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Question 1
Correct
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What is the equivalent of cardiac preload?
Your Answer: End diastolic volume
Explanation:Preload, also known as end diastolic volume, follows the Frank Starling principle where a slight increase results in an increase in cardiac output. However, if preload is significantly increased, such as exceeding 250ml, it can lead to a decrease in cardiac output.
The heart has four chambers and generates pressures of 0-25 mmHg on the right side and 0-120 mmHg on the left. The cardiac output is the product of heart rate and stroke volume, typically 5-6L per minute. The cardiac impulse is generated in the sino atrial node and conveyed to the ventricles via the atrioventricular node. Parasympathetic and sympathetic fibers project to the heart via the vagus and release acetylcholine and noradrenaline, respectively. The cardiac cycle includes mid diastole, late diastole, early systole, late systole, and early diastole. Preload is the end diastolic volume and afterload is the aortic pressure. Laplace’s law explains the rise in ventricular pressure during the ejection phase and why a dilated diseased heart will have impaired systolic function. Starling’s law states that an increase in end-diastolic volume will produce a larger stroke volume up to a point beyond which stroke volume will fall. Baroreceptor reflexes and atrial stretch receptors are involved in regulating cardiac output.
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This question is part of the following fields:
- Cardiovascular System
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Question 2
Incorrect
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Which one of the following vessels does not directly drain into the inferior vena cava?
Your Answer: Right common iliac
Correct Answer: Superior mesenteric vein
Explanation:The portal vein receives drainage from the superior mesenteric vein, while the right and left hepatic veins directly drain into it. This can result in significant bleeding in cases of severe liver lacerations.
Anatomy of the Inferior Vena Cava
The inferior vena cava (IVC) originates from the fifth lumbar vertebrae and is formed by the merging of the left and right common iliac veins. It passes to the right of the midline and receives drainage from paired segmental lumbar veins throughout its length. The right gonadal vein empties directly into the cava, while the left gonadal vein usually empties into the left renal vein. The renal veins and hepatic veins are the next major veins that drain into the IVC. The IVC pierces the central tendon of the diaphragm at the level of T8 and empties into the right atrium of the heart.
The IVC is related anteriorly to the small bowel, the first and third parts of the duodenum, the head of the pancreas, the liver and bile duct, the right common iliac artery, and the right gonadal artery. Posteriorly, it is related to the right renal artery, the right psoas muscle, the right sympathetic chain, and the coeliac ganglion.
The IVC is divided into different levels based on the veins that drain into it. At the level of T8, it receives drainage from the hepatic vein and inferior phrenic vein before piercing the diaphragm. At the level of L1, it receives drainage from the suprarenal veins and renal vein. At the level of L2, it receives drainage from the gonadal vein, and at the level of L1-5, it receives drainage from the lumbar veins. Finally, at the level of L5, the common iliac vein merges to form the IVC.
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This question is part of the following fields:
- Cardiovascular System
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Question 3
Incorrect
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Sarah is a 60-year-old female who has been recently diagnosed with hypertension. After a 3-month trial of improving diet and increasing exercise, her blood pressure is still elevated at 160/100 mmHg. Her doctor decides to start her on enalapril, an ACE inhibitor, to treat her hypertension.
At what location in the body is enalapril activated to its pharmacologically active compound?Your Answer: At site of therapeutic target tissues/cells
Correct Answer: Under phase 1 metabolism in the liver
Explanation:ACE inhibitors are prodrugs that require activation through phase 1 metabolism in the liver, except for captopril and lisinopril which are administered as active drugs. The hepatic esterolysis process converts ACE inhibitors into their active metabolite, allowing them to function as subtype 1B prodrugs. It is important to note that ACE inhibitors are not activated at the site of therapeutic action, and belong to subtype 1A and 2C prodrugs that are activated intracellularly or extracellularly at the therapeutic site, respectively. Answer 3 is a distractor, as ACE inhibitors do not activate ACE in the lung, but rather inhibit its activity. Answer 5 is also incorrect, as most ACE inhibitors require activation through metabolism.
Angiotensin-converting enzyme (ACE) inhibitors are commonly used as the first-line treatment for hypertension and heart failure in younger patients. However, they may not be as effective in treating hypertensive Afro-Caribbean patients. ACE inhibitors are also used to treat diabetic nephropathy and prevent ischaemic heart disease. These drugs work by inhibiting the conversion of angiotensin I to angiotensin II and are metabolized in the liver.
While ACE inhibitors are generally well-tolerated, they can cause side effects such as cough, angioedema, hyperkalaemia, and first-dose hypotension. Patients with certain conditions, such as renovascular disease, aortic stenosis, or hereditary or idiopathic angioedema, should use ACE inhibitors with caution or avoid them altogether. Pregnant and breastfeeding women should also avoid these drugs.
