-
Question 1
Incorrect
-
A 26-year-old male patient comes to the follow-up clinic after undergoing surgery to remove an endocrine gland. He had been experiencing symptoms such as profuse sweating, headaches, palpitations, and high blood pressure (200/120mmHg) prior to the decision for surgery. What type of cells would be revealed through histological staining of the removed organ?
Your Answer: Thyrotrope cells
Correct Answer: Chromaffin cells
Explanation:The man’s initial symptoms are consistent with a diagnosis of phaeochromocytoma, a type of neuroendocrine tumor that affects the chromaffin cells in the adrenal medulla. This condition leads to an overproduction of adrenaline and noradrenaline, resulting in an excessive sympathetic response.
Calcitonin is secreted by the parafollicular C cells in the thyroid gland.
The anterior pituitary gland contains gonadotropes, lactotropes, and thyrotropes, which secrete gonadotropins (FSH, LH), prolactin, and TSH, respectively.
Phaeochromocytoma: A Rare Tumor that Secretes Catecholamines
Phaeochromocytoma is a type of tumor that secretes catecholamines and is considered rare. It is familial in about 10% of cases and may be associated with certain syndromes such as MEN type II, neurofibromatosis, and von Hippel-Lindau syndrome. This tumor can be bilateral in 10% of cases and malignant in 10%. It can also occur outside of the adrenal gland, with the most common site being the organ of Zuckerkandl, which is adjacent to the bifurcation of the aorta.
The symptoms of phaeochromocytoma are typically episodic and include hypertension (which is present in around 90% of cases and may be sustained), headaches, palpitations, sweating, and anxiety. To diagnose this condition, a 24-hour urinary collection of metanephrines is preferred over a 24-hour urinary collection of catecholamines due to its higher sensitivity (97%).
Surgery is the definitive management for phaeochromocytoma. However, before surgery, the patient must first be stabilized with medical management, which includes an alpha-blocker (such as phenoxybenzamine) given before a beta-blocker (such as propranolol).
-
This question is part of the following fields:
- Endocrine System
-
-
Question 2
Incorrect
-
Which of the following most accurately explains how glucocorticoids work?
Your Answer: Binding of cell wall receptors and intracellular tyrosine kinase activation
Correct Answer: Binding of intracellular receptors that migrate to the nucleus to then affect gene transcription
Explanation:The effects of glucocorticoids are mediated by intracellular receptors that bind to them and are subsequently transported to the nucleus, where they modulate gene transcription.
Corticosteroids are commonly prescribed medications that can be taken orally or intravenously, or applied topically. They mimic the effects of natural steroids in the body and can be used to replace or supplement them. However, the use of corticosteroids is limited by their numerous side effects, which are more common with prolonged and systemic use. These side effects can affect various systems in the body, including the endocrine, musculoskeletal, gastrointestinal, ophthalmic, and psychiatric systems. Some of the most common side effects include impaired glucose regulation, weight gain, osteoporosis, and increased susceptibility to infections. Patients on long-term corticosteroids should have their doses adjusted during intercurrent illness, and the medication should not be abruptly withdrawn to avoid an Addisonian crisis. Gradual withdrawal is recommended for patients who have received high doses or prolonged treatment.
-
This question is part of the following fields:
- Endocrine System
-
-
Question 3
Incorrect
-
The acute phase response to injury in elderly patients does not involve which of the following?
Your Answer: Increased serum amyloid A
Correct Answer: Increased transferrin
Explanation:The acute phase response is characterized by various physiological changes, such as the production of acute phase proteins, decreased levels of transport proteins like albumin and transferrin, hepatic retention of cations, fever, an increase in neutrophil count, elevated muscle proteolysis, and alterations in vascular permeability.
Surgery triggers a stress response that causes hormonal and metabolic changes in the body. This response is characterized by substrate mobilization, muscle protein loss, sodium and water retention, suppression of anabolic hormone secretion, activation of the sympathetic nervous system, and immunological and haematological changes. The hypothalamic-pituitary axis and the sympathetic nervous systems are activated, and the normal feedback mechanisms of control of hormone secretion fail. The stress response is associated with increased growth hormone, cortisol, renin, adrenocorticotrophic hormone (ACTH), aldosterone, prolactin, antidiuretic hormone, and glucagon, while insulin, testosterone, oestrogen, thyroid stimulating hormone, luteinizing hormone, and follicle stimulating hormone are decreased or remain unchanged. The metabolic effects of cortisol are enhanced, including skeletal muscle protein breakdown, stimulation of lipolysis, anti-insulin effect, mineralocorticoid effects, and anti-inflammatory effects. The stress response also affects carbohydrate, protein, lipid, salt and water metabolism, and cytokine release. Modifying the response can be achieved through opioids, spinal anaesthesia, nutrition, growth hormone, anabolic steroids, and normothermia.
