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  • Question 1 - A woman in her 30s experiences dehydration from diarrhoea and vomiting, leading to...

    Incorrect

    • A woman in her 30s experiences dehydration from diarrhoea and vomiting, leading to activation of the renin-angiotensin-aldosterone system by her kidneys. This increases the pressure across the glomerulus and maintains glomerular filtration rate. What is the normal passage of blood through this area?

      Your Answer: afferent arteriole- glomerular capillary bed- peritubular capillaries and medullary vasa recta- efferent arteriole

      Correct Answer: afferent arteriole- glomerular capillary bed- efferent arteriole- peritubular capillaries and medullary vasa recta

      Explanation:

      The journey of blood to a nephron begins with the afferent arteriole, followed by the glomerular capillary bed, efferent arteriole, and finally the peritubular capillaries and medullary vasa recta.

      The afferent arteriole is the first stage, where blood enters the nephron. From there, it flows through the glomerulus and exits through the efferent arteriole.

      If the efferent arteriole is constricted, it can increase pressure across the glomerulus, leading to a higher filtration fraction and maintaining eGFR.

      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.

    • This question is part of the following fields:

      • Renal System
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  • Question 2 - A 90-year-old man is discovered unconscious in his residence. He is transported to...

    Incorrect

    • A 90-year-old man is discovered unconscious in his residence. He is transported to the hospital for further evaluation and is diagnosed with dehydration-induced hypotension. What is the most probable physiological response?

      Your Answer: Increased parasympathetic tone due to baroreceptor reflex

      Correct Answer: Renin release due to reduced perfusion of organs

      Explanation:

      Renin is released when there is a decrease in renal perfusion.

      The secretion of aldosterone would increase due to elevated levels of angiotensin II.

      Angiotensin II causes vasoconstriction of the efferent arteriole to the glomerulus, which increases the pressure across the glomerulus and filtration fraction, ultimately preserving GFR.

      Angiotensin II stimulates the pituitary gland to secrete more ADH, which acts on the collecting duct to increase water absorption.

      The baroreceptor reflex is another mechanism that helps maintain blood pressure homeostasis, along with the renin-angiotensin-aldosterone system. When blood pressure increases, baroreceptors in the aortic arch/carotid sinus detect the stretching of the vessel, leading to inhibition of sympathetic tone and increased parasympathetic tone, which decreases blood pressure. In hypotension, the baroreceptors detect less stretching in the vessel, leading to increased sympathetic tone and decreased parasympathetic tone. In this case, increased sympathetic tone would result in an increase in heart rate.

      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.

    • This question is part of the following fields:

      • Renal System
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  • Question 3 - Sarah, who is in her 50s, has recently undergone a kidney transplant. A...

    Correct

    • 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: 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.

    • This question is part of the following fields:

      • Renal System
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  • Question 4 - A 65-year-old man visits the haemofiltration unit thrice a week for treatment. What...

    Correct

    • A 65-year-old man visits the haemofiltration unit thrice a week for treatment. What is responsible for detecting alterations in salt concentrations, such as sodium chloride, in normally functioning kidneys and adjusting the glomerular filtration rate accordingly?

      Your Answer: Macula densa

      Explanation:

      The macula densa is a specialized area of columnar tubule cells located in the final part of the ascending loop of Henle. These cells are in contact with the afferent arteriole and play a crucial role in detecting the concentration of sodium chloride in the convoluted tubules and ascending loop of Henle. This detection is affected by the glomerular filtration rate (GFR), which is increased by an increase in blood pressure. When the macula densa detects high sodium chloride levels, it releases ATP and adenosine, which constrict the afferent arteriole and lower GFR. Conversely, when low sodium chloride levels are detected, the macula densa releases nitric oxide, which acts as a vasodilator. The macula densa can also increase renin production from the juxtaglomerular cells.

      Juxtaglomerular cells are smooth muscle cells located mainly in the walls of the afferent arteriole. They act as baroreceptors to detect changes in blood pressure and can secrete renin.

      Mesangial cells are located at the junction of the afferent and efferent arterioles and, together with the juxtaglomerular cells and the macula densa, form the juxtaglomerular apparatus.

      Podocytes, which are modified simple squamous epithelial cells with foot-like projections, make up the innermost layer of the Bowman’s capsule surrounding the glomerular capillaries. They assist in glomerular filtration.

      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.

    • This question is part of the following fields:

      • Renal System
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  • Question 5 - A 26-year-old man is involved in a car crash and develops oliguria with...

    Correct

    • A 26-year-old man is involved in a car crash and develops oliguria with worsening renal function. How can acute tubular necrosis be differentiated from pre-renal azotemia in this case?

      Your Answer: No response to intravenous fluids

      Explanation:

      Inability to respond to intravenous fluids is observed in acute tubular necrosis due to the damage originating from the renal system itself, rather than being caused by a reduction in volume.

      Understanding the Difference between Acute Tubular Necrosis and Prerenal Uraemia

      Acute kidney injury can be caused by various factors, including prerenal uraemia and acute tubular necrosis. It is important to differentiate between the two to determine the appropriate treatment. Prerenal uraemia occurs when the kidneys hold on to sodium to preserve volume, leading to decreased blood flow to the kidneys. On the other hand, acute tubular necrosis is caused by damage to the kidney tubules, which can be due to various factors such as toxins, infections, or ischemia.

      To differentiate between the two, several factors can be considered. In prerenal uraemia, the urine sodium level is typically less than 20 mmol/L, while in acute tubular necrosis, it is usually greater than 40 mmol/L. The urine osmolality is also higher in prerenal uraemia, typically above 500 mOsm/kg, while in acute tubular necrosis, it is usually below 350 mOsm/kg. The fractional sodium excretion is less than 1% in prerenal uraemia, while it is greater than 1% in acute tubular necrosis. Additionally, the response to fluid challenge is typically good in prerenal uraemia, while it is poor in acute tubular necrosis.

