Vasa vasorum are vessels found in the outermost layer of the blood vessel wall known as the tunica adventitia. They are the hallmark of Buerger’s disease, which presents with corkscrew vessels and can lead to amputation. The other answers do not contain the vasa vasorum.

Artery Histology: Layers of Blood Vessel Walls

The wall of a blood vessel is composed of three layers: the tunica intima, tunica media, and tunica adventitia. The innermost layer, the tunica intima, is made up of endothelial cells that are separated by gap junctions. The middle layer, the tunica media, contains smooth muscle cells and is separated from the intima by the internal elastic lamina and from the adventitia by the external elastic lamina. The outermost layer, the tunica adventitia, contains the vasa vasorum, fibroblast, and collagen. This layer is responsible for providing support and protection to the blood vessel. The vasa vasorum are small blood vessels that supply oxygen and nutrients to the larger blood vessels. The fibroblast and collagen provide structural support to the vessel wall. Understanding the histology of arteries is important in diagnosing and treating various cardiovascular diseases.

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.

The vertebral artery does not travel through the intervertebral foramen, but instead passes through the foramina found in the transverse processes of the cervical vertebrae.

Anatomy of the Vertebral Artery

The vertebral artery is a branch of the subclavian artery and can be divided into four parts. The first part runs to the foramen in the transverse process of C6 and is located anterior to the vertebral and internal jugular veins. On the left side, the thoracic duct is also an anterior relation. The second part runs through the foramina of the transverse processes of the upper six cervical vertebrae and is accompanied by a venous plexus and the inferior cervical sympathetic ganglion. The third part runs posteromedially on the lateral mass of the atlas and enters the sub occipital triangle. It then passes anterior to the edge of the posterior atlanto-occipital membrane to enter the vertebral canal. The fourth part passes through the spinal dura and arachnoid, running superiorly and anteriorly at the lateral aspect of the medulla oblongata. At the lower border of the pons, it unites to form the basilar artery.

The anatomy of the vertebral artery is important to understand as it plays a crucial role in supplying blood to the brainstem and cerebellum. Any damage or blockage to this artery can lead to serious neurological complications. Therefore, it is essential for healthcare professionals to have a thorough understanding of the anatomy and function of the vertebral artery.

The ophthalmic artery originates from the internal carotid artery, which is part of the Circle of Willis, a circular network of arteries that supply the brain. The anterior cerebral arteries, which supply the frontal and parietal lobes, as well as the corpus callosum and cingulate cortex of the brain, also arise from the internal carotid artery. A stroke of the ophthalmic artery or its branch, the central retinal artery, can cause painless loss of vision. The basilar artery, which forms part of the posterior cerebral circulation, is formed from the convergence of the two vertebral arteries and gives rise to many arteries, but not the ophthalmic artery. The posterior cerebral artery, which supplies the occipital lobe, arises from the basilar artery.

The Circle of Willis is an anastomosis formed by the internal carotid arteries and vertebral arteries on the bottom surface of the brain. It is divided into two halves and is made up of various arteries, including the anterior communicating artery, anterior cerebral artery, internal carotid artery, posterior communicating artery, and posterior cerebral arteries. The circle and its branches supply blood to important areas of the brain, such as the corpus striatum, internal capsule, diencephalon, and midbrain.

The vertebral arteries enter the cranial cavity through the foramen magnum and lie in the subarachnoid space. They then ascend on the anterior surface of the medulla oblongata and unite to form the basilar artery at the base of the pons. The basilar artery has several branches, including the anterior inferior cerebellar artery, labyrinthine artery, pontine arteries, superior cerebellar artery, and posterior cerebral artery.

The internal carotid arteries also have several branches, such as the posterior communicating artery, anterior cerebral artery, middle cerebral artery, and anterior choroid artery. These arteries supply blood to different parts of the brain, including the frontal, temporal, and parietal lobes. Overall, the Circle of Willis and its branches play a crucial role in providing oxygen and nutrients to the brain.

