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Question 1
Incorrect
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A 67-year-old woman visits the anticoagulation clinic for her regular INR test. She has a medical history of deep vein thrombosis and pulmonary embolism and is currently taking warfarin for life. During this visit, her INR level is found to be 4.4, which is higher than her target of 3.0. Upon further inquiry, she reveals that she had been prescribed antibiotics by her GP recently. Can you identify the clotting factors that warfarin affects?
Your Answer: Factors II, V, X
Correct Answer: Factors II, VII, IX, X
Explanation:Warfarin is an oral anticoagulant that is widely used to prevent blood clotting in various medical conditions, including stroke prevention in atrial fibrillation and venous thromboembolism. Warfarin primarily targets the Vitamin K dependent clotting factors, which include factors II, VII, IX, and X.
To monitor the effectiveness of warfarin therapy, the International Normalized Ratio (INR) is used. However, the INR can be affected by drug interactions, such as those with antibiotics. Therefore, it is important to be aware of the common drug interactions associated with warfarin.
Understanding Warfarin: Mechanism of Action, Indications, Monitoring, Factors, and Side-Effects
Warfarin is an oral anticoagulant that has been widely used for many years to manage venous thromboembolism and reduce stroke risk in patients with atrial fibrillation. However, it has been largely replaced by direct oral anticoagulants (DOACs) due to their ease of use and lack of need for monitoring. Warfarin works by inhibiting epoxide reductase, which prevents the reduction of vitamin K to its active hydroquinone form. This, in turn, affects the carboxylation of clotting factor II, VII, IX, and X, as well as protein C.
Warfarin is indicated for patients with mechanical heart valves, with the target INR depending on the valve type and location. Mitral valves generally require a higher INR than aortic valves. It is also used as a second-line treatment after DOACs for venous thromboembolism and atrial fibrillation, with target INRs of 2.5 and 3.5 for recurrent cases. Patients taking warfarin are monitored using the INR, which may take several days to achieve a stable level. Loading regimes and computer software are often used to adjust the dose.
Factors that may potentiate warfarin include liver disease, P450 enzyme inhibitors, cranberry juice, drugs that displace warfarin from plasma albumin, and NSAIDs that inhibit platelet function. Warfarin may cause side-effects such as haemorrhage, teratogenic effects, skin necrosis, temporary procoagulant state, thrombosis, and purple toes.
In summary, understanding the mechanism of action, indications, monitoring, factors, and side-effects of warfarin is crucial for its safe and effective use in patients. While it has been largely replaced by DOACs, warfarin remains an important treatment option for certain patients.
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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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A 57-year-old patient is being evaluated on the ward 3 days after experiencing a transmural myocardial infarction (MI). The patient reports experiencing sharp, severe retrosternal chest pain that worsens with inspiration.
During the assessment, the patient's vital signs are heart rate 82 beats/min, BP 132/90 mmHg, temperature 37.8ºC, and oxygen saturation 97% on room air. Upon auscultation, a pericardial friction rub is audible.
What is the histological change in the myocardial tissue that is consistent with this presentation?Your Answer: Caseous necrosis with eosinophil infiltration
Correct Answer: Coagulative necrosis with neutrophil infiltration
Explanation: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 3
Incorrect
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A 47-year-old woman is recuperating in the ICU after undergoing a Whipples surgery. She has a central venous line inserted. What will cause the 'y' descent on the waveform trace?
Your Answer: Opening of the pulmonary valve
Correct Answer: Emptying of the right atrium
Explanation:The JVP waveform consists of 3 upward deflections and 2 downward deflections. The upward deflections include the a wave, which represents atrial contraction, the c wave, which represents ventricular contraction, and the v wave, which represents atrial venous filling. The downward deflections include the x wave, which occurs when the atrium relaxes and the tricuspid valve moves down, and the y wave, which represents ventricular filling. The y descent in the waveform indicates the emptying of the atrium and the filling of the right ventricle.
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 4
Incorrect
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A 63-year-old man comes to the clinic for a hypertension follow-up. He was diagnosed with high blood pressure two months ago and started on amlodipine. However, his blood pressure remained uncontrolled, so ramipril was added four weeks ago. During his visit today, his blood pressure is measured at 155/92 mmHg. You decide to prescribe indapamide, a thiazide-like diuretic. Can you explain the mechanism of action of thiazide-like diuretics?
Your Answer:
Correct Answer: Inhibit Na+ Cl- cotransporter
Explanation:Thiazide-like drugs such as indapamide work by blocking the Na+-Cl− symporter at the beginning of the distal convoluted tubule, which inhibits sodium reabsorption. Loop diuretics, on the other hand, inhibit the Na+ K+ 2Cl- cotransporters in the thick ascending loop of Henle. Amiloride, a potassium-sparing diuretic, inhibits the epithelial sodium channels in the cortical collecting ducts, while spironolactone, another potassium-sparing diuretic, blocks the action of aldosterone on aldosterone receptors and inhibits the Na+/K+ exchanger in the cortical collecting ducts.
Thiazide diuretics are medications that work by blocking the thiazide-sensitive Na+-Cl− symporter, which inhibits sodium reabsorption at the beginning of the distal convoluted tubule (DCT). This results in the loss of potassium as more sodium reaches the collecting ducts. While thiazide diuretics are useful in treating mild heart failure, loop diuretics are more effective in reducing overload. Bendroflumethiazide was previously used to manage hypertension, but recent NICE guidelines recommend other thiazide-like diuretics such as indapamide and chlorthalidone.
Common side effects of thiazide diuretics include dehydration, postural hypotension, and electrolyte imbalances such as hyponatremia, hypokalemia, and hypercalcemia. Other potential adverse effects include gout, impaired glucose tolerance, and impotence. Rare side effects may include thrombocytopenia, agranulocytosis, photosensitivity rash, and pancreatitis.
