Hepatitis B surface antigen (HBsAg) is a protein on the surface of the hepatitis B virus, that is the first serologic marker to appear in a new acute infection.It can be detected as early as 1 week and as late as 9 weeks. It can be detected in high levels in serum during acute or chronic hepatitis B virus infection. The presence of HBsAg indicates that the person is infectious. The body normally produces antibodies to HBsAg as part of the normal immune response to infection. HBsAg is the antigen used to make hepatitis B vaccine.Hepatitis B surface antibody (anti-HBs) indicates recovery and immunity from the hepatitis B virus infection. Anti-HBs also develops in a person who has been successfully vaccinated against hepatitis B.Total hepatitis B core antibody (anti-HBc): Appears at the onset of symptoms in acute hepatitis B and persists for life. The presence of anti-HBc indicates previous or ongoing infection with hepatitis B virus in an undefined time frame. It is not present following hepatitis B vaccination.IgM antibody to hepatitis B core antigen (IgM anti-HBc) indicates recent infection with hepatitis B virus (<6 months). Its presence indicates acute infection.The following table summarises the presence of hepatitis B markers according to each situation:Susceptible to infection:HBsAg = NegativeAnti-HBc = NegativeAnti-HBs = NegativeImmune due to natural infection:HBsAg = NegativeAnti-HBc = PositiveAnti-HBs = PositiveImmune due to vaccination:HBsAg = NegativeAnti-HBc = NegativeAnti-HBs = PositiveAcute infection:HBsAg = PositiveAnti-HBc = PositiveAnti-HBs = NegativeIgM anti-HBc = PositiveChronic infection:HBsAg = PositiveAnti-HBc = PositiveAnti-HBs = NegativeIgM anti-HBc = Negative

Bone pain, pathologic fractures, weakness, anaemia, infection, hypercalcemia, spinal cord compression, and renal failure are all signs and symptoms of multiple myeloma (MM). The patient’s condition matched the signs and symptoms of myeloma.

The pressure measured in the right atrium or superior vena cava is known as central venous pressure (CVP). In a spontaneously breathing subject, the usual CVP value is 0-8 cmH2O (0-6 mmHg).At the conclusion of expiration, the CVP should be measured with the patient resting flat. The catheter’s tip should be at the intersection of the superior vena cava and the right atrium. An electronic transducer is installed and zeroed at the level of the right atrium to measure it (usually in the 4th intercostal space in the mid-axillary line).CVP is a good predictor of preload in the right ventricle. Hypovolaemia is indicated by a volume challenge of 250-500 mL crystalloid eliciting an increase in CVP that is not sustained for more than 10 minutes.CVP is influenced by a number of factors, including:Mechanical ventilation (and PEEP)Pulmonary hypertensionPulmonary embolismHeart failurePleural effusionDecreased cardiac outputCardiac tamponadeCVP is reduced by the following factors:Distributive shockNegative pressure ventilationHypovolaemiaDeep inhalation

Acetazolamide is a non-competitive, reversible inhibitor of carbonic anhydrase found in the cytosol of cells and on the brush border of the proximal convoluted tubule. Bicarbonate and hydrogen ions are converted to carbonic acid by carbonic anhydrase, which then converts carbonic acid to carbon dioxide and water. As a result, acetazolamide reduces the availability of hydrogen ions, causing sodium and bicarbonate ions to accumulate in the renal tubule, resulting in diuresis.The mechanism of action of the various types of diuretics is summarised below:1) Loop diuretics, e.g. furosemide, bumetanideAct on the Na.K.2Cl co-transporters in the ascending loop of Henlé to inhibit sodium, chloride and potassium reabsorption.2) Thiazide diuretics, e.g. Bendroflumethiazide, hydrochlorothiazideAct on the Na.Cl co-transporter in the distal convoluted tubule to inhibit sodium and chloride reabsorption.3) Osmotic diuretics, e.g. mannitolIncreases the osmolality of the glomerular filtrate and tubular fluid, increasing urinary volume by an osmotic effect.4) Aldosterone antagonists, e.g. spironolactoneActs in the distal convoluted tubule as a competitive aldosterone antagonist resulting in inhibition of sodium reabsorption and increasing potassium reabsorption.5) Carbonic anhydrase inhibitors, e.g. acetazolamideInhibit the enzyme carbonic anhydrase preventing the conversion of bicarbonate and hydrogen ions into carbonic acid.

Acute bronchiolitis is caused most commonly by respiratory syncytial virus, occurring mostly in children aged 6 months to 2 years. Children with bronchiolitis are febrile and tachypnoeic with a dry cough and difficulty feeding. Examination may reveal chest hyperinflation, respiratory distress, wheezing and fine end-inspiratory crepitations. Chest x-ray may show hyperinflation and increased peribronchial markings (although CXR should only performed if there is diagnostic uncertainty or an atypical course). Treatment is usually supportive, aerosolized ribavirin is reserved for severely ill or immunocompromised patients.