SLE patients should avoid taking hydralazine as it is known to cause drug-induced SLE, along with other medications such as isoniazid and procainamide.

Hydralazine: An Antihypertensive with Limited Use

Hydralazine is an antihypertensive medication that is not commonly used nowadays. It is still prescribed for severe hypertension and hypertension in pregnancy. The drug works by increasing cGMP, which leads to smooth muscle relaxation. However, there are certain contraindications to its use, such as systemic lupus erythematous and ischaemic heart disease/cerebrovascular disease.

Despite its potential benefits, hydralazine can cause adverse effects such as tachycardia, palpitations, flushing, fluid retention, headache, and drug-induced lupus. Therefore, it is not the first choice for treating hypertension in most cases. Overall, hydralazine is an older medication that has limited use due to its potential side effects and newer, more effective antihypertensive options available.

The likely diagnosis for a patient experiencing paroxysmal nocturnal dyspnoea is left-sided heart failure. This symptom, which involves sudden waking at night due to shortness of breath, is a common feature of heart failure, particularly on the left side. Aortic dissection, myocardial infarction, and pulmonary embolism are unlikely diagnoses as they present with different symptoms. Right-sided heart failure is also an unlikely diagnosis as it presents with different features such as raised JVP, ankle oedema, and hepatomegaly.

Features of Chronic Heart Failure

Chronic heart failure is a condition that affects the heart’s ability to pump blood effectively. It is characterized by several features that can help in its diagnosis. Dyspnoea, or shortness of breath, is a common symptom of chronic heart failure. Patients may also experience coughing, which can be worse at night and accompanied by pink or frothy sputum. Orthopnoea, or difficulty breathing while lying down, and paroxysmal nocturnal dyspnoea, or sudden shortness of breath at night, are also common symptoms.

Another feature of chronic heart failure is the presence of a wheeze, known as a cardiac wheeze. Patients may also experience weight loss, known as cardiac cachexia, which occurs in up to 15% of patients. However, this may be hidden by weight gained due to oedema. On examination, bibasal crackles may be heard, and signs of right-sided heart failure, such as a raised JVP, ankle oedema, and hepatomegaly, may be present.

In summary, chronic heart failure is a condition that can be identified by several features, including dyspnoea, coughing, orthopnoea, paroxysmal nocturnal dyspnoea, wheezing, weight loss, bibasal crackles, and signs of right-sided heart failure. Early recognition and management of these symptoms can help improve outcomes for patients with chronic heart failure.

Ranolazine is a medication that works by inhibiting persistent or late sodium current in various voltage-gated sodium channels in heart muscle. This results in a decrease in intracellular calcium levels, which in turn reduces tension in the heart muscle and lowers its oxygen demand.

Other medications used to treat angina include ivabradine, which inhibits funny channels, trimetazidine, which inhibits fatty acid metabolism, nitrates, which increase nitric oxide, and several drugs that reduce heart rate, such as beta blockers and calcium channel blockers.

It is important to note that ranolazine is not typically the first medication prescribed for angina. The drug management of angina may vary depending on the individual patient’s needs and medical history.

Angina pectoris can be managed through lifestyle changes, medication, percutaneous coronary intervention, and surgery. In 2011, NICE released guidelines for the management of stable angina. Medication is an important aspect of treatment, and all patients should receive aspirin and a statin unless there are contraindications. Sublingual glyceryl trinitrate can be used to abort angina attacks. NICE recommends using either a beta-blocker or a calcium channel blocker as first-line treatment, depending on the patient’s comorbidities, contraindications, and preferences. If a calcium channel blocker is used as monotherapy, a rate-limiting one such as verapamil or diltiazem should be used. If used in combination with a beta-blocker, a longer-acting dihydropyridine calcium channel blocker like amlodipine or modified-release nifedipine should be used. Beta-blockers should not be prescribed concurrently with verapamil due to the risk of complete heart block. If initial treatment is ineffective, medication should be increased to the maximum tolerated dose. If a patient is still symptomatic after monotherapy with a beta-blocker, a calcium channel blocker can be added, and vice versa. If a patient cannot tolerate the addition of a calcium channel blocker or a beta-blocker, long-acting nitrate, ivabradine, nicorandil, or ranolazine can be considered. If a patient is taking both a beta-blocker and a calcium-channel blocker, a third drug should only be added while awaiting assessment for PCI or CABG.

