Chickenpox (varicella zoster) is a highly contagious airborne disease and has an incubation period of between 7-21 days. It often has a prodromal phase when there is a fever, aches and headaches, dry cough, and sore throat before onset of rash.

Some recognized complications of chickenpox are:
Orchitis
Hepatitis
Pneumonia
Encephalitis
Infected spots
Otitis media
Myocarditis
Glomerulonephritis
Appendicitis
Pancreatitis

Treatment is symptomatic and includes using paracetamol to manage fever. There is a link between use of ibuprofen in patients with chicken-pox and necrotizing fasciitis so Ibuprofen should NOT be used.

An emollient and antihistamine can be used to ease the itchy rash and oral hydration is encouraged.

The current recommendation by NICE and the BNF is to use vancomycin as first-line in treatment of septicaemia related to vascular catheter. A broad-spectrum antipseudomonal beta-lactam antibiotic should be added to vancomycin if a Gram-negative sepsis is suspected especially in an immunocompromised patient.

In any patient that has had a central venous catheter in situ for a period longer than a week, it should be suspected as the source of sepsis.

The features suggesting the vascular catheter as the source of infection include:
Presence of the catheter before onset of fever.
The absence of another identifiable source of infection.
Presence of inflammation or purulent material at the insertion site or along the tunnel.
An immunocompetent patient without any underlying disease developing bacteraemia (or fungaemia).

Non-Hodgkin’s Lymphoma (NHL) causes neoplastic transformation of both B cell (85%) and T cell (15%) lines.

The most common presentation is with enlarged, rubbery, painless lymph nodes. The patient may also have B symptoms which consist of night sweats, weight loss and fevers. Multiple myeloma most commonly presents with bone pain, especially in the back and ribs.

The presence of Reed-Sternberg cells characterises Hodgkin’s lymphoma. Acute lymphoblastic leukaemia will present with features of anaemia, thrombocytopenia and leukopenia. The most common symptoms of chronic lymphocytic leukaemia are fatigue, night sweats and low-grade fever.

The peak incidence of NHL is in the 50-70 years age group, it affects men and women equally, but affects the Caucasian population more commonly than black and Asian ethnic groups.
The following are recognised risk factors for NHL:
Chromosomal translocations and molecular rearrangements
Epstein-Barr virus infection
Human T-cell leukaemia virus type-1 (HTLV-1)
Hepatitis C
Congenital and acquired immunodeficiency states
Autoimmune disorders, e.g. Sjogren’s syndrome and Hashimoto’s thyroiditis

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, bumetanide
Act 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, hydrochlorothiazide
Act on the Na.Cl co-transporter in the distal convoluted tubule to inhibit sodium and chloride reabsorption.

3) Osmotic diuretics, e.g. mannitol
Increases the osmolality of the glomerular filtrate and tubular fluid, increasing urinary volume by an osmotic effect.

4) Aldosterone antagonists, e.g. spironolactone
Acts 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. acetazolamide
Inhibit the enzyme carbonic anhydrase preventing the conversion of bicarbonate and hydrogen ions into carbonic acid.

Homonymous hemianopia is a visual field defect involving either the two right or the two left halves of the visual fields of both eyes. It is caused by lesions of the retrochiasmal visual pathways, ie, lesions of the optic tract, the lateral geniculate nucleus, the optic radiations, and the cerebral visual (occipital) cortex

Amoxicillin and Ampicillin are more hydrophilic (broad-spectrum) penicillins than benzylpenicillin and phenoxymethylpenicillin. Because they may penetrate through gaps in the outer phospholipid membrane, they are effective against Gram-negative bacteria. Amoxicillin and Ampicillin are resistant to penicillinase-producing microbes.

Community-acquired pneumonia, otitis media, sinusitis, oral infections, and urinary tract infections are among the most prevalent conditions for which they are prescribed. The normal adult oral dose of Amoxicillin is 500 mg three times/day, which can be increased to 1 g three times/day if necessary. Ampicillin is given to adults in doses of 0.5-1 g every 6 hours.

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:
Glycogenolysis
Gluconeogenesis
Lipolysis in adipose tissue
The secretion of glucagon is also stimulated by:
Adrenaline
Cholecystokinin
Arginine
Alanine
Acetylcholine
The secretion of glucagon is inhibited by:
Insulin
Somatostatin
Increased free fatty acids
Increased urea production

Glycolysis 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.

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.

CD8+ T-cells (Cytotoxic T cells)
Recognise antigen only in association with HLA Class I molecules (found on all nucleated cells; present endogenous antigens such as those found in cells infected by viruses or intracellular bacteria.)
Comprise about 25% of peripheral T-cells
Responsible for cytotoxic killing of target cells

Enoxaparin is a low molecular weight heparin (LMWH) that works in the same way as heparin by binding to and activating the enzyme inhibitor antithrombin III. Antithrombin III inactivates thrombin by forming a 1:1 complex with it. Factor Xa and a few other clotting proteases are also inhibited by the heparin-antithrombin III complex.

Nosocomial infections are defined as those occurring within 48 hours of hospital admission, 3 days of discharge or 30 days of an operation. They affect 1 in 10 patients admitted to hospital. Annually, this results in 5000 deaths with a cost to the National Health Service of a billion pounds. On average, a patient with hospital acquired infection spent 2.5-times longer in hospital, incurring additional costs of £3000 more than an uninfected patient. Intensive care units (ICU) have the highest prevalence of hospital-acquired infections in the hospital setting.
The current recommendations by NICE and the BNF on the treatment of hospital acquired pneumonia are:
Early onset infection(less than 5 days after admission to hospital): co-amoxiclav or cefuroxime for 7 days
Late-onset infection(more than 5 days after admission to hospital): an antipseudomonal penicillin (e.g. piperacillin with tazobactam), a broad-spectrum cephalosporin (e.g. ceftazidime), or a quinolone (e.g. ciprofloxacin)
If the patient developed a hospital-acquired pneumonia within 5 days of admission – co-amoxiclav would be the most appropriate choice.
If the patient has developed a hospital-acquired pneumonia > 5 days after admission – ciprofloxacin would be the most appropriate choice from the list of options available.

