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Question 1
Incorrect
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A 47-year-old man is under the care of an ophthalmologist for open angle glaucoma. He visits his GP to express his worries about the medication prescribed after reading online information. What is the medication that the ophthalmologist has prescribed, which can function as a diuretic by acting on the proximal convoluted tubule of the kidney?
Your Answer: Mannitol (osmotic diuretic)
Correct Answer: Acetazolamide (carbonic anhydrase inhibitor)
Explanation:Diuretic drugs are classified into three major categories based on the location where they inhibit sodium reabsorption. Loop diuretics act on the thick ascending loop of Henle, thiazide diuretics on the distal tubule and connecting segment, and potassium sparing diuretics on the aldosterone-sensitive principal cells in the cortical collecting tubule. Sodium is reabsorbed in the kidney through Na+/K+ ATPase pumps located on the basolateral membrane, which return reabsorbed sodium to the circulation and maintain low intracellular sodium levels. This ensures a constant concentration gradient.
The physiological effects of commonly used diuretics vary based on their site of action. furosemide, a loop diuretic, inhibits the Na+/K+/2Cl- carrier in the ascending limb of the loop of Henle and can result in up to 25% of filtered sodium being excreted. Thiazide diuretics, which act on the distal tubule and connecting segment, inhibit the Na+Cl- carrier and typically result in between 3 and 5% of filtered sodium being excreted. Finally, spironolactone, a potassium sparing diuretic, inhibits the Na+/K+ ATPase pump in the cortical collecting tubule and typically results in between 1 and 2% of filtered sodium being excreted.
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This question is part of the following fields:
- Renal System
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Question 2
Incorrect
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A 54-year-old man visits the outpatient clinic complaining of feeling generally unwell with increased diarrhoea and vomiting for the past week. He has a medical history of hypertension and type 2 diabetes mellitus and is currently taking amlodipine, candesartan, doxazosin, metformin, gliclazide, and insulin.
The following investigations were conducted:
Results today 3 months ago Reference ranges
Na+ 137 mmol/L 133 mmol/L (135 - 145)
K+ 6.1 mmol/L 3.6 mmol/L (3.5 - 5.0)
Urea 8.9 mmol/L 4.5 mmol/L (2.0 - 7.0)
Creatinine 155 µmol/L 65 µmol/L (55 - 120)
eGFR 35 mL/min/1.73m² 90 mL/min/1.73m² (> 60)
Which medication should be discontinued?Your Answer: Gliclazide
Correct Answer: Candesartan
Explanation:In cases of acute kidney injury, it is important to identify and treat the underlying cause while preventing further deterioration. However, certain medications must be discontinued, including angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, NSAIDs, and diuretics. Therefore, candesartan, an angiotensin receptor blocker, should be stopped in this patient. On the other hand, amlodipine, a calcium channel blocker, and doxazosin, an alpha antagonist, are safe to continue in patients with acute kidney injury.
Acute kidney injury (AKI) is a condition where there is a reduction in renal function following an insult to the kidneys. It was previously known as acute renal failure and can result in long-term impaired kidney function or even death. AKI can be caused by prerenal, intrinsic, or postrenal factors. Patients with chronic kidney disease, other organ failure/chronic disease, a history of AKI, or who have used drugs with nephrotoxic potential are at an increased risk of developing AKI. To prevent AKI, patients at risk may be given IV fluids or have certain medications temporarily stopped.
The kidneys are responsible for maintaining fluid balance and homeostasis, so a reduced urine output or fluid overload may indicate AKI. Symptoms may not be present in early stages, but as renal failure progresses, patients may experience arrhythmias, pulmonary and peripheral edema, or features of uraemia. Blood tests such as urea and electrolytes can be used to detect AKI, and urinalysis and imaging may also be necessary.
Management of AKI is largely supportive, with careful fluid balance and medication review. Loop diuretics and low-dose dopamine are not recommended, but hyperkalaemia needs prompt treatment to avoid life-threatening arrhythmias. Renal replacement therapy may be necessary in severe cases. Patients with suspected AKI secondary to urinary obstruction require prompt review by a urologist, and specialist input from a nephrologist is required for cases where the cause is unknown or the AKI is severe.
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This question is part of the following fields:
- Renal System
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Question 3
Incorrect
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You are requested to evaluate a 2-day-old infant in the neonatal unit following an abnormal newborn physical examination. The doctor conducting the examination encountered difficulty in palpating the testicles and documented ambiguous genitalia.
Subsequent investigations indicate an elevated level of 17-hydroxyprogesterone, which is linked to a deficiency in an enzyme responsible for converting progesterone to 11-deoxycorticosterone.
What is the name of the deficient enzyme in this newborn?Your Answer:
Correct Answer: 21-hydroxylase
Explanation:The renin-angiotensin-aldosterone system is a complex system that regulates blood pressure and fluid balance in the body. The adrenal cortex is divided into three zones, each producing different hormones. The zona glomerulosa produces mineralocorticoids, mainly aldosterone, which helps regulate sodium and potassium levels in the body. Renin is an enzyme released by the renal juxtaglomerular cells in response to reduced renal perfusion, hyponatremia, and sympathetic nerve stimulation. It hydrolyses angiotensinogen to form angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme in the lungs. Angiotensin II has various actions, including causing vasoconstriction, stimulating thirst, and increasing proximal tubule Na+/H+ activity. It also stimulates aldosterone and ADH release, which causes retention of Na+ in exchange for K+/H+ in the distal tubule.
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This question is part of the following fields:
- Renal System
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Question 4
Incorrect
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A 51-year-old man comes to the clinic to discuss the findings of his ambulatory blood pressure test, which revealed an average blood pressure of 156/94mmHg. As a first-line treatment for hypertension in this age group, you suggest starting him on ACE inhibitors. These medications work by inhibiting the activity of angiotensin-converting-enzyme. What is the primary location of angiotensin-converting-enzyme in the body?
Your Answer:
Correct Answer: Lungs
Explanation:The lungs contain the majority of angiotensin-converting-enzyme, with smaller amounts found in endothelial cells of the vasculature and kidney epithelial cells. Its role in the renin-angiotensin-aldosterone system involves converting angiotensin I to angiotensin II.
Aldosterone, produced in the zona glomerulosa of the adrenal cortex, is a crucial compound in the renin-angiotensin-aldosterone system. Angiotensinogen, the precursor to angiotensin I, is produced in the liver and converted by renin, which is produced in the juxtaglomerular cells of the kidneys.
The pancreas does not play a role in the renin-angiotensin-aldosterone system, but produces and releases insulin and glucagon among other hormones. Based on the World Health Organisation classification of hypertension, the patient in the question has mild hypertension. Current NICE guidelines recommend lifestyle advice and ACE inhibitors for patients under 55 years old with mild hypertension.
The renin-angiotensin-aldosterone system is a complex system that regulates blood pressure and fluid balance in the body. The adrenal cortex is divided into three zones, each producing different hormones. The zona glomerulosa produces mineralocorticoids, mainly aldosterone, which helps regulate sodium and potassium levels in the body. Renin is an enzyme released by the renal juxtaglomerular cells in response to reduced renal perfusion, hyponatremia, and sympathetic nerve stimulation. It hydrolyses angiotensinogen to form angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme in the lungs. Angiotensin II has various actions, including causing vasoconstriction, stimulating thirst, and increasing proximal tubule Na+/H+ activity. It also stimulates aldosterone and ADH release, which causes retention of Na+ in exchange for K+/H+ in the distal tubule.
