1. Neurology

NeurologyMigraine use mefenamic acid for perimenstrual prophylaxis of menstrually related migraines, with treatment starting 2 days prior to the onset of flow or 1 day prior to the expected onset of the headache and continuing for the duration of menstruation. Metoclopramide has been shown to have efficacy for both the pain and nausea associated with migraine. safely used in pregnancy Topiramate is second line prophlaxis for migraine after propranolol Oral contraceptive pills are contraindicated in women with migraine with aura, especially if the aura involves more than just simple visual aura, if there are additional stroke risk factors, or if the aura begins after the initiation of oral contraceptionTension-type headache is distinguished from migraine by the fact that patients with tension headache are not disabled and can carry out activities of daily living in a normal, expedient manner.

Medication overuse headache headache for more than 15 days per month and the use of acute headache medication on more than 10 days per month.

Trigeminal neuralgia. affects the right side of the face five times more frequently than the left. The number of attacks may vary from one a day up to a hundred per day, and patients are typically asymptomatic in between attacks Trigeminal neuralgia is a disease of middle-to-late age female We should evaluate for secondary causes of Trigeminal neuralgia if ito occur in a young patiento associated with any physical signs as reduced corneal reflex and reduced sensation in the mandibular and maxillary division of the trigeminal secondary causes of Trigeminal neuralgiao multiple sclerosis,o posterior fossa tumors, ando vascular or aneurysmal compression of the trigeminal nerve. Usual treatment for trigeminal neuralgia would be a titrated dose of carbamazepine, with addition of gabapentin or amitriptyline if needed. The disorder may cease spontaneously after 6-12 months.The trigeminal autonomic cephalalgias

Disease Duration Frequency TreatmentCluster headache 1 hour 1-3/day

prefer to be mobile, because resting causes worsening of the painprophylaxis1. verapamil2. Prednisone is the most appropriate treatment for episodic cluster headache.Paroxysmal hemicrania 15 minutes 11/day indomethacinSUNCT syndrome 60 seconds 30-200/day lamotrigineMigrain > 3hours Resting in a dark, quiet room results in improvement.

Thunderclap headache is head pain that begins suddenly and is severe at onset. TCH might be the first sign ofo subarachnoid haemorrhage,o unruptured intracranial aneurysm,o cerebral venous sinus thrombosis,o cervical artery dissection,o acute hypertensive crisis,o spontaneous intracranial hypotension,o ischaemic stroke,o retroclival haematoma,o pituitary apoplexy,o third ventricle colloid cyst, ando intracranial infection. CT of the head without enhancement is the most sensitive test for subarachnoid hemorrhage. A lumbar puncture is necessary if CT scan results are normal. If results of both the CT scan and lumbar puncture are normal, neurovascular imaging is indicated in these patients and should include magnetic resonance or CT angiography (or venography).

Vertebral artery dissection Typically presents witho neck or head pain,o Horner's syndrome,o dysarthria,o dysphagia,o decreased pain and temperature sensation,o dysmetria,o ataxia, ando vertigo. Magnetic resonance angiography is a sensitive diagnostic test for vertebral artery dissection as a cause of stroke. If MR angiography negative and suspicion is still high, 4 vessel cerebral angiography can be arranged. Where there is no evidence of sub-arachnoid haemorrhage, anti-coagulation is the management of choice to prevent thromboembolic sequelae as a result of the dissectionSubclavian steal syndrome is associated with retrograde flow in the vertebral artery due to a proximal subclavian artery stenosis. Neurological symptoms are precipitated by vigorous exercise with the arm above the head, such as painting a wall, they are in fact related to reduced blood flow. The diagnosis is often confused with transient ischaemic attacks or epilepsy. Duplex ultrasound and magnetic resonance angiography are the investigations of choice. Endarterectomy and stenting are common surgical methods involved in relieving symptoms associated with this condition.Subarachnoid hemorrhage CT brain imaging within the first 48 hours is approximately 95% sensitive at identifying SAH. However, a normal CT scan does not exclude SAH and a lumbar puncture should be performed if the CT scan is negative and SAH is still suspected. Since bilirubin is undetectable in the cerebrospinal fluid (CSF) until 12 hours after the onset of symptoms, a lumbar puncture should be delayed until after this time unless meningitis is suspected. Lumbar puncture is most sensitive in the initial period (12 hours after the onset of symptoms and up to 14 days later). Bilirubin may be detected in CSF by spectrophotometry visual inspection for the yellow discoloration (xanthochromia).from 12 hours up to 2 weeks Evidence clearly indicates that visual inspection is not a reliable method. CSF spectrophotometry detects the presence of both oxyhaemoglobin and bilirubin because either one or both of these pigments may contribute to xanthochromia following SAH. CSF supernatant is scanned CSF may be of thisAppearance Clear ClearOpening pressure 17 cm H20 (NR 4 - 18)CSF white cell count 0 cells/mL (NR 100 mmHg, start IV nitroglycerine 1020 g/min;o BP of 70100 mmHg, with no signs or symptoms of shock start IV dobutamine 220 g/min;o BP is 70100 mmHg with signs or symptoms of shock, start IV dopamine 515 g/min;o BP is less than 70 mmHg with signs or symptoms of shock, start IV noradrenaline 0.530 g/min.Flash pulmonary oedema Rapidly developing pulmonary congestion The most common cause of flash pulmonary oedema is myocardial ischaemia.Bilateral renal artery stenosis can also present with a similar clinical picture but is less common cause, as is acute aortic regurgitation.

