supplementation is usually not effective, and management focuses on ensuring adequate fluid intake to offset water loss and monitoring electrolyte levels. Causative drugs need to be stopped, and there is a risk of developing complications such as hydroureteronephrosis and an overdistended bladder.

    • This question is part of the following fields:

      • Endocrinology
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  • Question 4 - A 75 year old man with a long-standing history of hypothyroidism presents to...

    Incorrect

    • A 75 year old man with a long-standing history of hypothyroidism presents to the emergency department due to worsening confusion and fatigue. On examination you note diffuse non-pitting edema and decreased deep tendon reflexes. Observations are shown below:

      Blood pressure 98/66 mmHg
      Pulse 42 bpm
      Respiration rate 11 bpm
      Temperature 34.6ºC

      Bloods are sent for analysis. Which of the following laboratory abnormalities would you expect in a patient with this condition?

      Your Answer: Low TSH

      Correct Answer: Hyponatremia

      Explanation:

      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.

    • This question is part of the following fields:

      • Endocrinology
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  • Question 5 - A 40-year-old male patient presents with a history of dizziness and fainting episodes....

    Incorrect

    • A 40-year-old male patient presents with a history of dizziness and fainting episodes. He has also been suffering from a mild flu-like illness for the past few days. He had a syncopal episode in the department and was moved into the resuscitation area. His observations are as follows: Temperature 38.4°C, HR 112, BP 78/44, oxygen saturation 98% on high-flow oxygen, GCS 14/15, BM 1.5.
      His initial blood results are shown below:
      Na+: 118 mmol/l
      K+: 6.1 mmol/l
      Urea: 11.6 mmol/l
      Creatinine: 132 mmol/l
      Which of the following investigations is most appropriate to confirm the underlying diagnosis?

      Your Answer: 24-hour urinary cortisol collection

      Correct Answer: Synacthen test

      Explanation:

      This patient has presented with an Addisonian crisis, which is a rare but potentially catastrophic condition if not diagnosed promptly. It is more commonly seen in women than men and typically occurs between the ages of 30 and 50.

      Addison’s disease is caused by insufficient production of steroid hormones by the adrenal glands, affecting the production of glucocorticoids, mineralocorticoids, and sex steroids. The main causes of Addison’s disease include autoimmune adrenalitis (accounting for 80% of cases), bilateral adrenalectomy, Waterhouse-Friderichsen syndrome (hemorrhage into the adrenal glands), and tuberculosis.

      The most common trigger for an Addisonian crisis in patients with Addison’s disease is the intentional or accidental withdrawal of steroid therapy. Other factors that can precipitate a crisis include infection, trauma, myocardial infarction, cerebral infarction, asthma, hypothermia, and alcohol abuse.

      Clinical features of Addison’s disease include weakness, lethargy, hypotension (especially orthostatic hypotension), nausea, vomiting, weight loss, reduced axillary and pubic hair, depression, and hyperpigmentation (particularly in palmar creases, buccal mucosa, and exposed areas). In an Addisonian crisis, the main symptoms are usually hypoglycemia and shock, characterized by tachycardia, peripheral vasoconstriction, hypotension, altered consciousness, and even coma.

      Biochemical markers of Addison’s disease typically include increased ACTH levels (as a compensatory response to stimulate the adrenal glands), elevated serum renin levels, hyponatremia, hyperkalemia, hypercalcemia, hypoglycemia, and metabolic acidosis. Confirmatory investigations may involve the Synacthen test, plasma ACTH level measurement, plasma renin level measurement, and testing for adrenocortical antibodies.

      Management of Addison’s disease should be overseen by an Endocrinologist. Treatment usually involves the administration of hydrocortisone, fludrocortisone, and dehydroepiandrosterone. Some patients may also require thyroxine if there is concurrent hypothalamic-pituitary disease. Treatment is lifelong, and patients should carry a steroid card and MedicAlert bracelet to alert healthcare professionals about their condition and the potential for an Addisonian crisis.

    • This question is part of the following fields:

      • Endocrinology
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  • Question 6 - A 65-year-old diabetic man presents with a gradual decrease in consciousness and confusion...

    Incorrect

    • A 65-year-old diabetic man presents with a gradual decrease in consciousness and confusion over the past week. He normally controls his diabetes with metformin 500 mg twice a day. He recently received treatment for a urinary tract infection from his doctor, and his family reports that he has been excessively thirsty. He has vomited multiple times today. A urine dipstick test shows a small amount of white blood cells and 1+ ketones. His arterial blood gas results are as follows:
      pH: 7.29
      pO2: 11.1 kPa
      pCO2: 4.6 kPa
      HCO3-: 22 mmol/l
      Na+: 154 mmol/l
      K+: 3.2 mmol/l
      Cl-: 100 mmol/l
      Urea: 17.6 mmol/l
      Glucose: 32 mmol/l
      What is the SINGLE most likely diagnosis?

      Your Answer:

      Correct Answer: Hyperosmolar hyperglycaemic state

      Explanation:

      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.

    • This question is part of the following fields:

      • Endocrinology
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  • Question 7 - A 55-year-old man presents with a history of excessive urination and increased thirst....

    Incorrect

    • A 55-year-old man presents with a history of excessive urination and increased thirst. A diagnosis of type 2 diabetes mellitus is suspected.
      Select from the options below the SINGLE result that is most indicative of a diagnosis of diabetes mellitus.

      Your Answer:

      Correct Answer: An HbA1c of 50 mmol/mol

      Explanation:

      According to the 2011 recommendations from the World Health Organization (WHO), HbA1c can now be used as a diagnostic test for diabetes. However, this is only applicable if stringent quality assurance tests are in place and the assays are standardized to criteria aligned with international reference values. Additionally, accurate measurement of HbA1c is only possible if there are no conditions present that could hinder its accuracy.