Patients taking high-dose diuretics may be at increased risk of hypotension when using ACE inhibitors. Therefore, it is important to monitor urea and electrolyte levels before and after starting treatment, as well as any changes in creatinine and potassium levels. Acceptable changes include a 30% increase in serum creatinine from baseline and an increase in potassium up to 5.5 mmol/l. Patients with undiagnosed bilateral renal artery stenosis may experience significant renal impairment when using ACE inhibitors.
The current NICE guidelines recommend using a flow chart to manage hypertension, with ACE inhibitors as the first-line treatment for patients under 55 years old. However, individual patient factors and comorbidities should be taken into account when deciding on the best treatment plan.
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This question is part of the following fields:
- Cardiovascular System
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Question 4
Incorrect
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A 14-year-old male immigrant from India visits his primary care physician complaining of gradually worsening shortness of breath, particularly during physical exertion, and widespread joint pain. He had a severe untreated throat infection in the past, but his vaccination record is complete. During the physical examination, a high-pitched holosystolic murmur is heard at the apex with radiation to the axilla.
Hemoglobin: 135 g/L
Platelets: 150 * 10^9/L
White blood cells: 9.5 * 10^9/L
Anti-streptolysin O titers: >200 units/mL
What is the most probable histological finding in his heart?Your Answer: Schiller-Duval bodies
Correct Answer: Aschoff bodies
Explanation:Rheumatic heart fever is characterized by the presence of Aschoff bodies, which are granulomatous nodules. The mitral valve is commonly affected in this condition, and an elevated ASO titre indicates exposure to group A streptococcus bacteria. Rheumatic heart disease is also associated with the presence of Anitschkow cells, which are enlarged macrophages with an ovoid, wavy, rod-like nucleus. Other types of bodies seen in different conditions include Councilman bodies in hepatitis C and yellow fever, Mallory bodies in alcoholism affecting hepatocytes, and Call-Exner bodies in granulosa cell tumours.
Rheumatic fever is a condition that occurs as a result of an immune response to a recent Streptococcus pyogenes infection, typically occurring 2-4 weeks after the initial infection. The pathogenesis of rheumatic fever involves the activation of the innate immune system, leading to antigen presentation to T cells. B and T cells then produce IgG and IgM antibodies, and CD4+ T cells are activated. This immune response is thought to be cross-reactive, mediated by molecular mimicry, where antibodies against M protein cross-react with myosin and the smooth muscle of arteries. This response leads to the clinical features of rheumatic fever, including Aschoff bodies, which are granulomatous nodules found in rheumatic heart fever.
To diagnose rheumatic fever, evidence of recent streptococcal infection must be present, along with 2 major criteria or 1 major criterion and 2 minor criteria. Major criteria include erythema marginatum, Sydenham’s chorea, polyarthritis, carditis and valvulitis, and subcutaneous nodules. Minor criteria include raised ESR or CRP, pyrexia, arthralgia, and prolonged PR interval.
Management of rheumatic fever involves antibiotics, typically oral penicillin V, as well as anti-inflammatories such as NSAIDs as first-line treatment. Any complications that develop, such as heart failure, should also be treated. It is important to diagnose and treat rheumatic fever promptly to prevent long-term complications such as rheumatic heart disease.
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This question is part of the following fields:
- Cardiovascular System
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Question 5
Correct
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A 60-year-old woman who was discharged from the hospital 3 days ago presents to the emergency department with complaints of chest tightness and severe shortness of breath. While being evaluated, the patient suddenly becomes unresponsive and experiences cardiac arrest. Despite receiving appropriate life-saving measures, there is no return of spontaneous circulation and the patient is declared dead. Upon autopsy, a slit-like tear is discovered in the anterior wall of the left ventricle.
What factors may have contributed to the cardiac finding observed in this patient?Your Answer: Coronary atherosclerosis
Explanation:Left Ventricular Free Wall Rupture Post-MI
Following a myocardial infarction (MI), the weakened myocardial wall may be unable to contain high left ventricular (LV) pressures, leading to mechanical complications such as left ventricular free wall rupture. This occurs 3-14 days post-MI and is characterized by macrophages and granulation tissue at the margins. Patients are also at high risk of papillary muscle rupture and left ventricular pseudoaneurysm. The patient’s autopsy finding of a slit-like tear in the anterior LV wall is consistent with this complication.
Coronary atherosclerosis is the most likely cause of the patient’s MI, as it is a common underlying condition. Prolonged alcohol consumption and recent viral infection can lead to dilated cardiomyopathy, while recurrent bacterial pharyngitis can cause inflammatory damage to both the myocardium and valvular endocardium. Repeated blood transfusion is not a known risk factor for left ventricular free wall rupture.