      Other factors that can help differentiate between the two include the serum urea:creatinine ratio, fractional urea excretion, urine:plasma osmolality, urine:plasma urea, specific gravity, and urine sediment. By considering these factors, healthcare professionals can accurately diagnose and treat acute kidney injury.

    • This question is part of the following fields:

      • Renal System
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  • Question 6 - You have been requested to evaluate a 45-year-old Caucasian individual who has recently...

    Correct

    • You have been requested to evaluate a 45-year-old Caucasian individual who has recently been diagnosed with hypertension. Despite making dietary modifications and engaging in physical activity, their blood pressure remains above 160/100 mmHg, prompting you to recommend medication.

      During the consultation, the patient inquires about the drug's mechanism of action. You clarify that the medication obstructs an enzyme responsible for converting a peptide hormone into its active state.

      Based on the medication you have prescribed, which of the following alterations is expected to happen?

      Your Answer: Reduced ADH release

      Explanation:

      The drug in question is most likely an ACE inhibitor, which is commonly prescribed as first-line therapy for hypertension in older patients of certain races. ACE inhibitors work by inhibiting the enzyme responsible for converting angiotensin I to angiotensin II, which is a key component of the renin-angiotensin-aldosterone system that regulates blood pressure. Angiotensin II has several actions that help to counteract drops in blood pressure, including vasoconstriction, increased aldosterone secretion, and increased ADH release. ACE inhibitors have the opposite effect, leading to reduced levels of ADH. However, ACE inhibitors can also cause a buildup of bradykinin, which may result in a persistent dry cough as a side effect.

      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.

    • This question is part of the following fields:

      • Renal System
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  • Question 7 - A 75-year-old male is brought to the emergency department after falling at home....

    Incorrect

    • A 75-year-old male is brought to the emergency department after falling at home. Upon admission, his blood tests reveal a sodium level of 128 mmol/l. Which medication is the most probable cause of this?

      Your Answer: Simvastatin

      Correct Answer: Sertraline

      Explanation:

      Hyponatremia is a common side effect of SSRIs, including Sertraline, which can cause SIADH. However, medications such as Statins, Levothyroxine, and Metformin are not typically linked to hyponatremia.

      SIADH is a condition where the body retains too much water, leading to low sodium levels in the blood. This can be caused by various factors such as malignancy (particularly small cell lung cancer), neurological conditions like stroke or meningitis, infections like tuberculosis or pneumonia, certain drugs like sulfonylureas and SSRIs, and other factors like positive end-expiratory pressure and porphyrias. Treatment involves slowly correcting the sodium levels, restricting fluid intake, and using medications like demeclocycline or ADH receptor antagonists. It is important to correct the sodium levels slowly to avoid complications like central pontine myelinolysis.

    • This question is part of the following fields:

      • Renal System
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  • Question 8 - Which one of the following structures is not located behind the left kidney?...

    Incorrect

    • Which one of the following structures is not located behind the left kidney?

      Your Answer: Medial arcuate ligament

      Correct Answer: 10th rib

      Explanation:

      Renal Anatomy: Understanding the Structure and Relations of the Kidneys

      The kidneys are two bean-shaped organs located in a deep gutter alongside the vertebral bodies. They measure about 11cm long, 5cm wide, and 3 cm thick, with the left kidney usually positioned slightly higher than the right. The upper pole of both kidneys approximates with the 11th rib, while the lower border is usually alongside L3. The kidneys are surrounded by an outer cortex and an inner medulla, which contains pyramidal structures that terminate at the renal pelvis into the ureter. The renal sinus lies within the kidney and contains branches of the renal artery, tributaries of the renal vein, major and minor calyces, and fat.

      The anatomical relations of the kidneys vary depending on the side. The right kidney is in direct contact with the quadratus lumborum, diaphragm, psoas major, and transversus abdominis, while the left kidney is in direct contact with the quadratus lumborum, diaphragm, psoas major, transversus abdominis, stomach, pancreas, spleen, and distal part of the small intestine. Each kidney and suprarenal gland is enclosed within a common layer of investing fascia, derived from the transversalis fascia, which is divided into anterior and posterior layers (Gerotas fascia).

      At the renal hilum, the renal vein lies most anteriorly, followed by the renal artery (an end artery), and the ureter lies most posteriorly. Understanding the structure and relations of the kidneys is crucial in diagnosing and treating renal diseases and disorders.

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      • Renal System
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  • Question 9 - A 72-year-old man with confirmed heart failure visits the community cardiology clinic and...

    Correct

    • A 72-year-old man with confirmed heart failure visits the community cardiology clinic and complains of ankle swelling as his most bothersome symptom. He expresses reluctance to begin another diuretic due to a previous hospitalization for weakness, nausea, and abdominal cramps after starting one. The cardiologist proposes initiating an aldosterone receptor antagonist. What medication is the cardiologist recommending?

      Your Answer: Spironolactone (potassium-sparing diuretic)

      Explanation:

      Spironolactone is a medication that works as an aldosterone antagonist in the cortical collecting duct. It is used to treat various conditions such as ascites, hypertension, heart failure, nephrotic syndrome, and Conn’s syndrome. In patients with cirrhosis, spironolactone is often prescribed in relatively large doses of 100 or 200 mg to counteract secondary hyperaldosteronism. It is also used as a NICE ‘step 4’ treatment for hypertension. In addition, spironolactone has been shown to reduce all-cause mortality in patients with NYHA III + IV heart failure who are already taking an ACE inhibitor, according to the RALES study.

