Flecainide is an antiarrhythmic drug of class Ic that works by blocking the Nav1.5 sodium channel in the heart, prolonging the cardiac action potential and slowing cardiac impulse conduction. It has a significant impact on accessory pathway conduction, particularly retrograde conduction, and significantly reduces ventricular ectopic foci.Many different arrhythmias can be treated with flecainide, including:Pre-excitation syndromes (e.g. Wolff-Parkinson-White)Acute atrial arrhythmiasVentricular arrhythmiasChronic neuropathic painThe use of flecainide is contraindicated in the following situations:Abnormal left ventricular functionAtrial conduction defects (unless pacing rescue available)Bundle branch block (unless pacing rescue available)Distal block (unless pacing rescue available)Haemodynamically significant valvular heart diseaseHeart failureHistory of myocardial infarctionLong-standing atrial fibrillation where conversion to sinus rhythm not attemptedSecond-degree or greater AV block (unless pacing rescue available)Sinus node dysfunction (unless pacing rescue available)Flecainide should only be used in people who don’t have a structural heart problem. The CAST trial found a significant increase in sudden cardiac death and all-cause mortality in patients with an ejection fraction of less than 40% after a myocardial infarction, where it tended to be pro-arrhythmic.Anti-arrhythmic drugs have a limited and ineffective role in the treatment of atrial flutter. It’s important to keep in mind that flecainide shouldn’t be used by itself to treat atrial flutter. When used alone, there is a risk of inducing 1:1 atrioventricular conduction, which results in an increase in ventricular rate that is paradoxical. As a result, it should be used in conjunction with a beta-blocker or a calcium channel blocker with a rate-limiting effect.

Damage to the Wernicke’s speech area in the temporal lobe can result in a receptive dysphasia. Hemispatial neglect is most likely to occur in a lesion of the parietal lobe. Homonymous hemianopia is most likely to occur in a lesion of the occipital lobe. Expressive dysphasia is most likely to occur in a lesion of the Broca speech area in the frontal lobe. Conjugate eye deviation towards the side of the lesion is most likely to occur in a lesion of the frontal lobe.

Malaria is a protozoal infection of red blood cells and the liver. It is caused by the parasite belonging to the genus Plasmodium. It is transmitted by the female mosquito Anopheles.Several species with distinct features:P. vivax/P. ovaleP. malariaeP. falciparumThe common symptoms of malaria are:Paroxysms of fever – a cyclical occurrence of:1) a cold phase – the patient experiences intense chills2) a hot stage – the patient feels extremely hot3) a sweating stage – the fever declines and the patient sweats profusely- Fever recurs at regular intervals (48hrs, 72hrs): Variable by species of PlasmodiumAnaemia (RBC infection)- Severity varies by species of Plasmodium- Haemolytic: sometimes jaundiceSplenomegalyAlso nonspecific symptoms:- Sweating- fatigue- malaise- arthralgias- headache- Sometimes cough, vomiting, diarrhoea

Neutrophils are the most abundant peripheral blood leucocyte, comprising about 50 – 70% of circulating white cells. Neutrophils have a characteristic dense nucleus consisting of between two and five lobes, and a pale cytoplasm with an irregular outline containing many fine pink-blue or grey-blue granules. The granules are divided into primary, which appear at the promyelocyte stage, and secondary, which appear at the myelocyte stage and predominate in the mature nucleus. Both types of granule are lysosomal in origin; the primary contains myeloperoxidase and other acid hydrolases; the secondary contains lactoferrin, lysozyme and other enzymes. The lifespan of neutrophils in the blood is only 6 – 10 hours. In response to tissue damage, cytokines and complement proteins, neutrophils migrate from the bloodstream to the site of insult within minutes, where they destroy pathogens by phagocytosis.