Myocardial infarction (MI) can lead to various complications, which can occur immediately, early, or late after the event. Cardiac arrest is the most common cause of death following MI, usually due to ventricular fibrillation. Cardiogenic shock may occur if a large part of the ventricular myocardium is damaged, and it is difficult to treat. Chronic heart failure may result from ventricular myocardium dysfunction, which can be managed with loop diuretics, ACE-inhibitors, and beta-blockers. Tachyarrhythmias, such as ventricular fibrillation and ventricular tachycardia, are common complications. Bradyarrhythmias, such as atrioventricular block, are more common following inferior MI. Pericarditis is common in the first 48 hours after a transmural MI, while Dressler’s syndrome may occur 2-6 weeks later. Left ventricular aneurysm and free wall rupture, ventricular septal defect, and acute mitral regurgitation are other complications that may require urgent medical attention.
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This question is part of the following fields:
- Cardiovascular System
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Question 6
Incorrect
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A 70-year-old man visits his primary care physician complaining of paroxysmal nocturnal dyspnoea and increasing orthopnoea. The physician suspects heart failure and orders a chest X-ray. What signs on the chest X-ray would indicate heart failure?
Your Answer: Increased opacity in the left upper zone
Correct Answer: Upper zone vessel enlargement
Explanation:Diagnosis of Chronic Heart Failure
Chronic heart failure is a serious condition that requires prompt diagnosis and management. In 2018, the National Institute for Health and Care Excellence (NICE) updated its guidelines on the diagnosis and management of chronic heart failure. According to the new guidelines, all patients should undergo an N-terminal pro-B-type natriuretic peptide (NT‑proBNP) blood test as the first-line investigation, regardless of whether they have previously had a myocardial infarction or not.
Interpreting the NT-proBNP test is crucial in determining the severity of the condition. If the levels are high, specialist assessment, including transthoracic echocardiography, should be arranged within two weeks. If the levels are raised, specialist assessment, including echocardiogram, should be arranged within six weeks.
BNP is a hormone produced mainly by the left ventricular myocardium in response to strain. Very high levels of BNP are associated with a poor prognosis. The table above shows the different levels of BNP and NTproBNP and their corresponding interpretations.
It is important to note that certain factors can alter the BNP level. For instance, left ventricular hypertrophy, ischaemia, tachycardia, and right ventricular overload can increase BNP levels, while diuretics, ACE inhibitors, beta-blockers, angiotensin 2 receptor blockers, and aldosterone antagonists can decrease BNP levels. Therefore, it is crucial to consider these factors when interpreting the NT-proBNP test.
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This question is part of the following fields:
- Cardiovascular System
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Question 7
Incorrect
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A 40-year-old woman visits her GP complaining of muscle cramps, fatigue, and tingling in her fingers and toes for the past two weeks. Upon conducting a blood test, the doctor discovers low levels of serum calcium and parathyroid hormone. The patient is new to the clinic and seems a bit confused, possibly due to hypocalcemia, and is unable to provide a complete medical history. However, she mentions that she was recently hospitalized. What is the most probable cause of her hypoparathyroidism?
Your Answer: Vitamin D deficiency
Correct Answer: Thyroidectomy
Explanation:Due to their location behind the thyroid gland, the parathyroid glands are at risk of damage during a thyroidectomy, leading to iatrogenic hypoparathyroidism. This condition is characterized by low levels of both parathyroid hormone and calcium, indicating that the parathyroid glands are not responding to the hypocalcemia. The patient’s confusion and prolonged hospital stay are likely related to the surgery.
Hypocalcemia can also be caused by chronic kidney disease, which triggers an increase in parathyroid hormone production in an attempt to raise calcium levels, resulting in hyperparathyroidism. Additionally, a deficiency in vitamin D, which is activated by the kidneys and aids in calcium absorption in the terminal ileum, can also lead to hyperparathyroidism.
While a parathyroid adenoma is a common occurrence, it is more likely to cause hyperparathyroidism than hypoparathyroidism, which is a relatively rare side effect of thyroidectomy.
Anatomy and Development of the Parathyroid Glands
The parathyroid glands are four small glands located posterior to the thyroid gland within the pretracheal fascia. They develop from the third and fourth pharyngeal pouches, with those derived from the fourth pouch located more superiorly and associated with the thyroid gland, while those from the third pouch lie more inferiorly and may become associated with the thymus.
The blood supply to the parathyroid glands is derived from the inferior and superior thyroid arteries, with a rich anastomosis between the two vessels. Venous drainage is into the thyroid veins. The parathyroid glands are surrounded by various structures, with the common carotid laterally, the recurrent laryngeal nerve and trachea medially, and the thyroid anteriorly. Understanding the anatomy and development of the parathyroid glands is important for their proper identification and preservation during surgical procedures.
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This question is part of the following fields:
- Cardiovascular System
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Question 8
Incorrect
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A 68-year-old man arrives at the emergency department complaining of intense abdominal pain that spreads to his back. His medical history shows that he has an abdominal aortic aneurysm. During a FAST scan, it is discovered that the abdominal aorta is widely dilated, with the most significant expansion occurring at the point where it divides into the iliac arteries. What vertebral level corresponds to the location of the most prominent dilation observed in the FAST scan?