-
This question is part of the following fields:
- Endocrine System
-
-
Question 4
Incorrect
-
An aged woman with malabsorption and weight loss was diagnosed with small bowel amyloidosis. She was initially found to have osteomalacia and hypocalcemia. Despite receiving total parenteral nutrition with sufficient calcium replacement for the past seven days, she remained hypocalcemic. Which electrolyte deficiency is most likely responsible for this condition?
Your Answer: Phosphate
Correct Answer: Magnesium
Explanation:Magnesium deficiency may occur in patients with malabsorption, even if they receive magnesium through TPN feeds, as it may not be enough to compensate for their losses. Serum calcium levels are not affected by sodium, phosphate, and potassium.
The Importance of Magnesium and Calcium in the Body
Magnesium and calcium are essential minerals in the body. Magnesium plays a crucial role in the secretion and action of parathyroid hormone (PTH) on target tissues. However, a deficiency in magnesium can cause hypocalcaemia and make patients unresponsive to calcium and vitamin D supplementation.
The body contains 1000 mmol of magnesium, with half stored in bones and the rest in muscle, soft tissues, and extracellular fluid. Unlike calcium, there is no specific hormonal control of magnesium. Hormones such as PTH and aldosterone affect the renal handling of magnesium.
Magnesium and calcium also interact at a cellular level. A decrease in magnesium levels can affect the permeability of cellular membranes to calcium, leading to hyperexcitability. Therefore, it is essential to maintain adequate levels of both magnesium and calcium in the body for optimal health.
-
This question is part of the following fields:
- Endocrine System
-
-
Question 5
Incorrect
-
Which of the following is not secreted by the islets of Langerhans?
Your Answer: Pancreatic polypeptide
Correct Answer: Secretin
Explanation:Mucosal cells in the duodenum and jejunum release secretin.
Hormones Released from the Islets of Langerhans
The islets of Langerhans in the pancreas are responsible for the production and secretion of several hormones that play a crucial role in regulating blood glucose levels. The beta cells in the islets of Langerhans are responsible for producing insulin, which accounts for 70% of the total secretions. Insulin helps to lower blood glucose levels by promoting the uptake of glucose by cells and tissues throughout the body.
The alpha cells in the islets of Langerhans produce glucagon, which has the opposite effect of insulin. Glucagon raises blood glucose levels by stimulating the liver to release stored glucose into the bloodstream. The delta cells in the islets of Langerhans produce somatostatin, which helps to regulate the release of insulin and glucagon.
Finally, the F cells in the islets of Langerhans produce pancreatic polypeptide, which plays a role in regulating pancreatic exocrine function and appetite. Together, these hormones work to maintain a delicate balance of blood glucose levels in the body.
-
This question is part of the following fields:
- Endocrine System
-
-
Question 6
Incorrect
-
A 36-year-old woman visits her GP complaining of frequent urination. She has been waking up several times at night to urinate for the past two weeks and has been feeling more thirsty than usual. Her temperature is 37.3ºC. She has a history of bipolar disorder and is currently on lithium medication.
What could be the possible cause of her polyuria?Your Answer: Central diabetes insipidus
Correct Answer: Lithium reducing ADH-dependent water reabsorption in the collecting duct
Explanation:The site of action for antidiuretic hormone (ADH) is the collecting ducts. Lithium treatment for bipolar disorder can lead to diabetes insipidus, which is characterized by increased thirst (polydipsia) and increased urination (polyuria). Lithium use can cause nephrogenic diabetes insipidus, where the kidneys are unable to respond adequately to ADH. Normally, ADH induces the expression of aquaporin 2 channels in the collecting duct, which stimulates water reabsorption.
Central diabetes insipidus occurs when there is damage to the posterior pituitary gland, resulting in insufficient production and release of ADH. However, lithium use causes nephrogenic diabetes insipidus instead of central diabetes insipidus.
Although insulin resistance and hyperglycemia can also cause polyuria and polydipsia, as seen in diabetic ketoacidosis, the use of lithium suggests that the patient’s symptoms are due to diabetes insipidus rather than diabetes mellitus.
Lithium inhibits the expression of aquaporin channels in the renal collecting duct, rather than the distal convoluted tubule, which causes diabetes insipidus.