It is worth noting that while thiazide diuretics may cause hypercalcemia, they can also reduce the incidence of renal stones by decreasing urinary calcium excretion. According to current NICE guidelines, the management of hypertension involves the use of thiazide-like diuretics, along with other medications and lifestyle changes, to achieve optimal blood pressure control and reduce the risk of cardiovascular disease.
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This question is part of the following fields:
- Cardiovascular System
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Question 5
Incorrect
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A 65-year-old man was effectively cardioverted for an unstable broad complex tachycardia. The physician opts to initiate oral amiodarone at 200 mg thrice daily, and gradually decrease at weekly intervals until a maintenance dose of 200 mg once daily.
What is the rationale behind this dosing plan?Your Answer:
Correct Answer: Amiodarone has a very long half-life
Explanation:Amiodarone’s long half-life is due to its high lipophilicity and extensive tissue absorption, resulting in reduced bioavailability in serum. To achieve stable therapeutic levels, a prolonged loading regimen is necessary.
To quickly achieve therapeutic levels, high doses of oral amiodarone are required due to poor absorption. Once achieved, a once-daily regimen can be continued. Amiodarone’s plasma half-life ranges from 20 to 100 days, meaning its effects persist long after discontinuation. Patients should be counseled on this and advised to recognize adverse effects and avoid drugs that interact with amiodarone even after stopping it.
The statement that amiodarone has a short half-life is incorrect; it has a long half-life.
Patients do not need to stay admitted for monitoring during the loading regimen. However, thyroid and liver function tests should be performed every 6 months for up to 12 months after discontinuation due to the long half-life.
Amiodarone is excreted via the liver and biliary system, not rapidly metabolized and eliminated by the kidneys. Therefore, patients with amiodarone overdose or toxicity are not suitable for dialysis.
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 6
Incorrect
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A 25-year-old man comes to the clinic complaining of chest pain in the center of his chest. Based on his symptoms, pericarditis is suspected as the cause. The patient is typically healthy, but recently had a viral throat infection according to his primary care physician.
What is the most probable observation in this patient?Your Answer:
Correct Answer: Chest pain which is relieved on leaning forwards
Explanation:Pericarditis is inflammation of the pericardium, a sac surrounding the heart. It can be caused by various factors, including viral infections. The typical symptom of pericarditis is central chest pain that is relieved by sitting up or leaning forward. ST-segment depression on a 12-lead ECG is not a sign of pericarditis, but rather a sign of subendocardial tissue ischemia. A pansystolic cardiac murmur heard on auscultation is also not associated with pericarditis, as it is caused by valve defects. Additionally, pericarditis is not typically associated with bradycardia, but rather tachycardia.
Acute Pericarditis: Causes, Features, Investigations, and Management
Acute pericarditis is a possible diagnosis for patients presenting with chest pain. The condition is characterized by chest pain, which may be pleuritic and relieved by sitting forwards. Other symptoms include non-productive cough, dyspnoea, and flu-like symptoms. Tachypnoea and tachycardia may also be present, along with a pericardial rub.
The causes of acute pericarditis include viral infections, tuberculosis, uraemia, trauma, post-myocardial infarction, Dressler’s syndrome, connective tissue disease, hypothyroidism, and malignancy.
Investigations for acute pericarditis include ECG changes, which are often global/widespread, as opposed to the ‘territories’ seen in ischaemic events. The ECG may show ‘saddle-shaped’ ST elevation and PR depression, which is the most specific ECG marker for pericarditis. All patients with suspected acute pericarditis should have transthoracic echocardiography.
Management of acute pericarditis involves treating the underlying cause. A combination of NSAIDs and colchicine is now generally used as first-line treatment for patients with acute idiopathic or viral pericarditis.
In summary, acute pericarditis is a possible diagnosis for patients presenting with chest pain. The condition is characterized by chest pain, which may be pleuritic and relieved by sitting forwards, along with other symptoms. The causes of acute pericarditis are varied, and investigations include ECG changes and transthoracic echocardiography. Management involves treating the underlying cause and using a combination of NSAIDs and colchicine as first-line treatment.
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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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Evelyn is a 92-year-old woman who arrives at the hospital with severe chest pain, shortness of breath, and palpitations. Given her medical history of angina and diabetes mellitus, doctors suspect acute coronary syndrome. They order several tests, including a troponin I blood test. What is the function of this biomarker in the body?
Your Answer:
Correct Answer: Binds to actin to hold the troponin-tropomyosin complex in place
Explanation:Troponin I plays a crucial role in muscle contraction by binding to actin and holding the troponin-tropomyosin complex in place. This prevents the myosin-binding site on the actin from being exposed, thereby preventing muscle contraction. Troponin I is also used as a marker for myocardial muscle injury.
Unlike troponin C, troponin I does not bind to calcium. Instead, troponin C has several calcium-binding sites that, when occupied, cause a conformational change in the troponin-tropomyosin complex. This change exposes the myosin-binding site on the actin filament, allowing myosin to bind and initiate muscle contraction.
Although troponin I binds to actin, it does not perform the power stroke that shortens muscle fibers. This is the role of the myosin head, which uses energy from ATP.
It is troponin T, not troponin I, that binds with tropomyosin to form the troponin-tropomyosin complex. This complex allows tropomyosin to move in response to the conformational change induced by calcium binding to troponin C.
Finally, it is tropomyosin, not troponin I, that directly inhibits myosin-binding sites. Tropomyosin is a long fiber that runs along the side of actin filaments, blocking all myosin binding sites. When calcium concentrations within the cell increase, the conformational change in troponin moves tropomyosin, exposing these sites and allowing muscle contraction to occur.