A history of stroke and poor nutritional status points towards a nutritional deficiency as the most likely cause of her symptoms. The examination would differentiate between Vitamin B12 and Folic acid deficiency as in the former. The patient has a beefy red tongue and symptoms indicating peripheral nervous system involvement or subacute combined spinal cord degeneration. The patient may also have a lemon-yellow skin colour, loss of proprioception and vibratory sense and oral ulceration. Investigations in B12 deficiency can reveal the following:1. Macrocytic anaemia2. Neutropoenia3. Thrombocytopaenia4. Blood film: anisocytosis, poikilocytosis5. Low serum B126. Raised serum bilirubin (haemolysis)7. Intrinsic factor antibodies8. Positive Schilling test

If the complement sequence is completed, an active phospholipase (the membrane attack complex, MAC) is produced, which punches holes in the cell membrane and causes cell lysis. Because the MAC appears to be the sole means to destroy the Neisseria family of bacteria, C5 – C9 deficiency increases susceptibility to Neisseria infections.

Glucagon binds to class B G-protein coupled receptors and activates adenylate cyclase, increasing cAMP intracellularly. This activates protein kinase A. Protein kinase A phosphorylates and activates important enzymes in target cells.

Central cord syndrome is the most common type of incomplete cord injury and almost always occurs due to a traumatic injury. It results in motor deficits that are worse in the upper extremities as compared to the lower extremities. It may also cause bladder dysfunction (retention) and variable sensory deficits below the level of injury.The majority of these patients will be older and present with symptoms after a fall with hyperextension of their neck. On examination, patients will have more significant strength impairments in the upper extremities (especially the hands) compared to the lower extremities. Patients often complain of sensory deficits below the level of injury, but this is variable. Pain and temperature sensations are typically affected, but the sensation of light touch can also be impaired. The most common sensory deficits are in a cape-like distribution across their upper back and down their posterior upper extremities. They will often have neck pain at the site of spinal cord impingement.Bladder dysfunction (most commonly urinary retention) and priapism can also be signs of upper motor neuron dysfunction. The sacral sensation is usually preserved, but the clinician should assess the rectal tone to evaluate the severity of the compression.

The brachialis muscle is a prime flexor of the forearm at the elbow joint. It is fusiform in shape and located in the anterior (flexor) compartment of the arm, deep to the biceps brachii. The brachialis is a broad muscle, with its broadest part located in the middle rather than at either of its extremities. It is sometimes divided into two parts, and may fuse with the fibres of the biceps brachii, coracobrachialis, or pronator teres muscles. It also functions to form part of the floor of the cubital fossa.The brachialis is primarily supplied by the musculocutaneous nerve (C5, C6). In addition, a small lateral portion of the muscle is innervated by the radial nerve (C7).

All of the above answers are non-parametric tests.

Causes of a raised anion gap acidosis can be remember using the mnemonic MUDPILES:-Methanol-Uraemia (in renal failure)-Diabetic ketoacidosis-Propylene glycol overdose-Infection/Iron overdose/Isoniazid/Inborn errors of metabolism-Lactic acidosis-Ethylene glycol overdose-Salicylate overdose

If SBP is less than 90 mmHg , 500 mL sodium chloride 0.9 percent should be administered intravenously over 10–15 minutes, and repeated if SBP remains less than 90 mmHg. When SBP is greater than 90 mmHg, sodium chloride infusion must be maintained at a rate that replaces the deficit.

An exudate is an inflammatory fluid emanating from the intravascular space due to changes in the permeability of the surrounding microcirculation.Some common causes of exudates are: pneumonia, empyema, lung cancer, breast cancer, cancer of the pleura, SLE, rheumatoid arthritis, pericarditis, subphrenic abscess, chylothorax.Myxoedema, nephrotic syndrome, congestive cardiac failure, and liver cirrhosis all cause TRANSUDATE.

Dorsiflexion and eversion of the foot are innervated by the deep fibular nerve and the superficial fibular nerve, respectively. The common fibular nerve runs obliquely downward along the lateral border of the popliteal fossa (medial to the biceps femoris) before branching at the neck of the fibula. Thus, it is prone to being affected during an impact injury or fracture to the bone or leg. Casts that are placed too high can also compress the fibular nerve.