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This question is part of the following fields:
- Renal System
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Question 5
Incorrect
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At which of the following locations is the highest amount of water absorbed?
Your Answer:
Correct Answer: Jejunum
Explanation:The small bowel, specifically the jejunum and ileum, is the primary location for water absorption in the gastrointestinal tract. While the colon does play a role in water absorption, its contribution is minor in comparison. However, if there is a significant removal of the small bowel, the importance of the colon in water absorption may become more significant.
Water Absorption in the Human Body
Water absorption in the human body is a crucial process that occurs in the small bowel and colon. On average, a person ingests up to 2000ml of liquid orally within a 24-hour period. Additionally, gastrointestinal secretions contribute to a further 8000ml of fluid entering the small bowel. The process of intestinal water absorption is passive and is dependent on the solute load. In the jejunum, the active absorption of glucose and amino acids creates a concentration gradient that facilitates the flow of water across the membrane. On the other hand, in the ileum, most water is absorbed through facilitated diffusion, which involves the movement of water molecules with sodium ions.
The colon also plays a significant role in water absorption, with approximately 150ml of water entering it daily. However, the colon can adapt and increase this amount following resection. Overall, water absorption is a complex process that involves various mechanisms and is essential for maintaining proper hydration levels in the body.
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This question is part of the following fields:
- Renal System
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Question 6
Incorrect
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A 40-year-old man visits his doctor for a routine check-up and is informed that his cholesterol levels are elevated. He has a significant family history of high cholesterol and genetic testing reveals that he is heterozygous for the affected allele. If he has a child with a woman who does not carry the affected allele, what is the probability that their child will inherit the condition?
Your Answer:
Correct Answer: 50%
Explanation:Familial Hypercholesterolaemia: Causes, Diagnosis, and Management
Familial hypercholesterolaemia (FH) is a genetic condition that affects approximately 1 in 500 people. It is an autosomal dominant disorder that results in high levels of LDL-cholesterol, which can lead to early cardiovascular disease if left untreated. FH is caused by mutations in the gene that encodes the LDL-receptor protein.
To diagnose FH, NICE recommends suspecting it as a possible diagnosis in adults with a total cholesterol level greater than 7.5 mmol/l and/or a personal or family history of premature coronary heart disease. For children of affected parents, testing should be arranged by age 10 if one parent is affected and by age 5 if both parents are affected.
The Simon Broome criteria are used for clinical diagnosis, which includes a total cholesterol level greater than 7.5 mmol/l and LDL-C greater than 4.9 mmol/l in adults or a total cholesterol level greater than 6.7 mmol/l and LDL-C greater than 4.0 mmol/l in children. Definite FH is diagnosed if there is tendon xanthoma in patients or first or second-degree relatives or DNA-based evidence of FH. Possible FH is diagnosed if there is a family history of myocardial infarction below age 50 years in second-degree relatives, below age 60 in first-degree relatives, or a family history of raised cholesterol levels.
Management of FH involves referral to a specialist lipid clinic and the use of high-dose statins as first-line treatment. CVD risk estimation using standard tables is not appropriate in FH as they do not accurately reflect the risk of CVD. First-degree relatives have a 50% chance of having the disorder and should be offered screening, including children who should be screened by the age of 10 years if there is one affected parent. Statins should be discontinued in women 3 months before conception due to the risk of congenital defects.
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This question is part of the following fields:
- Renal System
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Question 7
Incorrect
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A 28-year-old rugby player complains of polyuria and polydipsia. He reports being hospitalized 5 months ago due to a head injury sustained while playing rugby. Central diabetes insipidus is confirmed through biochemistry and a water-deprivation test. A pituitary MRI reveals a thickened pituitary stalk, supporting the diagnosis. What is the appropriate medication for this patient?
Your Answer:
Correct Answer: Desmopressin
Explanation:Desmopressin is an effective treatment for central diabetes insipidus, which is a rare condition caused by damage or dysfunction of the posterior pituitary gland resulting in a lack of ADH production. Carbimazole is used to treat hyperthyroidism, while goserelin is used to treat prostate cancer. Indapamide, a thiazide-like diuretic, is used to manage hypertension and heart failure.
Diabetes insipidus is a medical condition that can be caused by either a decreased secretion of antidiuretic hormone (ADH) from the pituitary gland (cranial DI) or an insensitivity to ADH (nephrogenic DI). Cranial DI can be caused by various factors such as head injury, pituitary surgery, and infiltrative diseases like sarcoidosis. On the other hand, nephrogenic DI can be caused by genetic factors, electrolyte imbalances, and certain medications like lithium and demeclocycline. The common symptoms of DI are excessive urination and thirst. Diagnosis is made through a water deprivation test and checking the osmolality of the urine. Treatment options include thiazides and a low salt/protein diet for nephrogenic DI, while central DI can be treated with desmopressin.
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This question is part of the following fields:
- Renal System
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Question 8
Incorrect
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Sarah, who is in her 50s, has recently undergone a kidney transplant. A few hours after the surgery, she begins to feel extremely sick, experiencing a fever of 39°C and overall discomfort. She also reports pain at the site of the transplant, and the medical staff have noted a significant decrease in her urine output. The consultant suggests that this could be due to pre-existing antibodies, given the timing of the symptoms.
What is the most probable diagnosis in Sarah's case?Your Answer:
Correct Answer: Hyperacute transplant rejection
Explanation:Based on the symptoms and timeframe, it is likely that the patient is experiencing hyperacute transplant rejection. This type of rejection is classified as a type II hypersensitivity reaction, which occurs when pre-existing IgG or IgM antibodies attack HLA or ABO antigens. This autoimmune response causes thrombosis in the vascular supply to the transplanted organ, leading to ischemia and necrosis. Unfortunately, the only treatment option is to remove the graft.
Acute graft failure, on the other hand, typically occurs over several months and is often caused by HLA mismatch. This condition can be treated with immunosuppressants and steroids.
Chronic graft failure is characterized by antibody- and cell-mediated mechanisms that lead to fibrosis of the transplanted organ over time. This process usually takes more than six months to develop.
Post-transplant acute tubular necrosis is another possible complication that can cause reduced urine output and muddy brown casts on urinalysis. However, it does not typically present with the hyperacute symptoms described above.
Lymphocele is a common post-transplant complication that is usually asymptomatic but can cause a mass and compress the ureter if it becomes large enough. It can be drained through percutaneous or intraperitoneal methods.
The HLA system, also known as the major histocompatibility complex (MHC), is located on chromosome 6 and is responsible for human leucocyte antigens. Class 1 antigens include A, B, and C, while class 2 antigens include DP, DQ, and DR. When matching for a renal transplant, the importance of HLA antigens is ranked as DR > B > A.
Graft survival rates for renal transplants are high, with a 90% survival rate at one year and a 60% survival rate at ten years for cadaveric transplants. Living-donor transplants have even higher survival rates, with a 95% survival rate at one year and a 70% survival rate at ten years. However, postoperative problems can occur, such as acute tubular necrosis of the graft, vascular thrombosis, urine leakage, and urinary tract infections.