Understanding Troponin: The Proteins Involved in Muscle Contraction
Troponin is a group of three proteins that play a crucial role in the contraction of skeletal and cardiac muscles. These proteins work together to regulate the interaction between actin and myosin, which is essential for muscle contraction. The three subunits of troponin are troponin C, troponin T, and troponin I.
Troponin C is responsible for binding to calcium ions, which triggers the contraction of muscle fibers. Troponin T binds to tropomyosin, forming a complex that helps regulate the interaction between actin and myosin. Finally, troponin I binds to actin, holding the troponin-tropomyosin complex in place and preventing muscle contraction when it is not needed.
Understanding the role of troponin is essential for understanding how muscles work and how they can be affected by various diseases and conditions. By regulating the interaction between actin and myosin, troponin plays a critical role in muscle contraction and is a key target for drugs used to treat conditions such as heart failure and skeletal muscle disorders.
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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:
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 medical resident has been instructed by the geriatric consultant to review the medication chart of an elderly patient with a history of hypertension, heart failure, and biliary colic. The resident noticed a significant drop in systolic blood pressure upon standing and discontinued a medication that may have contributed to the postural hypotension. However, a few hours later, the patient's continuous cardiac monitoring showed tachycardia. Which medication cessation could have caused the tachycardia in this elderly patient?
Your Answer:
Correct Answer: Atenolol
Explanation:Abruptly stopping atenolol, a beta blocker, can lead to ‘rebound tachycardia’. None of the other drugs listed have been associated with this condition. While ramipril, an ace-inhibitor, may have contributed to the patient’s postural hypotension, it is not known to cause tachycardia upon cessation. Furosemide, a loop diuretic, can worsen postural hypotension by causing volume depletion, but it is not known to cause tachycardia upon discontinuation. Aspirin and clopidogrel, both antiplatelet drugs, are unlikely to be stopped abruptly and are not associated with either ‘rebound tachycardia’ or postural hypotension.
Beta-blockers are a class of drugs that are primarily used to manage cardiovascular disorders. They have a wide range of indications, including angina, post-myocardial infarction, heart failure, arrhythmias, hypertension, thyrotoxicosis, migraine prophylaxis, and anxiety. Beta-blockers were previously avoided in heart failure, but recent evidence suggests that certain beta-blockers can improve both symptoms and mortality. They have also replaced digoxin as the rate-control drug of choice in atrial fibrillation. However, their role in reducing stroke and myocardial infarction has diminished in recent years due to a lack of evidence.
Examples of beta-blockers include atenolol and propranolol, which was one of the first beta-blockers to be developed. Propranolol is lipid-soluble, which means it can cross the blood-brain barrier.
Like all drugs, beta-blockers have side-effects. These can include bronchospasm, cold peripheries, fatigue, sleep disturbances (including nightmares), and erectile dysfunction. There are also some contraindications to using beta-blockers, such as uncontrolled heart failure, asthma, sick sinus syndrome, and concurrent use with verapamil, which can precipitate severe bradycardia.
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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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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:
Correct 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 11
Incorrect
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A 32-year-old woman arrives at the emergency department with a sudden and severe headache, describing it as the worst she has ever experienced. She has a medical history of hypertension and polycystic kidney disease (PKD). The emergency physician diagnoses a subarachnoid hemorrhage, which is a common complication of her PKD.
What is the gold standard investigation for intracranial vascular disease?Your Answer:
Correct Answer: Cerebral angiography
Explanation:The gold standard investigation for intracranial vascular disease is cerebral angiography, which can diagnose intracranial aneurysms and other vascular diseases by visualizing arteries and veins using contrast dye injected into the bloodstream. This technique can also create 3-D reconstructed images that allow for a comprehensive view of the cerebral vessels and accompanying pathology from all angles.
Individuals with PKD are at an increased risk of cerebral aneurysms, which can lead to subarachnoid hemorrhages.
Flow-Sensitive MRI (FS MRI) is a useful tool that combines functional MRI with images of cerebrospinal fluid (CSF) flow. It can aid in planning the surgical removal of skull base tumors, spinal cord tumors, or tumors causing hydrocephalus.
While contrast and non-contrast CT scans are commonly used as the first line of investigation for intracranial lesions, they are not the gold standard and are superseded by cerebral angiography.
Understanding Cerebral Blood Flow and Angiography
Cerebral blood flow is regulated by the central nervous system, which can adjust its own blood supply. Various factors can affect cerebral pressure, including CNS metabolism, trauma, pressure, and systemic carbon dioxide levels. The most potent mediator is PaCO2, while acidosis and hypoxemia can also increase cerebral blood flow to a lesser degree. In patients with head injuries, increased intracranial pressure can impair blood flow. The Monro-Kelly Doctrine governs intracerebral pressure, which considers the brain as a closed box, and changes in pressure are offset by the loss of cerebrospinal fluid. However, when this is no longer possible, intracranial pressure rises.
Cerebral angiography is an invasive test that involves injecting contrast media into the carotid artery using a catheter. Radiographs are taken as the dye works its way through the cerebral circulation. This test can be used to identify bleeding aneurysms, vasospasm, and arteriovenous malformations, as well as differentiate embolism from large artery thrombosis. Understanding cerebral blood flow and angiography is crucial in diagnosing and treating various neurological conditions.
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This question is part of the following fields:
- Cardiovascular System
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Question 12
Incorrect
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Which segment of the ECG waveform corresponds to the shutting of the mitral valve?
Your Answer:
Correct Answer: QRS complex
Explanation:A diagram depicting the various stages of the cardiac cycle can be accessed through the external link provided.
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 13
Incorrect
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A patient with a history of peripheral vascular disease visits their GP with essential hypertension. Which of the following medications could worsen their peripheral vascular symptoms?