      However, spironolactone can cause adverse effects such as hyperkalaemia and gynaecomastia, although the latter is less common with eplerenone. It is important to monitor potassium levels in patients taking spironolactone to prevent hyperkalaemia, which can lead to serious complications such as cardiac arrhythmias. Overall, spironolactone is a useful medication for treating various conditions, but its potential adverse effects should be carefully considered and monitored.

    • This question is part of the following fields:

      • Renal System
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  • Question 10 - A 65-year-old man presents to the emergency department with a 4-hour history of...

    Incorrect

    • A 65-year-old man presents to the emergency department with a 4-hour history of palpitations. He has been experiencing vomiting and diarrhoea for the past few days and feels increasingly lethargic. The patient has a medical history of type 2 diabetes mellitus and chronic kidney disease.

      The following routine blood tests are taken:

      - Hb 150 g/L (135-180)
      - Platelets 308 * 109/L (150 - 400)
      - WBC 12.4 * 109/L (4.0 - 11.0)
      - Na+ 139 mmol/L (135 - 145)
      - K+ 7.1 mmol/L (3.5 - 5.0)
      - Urea 12.6 mmol/L (2.0 - 7.0)
      - Creatinine 204 µmol/L (55 - 120)
      - CRP 56 mg/L (< 5)

      The patient's ECG shows sinus tachycardia and tall tented T waves.

      What is the most appropriate initial management for this patient?

      Your Answer: Intravenous fluids

      Correct Answer: Calcium gluconate

      Explanation:

      To stabilize the cardiac membrane in a patient with hyperkalemia and ECG changes, the priority is to administer intravenous calcium gluconate. This is because hyperkalemia can lead to life-threatening arrhythmias and cardiac arrest if left untreated. ECG changes associated with hyperkalemia include tall tented T waves, P wave flattening and prolongation, and broad QRS complexes. Haemofiltration is generally reserved for refractory hyperkalemia, while insulin and dextrose infusion would treat hyperkalemia but not protect the heart from the risk of arrhythmia and death. Intravenous fluids play no role in the management of hyperkalemia or stabilizing the cardiac membrane.

      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.

    • This question is part of the following fields:

      • Renal System
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  • Question 11 - A 70-year-old man is receiving treatment for pneumonia and is currently experiencing delirium....

    Correct

    • A 70-year-old man is receiving treatment for pneumonia and is currently experiencing delirium. He has been catheterized and is receiving IV antibiotics. The nurse has observed that he has not urinated overnight, despite attempts to flush the catheter.

      The patient has a medical history of hypertension, chronic back pain, and type 2 diabetes, for which he takes ramipril, furosemide, naproxen, and gliclazide. His daily blood tests are pending, and the morning medication round has begun.

      What is the appropriate course of action regarding his medications?

      Your Answer: Withhold furosemide, naproxen, and ramipril, continue gliclazide and IV antibiotics

      Explanation:

      When a patient is suspected to have acute kidney injury (AKI), it is important to stop nephrotoxic medications such as ACE inhibitors, ARBs, diuretics, and NSAIDs. In this case, the patient is on ramipril, furosemide, and naproxen, which should be withheld. Gliclazide and IV antibiotics can be continued, but blood sugar levels should be monitored closely due to the increased risk of hypoglycemia in renal impairment. It is incorrect to give morning medication and wait for blood test results, increase furosemide, withhold all regular medications, or withhold only furosemide and gliclazide while continuing everything else. The appropriate action is to withhold all nephrotoxic medications and continue necessary treatments while monitoring the patient’s condition closely.

      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.

    • This question is part of the following fields:

      • Renal System
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  • Question 12 - A 35-year-old male presents with gynaecomastia. Upon examination, a nodule is detected in...

    Incorrect

    • A 35-year-old male presents with gynaecomastia. Upon examination, a nodule is detected in his right testis. What is the probable diagnosis?

      Your Answer: Oestrogen abuse

      Correct Answer: Leydig cell tumour

      Explanation:

      Overview of Testicular Disorders

      Testicular disorders can range from benign conditions to malignant tumors. Testicular cancer is the most common malignancy in men aged 20-30 years, with germ-cell tumors accounting for 95% of cases. Seminomas are the most common subtype, while non-seminomatous germ cell tumors include teratoma, yolk sac tumor, choriocarcinoma, and mixed germ cell tumors. Risk factors for testicular cancer include cryptorchidism, infertility, family history, Klinefelter’s syndrome, and mumps orchitis. The most common presenting symptom is a painless lump, but pain, hydrocele, and gynecomastia may also be present.

      Benign testicular disorders include epididymo-orchitis, which is an acute inflammation of the epididymis often caused by bacterial infection. Testicular torsion, which results in testicular ischemia and necrosis, is most common in males aged between 10 and 30. Hydrocele presents as a mass that transilluminates and may occur as a result of a patent processus vaginalis in children. Treatment for these conditions varies, with orchidectomy being the primary treatment for testicular cancer. Surgical exploration is necessary for testicular torsion, while epididymo-orchitis and hydrocele may require medication or surgical procedures depending on the severity of the condition.

    • This question is part of the following fields:

      • Renal System
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  • Question 13 - A 79-year-old male is admitted to hospital with dehydration. Blood tests are sent...

    Incorrect

    • A 79-year-old male is admitted to hospital with dehydration. Blood tests are sent to assess his renal function. The results are below. He is diagnosed with an acute kidney injury.