      To diagnose diabetes using HbA1c, a value of 48 mmol/mol (6.5%) is recommended as the cut-off point. It’s important to note that a value lower than 48 mmol/mol (6.5%) does not exclude the possibility of diabetes, as glucose tests are still necessary for a definitive diagnosis.

      When using glucose tests, the following criteria are considered diagnostic for diabetes mellitus:
      – A random venous plasma glucose concentration greater than 11.1 mmol/l
      – A fasting plasma glucose concentration greater than 7.0 mmol/l
      – A two-hour plasma glucose concentration greater than 11.1 mmol/l, two hours after consuming 75g of anhydrous glucose in an oral glucose tolerance test (OGTT)

      However, there are certain circumstances where HbA1c is not appropriate for diagnosing diabetes mellitus. These include:
      – ALL children and young people
      – Patients of any age suspected of having Type 1 diabetes
      – Patients with symptoms of diabetes for less than two months
      – Patients at high risk of diabetes who are acutely ill, such as those requiring hospital admission
      – Patients taking medication that may cause a rapid rise in glucose levels, such as steroids or antipsychotics
      – Patients with acute pancreatic damage, including those who have undergone pancreatic surgery
      – Pregnant individuals
      – Presence of genetic, hematologic, and illness-related factors that can influence HbA1c and its measurement.

    • This question is part of the following fields:

      • Endocrinology
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  • Question 8 - A 60 year old male presents to the emergency department complaining of palpitations...

    Incorrect

    • A 60 year old male presents to the emergency department complaining of palpitations and a headache. The patient appears distressed and is observed to be trembling and sweating excessively. The patient has no regular medication and no significant medical history. The patient mentions experiencing similar episodes in the past few months, but none as severe as this one. The patient's vital signs are as follows:

      Blood pressure: 212/100 mmHg
      Pulse: 98 bpm
      Respiration: 16 bpm
      Oxygen saturations: 97% on room air

      What is the most likely diagnosis?

      Your Answer:

      Correct Answer: Phaeochromocytoma

      Explanation:

      Phaeochromocytoma is characterized by certain clinical features, including paroxysmal hypertension, palpitations, headache, tremor, and profuse sweating. This patient exhibits paroxysmal symptoms that align with phaeochromocytoma, such as high blood pressure (systolic readings exceeding 220 mmHg are common), headache, sweating, and feelings of anxiety and fear. It is important to note that individuals with conditions like congenital adrenal hyperplasia, diabetes insipidus, and Addisonian crisis typically experience low blood pressure.

      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.

    • This question is part of the following fields:

      • Endocrinology
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  • Question 9 - A 45-year-old woman presents with overall fatigue and increased skin pigmentation. She has...

    Incorrect

    • A 45-year-old woman presents with overall fatigue and increased skin pigmentation. She has a history of bilateral adrenalectomy for Cushing's syndrome 10 years ago. During the examination of her visual fields, a bitemporal hemianopia is discovered.

      What is the MOST LIKELY single biochemical finding in this scenario?

      Your Answer:

      Correct Answer: Elevated ACTH levels

      Explanation:

      Nelson’s syndrome is a rare condition that occurs many years after a bilateral adrenalectomy for Cushing’s syndrome. It is believed to develop due to the loss of the normal negative feedback control that suppresses high cortisol levels. As a result, the hypothalamus starts producing CRH again, which stimulates the growth of a pituitary adenoma that produces adrenocorticotropic hormone (ACTH).

      Only 15-20% of patients who undergo bilateral adrenalectomy will develop this condition, and it is now rarely seen as the procedure is no longer commonly performed.

      The symptoms and signs of Nelson’s syndrome are related to the growth of the pituitary adenoma and the increased production of ACTH and melanocyte-stimulating hormone (MSH) from the adenoma. These may include headaches, visual field defects (up to 50% of cases), increased skin pigmentation, and the possibility of hypopituitarism.

      ACTH levels will be significantly elevated (usually >500 ng/L). Thyroxine, TSH, gonadotrophin, and sex hormone levels may be low. Prolactin levels may be high, but not as high as with a prolactin-producing tumor. MRI or CT scanning can be helpful in identifying the presence of an expanding pituitary mass.

      The treatment of choice for Nelson’s syndrome is trans-sphenoidal surgery.

    • This question is part of the following fields:

      • Endocrinology
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  • Question 10 - You are managing a patient in the resuscitation bay with suspected myxoedema coma....

    Incorrect

    • You are managing a patient in the resuscitation bay with suspected myxoedema coma. A member of the nursing team hands you the patient's ECG. What ECG findings would you anticipate in a patient with myxoedema coma?

      Your Answer:

      Correct Answer: Prolonged QT interval

      Explanation:

      Patients with myxoedema coma often exhibit several common ECG abnormalities. These include bradycardia, a prolonged QT interval, and T wave flattening or inversion. Additionally, severe hypothyroidism (myxoedema) is associated with other ECG findings such as low QRS voltage, conduction blocks, and T wave inversions without ST deviation.

      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.

    • This question is part of the following fields:

      • Endocrinology
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  • Question 11 - A 2-week-old baby comes in with vomiting, decreased weight, and an electrolyte imbalance....

    Incorrect

    • A 2-week-old baby comes in with vomiting, decreased weight, and an electrolyte imbalance. After being referred to the pediatricians, they are diagnosed with congenital adrenal hyperplasia (CAH).
      Which ONE statement is correct about this condition?