Your Answer:
Correct Answer: Atenolol
Explanation:Patients with peripheral vascular disease may experience worsened symptoms when taking beta-blockers, and caution should be exercised when prescribing this medication. Additionally, those with Raynaud disease may also experience aggravated symptoms. Monitoring for signs of progressive arterial obstruction is recommended.
Beta-blockers are a class of drugs that are primarily used to manage cardiovascular disorders. They have a wide range of indications, including angina, post-myocardial infarction, heart failure, arrhythmias, hypertension, thyrotoxicosis, migraine prophylaxis, and anxiety. Beta-blockers were previously avoided in heart failure, but recent evidence suggests that certain beta-blockers can improve both symptoms and mortality. They have also replaced digoxin as the rate-control drug of choice in atrial fibrillation. However, their role in reducing stroke and myocardial infarction has diminished in recent years due to a lack of evidence.
Examples of beta-blockers include atenolol and propranolol, which was one of the first beta-blockers to be developed. Propranolol is lipid-soluble, which means it can cross the blood-brain barrier.
Like all drugs, beta-blockers have side-effects. These can include bronchospasm, cold peripheries, fatigue, sleep disturbances (including nightmares), and erectile dysfunction. There are also some contraindications to using beta-blockers, such as uncontrolled heart failure, asthma, sick sinus syndrome, and concurrent use with verapamil, which can precipitate severe bradycardia.
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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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As a medical student in general practice, you encounter a 68-year-old female patient who has come in for her routine blood pressure check. She informs you that she has GTN spray at home. Can you explain how nitric oxide leads to vasodilation?
Your Answer:
Correct Answer: Activates guanylate cyclase
Explanation:Smooth muscle relaxation and vasodilation are caused by the release of nitric oxide in response to nitrates. Nitric oxide activates guanylate cyclase, which converts GTP to cGMP. This leads to the opening of K+ channels and hyperpolarization of the cell membrane, causing the closure of voltage-gated Ca2+ channels and pumping of Ca2+ out of the smooth muscle. This results in vasodilation. Nitric oxide does not inhibit the release of Bradykinin.
Understanding Nitrates and Their Effects on the Body
Nitrates are a type of medication that can cause blood vessels to widen, which is known as vasodilation. They are commonly used to manage angina and treat heart failure. One of the most frequently prescribed nitrates is sublingual glyceryl trinitrate, which is used to relieve angina attacks in patients with ischaemic heart disease.
The mechanism of action for nitrates involves the release of nitric oxide in smooth muscle, which activates guanylate cyclase. This enzyme then converts GTP to cGMP, leading to a decrease in intracellular calcium levels. In the case of angina, nitrates dilate the coronary arteries and reduce venous return, which decreases left ventricular work and reduces myocardial oxygen demand.
However, nitrates can also cause side effects such as hypotension, tachycardia, headaches, and flushing. Additionally, many patients who take nitrates develop tolerance over time, which can reduce their effectiveness. To combat this, the British National Formulary recommends that patients who develop tolerance take the second dose of isosorbide mononitrate after 8 hours instead of 12 hours. This allows blood-nitrate levels to fall for 4 hours and maintains effectiveness. It’s important to note that this effect is not seen in patients who take modified release isosorbide mononitrate.
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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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An 80-year-old man is admitted to the acute medical ward after experiencing a myocardial infarction. During examination, it is discovered that his heart rate is 40 beats per minute. The consultant explains that this is due to damage to the conduction pathways between the sinoatrial and atrioventricular (AV) node, resulting in the AV node pacing his ventricles exclusively.
In most patients, what is the blood supply to the AV node?Your Answer:
Correct Answer: Right coronary artery
Explanation:The AV node is typically supplied by the right coronary artery in right-dominant hearts, while in left-dominant hearts it is supplied by the left circumflex artery. The left circumflex artery also supplies the left atrium and some of the left ventricle, while the right marginal artery supplies the right ventricle, the posterior descending artery supplies the posterior third of the interventricular septum, and the left anterior descending artery supplies the left ventricle.
The walls of each cardiac chamber are made up of the epicardium, myocardium, and endocardium. The heart and roots of the great vessels are related anteriorly to the sternum and the left ribs. The coronary sinus receives blood from the cardiac veins, and the aortic sinus gives rise to the right and left coronary arteries. The left ventricle has a thicker wall and more numerous trabeculae carnae than the right ventricle. The heart is innervated by autonomic nerve fibers from the cardiac plexus, and the parasympathetic supply comes from the vagus nerves. The heart has four valves: the mitral, aortic, pulmonary, and tricuspid valves.
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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 50-year-old man is having a lymph node biopsy taken from the posterior triangle of his neck. What structure creates the posterior boundary of this area?
Your Answer:
Correct Answer: Trapezius muscle
Explanation:The posterior triangle of the neck is an area that is bound by the sternocleidomastoid and trapezius muscles, the occipital bone, and the middle third of the clavicle. Within this triangle, there are various nerves, vessels, muscles, and lymph nodes. The nerves present include the accessory nerve, phrenic nerve, and three trunks of the brachial plexus, as well as branches of the cervical plexus such as the supraclavicular nerve, transverse cervical nerve, great auricular nerve, and lesser occipital nerve. The vessels found in this area are the external jugular vein and subclavian artery. Additionally, there are muscles such as the inferior belly of omohyoid and scalene, as well as lymph nodes including the supraclavicular and occipital nodes.
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This question is part of the following fields:
- Cardiovascular System
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Question 17
Incorrect
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A 75-year-old man is experiencing symptoms of mesenteric ischemia. During his diagnostic evaluation, a radiologist is attempting to cannulate the coeliac axis from the aorta. Typically, at which vertebral level does this artery originate?
