When there is a high suspicion of gonorrhoea from clinical features, empiric treatment should be commenced whilst waiting for laboratory confirmation. The first line treatment for uncomplicated anogenital and pharyngeal disease includes ceftriaxone 500 mg IM (single dose) + azithromycin 1 g orally as a single dose. This covers concomitant chlamydia infection. For all people who have been treated for gonorrhoea, a test of cure is recommended

All of the organisms listed above can cause pneumonia in immunocompromised individuals but the most likely cause in this patient is Pneumocystis jirovecii.It is a leading AIDS-defining infection in HIV-infected individuals and causes opportunistic infection in immunocompromised individuals. HIV patients with a CD4 count less than 200 cells/mm3 are more prone.The clinical features of pneumonia caused by Pneumocystis jirovecii are:Fever, chest pain, cough (usually non-productive), exertional dyspnoea, tachypnoea, crackles and wheeze.Desaturation on exertion is a very sensitive sign of Pneumocystis jirovecii pneumonia.Chest X-ray can show perihilar fluffy shadowing (as is seen in this case) but can also be normal.

The Likelihood Ratio (LR) is the likelihood that a given test result would be expected in a patient with the target disorder compared to the likelihood that that same result would be expected in a patient without the target disorder.The LR is used to assess how good a diagnostic test is and to help in selecting an appropriate diagnostic tests or sequence of tests. They have advantages over sensitivity and specificity because they are less likely to change with the prevalence of the disorder, they can be calculated for several levels of the symptom/sign or test, they can be used to combine the results of multiple diagnostic test and they can be used to calculate post-test probability for a target disorder.A LR greater than 1 produces a post-test probability which is higher than the pre-test probability. An LR less than 1 produces a post-test probability which is lower than the pre-test probability. When the pre-test probability lies between 30 and 70 per cent, test results with a very high LR (say, above 10) rule in disease. An LR below 1 produces a post-test probability les than the pre-test probability. A very low LR (say, below 0.1) virtually rules out the chance that the patient has the disease.

Fibrinolysis is a normal haemostatic response to vascular injury. Plasminogen, a proenzyme in blood and tissue fluid, is converted to plasmin by activators either from the vessel wall (intrinsic activation) or from the tissues (extrinsic activation). The most important route follows the release of tissue plasminogen activator (TPA) from endothelial cells.

Cerebellar injury causes delayed and disorganized motions. When walking, people with cerebellar abnormalities sway and stagger. Damage to the cerebellum can cause asynergia, the inability to judge distance and when to stop, dysmetria, the inability to perform rapid alternating movements or adiadochokinesia, movement tremors, staggering, wide-based walking or ataxic gait, a proclivity to fall, weak muscles or hypotonia, slurred speech or ataxic dysarthria, and abnormal eye movements or nystagmus.

Hypocalcaemia occurs when there is abnormally low level of serum calcium ( >2.2 mmol/l) after correction for the serum albumin concentration.Rhabdomyolysis causes hyperphosphatemia, and this leads to a reduction in ionised calcium levels.Patients with rhabdomyolysis are commonly cared for in a high dependency care setting. Addison’s disease, hyperthyroidism, thiazide diuretics and lithium all cause hypercalcaemia.

Granulomatous inflammation is a distinctive pattern of chronic inflammation that is encountered in a limited number of infectious and some non-infectious conditions. Briefly, a granuloma is a cellular attempt to contain an offending agent that is difficult to eradicate. In this attempt, there is often strong activation of T lymphocytes leading to macrophage activation, which can cause injury to normal tissues. IL-1 is important in initiating granuloma formation, IL-2 can cause them to enlarge and TNF-α maintains them.

Neutrophil polymorphs are the predominant type of white cells in an acute reaction. They pass between endothelial cell junctions to invade damaged tissue so that the effects of injury can be combated. Extravasation occurs with the movement of leukocytes out of the vessel lumen, and is achieved in five phases which are margination, ‘rolling’, adhesion, transmigration and chemotaxis.

Fluid filtration out of the capillaries is usually slightly greater than fluid absorption into the capillaries. About 8 L of fluid per day is filtered by the microcirculation and returns to the circulation by the lymphatic system. Lymphatic capillaries drain into collecting lymphatics, then into larger lymphatic vessels. Both of these containing smooth muscle and unidirectional valves. From this point, lymph is propelled by smooth muscle constriction and vessel compression by body movements into afferent lymphatics. It then goes to the lymph nodes where phagocytes remove bacteria and foreign materials. It is here that most fluid is reabsorbed by capillaries, and the remainder returns to the subclavian veins via efferent lymphatics and the thoracic duct. The lymphatic system has a major role to play in the body’s immune defence and also has a very important role in the absorption and transportation of fats.