Tocolysis-associated pulmonary oedema Tocolytics are medications administered for the suppression of premature contractions. Acute pulmonary oedema can occur with administration of 2 agonists for tocolysis in up to 515% of cases. It usually occurs after 24 h of administration of these agents. The chest X-ray reveals pulmonary infiltrates and normal heart size. Concomitant use of corticosteroids that are often administered for lung maturation have also been implicated as risk factor for development of tocolysis-associated pulmonary oedema.Treatment involves stopping the tocolytics, oxygen and careful volume control.

Ventricular free wall rupture Autopsy studies reveal that ventricular free wall rupture occurs about 10 times more frequently than postinfarction ventricular septal rupture, occurring in about 11% of patients following acute myocardial infarction. Ventricular rupture and cardiogenic shock are now the leading causes of death following acute myocardial infarction, and together account for over two-thirds of early deaths in patients suffering their first acute infarction.

Coronary stents re-stenosis Studies have shown that in patients with type-2 diabetes, coronary stents are liable to re-stenosis at a rate of 4050% by the end of a 6-month follow-up period. Drug eluting stents have been shown to reduce the relative risk of re-stenosis by around 80%, but only where dual anti-platelet therapy with clopidogrel and aspirin is continued for at least 1 year. Whilst there is evidence that both rosiglitazone and pioglitazone both reduce in-stent re-stenosis, rosiglitazone is not recommended in patients who have a history of previous myocardial infarctionRisk factors for torsade de pointes include: bradycardia, hypokalaemia, congestive heart failure, digitalis therapy, subclinical long-QT syndrome, baseline QT prolongation, severe hypomagnesaemia, severe alkalosis and recent conversion from atrial fibrillation. Female sex is a powerful predictor of the risk of torsade de pointes in patients with congenital and acquired long-QT syndromes. How or whether variability in the expression of genes that determine normal cardiac electrophysiology explain the sex-dependent risk of torsade de pointes is not yet clear.

Ventricular tachycardia (VT) If secondary to digoxin toxicity and unstable haemodynamically. In the setting of digoxin toxicity DC cardioversion is not used unless all other measures have been exhausted because it is unusually unsuccessful. The most useful drugs in this setting are lidocaine and phenytoin. Amiodarone and procainamide may increase digoxin levels and should be avoided.

Prolonged QT Interval Six mutations (LQT16) have been identified in association with the RomanoWard syndrome. LQT1 and LQT2 mutations make up around 87% of cases of RomanoWard syndrome and are associated with cardiac potassium-channel gene mutations. JLN mutations (JervellLange-Nielsen syndrome) tend to be associated with deafness. Although sudden death usually occurs in symptomatic patients, it happens with the first episode of syncope in about 30% of the patients. LQT4 is associated with paroxysmal atrial fibrillation. Studies have shown an improved response to pharmacologic treatment with a lowered rate of sudden cardiac death in LQT1 and LQT2 compared with LQT3. Triggering events are somewhat different by genotype. Patients with LQT1 usually have cardiac events preceded byo exercise or swimming.o Sudden exposure of the patient's face to cold water is thought to elicit a vagotonic reflex. Patients with LQT2 may have arrhythmic events aftero an emotional event,o exercise, oro exposure to auditory stimuli (eg, door bells, telephone ring). Patients with LQT3 usually have events during night sleep. Diagnosis is based upon the QTc (corrected QT interval), although this may be within the normal range at rest; hence, Holter monitoring is recommended. Genetic testing for known mutations in DNA samples from patients is becoming accessible in specialized centers. Identification of an LQTS genetic mutation confirms the diagnosis. However, a negative result on genetic testing is of limited diagnostic value because only approximately 50% of patients with LQTS have known mutations. The remaining half of patients with LQTS may have mutations of yet unknown genes. Therefore, genetic testing has high specificity but a low sensitivity. Beta-blockade is seen as the treatment of choice for most cases of long QT syndrome, which is thought to work through reducing adrenergic demand. Beta-blockers decrease sympathetic activation from the left stellate ganglion. Beta-blockers also decrease the maximal heart rate achieved during exertion and thereby prevent exercise-related arrhythmic events that occur in long QT syndrome. Implantable defibrillators are also used in the management of these patients. The activity of the left stellate ganglion is greater compared to the right stellate ganglion in normal individuals. Animal and human studies have shown that right stellectomy or primary increase in the output of the left stellate ganglion increases the QT interval. Patients who experience ventricular arrhythmias or aborted sudden cardiac death despite beta-blocker therapy should have an implantable cardioverter defibrillator (ICD) in addition to beta-blockers. Left stellate cardiac ganglionectomy is an invasive procedure and results in Horners syndrome. It is performed in patients who have symptoms despite beta-blockers and have frequent shocks with ICD.Dual chamber pacing might be beneficial in subset of patients with long QT syndrome type 3. Management of drug-induced long QT syndrome is too stop the precipitating drug,o correction of any electrolyte disturbance like hypokalaemia or hypomagnesaemiao treatment of associated ventricular arrhythmia.o First-line pharmacological therapy for drug-induced long QT syndrome is intravenous magnesium sulphate 2 g administered as bolus over 12 min, followed by another bolus in 15 min if required, or continuous infusion at a rate of 520 mg/min.