While a urinary tract infection can also present with polyuria and nocturia, the presence of lithium in the patient’s drug history and the fact that the patient also has polydipsia suggest nephrogenic diabetes insipidus. Diabetes insipidus causes increased thirst due to the excessive volume of urine produced, leading to water loss from the body. In addition, a urinary tract infection would likely cause dysuria (burning or stinging when passing urine) and lower abdominal pain.
Understanding Antidiuretic Hormone (ADH)
Antidiuretic hormone (ADH) is a hormone that is produced in the supraoptic nuclei of the hypothalamus and released by the posterior pituitary gland. Its primary function is to conserve body water by promoting water reabsorption in the collecting ducts of the kidneys through the insertion of aquaporin-2 channels.
ADH secretion is regulated by various factors. An increase in extracellular fluid osmolality, a decrease in volume or pressure, and the presence of angiotensin II can all increase ADH secretion. Conversely, a decrease in extracellular fluid osmolality, an increase in volume, a decrease in temperature, or the absence of ADH can decrease its secretion.
Diabetes insipidus (DI) is a condition that occurs when there is either a deficiency of ADH (cranial DI) or an insensitivity to ADH (nephrogenic DI). Cranial DI can be treated with desmopressin, which is an analog of ADH.
Overall, understanding the role of ADH in regulating water balance in the body is crucial for maintaining proper hydration and preventing conditions like DI.
-
This question is part of the following fields:
- Endocrine System
-
-
Question 7
Correct
-
A 30-year-old woman complains of menstrual irregularity and galactorrhoea for the past year. She also experiences occasional headaches. During examination, she was found to have bitemporal superior quadrantanopia. What is the most probable diagnosis?
Your Answer: Prolactinoma
Explanation:Prolactinomas cause amenorrhoea, infertility, and galactorrhoea. If the tumour extends outside the sella, visual field defects or other mass effects may occur. Other types of tumours will produce different symptoms depending on their location and structure involved. Craniopharyngiomas originate from the pituitary gland and will produce poralhemianopia if large enough, as well as symptoms related to pituitary hormones. Non-functioning pituitary tumours will have similar symptoms without the pituitary hormone side effects. Tumours of the hypothalamus will present with symptoms of euphoria, headache, weight loss, and mass effect if large enough.
-
This question is part of the following fields:
- Endocrine System
-
-
Question 8
Incorrect
-
For individuals with multiple endocrine neoplasia type IIb, what is the most probable clinical presentation they will exhibit?
Your Answer: Turners type features
Correct Answer: Marfanoid features
Explanation:Understanding Multiple Endocrine Neoplasia
Multiple endocrine neoplasia (MEN) is an autosomal dominant disorder that affects the endocrine system. There are three main types of MEN, each with its own set of associated features. MEN type I is characterized by the 3 P’s: parathyroid hyperplasia leading to hyperparathyroidism, pituitary tumors, and pancreatic tumors such as insulinomas and gastrinomas. MEN type IIa is associated with the 2 P’s: parathyroid hyperplasia leading to hyperparathyroidism and phaeochromocytoma, as well as medullary thyroid cancer. MEN type IIb is characterized by phaeochromocytoma, medullary thyroid cancer, and a marfanoid body habitus.
The most common presentation of MEN is hypercalcaemia, which is often seen in MEN type I due to parathyroid hyperplasia. MEN type IIa and IIb are both associated with medullary thyroid cancer, which is caused by mutations in the RET oncogene. MEN type I is caused by mutations in the MEN1 gene. Understanding the different types of MEN and their associated features is important for early diagnosis and management of this rare but potentially serious condition.
-
This question is part of the following fields:
- Endocrine System
-
-
Question 9
Correct
-
A 20-year-old woman arrives at the emergency department complaining of abdominal pain, nausea, and vomiting. She reports having a cough and fever for the past few days. Upon examination, she has dry mucous membranes and her breath has a fruity odor. Her vital signs are as follows: blood pressure 95/55 mmHg, heart rate 120/min, respiratory rate 29/min, temperature 37.8ºC (100ºF), and oxygen saturation 98% on room air. Laboratory results show:
- Sodium (Na+): 124 mmol/L (135 - 145)
- Potassium (K+): 5.5 mmol/L (3.5 - 5.0)
- Bicarbonate: 13 mmol/L (22 - 29)
- Serum glucose: 30 mmol/L (4 - 7.8)
- pH: 7.15 (7.35 - 7.45)
- Serum ketones: 3.5 mmol/L (0 - 0.6)
What is the most likely cause of the increased ketones in this patient?Your Answer: Lipolysis
Explanation:DKA is a condition that arises due to uncontrolled lipolysis, leading to an excess of free fatty acids that are converted to ketone bodies. This life-threatening complication of diabetes is characterized by elevated levels of blood glucose, ketones, and acidosis, with symptoms such as nausea, vomiting, abdominal pain, dehydration, and fruity breath odor. DKA is commonly observed in type 1 diabetes mellitus and can be triggered by non-compliance with treatment or an infection. Insulin deficiency and increased levels of counterregulatory hormones cause lipolysis in adipose tissue, leading to the release of free fatty acids that undergo hepatic oxidation to form ketone bodies. In DKA, increased gluconeogenesis and glycogenolysis occur due to insulin deficiency and counterregulatory hormones, leading to the synthesis of glucose from non-carbohydrate precursors and breakdown of glycogen, respectively. Glycolysis is not involved in DKA as it does not lead to the breakdown of fatty acids.