Your Answer: T12
Correct Answer: L4
Explanation:The abdominal aorta divides into two branches at the level of the fourth lumbar vertebrae. At the level of T12, the coeliac trunk arises, while at L1, the superior mesenteric artery branches off. The testicular artery and renal artery originate at L2, and at L3, the inferior mesenteric artery is formed.
The aorta is a major blood vessel that carries oxygenated blood from the heart to the rest of the body. At different levels along the aorta, there are branches that supply blood to specific organs and regions. These branches include the coeliac trunk at the level of T12, which supplies blood to the stomach, liver, and spleen. The left renal artery, at the level of L1, supplies blood to the left kidney. The testicular or ovarian arteries, at the level of L2, supply blood to the reproductive organs. The inferior mesenteric artery, at the level of L3, supplies blood to the lower part of the large intestine. Finally, at the level of L4, the abdominal aorta bifurcates, or splits into two branches, which supply blood to the legs and pelvis.
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This question is part of the following fields:
- Cardiovascular System
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Question 9
Incorrect
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A 55-year-old man is having a radical gastrectomy for stomach cancer. What structure must be divided to access the coeliac axis during the procedure?
Your Answer: Gastrosplenic ligament
Correct Answer: Lesser omentum
Explanation:The division of the lesser omentum is necessary during a radical gastrectomy as it constitutes one of the nodal stations that must be removed.
The Coeliac Axis and its Branches
The coeliac axis is a major artery that supplies blood to the upper abdominal organs. It has three main branches: the left gastric, hepatic, and splenic arteries. The hepatic artery further branches into the right gastric, gastroduodenal, right gastroepiploic, superior pancreaticoduodenal, and cystic arteries. Meanwhile, the splenic artery gives off the pancreatic, short gastric, and left gastroepiploic arteries. Occasionally, the coeliac axis also gives off one of the inferior phrenic arteries.
The coeliac axis is located anteriorly to the lesser omentum and is related to the right and left coeliac ganglia, as well as the caudate process of the liver and the gastric cardia. Inferiorly, it is in close proximity to the upper border of the pancreas and the renal vein.
Understanding the anatomy and branches of the coeliac axis is important in diagnosing and treating conditions that affect the upper abdominal organs, such as pancreatic cancer or gastric ulcers.
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This question is part of the following fields:
- Cardiovascular System
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Question 10
Incorrect
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A 75-year-old man presents to the emergency department with chest pain and shortness of breath while gardening. He reports that the pain has subsided and is able to provide a detailed medical history. He mentions feeling breathless while gardening and walking in the park, and occasionally feeling like he might faint. He has a history of hypertension, is a retired construction worker, and a non-smoker. On examination, the doctor detects a crescendo-decrescendo systolic ejection murmur. The ECG shows no ST changes and the troponin test is negative. What is the underlying pathology responsible for this man's condition?
Your Answer: Fibrous plaque formation in the coronary arteries
Correct Answer: Old-age related calcification of the aortic valves
Explanation:The patient’s symptoms suggest an ischemic episode of the myocardium, which could indicate an acute coronary syndrome (ACS). However, the troponin test and ECG results were negative, and there are no known risk factors for coronary artery disease. Instead, the presence of a crescendo-decrescendo systolic ejection murmur and the triad of breathlessness, chest pain, and syncope suggest a likely diagnosis of aortic stenosis, which is commonly caused by calcification of the aortic valves in older adults or abnormal valves in younger individuals.
Arteriolosclerosis in severe systemic hypertension leads to hyperplastic proliferation of smooth muscle cells in the arterial walls, resulting in an onion-skin appearance. This is distinct from hyaline arteriolosclerosis, which is associated with diabetes mellitus and hypertension. Atherosclerosis, characterized by fibrous plaque formation in the coronary arteries, can lead to cardiac ischemia and myocyte death if the plaque ruptures and forms a thrombus.
After a myocardial infarction, the rupture of the papillary muscle can cause mitral regurgitation, which is most likely to occur between days 2 and 7 as macrophages begin to digest necrotic myocardial tissue. The posteromedial papillary muscle is particularly at risk due to its single blood supply from the posterior descending artery.
Aortic stenosis is a condition characterized by the narrowing of the aortic valve, which can lead to various symptoms. These symptoms include chest pain, dyspnea, syncope or presyncope, and a distinct ejection systolic murmur that radiates to the carotids. Severe aortic stenosis can cause a narrow pulse pressure, slow rising pulse, delayed ESM, soft/absent S2, S4, thrill, duration of murmur, and left ventricular hypertrophy or failure. The condition can be caused by degenerative calcification, bicuspid aortic valve, William’s syndrome, post-rheumatic disease, or subvalvular HOCM.