Gastrin is a peptide hormone that aids in gastric motility by stimulating the generation of gastric acid by the parietal cells of the stomach. G-cells in the stomach’s pyloric antrum, the duodenum, and the pancreas release it.The following stimuli cause the release of gastrin:Stimulation of the vagus nerveHypercalcaemiastomach bloatingProteins that have been partially digested, particularly amino acids.The presence of acid and somatostatin inhibits the release of gastrin.Gastrin’s main actions are as follows:Gastric parietal cells are stimulated to release hydrochloric acid.ECL cells are stimulated to produce histamine.Gastric parietal cell maturation and fundal growth stimulationCauses the secretion of pepsinogen by the gastric chief cells.Improves antral muscle mobility stimulates gastric contractionsIncreases gastric emptying rate and stimulates pancreatic secretionGallbladder emptying is induced.

Lactic acidosis is a common finding in critically ill patients and commonly associated with other serious underlying pathologies. It occurs when pH is 5 mmol/L. Anion gap is increased in lactic acidosis.Acquired lactic acidosis is classified into two subtypes:Type A: lactic acidosis due to tissue hypoxia andType B: due to non-hypoxic processes affecting the production and elimination of lactateSome causes of type A and type B lactic acidosis include:Type A lactic acidosisLeft ventricular failureSevere anaemiaShock (including septic shock)AsphyxiaCardiac arrestCO poisoningRespiratory failureSevere asthma and COPDType B lactic acidosis:Regional hypoperfusionRenal failureLiver failureSepsis (non-hypoxic sepsis)Thiamine deficiencyAlcoholic ketoacidosisDiabetic ketoacidosisCyanide poisoningMethanol poisoningBiguanide poisoning

In the posterior mediastinum where the oesophagus is crossed by the pulmonary trunk offers the least resistance when nasogastric tube is inserted from the nose to the stomach.

Amiodarone is an anti-arrhythmic medication that can be used to treat both ventricular and atrial arrhythmias. It’s a class III anti-arrhythmic that works by blocking a variety of channels, including Na+ and K+ channels, as well as beta-adrenoreceptors. As a result, it slows conduction through the SA and AV nodes and prolongs phase 3 of the cardiac action potential (slowing repolarisation).

CML is a myeloproliferative disorder characterised by an abnormal pluripotent haemopoietic stem cell. A cytogenetic abnormality known as the Philadelphia chromosome, which results from a reciprocal translocation between the long arms of chromosomes 9 and 22, causes more than 80% of cases of CML.CML is a disease that develops slowly over several years. This is known as the ‘chronic stage.’ This stage is usually asymptomatic, and 90 percent of patients are diagnosed at this point, with the disease being discovered frequently as a result of a routine blood test. During this stage, the bone marrow contains less than 10% immature white cells (blasts).When CML cells expand, symptoms typically begin to appear. The ‘accelerated stage’ is what it’s called. Approximately 10% of people are diagnosed at this point. During this stage, between 10% and 30% of blood cells in the bone marrow are blasts. During this stage, common clinical features include:Fatigue and exhaustionNight sweats and feverDistension of the abdomenPain in the left upper quadrant (splenic infarction)Splenomegaly (commonest examination finding)HepatomegalyBruising is simple.Gout is a type of arthritis that affects (rapid cell turnover)Hyperviscosity is a condition in which the viscosity of (CVA, priapism)A small percentage of patients experience a ‘blast crisis’ (blast stage). More than 30% of the blood cells in the bone marrow are immature blast cells at this stage. Patients with severe constitutional symptoms (fever, weight loss, bone pain), infections, and bleeding diathesis typically present at this stage.In CML, laboratory findings include:White cell count is abnormally high (often greater than 100 x 109/l).Increased number of immature leukocytes causes a left shift.Anaemia that is mild to moderately normochromic and normocytic.Platelets can be low, normal, or elevated, and the Philadelphia chromosome can be found in > 80% of patients. Serum uric acid and ALP levels are frequently elevated. Tyrosine kinase inhibitors (TKIs), such as imatinib and dasatinib, are the current mainstay of CML treatment. Allogenic bone marrow transplantation is now only used in cases where TKIs have failed to work.