Diabetic ketoacidosis (DKA) is a serious complication of type 1 diabetes mellitus, accounting for around 6% of cases. It can also occur in rare cases of extreme stress in patients with type 2 diabetes mellitus. DKA is caused by uncontrolled lipolysis, resulting in an excess of free fatty acids that are converted to ketone bodies. The most common precipitating factors of DKA are infection, missed insulin doses, and myocardial infarction. Symptoms include abdominal pain, polyuria, polydipsia, dehydration, Kussmaul respiration, and breath that smells like acetone. Diagnostic criteria include glucose levels above 11 mmol/l or known diabetes mellitus, pH below 7.3, bicarbonate below 15 mmol/l, and ketones above 3 mmol/l or urine ketones ++ on dipstick.
Management of DKA involves fluid replacement, insulin, and correction of electrolyte disturbance. Fluid replacement is necessary as most patients with DKA are deplete around 5-8 litres. Isotonic saline is used initially, even if the patient is severely acidotic. Insulin is administered through an intravenous infusion, and correction of electrolyte disturbance is necessary. Long-acting insulin should be continued, while short-acting insulin should be stopped. Complications may occur from DKA itself or the treatment, such as gastric stasis, thromboembolism, arrhythmias, acute respiratory distress syndrome, acute kidney injury, and cerebral edema. Children and young adults are particularly vulnerable to cerebral edema following fluid resuscitation in DKA and often need 1:1 nursing to monitor neuro-observations, headache, irritability, visual disturbance, focal neurology, etc.
-
This question is part of the following fields:
- Endocrine System
-
-
Question 10
Incorrect
-
A 65-year-old man with type 2 diabetes mellitus has been taking metformin 1g twice daily for the past 6 months. Despite this, his HbA1c has remained above target at 64 mmol/mol (8.0%).
He has a history of left ventricular failure following a myocardial infarction 2 years ago. He has been trying to lose weight since but still has a body mass index of 33 kg/m². He is also prone to recurrent urinary tract infections.
You intend to intensify treatment by adding a second medication.
What is the mechanism of action of the most appropriate anti-diabetic drug for him?Your Answer: Inhibition of renal sodium-glucose co-transporter-2 (SGLT2) to increase glucose excretion
Correct Answer: Inhibition of dipeptidyl peptidase-4 (DPP-4) to increase incretin levels
Explanation:Diabetes mellitus is a condition that has seen the development of several drugs in recent years. One hormone that has been the focus of much research is glucagon-like peptide-1 (GLP-1), which is released by the small intestine in response to an oral glucose load. In type 2 diabetes mellitus (T2DM), insulin resistance and insufficient B-cell compensation occur, and the incretin effect, which is largely mediated by GLP-1, is decreased. GLP-1 mimetics, such as exenatide and liraglutide, increase insulin secretion and inhibit glucagon secretion, resulting in weight loss, unlike other medications. They are sometimes used in combination with insulin in T2DM to minimize weight gain. Dipeptidyl peptidase-4 (DPP-4) inhibitors, such as vildagliptin and sitagliptin, increase levels of incretins by decreasing their peripheral breakdown, are taken orally, and do not cause weight gain. Nausea and vomiting are the major adverse effects of GLP-1 mimetics, and the Medicines and Healthcare products Regulatory Agency has issued specific warnings on the use of exenatide, reporting that it has been linked to severe pancreatitis in some patients. NICE guidelines suggest that a DPP-4 inhibitor might be preferable to a thiazolidinedione if further weight gain would cause significant problems, a thiazolidinedione is contraindicated, or the person has had a poor response to a thiazolidinedione.
