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Question 1
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A 26-year-old man collapses during a game of cricket. He has previously experienced chest pain and shortness of breath while running, which subsides on rest. Upon examination, he is found to have an ejection systolic murmur that intensifies with Valsalva maneuvers and diminishes with squatting. His echocardiogram reveals mitral regurgitation, asymmetric hypertrophy, and systolic anterior motion of the anterior mitral valve leaflet. What is the expected inheritance pattern for this diagnosis?
Your Answer: Autosomal dominant
Explanation:The inheritance pattern of HOCM is autosomal dominant, which means that it can be passed down from generation to generation. Symptoms of HOCM may include exertional dyspnoea, angina, syncope, and an ejection systolic murmur. It is important to note that there may be a family history of similar cardiac problems or sudden death due to ventricular arrhythmias. Autosomal recessive, mitochondrial inheritance, and X-linked dominant inheritance are not applicable to HOCM.
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 2
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: Left Ventricle
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 3
Incorrect
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A 68-year-old man is diagnosed with a transient ischaemic attack and started on modified-release dipyridamole as part of combination antiplatelet treatment. He already takes a statin. After a week of treatment, he visits his GP with concerns of the drug's mechanism of action.
What is the mechanism of action of modified-release dipyridamole?Your Answer: P2Y12 inhibitor
Correct Answer: Phosphodiesterase inhibitor
Explanation:Dipyridamole is a medication that inhibits phosphodiesterase in a non-specific manner and reduces the uptake of adenosine by cells.
As an antiplatelet agent, dipyridamole works by inhibiting phosphodiesterase. It can be used in combination with aspirin to prevent secondary transient ischemic attacks if clopidogrel is not well-tolerated.
Tirofiban is a drug that inhibits the platelet glycoprotein IIb/IIIa receptor, which binds to collagen.
The platelet receptor glycoprotein VI interacts with subendothelial collagen.
Glycoprotein 1b is the platelet receptor for von Willebrand Factor. Although there is no specific drug that targets this interaction, autoantibodies to glycoprotein Ib are the basis of immune thrombocytopenic purpura (ITP).
Clopidogrel targets the platelet receptor P2Y12, which interacts with adenosine diphosphate.
Understanding the Mechanism of Action of Dipyridamole
Dipyridamole is a medication that is commonly used in combination with aspirin to prevent the formation of blood clots after a stroke or transient ischemic attack. The drug works by inhibiting phosphodiesterase, which leads to an increase in the levels of cyclic adenosine monophosphate (cAMP) in platelets. This, in turn, reduces the levels of intracellular calcium, which is necessary for platelet activation and aggregation.
Apart from its antiplatelet effects, dipyridamole also reduces the cellular uptake of adenosine, a molecule that plays a crucial role in regulating blood flow and oxygen delivery to tissues. By inhibiting the uptake of adenosine, dipyridamole can increase its levels in the bloodstream, leading to vasodilation and improved blood flow.
Another mechanism of action of dipyridamole is the inhibition of thromboxane synthase, an enzyme that is involved in the production of thromboxane A2, a potent platelet activator. By blocking this enzyme, dipyridamole can further reduce platelet activation and aggregation, thereby preventing the formation of blood clots.
In summary, dipyridamole exerts its antiplatelet effects through multiple mechanisms, including the inhibition of phosphodiesterase, the reduction of intracellular calcium levels, the inhibition of thromboxane synthase, and the modulation of adenosine uptake. These actions make it a valuable medication for preventing thrombotic events in patients with a history of stroke or transient ischemic attack.
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This question is part of the following fields:
- Cardiovascular System
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Question 4
Correct
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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: 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 5
Incorrect
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A 50-year-old male is brought to the trauma unit following a car accident, with an estimated blood loss of 1200ml. His vital signs are as follows: heart rate of 125 beats per minute, blood pressure of 125/100 mmHg, and he feels cold to the touch.
Which component of his cardiovascular system has played the biggest role in maintaining his blood pressure stability?Your Answer: Venules
Correct Answer: Arterioles
Explanation:The highest resistance in the cardiovascular system is found in the arterioles, which means they contribute the most to the total peripheral resistance. In cases of compensated hypovolaemic shock, such as in this relatively young patient, the body compensates by increasing heart rate and causing peripheral vasoconstriction to maintain blood pressure.
Arteriole vasoconstriction in hypovolaemic shock patients leads to an increase in total peripheral resistance, which in turn increases mean arterial blood pressure. This has a greater effect on diastolic blood pressure, resulting in a narrowing of pulse pressure and clinical symptoms such as cold peripheries and delayed capillary refill time.
Capillaries are microscopic channels that provide blood supply to the tissues and are the primary site for gas and nutrient exchange. Venules, on the other hand, are small veins with diameters ranging from 8-100 micrometers and join multiple capillaries exiting from a capillary bed.
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 6
Incorrect
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A 46-year-old man with a history of hypertrophic cardiomyopathy (HOCM) presents for evaluation at the cardiology clinic. During the assessment, a fourth heart sound is detected.
What characteristic is associated with this clinical observation?Your Answer: It occurs during passive left ventricular filling
Correct Answer: It coincides with the P wave of the ECG
Explanation:The S4 heart sound occurs simultaneously with the P wave on an ECG. This sound is heard during late diastole when the left ventricle is being actively filled and the atrial contraction is forcing blood into a noncompliant left ventricle. The P wave on the ECG represents the depolarization of the left and right atrium, which results in atrial contraction. Therefore, the S4 heart sound coincides with the P wave on the ECG.