Management of aortic stenosis depends on the severity of the condition and the presence of symptoms. Asymptomatic patients are usually observed, while symptomatic patients require valve replacement. Surgical AVR is the preferred treatment for young, low/medium operative risk patients, while TAVR is used for those with a high operative risk. Balloon valvuloplasty may be used in children without aortic valve calcification and in adults with critical aortic stenosis who are not fit for valve replacement. If the valvular gradient is greater than 40 mmHg and there are features such as left ventricular systolic dysfunction, surgery may be considered even if the patient is asymptomatic.
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This question is part of the following fields:
- Cardiovascular System
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Question 11
Incorrect
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A 30-year-old male arrives at the emergency department complaining of sudden dizziness and palpitations. His medical history reveals that he had infectious diarrhea a week ago and was prescribed a 10-day course of erythromycin. Upon examination, an ECG confirms fast atrial fibrillation. The physician decides to use amiodarone to convert the patient into sinus rhythm. What is one potential risk associated with the use of amiodarone in this patient?
Your Answer: Wolff-Parkinson-White (WPW) syndrome
Correct Answer: Ventricular arrhythmias
Explanation:The risk of ventricular arrhythmias is increased when amiodarone and erythromycin are used together due to their ability to prolong the QT interval. Manufacturers advise against using multiple drugs that prolong QT interval to avoid this risk. WPW syndrome is a congenital condition that involves abnormal conductive cardiac tissue and can lead to reentrant tachycardia circuit in association with SVT. Amiodarone can cause a slate-grey appearance of the skin, while drugs like rifampicin can cause orange discoloration of body fluids. COPD is associated with multifocal atrial tachycardia.
Amiodarone is a medication used to treat various types of abnormal heart rhythms. It works by blocking potassium channels, which prolongs the action potential and helps to regulate the heartbeat. However, it also has other effects, such as blocking sodium channels. Amiodarone has a very long half-life, which means that loading doses are often necessary. It should ideally be given into central veins to avoid thrombophlebitis. Amiodarone can cause proarrhythmic effects due to lengthening of the QT interval and can interact with other drugs commonly used at the same time. Long-term use of amiodarone can lead to various adverse effects, including thyroid dysfunction, corneal deposits, pulmonary fibrosis/pneumonitis, liver fibrosis/hepatitis, peripheral neuropathy, myopathy, photosensitivity, a ‘slate-grey’ appearance, thrombophlebitis, injection site reactions, and bradycardia. Patients taking amiodarone should be monitored regularly with tests such as TFT, LFT, U&E, and CXR.
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This question is part of the following fields:
- Cardiovascular System
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Question 12
Correct
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A 65-year-old man arrives at the emergency department via ambulance complaining of chest pain. He reports that the pain started suddenly a few minutes ago and describes it as a sharp sensation that extends to his back.
The patient has a history of uncontrolled hypertension.
A CT scan reveals an enlarged mediastinum.
What is the most likely cause of the diagnosis?Your Answer: Tear in the tunica intima of the aorta
Explanation:An aortic dissection is characterized by a tear in the tunica intima of the aortic wall, which is a medical emergency. Patients typically experience sudden-onset, central chest pain that radiates to the back. This condition is more common in patients with hypertension and is associated with a widened mediastinum on a CT scan.
Aortic dissection is a serious condition that can cause chest pain. It occurs when there is a tear in the inner layer of the aorta’s wall. Hypertension is the most significant risk factor, but it can also be associated with trauma, bicuspid aortic valve, and certain genetic disorders. Symptoms of aortic dissection include severe and sharp chest or back pain, weak or absent pulses, hypertension, and aortic regurgitation. Specific arteries’ involvement can cause other symptoms such as angina, paraplegia, or limb ischemia. The Stanford classification divides aortic dissection into type A, which affects the ascending aorta, and type B, which affects the descending aorta. The DeBakey classification further divides type A into type I, which extends to the aortic arch and beyond, and type II, which is confined to the ascending aorta. Type III originates in the descending aorta and rarely extends proximally.
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This question is part of the following fields:
- Cardiovascular System
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Question 13
Correct
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A 67-year-old man with a stable angina history for two years visits his cardiologist for a regular check-up. During the review, the cardiologist observes that the patient's heart rate is low at 46 bpm. As a result, the cardiologist decides to replace his beta-blocker with a new anti-anginal drug called nicorandil.
What is the mode of action of the patient's new medication?Your Answer: Potassium channel activator through activation of guanylyl cyclase
Explanation:Nicorandil activates potassium channels, leading to vasodilation. This activation triggers guanylyl cyclase, which increases the production of cyclic GMP (cGMP) and activates protein kinase G (PKG). PKG phosphorylates and inhibits GTPase RhoA, reducing Rho-kinase activity and increasing myosin phosphatase activity. As a result, the smooth muscle becomes less sensitive to calcium, leading to dilation of the large coronary arteries and improved perfusion. Nicorandil does not significantly affect calcium or sodium channels. This mechanism helps alleviate anginal symptoms.