Nitrate tolerance is a common issue for patients who take nitrates, leading to reduced efficacy. NICE advises patients who take standard-release isosorbide mononitrate to use an asymmetric dosing interval to maintain a daily nitrate-free time of 10-14 hours to minimize the development of nitrate tolerance. However, this effect is not seen in patients who take once-daily modified-release isosorbide mononitrate.

To accentuate the sound of a left-sided murmur consistent with mitral stenosis during a cardiovascular examination, the patient should be asked to exhale. Conversely, a right-sided murmur is louder during inspiration. Listening in the left lateral position while the patient is lying down can also emphasize a mitral stenosis. To identify a mitral regurgitation murmur, listening in the axilla is helpful as it radiates. Diastolic murmurs can be heard better with a position change, while systolic murmurs tend to radiate and can be distinguished by listening in different anatomical landmarks. For example, an aortic stenosis may radiate to the carotids, while an aortic regurgitation may be heard better with the patient leaning forward.

Understanding Mitral Stenosis

Mitral stenosis is a condition where the mitral valve, which controls blood flow from the left atrium to the left ventricle, becomes obstructed. This leads to an increase in pressure within the left atrium, pulmonary vasculature, and right side of the heart. The most common cause of mitral stenosis is rheumatic fever, but it can also be caused by other rare conditions such as mucopolysaccharidoses, carcinoid, and endocardial fibroelastosis.

Symptoms of mitral stenosis include dyspnea, hemoptysis, a mid-late diastolic murmur, a loud S1, and a low volume pulse. Severe cases may also present with an increased length of murmur and a closer opening snap to S2. Chest x-rays may show left atrial enlargement, while echocardiography can confirm a cross-sectional area of less than 1 sq cm for a tight mitral stenosis.

Management of mitral stenosis depends on the severity of the condition. Asymptomatic patients are monitored with regular echocardiograms, while symptomatic patients may undergo percutaneous mitral balloon valvotomy or mitral valve surgery. Patients with associated atrial fibrillation require anticoagulation, with warfarin currently recommended for moderate/severe cases. However, there is an emerging consensus that direct-acting anticoagulants may be suitable for mild cases with atrial fibrillation.

Overall, understanding mitral stenosis is important for proper diagnosis and management of this condition.

The Purkinje fibres have the highest conduction velocities in the heart’s electrical conduction system. The process starts with the SA node generating spontaneous action potentials, which are then conducted across both atria through cell to cell conduction at a speed of approximately 1 m/s. The only pathway for the action potential to enter the ventricles is through the AV node, which has a slow conduction speed of 0.05ms to allow for complete atrial contraction and ventricular filling. The action potentials are then conducted through the Bundle of His, which splits into the left and right bundle branches, with a conduction speed of approximately 2m/s. Finally, the action potential reaches the Purkinje fibres, which are specialized conducting cells that allow for a faster conduction speed of 2-4m/s. This fast conduction speed is crucial for a synchronized and efficient contraction of the ventricle, generating pressure during systole.

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.

The patient is exhibiting symptoms that are indicative of infective endocarditis and has a past of using intravenous drugs. Infective endocarditis can be caused by various factors, but in developed countries, S. aureus is the most prevalent cause. This is especially true for individuals who use intravenous drugs, as in this case.