Hyperacute rejection can occur within minutes to hours after a transplant and is caused by pre-existing antibodies against ABO or HLA antigens. This type of rejection is an example of a type II hypersensitivity reaction and leads to widespread thrombosis of graft vessels, resulting in ischemia and necrosis of the transplanted organ. Unfortunately, there is no treatment available for hyperacute rejection, and the graft must be removed.
Acute graft failure, which occurs within six months of a transplant, is usually due to mismatched HLA and is caused by cell-mediated cytotoxic T cells. This type of failure is usually asymptomatic and is detected by a rising creatinine, pyuria, and proteinuria. Other causes of acute graft failure include cytomegalovirus infection, but it may be reversible with steroids and immunosuppressants.
Chronic graft failure, which occurs after six months of a transplant, is caused by both antibody and cell-mediated mechanisms that lead to fibrosis of the transplanted kidney, known as chronic allograft nephropathy. The recurrence of the original renal disease, such as MCGN, IgA, or FSGS, can also cause chronic graft failure.
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This question is part of the following fields:
- Renal System
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Question 9
Incorrect
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A 45-year-old patient presents to the clinic with complaints of abdominal pain. Upon routine blood tests, the following results were obtained:
Na+ 142 mmol/l
K+ 4.0 mmol/l
Chloride 104 mmol/l
Bicarbonate 19 mmol/l
Urea 7.0 mmol/l
Creatinine 112 µmol/l
What is the calculated anion gap?Your Answer:
Correct Answer: 23 mmol/L
Explanation:Understanding Anion Gap in Metabolic Acidosis
Metabolic acidosis is a condition where the body produces too much acid or loses too much bicarbonate. Anion gap is a useful tool in diagnosing metabolic acidosis. It is calculated by subtracting the sum of bicarbonate and chloride from the sum of sodium and potassium. A normal anion gap is between 8-14 mmol/L.
There are two types of metabolic acidosis: normal anion gap and raised anion gap. Normal anion gap or hyperchloraemic metabolic acidosis can be caused by gastrointestinal bicarbonate loss, renal tubular acidosis, drugs like acetazolamide, ammonium chloride injection, and Addison’s disease. On the other hand, raised anion gap metabolic acidosis can be caused by lactate due to shock or hypoxia, ketones in diabetic ketoacidosis or alcohol, urate in renal failure, acid poisoning from salicylates or methanol, and 5-oxoproline from chronic paracetamol use.
Understanding anion gap in metabolic acidosis is crucial in identifying the underlying cause of the condition. It helps healthcare professionals in providing appropriate treatment and management to patients.
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This question is part of the following fields:
- Renal System
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Question 10
Incorrect
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A 70-year-old man visits the endocrinology clinic complaining of muscle cramps, headaches, and lethargy. During the clinic visit, his vital signs are heart rate 80/min, respiratory rate 18/min, blood pressure 150/100 mmHg, temperature 36.5ºC, and saturations 99% on air. Recent blood tests reveal:
- Na+ 147 mmol/L (135 - 145)
- K+ 3.2 mmol/L (3.5 - 5.0)
- Bicarbonate 28 mmol/L (22 - 29)
- Urea 6.0 mmol/L (2.0 - 7.0)
- Creatinine 95 µmol/L (55 - 120)
An adrenal mass is detected on his abdominal CT scan. Can you identify where the hormone responsible for his symptoms is produced?Your Answer:
Correct Answer: Zona glomerulosa
Explanation:The correct answer is the zona glomerulosa. This patient is experiencing symptoms of hyperaldosteronism, which is likely caused by an adenoma in the zona glomerulosa, as indicated by the mass seen on CT scan (also known as Conn’s syndrome). The adenoma stimulates the production of aldosterone, leading to hypertension and hypokalemia.
The adrenal medulla produces catecholamines, such as adrenaline and noradrenaline.
The juxtaglomerular apparatus is located in the kidney and produces renin in response to decreased renal perfusion.
The zona fasciculata is the middle layer of the adrenal cortex and is responsible for producing glucocorticoids, such as cortisol.
The zona reticularis is the innermost layer of the adrenal cortex and produces androgens, such as dehydroepiandrosterone (DHEA).
The renin-angiotensin-aldosterone system is a complex system that regulates blood pressure and fluid balance in the body. The adrenal cortex is divided into three zones, each producing different hormones. The zona glomerulosa produces mineralocorticoids, mainly aldosterone, which helps regulate sodium and potassium levels in the body. Renin is an enzyme released by the renal juxtaglomerular cells in response to reduced renal perfusion, hyponatremia, and sympathetic nerve stimulation. It hydrolyses angiotensinogen to form angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme in the lungs. Angiotensin II has various actions, including causing vasoconstriction, stimulating thirst, and increasing proximal tubule Na+/H+ activity. It also stimulates aldosterone and ADH release, which causes retention of Na+ in exchange for K+/H+ in the distal tubule.
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This question is part of the following fields:
- Renal System
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Question 11
Incorrect
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You have been requested to evaluate a patient in the endocrinology clinic who is postmenopausal and has presented with generalized hair thinning on the scalp, changes in the tone of her voice, and troublesome acne on her back and upper chest. The patient's serum testosterone is within the normal range, but FSH and LH are elevated, consistent with her postmenopausal status. However, her serum levels of dehydroepiandrosterone (DHEA) are above the normal range, prompting a CT scan that reveals a 4 cm mass in the left adrenal gland.
Based on the blood results, which part of the adrenal gland is the tumor most likely to originate from?Your Answer:
Correct Answer: Zona reticularis
Explanation:A tumor in the zona reticularis of the adrenal cortex is causing excessive production of dehydroepiandrosterone (DHEA), an androgen hormone that can be converted into testosterone. This can lead to hyper-androgenic effects such as hirsutism, deepening of the voice, and increased libido. The zona glomerulosa and zona fasciculata are other areas of the adrenal cortex that produce aldosterone and cortisol respectively. The adrenal medulla produces catecholamines such as adrenaline and noradrenaline. The adrenal gland is supplied by the superior, middle, and inferior adrenal arteries, which are not involved in hormone production. A useful mnemonic for remembering which section of the cortex produces which hormones is GFR – ACD.
The renin-angiotensin-aldosterone system is a complex system that regulates blood pressure and fluid balance in the body. The adrenal cortex is divided into three zones, each producing different hormones. The zona glomerulosa produces mineralocorticoids, mainly aldosterone, which helps regulate sodium and potassium levels in the body. Renin is an enzyme released by the renal juxtaglomerular cells in response to reduced renal perfusion, hyponatremia, and sympathetic nerve stimulation. It hydrolyses angiotensinogen to form angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme in the lungs. Angiotensin II has various actions, including causing vasoconstriction, stimulating thirst, and increasing proximal tubule Na+/H+ activity. It also stimulates aldosterone and ADH release, which causes retention of Na+ in exchange for K+/H+ in the distal tubule.
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This question is part of the following fields:
- Renal System
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Question 12
Incorrect
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A 24-year-old male patient visits his GP after observing swelling in his legs. He mentions that his urine has turned frothy. Upon conducting blood tests, the doctor discovers elevated cholesterol levels and reduced albumin.
What type of electrolyte imbalances should the GP anticipate in this individual?Your Answer:
Correct Answer: Hypervolaemic hyponatraemia
Explanation:Hypervolaemic hyponatraemia can be caused by nephrotic syndrome.