      Na+ 143 mmol/l
      K+ 4.8 mmol/l
      Urea 32 mmol/l
      Creatinine 383 mmol/l
      eGFR 15 ml/min

      What electrolyte should be monitored closely?

      Your Answer: Sodium

      Correct Answer: Potassium

      Explanation:

      The nephron plays a crucial role in maintaining the balance of electrolytes in the bloodstream, particularly potassium and hydrogen ions, which are regulated in the distal convoluted tubule (DCT) and collecting duct (CD).

      Dehydration-induced acute kidney injury (AKI) is considered a pre-renal cause that reduces the glomerular filtration rate (GFR). In response, the kidney attempts to reabsorb as much fluid as possible to compensate for the body’s fluid depletion. As a result, minimal filtrate reaches the DCT and CD, leading to reduced potassium excretion. High levels of potassium can be extremely hazardous, especially due to its impact on the myocardium. Therefore, monitoring potassium levels is crucial in such situations, which can be done quickly through a venous blood gas (VBG) test.

      Hyperkalaemia is a condition where there is an excess of potassium in the blood. The levels of potassium in the plasma are regulated by various factors such as aldosterone, insulin levels, and acid-base balance. When there is metabolic acidosis, hyperkalaemia can occur as hydrogen and potassium ions compete with each other for exchange with sodium ions across cell membranes and in the distal tubule. The ECG changes that can be seen in hyperkalaemia include tall-tented T waves, small P waves, widened QRS leading to a sinusoidal pattern, and asystole.

      There are several causes of hyperkalaemia, including acute kidney injury, drugs such as potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin, and heparin, metabolic acidosis, Addison’s disease, rhabdomyolysis, and massive blood transfusion. Foods that are high in potassium include salt substitutes, bananas, oranges, kiwi fruit, avocado, spinach, and tomatoes.

      It is important to note that beta-blockers can interfere with potassium transport into cells and potentially cause hyperkalaemia in renal failure patients. In contrast, beta-agonists such as Salbutamol are sometimes used as emergency treatment. Additionally, both unfractionated and low-molecular weight heparin can cause hyperkalaemia by inhibiting aldosterone secretion.

    • This question is part of the following fields:

      • Renal System
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  • Question 14 - A 58-year-old male comes to the rheumatology clinic complaining of persistent pain caused...

    Incorrect

    • A 58-year-old male comes to the rheumatology clinic complaining of persistent pain caused by his rheumatoid arthritis. He is prescribed an NSAID for pain management. How does this medication impact his kidneys?

      Your Answer: Afferent arterial dilation

      Correct Answer: Afferent arteriole constriction

      Explanation:

      NSAIDs are commonly used drugs that have anti-inflammatory properties. They work by inhibiting the enzymes COX-1 and COX-2, which are responsible for synthesizing prostanoids such as prostaglandins and thromboxanes.

      Prostaglandins play a crucial role in the kidney by causing vasodilation of the afferent arterioles in the glomeruli. This increases blood flow into the glomerulus and leads to an increase in the glomerular filtration rate (GFR).

      When NSAIDs inhibit the COX enzymes, they reduce the levels of prostaglandins in the body. This results in a loss of vasodilation in the afferent arterioles, which leads to reduced renal perfusion and a decrease in GFR.

      The Impact of NSAIDs on Kidney Function

      NSAIDs are commonly used anti-inflammatory drugs that work by inhibiting the enzymes COX-1 and COX-2, which are responsible for the synthesis of prostanoids such as prostaglandins and thromboxanes. In the kidneys, prostaglandins play a crucial role in vasodilating the afferent arterioles of the glomeruli, allowing for increased blood flow and a higher glomerular filtration rate (GFR).

      However, when NSAIDs inhibit the COX enzymes, the levels of prostaglandins decrease, leading to a reduction in afferent arteriole vasodilation and subsequently, a decrease in renal perfusion and GFR. This can have negative consequences for kidney function, particularly in individuals with pre-existing kidney disease or those taking high doses of NSAIDs for prolonged periods of time.

      It is important for healthcare providers to consider the potential impact of NSAIDs on kidney function and to monitor patients accordingly, especially those at higher risk for kidney damage. Alternative treatments or lower doses of NSAIDs may be recommended to minimize the risk of kidney injury.

    • This question is part of the following fields:

      • Renal System
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  • Question 15 - A 9-year-old boy comes to the GP after experiencing bloody diarrhoea for the...

    Incorrect

    • A 9-year-old boy comes to the GP after experiencing bloody diarrhoea for the past 6 days. He complains of abdominal pain and has been urinating very little. His mother has also noticed multiple bruises on his body without any known cause. What is the most probable organism responsible for his symptoms?

      Your Answer: Leptospirosis spp

      Correct Answer: E. coli

      Explanation:

      The patient’s symptoms suggest that they may be suffering from haemolytic uraemic syndrome (HUS), which is often caused by an infection with E.coli 0157:H7.

      HUS is characterized by a combination of haemolytic anaemia, thrombocytopaenia, and acute kidney injury, which can ultimately lead to renal failure.

      The presence of bloody diarrhoea in the patient’s medical history is a significant indicator of HUS. Additionally, the reduced urine output is likely due to the acute kidney injury, while the bruising may be a result of the thrombocytopaenia associated with HUS.

      Understanding Haemolytic Uraemic Syndrome

      Haemolytic uraemic syndrome (HUS) is a condition that primarily affects young children and is characterized by a triad of symptoms, including acute kidney injury, microangiopathic haemolytic anaemia, and thrombocytopenia. The most common cause of HUS in children is Shiga toxin-producing Escherichia coli (STEC) 0157:H7, which accounts for over 90% of cases. Other causes of HUS include pneumococcal infection, HIV, systemic lupus erythematosus, drugs, and cancer.