      Your Answer:

      Correct Answer: Diagnosis can be made by finding elevated 17-hydroxyprogesterone levels

      Explanation:

      Congenital adrenal hyperplasia (CAH) is a group of inherited disorders that are caused by autosomal recessive genes. The majority of affected patients, over 90%, have a deficiency of the enzyme 21-hydroxylase. This enzyme is encoded by the 21-hydroxylase gene, which is located on chromosome 6p21 within the HLA histocompatibility complex. The second most common cause of CAH is a deficiency of the enzyme 11-beta-hydroxylase. The condition is rare, with an incidence of approximately 1 in 500 births in the UK. It is more prevalent in the offspring of consanguineous marriages.

      The deficiency of 21-hydroxylase leads to a deficiency of cortisol and/or aldosterone, as well as an excess of precursor steroids. As a result, there is an increased secretion of ACTH from the anterior pituitary, leading to adrenocortical hyperplasia.

      The severity of CAH varies depending on the degree of 21-hydroxylase deficiency. Female infants often exhibit ambiguous genitalia, such as clitoral hypertrophy and labial fusion. Male infants may have an enlarged scrotum and/or scrotal pigmentation. Hirsutism, or excessive hair growth, occurs in 10% of cases.

      Boys with CAH often experience a salt-losing adrenal crisis at around 1-3 weeks of age. This crisis is characterized by symptoms such as vomiting, weight loss, floppiness, and circulatory collapse.

      The diagnosis of CAH can be made by detecting markedly elevated levels of the metabolic precursor 17-hydroxyprogesterone. Neonatal screening is possible, primarily through the identification of persistently elevated 17-hydroxyprogesterone levels.

      In infants presenting with a salt-losing crisis, the following biochemical abnormalities are observed: hyponatremia (low sodium levels), hyperkalemia (high potassium levels), metabolic acidosis, and hypoglycemia.

      Boys experiencing a salt-losing crisis will require fluid resuscitation, intravenous dextrose, and intravenous hydrocortisone.

      Affected females will require corrective surgery for their external genitalia. However, they have an intact uterus and ovaries and are capable of having children.

      The long-term management of both sexes involves lifelong replacement of hydrocortisone (to suppress ACTH levels).

    • This question is part of the following fields:

      • Endocrinology
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  • Question 12 - A 45-year-old woman presents with overall fatigue and increased skin pigmentation. She has...

    Incorrect

    • A 45-year-old woman presents with overall fatigue and increased skin pigmentation. She has a history of bilateral adrenalectomy for Cushing's syndrome 10 years ago. During the examination of her visual fields, a bitemporal hemianopia is discovered.

      What is the SINGLE most probable diagnosis?

      Your Answer:

      Correct Answer: Nelson’s syndrome

      Explanation:

      Nelson’s syndrome is a rare condition that occurs many years after a bilateral adrenalectomy for Cushing’s syndrome. It is believed to develop due to the loss of the normal negative feedback control that suppresses high cortisol levels. As a result, the hypothalamus starts producing CRH again, which stimulates the growth of a pituitary adenoma that produces adrenocorticotropic hormone (ACTH).

      Only 15-20% of patients who undergo bilateral adrenalectomy will develop this condition, and it is now rarely seen as the procedure is no longer commonly performed.

      The symptoms and signs of Nelson’s syndrome are related to the growth of the pituitary adenoma and the increased production of ACTH and melanocyte-stimulating hormone (MSH) from the adenoma. These may include headaches, visual field defects (up to 50% of cases), increased skin pigmentation, and the possibility of hypopituitarism.

      ACTH levels will be significantly elevated (usually >500 ng/L). Thyroxine, TSH, gonadotrophin, and sex hormone levels may be low. Prolactin levels may be high, but not as high as with a prolactin-producing tumor. MRI or CT scanning can be helpful in identifying the presence of an expanding pituitary mass.

      The treatment of choice for Nelson’s syndrome is trans-sphenoidal surgery.

    • This question is part of the following fields:

      • Endocrinology
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  • Question 13 - A 36 year old male is brought into the emergency department following a...

    Incorrect

    • A 36 year old male is brought into the emergency department following a syncopal episode. The patient reports several weeks of generalized weakness, muscle aches, and feeling dizzy when standing which has been gradually worsening. On examination, you note pigmented areas on the lips, tongue, and gums with patches of vitiligo around the hands and wrists. Observation and blood test results are shown below:

      Hb 132 g/l
      Platelets 124 * 109/l
      WBC 8.0 * 109/l
      Na+ 128 mmol/l
      K+ 6.2 mmol/l
      Urea 8.9 mmol/l
      Creatinine 95 µmol/l
      Glucose 3.1 mmol/l

      Blood pressure 94/56 mmHg
      Pulse 102 bpm
      Respirations 18 bpm
      Oxygen sats 97% on air

      What is the most likely diagnosis?

      Your Answer:

      Correct Answer: Addison's disease

      Explanation:

      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.

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      • Endocrinology
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  • Question 14 - A 42-year-old is brought into the emergency department after becoming drowsy following a...

    Incorrect

    • A 42-year-old is brought into the emergency department after becoming drowsy following a 5 day illness. Upon checking the patient's records you note a history of Addison's disease. Which of the following features would you expect in a patient with Addison's disease?

      Your Answer:

      Correct Answer: Hypotension

      Explanation:

      Addison’s disease is characterized by hypotension, which is caused by a deficiency of glucocorticoids (mainly cortisol) and mineralocorticoids (mainly aldosterone). This deficiency leads to low blood pressure. If left untreated, it can progress to hypovolemic shock (also known as Addisonian or adrenal crisis) and can be fatal. Metabolic disturbances associated with Addison’s disease include hyponatremia, hypoglycemia, hyperkalemia, hypercalcemia, and low serum cortisol 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.

    • This question is part of the following fields:

      • Endocrinology
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  • Question 15 - A 52 year old female presents to the emergency department due to increasing...