Nephrotic syndrome is characterized by oedema, proteinuria, hypercholesterolaemia, and hypoalbuminaemia. It results in fluid retention, which can lead to hypervolaemic hyponatraemia. Urinary sodium levels would not show an increase if tested.
Understanding Hyponatraemia: Causes and Diagnosis
Hyponatraemia is a condition that can be caused by either an excess of water or a depletion of sodium in the body. However, it is important to note that there are also cases of pseudohyponatraemia, which can be caused by factors such as hyperlipidaemia or taking blood from a drip arm. To diagnose hyponatraemia, doctors often look at the levels of urinary sodium and osmolarity.
If the urinary sodium level is above 20 mmol/l, it may indicate sodium depletion due to renal loss or the use of diuretics such as thiazides or loop diuretics. Other possible causes include Addison’s disease or the diuretic stage of renal failure. On the other hand, if the patient is euvolaemic, it may be due to conditions such as SIADH (urine osmolality > 500 mmol/kg) or hypothyroidism.
If the urinary sodium level is below 20 mmol/l, it may indicate sodium depletion due to extrarenal loss caused by conditions such as diarrhoea, vomiting, sweating, burns, or adenoma of rectum. Alternatively, it may be due to water excess, which can cause the patient to be hypervolaemic and oedematous. This can be caused by conditions such as secondary hyperaldosteronism, nephrotic syndrome, IV dextrose, or psychogenic polydipsia.
In summary, hyponatraemia can be caused by a variety of factors, and it is important to diagnose the underlying cause in order to provide appropriate treatment. By looking at the levels of urinary sodium and osmolarity, doctors can determine the cause of hyponatraemia and provide the necessary interventions.
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This question is part of the following fields:
- Renal System
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Question 13
Incorrect
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A 35-year-old female patient complains of chronic flank pain. Her family history reveals a brother with similar symptoms and a mother who died from a subarachnoid haemorrhage. Bilateral renal ultrasound shows multiple cysts. Which chromosome is most likely to be affected in this genetic disorder?
Your Answer:
Correct Answer: 16
Explanation:Autosomal dominant polycystic kidney disease (ADPKD) is a commonly inherited kidney disease that affects 1 in 1,000 Caucasians. The disease is caused by mutations in two genes, PKD1 and PKD2, which produce polycystin-1 and polycystin-2 respectively. ADPKD type 1 accounts for 85% of cases, while ADPKD type 2 accounts for 15% of cases. ADPKD type 1 is caused by a mutation in the PKD1 gene on chromosome 16, while ADPKD type 2 is caused by a mutation in the PKD2 gene on chromosome 4. ADPKD type 1 tends to present with renal failure earlier than ADPKD type 2.
To screen for ADPKD in relatives of affected individuals, an abdominal ultrasound is recommended. The diagnostic criteria for ultrasound include the presence of two cysts, either unilateral or bilateral, if the individual is under 30 years old. If the individual is between 30-59 years old, two cysts in both kidneys are required for diagnosis. If the individual is over 60 years old, four cysts in both kidneys are necessary for diagnosis.
For some patients with ADPKD, tolvaptan, a vasopressin receptor 2 antagonist, may be an option to slow the progression of cyst development and renal insufficiency. However, NICE recommends tolvaptan only for adults with ADPKD who have chronic kidney disease stage 2 or 3 at the start of treatment, evidence of rapidly progressing disease, and if the company provides it with the agreed discount in the patient access scheme.
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This question is part of the following fields:
- Renal System
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Question 14
Incorrect
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A 32-year-old single mum has been recommended for genetic testing after her 10-months-old daughter was diagnosed with congenital nephrogenic diabetes insipidus. She has no symptoms and does not know of any family history of this disorder.
Which part of the kidney is frequently impacted in this condition?Your Answer:
Correct Answer: Vasopressin receptor
Explanation:Diabetes insipidus is a medical condition that can be caused by either a decreased secretion of antidiuretic hormone (ADH) from the pituitary gland (cranial DI) or an insensitivity to ADH (nephrogenic DI). Cranial DI can be caused by various factors such as head injury, pituitary surgery, and infiltrative diseases like sarcoidosis. On the other hand, nephrogenic DI can be caused by genetic factors, electrolyte imbalances, and certain medications like lithium and demeclocycline. The common symptoms of DI are excessive urination and thirst. Diagnosis is made through a water deprivation test and checking the osmolality of the urine. Treatment options include thiazides and a low salt/protein diet for nephrogenic DI, while central DI can be treated with desmopressin.
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This question is part of the following fields:
- Renal System
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Question 15
Incorrect
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A 20-year-old man is brought to the Emergency Department in an unconscious state, lying in a pool of blood with several stab wounds in his abdomen. How does the physiological compensatory mechanism differ in the short-term for a venous bleed versus an arterial bleed?
Your Answer:
Correct Answer: A venous bleed causes reduced preload before reducing blood pressure and being detected by baroreceptors whilst an arterial bleed causes an instant blood pressure drop
Explanation:A venous bleed is compensated for in a less direct manner compared to an arterial bleed. The reduction in preload caused by a venous bleed results in a decrease in cardiac output and subsequently, blood pressure. Baroreceptors detect this drop in blood pressure and trigger a physiological compensation response.
In contrast, an arterial bleed causes an immediate drop in blood pressure, which is detected directly by baroreceptors.
Both types of bleeding result in increased levels of angiotensin II and a heightened thirst drive. However, these compensatory mechanisms take longer to take effect than the immediate response triggered by baroreceptors.
Understanding Bleeding and its Effects on the Body
Bleeding, even if it is of a small volume, triggers a response in the body that causes generalised splanchnic vasoconstriction. This response is mediated by the activation of the sympathetic nervous system. The process of vasoconstriction is usually enough to maintain renal perfusion and cardiac output if the volume of blood lost is small. However, if greater volumes of blood are lost, the renin angiotensin system is activated, resulting in haemorrhagic shock.
The body’s physiological measures can restore circulating volume if the source of bleeding ceases. Ongoing bleeding, on the other hand, will result in haemorrhagic shock. Blood loss is typically quantified by the degree of shock produced, which is determined by parameters such as blood loss volume, pulse rate, blood pressure, respiratory rate, urine output, and symptoms. Understanding the effects of bleeding on the body is crucial in managing and treating patients who experience blood loss.
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This question is part of the following fields:
- Renal System
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Question 16
Incorrect
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A 70-year-old male was admitted to the hospital due to delirium observed in the nursing home. Upon diagnosis, he was found to have a lower respiratory tract infection which progressed to sepsis. During his stay in the ICU, he was discovered to have severe hyponatremia. The medical team has prescribed tolvaptan along with other medications.
What is the mechanism of action of tolvaptan?Your Answer:
Correct Answer: Vasopressin V2 receptor antagonist
Explanation:Tolvaptan is a drug that blocks the action of vasopressin at the V2 receptor, which reduces water absorption and increases aquaresis without sodium loss. Vasopressin is a hormone that regulates water balance in the body.