Nicorandil is a medication that is commonly used to treat angina. It works by activating potassium channels, which leads to vasodilation. This process is achieved through the activation of guanylyl cyclase, which results in an increase in cGMP. However, there are some adverse effects associated with the use of nicorandil, including headaches, flushing, and the development of ulcers on the skin, mucous membranes, and eyes. Additionally, gastrointestinal ulcers, including anal ulceration, may also occur. It is important to note that nicorandil should not be used in patients with left ventricular failure.
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This question is part of the following fields:
- Cardiovascular System
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Question 14
Incorrect
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The cephalic vein penetrates the clavipectoral fascia to end in which of the following veins mentioned below?
Your Answer: Azygos
Correct Answer: Axillary
Explanation:The Cephalic Vein: Path and Connections
The cephalic vein is a major blood vessel that runs along the lateral side of the arm. It begins at the dorsal venous arch, which drains blood from the hand and wrist, and travels up the arm, crossing the anatomical snuffbox. At the antecubital fossa, the cephalic vein is connected to the basilic vein by the median cubital vein. This connection is commonly used for blood draws and IV insertions.
After passing through the antecubital fossa, the cephalic vein continues up the arm and pierces the deep fascia of the deltopectoral groove to join the axillary vein. This junction is located near the shoulder and marks the end of the cephalic vein’s path.
Overall, the cephalic vein plays an important role in the circulation of blood in the upper limb. Its connections to other major veins in the arm make it a valuable site for medical procedures, while its path through the deltopectoral groove allows it to contribute to the larger network of veins that drain blood from the upper body.
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This question is part of the following fields:
- Cardiovascular System
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Question 15
Incorrect
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A 78-year-old woman visits her doctor complaining of increasing breathlessness at night and swollen ankles over the past 10 months. She has a medical history of ischaemic heart disease, but an echocardiogram reveals normal valve function. During the examination, the doctor detects a low-pitched sound at the start of diastole, following S2. What is the probable reason for this sound?
Your Answer: Aortic regurgitation
Correct Answer: Rapid movement of blood entering ventricles from atria
Explanation:S3 is an unusual sound that can be detected in certain heart failure patients. It is caused by the rapid movement and oscillation of blood into the ventricles.
Another abnormal heart sound, S4, is caused by forceful atrial contraction and occurs later in diastole.
While aortic regurgitation causes an early diastolic decrescendo murmur and mitral stenosis can cause a mid-diastolic rumble with an opening snap, these conditions are less likely as the echocardiogram reported normal valve function.
A patent ductus arteriosus typically causes a continuous murmur and would present earlier in life.
Heart sounds are the sounds produced by the heart during its normal functioning. The first heart sound (S1) is caused by the closure of the mitral and tricuspid valves, while the second heart sound (S2) is due to the closure of the aortic and pulmonary valves. The intensity of these sounds can vary depending on the condition of the valves and the heart. The third heart sound (S3) is caused by the diastolic filling of the ventricle and is considered normal in young individuals. However, it may indicate left ventricular failure, constrictive pericarditis, or mitral regurgitation in older individuals. The fourth heart sound (S4) may be heard in conditions such as aortic stenosis, HOCM, and hypertension, and is caused by atrial contraction against a stiff ventricle. The different valves can be best heard at specific sites on the chest wall, such as the left second intercostal space for the pulmonary valve and the right second intercostal space for the aortic valve.
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This question is part of the following fields:
- Cardiovascular System
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Question 16
Incorrect
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A 68-year-old woman comes into the emergency department with her daughter after experiencing shortness of breath for 2 hours. She is in poor condition with a heart rate of 128/min, blood pressure of 90/66 mmHg, O2 saturation of 94% on air, respiratory rate of 29/min, and temperature of 36.3ºC. Her legs are swollen up to her knees, and her JVP is visible at her ear lobe. She has a history of myocardial infarction 4 years ago, angina, and a smoking history of 20 packs per year.
What is the underlying cause of her presentation?Your Answer: Supply demand mismatch of the coronary circulation
Correct Answer: Reduced cardiac output
Explanation:The cause of the patient’s acute heart failure is a decrease in cardiac output, which may be due to biventricular failure. This is evidenced by peripheral edema and respiratory distress, including shortness of breath, high respiratory rate, and low oxygen saturation. These symptoms are likely caused by inadequate heart filling, leading to peripheral congestion and pulmonary edema or pleural effusion.
The pathophysiology of myocardial infarction is not relevant to the patient’s condition, as it is not explained by her peripheral edema and elevated JVP.
While shortness of breath in heart failure may be caused by reduced ventilation/perfusion due to pulmonary edema, this is only one symptom and not the underlying mechanism of the condition.
The overactivity of the renin-angiotensin system is a physiological response to decreased blood pressure or increased renal sympathetic firing, but it is not necessarily related to the patient’s current condition.