    Incorrect

    • A 52 year old female presents to the emergency department due to increasing confusion and restlessness over the past 48 hours. The patient's family inform you that she had complained of feeling anxious and having loose stools yesterday but had attributed it to the antibiotics prescribed by her dentist for a tooth infection a few days ago. It is important to note that the patient has a history of Graves disease. The patient's vital signs are as follows:

      Blood pressure: 152/78 mmHg
      Pulse: 128 bpm
      Respiration rate: 24 bpm
      Temperature: 39.8ºC

      What is the most likely diagnosis?

      Your Answer:

      Correct Answer: Thyroid storm

      Explanation:

      Thyroid storm, also known as thyrotoxic crisis, is a rare and potentially life-threatening complication of hyperthyroidism. The most common cause of thyroid storm is infection. Please refer to the yellow box at the bottom of the notes for additional information on 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.

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  • Question 16 - A 58 year old male comes to the emergency department complaining of palpitations,...

    Incorrect

    • A 58 year old male comes to the emergency department complaining of palpitations, swollen legs, and excessive sweating. Thyroid function tests are requested and reveal low TSH and elevated free T4 levels. Which of the following medications is most likely responsible for these symptoms?

      Your Answer:

      Correct Answer: Amiodarone

      Explanation:

      Amiodarone, a medication used to treat heart rhythm problems, can have effects on the thyroid gland. It can either cause hypothyroidism (low thyroid hormone levels) or hyperthyroidism (high thyroid hormone levels). Amiodarone is a highly fat-soluble drug that accumulates in various tissues, including the thyroid. Even after stopping the medication, its effects can still be seen due to its long elimination half-life of around 100 days.

      The reason behind amiodarone impact on the thyroid is believed to be its high iodine content. In patients with sufficient iodine levels, amiodarone-induced hypothyroidism is more likely to occur. On the other hand, in populations with low iodine levels, amiodarone can lead to a condition called iodine-induced thyrotoxicosis, which is characterized by hyperthyroidism.

      The mechanism of amiodarone-induced hypothyroidism involves the release of iodide from the drug, which blocks the uptake of further iodide by the thyroid gland and hampers the production of thyroid hormones. Additionally, amiodarone inhibits the conversion of the inactive thyroid hormone T4 to the active form T3.

      Amiodarone-induced hyperthyroidism, on the other hand, is thought to occur in individuals with abnormal thyroid glands, such as those with nodular goiters, autonomous nodules, or latent Graves’ disease. In these cases, the excess iodine from amiodarone overwhelms the thyroid’s normal regulatory mechanisms, leading to hyperthyroidism.

      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. hypotension, hypoventilation, altered mental state, seizures and/or coma.

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      • Endocrinology
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  • Question 17 - A 65 year old male is brought to the emergency department after experiencing...

    Incorrect

    • A 65 year old male is brought to the emergency department after experiencing a sudden decline in health over the past 72 hours. The patient appears slightly confused and restless. Here are the observations:

      Blood pressure: 178/94 mmHg
      Pulse: 122 bpm
      Respiration rate: 24 bpm
      Temperature: 39.5ºC

      An ECG is conducted, revealing rapid atrial fibrillation. During the examination, 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 GP office is contacted to obtain further information about their medical history. The patient is prescribed carbimazole and bisoprolol, but they have not renewed their prescription on time. What is the most probable diagnosis?

      Your Answer:

      Correct Answer: Thyroid storm

      Explanation:

      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.

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      • Endocrinology
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  • Question 18 - A 35 year old male presents to the emergency department complaining of palpitations....

    Incorrect

    • A 35 year old male presents to the emergency department complaining of palpitations. The triage nurse requests an urgent review as she is concerned about the patient's blood pressure. The patient's vital signs are as follows:

      Blood pressure: 226/120 mmHg
      Pulse: 122 bpm
      Respiration rate: 18
      Oxygen saturations: 97% on room air

      You consider secondary causes of hypertension, such as phaeochromocytoma. Which of the following biochemical abnormalities is most commonly associated with phaeochromocytoma?

      Your Answer:

      Correct Answer: Hypergylcaemia

      Explanation:

      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.

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      • Endocrinology
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  • Question 19 - You assess a 58-year-old individual who has arrived at the emergency department complaining...

    Incorrect

    • You assess a 58-year-old individual who has arrived at the emergency department complaining of chest pain resembling a cardiac condition. Upon reviewing the patient's medical history, you discover a previous diagnosis of hyperaldosteronism. In terms of aldosterone production, where is it typically synthesized?

      Your Answer:

      Correct Answer: Zona glomerulosa of the adrenal cortex

      Explanation:

      The secretion of aldosterone occurs in the zona glomerulosa of the adrenal cortex.

      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.

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      • Endocrinology
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  • Question 20 - A 22 year old female presents to the emergency department with symptoms of...

    Incorrect

    • A 22 year old female presents to the emergency department with symptoms of headache, nausea, and vomiting. The patient has a history of being insulin dependent due to diabetes. Initial tests indicate that the patient is likely experiencing diabetic ketoacidosis. As part of the patient's treatment plan, you order an insulin infusion. What is an expected outcome of administering insulin in this situation?

      Your Answer:

      Correct Answer: Increase blood pH

      Explanation:

      Insulin is known to have several effects on the body. One of its important functions is to increase blood pH. In patients with diabetic ketoacidosis (DKA), their blood pH is low due to acidosis. Insulin helps to correct this by reducing the levels of free fatty acids in the blood, which are responsible for the production of ketone bodies that contribute to acidosis. By doing so, insulin can increase the blood pH.

      Additionally, insulin plays a role in regulating glucose levels. It facilitates the movement of glucose from the blood into cells, leading to a decrease in blood glucose levels and an increase in intracellular glucose.

      Furthermore, insulin affects the balance of sodium and potassium in the body. It decreases the excretion of sodium by the kidneys and drives potassium from the blood into cells, resulting in a reduction in blood potassium levels. However, it is important to monitor potassium levels closely during insulin infusions, as if they become too low (hypokalemia), the infusion may need to be stopped.