Hypoxia, hypercalcaemia, hypokalaemia and hypomagnesaemia predispose to digoxin toxicity. Care should also be taken in the elderly who are particularly susceptible to digoxin toxicity. Hypokalaemia may be precipitated by use of diuretics. Although hyponatremia can result in the development of other pathological disturbances, it does not potentiate digoxin toxicity.

Mycobacterium tuberculosis are part of the Mycobacteriaceae family. They are described to have the characteristics of a Gram-positive cell wall but they are not easily stained with Gram stain. This is because their cell wall contains a high lipid content, and this lipid allows the Mycobacteria to bind to alkaline stains with the application and help of heat. Once stained, they are able to resist decolorization even with the use of acid alcohol as the decolourizer, making them very difficult to decolorize, that is why they are known to be acid-fast.The Ghon complex is a non-pathognomonic radiographic finding on a chest x-ray that is significant for pulmonary infection of tuberculosis. The location of the Ghon’s focus is usually subpleural and predominantly in the upper part of the lower lobe and lower part of the middle or upper lobe. Skeletal tuberculosis of the spine is referred to as Pott disease.The risk of reactivation TB is about 3.3% during the first year after a positive PPD skin test and a total of 5% to 15% thereafter in the person’s lifetime. Progression from infection to active disease varies with age and the intensity and duration of exposure. Reactivation TB occurs when there is an alteration or suppression of the cellular immune system in the infected host that favoursreplication of the bacilli and progression to disease.

An opsonin is any molecule that enhances phagocytosis by marking an antigen for an immune response, for example, immunoglobulin or complement. Opsonisation is the molecular mechanism whereby molecules, microbes, or apoptotic cells are chemically modified to have a stronger attraction to the cell surface receptors on phagocytes and natural killer cells. With the antigen coated in opsonins, binding to immune cells is greatly enhanced. Opsonisation also mediates phagocytosis via signal cascades from cell surface receptors.

Heparin-induced thrombocytopenia (HIT) is a prothrombotic disorder caused by antibodies that recognize complexes of platelet factor 4 (PF4) and heparin. HIT is frequently considered in the differential diagnosis of thrombocytopenia occurring in patients on heparin therapy. HIT is a challenging diagnosis because of routine heparin use in hospitalized patients, the common occurrence of thrombocytopenia. The process of heparin dependent IgG antibodies binding to heparin/platelet factor 4 complexes activates platelets and produces a hypercoagulable state. This syndrome typically develops 5-10 days (range 4-15 days) after heparin is commenced. It can occur with unfractionated heparin, low molecular weight heparin, or, rarely, fondaparinux. The diagnosis of HIT requires the combination of a compatible clinical picture and laboratory confirmation of the presence of heparin dependent platelet activating HIT antibodies. Discontinuation of heparin alone or initiation of a vitamin K antagonist alone like warfarin, is not sufficient to stop the development of thrombosis in patients with acute HIT. If there is moderate clinical suspicion for HIT, all sources of heparin must be discontinued and there must be consideration of anticoagulant treatment with a non-heparin drug.

Glucagon is a peptide hormone that is produced and secreted by alpha cells of the islets of Langerhans, which are located in the endocrine portion of the pancreas. The main physiological role of glucagon is to stimulate hepatic glucose output, thereby leading to increases in glycaemia. It provides the major counter-regulatory mechanism to insulin in maintaining glucose homeostasis.Hypoglycaemia is the principal stimulus for the secretion of glucagon but may also be used as an antidote in beta-blocker overdose and in anaphylaxis in patients on beta-blockers that fail to respond to adrenaline. Glucagon then causes:GlycogenolysisGluconeogenesisLipolysis in adipose tissueThe secretion of glucagon is also stimulated by:AdrenalineCholecystokininArginineAlanineAcetylcholineThe secretion of glucagon is inhibited by:InsulinSomatostatinIncreased free fatty acidsIncreased urea productionGlycolysis is the metabolic pathway that converts glucose into pyruvate. The free energy released by this process is used to form ATP and NADH. Glycolysis is inhibited by glucagon, and glycolysis and gluconeogenesis are reciprocally regulated so that when one cell pathway is activated, the other is inactive and vice versa.Glucagon has a minor effect of enhancing lipolysis in adipose tissue. Lipolysis is the breakdown of lipids and involves the hydrolysis of triglycerides into glycerol and free fatty acids. It makes fatty acids available for oxidation.