      To diagnose HUS, doctors may perform a full blood count, check for evidence of STEC infection in stool culture, and conduct PCR for Shiga toxins. Treatment for HUS is supportive and may include fluids, blood transfusion, and dialysis if required. Antibiotics are not recommended, despite the preceding diarrhoeal illness in many patients. The indications for plasma exchange in HUS are complicated, and as a general rule, plasma exchange is reserved for severe cases of HUS not associated with diarrhoea. Eculizumab, a C5 inhibitor monoclonal antibody, has shown greater efficiency than plasma exchange alone in the treatment of adult atypical HUS.

      In summary, HUS is a serious condition that primarily affects young children and is characterized by a triad of symptoms. The most common cause of HUS in children is STEC 0157:H7, and diagnosis may involve various tests. Treatment is supportive, and antibiotics are not recommended. The indications for plasma exchange are complicated, and eculizumab may be more effective in treating adult atypical HUS.

    • This question is part of the following fields:

      • Renal System
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  • Question 16 - A 75-year-old man has been diagnosed with glomerulonephritis. He has a medical history...

    Incorrect

    • A 75-year-old man has been diagnosed with glomerulonephritis. He has a medical history of systemic lupus erythematosus and chronic heart failure. Currently, he is taking statins, paracetamol, ramipril, prednisolone, and verapamil. Which of these medications will need to be discontinued due to his recent diagnosis?

      Your Answer: Prednisolone

      Correct Answer: Ramipril

      Explanation:

      When a patient is experiencing acute kidney injury (AKI), it is important to discontinue certain medications that can exacerbate the condition. These medications include ACE inhibitors/ARBs, NSAIDs, and diuretics, which can all have a negative impact on glomerular filtration rate and pressure. A helpful mnemonic to remember these nephrotoxic drugs is DAMN (Diuretics, ACE inhibitors/ARBs, Metformin, NSAIDs). However, medications such as paracetamol, prednisolone, and statins are usually safe to continue during AKI as they do not significantly affect renal function.

      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.

    • This question is part of the following fields:

      • Renal System
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  • Question 17 - A 38-year-old female visits her doctor complaining of tingling sensations around her mouth...

    Correct

    • 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: 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.

    • This question is part of the following fields:

      • Renal System
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  • Question 18 - Which one of the following statements are not typically true in hypokalaemia? ...

    Incorrect

    • Which one of the following statements are not typically true in hypokalaemia?

      Your Answer: It may cause hyponatraemia

      Correct Answer: It often accompanies acidosis

      Explanation:

      Potassium depletion can occur through the gastrointestinal tract or the kidneys. Chronic vomiting is less likely to cause potassium loss than diarrhea because gastric secretions contain less potassium than lower GI secretions. However, if vomiting leads to metabolic alkalosis, renal potassium wasting may occur as the body excretes potassium instead of hydrogen ions. Conversely, potassium depletion can result in acidic urine.

      Hypokalemia is often associated with metabolic alkalosis due to two factors. Firstly, common causes of metabolic alkalosis, such as vomiting and diuretics, directly cause loss of H+ and K+ (via aldosterone), leading to hypokalemia. Secondly, hypokalemia can cause metabolic alkalosis through three mechanisms. Firstly, it causes a transcellular shift where K+ leaves and H+ enters cells, raising extracellular pH. Secondly, it causes an intracellular acidosis in the proximal tubules, promoting ammonium production and excretion. Thirdly, in the presence of hypokalemia, hydrogen secretion in the proximal and distal tubules increases, leading to further reabsorption of HCO3-. Overall, this results in an increase in net acid excretion.

      Understanding Hypokalaemia and its Causes

      Hypokalaemia is a condition characterized by low levels of potassium in the blood. Potassium and hydrogen ions are competitors, and as potassium levels decrease, more hydrogen ions enter the cells. Hypokalaemia can occur with either alkalosis or acidosis. In cases of alkalosis, hypokalaemia may be caused by vomiting, thiazide and loop diuretics, Cushing’s syndrome, or Conn’s syndrome. On the other hand, hypokalaemia with acidosis may be caused by diarrhoea, renal tubular acidosis, acetazolamide, or partially treated diabetic ketoacidosis.

      It is important to note that magnesium deficiency may also cause hypokalaemia. In such cases, normalizing potassium levels may be difficult until the magnesium deficiency has been corrected. Understanding the causes of hypokalaemia can help in its diagnosis and treatment.

    • This question is part of the following fields:

      • Renal System
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  • Question 19 - A 25-year-old suffers a groin stab wound resulting in hypovolaemic shock. What would...

    Correct

    • A 25-year-old suffers a groin stab wound resulting in hypovolaemic shock. What would be the probable observation on examining his urine?

      Your Answer: Increased specific gravity

      Explanation:

      When blood pressure drops below the level at which the kidney can regulate its blood flow, hypovolemic shock can lead to a reduction in renal blood flow. This can cause an increase in specific gravity as the body tries to retain water to maintain blood volume.

      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.

    • This question is part of the following fields:

      • Renal System
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  • Question 20 - In individuals experiencing abdominal discomfort and nausea, along with recurrent kidney stones and...

    Incorrect

    • In individuals experiencing abdominal discomfort and nausea, along with recurrent kidney stones and urinary tract infections, what structural anomaly might be detected on imaging?

      Your Answer: Kidneys with multiple cysts

      Correct Answer: Fused kidneys crossing anterior to the aorta

      Explanation:

      The presence of abdominal pain, nausea, and recurrent kidney stones and urinary tract infections raises the possibility of a horseshoe kidney, where two kidneys are fused in the midline and pass in front of the aorta. This is a congenital condition that is more prevalent in males and is linked to a higher incidence of urinary tract infections. Unfortunately, there is no cure for this condition, and treatment is focused on managing symptoms.

