IgA is the major Ig in secretions, particularly from the gastrointestinal tract (but also in saliva, tears, sweat and breast milk).IgE is important for mast cell degranulation in allergic and antiparasitic response. In the allergic response, the plasma cell produces IgE-antibodies, which, like antibodies of other immunoglobulin isotypes, are capable of binding a specific allergen via its Fab portion.IgG is the most abundant in plasma (comprising 80% of normal serum immunoglobulin) and the main circulatory Ig for the secondary immune response.

CSF analysis typically shows: cloudy turbid appearanceraised WCC – predominantly neutrophilshigh proteinlow glucose (typically < 40% of serum glucose)Gram-negative diplococci seen under microscopy

Cholera is caused by Vibrio cholerae, a motile, Gram-negative, curved bacillus. It is transmitted through water and food (especially seafood) and is primarily a disease seen in developing countries where there is poor sanitation and lack of safe water supplies.The cholera toxin leads to stimulation of adenyl cyclase, ADP-ribosylation of the G regulatory protein, inactivation of GTPase leading to active outpouring of NaCl. The cholera toxin consists of an A (the toxin) and B subunit. The B subunit attaches to the gut mucosa and presents the A subunit to the cell. The toxin stimulates adenyl cyclase by irreversible ADP-ribosylation of the GTP binding domain of adenyl cyclase leading to the opening of chloride channels resulting in an outpouring of NaCl and water into the lumen of the gut and causing secretory diarrhoea.Incubation period is between 2 and 5 days, but can be as short as just a few hours.

Adverse effects of warfarin:The most common adverse effect of warfarin is bleedingOther common adverse effects of warfarin include nausea, vomiting, diarrhoea, jaundice, hepatic dysfunction, pancreatitis, pyrexia, alopecia, purpura, and rashSkin necrosis is a rare but serious adverse effect of warfarin; treatment with warfarin should be stopped if warfarin related skin necrosis is suspectedCalciphylaxis is a rare, but a very serious condition that causes vascular calcification and cutaneous necrosis

Paroxysmal supraventricular tachycardia is an intermittent tachycardia (HR > 100 bpm) and has the following characteristics:1. Sudden onset/offset (Contrast with sinus tachycardia)2. Electrical activity originates above the ventricle (Contrast with ventricular tachycardia)3. Produces narrow QRS complex (<120ms) The most common cause of PSVT is Atrioventricular nodal re-entrant tachycardia (AVNRT), most common in young women with a mean age onset of 32 years old. There are recurrent episodes of palpitations, and most of the episodes spontaneously. Sometimes, some vagal manoeuvres are required:1. Valsalva manoeuvre2. immersing the face in ice-cold water3. carotid sinus massage.If PSVT keeps persisting or is causing severe symptoms, the treatment of choice is intravenous adenosine. The patient’s ECG should be continuously monitored throughout the treatment. The recommended doses in adults are as follows:- Initial dose of adenosine is 6 mg by rapid IV bolus- If unsuccessful, give another dose of adenosine 12 mg by rapid IV bolus- If unsuccessful, give a further dose of adenosine 12 mg by rapid IV bolusThe latest ALS guidelines advocate 18 mg for the third dose, whereas the BNF/NICE guidelines advocate 12 mg.If adenosine fails or is contraindicated, intravenous verapamil can be used as an alternative, but it should be avoided in patients recently treated with beta-blockers.Synchronized electrical cardioversion will be necessary with signs of hemodynamic instability or if drug treatment has failed to restore sinus rhythm.Recurrent episodes of paroxysmal supraventricular tachycardia can be treated by catheter ablation or prevented with drugs such as flecainide, sotalol, diltiazem, or verapamil.