Prosthetic valve thrombosis (PVT) May resulting in shock. This complication occurs in 0.03 to 5.5% annually with equal frequency in bioprosthesis and mechanical valves. It is more common in mitral prosthesis and with subtherapeutic anticoagulation. The best diagnostic modality is transoesophageal echocardiography; however transthoracic echocardiography is the initial choice in sick patients, and if adequate visualisation is not obtained TEE can be done. Thrombolytic therapy for patientso pulmonary oedema oro hypotension.o right-sided PVT should be treated with thrombolytic agents surgery Ino stable patients,o is a better option for left-sided PVT, whileSerial echocardiography should be performed, and if the response is inadequate repeat thrombolytic therapy can be given.

Complications of prosthetic valves include structural valve deterioration, symptoms of heart failure with significant valve regurgitation. valve thrombosis, embolism, bleeding, pannus formation, is a slowly growing fibrous overgrowth fixed on the prosthesis, causing valve dysfunction endocarditis. prosthesis mismatch may occur when the inserted valve prosthesis is too small relative to patient size, recreating the outflow obstruction present preoperatively. The main hemodynamic consequence is persistence of significant transvalvular gradients through what is otherwise a normally functioning prosthesis. Mild hemolytic anemia is common in patients with prosthetic heart valves, but can be more severe in up to 10% to 20% of patients.o Hemolytic anemia is more common in those with paravalvular regurgitation and with mechanical valves.o Clinical features include fatigue, anemia, new murmur, and, in more severe cases, jaundice and heart failure.o Most cases of hemolytic anemia are subclinical, identified only by laboratory data.o Symptomatic hemolytic anemia can usually be treated with oral iron and folate replacement, although more severe cases may warrant blood transfusion or recombinant human erythropoietin

Anticoagulation for the pregnant patient with a mechanical valve prosthesis when the dose of warfarin is less than 5 mg daily, the risk of embryopathy decreases to below 10%.So Continue warfarin, adjusted to INR

Aortic stenosis severe aortic stenosiso An absent aortic component of S2,o a long and late-peaking systolic murmur,o a sustained apical impulse An overestimation of the severity of aortic stenosis can occur due to large volumes of blood passing over the valve at high velocities, which occurs in aortic regurgitation. Aortic valve replacement is not performed in asymptomatic patients because of the increased surgical risk Patient with severe left ventricular (LV) dysfunction, and calculated valve area in such patients can be falsely low because low cardiac output reduces the valve opening forces. It is important to distinguish patients with true severe aortic stenosis (AS) with secondary LV dysfunction from those who have a falsely low calculated aortic valve area because of low cardiac output. An important method of distinguishing between the two conditions is to assess the haemodynamics after increasing the cardiac output by dobutamine infusion during echocardiography or cardiac catheterisation. Patients with truly severe AS manifest an increase in transaortic pressure gradient while the valve surface area remains the same during dobutamine infusion; while those with falsely low calculated valve area manifest an increase in calculated valve surface area. Dobutamine echocardiography is also important to assess LV contractile reserve. Patients who have 20% or more increase in stroke volume after dobutamine infusion have a much better prognosis after surgery compared to those who do not have LV contractile reserve.

Aortic stenosis with acutely ill elderly patient with heart failure The ultimate treatment is valve replacement but in a patient who is acutely unwell, a valvuloplasty is used as a bridging procedure. An aortic balloon pump would improve the cardiac failure and also increase coronary perfusion, and is necessary in such a high-risk procedure. Noradrenaline has no place here as it can worsen the left ventricular failure as raising the afterload may cause the ventricle to fail further. Milrinone, a phosphodiesterase III inhibitor, appears to be useful in moderate ventricular dysfunction with small doses of adrenaline. This increases the cardiac output as well as raising the mean arterial pressure.

Microcytic anaemia and severe calcific aortic stenosis This is Heydes syndrome The treatment is to replace the valve after blood transfusion " No further gastro-endoscopies are needed", as the mechanism is thought to be due to destruction of von Willebrands factor as the platelets traverse the stenosed valve resulting in bleeding per rectum. several gastric endoscopies and colonoscopies in search of an underlying cause of his anaemia may be done with ve results The investigation of choice after valve replacement is mesenteric angiography as the bleeding vessels are poorly visualised on colonoscopy. This would look for the presence of angiodysplasia, which may be associated with aortic stenosis. Resection of the diseased bowel has also been described as a treatment

Mitral stenosis Clinical markers consistent with severe mitral stenosis are transmitral pressure gradients greater than 10 mm Hg, enlargement of the left atrium, mitral valve area less than 1.5 cm2, and pulmonary pressures greater than 50 mm Hg.Clinical outcome in asymptomatic or minimally symptomatic patients with mitral stenosis is excellent (>80% survival at 10 years), but once patients are symptomatic, 10-year survival is less than 15%. Morbidity associated with untreated mitral stenosis includeso pulmonary hypertension,o right-sided heart failure,o systemic embolism from atrial fibrillation, ando valve infection.Management In symptomatic patients, percutaneous valvuloplasty is the preferred less invasive than surgical intervention avoids the need for lifelong anticoagulation.o Major complications of percutaneous valvuloplasty include severe mitral regurgitation (1%-8%) systemic embolization (1%-3%) tamponade (1%-2%). Procedural mortality rate is 1%.o Valve characteristics that favor successful valvuloplasty include pliable mitral valve leaflets, minimal commissural fusion, and minimal valvular/subvalvular calcification,o These are contraindications: severely calcified or rigid valve leaflets, concomitant coronary artery or other valve disease requiring surgery. concomitant mitral regurgitation. atrial thrombus In patients under consideration for valvuloplasty, transesophageal echocardiography is necessary to definitively exclude a left atrial thrombus because of the risk of thrombus dislodgement and embolization during the procedure. If thrombus present These patients should undergo mitral valve replacement.