      Further Reading:

      Diabetic ketoacidosis (DKA) is a serious complication of diabetes that occurs due to a lack of insulin in the body. It is most commonly seen in individuals with type 1 diabetes but can also occur in type 2 diabetes. DKA is characterized by hyperglycemia, acidosis, and ketonaemia.

      The pathophysiology of DKA involves insulin deficiency, which leads to increased glucose production and decreased glucose uptake by cells. This results in hyperglycemia and osmotic diuresis, leading to dehydration. Insulin deficiency also leads to increased lipolysis and the production of ketone bodies, which are acidic. The body attempts to buffer the pH change through metabolic and respiratory compensation, resulting in metabolic acidosis.

      DKA can be precipitated by factors such as infection, physiological stress, non-compliance with insulin therapy, acute medical conditions, and certain medications. The clinical features of DKA include polydipsia, polyuria, signs of dehydration, ketotic breath smell, tachypnea, confusion, headache, nausea, vomiting, lethargy, and abdominal pain.

      The diagnosis of DKA is based on the presence of ketonaemia or ketonuria, blood glucose levels above 11 mmol/L or known diabetes mellitus, and a blood pH below 7.3 or bicarbonate levels below 15 mmol/L. Initial investigations include blood gas analysis, urine dipstick for glucose and ketones, blood glucose measurement, and electrolyte levels.

      Management of DKA involves fluid replacement, electrolyte correction, insulin therapy, and treatment of any underlying cause. Fluid replacement is typically done with isotonic saline, and potassium may need to be added depending on the patient’s levels. Insulin therapy is initiated with an intravenous infusion, and the rate is adjusted based on blood glucose levels. Monitoring of blood glucose, ketones, bicarbonate, and electrolytes is essential, and the insulin infusion is discontinued once ketones are below 0.3 mmol/L, pH is above 7.3, and bicarbonate is above 18 mmol/L.

      Complications of DKA and its treatment include gastric stasis, thromboembolism, electrolyte disturbances, cerebral edema, hypoglycemia, acute respiratory distress syndrome, and acute kidney injury. Prompt medical intervention is crucial in managing DKA to prevent potentially fatal outcomes.

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      • Endocrinology
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  • Question 21 - A 2-month-old baby comes in with symptoms of vomiting, decreased weight, and an...

    Incorrect

    • A 2-month-old baby comes in with symptoms of vomiting, decreased weight, and an electrolyte imbalance. Upon consulting with the pediatricians, the baby is diagnosed with congenital adrenal hyperplasia (CAH). Which of the following is NOT a characteristic biochemical finding associated with this condition?

      Your Answer:

      Correct Answer: Hyperglycaemia

      Explanation:

      Congenital adrenal hyperplasia (CAH) is a group of inherited disorders that are caused by autosomal recessive genes. The majority of affected patients, over 90%, have a deficiency of the enzyme 21-hydroxylase. This enzyme is encoded by the 21-hydroxylase gene, which is located on chromosome 6p21 within the HLA histocompatibility complex. The second most common cause of CAH is a deficiency of the enzyme 11-beta-hydroxylase. The condition is rare, with an incidence of approximately 1 in 500 births in the UK. It is more prevalent in the offspring of consanguineous marriages.

      The deficiency of 21-hydroxylase leads to a deficiency of cortisol and/or aldosterone, as well as an excess of precursor steroids. As a result, there is an increased secretion of ACTH from the anterior pituitary, leading to adrenocortical hyperplasia.

      The severity of CAH varies depending on the degree of 21-hydroxylase deficiency. Female infants often exhibit ambiguous genitalia, such as clitoral hypertrophy and labial fusion. Male infants may have an enlarged scrotum and/or scrotal pigmentation. Hirsutism, or excessive hair growth, occurs in 10% of cases.

      Boys with CAH often experience a salt-losing adrenal crisis at around 1-3 weeks of age. This crisis is characterized by symptoms such as vomiting, weight loss, floppiness, and circulatory collapse.

      The diagnosis of CAH can be made by detecting markedly elevated levels of the metabolic precursor 17-hydroxyprogesterone. Neonatal screening is possible, primarily through the identification of persistently elevated 17-hydroxyprogesterone levels.

      In infants presenting with a salt-losing crisis, the following biochemical abnormalities are observed: hyponatremia (low sodium levels), hyperkalemia (high potassium levels), metabolic acidosis, and hypoglycemia.

      Boys experiencing a salt-losing crisis will require fluid resuscitation, intravenous dextrose, and intravenous hydrocortisone.

      Affected females will require corrective surgery for their external genitalia. However, they have an intact uterus and ovaries and are capable of having children.

      The long-term management of both sexes involves lifelong replacement of hydrocortisone (to suppress ACTH levels).

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  • Question 22 - A 52-year-old woman arrives at the emergency department complaining of worsening dizziness and...

    Incorrect

    • A 52-year-old woman arrives at the emergency department complaining of worsening dizziness and weakness in the past few days. She reports experiencing abdominal discomfort, nausea, muscle aches, and weight loss over the last month. To investigate potential underlying causes of her symptoms, you order blood tests. What biochemical abnormalities would you anticipate if the patient is suffering from adrenal insufficiency?

      Your Answer:

      Correct Answer: Hyponatraemia and hyperkalaemia

      Explanation:

      If the patient is suffering from adrenal insufficiency, it is likely that she will have hyponatremia and hyperkalemia. Adrenal insufficiency occurs when the adrenal glands do not produce enough hormones, particularly cortisol. This can lead to imbalances in electrolytes, such as sodium and potassium. Hyponatremia refers to low levels of sodium in the blood, while hyperkalemia refers to high levels of potassium in the blood. These abnormalities can cause symptoms such as dizziness, weakness, abdominal discomfort, and muscle aches. Additionally, the patient’s reported weight loss and other symptoms are consistent with adrenal insufficiency.