Your Answer:
Correct Answer: T12
Explanation:The coeliac trunk is a major artery that arises from the aorta and gives off three branches on the left-hand side: the left gastric, hepatic, and splenic arteries.
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 18
Incorrect
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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:
Correct 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 19
Incorrect
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A 72-year-old male with urinary incontinence visits the urogynaecology clinic and is diagnosed with overactive bladder incontinence. He is prescribed a medication that works by blocking the parasympathetic pathway. What other drugs have a similar mechanism of action to the one he was prescribed?
Your Answer:
Correct Answer: Atropine
Explanation:Atropine is classified as an antimuscarinic drug that works by inhibiting the M1 to M5 muscarinic receptors. While oxybutynin is commonly prescribed for urinary incontinence due to its ability to block the M3 muscarinic receptors, atropine is more frequently used in anesthesia to reduce salivation before intubation.
Alfuzosin, on the other hand, is an alpha blocker that is primarily used to treat benign prostate hyperplasia.
Meropenem is an antibiotic that is reserved for infections caused by bacteria that are resistant to most beta-lactams. However, it is typically used as a last resort due to its potential adverse effects.
Mirabegron is another medication used to treat urinary incontinence, but it works by activating the β3 adrenergic receptors.
Understanding Atropine and Its Uses
Atropine is a medication that works against the muscarinic acetylcholine receptor. It is commonly used to treat symptomatic bradycardia and organophosphate poisoning. In cases of bradycardia with adverse signs, IV atropine is the first-line treatment. However, it is no longer recommended for routine use in asystole or pulseless electrical activity (PEA) during advanced life support.
Atropine has several physiological effects, including tachycardia and mydriasis. However, it is important to note that it may trigger acute angle-closure glaucoma in susceptible patients. Therefore, it is crucial to use atropine with caution and under the guidance of a healthcare professional. Understanding the uses and effects of atropine can help individuals make informed decisions about their healthcare.
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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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Electrophysiology studies are being conducted in a young boy with suspected Wolff-Parkinson-White syndrome, who has experienced recurrent episodes of sudden palpitations. The procedure involves catheterization within the heart to evaluate the electrical activity and determine the conduction velocity of various parts of the conduction pathway.
Which segment of this pathway exhibits the highest conduction velocity?Your Answer:
Correct Answer: Purkinje fibres
Explanation:The Purkinje fibres have the fastest conduction velocities in the heart, at approximately 4m/sec, due to different connexins in their gap junctions. They allow depolarisation throughout the ventricular muscle. Atrial muscle conducts at around 0.5m/sec, the atrioventricular node conducts at a slow rate, and the Bundle of His conducts at 2m/sec, but not as rapidly as the Purkinje fibres.
Understanding the Cardiac Action Potential and Conduction Velocity
The cardiac action potential is a series of electrical events that occur in the heart during each heartbeat. It is responsible for the contraction of the heart muscle and the pumping of blood throughout the body. The action potential is divided into five phases, each with a specific mechanism. The first phase is rapid depolarization, which is caused by the influx of sodium ions. The second phase is early repolarization, which is caused by the efflux of potassium ions. The third phase is the plateau phase, which is caused by the slow influx of calcium ions. The fourth phase is final repolarization, which is caused by the efflux of potassium ions. The final phase is the restoration of ionic concentrations, which is achieved by the Na+/K+ ATPase pump.
Conduction velocity is the speed at which the electrical signal travels through the heart. The speed varies depending on the location of the signal. Atrial conduction spreads along ordinary atrial myocardial fibers at a speed of 1 m/sec. AV node conduction is much slower, at 0.05 m/sec. Ventricular conduction is the fastest in the heart, achieved by the large diameter of the Purkinje fibers, which can achieve velocities of 2-4 m/sec. This allows for a rapid and coordinated contraction of the ventricles, which is essential for the proper functioning of the heart. Understanding the cardiac action potential and conduction velocity is crucial for diagnosing and treating heart conditions.
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This question is part of the following fields:
- Cardiovascular System
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Question 21
Incorrect
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A 68-year-old man visits his doctor complaining of exertional dyspnea and is diagnosed with heart failure. Afterload-induced increases can lead to systolic dysfunction in heart failure.
What factors worsen his condition by increasing afterload?Your Answer:
Correct Answer: Ventricular dilatation
Explanation:Ventricular dilation can increase afterload, which is the resistance the heart must overcome during contraction. Afterload is often measured as ventricular wall stress, which is influenced by ventricular pressure, radius, and wall thickness. As the ventricle dilates, the radius increases, leading to an increase in wall stress and afterload. This can eventually lead to heart failure if the heart is unable to compensate. Conversely, decreased systemic vascular resistance and hypotension can decrease afterload, while increased venous return can increase preload. Mitral valve stenosis, on the other hand, can decrease preload.
The stroke volume refers to the amount of blood that is pumped out of the ventricle during each cycle of cardiac contraction. This volume is usually the same for both ventricles and is approximately 70ml for a man weighing 70Kg. To calculate the stroke volume, the end systolic volume is subtracted from the end diastolic volume. Several factors can affect the stroke volume, including the size of the heart, its contractility, preload, and afterload.
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This question is part of the following fields:
- Cardiovascular System
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Question 22
Incorrect
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A 23-year-old male university student presents to the emergency department with lightheadedness and a fall an hour earlier, associated with loss of consciousness. He admits to being short of breath on exertion with chest pain for several months. The patient denies vomiting or haemoptysis. The symptoms are not exacerbated or relieved by any positional changes or during phases of respiration.
He has no relevant past medical history, is not on any regular medications, and has no documented drug allergies. There is no relevant family history. He is a non-smoker and drinks nine unite of alcohol a week. He denies any recent travel or drug use.