Autosomal dominant polycystic kidney disease (ADPKD) is a commonly inherited kidney disease that affects 1 in 1,000 Caucasians. The disease is caused by mutations in two genes, PKD1 and PKD2, which produce polycystin-1 and polycystin-2 respectively. ADPKD type 1 accounts for 85% of cases, while ADPKD type 2 accounts for 15% of cases. ADPKD type 1 is caused by a mutation in the PKD1 gene on chromosome 16, while ADPKD type 2 is caused by a mutation in the PKD2 gene on chromosome 4. ADPKD type 1 tends to present with renal failure earlier than ADPKD type 2.
To screen for ADPKD in relatives of affected individuals, an abdominal ultrasound is recommended. The diagnostic criteria for ultrasound include the presence of two cysts, either unilateral or bilateral, if the individual is under 30 years old. If the individual is between 30-59 years old, two cysts in both kidneys are required for diagnosis. If the individual is over 60 years old, four cysts in both kidneys are necessary for diagnosis.
For some patients with ADPKD, tolvaptan, a vasopressin receptor 2 antagonist, may be an option to slow the progression of cyst development and renal insufficiency. However, NICE recommends tolvaptan only for adults with ADPKD who have chronic kidney disease stage 2 or 3 at the start of treatment, evidence of rapidly progressing disease, and if the company provides it with the agreed discount in the patient access scheme.
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This question is part of the following fields:
- Renal System
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Question 17
Incorrect
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A 20-year-old patient visits their GP complaining of non-specific malaise. The patient has a medical history of recurrent haematuria during childhood with infections and fever, as well as bilateral mild sensorineural hearing loss. Due to frequent moves between countries, the patient has never had continuous medical care. Further investigations reveal proteinuria and haematuria, leading to a referral to secondary care and a subsequent renal biopsy. The biopsy results show splitting of the lamina densa on electron microscopy.
What is the most common mode of inheritance for this likely diagnosis?Your Answer:
Correct Answer: X-linked dominant
Explanation:Alport’s syndrome is a genetic disorder that is typically inherited in an X-linked dominant pattern. It is caused by a defect in the gene responsible for producing type IV collagen, which leads to an abnormal glomerular-basement membrane (GBM). The disease is more severe in males, with females rarely developing renal failure. Symptoms usually present in childhood and may include microscopic haematuria, progressive renal failure, bilateral sensorineural deafness, lenticonus, retinitis pigmentosa, and splitting of the lamina densa seen on electron microscopy. In some cases, an Alport’s patient with a failing renal transplant may have anti-GBM antibodies, leading to a Goodpasture’s syndrome-like picture. Diagnosis can be made through molecular genetic testing, renal biopsy, or electron microscopy. In around 85% of cases, the syndrome is inherited in an X-linked dominant pattern, while 10-15% of cases are inherited in an autosomal recessive fashion, with rare autosomal dominant variants existing.
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This question is part of the following fields:
- Renal System
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Question 18
Incorrect
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A 25-year-old woman visits her GP, reporting excessive urination and constant thirst for the past few months. She has a history of bipolar disorder and is taking lithium. The symptoms suggest nephrogenic diabetes insipidus, which occurs when the kidneys fail to respond to vasopressin. What is the primary site in the kidney responsible for most of the water reabsorption?
Your Answer:
Correct Answer: Proximal tubule
Explanation:The proximal tubule is responsible for reabsorbing the majority of water in the kidneys. However, in cases of nephrogenic diabetes insipidus, which is often a result of taking lithium, the collecting ducts do not properly respond to antidiuretic hormone (ADH). This means that even with increased ADH, aquaporin-2 channels are not inserted in the collecting ducts, resulting in decreased water reabsorption.
The Loop of Henle and its Role in Renal Physiology
The Loop of Henle is a crucial component of the renal system, located in the juxtamedullary nephrons and running deep into the medulla. Approximately 60 litres of water containing 9000 mmol sodium enters the descending limb of the loop of Henle in 24 hours. The osmolarity of fluid changes and is greatest at the tip of the papilla. The thin ascending limb is impermeable to water, but highly permeable to sodium and chloride ions. This loss means that at the beginning of the thick ascending limb the fluid is hypo osmotic compared with adjacent interstitial fluid. In the thick ascending limb, the reabsorption of sodium and chloride ions occurs by both facilitated and passive diffusion pathways. The loops of Henle are co-located with vasa recta, which have similar solute compositions to the surrounding extracellular fluid, preventing the diffusion and subsequent removal of this hypertonic fluid. The energy-dependent reabsorption of sodium and chloride in the thick ascending limb helps to maintain this osmotic gradient. Overall, the Loop of Henle plays a crucial role in regulating the concentration of solutes in the renal system.
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This question is part of the following fields:
- Renal System
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Question 19
Incorrect
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A woman presents with symptoms of agalactorrhoea, amenorrhoea, intolerance to cold, constipation, and weight loss six months after giving birth. She experienced postpartum bleeding during delivery and has now been diagnosed with hypopituitarism. What could be the possible reason for this condition?
Your Answer:
Correct Answer: Sheehan's syndrome
Explanation:Sheehan’s syndrome is a condition that arises from pituitary ischaemia, which is caused by blood loss during or after childbirth. The syndrome is characterized by symptoms that indicate global hypopituitarism, including agalactorrhoea (lack of prolactin), amenorrhoea (lack of FSH and LH), cold intolerance and constipation (lack of thyroid hormones), and weight loss (lack of steroid hormones).
Malignancy is an uncommon cause of hypopituitarism.
While pituitary adenoma is a frequent cause of hypopituitarism, it is unlikely to be the cause of this patient’s symptoms, given that they occurred after childbirth. Pituitary adenoma may also present with symptoms related to mass effect, such as headache and bilateral hemianopia.
Understanding Hypopituitarism: Causes, Symptoms, and Management
Hypopituitarism is a medical condition that occurs when the pituitary gland fails to produce enough hormones. This can be caused by various factors such as compression of the gland by non-secretory pituitary macroadenoma, pituitary apoplexy, Sheehan’s syndrome, hypothalamic tumors, trauma, iatrogenic irradiation, and infiltrative diseases like hemochromatosis and sarcoidosis. The symptoms of hypopituitarism depend on which hormones are deficient. For instance, low ACTH can cause tiredness and postural hypotension, while low FSH/LH can lead to amenorrhea, infertility, and loss of libido. Low TSH can cause constipation and feeling cold, while low GH can result in short stature if it occurs during childhood. Low prolactin can cause problems with lactation.
To diagnose hypopituitarism, hormone profile testing and imaging are usually conducted. Treatment involves addressing the underlying cause, such as surgical removal of pituitary macroadenoma, and replacement of deficient hormones. It is important to manage hypopituitarism promptly to prevent complications and improve the patient’s quality of life.
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This question is part of the following fields:
- Renal System
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Question 20
Incorrect
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A 65-year-old man is undergoing assessment for polycythemia and has no history of smoking. What type of solid-organ cancer could be a possible cause?
Your Answer:
Correct Answer: Renal cell carcinoma
Explanation:Renal cell carcinoma has the potential to secrete various hormones such as erythropoietin, PTHrP, renin, or ACTH. This can lead to secondary polycythemia, hypercalcemia, or other related conditions. On the other hand, small cell lung cancer can cause ectopic secretion of ACTH or ADH, but not erythropoietin. Pituitary tumors, on the other hand, may secrete prolactin.