Aetiology of Infective Endocarditis

Infective endocarditis is a condition that affects patients with previously normal valves, rheumatic valve disease, prosthetic valves, congenital heart defects, intravenous drug users, and those who have recently undergone piercings. The strongest risk factor for developing infective endocarditis is a previous episode of the condition. The mitral valve is the most commonly affected valve.

The most common cause of infective endocarditis is Staphylococcus aureus, particularly in acute presentations and intravenous drug users. Historically, Streptococcus viridans was the most common cause, but this is no longer the case except in developing countries. Coagulase-negative Staphylococci such as Staphylococcus epidermidis are commonly found in indwelling lines and are the most common cause of endocarditis in patients following prosthetic valve surgery. Streptococcus bovis is associated with colorectal cancer, with the subtype Streptococcus gallolyticus being most linked to the condition.

Culture negative causes of infective endocarditis include prior antibiotic therapy, Coxiella burnetii, Bartonella, Brucella, and HACEK organisms (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella). It is important to note that systemic lupus erythematosus and malignancy, specifically marantic endocarditis, can also cause non-infective endocarditis.

The presence of intermittent palpitations and lightheadedness can be indicative of various conditions, but the detection of a shortened PR interval and delta wave on an ECG suggests the possibility of Wolff-Parkinson-White syndrome. This syndrome arises from an additional pathway connecting the atrium and ventricle.

Understanding Wolff-Parkinson White Syndrome

Wolff-Parkinson White (WPW) syndrome is a condition that occurs due to a congenital accessory conducting pathway between the atria and ventricles, leading to atrioventricular re-entry tachycardia (AVRT). This condition can cause AF to degenerate rapidly into VF as the accessory pathway does not slow conduction. The ECG features of WPW include a short PR interval, wide QRS complexes with a slurred upstroke known as a delta wave, and left or right axis deviation depending on the location of the accessory pathway. WPW is associated with various conditions such as HOCM, mitral valve prolapse, Ebstein’s anomaly, thyrotoxicosis, and secundum ASD.

The definitive treatment for WPW is radiofrequency ablation of the accessory pathway. Medical therapy options include sotalol, amiodarone, and flecainide. However, sotalol should be avoided if there is coexistent atrial fibrillation as it may increase the ventricular rate and potentially deteriorate into ventricular fibrillation. WPW can be differentiated into type A and type B based on the presence or absence of a dominant R wave in V1. It is important to understand WPW and its associations to provide appropriate management and prevent potential complications.

The man is experiencing critical ischemia, which is a severe form of peripheral arterial disease. He has progressed from experiencing claudication (similar to angina of the leg) to experiencing pain even at rest. While lifestyle changes and medication such as aspirin and statins are important, surgical intervention is necessary in this case. His ABPI is very low, indicating arterial disease, and percutaneous transluminal angioplasty is the preferred surgical option due to its minimally invasive nature. Amputation is not recommended at this stage as the tissue is still viable.

Symptoms of peripheral arterial disease include no symptoms, claudication, leg pain at rest, ulceration, and gangrene. Signs include absent leg and foot pulses, cold white legs, atrophic skin, arterial ulcers, and long capillary filling time (over 15 seconds in severe ischemia). The first line investigation is ABPI, and imaging options include colour duplex ultrasound and MR/CT angiography if intervention is being considered.

Management involves modifying risk factors such as smoking cessation, treating hypertension and high cholesterol, and prescribing clopidogrel. Supervised exercise programs can also help increase blood flow. Surgical options include percutaneous transluminal angioplasty and surgical reconstruction using the saphenous vein as a bypass graft. Amputation may be necessary in severe cases.

Understanding Ankle Brachial Pressure Index (ABPI)

Ankle Brachial Pressure Index (ABPI) is a non-invasive test used to assess the blood flow in the legs. It is a simple and quick test that compares the blood pressure in the ankle with the blood pressure in the arm. The result is expressed as a ratio, with the normal value being 1.0.