On examination, the patient appears to be comfortable at rest. His heart rate is 68/min, blood pressure 112/84 mmHg, oxygen saturation 99% on air, respiratory rate of 16 breaths per minute, temperature 36.7ºC.
An ejection systolic murmur is audible throughout the praecordium, loudest over the sternum bilaterally. No heaves or thrills are palpable, and there are no radiations. The murmur gets louder when the patient is asked to perform the Valsalva manoeuvre. The murmur is noted as grade II. Lung fields are clear on auscultation. The abdomen is soft and non-tender, with bowel sounds present. His body mass index is 20 kg/m².
His ECG taken on admission reveals sinus rhythm, with generalised deep Q waves and widespread T waves. There is evidence of left ventricular hypertrophy.
What is the most likely diagnosis?Your Answer:
Correct Answer: Hypertrophic obstructive cardiomyopathy
Explanation:The patient’s symptoms and findings suggest the possibility of hypertrophic obstructive cardiomyopathy (HOCM), which is characterized by exertional dyspnea, chest pain, syncope, and ejection systolic murmur that is louder during Valsalva maneuver and quieter during squatting. The ECG changes observed are also consistent with HOCM. Given the patient’s young age, it is crucial to rule out this diagnosis as HOCM is a leading cause of sudden cardiac death in young individuals.
Brugada syndrome, an autosomal dominant cause of sudden cardiac death in young people, may also present with unexplained falls. However, the absence of a family history of cardiac disease and the unlikely association with the murmur and ECG changes described make this diagnosis less likely. It is important to note that performing Valsalva maneuver in a patient with Brugada syndrome can be life-threatening due to the risk of arrhythmias such as ventricular fibrillation.
Chagas disease, a parasitic disease prevalent in South America, is caused by an insect bite and has a long dormant period before causing ventricular damage. However, the patient’s age and absence of exposure to the disease make this diagnosis less likely.
Myocardial infarction can cause central chest pain and ECG changes, but it is rare for it to present with falls. Moreover, the ECG changes observed are not typical of myocardial infarction. The patient’s young age and lack of cardiac risk factors also make this diagnosis less likely.
Hypertrophic obstructive cardiomyopathy (HOCM) is a genetic disorder that affects muscle tissue and is inherited in an autosomal dominant manner. It is caused by mutations in genes that encode contractile proteins, with the most common defects involving the β-myosin heavy chain protein or myosin-binding protein C. HOCM is characterized by left ventricle hypertrophy, which leads to decreased compliance and cardiac output, resulting in predominantly diastolic dysfunction. Biopsy findings show myofibrillar hypertrophy with disorganized myocytes and fibrosis. HOCM is often asymptomatic, but exertional dyspnea, angina, syncope, and sudden death can occur. Jerky pulse, systolic murmurs, and double apex beat are also common features. HOCM is associated with Friedreich’s ataxia and Wolff-Parkinson White. ECG findings include left ventricular hypertrophy, non-specific ST segment and T-wave abnormalities, and deep Q waves. Atrial fibrillation may occasionally be seen.
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This question is part of the following fields:
- Cardiovascular System
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Question 23
Incorrect
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A senior gentleman visits the GP for his routine INR check. He was prescribed warfarin five years ago upon being diagnosed with atrial fibrillation.
Which enzyme does warfarin inhibit?Your Answer:
Correct Answer: Epoxide reductase
Explanation:Warfarin prevents the activation of Vitamin K by inhibiting epoxide reductase. This enzyme is responsible for converting Vitamin K epoxide to Vitamin K quinone, a necessary step in the Vitamin K metabolic pathway. Without this conversion, the production of clotting factors (10, 9, 7 and 2) is decreased.
Gamma-glutamyl carboxylase is the enzyme responsible for carboxylating glutamic acid to produce clotting factors. Warfarin does not directly inhibit this enzyme.
CYP2C9 is an enzyme involved in the metabolism of many drugs, including warfarin.
Protein C is a plasma protein that functions as an anticoagulant. It is dependent on Vitamin K for activation and works by inhibiting factor 5 and 8. Protein C is produced as an inactive precursor enzyme, which is then activated to exert its anticoagulant effects.
Understanding Warfarin: Mechanism of Action, Indications, Monitoring, Factors, and Side-Effects
Warfarin is an oral anticoagulant that has been widely used for many years to manage venous thromboembolism and reduce stroke risk in patients with atrial fibrillation. However, it has been largely replaced by direct oral anticoagulants (DOACs) due to their ease of use and lack of need for monitoring. Warfarin works by inhibiting epoxide reductase, which prevents the reduction of vitamin K to its active hydroquinone form. This, in turn, affects the carboxylation of clotting factor II, VII, IX, and X, as well as protein C.
Warfarin is indicated for patients with mechanical heart valves, with the target INR depending on the valve type and location. Mitral valves generally require a higher INR than aortic valves. It is also used as a second-line treatment after DOACs for venous thromboembolism and atrial fibrillation, with target INRs of 2.5 and 3.5 for recurrent cases. Patients taking warfarin are monitored using the INR, which may take several days to achieve a stable level. Loading regimes and computer software are often used to adjust the dose.
Factors that may potentiate warfarin include liver disease, P450 enzyme inhibitors, cranberry juice, drugs that displace warfarin from plasma albumin, and NSAIDs that inhibit platelet function. Warfarin may cause side-effects such as haemorrhage, teratogenic effects, skin necrosis, temporary procoagulant state, thrombosis, and purple toes.
In summary, understanding the mechanism of action, indications, monitoring, factors, and side-effects of warfarin is crucial for its safe and effective use in patients. While it has been largely replaced by DOACs, warfarin remains an important treatment option for certain patients.