Renal cell cancer, also known as hypernephroma, is a primary renal neoplasm that accounts for 85% of cases. It originates from the proximal renal tubular epithelium and is commonly associated with smoking and conditions such as von Hippel-Lindau syndrome and tuberous sclerosis. The clear cell subtype is the most prevalent, comprising 75-85% of tumors.
Renal cell cancer is more common in middle-aged men and may present with classical symptoms such as haematuria, loin pain, and an abdominal mass. Other features include endocrine effects, such as the secretion of erythropoietin, parathyroid hormone-related protein, renin, and ACTH. Metastases are present in 25% of cases at presentation, and paraneoplastic syndromes such as Stauffer syndrome may also occur.
The T category criteria for renal cell cancer are based on tumor size and extent of invasion. Management options include partial or total nephrectomy, depending on the tumor size and extent of disease. Patients with a T1 tumor are typically offered a partial nephrectomy, while alpha-interferon and interleukin-2 may be used to reduce tumor size and treat metastases. Receptor tyrosine kinase inhibitors such as sorafenib and sunitinib have shown superior efficacy compared to interferon-alpha.
In summary, renal cell cancer is a common primary renal neoplasm that is associated with various risk factors and may present with classical symptoms and endocrine effects. Management options depend on the extent of disease and may include surgery and targeted therapies.
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This question is part of the following fields:
- Renal System
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Question 21
Incorrect
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A 50-year-old male is brought back to a surgical ward after a renal transplant. Diuresis suddenly decreases 2 hours after the transplantation. The patient is quickly transferred back to surgery where the transplanted kidney displays signs of hyperacute rejection and is removed. Histopathological examination confirms hyperacute rejection.
What type of reaction has this patient undergone?Your Answer:
Correct Answer: Type II hypersensitivity
Explanation:Hyperacute transplant rejection is a type II hypersensitivity reaction, which is characterized by a cytotoxic response caused by pre-existing antibodies to the ABO or HLA antigens. This reaction leads to widespread thrombosis and ischaemia/necrosis within the transplanted organ, necessitating its surgical removal.
In contrast, type I hypersensitivity is an immediate IgE-mediated reaction that occurs within minutes, while type III hypersensitivity is an IgM-mediated reaction that involves the formation of circulating immune complexes. Type IV hypersensitivity is a cell-mediated response that takes weeks to develop and is seen in chronic graft rejections. Finally, type V hypersensitivity is an autoimmune reaction that involves the binding of auto-antibodies to cell surface receptors, either preventing the intended ligand binding or mimicking its effects.
The HLA system, also known as the major histocompatibility complex (MHC), is located on chromosome 6 and is responsible for human leucocyte antigens. Class 1 antigens include A, B, and C, while class 2 antigens include DP, DQ, and DR. When matching for a renal transplant, the importance of HLA antigens is ranked as DR > B > A.
Graft survival rates for renal transplants are high, with a 90% survival rate at one year and a 60% survival rate at ten years for cadaveric transplants. Living-donor transplants have even higher survival rates, with a 95% survival rate at one year and a 70% survival rate at ten years. However, postoperative problems can occur, such as acute tubular necrosis of the graft, vascular thrombosis, urine leakage, and urinary tract infections.
Hyperacute rejection can occur within minutes to hours after a transplant and is caused by pre-existing antibodies against ABO or HLA antigens. This type of rejection is an example of a type II hypersensitivity reaction and leads to widespread thrombosis of graft vessels, resulting in ischemia and necrosis of the transplanted organ. Unfortunately, there is no treatment available for hyperacute rejection, and the graft must be removed.
Acute graft failure, which occurs within six months of a transplant, is usually due to mismatched HLA and is caused by cell-mediated cytotoxic T cells. This type of failure is usually asymptomatic and is detected by a rising creatinine, pyuria, and proteinuria. Other causes of acute graft failure include cytomegalovirus infection, but it may be reversible with steroids and immunosuppressants.
Chronic graft failure, which occurs after six months of a transplant, is caused by both antibody and cell-mediated mechanisms that lead to fibrosis of the transplanted kidney, known as chronic allograft nephropathy. The recurrence of the original renal disease, such as MCGN, IgA, or FSGS, can also cause chronic graft failure.
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This question is part of the following fields:
- Renal System
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Question 22
Incorrect
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Which one of the following decreases the production of renin?
Your Answer:
Correct Answer: Beta-blockers
Explanation:Renin and its Factors
Renin is a hormone that is produced by juxtaglomerular cells. Its main function is to convert angiotensinogen into angiotensin I. There are several factors that can stimulate or reduce the secretion of renin.
Factors that stimulate renin secretion include hypotension, which can cause reduced renal perfusion, hyponatremia, sympathetic nerve stimulation, catecholamines, and erect posture. On the other hand, there are also factors that can reduce renin secretion, such as beta-blockers and NSAIDs.
It is important to understand the factors that affect renin secretion as it plays a crucial role in regulating blood pressure and fluid balance in the body. By knowing these factors, healthcare professionals can better manage and treat conditions related to renin secretion.
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This question is part of the following fields:
- Renal System
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Question 23
Incorrect
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A 26-year-old male visits his doctor complaining of fever and coryzal symptoms. He has no significant medical history and is not sexually active.
During the physical examination, the doctor notes a soft, slightly tender abdomen with no guarding. The patient's temperature is 38.2 ºC.
To investigate further, the doctor orders a complete blood count, urea and electrolytes, and C-reactive protein. Additionally, a mid-stream urine sample is sent for microscopy, culture, and sensitivity.
What might be observed in the urine on microscopy?Your Answer:
Correct Answer: Hyaline casts
Explanation:During fever, exercise, or use of loop diuretics, it is normal to observe hyaline casts in urine. Nephritic syndrome is associated with red cell casts, while gout is characterized by needle-shaped crystals. Acute tubular necrosis is indicated by brown granular casts, and pseudogout is identified by rhomboid-shaped crystals.
Different Types of Urinary Casts and Their Significance
Urine contains various types of urinary casts that can provide important information about the underlying condition of the patient. Hyaline casts, for instance, are composed of Tamm-Horsfall protein that is secreted by the distal convoluted tubule. These casts are commonly seen in normal urine, after exercise, during fever, or with loop diuretics. On the other hand, brown granular casts in urine are indicative of acute tubular necrosis.
In prerenal uraemia, the urinary sediment appears ‘bland’, which means that there are no significant abnormalities in the urine. Lastly, red cell casts are associated with nephritic syndrome, which is a condition characterized by inflammation of the glomeruli in the kidneys. By analyzing the type of urinary casts present in the urine, healthcare professionals can diagnose and manage various kidney diseases and disorders. Proper identification and interpretation of urinary casts can help in the early detection and treatment of kidney problems.
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This question is part of the following fields:
- Renal System
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Question 24
Incorrect
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A 87-year-old woman, Gwen, has been admitted to the geriatric ward with a suspected UTI.
Gwen is disoriented, visibly dehydrated and overall in poor health. She has a medical history of hypertension and takes ramipril.
The resident orders an ECG, which reveals tented T waves and wide QRS complexes. As a result, they prescribe calcium gluconate.