Understanding Acute Heart Failure: Symptoms and Diagnosis
Acute heart failure (AHF) is a medical emergency that can occur suddenly or worsen over time. It can affect individuals with or without a history of pre-existing heart failure. Decompensated AHF is more common and is characterized by a background history of HF. AHF is typically caused by a reduced cardiac output resulting from a functional or structural abnormality. De-novo heart failure, on the other hand, is caused by increased cardiac filling pressures and myocardial dysfunction, usually due to ischaemia.
The most common precipitating causes of acute AHF are acute coronary syndrome, hypertensive crisis, acute arrhythmia, and valvular disease. Patients with heart failure may present with signs of fluid congestion, weight gain, orthopnoea, and breathlessness. They are broadly classified into four groups based on whether they present with or without hypoperfusion and fluid congestion. This classification is clinically useful in determining the therapeutic approach.
The symptoms of AHF include breathlessness, reduced exercise tolerance, oedema, fatigue, chest signs, and an S3-heart sound. Signs of AHF include cyanosis, tachycardia, elevated jugular venous pressure, and a displaced apex beat. Over 90% of patients with AHF have a normal or increased blood pressure.
The diagnostic workup for patients with AHF includes blood tests, chest X-ray, echocardiogram, and B-type natriuretic peptide. Blood tests are used to identify any underlying abnormalities, while chest X-ray findings include pulmonary venous congestion, interstitial oedema, and cardiomegaly. Echocardiogram is used to identify pericardial effusion and cardiac tamponade, while raised levels of B-type natriuretic peptide (>100mg/litre) indicate myocardial damage and support the diagnosis.
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This question is part of the following fields:
- Cardiovascular System
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Question 17
Correct
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As a certified physician, you are standing at the bus stop waiting to head to work. A 78-year-old woman is standing next to you and suddenly begins to express discomfort in her chest. She then collapses and loses consciousness. Fortunately, there is no threat to your safety. What steps do you take in this situation?
Your Answer: Perform basic life support for the lady, ask the husband to call 999
Explanation:In accordance with the Good Medical Practice 2013, it is your responsibility to provide assistance in the event of emergencies occurring in clinical settings or within the community. However, you must consider your own safety, level of expertise, and the availability of alternative care options before offering aid. This obligation encompasses providing basic life support and administering first aid. In situations where you are the sole individual present, it is incumbent upon you to fulfill this duty.
The 2015 Resus Council guidelines for adult advanced life support outline the steps to be taken in the event of a cardiac arrest. Patients are divided into those with ‘shockable’ rhythms (ventricular fibrillation/pulseless ventricular tachycardia) and ‘non-shockable’ rhythms (asystole/pulseless-electrical activity). Key points include the ratio of chest compressions to ventilation (30:2), continuing chest compressions while a defibrillator is charged, and delivering drugs via IV access or the intraosseous route. Adrenaline and amiodarone are recommended for non-shockable rhythms and VF/pulseless VT, respectively. Thrombolytic drugs should be considered if a pulmonary embolism is suspected. Atropine is no longer recommended for routine use in asystole or PEA. Following successful resuscitation, oxygen should be titrated to achieve saturations of 94-98%. The ‘Hs’ and ‘Ts’ outline reversible causes of cardiac arrest, including hypoxia, hypovolaemia, and thrombosis.
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This question is part of the following fields:
- Cardiovascular System
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Question 18
Correct
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Which one of the following statements relating to the basilar artery and its branches is false?
Your Answer: The posterior inferior cerebellar artery is the largest of the cerebellar arteries arising from the basilar artery
Explanation:The largest of the cerebellar arteries that originates from the vertebral artery is the posterior inferior cerebellar artery. The labyrinthine artery, which is thin and lengthy, may emerge from the lower section of the basilar artery. It travels alongside the facial and vestibulocochlear nerves into the internal auditory meatus. The posterior cerebral artery is frequently bigger than the superior cerebellar artery and is separated from the vessel, close to its source, by the oculomotor nerve. Arterial decompression is a widely accepted treatment for trigeminal neuralgia.
The Circle of Willis is an anastomosis formed by the internal carotid arteries and vertebral arteries on the bottom surface of the brain. It is divided into two halves and is made up of various arteries, including the anterior communicating artery, anterior cerebral artery, internal carotid artery, posterior communicating artery, and posterior cerebral arteries. The circle and its branches supply blood to important areas of the brain, such as the corpus striatum, internal capsule, diencephalon, and midbrain.
The vertebral arteries enter the cranial cavity through the foramen magnum and lie in the subarachnoid space. They then ascend on the anterior surface of the medulla oblongata and unite to form the basilar artery at the base of the pons. The basilar artery has several branches, including the anterior inferior cerebellar artery, labyrinthine artery, pontine arteries, superior cerebellar artery, and posterior cerebral artery.