Mitral stenosis with paroxysmal AF A beta-blocker can be used as first-line treatment, as it might prevent atrial tachyarrhythmias. It will also slow down the heart rate in sinus rhythm, thus increasing diastolic time and augmenting cardiac output. Digoxin is not particularly helpful in paroxysmal AF, and amiodarone should be reserved for resistant cases.

Mitral regurgitation Clinical markers that should prompt surgical intervention includeo left ventricular enlargement or dysfunction (end-systolic dimension >40 mm and ejection fraction 50 mm Hg, oro an exercise-associated increase in pulmonary pressures (increase of approximately 25 mm Hg over baseline). Otherwise, asymptomatic patients with severe, chronic mitral regurgitation but normal left ventricular size and function can be reevaluated with periodic 6- to 12-month monitoring.

Decompensated rheumatic mitral valve disease in pregnancy optimization of medical management is preferred over urgent percutaneous mitral balloon valvuloplasty. A transthoracic echocardiogram aids in evaluating the severity of mitral stenosis, pulmonary pressures, involvement of other cardiac valves, and the presence of concurrent mitral regurgitation. If the patient can be treated medically and the pregnancy carried to term, valvuloplasty can be delayed until after delivery to reduce radiation exposure to the fetus and provide an opportunity to reassess the patient. With the decrease in volume load, a previously symptomatic pregnant patient may improve following delivery, delaying or eliminating the need for valvuloplasty. If despite aggressive medical therapy, the pregnant patient remains severely symptomatic, however, percutaneous balloon valvuloplasty may be performed (preferred gestational age >8 weeks) if significant mitral regurgitation is absent and a left atrial thrombus is excluded by transesophageal echocardiography.Peripartum cardiomyopathy Peripartum cardiomyopathy is defined as heart failure with a left ventricular ejection fraction less than 45% that is diagnosed between 3 months before and 6 months after delivery in the absence of an identifiable cause. Risk factors for peripartum cardiomyopathy include age (>30 years at the time of the pregnancy), race (black, African, Haitian), and the presence of gestational hypertension. With a maternal mortality rate of approximately 10%, Improvement in left ventricular function occurs in about 50% of women with peripartum cardiomyopathy within 6 months after delivery. Treatment is the same as for the non-pregnant patient with cardiac failure, although angiotensin-converting enzyme inhibitors should be avoided. The mainstay of medical treatment is digoxin and loop diuretics. Nitrates are generally not recommended during pregnancy. If indicated nitrates and inotropic support with dobutamine should be used. Beta-blockers should be added once the patients volume status is optimised. Patients with PPCM are at risk of thromboembolism due to both hypercoagulable state of pregnancy and stasis of blood in the left ventricle. Therefore, anticoagulation with heparin or warfarin is recommended "when left ventricular ejection fraction is less than 35%". Heparin is preferable in late pregnancy because it has short half-life and can be discontinued prior to delivery. Intravenous immune globulin and pentoxifylline have been shown to improve outcomes in some studies.Dilated cardiomyopathy The prevalence of is approximately 1%, and incidence increases with age and approaches 10% at the age of 80 years. Annual mortality associated with cardiomyopathy and moderate heart failure is 20% Signs at clinical presentation include increased jugular venous pressure (JVP), small pulse pressure, hepatomegaly and peripheral oedema, and functional mitral regurgitation is often present. Predisposing factors includeo alcoholism,o viral myocarditis,o cocaine abuse, and toxins such as cobalt, lead, phosphorus and carbon monoxide. Heart failure should be managed with diuretic therapy, sodium restriction and ACE inhibition. Crucial to the management of alcoholic cardiomyopathy is cessation of alcohol use. Patients who succeed in giving up ethanol often gain rapid improvement in their symptoms.Hypertrophic obstructive cardiomyopathy The disease exists in two major forms:o a familial one that presents in young patients and has been mapped to chromosome 14q, ando a sporadic form usually found in the elderly. Symptoms of cardiac failure respond to medical therapy witho b-blockade use metoprolol ,,,,BUT Carvedilol has vasodilator properties that could further lower blood pressure as well as potentially exacerbate outflow gradient.o but where the outflow gradient is greater than 50 mmHg, surgical myomectomy is usually recommended.o Unfortunately surgery does not reduce the risk of arrhythmia.o Surgical septal myectomy should be considered in patients with outflow obstruction who are NYHA functional class III or IV and whose symptoms are refractory to medical therapy. Patients prone to ventricular arrhythmias may be considered for implantable defibrillator.Common ECG findings in patients with HOCM include1. LV hypertrophy,2. atrial enlargement,3. ST-T segment abnormalities,4. right or left axis deviation,5. PR prolongation,6. sinus bradycardia with ectopic atrial rhythm and bundle branch block.7. Ventricular fibrillation is responsible for the sudden death in 80% of these patients.8. HOCM can also be associated with WolffParkinsonWhite syndrome