The presence of an S4 heart sound can indicate diastolic heart failure, which is caused by severe left ventricular hypertrophy. This condition can be found in patients with HOCM or can develop as a complication of hypertension or aortic stenosis.
In contrast, the S3 heart sound occurs during early diastole when the left ventricle is being passively filled.
During diastole, the T wave on the ECG represents the repolarization of the ventricles and marks the beginning of ventricular relaxation.
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 7
Incorrect
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As the physician in charge of the health of a 70-year-old man who came in for his yearly check-up, you discover that he smokes 15 cigarettes daily and has a medical history of hypertension and hypercholesterolemia. During the examination, you hear a left-sided carotid bruit while auscultating. A recent duplex ultrasound showed that the left internal carotid artery has a 50% stenosis. What is the final step in the pathogenesis of this man's condition?
Your Answer: Endothelial dysfunction allowing deposition into the tunica intima
Correct Answer: Smooth muscle proliferation and migration into the tunica intima
Explanation:Understanding Atherosclerosis and its Complications
Atherosclerosis is a complex process that occurs over several years. It begins with endothelial dysfunction triggered by factors such as smoking, hypertension, and hyperglycemia. This leads to changes in the endothelium, including inflammation, oxidation, proliferation, and reduced nitric oxide bioavailability. As a result, low-density lipoprotein (LDL) particles infiltrate the subendothelial space, and monocytes migrate from the blood and differentiate into macrophages. These macrophages then phagocytose oxidized LDL, slowly turning into large ‘foam cells’. Smooth muscle proliferation and migration from the tunica media into the intima result in the formation of a fibrous capsule covering the fatty plaque.
Once a plaque has formed, it can cause several complications. For example, it can form a physical blockage in the lumen of the coronary artery, leading to reduced blood flow and oxygen to the myocardium, resulting in angina. Alternatively, the plaque may rupture, potentially causing a complete occlusion of the coronary artery and resulting in a myocardial infarction. It is essential to understand the process of atherosclerosis and its complications to prevent and manage cardiovascular diseases effectively.
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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 28-year-old, gravida 2 para 1, presents to the emergency department with pelvic pain. She delivered a healthy baby at 37 weeks gestation 13 days ago.
During the examination, it was found that she has right lower quadrant pain and her temperature is 37.8º C. Further tests revealed a left gonadal (ovarian) vein thrombosis. The patient was informed about the risk of the thrombus lodging in the venous system from the left gonadal vein.
What is the first structure that the thrombus will go through if lodged from the left gonadal vein?Your Answer: Superior vena cava
Correct Answer: Left renal vein
Explanation:The left gonadal veins empty into the left renal vein, meaning that any thrombus originating from the left gonadal veins would travel to the left renal vein. However, if the thrombus originated from the right gonadal vein, it would flow into the inferior vena cava (IVC) since the right gonadal vein directly drains into the IVC.
The portal vein is typically formed by the merging of the superior mesenteric and splenic veins, and it also receives blood from the inferior mesenteric, gastric, and cystic veins.
The superior vena cava collects venous drainage from the upper half of the body, specifically above the diaphragm.
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 9
Incorrect
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A 67-year-old woman visited her physician complaining of palpitations. She has a medical history of type 2 diabetes, hypertension, and ischemic heart disease. Her current medications include Metformin, insulin injections, candesartan, and metoprolol. The doctor reviewed her medical records and decided to prescribe a medication to prevent complications related to the underlying cause of her palpitations. The doctor informed her that she would need to visit the hospital laboratory regularly to have her blood checked due to the medication's risk of bleeding. Which blood clotting factors are affected by this condition?
Your Answer: Factor VIII
Correct Answer: Factor IX
Explanation:This patient with a medical history of diabetes, hypertension, and diabetes is likely experiencing atrial fibrillation, which increases the risk of stroke due to the formation of blood clots in the left atrium. To minimize this risk, the anticoagulant warfarin is commonly prescribed, but it also increases the risk of bleeding. Regular monitoring of the International Normalized Ratio is necessary to ensure the patient’s safety. Warfarin works by inhibiting Vitamin K epoxide reductase, which affects the synthesis of clotting factors II, VII, IX, and X, as well as protein C and S. Factor IX is a vitamin K dependent clotting factor and is deficient in Hemophilia B. Factors XI and V are not vitamin K dependent clotting factors, while Factor I is not a clotting factor at all.
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 10
Incorrect
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A 48-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 ramipril. However, his blood pressure remained uncontrolled, so amlodipine was added to his treatment four weeks ago. Today, his blood pressure reading is 161/91mmHg. You decide to prescribe indapamide, a thiazide diuretic. Can you identify the primary site of action of thiazides in the nephron?
Your Answer: Descending limb of the loop of Henle
Correct Answer: Distal convoluted tubule
Explanation:Thiazide diuretics, 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 Na+/K+ 2Cl- channels in the thick ascending loop of Henle. There are currently no diuretic agents that specifically target the descending limb of the loop of Henle. Carbonic anhydrase inhibitors prevent the exchange of luminal Na+ for cellular H+ in both the proximal and distal tubules. Potassium-sparing diuretics, such as amiloride, inhibit the Na+/K+ ATPase in the cortical collecting ducts either directly or by blocking aldosterone receptors, as seen in spironolactone.
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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