Helicobacter pylori is a ubiquitous organism that is present in about 50% of the global population. Chronic infection with H pylori causes atrophic and even metaplastic changes in the stomach, and it has a known association with peptic ulcer disease. The most common route of H pylori infection is either oral-to-oral or faecal-to-oral contact.

Piriformis syndrome is a clinical condition of sciatic nerve entrapment at the level of the ischial tuberosity. While there are multiple factors potentially contributing to piriformis syndrome, the clinical presentation is fairly consistent, with patients often reporting pain in the gluteal/buttock region that may shoot, burn or ache down the back of the leg (i.e. sciatic-like pain). In addition, numbness in the buttocks and tingling sensations along the distribution of the sciatic nerve is not uncommon.

The sciatic nerve runs just adjacent to the piriformis muscle, which functions as an external rotator of the hip. Hence, whenever the piriformis muscle is irritated or inflamed, it also affects the sciatic nerve, which then results in sciatica-like pain.

Exposure to nitrous oxide for prolonged periods, either by continuous or by intermittent administration, may result in megaloblastic anaemia as a result of interference with the action of vitamin B12; neurological toxic effects can occur without preceding overt haematological changes. Depression of white cell formation may also occur.

JVP Waveform in Cardiac Cycle Physiology: a wave Right atrial contraction causes atrial systole (end diastole). the c wave During right isovolumetric ventricular contraction, the tricuspid valve bulges into the right atrium, resulting in isovolumetric contraction (early systole). descent by x Rapid ventricular ejection (mid systole) is caused by a combination of right atrial relaxation, tricuspid valve downward movement during right ventricular contraction, and blood ejection from both ventricles. the v-wave Ventricular ejection and isovolumetric relaxation (late systole) occur as a result of venous return filling the right atrium. y lineage Ventricular filling occurs when the tricuspid valve opens, allowing blood to flow rapidly from the right atrium to the right ventricle.

HIV mainly infects CD4+ T helper cells. Viral replication results in progressive T-cell depletion and impaired cell-mediated immunity with subsequent secondary opportunistic infections and increased risk of malignancy. B-cell function is also reduced as a result of lack of T-cell stimulation.
HIV is not a notifiable disease.

The ventilation/perfusion ratio (V/Q ratio) is a ratio used to assess the efficiency and adequacy of the matching ventilation and perfusion.

A pulmonary artery carries deoxygenated blood from the right side of the heart to the lungs. When a large pulmonary embolus completed blocked a pulmonary artery the alveoli were ventilated but not perfused at all, then the V/Q ratio would be infinity.

Pancreatic exocrine secretion is controlled by:
Parasympathetic stimulation which enhances secretion of both the enzyme and aqueous components
Sympathetic stimulation which inhibits pancreatic secretion
Secretin which stimulates secretion of the alkaline-rich fluid from ductal cells
Cholecystokinin which stimulates secretion of the enzyme-rich fluid from acinar cellsSomatostatin which inhibits secretion from both acinar and ductal cells
Gastrin which stimulates pancreatic acinar cells to secrete digestive enzymes

Impetigo is a highly contagious infection of the superficial epidermis that most commonly affects young children but can occur in any age group. In children it is the most common bacterial skin infection and it is the third most common skin disease overall, behind dermatitis and viral warts.
The commonest causative organism is Staphylococcus aureus. Streptococcus pyogenesis the second commonest and causes fewer cases, either alone or in combination withS. aureus.The streptococcal form tends to be commoner in warmer, more humid climates. (Hirschmann JV. Impetigo: etiology and therapy. Curr Clin Top Infect Dis. 2002;22:42–51.)
Impetigo is most commonly spread by direct person-to-person contact, and can spread rapidly through families and school classes. It can also, less commonly, be spread by indirect contact.
There are two main forms of impetigo:
Non-bullous impetigo – lesions usually start as tiny pustules or vesicles that evolve rapidly into honey-crusted plaques that tend to be under 2 cm in diameter. These can be itchy but are rarely painful.
Bullous impetigo – lesions have a thin roof and tend to rupture spontaneously. This type is more likely to be painful and may be associated with systemic upset.

Anaemia is defined as a reduction in haemoglobin concentration below the normal range for the age and sex of the individual. Children tend to have lower haemoglobin than adults, and women tend to have lower haemoglobin than men. Anaemia may occur from an actual reduction in total circulating haemoglobin mass, or with an increase in plasma volume e.g. in pregnancy, causing a dilutional anaemia. After acute major blood loss, anaemia is not immediately apparent because total blood volume is reduced and it takes up to a day for plasma volume to be replaced and hence the degree of anaemia to become apparent. The initial clinical features in acute haemorrhage are therefore a result of reduction in blood volume rather than that of anaemia. When anaemia develops slowly, the associated symptoms are often very mild as the body has time to adapt to the fall in haemoglobin. This involves mechanisms such as an increase in red cell 2,3 -diphosphoglycerate (2,3 – DPG), which shifts the oxygen dissociation curve to the right, allowing enhanced delivery of O2 to the tissues, and an increase in stroke volume and heart rate.