Cardiac amyloidosis most commonly presents as restrictive cardiomyopathy. The clinical findings are those of right heart failure ie jugular venous distension and peripheral oedema, whereas orthopnoea and paroxysmal nocturnal dyspnoea are typically absent. In more advanced stages systolic dysfunction also occurs. Postural hypotension can occur as a result ofo poor ventricular filling oro associated autonomic neuropathy. Combination of low-voltage electrocardiogram (ECG) and thickened ventricular walls is one of the characteristic features of cardiac amyloidosis. The most distinctive feature of cardiac amyloidosis is a sparkling, granular appearance of the myocardium, but this is a relatively insensitive feature occurring only in about 25% of cases. Other echocardiographic abnormalities include dilatation of atria, thickened interatrial septum, diastolic dysfunction and small-volume ventricles. Cardiac amyloidosis usually occurs in setting of light chain amyloidosis (AL) and hereditary amyloidosis, and rarely in secondary amyloidosis.

Hypertension beta-blocker diuretic combination is not recommended due to an association with incident diabetes in BP lowering meta-analyses. Every patiente with type 2 diabetes above 40 years of age should be treated with a statin unless contraindicated. Lowering diastolic blood pressure should be gradual and cautious in patients with coronary artery disease or diabetes mellitus and in those who are older than 60 years, to avoid the possibility of inducing myocardial ischemia. Although lower systolic blood pressure measurements are associated with better outcomes in ischemic heart disease, there is inconsistent evidence that excessive diastolic blood pressure lowering may worsen cardiac outcomes. accelerated hypertensiono should be admitted to hospitalo Initial treatment can be with ORAL nifedipine or atenolol, escalating to intravenous therapy with nitrates if there is no effect.o Sublingual nifedipine should be avoided as it might lead to a sudden drop in blood pressure, which could interfere with the autoregulatory mechanism of cerebral perfusion leading to an ischaemic stroke. Hypertensive encephalopathy with a deteriorating level of consciousness conscious level.o condition is too advanced for oral therapy and requires intravenous (iv) blood pressure lowering therapy with sodium nitroprusside.o The aim of treatment is to lower blood pressure to around 110115 mmHg diastolic within 24 h.o Nitroprusside therapy is usually accompanied by iv furosemide.

How should I manage a woman with chronic hypertension?Advise the woman that: She should restrict her dietary intake of salt (sodium).. Bed rest is not recommended. For uncomplicated hypertension, keep the blood pressure less than 150/100 mmHg (but diastolic pressure no less than 80 mmHg). If there is evidence of target-organ damage (for example kidney disease), keep the blood pressure less than 140/90 mmHg. Warn about symptoms of pre-eclampsia and that she should seek immediate advice if she develops any symptoms after 20 weeks' gestation (including during the postpartum period). Prescribe aspirin 75 mg daily from 12 weeks' gestation. Explain that this is believed to help prevent the development of pre-eclampsia.

Acute mountain sickness,o one manifestation of which is acute pulmonary oedema.o oxygen would be initiated first, particularly in view of persistent hypoxiao Nifedipine reduces pulmonary hypertension and is the treatment of choice for pulmonary oedema in cases where high-flow oxygen is not available.o Acetazolamide may be of some value in prophylaxis in preventing acute mountain sickness, but the best prevention is slow acclimatisation.o Patients may also present with high altitude cerebral oedema, the treatment for which is dexamethasone. Where available, portable pressure bags are a useful adjunct to therapy.