      Moreover, the identification of numerous cysts in the kidneys suggests the presence of polycystic kidney disease, which is associated with diverticulosis and cerebral aneurysms.

      Understanding the Risk Factors for Renal Stones

      Renal stones, also known as kidney stones, are solid masses that form in the kidneys and can cause severe pain and discomfort. There are several risk factors that can increase the likelihood of developing renal stones. Dehydration is a significant risk factor, as it can lead to concentrated urine and the formation of stones. Other factors include hypercalciuria, hyperparathyroidism, hypercalcaemia, cystinuria, high dietary oxalate, renal tubular acidosis, medullary sponge kidney, polycystic kidney disease, and exposure to beryllium or cadmium.

      Urate stones, a type of renal stone, are caused by the precipitation of uric acid. Risk factors for urate stones include gout and ileostomy, which can result in acidic urine due to the loss of bicarbonate and fluid.

      In addition to these factors, certain medications can also contribute to the formation of renal stones. Loop diuretics, steroids, acetazolamide, and theophylline can promote the formation of calcium stones, while thiazides can prevent them by increasing distal tubular calcium resorption.

      It is important to understand these risk factors and take steps to prevent the formation of renal stones, such as staying hydrated, maintaining a healthy diet, and avoiding medications that may contribute to their formation.

    • This question is part of the following fields:

      • Renal System
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  • Question 21 - A 54-year-old male comes to the emergency surgical department complaining of intense abdominal...

    Incorrect

    • A 54-year-old male comes to the emergency surgical department complaining of intense abdominal pain. He has no history of malignancy and is generally healthy. The biochemistry lab contacts the ward with an urgent message that his corrected calcium level is 3.6 mmol/l. What is the preferred medication for treating this abnormality?

      Your Answer: Dexamethasone

      Correct Answer: IV Pamidronate

      Explanation:

      Pamidronate is the preferred drug due to its high efficacy and prolonged effects. If using calcitonin, it should be combined with another medication to ensure continued treatment of hypercalcemia after its short-term effects wear off. Zoledronate is the preferred option for cases related to cancer.

      Managing Hypercalcaemia

      Hypercalcaemia can be managed through various methods. The first step is to rehydrate the patient with normal saline, usually at a rate of 3-4 litres per day. Once rehydration is achieved, bisphosphonates can be administered. These drugs take 2-3 days to work, with maximum effect seen at 7 days.

      Calcitonin is another option that can be used for quicker effect than bisphosphonates. In cases of sarcoidosis, steroids may also be used. However, loop diuretics such as furosemide should be used with caution as they may worsen electrolyte derangement and volume depletion. They are typically reserved for patients who cannot tolerate aggressive fluid rehydration.

      In summary, the management of hypercalcaemia involves rehydration with normal saline followed by the use of bisphosphonates, calcitonin, or steroids in certain cases. Loop diuretics may also be used, but with caution. It is important to monitor electrolyte levels and adjust treatment accordingly.

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      • Renal System
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  • Question 22 - A 45-year-old woman visits her doctor complaining of muscle cramps and fatigue. Upon...

    Incorrect

    • A 45-year-old woman visits her doctor complaining of muscle cramps and fatigue. Upon ruling out any musculoskeletal issues, a blood test is conducted which reveals hyperparathyroidism and low serum phosphate levels. It is suspected that the low phosphate levels are due to the inhibitory effect of parathyroid hormone on renal phosphate reabsorption. Which site in the kidney is most likely affected by parathyroid hormone to cause these blood results?

      Your Answer: Distal convoluted tubule

      Correct Answer: Proximal convoluted tubule

      Explanation:

      The proximal convoluted tubule is responsible for the majority of renal phosphate reabsorption. This occurs through co-transport with sodium and up to two thirds of filtered water. The thin ascending limb of the Loop of Henle is impermeable to water but highly permeable to sodium and chloride, while reabsorption of these ions occurs in the thick ascending limb. Parathyroid hormone is most effective at the proximal convoluted tubule due to its role in regulating phosphate 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.

    • This question is part of the following fields:

      • Renal System
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  • Question 23 - A 65-year-old woman is admitted to the ICU with a multidrug-resistant urinary tract...

    Correct

    • A 65-year-old woman is admitted to the ICU with a multidrug-resistant urinary tract infection. She has a medical history of type 2 diabetes, hypertension, and a previous cerebrovascular accident. After three days, she experiences an altered sensorium and her urine output has been 100 ml over the past 12 hours. Her creatinine level has increased from 1 mg/dl to almost 5 mg/dl, and her blood pressure is currently 180/100 mmHg. The patient is currently taking amikacin, insulin, atorvastatin, atenolol, ramipril, and clopidogrel.

      Which medication, other than ramipril, should be discontinued for this patient?

      Your Answer: Amikacin

      Explanation:

      The patient’s symptoms suggest that they may be experiencing acute kidney injury (AKI) as a result of a severe urinary tract infection and potential sepsis. It is important to note that ACE inhibitors such as ramipril should not be used in cases of AKI, and aminoglycosides like amikacin should also be discontinued. Beta-blockers like atenolol, on the other hand, are generally safe to use in AKI patients and may be preferred over ACE inhibitors and ARBs as antihypertensives. While statins like atorvastatin are generally safe in AKI, they can rarely cause rhabdomyolysis, which can worsen renal function and lead to renal failure. Therefore, patients who experience muscle pain should be evaluated further to rule out the possibility of rhabdomyolysis.

      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.