-
This question is part of the following fields:
- Endocrine System
-
-
Question 11
Correct
-
A 65-year-old male with a diagnosis of lung cancer presents with fatigue and lightheadedness. Upon examination, the following results are obtained:
Plasma sodium concentration 115 mmol/L (137-144)
Potassium 3.5 mmol/L (3.5-4.9)
Urea 3.2 mmol/L (2.5-7.5)
Creatinine 67 µmol/L (60-110)
What is the probable reason for his symptoms based on these findings?Your Answer: Syndrome of inappropriate ADH secretion
Explanation:Syndrome of Inappropriate ADH Secretion
Syndrome of inappropriate ADH secretion (SIADH) is a condition characterized by low levels of sodium in the blood. This is caused by the overproduction of antidiuretic hormone (ADH) by the posterior pituitary gland. Tumors such as bronchial carcinoma can cause the ectopic elaboration of ADH, leading to dilutional hyponatremia. The diagnosis of SIADH is one of exclusion, but it can be supported by a high urine sodium concentration with high urine osmolality.
Hypoadrenalism is less likely to cause hyponatremia, as it is usually associated with hyperkalemia and mild hyperuricemia. On the other hand, diabetes insipidus is a condition where the kidneys are unable to reabsorb water, leading to excessive thirst and urination.
It is important to diagnose and treat SIADH promptly to prevent complications such as seizures, coma, and even death. Treatment options include fluid restriction, medications to block the effects of ADH, and addressing the underlying cause of the condition.
In conclusion, SIADH is a condition that can cause low levels of sodium in the blood due to the overproduction of ADH. It is important to differentiate it from other conditions that can cause hyponatremia and to treat it promptly to prevent complications.
-
This question is part of the following fields:
- Endocrine System
-
-
Question 12
Incorrect
-
A 43-year-old obese man comes to your clinic for a diabetes check-up. Despite being treated with metformin and gliclazide, his HbA1c remains elevated at 55 mmol/mol. He has previously found it difficult to follow dietary advice and lose weight. To enhance his diabetic management, you prescribe sitagliptin, a DPP-4 inhibitor. What is the mode of action of this novel medication?
Your Answer: Modulates genes involved in glucose homeostasis and lipid metabolism
Correct Answer: Inhibits the breakdown of incretins
Explanation:DPP-4 inhibitors, GLP-1 agonists, SGLT-2 inhibitors, thiazolidinediones, and sulfonylureas are all medications used to treat diabetes. DPP-4 inhibitors work by inhibiting the breakdown of incretins such as GLP-1 and GIP, which are released in response to food and help to lower blood glucose levels. GLP-1 agonists directly stimulate incretin receptors, while SGLT-2 inhibitors increase the urinary secretion of glucose. Thiazolidinediones stimulate intracellular signaling molecules responsible for glucose and lipid metabolism, and sulfonylureas stimulate beta cells to secrete more insulin. However, sulfonylureas may be less effective in long-standing diabetes as many beta cells may no longer function properly.
Diabetes mellitus is a condition that has seen the development of several drugs in recent years. One hormone that has been the focus of much research is glucagon-like peptide-1 (GLP-1), which is released by the small intestine in response to an oral glucose load. In type 2 diabetes mellitus (T2DM), insulin resistance and insufficient B-cell compensation occur, and the incretin effect, which is largely mediated by GLP-1, is decreased. GLP-1 mimetics, such as exenatide and liraglutide, increase insulin secretion and inhibit glucagon secretion, resulting in weight loss, unlike other medications. They are sometimes used in combination with insulin in T2DM to minimize weight gain. Dipeptidyl peptidase-4 (DPP-4) inhibitors, such as vildagliptin and sitagliptin, increase levels of incretins by decreasing their peripheral breakdown, are taken orally, and do not cause weight gain. Nausea and vomiting are the major adverse effects of GLP-1 mimetics, and the Medicines and Healthcare products Regulatory Agency has issued specific warnings on the use of exenatide, reporting that it has been linked to severe pancreatitis in some patients. NICE guidelines suggest that a DPP-4 inhibitor might be preferable to a thiazolidinedione if further weight gain would cause significant problems, a thiazolidinedione is contraindicated, or the person has had a poor response to a thiazolidinedione.
-
This question is part of the following fields:
- Endocrine System
-
-
Question 13
Correct
-
Which of the following explains the mechanism by which PTH increases serum calcium levels?
Your Answer: Activation of vitamin D to increase absorption of calcium from the small intestine.