      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.

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      • Endocrinology
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  • Question 23 - You evaluate a 4-year-old girl who has been diagnosed with diabetic ketoacidosis (DKA)....

    Incorrect

    • You evaluate a 4-year-old girl who has been diagnosed with diabetic ketoacidosis (DKA). She had initially improved after receiving fluids, but her condition has worsened in the past hour. She is now expressing discomfort due to a headache and is displaying irritability. She has started vomiting again, and the nursing staff has observed an increase in her blood pressure and a decrease in her heart rate.
      What complication has developed?

      Your Answer:

      Correct Answer: Cerebral oedema

      Explanation:

      Cerebral edema is the most significant complication of diabetic ketoacidosis (DKA), leading to death in many cases. It occurs in approximately 0.2-1% of DKA cases. The high blood glucose levels cause an osmolar gradient, resulting in the movement of water from the intracellular fluid (ICF) to the extracellular fluid (ECF) space and a decrease in cell volume. When insulin and intravenous fluids are administered to correct the condition, the effective osmolarity decreases rapidly, causing a reversal of the fluid shift and the development of cerebral edema.

      Cerebral edema is associated with a higher mortality rate and poor neurological outcomes. To prevent its occurrence, it is important to slowly normalize osmolarity over a period of 48 hours, paying attention to glucose and sodium levels, as well as ensuring proper hydration. Monitoring the child for symptoms such as headache, recurrent vomiting, irritability, changes in Glasgow Coma Scale (GCS), abnormal slowing of heart rate, and increasing blood pressure is crucial.

      If cerebral edema does occur, it should be treated with either a hypertonic (3%) saline solution at a dosage of 3 ml/kg or a mannitol infusion at a dosage of 250-500 mg/kg over a 20-minute period.

      In addition to cerebral edema, there are other complications associated with DKA in children, including cardiac arrhythmias, pulmonary edema, and acute renal failure.

    • This question is part of the following fields:

      • Endocrinology
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  • Question 24 - You organize a teaching session for the junior doctors on the syndrome of...

    Incorrect

    • You organize a teaching session for the junior doctors on the syndrome of inappropriate antidiuretic hormone secretion. Which of the following biochemical abnormalities is typical of SIADH?

      Your Answer:

      Correct Answer: Hyponatraemia

      Explanation:

      SIADH is characterized by hyponatremia, which is a condition where there is a low level of sodium in the blood. This occurs because the body is unable to properly excrete excess water, leading to a dilution of sodium levels. SIADH is specifically classified as euvolemic, meaning that there is a normal amount of fluid in the body, and hypotonic, indicating that the concentration of solutes in the blood is lower than normal.

      Further Reading:

      Syndrome of inappropriate antidiuretic hormone (SIADH) is a condition characterized by low sodium levels in the blood due to excessive secretion of antidiuretic hormone (ADH). ADH, also known as arginine vasopressin (AVP), is responsible for promoting water and sodium reabsorption in the body. SIADH occurs when there is impaired free water excretion, leading to euvolemic (normal fluid volume) hypotonic hyponatremia.

      There are various causes of SIADH, including malignancies such as small cell lung cancer, stomach cancer, and prostate cancer, as well as neurological conditions like stroke, subarachnoid hemorrhage, and meningitis. Infections such as tuberculosis and pneumonia, as well as certain medications like thiazide diuretics and selective serotonin reuptake inhibitors (SSRIs), can also contribute to SIADH.

      The diagnostic features of SIADH include low plasma osmolality, inappropriately elevated urine osmolality, urinary sodium levels above 30 mmol/L, and euvolemic. Symptoms of hyponatremia, which is a common consequence of SIADH, include nausea, vomiting, headache, confusion, lethargy, muscle weakness, seizures, and coma.

      Management of SIADH involves correcting hyponatremia slowly to avoid complications such as central pontine myelinolysis. The underlying cause of SIADH should be treated if possible, such as discontinuing causative medications. Fluid restriction is typically recommended, with a daily limit of around 1000 ml for adults. In severe cases with neurological symptoms, intravenous hypertonic saline may be used. Medications like demeclocycline, which blocks ADH receptors, or ADH receptor antagonists like tolvaptan may also be considered.

      It is important to monitor serum sodium levels closely during treatment, especially if using hypertonic saline, to prevent rapid correction that can lead to central pontine myelinolysis. Osmolality abnormalities can help determine the underlying cause of hyponatremia, with increased urine osmolality indicating dehydration or renal disease, and decreased urine osmolality suggesting SIADH or overhydration.

    • This question is part of the following fields:

      • Endocrinology
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  • Question 25 - A 70-year-old woman from a retirement community experiences a sudden collapse. Her blood...

    Incorrect

    • A 70-year-old woman from a retirement community experiences a sudden collapse. Her blood sugar level is measured and found to be 2.2. She has a medical history of diabetes mellitus.
      Which ONE medication is the LEAST probable cause of her hypoglycemic episode?

      Your Answer:

      Correct Answer: Metformin

      Explanation:

      Metformin is a type of biguanide medication that, when taken alone, does not lead to low blood sugar levels (hypoglycemia). However, it can potentially worsen hypoglycemia when used in combination with other drugs like sulphonylureas.

      Gliclazide, on the other hand, is a sulphonylurea medication known to cause hypoglycemia. Pioglitazone, a thiazolidinedione drug, is also recognized as a cause of hypoglycemia.

      It’s important to note that Actrapid and Novomix are both forms of insulin, which can also result in hypoglycemia.

