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Question 1
Incorrect
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As a curious fourth-year medical student, you observe the birth of a full-term baby delivered vaginally to a mother who has given birth once before. The infant's Apgar score is 9 at 1 minute and 10 at 10 minutes, and the delivery is uncomplicated. However, a postnatal examination reveals that the ductus arteriosus has not closed properly. Can you explain the process by which this structure normally closes?
Your Answer: Increased oxygen tension which increases the concentration of prostaglandins
Correct Answer: Decreased prostaglandin concentration
Explanation:The ductus arteriosus, which is a shunt connecting the pulmonary artery with the descending aorta in utero, closes with the first breaths of life. This is due to an increase in pulmonary blood flow, which helps to clear local vasodilating prostaglandins that keep the duct open during fetal development. The opening of the lung alveoli with the first breath of life leads to an increase in oxygen tension in the blood, but this is not the primary mechanism behind the closure of the ductus arteriosus. It is important to note that oxygen tension in the blood increases after birth when the infant breathes in air and no longer receives mixed oxygenated blood via the placenta.
Understanding Patent Ductus Arteriosus
Patent ductus arteriosus is a type of congenital heart defect that is generally classified as ‘acyanotic’. However, if left uncorrected, it can eventually result in late cyanosis in the lower extremities, which is termed differential cyanosis. This condition is caused by a connection between the pulmonary trunk and descending aorta. Normally, the ductus arteriosus closes with the first breaths due to increased pulmonary flow, which enhances prostaglandins clearance. However, in some cases, this connection remains open, leading to patent ductus arteriosus.
This condition is more common in premature babies, those born at high altitude, or those whose mothers had rubella infection in the first trimester. The features of patent ductus arteriosus include a left subclavicular thrill, continuous ‘machinery’ murmur, large volume, bounding, collapsing pulse, wide pulse pressure, and heaving apex beat.
The management of patent ductus arteriosus involves the use of indomethacin or ibuprofen, which are given to the neonate. These medications inhibit prostaglandin synthesis and close the connection in the majority of cases. If patent ductus arteriosus is associated with another congenital heart defect amenable to surgery, then prostaglandin E1 is useful to keep the duct open until after surgical repair. Understanding patent ductus arteriosus is important for early diagnosis and management of this condition.
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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 man presents to the emergency department with acute, severe shortness of breath.
During the clinical examination, an elevated JVP is noted, and bilateral basal crackles are heard on auscultation. An S3 gallop is also heard on auscultation of his heart.
The physician places him on high flow oxygen and positions him upright. You are asked to review the patient's medication chart and discontinue any medications that may be contraindicated in his current condition.
Which medication should you discontinue?Your Answer: Morphine
Correct Answer: Nicorandil
Explanation:Nicorandil is a medication that is commonly used to treat angina. It works by activating potassium channels, which leads to vasodilation. This process is achieved through the activation of guanylyl cyclase, which results in an increase in cGMP. However, there are some adverse effects associated with the use of nicorandil, including headaches, flushing, and the development of ulcers on the skin, mucous membranes, and eyes. Additionally, gastrointestinal ulcers, including anal ulceration, may also occur. It is important to note that nicorandil should not be used in patients with left ventricular failure.
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This question is part of the following fields:
- Cardiovascular System
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Question 3
Correct
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A 67-year-old man with a stable angina history for two years visits his cardiologist for a regular check-up. During the review, the cardiologist observes that the patient's heart rate is low at 46 bpm. As a result, the cardiologist decides to replace his beta-blocker with a new anti-anginal drug called nicorandil.
What is the mode of action of the patient's new medication?Your Answer: Potassium channel activator through activation of guanylyl cyclase
Explanation:Nicorandil activates potassium channels, leading to vasodilation. This activation triggers guanylyl cyclase, which increases the production of cyclic GMP (cGMP) and activates protein kinase G (PKG). PKG phosphorylates and inhibits GTPase RhoA, reducing Rho-kinase activity and increasing myosin phosphatase activity. As a result, the smooth muscle becomes less sensitive to calcium, leading to dilation of the large coronary arteries and improved perfusion. Nicorandil does not significantly affect calcium or sodium channels. This mechanism helps alleviate anginal symptoms.
Nicorandil is a medication that is commonly used to treat angina. It works by activating potassium channels, which leads to vasodilation. This process is achieved through the activation of guanylyl cyclase, which results in an increase in cGMP. However, there are some adverse effects associated with the use of nicorandil, including headaches, flushing, and the development of ulcers on the skin, mucous membranes, and eyes. Additionally, gastrointestinal ulcers, including anal ulceration, may also occur. It is important to note that nicorandil should not be used in patients with left ventricular failure.