As the contents of the intestine are isotonic with body fluids and mostly have the same concentration of the major electrolytes, their absorption is active. Water cannot be moved directly, but follows osmotic gradients set up by the transport of ions, primarily mediated by the sodium pump.Na+/K+ ATPase located on the basolateral membrane of the epithelial cells pumps three Na+ ions from the cell in exchange for two K+ ions, against their respective concentration gradients. This leads to a low intracellular concentration of Na+ and a high intracellular concentration of K+. The low intracellular concentration of Na+ ensures a movement of Na+ from the intestinal contents into the cell down its concentration gradient by both membrane channels and transporter protein mechanisms. Na+ is then rapidly pumped again by the basolateral sodium pump. K+ leaves the cell across the basolateral membrane down its concentration gradient linked to an outward movement of Cl- against its concentration gradient (Cl- having entered the cell across the luminal membrane down its concentration gradient).

Pilocytic astrocytoma (PCA), previously known as cystic cerebellar astrocytoma or juvenile pilocytic astrocytoma, was first described in 1931 by Harvey Cushing, based on a case series of cerebellar astrocytomas; though he never used these terms but rather described a spongioblastoma. They are low-grade, and usually well-circumscribed tumours, which tend to occur in young patients. By the World Health Organization (WHO) classification of central nervous system tumours, they are considered grade I gliomas and have a good prognosis.PCA most commonly occurs in the cerebellum but can also occur in the optic pathway, hypothalamus, and brainstem. They can also occur in the cerebral hemispheres, although this tends to be the case in young adults. Presentation and treatment vary for PCA in other locations. Glial cells include astrocytes, oligodendrocytes, ependymal cells, and microglia. Astrocytic tumours arise from astrocytes and are the most common tumour of glial origin. The WHO 2016 categorized these tumours as either diffuse gliomas or other astrocytic tumours. Diffuse gliomas include grade II and III diffuse astrocytomas, grade IV glioblastoma, and diffuse gliomas of childhood. The other astrocytic tumours group include PCA, pleomorphic xanthoastrocytoma, subependymal giant cell astrocytoma, and anaplastic pleomorphic xanthoastrocytoma.PCA can present with symptoms secondary to the posterior fossa mass effect. This may include obstructive hydrocephalus, with resultant headache, nausea and vomiting, and papilledema. If hydrocephalus occurs before the fusion of the cranial sutures (<18-months-of-age), then an increase in head circumference will likely occur. Lesions of the cerebellar hemisphere result in peripheral ataxia, dysmetria, intention tremor, nystagmus, and dysarthria. In contrast, lesions of the vermis cause a broad-based gait, truncal ataxia, and titubation. Posterior fossa lesions can also cause cranial nerve palsies. Diplopia may occur due to abducens palsy from the stretching of the nerve. They may also have blurred vision due to papilledema. Seizures are rare with posterior fossa lesions.

Erythrocytes have a normal lifespan of about 120 days. Mature erythrocytes are biconcave discs with no nucleus, ribosomes or mitochondria but with the ability to generate energy as ATP by the anaerobic glycolytic pathway. The red cell membrane consists of a bipolar lipid layer with a membrane skeleton of penetrating and integral proteins anchoring carbohydrate surface antigens. The shape and flexibility of red cells allows them to deform easily and pass through capillaries.

Metronidazole and the other 5-nitroimidazole agents inhibit nucleic acid synthesis by forming toxic free radical metabolites in the bacterial cell that damage DNA. Vancomycin inhibits cell wall peptidoglycan formation by binding the D-Ala-D-Ala portion of cell wall precursors. Erythromycin inhibits protein synthesis and blocks translocation by binding to the 23S rRNA of the 50S ribosomal subunit.Chloramphenicol blocks peptidyl transferase at 50S ribosomal subunit.Gentamicin, an aminoglycoside antibiotic, acts by binding to the 30S subunit of the bacterial ribosome inhibiting the binding of aminoacyl-tRNA and thus preventing initiation of protein synthesis.An overview of the different mechanisms of action of the various types of antimicrobial agents is shown below:1. Inhibition of cell wall synthesis- Penicillins- Cephalosporins- Vancomycin2. Disruption of cell membrane function- Polymyxins- Nystatin- Amphotericin B3. Inhibition of protein synthesis- Macrolides- Aminoglycosides- Tetracyclines- Chloramphenicol4. Inhibition of nucleic acid synthesis- Quinolones- Trimethoprim- 5-nitroimidazoles- Rifampicin5. Anti-metabolic activity- Sulphonamides- Isoniazid