    • This question is part of the following fields:

      • Renal System
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  • Question 24 - A 62-year-old male with type 2 diabetes is urgently referred by his GP...

    Correct

    • A 62-year-old male with type 2 diabetes is urgently referred by his GP due to poor glycaemic control for the past three days, with home blood glucose readings around 25 mmol/L. He is currently being treated with metformin and lisinopril. Yesterday, his GP checked his U+E and found that his serum sodium was 138 mmol/L (137-144), serum potassium was 5.8 mmol/L (3.5-4.9), serum urea was 20 mmol/L (2.5-7.5), and serum creatinine was 350 µmol/L (60-110). On examination, he has a temperature of 39°C, a pulse of 108 bpm, a blood pressure of 96/60 mmHg, a respiratory rate of 32/min, and oxygen saturations of 99% on air. His cardiovascular, respiratory, and abdominal examination are otherwise normal. Further investigations reveal a plasma glucose level of 17 mmol/L (3.0-6.0) and urine analysis showing blood ++ and protein ++, but ketones are negative. What is the likely diagnosis?

      Your Answer: Sepsis

      Explanation:

      The causes of septic shock are important to understand in order to provide appropriate treatment and improve patient outcomes. Septic shock can cause fever, hypotension, and renal failure, as well as tachypnea due to metabolic acidosis. However, it is crucial to rule out other conditions such as hyperosmolar hyperglycemic state or diabetic ketoacidosis, which have different symptoms and diagnostic criteria.

      While metformin can contribute to acidosis, it is unlikely to be the primary cause in this case. Diabetic patients may be prone to renal tubular acidosis, but this is not likely to be the cause of an acute presentation. Instead, a type IV renal tubular acidosis, characterized by hyporeninaemic hypoaldosteronism, may be a more likely association.

      Overall, it is crucial to carefully evaluate patients with septic shock and consider all possible causes of their symptoms. By ruling out other conditions and identifying the underlying cause of the acidosis, healthcare providers can provide targeted treatment and improve patient outcomes. Further research and education on septic shock and its causes can also help to improve diagnosis and treatment in the future.

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      • Renal System
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  • Question 25 - A 50-year-old man visits his doctor complaining of pain in his lower back....

    Correct

    • A 50-year-old man visits his doctor complaining of pain in his lower back. He reports seeing blood in his urine and feeling a lump in his left flank, causing him great concern. The doctor plans to perform an ultrasound.
      What is the probable diagnosis at this point?

      Your Answer: Renal cell carcinoma

      Explanation:

      Common Kidney Conditions and Their Symptoms

      Haematuria, loin pain, and an abdominal mass are the three main symptoms associated with renal cell carcinoma. Patients may also experience weight loss and malaise. Diagnostic tests such as ultrasonography and excretion urography can reveal the presence of a solid lesion or space-occupying lesion. CT and MRI scans may be used to determine the stage of the tumour. Nephrectomy is the preferred treatment option, unless the patient’s second kidney is not functioning properly.

      Nephrotic syndrome is a kidney condition that causes excessive protein excretion. Patients typically experience swelling around the eyes and legs.

      Renal calculi, or kidney stones, can cause severe flank pain and haematuria. Muscle spasms occur as the body tries to remove the stone.

      Urinary tract infections are more common in women and present with symptoms such as frequent urination, painful urination, suprapubic pain, and haematuria.

      In summary, these common kidney conditions can cause a range of symptoms and require different diagnostic tests and treatment options. It is important to seek medical attention if any of these symptoms are present.

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      • Renal System
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  • Question 26 - A 35-year-old man with end-stage renal failure due to polycystic kidney disease is...

    Incorrect

    • A 35-year-old man with end-stage renal failure due to polycystic kidney disease is being evaluated for a possible kidney transplant. Donor screening, which involves human leukocyte antigen (HLA) testing, has been conducted on several family members. Which HLA class is the most crucial in minimizing rejection risk for this patient?

      Your Answer: DQ

      Correct Answer: DR

      Explanation:

      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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      • Renal System
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  • Question 27 - A 67-year-old retired farmer presents to the emergency department with complaints of abdominal...

    Incorrect

    • A 67-year-old retired farmer presents to the emergency department with complaints of abdominal pain and inability to urinate for the past 24 hours. He reports a history of slow urine flow and difficulty emptying his bladder for the past few years. The patient has a medical history of type 2 diabetes mellitus, hypertension, and lower back pain, and underwent surgery for an inguinal hernia 2 years ago. Ultrasound reveals a distended bladder and hydronephrosis, and the patient undergoes urethral catheterization. Further investigation shows an enlarged prostate and an increase in free prostate-specific antigen (PSA), and a prostate biopsy is scheduled. Which part of the prostate is most likely causing bladder obstruction in this patient?

      Your Answer: Lateral and posterior lobe

      Correct Answer: Lateral and middle lobe lobe

      Explanation:

      A man presented with symptoms of acute urinary retention and a history of poor urine flow and straining to void, suggesting bladder outlet obstruction possibly due to an enlarged prostate. While prostatic adenocarcinoma is common in men over 50, it is unlikely to cause urinary symptoms. However, patients should still be screened for it to allow for early intervention if necessary. The man’s increased levels of free PSA indicate BPH rather than prostatic adenocarcinoma, as the latter would result in decreased free PSA and increased bound-PSA levels.

      The lateral and middle lobes of the prostate are closest to the urethra and their hyperplasia can compress it, leading to urinary and voiding symptoms. If the urethra is completely compressed, acute urinary retention and bladder outlet obstruction can occur. The anterior lobe is rarely enlarged in BPH and is not positioned to obstruct the urethra, while the posterior lobe is mostly involved in prostatic adenocarcinoma but does not typically cause urinary symptoms due to its distance from the urethra.