ABPI is particularly useful in the assessment of peripheral arterial disease (PAD), which is a condition that affects the blood vessels outside the heart and brain. PAD can cause intermittent claudication, which is a cramping pain in the legs that occurs during exercise and is relieved by rest.

The interpretation of ABPI results is as follows: a ratio between 0.6 and 0.9 is indicative of claudication, while a ratio between 0.3 and 0.6 suggests rest pain. A ratio below 0.3 indicates impending limb loss and requires urgent intervention.

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.

The atrioventricular node is most likely supplied by the right coronary artery.

The left coronary artery gives rise to the left anterior descending and circumflex arteries.

An anterior myocardial infarction is caused by occlusion of the left anterior descending artery.

The coronary sinus is a venous structure that drains blood from the heart and returns it to the right atrium.

Understanding Coronary Circulation

Coronary circulation refers to the blood flow that supplies the heart with oxygen and nutrients. The arterial supply of the heart is divided into two main branches: the left coronary artery (LCA) and the right coronary artery (RCA). The LCA originates from the left aortic sinus, while the RCA originates from the right aortic sinus. The LCA further divides into two branches, the left anterior descending (LAD) and the circumflex artery, while the RCA supplies the posterior descending artery.

The LCA supplies the left ventricle, left atrium, and interventricular septum, while the RCA supplies the right ventricle and the inferior wall of the left ventricle. The SA node, which is responsible for initiating the heartbeat, is supplied by the RCA in 60% of individuals, while the AV node, which is responsible for regulating the heartbeat, is supplied by the RCA in 90% of individuals.

On the other hand, the venous drainage of the heart is through the coronary sinus, which drains into the right atrium. During diastole, the coronary arteries fill with blood, allowing for the delivery of oxygen and nutrients to the heart muscles. Understanding the coronary circulation is crucial in the diagnosis and management of various heart diseases.

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.

According to the 2021 NICE guidelines on preventing stroke in individuals with atrial fibrillation, DOACs should be the first-line anticoagulant therapy offered. The correct answer is ‘edoxaban’. ‘Aspirin’ is not appropriate for managing atrial fibrillation as it is an antiplatelet agent. ‘Low molecular weight heparin’ and ‘unfractionated heparin’ are not recommended for long-term anticoagulation in this case as they require subcutaneous injections.

Atrial fibrillation (AF) is a condition that requires careful management, including the use of anticoagulation therapy. The latest guidelines from NICE recommend assessing the need for anticoagulation in all patients with a history of AF, regardless of whether they are currently experiencing symptoms. The CHA2DS2-VASc scoring system is used to determine the most appropriate anticoagulation strategy, with a score of 2 or more indicating the need for anticoagulation. However, it is important to ensure a transthoracic echocardiogram has been done to exclude valvular heart disease, which is an absolute indication for anticoagulation.

When considering anticoagulation therapy, doctors must also assess the patient’s bleeding risk. NICE recommends using the ORBIT scoring system to formalize this risk assessment, taking into account factors such as haemoglobin levels, age, bleeding history, renal impairment, and treatment with antiplatelet agents. While there are no formal rules on how to act on the ORBIT score, individual patient factors should be considered. The risk of bleeding increases with a higher ORBIT score, with a score of 4-7 indicating a high risk of bleeding.

For many years, warfarin was the anticoagulant of choice for AF. However, the development of direct oral anticoagulants (DOACs) has changed this. DOACs have the advantage of not requiring regular blood tests to check the INR and are now recommended as the first-line anticoagulant for patients with AF. The recommended DOACs for reducing stroke risk in AF are apixaban, dabigatran, edoxaban, and rivaroxaban. Warfarin is now used second-line, in patients where a DOAC is contraindicated or not tolerated. Aspirin is not recommended for reducing stroke risk in patients with AF.