Lymphoma is a cancer of the lymphatic system, which is part of the body’s germ-fighting network. They are a group of diseases that are caused by malignant lymphocytes. These malignant cells accumulate in lymph nodes and other lymphoid tissue, giving rise to the characteristic clinical feature of lymphadenopathy. They can be subdivided into Hodgkin lymphoma (HL) which are characterised by the presence of Reed-Sternberg cells, and non-Hodgkin lymphoma (NHL). Characteristics of HL include:1. can present at any age but is rare in children and has a peak incidence in young adults, 2. almost 2:1 male predominance. 3. presents with painless, asymmetrical, firm and discrete enlargement of superficial lymph nodes. 4. cervical node involvement in 60-70% of cases, 5. axillary node involvement in 10-15% 6. inguinal node involvement in 6-12%. 7. modest splenomegaly during the course of the disease in 50% of patients8. may occasionally have liver enlargement9. bone marrow failure involvement is unusual in early disease. Approximately 85% of patients are cured, but the prognosis depends on age, stage and histology. Two well‐known but rare symptoms in HL are alcohol‐induced pain and pruritus.

Hypothyroidism occurs when there is a deficiency of circulating thyroid hormones. It is commoner in women and is most frequently seen in the age over 60.Iodine deficiency is the commonest cause of hypothyroidism worldwide.In the UK and other developed countries, iodine deficiency is not a problem and autoimmune thyroiditis is the commonest cause.

Fracture dislocations of the elbow appear extremely complex, and identification of the basic injury patterns can facilitate management. The simplest pattern of elbow fracture dislocation is posterior dislocation of the elbow with fracture of the radial head. Addition of a coronoid fracture, no matter how small, to elbow dislocation and radial head fracture is called the terrible triad of the elbow.

Cushing’s syndrome is a group of symptoms and signs brought on by long-term exposure to high amounts of endogenous or exogenous glucocorticoids. Cushing’s syndrome affects about 10-15 persons per million, and it is more common in those who have had a history of obesity, hypertension, or diabetes.Cushing’s syndrome has a wide range of clinical manifestations that are dependent on the degree of cortisol overproduction. The appearance might be vague and the diagnosis difficult to detect when cortisol levels are just somewhat elevated. On the other hand, in long-term cases of severely increased cortisol levels, the presentation might be colourful and the diagnosis simple.Cushing’s syndrome has the following clinical features:Obesity and weight growth in the true senseSupraclavicular fat pads are fat pads that are located above the clavicle.Buffalo humpFullness and plethora of the face (‘moon facies’)Muscle atrophy and weakening at the proximal levelDiabetes mellitus, also known as impaired glucose toleranceHypertensionSkin thinning and bruisingDepressionHirsutismAcneOsteoporosisAmenorrhoea or oligomenorrhoeaCortisol levels fluctuate throughout the day, with the greatest levels occurring around 0900 hours and the lowest occurring at 2400 hrs during sleep. The diurnal swing of cortisol levels is lost in Cushing’s syndrome, and levels are greater during the whole 24-hour period. In the morning, levels may be normal, but they may be high at night-time, when they are generally repressed. As a result, random cortisol testing is not an effective screening technique and is not advised.The following are the two most common first-line screening tests:Cortisol levels in the urine are measured every 24 hours.A diagnosis of Cushing’s syndrome can be made if more than two collections measure cortisol excretion more than three times the upper limit of normal.Physical stress (e.g., excessive exercise, trauma), mental stress (e.g., sadness), alcohol or drug misuse, complex diabetes, and pregnancy can all cause false positives.Renal dysfunction, inadequate collection, and cyclical Cushing’s disease can all cause false negatives.The overnight low-dose dexamethasone suppression test (LDDST) involves giving 1 mg of dexamethasone at 11 p.m. and measuring blood cortisol levels at 8 a.m. the next day.Cushing’s syndrome is diagnosed when cortisol is not suppressed to less than 50 nmol/L.It might be difficult to tell the difference between mild Cushing’s disease and normal cortisol production.False positives can occur as a result of depression, severe systemic sickness, renal failure, prolonged alcohol misuse, old age, and the use of hepatic enzyme-inducing medicines, among other things.False negatives are extremely uncommon in Cushing’s disease patients.A characteristic biochemical picture might also be helpful in confirming the diagnosis of Cushing’s syndrome. The following are the primary characteristics:HypokalaemiaAlkalosis metabolique