The ventilation/perfusion ratio (V/Q ratio) is a ratio used to assess the efficiency and adequacy of the matching ventilation and perfusion. The ideal V/Q ratio is 1. In an average healthy male, the ventilation value is approximately 5 L/min and the perfusion value is approximately 5 L/min. Any mismatch between ventilation and perfusion will be evident in the V/Q ratio. If perfusion is normal but ventilation is reduced, the V/Q ratio will be less than 1, whereas if ventilation is normal but perfusion is reduced, the V/Q ratio will be greater than 1. If the alveoli were ventilated but not perfused at all, then the V/Q ratio would be infinity.

Achlorhydria is an autoimmune illness of the gastric parietal cells that causes insufficient stomach acid production. The parietal cells that have been injured are unable to create the necessary amount of stomach acid. As a result, the pH of the stomach rises, food digestion suffers, and the risk of gastroenteritis rises.The secretion of hydrochloric acid and intrinsic factor is controlled by the gastric parietal cells, which are epithelial cells in the stomach. These cells can be found in the gastric glands, the fundus lining, and the stomach body.In response to the following three stimuli, the stomach parietal cells release hydrochloric acid:H2 Histamine receptors are stimulated by histamine (most significant contribution)Acetylcholine stimulates M3 Receptors via parasympathetic action.CCK2 receptors are stimulated by Gastrin.Intrinsic factor, which is essential for vitamin B12 absorption, is also produced by stomach parietal cells.Omeprazole is a proton pump inhibitor that is both selective and irreversible. It inhibits the H+/K+-ATPase system present on the secretory membrane of gastric parietal cells, which lowers stomach acid secretion.Ranitidine inhibits histamine H2-receptors in a competitive manner. The reversible inhibition of H2-receptors in gastric parietal cells reduces both the volume and concentration of gastric acid.

Prevention of spread of measles is extremely important and infected patients should be isolated. The infectious stage is from 3 days before the rash emerges and patients are advised to stay away from school/nursery/work for 4 days from onset of the rash.

By combining with haemoglobin to form carboxyhaemoglobin, carbon monoxide (CO) disrupts the blood’s oxygen transport function. CO binds to haemoglobin with a 240-fold higher affinity than oxygen. As a result, even small amounts of CO can bind a large portion of the blood’s haemoglobin, making it unavailable for oxygen transport. During a suspected carbon monoxide poisoning, the blood PO2 and haemoglobin concentrations will be normal, but the oxygen concentration will be drastically reduced. The oxygen dissociation curve will also shift to the left in the presence of Carboxyhaemoglobin ( haemoglobin and carbon monoxide combination), interfering with oxygen unloading.

Neisseria meningitidisis is a Gram-negative diplococcusc that can cause meningococcal meningitis.Carriage of Neisseria meningitidisis very common and it exists in the normal flora in the nasopharynx in 5 – 15% of adults. Actual disease only develops in a very small percentage of individuals. Infection is most common in the winter months and epidemics tend to occur about once every 10 years.Most invasive infections are caused by serotypes A, B or C. In the UK, most cases of meningococcal septicaemia are caused byNeisseria meningitidisgroup B. The vaccination programme forNeisseria meningitidisgroup C has made this type much less common. A vaccine for group B disease has now been initiated in children.The main determinant of the pathogenicity of Neisseria meningitidisis the antiphagocytic polysaccharide capsule. Meningococci cross mucosal epithelium by endocytosis and the capsule allows survival in the bloodstream. Lipo-oligosaccharide activates complement activation and cytokine release, resulting in shock and disseminated intravascular coagulation (DIC).Theclinical featuresof meningococcal meningitis include:Non-blanching rashNeck stiffnessHeadachePhotophobiaAltered mental state (drowsiness, confusion)Focal neurological deficitsSeizuresSeptic shockThe diagnosis is usually made clinically and confirmed by culture of blood, aspirate from the rash and CSF. Rapid antigen detection or nucleic acid amplification testing (NAAT) on blood and CSF are both sensitive and reliable.Due to the potentially life-threatening nature of the disease treatment should not wait for laboratory confirmation and antibiotics should be started immediately. In the hospital setting IV ceftriaxone (2 g adult; 80 mg/kg child) or IV cefotaxime (2 g adult; 80 mg/kg child) are the preferred agents. IM benzylpenicillin can be given as an alternative in the pre-hospital setting and chloramphenicol is a suitable alternative if there is a history of anaphylaxis to cephalosporins. Treatment does not eradicate carriage and the patient should be given ‘prophylaxis’ following recovery.