What is the purpose of administering calcium gluconate in this patient's treatment?Your Answer:
Correct Answer: Stabilises the myocardium to protect against hyperkalaemia
Explanation:Calcium gluconate is not used to lower potassium levels, but rather to stabilize the myocardium and prevent life-threatening arrhythmias. In this patient with a UTI and likely AKI, hyperkalaemia is a common electrolyte imbalance that can disrupt the electrical gradient across the myocardial cells. Insulin and glucose are used to lower blood potassium levels by driving potassium into the cells. Calcium gluconate may be used to treat hypocalcaemia, but this is not a concern in this patient. Additionally, calcium gluconate does not affect the excretion of calcium from the kidneys. IV fluids would be used to manage the patient’s dehydration, but calcium gluconate is not used to increase fluid retention by the kidneys.
Managing Hyperkalaemia: A Step-by-Step Guide
Hyperkalaemia is a serious condition that can lead to life-threatening arrhythmias if left untreated. To manage hyperkalaemia, it is important to address any underlying factors that may be contributing to the condition, such as acute kidney injury, and to stop any aggravating drugs, such as ACE inhibitors. Treatment can be categorised based on the severity of the hyperkalaemia, which is classified as mild, moderate, or severe based on the patient’s potassium levels.
ECG changes are also important in determining the appropriate management for hyperkalaemia. Peaked or ‘tall-tented’ T waves, loss of P waves, broad QRS complexes, and a sinusoidal wave pattern are all associated with hyperkalaemia and should be evaluated in all patients with new hyperkalaemia.
The principles of treatment modalities for hyperkalaemia include stabilising the cardiac membrane, shifting potassium from extracellular to intracellular fluid compartments, and removing potassium from the body. IV calcium gluconate is used to stabilise the myocardium, while insulin/dextrose infusion and nebulised salbutamol can be used to shift potassium from the extracellular to intracellular fluid compartments. Calcium resonium, loop diuretics, and dialysis can be used to remove potassium from the body.
In practical terms, all patients with severe hyperkalaemia or ECG changes should receive emergency treatment, including IV calcium gluconate to stabilise the myocardium and insulin/dextrose infusion to shift potassium from the extracellular to intracellular fluid compartments. Other treatments, such as nebulised salbutamol, may also be used to temporarily lower serum potassium levels. Further management may involve stopping exacerbating drugs, treating any underlying causes, and lowering total body potassium through the use of calcium resonium, loop diuretics, or dialysis.
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This question is part of the following fields:
- Renal System
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Question 25
Incorrect
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A patient with compromised kidney function is given a new medication that is typically eliminated through renal excretion. What factors might impact the excretion of the medication?
Your Answer:
Correct Answer: Diffusivity across the basement membrane and tubular secretion/reabsorption
Explanation:The clearance of a substance in the kidneys is influenced by two important factors: diffusivity across the basement membrane and tubular secretion/reabsorption. Additionally, the Loop of Henle plays a crucial role in generating a significant osmotic gradient, while the primary function of the collecting duct is to facilitate the reabsorption of water.
The Loop of Henle and its Role in Renal Physiology
The Loop of Henle is a crucial component of the renal system, located in the juxtamedullary nephrons and running deep into the medulla. Approximately 60 litres of water containing 9000 mmol sodium enters the descending limb of the loop of Henle in 24 hours. The osmolarity of fluid changes and is greatest at the tip of the papilla. The thin ascending limb is impermeable to water, but highly permeable to sodium and chloride ions. This loss means that at the beginning of the thick ascending limb the fluid is hypo osmotic compared with adjacent interstitial fluid. In the thick ascending limb, the reabsorption of sodium and chloride ions occurs by both facilitated and passive diffusion pathways. The loops of Henle are co-located with vasa recta, which have similar solute compositions to the surrounding extracellular fluid, preventing the diffusion and subsequent removal of this hypertonic fluid. The energy-dependent reabsorption of sodium and chloride in the thick ascending limb helps to maintain this osmotic gradient. Overall, the Loop of Henle plays a crucial role in regulating the concentration of solutes in the renal system.
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This question is part of the following fields:
- Renal System
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Question 26
Incorrect
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A 50-year-old woman comes to the GP clinic with her husband after attempting a dehydration detox. She appears confused and drowsy, and reports having vomited three times in the past 12 hours without passing urine. The patient has a medical history of allergic rhinitis, anxiety, hypothyroidism, type 2 diabetes mellitus, and chronic lower back pain.
During the examination, you observe dry mucous membranes, a pulse rate of 112/min, a respiratory rate of 24/min, a blood pressure of 97/65 mmHg, a temperature of 37.1ºC, and O2 saturation of 98%.
Given the patient's condition, you suspect that she requires immediate hospital care and refer her to the emergency department.
What medication should be stopped immediately for this patient?Your Answer:
Correct Answer: Losartan
Explanation:In cases of AKI, it is recommended to discontinue the use of angiotensin II receptor antagonists such as Losartan as they can worsen renal function by reducing renal perfusion. This is because angiotensin II plays a role in constricting systemic blood vessels and the efferent arteriole of the glomerulus, which increases GFR. Blocking angiotensin II can lead to a drop in systemic blood pressure and dilation of the efferent glomerular arteriole, which can exacerbate kidney impairment.
Cetirizine is not the most important medication to discontinue in AKI, as it is a non-sedating antihistamine and is unlikely to be a major cause of drowsiness. Diazepam may be contributing to drowsiness and is excreted in the urine, but sudden discontinuation can result in withdrawal symptoms. Levothyroxine does not need to be stopped in AKI as thyroid hormones are primarily metabolized in the liver and are not considered high risk in renal impairment.
Acute kidney injury (AKI) is a condition where there is a reduction in renal function following an insult to the kidneys. It was previously known as acute renal failure and can result in long-term impaired kidney function or even death. AKI can be caused by prerenal, intrinsic, or postrenal factors. Patients with chronic kidney disease, other organ failure/chronic disease, a history of AKI, or who have used drugs with nephrotoxic potential are at an increased risk of developing AKI. To prevent AKI, patients at risk may be given IV fluids or have certain medications temporarily stopped.
The kidneys are responsible for maintaining fluid balance and homeostasis, so a reduced urine output or fluid overload may indicate AKI. Symptoms may not be present in early stages, but as renal failure progresses, patients may experience arrhythmias, pulmonary and peripheral edema, or features of uraemia. Blood tests such as urea and electrolytes can be used to detect AKI, and urinalysis and imaging may also be necessary.
Management of AKI is largely supportive, with careful fluid balance and medication review. Loop diuretics and low-dose dopamine are not recommended, but hyperkalaemia needs prompt treatment to avoid life-threatening arrhythmias. Renal replacement therapy may be necessary in severe cases. Patients with suspected AKI secondary to urinary obstruction require prompt review by a urologist, and specialist input from a nephrologist is required for cases where the cause is unknown or the AKI is severe.
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This question is part of the following fields:
- Renal System
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Question 27
Incorrect
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A 45-year-old female is admitted to the hospital for investigation of recently developed hypertension, myalgia, and a facial rash. She experiences a decline in kidney function and complains of muscle aches and ankle swelling during her hospital stay. A kidney biopsy and urine sample are taken, revealing a proliferative 'wire-loop' glomerular lesion on histopathological assessment. The urinalysis shows proteinuria but no presence of leukocytes or nitrites. What is the most probable diagnosis?