The internal carotid arteries also have several branches, such as the posterior communicating artery, anterior cerebral artery, middle cerebral artery, and anterior choroid artery. These arteries supply blood to different parts of the brain, including the frontal, temporal, and parietal lobes. Overall, the Circle of Willis and its branches play a crucial role in providing oxygen and nutrients to the brain.
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This question is part of the following fields:
- Cardiovascular System
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Question 19
Incorrect
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A 12-year-old child presents to the emergency department with polyarthritis and chest pain that is relieved by leaning forward. Blood tests reveal a raised ESR and leucocytosis, but are otherwise normal. The child's parents mention that they have never vaccinated their child as they themselves are unvaccinated and rarely fall ill. In light of this information, you decide to order an anti-streptolysin-O-titre to investigate for recent streptococcal infection. What is the immunological term used to describe the mechanism behind the development of this condition?
Your Answer: Viral persistence
Correct Answer: Molecular mimicry
Explanation:Rheumatic fever is caused by molecular mimicry, where the M protein on the cell wall of Streptococcus pyogenes cross-reacts with myosin in the smooth muscles of arteries, leading to autoimmunity. This is evidenced by the patient’s symptoms of polyarthritis and chest pain, as well as the presence of anti-streptolysin-O-titre in their blood. Bystander activation, exposure to cryptic antigens, and super-antigens are all pathophysiological mechanisms that can lead to autoimmune destruction of tissues.
Rheumatic fever is a condition that occurs as a result of an immune response to a recent Streptococcus pyogenes infection, typically occurring 2-4 weeks after the initial infection. The pathogenesis of rheumatic fever involves the activation of the innate immune system, leading to antigen presentation to T cells. B and T cells then produce IgG and IgM antibodies, and CD4+ T cells are activated. This immune response is thought to be cross-reactive, mediated by molecular mimicry, where antibodies against M protein cross-react with myosin and the smooth muscle of arteries. This response leads to the clinical features of rheumatic fever, including Aschoff bodies, which are granulomatous nodules found in rheumatic heart fever.
To diagnose rheumatic fever, evidence of recent streptococcal infection must be present, along with 2 major criteria or 1 major criterion and 2 minor criteria. Major criteria include erythema marginatum, Sydenham’s chorea, polyarthritis, carditis and valvulitis, and subcutaneous nodules. Minor criteria include raised ESR or CRP, pyrexia, arthralgia, and prolonged PR interval.
Management of rheumatic fever involves antibiotics, typically oral penicillin V, as well as anti-inflammatories such as NSAIDs as first-line treatment. Any complications that develop, such as heart failure, should also be treated. It is important to diagnose and treat rheumatic fever promptly to prevent long-term complications such as rheumatic heart disease.
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This question is part of the following fields:
- Cardiovascular System
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Question 20
Incorrect
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A 60-year-old male is referred to the medical assessment unit by his physician suspecting a UTI. He has a permanent catheter in place due to urinary retention caused by benign prostatic hypertrophy. His blood test results reveal hypercalcemia. An ultrasound Doppler scan of his neck displays a distinct sonolucent signal indicating hyperactive parathyroid tissue and noticeable vasculature, which is likely the parathyroid veins. What is the structure that the parathyroid veins empty into?
Your Answer: Brachiocephalic veins
Correct Answer: Thyroid plexus of veins
Explanation:The veins of the parathyroid gland drain into the thyroid plexus of veins, as opposed to other possible drainage routes.
The cavernous sinus is a dural venous sinus that creates a cavity called the lateral sellar compartment, which is bordered by the temporal and sphenoid bones.
The brachiocephalic vein is formed by the merging of the subclavian and internal jugular veins, and also receives drainage from the left and right internal thoracic vein.
The external vertebral venous plexuses, which are most prominent in the cervical region, consist of anterior and posterior plexuses that freely anastomose with each other. The anterior plexuses are located in front of the vertebrae bodies, communicate with the basivertebral and intervertebral veins, and receive tributaries from the vertebral bodies. The posterior plexuses are situated partly on the posterior surfaces of the vertebral arches and their processes, and partly between the deep dorsal muscles.
The suboccipital venous plexus is responsible for draining deoxygenated blood from the back of the head, and is connected to the external vertebral venous plexuses.
Anatomy and Development of the Parathyroid Glands
The parathyroid glands are four small glands located posterior to the thyroid gland within the pretracheal fascia. They develop from the third and fourth pharyngeal pouches, with those derived from the fourth pouch located more superiorly and associated with the thyroid gland, while those from the third pouch lie more inferiorly and may become associated with the thymus.
The blood supply to the parathyroid glands is derived from the inferior and superior thyroid arteries, with a rich anastomosis between the two vessels. Venous drainage is into the thyroid veins. The parathyroid glands are surrounded by various structures, with the common carotid laterally, the recurrent laryngeal nerve and trachea medially, and the thyroid anteriorly. Understanding the anatomy and development of the parathyroid glands is important for their proper identification and preservation during surgical procedures.
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This question is part of the following fields:
- Cardiovascular System
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