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This question is part of the following fields:
- Cardiovascular System
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Question 24
Incorrect
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A 65-year-old farmer arrives at the Emergency department with complaints of intense chest pain that spreads to his left arm and causes breathing difficulties. His heart rate is 94 bpm. What ECG changes would you expect to observe based on the probable diagnosis?
Your Answer:
Correct Answer: ST elevation in leads II, III, aVF
Explanation:ECG Changes in Myocardial Infarction
When interpreting an electrocardiogram (ECG) in a patient with suspected myocardial infarction (MI), it is important to consider the specific changes that may be present. In the case of a ST-elevation MI (STEMI), the ECG may show ST elevation in affected leads, such as II, III, and aVF. However, it is possible to have a non-ST elevation MI (NSTEMI) with a normal ECG, or with T wave inversion instead of upright T waves.
Other ECG changes that may be indicative of cardiac issues include a prolonged PR interval, which could suggest heart block, and ST depression, which may reflect ischemia. Additionally, tall P waves may be seen in hyperkalemia.
It is important to note that a patient may have an MI without displaying any ECG changes at all. In these cases, checking cardiac markers such as troponin T can help confirm the diagnosis. Overall, the various ECG changes that may be present in MI can aid in prompt and accurate diagnosis and treatment.
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This question is part of the following fields:
- Cardiovascular System
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Question 25
Incorrect
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These thyroid function tests were obtained on a 55-year-old female who has recently been treated for hypertension:
Free T4 28.5 pmol/L (9.8-23.1)
TSH <0.02 mU/L (0.35-5.5)
Free T3 10.8 pmol/L (3.5-6.5)
She now presents with typical symptoms of hyperthyroidism.
Which medication is likely to have caused this?Your Answer:
Correct Answer: Amiodarone
Explanation:Amiodarone and its Effects on Thyroid Function
Amiodarone is a medication that can have an impact on thyroid function, resulting in both hypo- and hyperthyroidism. This is due to the high iodine content in the drug, which contributes to its antiarrhythmic effects. Atenolol, on the other hand, is a beta blocker that is commonly used to treat thyrotoxicosis. Warfarin is another medication that is used to treat atrial fibrillation.
There are two types of thyrotoxicosis that can be caused by amiodarone. Type 1 results in excess thyroxine synthesis, while type 2 leads to the release of excess thyroxine but normal levels of synthesis. It is important for healthcare professionals to monitor thyroid function in patients taking amiodarone and adjust treatment as necessary to prevent complications.
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This question is part of the following fields:
- Cardiovascular System
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Question 26
Incorrect
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A 68-year-old man presents to the emergency department after experiencing a syncopal episode. His ECG reveals a prolonged PR interval, with every other QRS complex being dropped. The QRS complex width is within normal limits.
From which area of the heart is the conduction delay most likely originating?Your Answer:
Correct Answer: Atrio-Ventricular node
Explanation:The PR interval is the duration between the depolarization of the atria and the depolarization of the ventricles. In this case, the man is experiencing a 2:1 block, which is a type of second-degree heart block. Since his PR interval is prolonged, the issue must be occurring in the pathway between the atria and ventricles. However, since his QRS complex is normal, it is likely that the problem is in the AV node rather than the bundles of His. If the issue were in the sino-atrial node, it would not cause a prolonged PR interval with dropped QRS complexes. Similarly, if there were a slowing of conduction in the ventricles, it would cause a wide QRS complex but not a prolonged PR interval.
Understanding the Normal ECG
The electrocardiogram (ECG) is a diagnostic tool used to assess the electrical activity of the heart. The normal ECG consists of several waves and intervals that represent different phases of the cardiac cycle. The P wave represents atrial depolarization, while the QRS complex represents ventricular depolarization. The ST segment represents the plateau phase of the ventricular action potential, and the T wave represents ventricular repolarization. The Q-T interval represents the time for both ventricular depolarization and repolarization to occur.
The P-R interval represents the time between the onset of atrial depolarization and the onset of ventricular depolarization. The duration of the QRS complex is normally 0.06 to 0.1 seconds, while the duration of the P wave is 0.08 to 0.1 seconds. The Q-T interval ranges from 0.2 to 0.4 seconds depending upon heart rate. At high heart rates, the Q-T interval is expressed as a ‘corrected Q-T (QTc)’ by taking the Q-T interval and dividing it by the square root of the R-R interval.
Understanding the normal ECG is important for healthcare professionals to accurately interpret ECG results and diagnose cardiac conditions. By analyzing the different waves and intervals, healthcare professionals can identify abnormalities in the electrical activity of the heart and provide appropriate treatment.
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This question is part of the following fields:
- Cardiovascular System
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Question 27
Incorrect
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A 39-year-old woman is being evaluated for progressive dyspnea and is found to have primary pulmonary hypertension. She is prescribed bosentan. What is the mode of action of bosentan?
Your Answer:
Correct Answer: Endothelin receptor antagonist
Explanation:Bosentan is an antagonist of the endothelin-1 receptor.
Pulmonary arterial hypertension (PAH) is a condition where the resting mean pulmonary artery pressure is equal to or greater than 25 mmHg. The pathogenesis of PAH is thought to involve endothelin. It is more common in females and typically presents between the ages of 30-50 years. PAH is diagnosed in the absence of chronic lung diseases such as COPD, although certain factors increase the risk. Around 10% of cases are inherited in an autosomal dominant fashion.
The classical presentation of PAH is progressive exertional dyspnoea, but other possible features include exertional syncope, exertional chest pain, peripheral oedema, and cyanosis. Physical examination may reveal a right ventricular heave, loud P2, raised JVP with prominent ‘a’ waves, and tricuspid regurgitation.