Congestive cardiac failure BNP may be elevated with heart failure, acute myocardial infarction pulmonary embolism.Obesity is associated with lower BNP levelsBNP levels are higher in the settings of renal failure, older age, and female sex. A calcium antagonist such as amlodipine precipitates peripheral oedema and fluid retention and should be withdrawn. Digoxin is a last resort in patients with no evidence of atrial fibrillation. A beta-blocker such as bisoprolol offers great prognostic benefit but should be initiated during a stable stage of the condition.o Beta-blocker should be initiated in small doses and in stable patients who have little or no evidence of fluid overload. Once started, patients should be monitored for worsening of symptoms or fluid retention.o Patients should be educated about possible worsening of symptoms and to weigh themselves daily.o If worsening of symptoms or fluid retention occurs, it should be managed by increasing the dose of diureticso Stopping the beta-blocker is only required if there is heart block, hypotension or severe pulmonary oedema.o It is better to try and continue the beta-blocker if possible. For patients intolerant of ACE inhibitors due to hyperkalemia or renal insufficiency, the combination of hydralazine and a nitrate is a suitable alternative, with hemodynamic effects of vasodilation and afterload reduction. Treatment with this combination is also associated with a reduction in mortality The addition of hydralazine and isosorbide dinitrate to standard medical therapy is indicated for treatment of black patients with systolic heart failure and New York Heart Association functional class III or IV symptoms. Thiazide diuretics should be used very cautiously if there is no satisfactory diuresis on furosemide alone Spironolactone combines a good diuretic effect with prognostic benefit. In this case it will also help raise the patients potassium. Alpha-blockers and nitrates are alternatives for patients who do not tolerate first-line agents. Clinical studies have not demonstrated that the combination of captopril and valsartan improves survival, and the combination is associated with an increased incidence of side effects. Endomyocardial biopsy is recommended in patients witho new-onset heart failure (120 ms. biventricular implantable cardiac defibrillator (ICD)o if there is evidence of previous ischaemic heart disease and ventricular arrhythmias.o Current guidelines recommend implantable cardioverter-defibrillator (ICD) placement in patients with ischemic or nonischemic cardiomyopathy and an ejection fraction of less than or equal to 35%. ICD placement is, therefore, indicated in this setting (primary prevention), regardless of symptoms or functional status Biventricular pacemaker-defibrillator placemento Approximately 70% of patients who undergo biventricular device placement obtain a symptomatic benefit, thought to result from mechanical resynchronization of the timing of right and left ventricular contraction.o These devices have been shown to improve ejection fraction, quality of life, and functional status, decrease heart failure hospitalizations and mortality. A ventricular assist device is an alternative to transplantation. The criteria includeso history of cardiogenic shock,o pulmonary capillary wedge pressure >20 mmHg, ando either a cardiac index 20 mm Hg) variation in systolic blood pressure in the arms may be present. Descending thoracic aortic aneurysm is more commonly associated witho splanchnic ischemia,o renal insufficiency,o lower extremity ischemia, oro focal neurologic deficit due to spinal cord ischemia. The absence of a widened mediastinum on chest X-ray does not rule out dissection. The diagnosis can be further suggested by the finding of aortic regurgitation and pericardial effusion, or even a dissection flap, in the echocardiogram. This can be done by the bedside while steps are taken to prepare the patient for theatre, and as such is much safer than a computerised tomography with contrast in the first instance. Patients with type A aortic dissection should have emergency surgery because of the high risk of mortality and complication such aso aortic regurgitation,o myocardial infarction ando cardiac tamponade. Most patients with type B dissection should be treated medically unless they have complications such as persistent leak, rupture or compromised blood flow to renal, mesenteric or limb circulation.o Beta-blockers are the mainstay of medical therapy, as they reduce the rate of left ventricular ejection and shear on the aortic wall. The aim is to reduce blood pressure to 100120 mmHg and the pulse to near 60 mmHg.o Sodium nitroprusside can be added if blood pressure is not controlled with beta-blockers but should not be used alone as it may increase rate of left ventricular ejection. Hydralazine should be avoided for the same reason.

Features that favour oesophageal rupture over aortic dissection include: The history of onset while eating Blood pressure equal in both arms No diastolic murmur Good peripheral pulses Presence of a pleural effusion.

Carcinoid syndrome Markedly elevated HIAA concentrations are typically found and do not reflect a worse prognosis. Mild derangement of AST/ALT is typically found and alkaline phosphatase is often elevated as a consequence of carcinoid infiltration and mild obstruction. Liver function is usually quite normal despite often heavy hepatic infiltration. Wheeze, again, is a typical feature as a consequence of the release of vasoactive compounds such as 5-HT and bradykinin. Symptoms usually improve following treatment with somatostatin analogues. Relative youth actually reflects a better prognosis. Cardiac lesions are not reversible with treatment, deteriorate with time and frequently require replacement. Patients with carcinoid heart disease,,,most die of progressive right heart failure within one year after onset of symptoms. The prognosis of patients with recognised carcinoid heart disease has improved over the past two decades [and] may be related to valve replacement surgeryDigoxin Toxicity Indications for administration of Digoxin specific Fab Fragment are:o haemodynamic instabilityo life-threatening arrhythmiaso serum potassium >5 mmol/l in acute toxicityo plasma digoxin level >13nmol/lo ingestion of more than 10 mg digoxin in adults and 4 mg in children

Deep venous thrombosis Thrombosis involving the popliteal veins are considered to be proximal DVT, while thrombosis involving veins distal to popliteal veins are considered distal. Anticoagulation for distal DVT is controversial as the incidence of pulmonary embolism in such a setting is very low. However, patients with distal DVT should be followed by serial Doppler studies, if not anticoagulated, because proximal extension of thrombosis can occur.Clopidogrel causing thrombotic thrombocytopenic purpura fever, altered mental status, hemiparesis, anaemia, thrombocytopenia and renal impairment This disorder can occur in less than 1% of patients receiving clopidogrel or ticlodipine. The peripheral blood smear reveals fragmented RBCs (schistocytes, eg, spherocytes, segmented RBCs, burr cells, or helmet cells). While further imaging with MRI would certainly be indicated, cerebral angiography would not be performed here as a next step, and in any case the low platelet count would give cause for caution with invasive procedures including lumbar puncture.

Hyperlipidemiadysbetalipoproteinaemia (type III hyperlipoproteinaemia) Palmar xanthomas are pathognomonic It is caused by mutation in apoprotein E, transmitted as an autosomal recessive trait usually requires a secondary exacerbating metabolic factor for expression of the phenotype. Therefore, secondary causes of hyperlipidaemia such aso hypothyroidism,o obesity,o diabetes mellitus,o renal insufficiency,o high-calorie,o high-fat diet oro alcohol are often encountered at diagnosis, Patients are predisposed to peripheral vascular disease and coronary artery disease. Lipid profile in these patients revealso elevated cholesterol and triglycerides while high-density lipoprotein (HDL) is normal and low-density lipoprotein(LDL) low.o Definitive diagnosis can be made by lipoprotein electrophoresis or genotyping of apoprotein E. Treatment involveso management of secondary causes