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This question is part of the following fields:
- Cardiovascular System
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Question 4
Incorrect
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A 65-year-old man is admitted after experiencing an acute coronary syndrome. He is prescribed aspirin, clopidogrel, nitrates, and morphine. Due to his high 6-month risk score, percutaneous coronary intervention is planned and he is given intravenous tirofiban. What is the mechanism of action of this medication?
Your Answer: Activates antithrombin III
Correct Answer: Glycoprotein IIb/IIIa receptor antagonist
Explanation:Glycoprotein IIb/IIIa Receptor Antagonists
Glycoprotein IIb/IIIa receptor antagonists are a class of drugs that inhibit the function of the glycoprotein IIb/IIIa receptor, which is found on the surface of platelets. These drugs are used to prevent blood clots from forming in patients with acute coronary syndrome, unstable angina, or during percutaneous coronary intervention (PCI).
Examples of glycoprotein IIb/IIIa receptor antagonists include abciximab, eptifibatide, and tirofiban. These drugs work by blocking the binding of fibrinogen to the glycoprotein IIb/IIIa receptor, which prevents platelet aggregation and the formation of blood clots.
Glycoprotein IIb/IIIa receptor antagonists are typically administered intravenously and are used in combination with other antiplatelet agents, such as aspirin and clopidogrel. While these drugs are effective at preventing blood clots, they can also increase the risk of bleeding. Therefore, careful monitoring of patients is necessary to ensure that the benefits of these drugs outweigh the risks.
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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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Sophie, a 6-week-old baby, presents to the emergency department for evaluation. Her mother has observed that Sophie has been experiencing shortness of breath for the past 3 weeks, particularly during feeding. Sophie was born at 36 weeks and her mother reports no other issues since birth.
During the examination, a continuous machinery murmur with a left-sided sub-clavicular thrill is detected, and a diagnosis of patent ductus arteriosus is made. Surgery is not deemed necessary, but a medication that inhibits prostaglandin synthesis is recommended.
What is the most probable pharmacological treatment that will be offered?Your Answer: Prostaglandin E1
Correct Answer: Indomethacin
Explanation:The inhibition of prostaglandin synthesis in infants with patent ductus arteriosus is achieved through the use of indomethacin. This medication (or ibuprofen) is effective in promoting closure of the ductus arteriosus by inhibiting prostaglandin synthesis.
Beta-blockers such as bisoprolol are not used in the management of PDA, making this answer incorrect.
Steroids like dexamethasone and prednisolone are not typically used in the treatment of PDA, although they may be given to the mother if premature delivery is expected. Therefore, these answers are also incorrect.
Understanding Patent Ductus Arteriosus
Patent ductus arteriosus is a type of congenital heart defect that is generally classified as ‘acyanotic’. However, if left uncorrected, it can eventually result in late cyanosis in the lower extremities, which is termed differential cyanosis. This condition is caused by a connection between the pulmonary trunk and descending aorta. Normally, the ductus arteriosus closes with the first breaths due to increased pulmonary flow, which enhances prostaglandins clearance. However, in some cases, this connection remains open, leading to patent ductus arteriosus.
This condition is more common in premature babies, those born at high altitude, or those whose mothers had rubella infection in the first trimester. The features of patent ductus arteriosus include a left subclavicular thrill, continuous ‘machinery’ murmur, large volume, bounding, collapsing pulse, wide pulse pressure, and heaving apex beat.
The management of patent ductus arteriosus involves the use of indomethacin or ibuprofen, which are given to the neonate. These medications inhibit prostaglandin synthesis and close the connection in the majority of cases. If patent ductus arteriosus is associated with another congenital heart defect amenable to surgery, then prostaglandin E1 is useful to keep the duct open until after surgical repair. Understanding patent ductus arteriosus is important for early diagnosis and management of this condition.
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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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Where are the arterial baroreceptors situated?
Your Answer: None of the above
Correct Answer: Carotid sinus and aortic arch
Explanation: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 7
Incorrect
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An 80-year-old patient who recently had a TIA is admitted to the vascular ward in preparation for a carotid endarterectomy tomorrow. During her pre-operative consultation, the surgeon explained that the artery will be tied during the procedure. The patient asks about the different arteries and their functions. You inform her that the internal carotid artery supplies the brain, while the external carotid artery divides into two arteries after ascending the neck. One of these arteries is the superficial temporal artery, but what is the other?