Syncope and sudden death due to ventricular tachycardia, particularly Torsades-des-pointes is seen in prolongation of the QT interval.The causes of a prolonged QT interval include:ErythromycinAmiodaroneQuinidineMethadoneProcainamideSotalolTerfenadineTricyclic antidepressantsJervell-Lange-Nielsen syndrome (autosomal dominant)Romano Ward syndrome (autosomal recessive)HypothyroidismHypocalcaemiaHypokalaemiaHypomagnesaemiaHypothermiaRheumatic carditisMitral valve prolapseIschaemic heart disease

Poststreptococcal glomerulonephritis (PSGN) is caused by prior infection with specific nephritogenic strains of group A beta-haemolytic streptococcus. The clinical presentation of PSGN varies from asymptomatic, microscopic haematuria to the full-blown acute nephritic syndrome, characterized by red to brown urine, proteinuria (which can reach the nephrotic range), oedema, hypertension, and acute kidney injury.

High-dose inhaled short-acting beta2-agonists are the first line treatment for acute asthma(salbutamol or terbutaline). Oxygen should only been given to hypoxaemic patients (to maintain oxygen saturations of 94 – 98%). A pressurised metered dose inhaler with spacer device is preferred in patients with moderate to severe asthma (4 puffs initially, followed by 2 puffs every 2 minutes according to response, up to 10 puffs, whole process repeated every 10 – 20 minutes if necessary). The oxygen-driven nebuliser route is recommended for patients with life-threatening features or poorly responsive severe asthma (salbutamol 5 mg at 15 – 30 minute intervals). Continuous nebulisation should be considered in patients with severe acute asthma that is poorly responsive to initial bolus dose (salbutamol at 5 – 10 mg/hour) The intravenous route should be reserved for those in whom inhaled therapy cannot be used reliably.

A plasma potassium less than 3.5 mmol/L defines hypokalaemia.Excessive liquorice ingestion causes hypermineralocorticoidism and leads to hypokalaemia.Gitelman’s syndrome causes metabolic alkalosis with hypokalaemia and hypomagnesaemia. It is an inherited defect of the distal convoluted tubules.Bartter’s syndrome causes hypokalaemic alkalosis. It is a rare inherited defect in the ascending limb of the loop of Henle.Type 1 and 2 renal tubular acidosis both cause hypokalaemia Type 4 renal tubular acidosis causes hyperkalaemia.

Clinical features of haemolytic anaemia include:AnaemiaJaundice (caused by unconjugated bilirubin in plasma, bilirubin is absent from urine)Pigment gallstonesSplenomegalyAnkle ulcersExpansion of marrow with, in children, bone expansion e.g. frontal bossing in beta-thalassaemia majorAplastic crisis caused by parvovirus

Diabetes ketoacidosis is an acute complication of diabetes mellitus. Insulin is administered to achieve euglycemia, and crystalloids or colloidal solution is administered to achieve euvolemia and euelectrolytaemia. Potassium levels severely fluctuate during the treatment of DKA, hypokalaemia being more common. Insulin promotes the cell to take up potassium from the extracellular space via increased sodium-potassium pump activity. It is important to monitor potassium levels during the treatment of DKA regularly. It is widely suggested that the normal saline shall be used for initial resuscitation, and once the potassium level is retrieved, the patient can be started on potassium replacement should the serum potassium level be between 3.3 and 4.5 mmol/L If potassium levels fall below 3.3 mmol/l, insulin administration may need to be interrupted to correct the hypokalaemia.