    • This question is part of the following fields:

      • Endocrinology
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  • Question 26 - A 70 year old type 2 diabetic visits the emergency department with a...

    Incorrect

    • A 70 year old type 2 diabetic visits the emergency department with a foot injury. You suspect neuropathy and conduct sensory testing. Which of the following senses is usually the first to be lost in diabetic neuropathy?

      Your Answer:

      Correct Answer: Vibration

      Explanation:

      The initial noticeable abnormality in sensory testing for diabetic neuropathy is often the loss of vibration sense. Reduced sensation, particularly in vibration sense, is typically the first symptom to be observed in diabetic neuropathy.

      Further Reading:

      Diabetic foot is a complication that can occur in individuals with diabetes due to long-standing high blood sugar levels. This leads to a process called glycation or glycosylation, where glucose binds to proteins and lipids in the body. Abnormal protein glycation can cause cellular dysfunction and various complications.

      One of the main problems in diabetic foot is peripheral vascular disease and peripheral neuropathy. These conditions can result in significant foot issues, as trauma to the feet may go unnoticed and untreated. Vascular disease also impairs wound healing and increases the risk of developing ulcers.

      Clinical features of diabetic foot include reduced sensation, especially to vibration, non-dermatomal sensory loss, foot deformities such as pes cavus and claw toes, and weak or absent foot pulses. It is important for diabetic patients to have their feet assessed regularly, at least annually, to identify any potential problems. Additional foot assessments should also be conducted during hospital admissions.

      During a diabetic foot assessment, the healthcare provider should remove shoes, socks, and any bandages or dressings to examine both feet. They should assess for neuropathy using a 10 g monofilament to test foot sensation and check for limb ischemia by examining pulses and performing ankle brachial pressure index (ABPI) measurements. Any abnormal tissue, such as ulcers, calluses, infections, inflammation, deformities, or gangrene, should be documented. The risk of Charcot arthropathy should also be assessed.

      The severity of foot ulcers in diabetic patients can be documented using standardized systems such as SINBAD or the University of Texas classification. The presence and severity of diabetic foot infection can be determined based on criteria such as local swelling, induration, erythema, tenderness, pain, warmth, and purulent discharge.

      Management of foot ulcers involves offloading, control of foot infection, control of ischemia, wound debridement, and appropriate wound dressings. Antibiotics may be necessary depending on the severity of the infection. Diabetic patients with foot ulcers should undergo initial investigations including blood tests, wound swabs, and imaging to assess for possible osteomyelitis.

      Charcot foot is a serious complication of diabetic peripheral neuropathy that results in progressive destructive arthropathy and foot deformity. Signs of Charcot foot include redness, swelling, warm skin, pain, and deformity. The hallmark deformity is midfoot collapse, known as the rocker-bottom foot.

    • This question is part of the following fields:

      • Endocrinology
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  • Question 27 - A 68 year old is brought into the emergency department by ambulance after...

    Incorrect

    • A 68 year old is brought into the emergency department by ambulance after experiencing a seizure. The nursing home staff inform the patient has been exhibiting increased lethargy in recent days. Blood samples are sent to the laboratory and the lab calls shortly after to report the abnormal sodium level (shown below):

      Na+ 116 mmol/l
      K+ 4.9 mmol/l
      Urea 10.5 mmol/l
      Creatinine 109 µmol/l

      What is the most suitable course of action for managing this patient?

      Your Answer:

      Correct Answer: Intravenous infusion 3% sodium chloride solution

      Explanation:

      To treat low sodium levels, a solution of sodium chloride is administered. It is important to regularly monitor plasma sodium levels every 2 hours during this treatment, but it is crucial to avoid taking samples from the arm where the IV is inserted. The increase in serum sodium should not exceed 2 mmol/L per hour and should not exceed 8 to 10 mmol/L within a 24-hour period. Hypertonic saline is administered intravenously until neurological symptoms improve.

      Further Reading:

      Syndrome of inappropriate antidiuretic hormone (SIADH) is a condition characterized by low sodium levels in the blood due to excessive secretion of antidiuretic hormone (ADH). ADH, also known as arginine vasopressin (AVP), is responsible for promoting water and sodium reabsorption in the body. SIADH occurs when there is impaired free water excretion, leading to euvolemic (normal fluid volume) hypotonic hyponatremia.

      There are various causes of SIADH, including malignancies such as small cell lung cancer, stomach cancer, and prostate cancer, as well as neurological conditions like stroke, subarachnoid hemorrhage, and meningitis. Infections such as tuberculosis and pneumonia, as well as certain medications like thiazide diuretics and selective serotonin reuptake inhibitors (SSRIs), can also contribute to SIADH.

      The diagnostic features of SIADH include low plasma osmolality, inappropriately elevated urine osmolality, urinary sodium levels above 30 mmol/L, and euvolemic. Symptoms of hyponatremia, which is a common consequence of SIADH, include nausea, vomiting, headache, confusion, lethargy, muscle weakness, seizures, and coma.

      Management of SIADH involves correcting hyponatremia slowly to avoid complications such as central pontine myelinolysis. The underlying cause of SIADH should be treated if possible, such as discontinuing causative medications. Fluid restriction is typically recommended, with a daily limit of around 1000 ml for adults. In severe cases with neurological symptoms, intravenous hypertonic saline may be used. Medications like demeclocycline, which blocks ADH receptors, or ADH receptor antagonists like tolvaptan may also be considered.

      It is important to monitor serum sodium levels closely during treatment, especially if using hypertonic saline, to prevent rapid correction that can lead to central pontine myelinolysis. Osmolality abnormalities can help determine the underlying cause of hyponatremia, with increased urine osmolality indicating dehydration or renal disease, and decreased urine osmolality suggesting SIADH or overhydration.

    • This question is part of the following fields:

      • Endocrinology
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  • Question 28 - A 5-year-old girl is brought into the Emergency Department with stomach pain and...