Here is a mnemonic to remember the order in which the branches of the external carotid artery originate: Some Attendings Like Freaking Out Potential Medical Students. The first branch is the superior thyroid artery, followed by the ascending pharyngeal, lingual, facial, occipital, post auricular, and finally the maxillary and superficial temporal arteries.

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.

Patients taking ACE-inhibitors should be cautious when using trimethoprim as it can lead to life-threatening hyperkalaemia, which may result in sudden death. Therefore, it is essential to monitor the potassium levels regularly by conducting urea and electrolyte tests.

When using trimethoprim with methotrexate, it is crucial to monitor the complete blood count regularly due to the increased risk of myelosuppression. However, if the patient is only taking trimethoprim, there is no need to monitor troponins and creatine kinase.

Angiotensin-converting enzyme (ACE) inhibitors are commonly used as the first-line treatment for hypertension and heart failure in younger patients. However, they may not be as effective in treating hypertensive Afro-Caribbean patients. ACE inhibitors are also used to treat diabetic nephropathy and prevent ischaemic heart disease. These drugs work by inhibiting the conversion of angiotensin I to angiotensin II and are metabolized in the liver.

While ACE inhibitors are generally well-tolerated, they can cause side effects such as cough, angioedema, hyperkalaemia, and first-dose hypotension. Patients with certain conditions, such as renovascular disease, aortic stenosis, or hereditary or idiopathic angioedema, should use ACE inhibitors with caution or avoid them altogether. Pregnant and breastfeeding women should also avoid these drugs.

Patients taking high-dose diuretics may be at increased risk of hypotension when using ACE inhibitors. Therefore, it is important to monitor urea and electrolyte levels before and after starting treatment, as well as any changes in creatinine and potassium levels. Acceptable changes include a 30% increase in serum creatinine from baseline and an increase in potassium up to 5.5 mmol/l. Patients with undiagnosed bilateral renal artery stenosis may experience significant renal impairment when using ACE inhibitors.

The current NICE guidelines recommend using a flow chart to manage hypertension, with ACE inhibitors as the first-line treatment for patients under 55 years old. However, individual patient factors and comorbidities should be taken into account when deciding on the best treatment plan.

The anterior cerebral artery is responsible for supplying blood to a portion of the frontal and parietal lobes. While this type of stroke is uncommon and may be challenging to diagnose through clinical means, imaging techniques can reveal affected vessels or brain regions. Damage to the frontal and parietal lobes can result in significant mood, personality, and movement disorders.

It’s important to note that the occipital lobe and cerebellum receive their blood supply from the posterior cerebral artery and cerebellar arteries (which originate from the basilar and vertebral arteries), respectively. Therefore, they would not be impacted by an ACA stroke. Similarly, the middle cerebral artery is responsible for supplying blood to the temporal lobe, so damage to the ACA would not affect this area.

The Circle of Willis is an anastomosis formed by the internal carotid arteries and vertebral arteries on the bottom surface of the brain. It is divided into two halves and is made up of various arteries, including the anterior communicating artery, anterior cerebral artery, internal carotid artery, posterior communicating artery, and posterior cerebral arteries. The circle and its branches supply blood to important areas of the brain, such as the corpus striatum, internal capsule, diencephalon, and midbrain.

The vertebral arteries enter the cranial cavity through the foramen magnum and lie in the subarachnoid space. They then ascend on the anterior surface of the medulla oblongata and unite to form the basilar artery at the base of the pons. The basilar artery has several branches, including the anterior inferior cerebellar artery, labyrinthine artery, pontine arteries, superior cerebellar artery, and posterior cerebral artery.

The internal carotid arteries also have several branches, such as the posterior communicating artery, anterior cerebral artery, middle cerebral artery, and anterior choroid artery. These arteries supply blood to different parts of the brain, including the frontal, temporal, and parietal lobes. Overall, the Circle of Willis and its branches play a crucial role in providing oxygen and nutrients to the brain.

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.