During quiet respiration, the approximate position of the right oblique fissure can be marked by a line on the thoracic wall that begins at the spinous process of vertebra T4, crosses the fifth intercostal space laterally and then follows the contour of rib 6 anteriorly.

Avulsion fractures of the fibular head are rare and are so-called the arcuate signal. The “arcuate signal” is used to describe an avulsed bone fragment related to the insertion site of the tendon of the biceps femoris associated with the arcuate complex, which consists of the fabellofibular, popliteofibular, and arcuate ligaments. Such lesions are typically observed in direct trauma to the knee with excessive varus and internal rotation forces or indirect trauma with the same direction of the force.

Anaphylaxis is characterised by sudden onset and rapidly developing, life-threatening airway, breathing and circulation problems associated with skin and/or mucosal changes. Reactions can vary greatly, from hypotension alone, to reactions with predominantly asthmatic features, to cardiac/respiratory arrest. Skin or mucosal changes may be absent or subtle in up to 20% of cases but skin or mucosal changes alone are not a sign of an anaphylactic reaction.

A histogram is used to demonstrate the distribution of continuous quantitative data. It is a very familiar graphical display device for representing the distribution of a single batch of data. The range of the data is divided into class intervals or bins, and the number of values falling into each interval is counted. The histogram then consists of a series of rectangles whose widths are defined by the class limits implied by the binwidths, and whose heights depend on the number of values in each bin. Histograms quickly reveal such attributes of the data distribution as location, spread, and symmetry. If the data are multimodal (i.e., more than one “hump” in the distribution of the data), this is quickly evident as well.

Megaloblastic anemia results from inhibition of DNA synthesis during red blood cell production. When DNA synthesis is impaired, the cell cycle cannot progress from the growth stage to the mitosis stage. This leads to continuing cell growth without division, which presents as macrocytosis, with an increase in mean corpuscular volume (MCV). The defect in red cell DNA synthesis is most often due to hypovitaminosis, specifically vitamin B12 deficiency or folate deficiency.Folate is an essential vitamin found in most foods, especially liver, green vegetables and yeast. The normal daily diet contains 200 – 250 μg, of which about 50% is absorbed. Daily adult requirements are about 100 μg. Absorption of folate is principally from the duodenum and jejunum. Stores of folate are normally only adequate for 4 months and so features of deficiency may be apparent after this time.

Prednisolone is four times more potent than hydrocortisone, and therefore, a dose of 25 mg would be equivalent to 100 mg of hydrocortisone.The following table summarises the relative potency of the main corticosteroids compared with hydrocortisone:CorticosteroidPotency relative to hydrocortisonePrednisolone4 times more potentTriamcinolone5 times more potentMethylprednisolone5 times more potentDexamethasone25 times more potent

Foetal haemoglobin (HbF) makes up about 0.5 – 0.8 % of total adult haemoglobin and consists of two α and two gamma (γ) globin chains.

Factors decreasing FRC:Restrictive ventilatory defects e.g. pulmonary fibrosisPosture – lying supineIncreased intra-abdominal pressure (e.g. obesity, pregnancy, ascites)Reduced muscle tone of diaphragm e.g. muscle relaxants in anaesthesia, neuromuscular disease

Digestion of dietary protein begins in the stomach where pepsin hydrolyses protein to polypeptides, and continues in the duodenum where pancreatic proteases (trypsin and chymotrypsin) continue the process of hydrolysis forming oligopeptides. These are further broken down into small peptides and amino acids by pancreatic carboxypeptidases and aminopeptidases located on luminal membrane epithelial cells. Free amino acids are absorbed across the apical membrane by secondary active transport coupled with Na+transport into the cell. Amino acids cross the basal membrane into the capillaries by facilitated diffusion.