Explanation:The activity of the 1-α-hydroxylase enzyme, which converts 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol (the active form of vitamin D), is increased by PTH. Osteoblasts mediate the effects of PTH on osteoclasts, as osteoclasts do not have a PTH receptor.
Understanding Parathyroid Hormone and Its Effects
Parathyroid hormone is a hormone produced by the chief cells of the parathyroid glands. Its main function is to increase the concentration of calcium in the blood by stimulating the PTH receptors in the kidney and bone. This hormone has a short half-life of only 4 minutes.
The effects of parathyroid hormone are mainly seen in the bone, kidney, and intestine. In the bone, PTH binds to osteoblasts, which then signal to osteoclasts to resorb bone and release calcium. In the kidney, PTH promotes the active reabsorption of calcium and magnesium from the distal convoluted tubule, while decreasing the reabsorption of phosphate. In the intestine, PTH indirectly increases calcium absorption by increasing the activation of vitamin D, which in turn increases calcium absorption.
Overall, understanding the role of parathyroid hormone is important in maintaining proper calcium levels in the body. Any imbalances in PTH secretion can lead to various disorders such as hyperparathyroidism or hypoparathyroidism.
-
This question is part of the following fields:
- Endocrine System
-
-
Question 14
Incorrect
-
Which one of the following is not associated with excessive glucocorticoids?
Your Answer: Growth retardation in children
Correct Answer: Hyponatraemia
Explanation:Excessive levels of glucocorticoids can lead to various negative consequences such as skin thinning, osteonecrosis, and osteoporosis. Steroids can cause the body to retain sodium and water, while also resulting in potassium loss and potentially leading to hypokalaemic alkalosis.
Cortisol: Functions and Regulation
Cortisol is a hormone produced in the zona fasciculata of the adrenal cortex. It plays a crucial role in various bodily functions and is essential for life. Cortisol increases blood pressure by up-regulating alpha-1 receptors on arterioles, allowing for a normal response to angiotensin II and catecholamines. However, it inhibits bone formation by decreasing osteoblasts, type 1 collagen, and absorption of calcium from the gut, while increasing osteoclastic activity. Cortisol also increases insulin resistance and metabolism by increasing gluconeogenesis, lipolysis, and proteolysis. It inhibits inflammatory and immune responses, but maintains the function of skeletal and cardiac muscle.
The regulation of cortisol secretion is controlled by the hypothalamic-pituitary-adrenal (HPA) axis. The pituitary gland secretes adrenocorticotropic hormone (ACTH), which stimulates the adrenal cortex to produce cortisol. The hypothalamus releases corticotrophin-releasing hormone (CRH), which stimulates the pituitary gland to release ACTH. Stress can also increase cortisol secretion.
Excess cortisol in the body can lead to Cushing’s syndrome, which can cause a range of symptoms such as weight gain, muscle weakness, and high blood pressure. Understanding the functions and regulation of cortisol is important for maintaining overall health and preventing hormonal imbalances.
-
This question is part of the following fields:
- Endocrine System
-
-
Question 15
Correct
-
A 70-year-old man with chronic back pain and renal failure presents with the following blood test results:
Reference range
Ca2+ 2.10 2.15-2.55 mmol/l
Parathyroid hormone 9.8 1-6.5 pmol/l
Phosphate 0.75 0.6-1.25 mmol/l
What is the probable diagnosis?Your Answer: Secondary hyperparathyroidism
Explanation:Secondary hyperparathyroidism is characterized by elevated levels of PTH, while calcium levels are either normal or low. This condition occurs due to the parathyroid glands’ hyperplasia in response to chronic hypocalcemia or hyperphosphatemia, which is a natural physiological reaction. The body releases calcium from the kidneys, gastrointestinal system, and bones.
Parathyroid Glands and Disorders of Calcium Metabolism
The parathyroid glands play a crucial role in regulating calcium levels in the body. Hyperparathyroidism is a disorder that occurs when these glands produce too much parathyroid hormone (PTH), leading to abnormal calcium metabolism. Primary hyperparathyroidism is the most common form and is usually caused by a solitary adenoma. Secondary hyperparathyroidism occurs as a result of low calcium levels, often in the setting of chronic renal failure. Tertiary hyperparathyroidism is a rare condition that occurs when hyperplasia of the parathyroid glands persists after correction of underlying renal disorder.