Management of PAH should first involve treating any underlying conditions. Acute vasodilator testing is central to deciding on the appropriate management strategy. If there is a positive response to acute vasodilator testing, oral calcium channel blockers may be used. If there is a negative response, prostacyclin analogues, endothelin receptor antagonists, or phosphodiesterase inhibitors may be used. Patients with progressive symptoms should be considered for a heart-lung transplant.
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This question is part of the following fields:
- Cardiovascular System
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Question 28
Incorrect
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A nursing student is being consented for a parathyroidectomy for symptomatic hyperparathyroidism. The parathyroid gland consists of 2 superior and 2 inferior glands. The patient is informed that all four glands will be removed in order to achieve a complete resolution of her symptoms. You explain to her that the superior and inferior glands are derived from different structures.
From which one of the following embryological structures are the superior parathyroid glands derived from?Your Answer:
Correct Answer: Fourth pharyngeal pouch
Explanation:The superior parathyroid glands are formed from the fourth pharyngeal pouch during embryonic development. The pharyngeal pouches develop between the branchial arches, with the first pouch located between the first and second arches. There are four pairs of pouches, with the fifth pouch being either absent or very small. A helpful mnemonic to remember the derivatives of the four pharyngeal pouches is 1A, 2P, 3 TIP, 4 SUB. This stands for the auditory tube, middle ear cavity, and mastoid antrum for the first pouch; the crypts of the palatine tonsil for the second pouch; the thymus and inferior parathyroid gland for the third pouch; and the superior parathyroid gland and ultimobranchial body for the fourth pouch.
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 29
Incorrect
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An elderly man in his late 60s is admitted to the cardiology ward due to worsening shortness of breath. He has a medical history of hypertension and ischaemic heart disease. During examination, bibasal crackles and pitting oedema to the knees bilaterally are observed. Blood tests are conducted, and the results show a brain natriuretic peptide level of 4990 pg/mL (< 400). What is the most probable physiological change that occurs in response to this finding?
Your Answer:
Correct Answer: Decreased afterload
Explanation:BNP has several actions, including vasodilation which can decrease cardiac afterload, diuretic and natriuretic effects, and suppression of both sympathetic tone and the renin-angiotensin-aldosterone system. In the case of heart failure, BNP is primarily secreted by the ventricular myocardium to compensate for symptoms by promoting diuresis, natriuresis, vasodilation, and suppression of sympathetic tone and renin-angiotensin-aldosterone activity. Vasodilation of the peripheral vascular system leads to a decrease in afterload, reducing the force that the left ventricle has to contract against and lowering the risk of left ventricular failure progression. BNP also suppresses sympathetic tone and the RAAS, which would exacerbate heart failure symptoms, and contributes to natriuresis, aiding diuresis and improving dyspnea.
B-type natriuretic peptide (BNP) is a hormone that is primarily produced by the left ventricular myocardium in response to strain. Although heart failure is the most common cause of elevated BNP levels, any condition that causes left ventricular dysfunction, such as myocardial ischemia or valvular disease, may also raise levels. In patients with chronic kidney disease, reduced excretion may also lead to elevated BNP levels. Conversely, treatment with ACE inhibitors, angiotensin-2 receptor blockers, and diuretics can lower BNP levels.
BNP has several effects, including vasodilation, diuresis, natriuresis, and suppression of both sympathetic tone and the renin-angiotensin-aldosterone system. Clinically, BNP is useful in diagnosing patients with acute dyspnea. A low concentration of BNP (<100 pg/mL) makes a diagnosis of heart failure unlikely, but elevated levels should prompt further investigation to confirm the diagnosis. Currently, NICE recommends BNP as a helpful test to rule out a diagnosis of heart failure. In patients with chronic heart failure, initial evidence suggests that BNP is an extremely useful marker of prognosis and can guide treatment. However, BNP is not currently recommended for population screening for cardiac dysfunction.
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This question is part of the following fields:
- Cardiovascular System
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Question 30
Incorrect
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A 30-year-old man arrived at the emergency department following a syncopal episode during a game of basketball. He is typically healthy with no prior medical history, but he does mention experiencing occasional palpitations, which he believes may be due to alcohol or caffeine consumption. Upon further inquiry, he reveals that his father passed away suddenly at the age of 40 due to a heart condition. What is the underlying pathophysiological alteration in this patient?
Your Answer:
Correct Answer: Asymmetric septal hypertrophy
Explanation:When a young patient presents with symptoms of syncope and chest discomfort, along with a family history of hypertrophic cardiomyopathy (HOCM), it is important to consider the possibility of this condition. Asymmetric septal hypertrophy and systolic anterior movement (SAM) of the anterior leaflet of the mitral valve on echocardiogram or cMR are supportive of HOCM. This condition is caused by a genetic defect in the beta-myosin heavy chain protein gene. While Brugada syndrome may also be a consideration, it is not listed as a possible answer due to its underlying mechanism of sodium channelopathy.
Hypertrophic obstructive cardiomyopathy (HOCM) is a genetic disorder that affects muscle tissue and is inherited in an autosomal dominant manner. It is caused by mutations in genes that encode contractile proteins, with the most common defects involving the β-myosin heavy chain protein or myosin-binding protein C. HOCM is characterized by left ventricle hypertrophy, which leads to decreased compliance and cardiac output, resulting in predominantly diastolic dysfunction. Biopsy findings show myofibrillar hypertrophy with disorganized myocytes and fibrosis. HOCM is often asymptomatic, but exertional dyspnea, angina, syncope, and sudden death can occur. Jerky pulse, systolic murmurs, and double apex beat are also common features. HOCM is associated with Friedreich’s ataxia and Wolff-Parkinson White. ECG findings include left ventricular hypertrophy, non-specific ST segment and T-wave abnormalities, and deep Q waves. Atrial fibrillation may occasionally be seen.
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This question is part of the following fields:
- Cardiovascular System
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