Your Answer:
Correct Answer: Systemic lupus erythematosus
Explanation:Lupus nephritis is characterized by proliferative ‘wire-loop’ glomerular histology, proteinuria, and systemic symptoms. This condition occurs when autoimmune processes in SLE cause inflammation and damage to the glomeruli. Symptoms may include oedema, myalgia, arthralgia, hypertension, and foamy-appearing urine due to high levels of protein. Acute tubular necrosis primarily affects the tubules and does not typically present with proteinuria. Congestive heart failure and IgA nephropathy can cause proteinuria, but they do not result in the ‘wire-loop’ glomerular lesion seen in lupus nephritis. Pyelonephritis may also cause proteinuria, but it is an infectious process and would present with additional symptoms such as nitrites, leukocytes, and blood in the urine.
Renal Complications in Systemic Lupus Erythematosus
Systemic lupus erythematosus (SLE) can lead to severe renal complications, including lupus nephritis, which can result in end-stage renal disease. Regular check-ups with urinalysis are necessary to detect proteinuria in SLE patients. The WHO classification system categorizes lupus nephritis into six classes, with class IV being the most common and severe form. Renal biopsy shows characteristic findings such as endothelial and mesangial proliferation, a wire-loop appearance, and subendothelial immune complex deposits.
Management of lupus nephritis involves treating hypertension and using glucocorticoids with either mycophenolate or cyclophosphamide for initial therapy in cases of focal (class III) or diffuse (class IV) lupus nephritis. Mycophenolate is generally preferred over azathioprine for subsequent therapy to decrease the risk of developing end-stage renal disease. Early detection and proper management of renal complications in SLE patients are crucial to prevent irreversible damage to the kidneys.
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This question is part of the following fields:
- Renal System
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Question 28
Incorrect
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A 38-year-old female visits her doctor complaining of tingling sensations around her mouth and frequent muscle cramps. During the blood pressure check, her wrist and fingers start to cramp and flex. Despite these symptoms, she appears to be in good health.
What condition is the most probable diagnosis?Your Answer:
Correct Answer: Hypocalcaemia
Explanation:Hypocalcaemia is characterized by perioral paraesthesia, cramps, tetany, and convulsions. The female in this scenario is displaying these symptoms, along with a positive Trousseau’s sign and potentially a positive Chvostek’s sign. Hypocalcaemia is commonly caused by hyperparathyroidism, vitamin D deficiency, or phosphate infusions.
Hyperkalaemia is when there is an elevated level of potassium in the blood, which can be caused by chronic kidney disease, dehydration, and certain medications such as spironolactone. Symptoms may include muscle weakness, heart palpitations, and nausea and vomiting.
Hypermagnesaemia is rare and can cause decreased respiratory rate, muscle weakness, and decreased reflexes. It may be caused by renal failure, excessive dietary intake, or increased cell destruction.
Hypokalaemia is relatively common and can cause weakness, fatigue, and muscle cramps. It may be caused by diuretic use, low dietary intake, or vomiting.
Hyponatraemia may also cause cramps, but typically presents with nausea and vomiting, fatigue, confusion, and in severe cases, seizures or coma. Causes may include syndrome of inappropriate ADH release (SIADH), excessive fluid intake, and certain medications such as diuretics, SSRIs, and antipsychotics.
Hypocalcaemia: Symptoms and Signs
Hypocalcaemia is a condition characterized by low levels of calcium in the blood. As calcium is essential for proper muscle and nerve function, many of the symptoms and signs of hypocalcaemia are related to neuromuscular excitability. The most common features of hypocalcaemia include muscle twitching, cramping, and spasms, as well as perioral paraesthesia. In chronic cases, patients may experience depression and cataracts. An electrocardiogram (ECG) may show a prolonged QT interval.
Two specific signs that are commonly used to diagnose hypocalcaemia are Trousseau’s sign and Chvostek’s sign. Trousseau’s sign is observed when the brachial artery is occluded by inflating the blood pressure cuff and maintaining pressure above systolic. This causes wrist flexion and fingers to be drawn together, which is seen in around 95% of patients with hypocalcaemia and around 1% of normocalcaemic people. Chvostek’s sign is observed when tapping over the parotid gland causes facial muscles to twitch. This sign is seen in around 70% of patients with hypocalcaemia and around 10% of normocalcaemic people. Overall, hypocalcaemia can cause a range of symptoms and signs that are related to neuromuscular excitability, and specific diagnostic signs can be used to confirm the diagnosis.
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This question is part of the following fields:
- Renal System
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Question 29
Incorrect
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A 44-year-old woman arrives at the Emergency Department with intermittent sharp pain in her right flank and haematuria. She reports feeling slightly nauseous, but otherwise feels well. She has a medical history of hyperparathyroidism, but has never experienced these symptoms before. Her body mass index is 28kg/m² and she admits to regularly consuming takeaways. During examination, she appears restless and exhibits tenderness in her right flank.
What is the probable substance responsible for causing this patient's pain?Your Answer:
Correct Answer: Calcium oxalate
Explanation:Renal stones are predominantly made up of calcium phosphate, and individuals with renal tubular acidosis are at a higher risk of developing them. Uric acid stones, which make up only 5-10% of cases, are often associated with malignancies.
Renal stones can be classified into different types based on their composition. Calcium oxalate stones are the most common, accounting for 85% of all calculi. These stones are formed due to hypercalciuria, hyperoxaluria, and hypocitraturia. They are radio-opaque and may also bind with uric acid stones. Cystine stones are rare and occur due to an inherited recessive disorder of transmembrane cystine transport. Uric acid stones are formed due to purine metabolism and may precipitate when urinary pH is low. Calcium phosphate stones are associated with renal tubular acidosis and high urinary pH. Struvite stones are formed from magnesium, ammonium, and phosphate and are associated with chronic infections. The pH of urine can help determine the type of stone present, with calcium phosphate stones forming in normal to alkaline urine, uric acid stones forming in acidic urine, and struvate stones forming in alkaline urine. Cystine stones form in normal urine pH.
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This question is part of the following fields:
- Renal System
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Question 30
Incorrect
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A health-conscious 45-year-old presents with an unexplained acute kidney injury (AKI) and a kidney biopsy reveals the presence of calcium oxalate crystals in the renal tubules. The patient's calcium levels are normal, oxalate levels are elevated, and vitamin D levels are within normal range. Which vitamin overdose could potentially account for this condition?
Your Answer:
Correct Answer: Vitamin C
Explanation:The deposition of calcium oxalate in the renal tubules indicates that the patient is experiencing oxalate nephropathy, which is commonly caused by an overdose of vitamin C. Therefore, the correct answer is vitamin C overdose. It should be noted that elevated calcium levels are associated with vitamin D overdose, which is not applicable in this case.
Understanding Oxalate Nephropathy
Oxalate nephropathy is a type of sudden kidney damage that occurs when calcium oxalate crystals accumulate in the renal tubules. This condition can be caused by various factors, including the ingestion of ethylene glycol or an overdose of vitamin C. When these crystals build up in the renal tubules, they can cause damage to the tubular epithelium, leading to kidney dysfunction.
To better understand oxalate nephropathy, it is important to note that the renal tubules are responsible for filtering waste products from the blood and excreting them in the urine. When calcium oxalate crystals accumulate in these tubules, they can disrupt this process and cause damage to the tubular epithelium. This can lead to a range of symptoms, including decreased urine output, swelling in the legs and feet, and fatigue.
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This question is part of the following fields:
- Renal System
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