Atrial septal defect should be closed if there is evidence of a left-to-right shunt with a pulmonary flow to systemic flow ratio that is greater than or equal to 1.5:1.0, volume overload of right-sided cardiac chambers, or symptoms related to the defect.Atrial septal defect with atrial fibrillation The patient should be cardioverted to sinus rhythm prior to any intervention to close the atrial septal defect. A transoesophageal echocardiogram can give sufficient anatomical data as to the size and site of the defect. It is well worth patients undergoing electrophysiological studies prior to any closure procedure. Any abnormal pathways predisposing to atrial flutter , fibrillation should be considered for radiofrequency ablation which can be curative.Cardiac transplantation

Coronary artery disease (transplant vasculopathy) increases in frequency with time after cardiac transplantation and is present in almost half of all patients by 5 years after transplantation. coronary artery disease in a cardiac transplant patient often presents atypically and may manifest with new-onset heart failure symptoms, decreased exercise tolerance, syncope (usually due to arrhythmias or conduction defects), or cardiac arrest. Because transplant-related coronary artery disease is frequently asymptomatic or manifests with very atypical symptoms, regular screening with coronary angiography and/or noninvasive stress testing is generally performed, Traditional risk factors hypertension, diabetes mellitus, dyslipidemia, smoking immunologic factors Because the pathophysiology is a diffuse intimal thickening, standard revascularization methods are frequently not feasible. There is evidence that statins help prevent and retard progression of transplant vasculopathy. Prognosis is poor once significant transplant vasculopathy becomes symptomatic, and in appropriate candidates, another cardiac transplantation is a possible treatment option.

Side effects for cyclosporine includeo hypertension,o nephrotoxicity,o hypertriglyceridemia,o hirsutism,o gingival hyperplasia, ando tremor.o High levels of cyclosporine can cause seizures

-blockers and pregnancy All available -blockers cross the placenta and are present in human breast milk, resulting in significant levels in the fetus or newborn. Therefore, when used during pregnancy, fetal and newborn heart rate and blood glucose monitoring are indicated. Adverse fetal effects, have been associated with the use of atenolol, especially when initiated early in the pregnancy.o low birth weight,o early delivery, ando small size for gestational ageo The World Health Organization considers atenolol (U.S. Food and Drug Administration [FDA] pregnancy risk category D) unsafe during breastfeeding as it concentrates in breast milk, resulting in a significant dose to the breast-fed infant with associated risks for hypoglycemia and bradycardia.o Metoprolol (pregnancy risk category C) should be considered as an alternative.

Digoxin in pregnancy risk category C drug. Although it readily passes to the fetal circulation, no teratogenic effect has been reported in humans. Digoxin is often used as a maintenance medication in patients with heart failure or atrial arrhythmias during pregnancy. The indications for digoxin are identical to those for nonpregnant patients with heart failure. It is recommended for patients with New York Heart Association class III heart failure to improve symptoms and reduce hospitalization. It is not indicated in asymptomatic patient.

Diuretics in pregnancy Diuretics impair uterine blood flow and placental perfusion. Continuation of diuretic therapy initiated before conception does not seem to have unfavorable effects. Maternal use of furosemide during pregnancy has not been associated with toxic or teratogenic effects, although metabolic complications have been observed. Neonatal hyponatremia and fetal hyperuricemia have been reported. Use of diuretics should be limited to the treatment of symptomatic heart failure with clear evidence of elevated central venous pressure. Furosemide (pregnancy risk category C)

Central Retinal Vein Occlusion Patients usually present with painless loss of vision diffuse retinal hemorrhages in all four quadrants of the retina as well as dilated, tortuous veins. cotton-wool spots, disc edema, optociliary shunt vessels neovessels might also be present. Multiple etiologies should be considered including:o hypertension,o glaucoma,o optic disc edema,o hypercoagulable states,o vasculitis,o drug-induced, ando retrobulbar compression by tumors or grave's opthalmopathy

left Subclavian steal syndrome left upper extremity claudication precipitated by exertion Examination findings include theo low blood pressure in the left arm compared with the right,o the diminished left radial and brachial pulses, ando the systolic murmur in the left clavicular region. Another possible symptom is syncope or near-syncope due to subclavian steal syndrome, which occurs in the setting of significant stenosis of the subclavian artery and retrograde flow in the ipsilateral vertebral artery during upper extremity exertion.

Transient ischemic attack in complex ascending aortic atheromas. The presence of an ascending aortic atheroma of 4 mm or greater in diameter increases the risk of recurrent stroke. Treatment either warfarin or antiplatelet

Lyme carditis is manifested by acute-onset, high-grade atrioventricular conduction defects that may occasionally be associated with myocarditis. Carditis occurs in 5% to 10% of patients with Lyme disease, usually within a few weeks to months after infection. Cardiac involvement can occur in isolation or with other symptoms of the disease. Atrioventricular block can present in any degree, and progression to complete heart block is often rapid. Atrioventricular block is usually within the node, but sinoatrial and His-Purkinje involvement have also been described. Prognosis is good, with usual resolution of atrioventricular block within days to weeks. In some patients, heart block is the first and only manifestation of Lyme disease, but the diagnosis can be confirmed by a positive IgM and IgG antibody response to B. burgdorferi. Lyme serologic testing should be considered in any patient with unexplained high-grade atrioventricular block, particularly in patients with potential tick exposure living in endemic areas. Electrophysiology study is not indicated, since it does not provide additional prognostic information. The preferred antibiotic regimen is intravenous ceftriaxone until the heart block resolves, followed by a 21-day course of oral therapy. Erythromycin is considered a third-line agent for the treatment of Lyme disease, as it is less effective than penicillin or cephalosporin drugs. However, oral erythromycin can be used for patients with erythema migrans who are intolerant of amoxicillin, doxycycline, and cefuroxime. Most cases of Lyme carditis resolve spontaneously, and neither temporary nor permanent pacemaker therapy is needed. Temporary pacing would be required if the patient were hemodynamically unstable with bradycardia. However, this rarely occurs in the setting of Lyme carditis. Indications for permanent pacemaker placement would include persistent high-grade atrioventricular block.