      Benign prostatic hyperplasia (BPH) is a common condition that affects older men, with around 50% of 50-year-old men showing evidence of BPH and 30% experiencing symptoms. The risk of BPH increases with age, with around 80% of 80-year-old men having evidence of the condition. Ethnicity also plays a role, with black men having a higher risk than white or Asian men. BPH typically presents with lower urinary tract symptoms (LUTS), which can be categorised into obstructive (voiding) symptoms and irritative (storage) symptoms. Complications of BPH can include urinary tract infections, retention, and obstructive uropathy.

      Assessment of BPH may involve dipstick urine testing, U&Es, and PSA testing if obstructive symptoms are present or if the patient is concerned about prostate cancer. A urinary frequency-volume chart and the International Prostate Symptom Score (IPSS) can also be used to assess the severity of LUTS and their impact on quality of life. Management options for BPH include watchful waiting, alpha-1 antagonists, 5 alpha-reductase inhibitors, combination therapy, and surgery. Alpha-1 antagonists are considered first-line for moderate-to-severe voiding symptoms and can improve symptoms in around 70% of men, but may cause adverse effects such as dizziness and dry mouth. 5 alpha-reductase inhibitors may slow disease progression and reduce prostate volume, but can cause adverse effects such as erectile dysfunction and reduced libido. Combination therapy may be used for bothersome moderate-to-severe voiding symptoms and prostatic enlargement. Antimuscarinic drugs may be tried for persistent storage symptoms. Surgery, such as transurethral resection of the prostate (TURP), may also be an option.

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      • Renal System
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  • Question 28 - A 56-year-old man with end stage diabetic nephropathy is undergoing evaluation for a...

    Correct

    • A 56-year-old man with end stage diabetic nephropathy is undergoing evaluation for a renal transplant. In terms of HLA matching between donor and recipient, which HLA antigen is the most crucial to match?

      Your Answer: DR

      Explanation:

      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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      • Renal System
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  • Question 29 - A 70-year-old woman with bilateral pitting edema that extends above the knee is...

    Incorrect

    • A 70-year-old woman with bilateral pitting edema that extends above the knee is prescribed furosemide. What is the mechanism of action of this medication?

      Your Answer: Inhibits the sodium-chloride transporter

      Correct Answer: Inhibits the sodium-potassium-chloride cotransporter

      Explanation:

      Furosemide is a type of loop diuretic that works by inhibiting the cotransporter in the thick ascending loop of Henle, which prevents the reabsorption of sodium, chloride, and potassium. This results in significant diuresis.

      Mannitol is an osmotic diuretic that is commonly used to reduce intracranial pressure after a head injury. Spironolactone is an aldosterone antagonist, while bendroflumethiazide acts on the sodium-chloride transporter in the distal convoluted tubule. Acetazolamide is a carbonic anhydrase inhibitor that is often prescribed for the treatment of acute angle closure glaucoma.

      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.

    • This question is part of the following fields:

      • Renal System
      39.3
      Seconds
  • Question 30 - A 65-year-old patient is admitted to the hospital with a chief complaint of...

    Correct

    • A 65-year-old patient is admitted to the hospital with a chief complaint of lethargy and a vague medical history. As part of the assessment, a venous blood gas (VBG) is performed and the results are as follows:

      Na+ 137 mmol/L (135 - 145)
      K+ 3.0 mmol/L (3.5 - 5.0)
      Cl- 105 mEq/L (98 - 106)
      pH 7.29 (7.35-7.45)
      pO2 42mmHg (35 - 45)
      pCO2 46mmHg (42 - 48)
      HCO3- 19 mmol/L (22 - 26)
      BE -3 mmol/L (-2 to +2)

      What is the most likely cause of this patient's presentation?

      Your Answer: Diarrhoea

      Explanation:

      The likely cause of the patient’s normal anion gap metabolic acidosis is diarrhoea. The anion gap calculation shows a normal range of 14 mmol/L, which is within the normal range of 8-14 mmol/L. Diarrhoea causes a loss of bicarbonate from the GI tract, resulting in less alkali to balance out the acid in the blood. Additionally, diarrhoea causes hypokalaemia due to potassium ion loss from the GI tract. COPD, Cushing’s syndrome, and diabetic ketoacidosis are incorrect options as they would result in respiratory acidosis, metabolic alkalosis, and raised anion gap metabolic acidosis, respectively.

      Understanding Metabolic Acidosis

      Metabolic acidosis is a condition that can be classified based on the anion gap, which is calculated by subtracting the sum of chloride and bicarbonate from the sum of sodium and potassium. The normal range for anion gap is 10-18 mmol/L. If a question provides the chloride level, it may be an indication to calculate the anion gap.

      Hyperchloraemic metabolic acidosis is a type of metabolic acidosis with a normal anion gap. It can be caused by gastrointestinal bicarbonate loss, prolonged diarrhea, ureterosigmoidostomy, fistula, renal tubular acidosis, drugs like acetazolamide, ammonium chloride injection, and Addison’s disease. On the other hand, raised anion gap metabolic acidosis is caused by lactate, ketones, urate, acid poisoning, and other factors.

      Lactic acidosis is a type of metabolic acidosis that is caused by high lactate levels. It can be further classified into two types: lactic acidosis type A, which is caused by sepsis, shock, hypoxia, and burns, and lactic acidosis type B, which is caused by metformin. Understanding the different types and causes of metabolic acidosis is important in diagnosing and treating the condition.

    • This question is part of the following fields:

      • Renal System
      66.1
      Seconds

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