Parathyroid hormone (PTH) is a peptide hormone synthesised by the chief cells of the parathyroid glands, located immediately behind the thyroid gland. PTH is primarily released in response to decreasing plasma [Ca2+] concentration. PTH acts to increase plasma calcium levels and decrease plasma phosphate levels.Parathyroid hormone (PTH) acts to increase calcium reabsorption in the distal tubule of the nephron (by activating Ca2+entry channels in the apical membrane and the Ca2+ATPase pump in the basolateral membrane) and increase phosphate excretion by inhibiting reabsorption in the proximal tubule of the nephron.

The most common type of adult leukaemia is chronic lymphocytic leukaemia (CLL). It develops as a result of relatively mature lymphocytes clonally proliferating. The B-cell lineage accounts for approximately 95% of cases. CLL is primarily a disease of adult men, with men over the age of 50 accounting for more than 75% of CLL patients.It is the most indolent form of chronic leukaemia, and it is frequently discovered by chance when blood counts are taken for other reasons, such as ‘well man’ screening tests. The patient may develop lymphadenopathy, hepatosplenomegaly, anaemia, and infections as the disease progresses.The following are examples of CLL laboratory findings:Clonal B cell lymphocytosis (diagnosed at greater than 5 x 109/l, but can reach 300 x 109/l)In advanced disease, normocytic, normochromic anaemia is present.Patients with autoimmune-related haemolytic anaemias have a positive direct antiglobulin test (DAT).Although bone marrow aspiration is not always required, it can aid in the diagnosis of CLL. If there has been rapid lymph node enlargement, a lymph node biopsy is required to rule out Richter’s syndrome. This is the transition from low-grade lymphoma to high-grade lymphoma, which is characterised by fever, weight loss, and pain.Although there is no cure for CLL, it can be managed with chemotherapy regimens that help patients live longer. Early treatment has no benefit, and the standard treatment for early disease is to watch and wait, with examinations and blood counts every 3 to 12 months. Chemotherapy is usually reserved for patients who have a disease that is active and causing symptoms.The following is the overall prognosis for CLL:1/3 will not require treatment and will live a long time.1/3 will go through an indolent phase before the disease progresses.1/3 of patients will have an aggressive disease that requires immediate treatment.

In hypokalaemia, initial potassium replacement therapy should not involve glucose infusions, as glucose may cause a further decrease in the plasma-potassium concentration. Glucose infusions are used for the other indications like diabetic ketoacidosis, hypoglycaemia, routine fluid maintenance in patients who are nil by mouth (very important in children), and in hyperkalaemia.

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.

According to a 2018 audit conducted by the Royal College of Emergency Medicine (RCEM), the standard of care for children presenting to EDs with fractured limbs has deteriorated, with most patients waiting longer than ever before for pain relief. More than one-tenth of the children who came in with significant pain from a limb fracture received no pain relief at all.For all patients, including children, the Agency for Health Care Policy and Research (AHCPR) in the United States recommends using the ABCs of pain management:A – Ask about pain regularly. Assess pain systematically.B – Believe the patient and family in their reports of pain and what relieves it.C – Choose pain control options appropriate for the patient, family, and setting.D – Deliver interventions in a timely, logical, coordinated fashion.E – Empower patients and their families. Enable patients to control their course to the greatest extent possible.The RCEM guidelines recommend assessing a child’s pain within 15 minutes of arrival. This is a fundamental requirement. For the assessment of pain in children, a variety of rating scales are available; which one is used depends on the child’s age and ability to use the scale. These are some of them:Faces of Wong-Baker Scale for assessing painScale of numerical evaluationThe behavioural scale is a scale that measures how people behave.The RCEM has provided the following visual guide:The RCEM has established the following guidelines for when patients in severe pain should receive appropriate analgesia:100% within 60 minutes of arrival or triage, whichever is earliest75% within 30 minutes of arrival or triage, whichever is earliest50% within 20 minutes of arrival or triage, whichever is earliest