    Incorrect

    • A 5-year-old girl is brought into the Emergency Department with stomach pain and vomiting. Her mother informs you that she has been losing weight recently and has been drinking a lot of fluids and urinating frequently. During the examination, you observe that she is drowsy and visibly dehydrated. She is breathing deeply and rapidly. A blood glucose test reveals very high levels. The urine dipstick shows 3+ ketones, and a venous blood gas test indicates a pH of 7.14. The diagnosis is diabetic ketoacidosis.
      How long should it take to correct this fluid deficit?

      Your Answer:

      Correct Answer: 48 hours

      Explanation:

      The most probable diagnosis in this case is diabetic ketoacidosis (DKA). To confirm the diagnosis, it is necessary to establish that his blood glucose levels are elevated, he has significant ketonuria or ketonaemia, and that he is acidotic.

      DKA is a life-threatening condition that occurs when there is a lack of insulin, leading to an inability to metabolize glucose. This results in high blood sugar levels and an osmotic diuresis, causing excessive thirst and increased urine production. Dehydration becomes inevitable when the urine output exceeds the patient’s ability to drink. Additionally, without insulin, fat becomes the primary energy source, leading to the production of large amounts of ketones and metabolic acidosis.

      The key features of DKA include hyperglycemia (blood glucose > 11 mmol/l), ketonaemia (> 3 mmol/l) or significant ketonuria (> 2+ on urine dipstick), and acidosis (bicarbonate < 15 mmol/l and/or venous pH < 7.3). Clinical symptoms of DKA include nausea, vomiting, excessive thirst, excessive urine production, abdominal pain, signs of dehydration, a smell of ketones on breath (similar to pear drops), deep and rapid respiration (Kussmaul breathing), confusion or reduced consciousness, and tachycardia, hypotension, and shock. Investigations that should be performed include blood glucose measurement, urine dipstick (which will show marked glycosuria and ketonuria), blood ketone assay (more sensitive and specific than urine dipstick), blood tests (full blood count and urea and electrolytes), and arterial or venous blood gas analysis to assess for metabolic acidosis. The main principles of managing DKA are as follows: – Fluid boluses should only be given to reverse signs of shock and should be administered slowly in 10 ml/kg aliquots. If there are no signs of shock, fluid boluses should not be given, and specialist advice should be sought if a second bolus is required.
      – Rehydration should be done with replacement therapy over 48 hours after signs of shock have been reversed.
      – The first 20 ml/kg of fluid resuscitation should be given in addition to replacement fluid calculations and should not be subtracted from the calculations for the 48-hour fluid replacement.
      – If a child in DKA shows signs of hypotensive shock, the use of inotropes may be considered.

    • This question is part of the following fields:

      • Endocrinology
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  • Question 29 - You assess a patient who has been brought into the resuscitation room in...

    Incorrect

    • You assess a patient who has been brought into the resuscitation room in an obtunded state. The patient is wearing a MedicAlert bracelet, indicating a diagnosis of Addison's disease.
      Which ONE statement accurately describes this condition?

      Your Answer:

      Correct Answer: ACTH levels are usually elevated

      Explanation:

      Addison’s disease occurs when the adrenal glands do not produce enough steroid hormones. This includes glucocorticoids, mineralocorticoids, and sex steroids. The most common cause is autoimmune adrenalitis, which accounts for about 70-80% of cases. It is more prevalent in women and typically occurs between the ages of 30 and 50.

      The clinical symptoms of Addison’s disease include weakness, lethargy, low blood pressure (especially when standing up), nausea, vomiting, weight loss, reduced hair in the armpits and pubic area, depression, and hyperpigmentation (darkening of the skin in certain areas like the palms, mouth, and exposed skin).

      Biochemically, Addison’s disease is characterized by increased levels of ACTH (a hormone that tries to stimulate the adrenal glands), low sodium levels, high potassium levels, high calcium levels, low blood sugar, and metabolic acidosis.

      People with Addison’s disease have a higher risk of developing type 1 diabetes, Hashimoto’s thyroiditis, Grave’s disease, premature ovarian failure, pernicious anemia, vitiligo, and alopecia.

      Management of Addison’s disease should be overseen by an Endocrinologist. Treatment typically involves taking hydrocortisone, fludrocortisone, and dehydroepiandrosterone. Some patients may also need thyroxine if there is hypothalamic-pituitary disease present. Treatment is lifelong, and patients should carry a steroid card and a MedicAlert bracelet in case of an Addisonian crisis.

    • This question is part of the following fields:

      • Endocrinology
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  • Question 30 - You assess a patient who has been admitted to the resuscitation unit in...

    Incorrect

    • You assess a patient who has been admitted to the resuscitation unit in an obtunded state. The patient is wearing a MedicAlert bracelet, indicating a diagnosis of Addison's disease.
      Which ONE biochemical characteristic would you NOT anticipate observing in this particular condition?

      Your Answer:

      Correct Answer: Low serum renin level

      Explanation:

      Addison’s disease is characterized by several classical biochemical features. One of these features is an increase in ACTH levels, which is a hormone that stimulates the production of cortisol. Additionally, individuals with Addison’s disease often have elevated serum renin levels, which is an enzyme involved in regulating blood pressure. Another common biochemical feature is hyponatremia, which refers to low levels of sodium in the blood. Hyperkalemia, or high levels of potassium, is also frequently observed in individuals with Addison’s disease. Furthermore, hypercalcemia, an excess of calcium in the blood, may be present. Hypoglycemia, or low blood sugar levels, is another characteristic feature. Lastly, metabolic acidosis, a condition where the body produces too much acid or cannot eliminate it properly, is often seen in individuals with Addison’s disease.

    • This question is part of the following fields:

      • Endocrinology
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