Tetralogy of Fallot Women with tetralogy of Fallot have an increased risk of having offspring with congenital anomalies. Approximately 15% of women with tetralogy of Fallot have chromosome 22q11.2 microdeletion "DiGeorge Syndrome", which raises the risk of having a child with congenital heart disease substantially, from 4% to 6% in affected women without the microdeletion to approximately 50% in those with the microdeletion.

Peripheral arterial disease

A supervised program of regular, repeated exercise to the point of near-maximal pain significantly increases pain-free walking time and walking distance in patients with symptomatic peripheral arterial disease. In patients with class I acute limb ischemia (moderate to severe claudication but no rest pain, audible venous and arterial Doppler signals),o antiplatelet therapy along with systemic anticoagulation with heparin is indicated. Patients with transient sensory deficits and no motor weakness are typically considered for intra-arterial thrombolytic therapy. Patient with marked motor and sensory deficits; needs emergency surgical revascularization. Patients with anesthesia, paralysis, and loss of vascular flow signals have irreversible ischemia and prompt amputation is required. Patients with less dense sensorimotor defects and intact venous flow signals may obtain limb salvage, but only with immediate revascularization. Patients without sensorimotor loss and with evidence of intact vascular flow are more likely to obtain limb salvage, but only with prompt vascular intervention.

Traveler venous thrombosis There is no evidence for an association between dehydration and travel-associated VTE and so whilst maintaining good hydration is unlikely to be harmful it cannot be strongly recommended for prevention of thrombosis Travellers at the highest risk of travel-related thrombosis undertaking journeys of greater than 3 hours should wear well fitted below knee compressionDiabetes

Recommended goals for management of adults with diabetes are hemoglobin A1C 4 normal)o modest elevations in aspartate transaminase ( 100Long-term prophylaxis with hepatitis B immunoglobulin is associated with a significant lower risk of re-infection post transplant. Alternatives include use of nucleoside analogues such as famciclovir and lamivudine.Primary sclerosing cholangitis Jaundice tends to fluctuate in primary sclerosing cholangitis, unlike primary biliary cirrhosis, which is progressive If associated with ulcerative colitis,, Colectomy has no effect on the natural history of PSC development at all. Ultrasound is normal in 50% of patients at an early stage of disease. MRCP has an accuracy of diagnosis for PSC of 90%, compared to 97% for ERCP but with a much better safety profile. In addition, MRCP gives the possibility of visualising bile ducts proximal to any obstruction. Liver transplantation is best choice Survival post liver transplant however is around 90%, although the chance of rejection is higher in PSC patients. 10-15% of PSC patients eventually develop cholangiocarcinoma. cholangiocarcinoma to be a contraindication to liver transplantation When cholangiocarcinoma with local invasion occur, the treatment of choice is stenting via ERCP. The procedure is successful at relieving symptoms of jaundice

Sphincter of Oddi dysmotility (SOD) can cause backup of bile and pancreatic juices which can result in biliary colic. recurrent admissions for intermittent upper abdominal pain especially after fatty More prolonged obstruction may result in bile leaking back into the bloodstream, which can cause transient abnormal liver biochemistry. SOD most commonly occurs in young females especially those who have previously undergone cholecystectomy. At ERCP, delayed drainage of contrast is seen and SOD manometry can confirm the diagnosis,,,There is usually a high resting pressure with marked phasic contractions and often some retrograde peristalsis. Endoscopic sphincterotomy or balloon sphincteroplasty often relieves this conditionAscending cholangitis In the acute settingo the most important first steps in management are to exclude bowel perforation erect chest X ray evaluate the degree of metabolic compromise due to sepsis/shock (arterial blood gas, ABG) to Subsequent acute management would include ano abdominal ultrasound for any biliary dilatation, which may be a precursor too urgent ERCPo Blood cultures should also be taken prior to commencing antibiotics, but should not delay their administration.o Ultrasonography is excellent for gallstones and cholecystitis. assessing bile duct dilatation. However, it often misses stones in the distal bile ducto ERCP is both diagnostic and therapeutic and is considered the criterion standard for imaging the biliary system. ERCP should be reserved for patients who may require therapeutic intervention. Patients with a high clinical suspicion for cholangitis should proceed directly to ERCP. ERCP has a high success rate (98%) and is considered safer than surgical and percutaneous intervention. Diagnostic use of ERCP carries a complication rate of approximately 1.38% The major complication nclude pancreatitis, bleeding, and perforation.o For diagnostic purposes, ERCP has now generally been replaced by MRCPo MRCP is a noninvasive imaging modality that is increasingly being used in the diagnosis of biliary stones and other biliary pathology. MRCP is accurate for detecting choledocholithiasis, neoplasms, strictures, and dilations within the biliary system. Limitations of MRCP include the inability for invasive diagnostic tests such as bile sampling, cytologic testing, stone removal, or stenting. It has limited sensitivity for small stones (