Diagnosis of hyperparathyroidism is based on hormone profiles and clinical features. Treatment options vary depending on the type and severity of the disorder. Surgery is usually indicated for primary hyperparathyroidism if certain criteria are met, such as elevated serum calcium levels, hypercalciuria, and nephrolithiasis. Secondary hyperparathyroidism is typically managed with medical therapy, while surgery may be necessary for persistent symptoms such as bone pain and soft tissue calcifications. Tertiary hyperparathyroidism may resolve on its own within a year after transplant, but surgery may be required if an autonomously functioning parathyroid gland is present. It is important to consider differential diagnoses, such as benign familial hypocalciuric hypercalcaemia, which is a rare but relatively benign condition.
-
This question is part of the following fields:
- Endocrine System
-
-
Question 16
Incorrect
-
A 55-year-old woman comes to her doctor complaining of fatigue, difficulty passing stool, and muscle weakness. Her lab results show:
Free T4 6 pmol/l (9-18 pmol/l)
TSH 7.2 mu/l (0.5-5.5 mu/l)
Based on the probable diagnosis, which of the following tests is most likely to be positive in this patient?Your Answer: Anti-TSH antibodies
Correct Answer: Anti-thyroid peroxidase (anti-TPO) antibodies
Explanation:Rheumatoid factor is not the most suitable answer for a patient with hypothyroidism, despite its presence in various rheumatological conditions and healthy individuals.
Understanding Thyroid Autoantibodies
Thyroid autoantibodies are antibodies that attack the thyroid gland, causing various thyroid disorders. There are three main types of anti-thyroid autoantibodies: anti-thyroid peroxidase (anti-TPO) antibodies, TSH receptor antibodies, and thyroglobulin antibodies. Anti-TPO antibodies are present in 90% of Hashimoto’s thyroiditis cases and 75% of Graves’ disease cases. TSH receptor antibodies are found in 90-100% of Graves’ disease cases. Thyroglobulin antibodies are present in 70% of Hashimoto’s thyroiditis cases, 30% of Graves’ disease cases, and a small proportion of thyroid cancer cases.
Understanding the different types of thyroid autoantibodies is important in diagnosing and treating thyroid disorders. Hashimoto’s thyroiditis and Graves’ disease are the most common autoimmune thyroid disorders, and the presence of specific autoantibodies can help differentiate between the two. Additionally, monitoring the levels of these antibodies can help track the progression of the disease and the effectiveness of treatment. Overall, understanding thyroid autoantibodies is crucial in managing thyroid health.
-
This question is part of the following fields:
- Endocrine System
-
-
Question 17
Correct
-
A 32-year-old man has been admitted to the emergency department with severe hypocalcaemia that has not responded to calcium replacement therapy. What other serum electrolytes should be checked urgently?
Your Answer: Magnesium
Explanation:If a person has hypomagnesaemia, it can lead to hypocalcaemia and make it difficult to treat. Therefore, when dealing with hypocalcaemia, it is important to keep an eye on the levels of calcium, phosphate, and magnesium. The phosphate levels can provide insight into potential causes, as low calcium levels combined with high phosphate levels may indicate hypoparathyroidism.
The Importance of Magnesium and Calcium in the Body
Magnesium and calcium are essential minerals in the body. Magnesium plays a crucial role in the secretion and action of parathyroid hormone (PTH) on target tissues. However, a deficiency in magnesium can cause hypocalcaemia and make patients unresponsive to calcium and vitamin D supplementation.
The body contains 1000 mmol of magnesium, with half stored in bones and the rest in muscle, soft tissues, and extracellular fluid. Unlike calcium, there is no specific hormonal control of magnesium. Hormones such as PTH and aldosterone affect the renal handling of magnesium.
Magnesium and calcium also interact at a cellular level. A decrease in magnesium levels can affect the permeability of cellular membranes to calcium, leading to hyperexcitability. Therefore, it is essential to maintain adequate levels of both magnesium and calcium in the body for optimal health.
-
This question is part of the following fields:
- Endocrine System
-
-
Question 18
Incorrect
-
A 28-year-old female patient presents to her GP with concerns about the appearance of lumps in her lower abdomen. She has been diagnosed with type 1 diabetes and has been using insulin for more than a decade. The lumps have developed in the areas where she administers her insulin injections.
What is the probable cause of the lumps?Your Answer: Lipoma
Correct Answer: Lipodystrophy
Explanation:Small subcutaneous lumps at injection sites, known as lipodystrophy, can be caused by insulin.
The type and location of the lump suggest that lipodystrophy is the most probable cause.
Deposits of insulin and glucose are not responsible for the formation of these lumps.
While a lipoma could also cause similar lumps, it is less likely than lipodystrophy, which is a known complication of insulin injections, especially at the injection site. These lumps can occur in multiple locations.