Your Answer: Lingual artery
Correct Answer: Maxillary artery
Explanation:The correct answer is the maxillary artery, which is one of the two terminal branches of the external carotid artery. It supplies deep structures of the face and usually bifurcates within the parotid gland to form the superficial temporal artery and maxillary artery. The facial artery supplies superficial structures in the face, while the lingual artery supplies the tongue. The middle meningeal artery is a branch of the maxillary artery and supplies the dura mater and calvaria. There are also two deep temporal arteries that arise from the maxillary artery and supply the temporalis muscle. The patient is scheduled to undergo carotid endarterectomy, a surgical procedure that involves removing atherosclerotic plaque from the common carotid artery to reduce the risk of subsequent ischaemic strokes or transient ischaemic attacks.
Anatomy of the External Carotid Artery
The external carotid artery begins on the side of the pharynx and runs in front of the internal carotid artery, behind the posterior belly of digastric and stylohyoid muscles. It is covered by sternocleidomastoid muscle and passed by hypoglossal nerves, lingual and facial veins. The artery then enters the parotid gland and divides into its terminal branches within the gland.
To locate the external carotid artery, an imaginary line can be drawn from the bifurcation of the common carotid artery behind the angle of the jaw to a point in front of the tragus of the ear.
The external carotid artery has six branches, with three in front, two behind, and one deep. The three branches in front are the superior thyroid, lingual, and facial arteries. The two branches behind are the occipital and posterior auricular arteries. The deep branch is the ascending pharyngeal artery. The external carotid artery terminates by dividing into the superficial temporal and maxillary arteries within the parotid gland.
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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 65-year-old woman visits the clinic complaining of increasing fatigue and weakness. Upon examination, there are no notable symptoms except for a low serum potassium level found in her blood test. After informing her of the results, she reveals that she has been experiencing palpitations and dizziness for a few hours. You advise her to go to the emergency department for an ECG and treatment. What ECG indication is associated with hypokalaemia?
Your Answer: Tall tented T waves
Correct Answer: ST segment depression
Explanation:ECG changes indicating hypokalaemia include ST-segment depression, along with other signs such as small or absent P waves, tall tented T waves, and broad bizarre QRS complexes. On the other hand, hyperkalaemia can be identified through ECG signs such as a long PR interval and a sine wave pattern, as well as tall tented T waves and broad bizarre QRS complexes. Prolongation of the PR interval may be seen in both hypokalaemia and hyperkalaemia, while a short PR interval suggests pre-excitation or an AV nodal rhythm. Patients with hypokalaemia may present with symptoms such as fatigue, muscle weakness, myalgia, muscle cramps, constipation, hyporeflexia, and in rare cases, paralysis. It is worth noting that abnormalities in serum potassium levels are often discovered incidentally.
Hypokalaemia, a condition characterized by low levels of potassium in the blood, can be detected through ECG features. These include the presence of U waves, small or absent T waves (which may occasionally be inverted), a prolonged PR interval, ST depression, and a long QT interval. The ECG image provided shows typical U waves and a borderline PR interval. To remember these features, one user suggests the following rhyme: In Hypokalaemia, U have no Pot and no T, but a long PR and a long QT.
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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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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: Foam cell formation from macrophages
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 10
Incorrect
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A 56-year-old man visits his GP complaining of congestive heart failure, angina, and exertional syncope. During the examination, the doctor observes a forceful apex beat and a systolic ejection murmur at the upper right sternal border.
What condition is most likely causing these symptoms?Your Answer: Aortic regurgitation
Correct Answer: Aortic stenosis
Explanation:Symptoms and Diagnosis of Heart Valve Disorders
Heart valve disorders can cause a range of symptoms depending on the type and severity of the condition. Aortic stenosis, for example, can lead to obstruction of left ventricular emptying, resulting in slow rising carotid pulse and a palpated murmur that may radiate to the neck. Aortic valve replacement is necessary for symptomatic patients to prevent death within three years or those with severe valve narrowing on ECHO. On the other hand, aortic regurgitation may not show any symptoms for many years until dyspnoea and fatigue set in. A blowing early diastolic murmur is typically found at the left sternal edge, and a mid-diastolic murmur may also be present over the apex of the heart.
Mitral regurgitation, whether acute or chronic, can cause pulmonary oedema, exertional dyspnoea, and lethargy. A pansystolic murmur is audible at the apex. Mitral stenosis, meanwhile, initially presents with exertional dyspnoea, but haemoptysis and a productive cough may also occur. A rumbling mid-diastolic murmur is indicative of mitral stenosis. Finally, a prolapsing mitral valve is common in young women and is usually asymptomatic, although atypical chest pain may be present. Overall, proper diagnosis and treatment of heart valve disorders are crucial to prevent complications and improve quality of life.
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This question is part of the following fields:
- Cardiovascular System
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