One of the complications that polycystic kidney disease may cause is the development of a brain aneurysm. A berry aneurysm is the most common type of brain aneurysm. The Circle of Willis, where the major blood vessels meet at the base of the brain, is where it usually appears. The most common junctions of the Circle of Willis where an aneurysm may occur include the anterior communicating artery (35%), internal carotid artery (30%), the posterior communicating artery and the middle cerebral artery (22%), and finally, the posterior circulation sites, most commonly the basilar artery tip.

Adverse Effects of lithium IncludeLeucocytosis (most patients)Polyuria/polydipsia (30-50%)Dry mouth (20-50%)Hand tremor (45% initially, 10% after 1 year of treatment)Confusion (40%)Decreased memory (40%)Headache (40%)Muscle weakness (30% initially, 1% after 1 year of treatment)Electrocardiographic (ECG) changes (20-30%)Nausea, vomiting, diarrhoea (10-30% initially, 1-10% after 1-2 years of treatment)Hyperreflexia (15%)Muscle twitch (15%)Vertigo (15%)Extrapyramidal symptoms, goitre (5%)Hypothyroidism (1-4%)Acne (1%)Hair thinning (1%)

The correct administration of IV adrenaline 1 mg (10 mL of 1:10,000 solution) is that it should be given after 3 shocks and every 3 – 5 minutes/after alternate shocks thereafter.

The periurethral portion of the prostate gland increases in size during puberty and after the age of 55 years due to the growth of non-malignant cells in the transition zone of the prostate that surrounds the urethra. Most cancers develop in the posterior lobe, and cancers in this location may be palpated during a digital rectal examination (DRE).

Gas exchange between alveolar air and blood in the pulmonary capillaries takes place by diffusion across the alveolar-capillary membrane. Diffusion occurs from an area of high partial pressure to an area of low partial pressure, thus the driving force for diffusion is the alveolar-capillary partial pressure gradient. Diffusion occurs until equilibrium is reached, but random movement of particles continues to occur and this is known as dynamic equilibrium. The diffusing capacity for oxygen (DLO2) cannot be measured directly but the rate of diffusion in the lungs can be estimated by measuring the diffusing capacity of the lungs for carbon monoxide (DLCO), not by measuring total lung capacity. The rate of transfer of a gas may be diffusion or perfusion limited; carbon monoxide transfer is diffusion-limited, oxygen transfer is usually perfusion-limited.

Fludrocortisone has the most potent mineralocorticosteroid activity, making it ideal for mineralocorticoid replacement in adrenal insufficiency.

About 25% of filtered sodium is reabsorbed in the the loop of Henle.

Water-impermeable ascending loop of Henle plays a central role in maintaining salt-water balance by creating the cortico-medullary osmotic gradient to set up urinary concentrating ability and reabsorbing approximately 25% of the filtered NaCl load.

The Meissner’s plexus (submucosal plexus), an enteric nervous plexus, acts as the main control for gastrointestinal secretion and local blood flow within the gut.It is located in the submucosal layer on the inner surface of the muscularis externa.