Insulin therapy can have side-effects that patients should be aware of. One of the most common side-effects is hypoglycaemia, which can cause sweating, anxiety, blurred vision, confusion, and aggression. Patients should be taught to recognize these symptoms and take 10-20g of a short-acting carbohydrate, such as a glass of Lucozade or non-diet drink, three or more glucose tablets, or glucose gel. It is also important for every person treated with insulin to have a glucagon kit for emergencies where the patient is not able to orally ingest a short-acting carbohydrate. Patients who have frequent hypoglycaemic episodes may develop reduced awareness, and beta-blockers can further reduce hypoglycaemic awareness.
Another potential side-effect of insulin therapy is lipodystrophy, which typically presents as atrophy or lumps of subcutaneous fat. This can be prevented by rotating the injection site, as using the same site repeatedly can cause erratic insulin absorption. It is important for patients to be aware of these potential side-effects and to discuss any concerns with their healthcare provider. By monitoring their blood sugar levels and following their treatment plan, patients can manage the risks associated with insulin therapy and maintain good health.
-
This question is part of the following fields:
- Endocrine System
-
-
Question 19
Correct
-
A 23-year-old woman presents with clinical manifestations of hyperthyroidism and is diagnosed with Graves disease. What is the most appropriate explanation for the pathophysiology of this condition?
Your Answer: Formation of IgG antibodies to the TSH receptors on the thyroid gland
Explanation:Graves disease typically results in the formation of IgG antibodies that target the TSH receptors located on the thyroid gland, leading to a significant decrease in TSH levels.
Thyroid Hormones and LATS in Graves Disease
Thyroid hormones are produced by the thyroid gland and include triiodothyronine (T3) and thyroxine (T4), with T3 being the major hormone active in target cells. The synthesis and secretion of these hormones involves the active concentration of iodide by the thyroid, which is then oxidized and iodinated by peroxidase in the follicular cells. This process is stimulated by thyroid-stimulating hormone (TSH), which is released by the pituitary gland. The normal thyroid has approximately three months’ worth of reserves of thyroid hormones.
In Graves disease, patients develop IgG antibodies to the TSH receptors on the thyroid gland. This results in chronic and long-term stimulation of the gland with the release of thyroid hormones. As a result, individuals with Graves disease typically have raised thyroid hormones and low TSH levels. It is important to check for thyroid receptor autoantibodies in individuals presenting with hyperthyroidism, as they are present in up to 85% of cases. This condition is known as LATS (long-acting thyroid stimulator) and can lead to a range of symptoms and complications if left untreated.
-
This question is part of the following fields:
- Endocrine System
-
-
Question 20
Correct
-
A 33-year-old woman with a history of coeliac disease presents to the emergency department with palpitations, diaphoresis, and tremors. Upon examination, her vital signs reveal a heart rate of 110 bpm and respiratory rate of 24 per min. She displays hand tremors, bulging eyeballs, and diffuse swelling in her neck. Her blood tests show:
TSH 0.1 mU/l
Free T4 32.5 pmol/l
Free T3 12.5 pmol/l
What is the most probable underlying pathophysiology in this patient?Your Answer: Antibodies to TSH receptors
Explanation:Graves’ disease is the most probable cause of thyrotoxicosis in a middle-aged woman, particularly if she exhibits exophthalmos. This autoimmune disorder is characterised by the presence of antibodies to the thyroid stimulating hormone (TSH) receptors.
Graves’ Disease: Common Features and Unique Signs
Graves’ disease is the most frequent cause of thyrotoxicosis, which is commonly observed in women aged 30-50 years. The condition presents typical features of thyrotoxicosis, such as weight loss, palpitations, and heat intolerance. However, Graves’ disease also displays specific signs that are not present in other causes of thyrotoxicosis. These include eye signs, such as exophthalmos and ophthalmoplegia, as well as pretibial myxoedema and thyroid acropachy. The latter is a triad of digital clubbing, soft tissue swelling of the hands and feet, and periosteal new bone formation.
Graves’ disease is characterized by the presence of autoantibodies, including TSH receptor stimulating antibodies in 90% of patients and anti-thyroid peroxidase antibodies in 75% of patients. Thyroid scintigraphy reveals a diffuse, homogenous, and increased uptake of radioactive iodine. These features help distinguish Graves’ disease from other causes of thyrotoxicosis and aid in its diagnosis.
-
This question is part of the following fields:
- Endocrine System
-
00
Correct
00
Incorrect
00
:
00
:
00
Session Time
00
:
00
Average Question Time (
Mins)