Anaphylaxis is a type I hypersensitivity reaction that is severe and life-threatening. It is marked by the fast onset of life-threatening airway and/or circulatory issues, which are generally accompanied by skin and mucosal abnormalities. When an antigen attaches to specific IgE immunoglobulins on mast cells, degranulation and the release of inflammatory mediators takes place (e.g. histamine, prostaglandins, and leukotrienes).The most important medicine for treating anaphylactic responses is adrenaline. It decreases oedema and reverses peripheral vasodilation as an alpha-adrenergic receptor agonist. Its beta-adrenergic effects widen the bronchial airways, enhance the force of cardiac contraction, and inhibit the release of histamine and leukotriene. The first medicine to be given is adrenaline, and the IM route is optimal for most people.In anaphylaxis, age-related dosages of IM adrenaline are:150 mcg (0.15 mL of 1:1000) for a child under 6 years300 mcg (0.3 mL of 1:1000) for a child aged 6 to 12 years 500 mcg (0.5 mL of 1:1000) for children aged 12 and above 500 mcg for adults (0.5 mL of 1:1000)

Lidocaine is a tertiary amine that is primarily used as a local anaesthetic but can also be used intravenously in the treatment of ventricular dysrhythmias.Lidocaine works as a local anaesthetic by diffusing in its uncharged base form through neural sheaths and the axonal membrane to the internal surface of the cell membrane sodium channels. Here it alters signal conduction by blocking the fast voltage-gated sodium channels. With sufficient blockage, the membrane of the postsynaptic neuron will not depolarise and will be unable to transmit an action potential, thereby preventing the transmission of pain signals.Each 1 ml of plain 1% lidocaine solution contains 10 mg of lidocaine hydrochloride. The maximum safe dose of plain lidocaine is 3 mg/kg. When administered with adrenaline 1:200,000, the maximum safe dose is 7 mg/kg. Because of the risk of vasoconstriction and tissue necrosis, lidocaine should not be used in combination with adrenaline in extremities such as fingers, toes, and the nose.The half-life of lidocaine is 1.5-2 hours. Its onset of action is rapid within a few minutes, and it has a duration of action of 30-60 minutes when used alone. Its duration of action is prolonged by co-administration with adrenaline (about 90 minutes).Lidocaine tends to cause vasodilatation when used locally. This is believed to be due mainly to the inhibition of action potentials via sodium channel blocking in vasoconstrictor sympathetic nerves.

In the absence of any contra-indications, high-dose NSAIDs are the first-line treatment for acute gout. Naproxen 750 mg as a stat dose followed by 250 mg TDS is a commonly used and effective regime.Aspirin should not be used in gout as it reduces the urinary clearance of urate and interferes with the action of uricosuric agents. Naproxen, Diclofenac or Indomethacin are more appropriate choices.Allopurinol is used prophylactically, preventing future attacks by reducing serum uric acid levels. It should not be started in the acute phase as it increases the severity and duration of symptoms.Colchicine acts on the neutrophils, binding to tubulin to prevent neutrophil migration into the joint. It is as effective as NSAIDs in relieving acute attacks. It also has a role in prophylactic treatment if Allopurinol is not tolerated.NSAIDs are contra-indicated in heart failure as they can cause fluid retention and congestive cardiac failure. Colchicine is the preferred treatment in patients with heart failure or those who are intolerant of NSAIDs.

The following structures are the layers of the anterior abdominal wall from the most superficial to the deepest layer:SkinFatty layer of the superficial fascia (Camper’s fascia)Membranous layer of the superficial fascia (Scarpa’s fascia)Aponeurosis of the external and internal oblique musclesRectus abdominis muscleAponeurosis of the internal oblique and transversus abdominisFascia transversalisExtraperitoneal fatParietal peritoneum

Meckel’s lies on the antimesenteric surface of the middle-to-distal ileum, approximately 2 feet proximal to the ileocaecal junction. It appears as a blind-ended tubular outpouching of bowel, about 2 inches long, occurring in about 2% of the population, and may contain two types of ectopic tissue (gastric and pancreatic). The rich blood supply to the diverticulum is provided by the superior mesenteric artery.Proximal to the major duodenal papilla the duodenum is supplied by the gastroduodenal artery (branch of the coeliac trunk) and distal to the major duodenal papilla it is supplied by the inferior pancreaticoduodenal artery (branch of superior mesenteric artery). The arterial supply to the jejunoileum is from the superior mesenteric artery.

Absolute risk reduction (ARR) of treatment = risk of death in control group – risk of death in treatment groupARR = (10/1000) – (5/1000) = 5/1000 = 0.005Number needed to treat (NNT) = 1/ARR = 1/0.005 = 200Therefore 200 people would need to be treated to prevent one extra death.

The clinical and laboratory findings, in this case, support a diagnosis of polycythaemia vera. A plethoric appearance, lethargy, splenomegaly and itching are common in this disease. Patients may also have gouty arthritis, Budd-Chiari syndrome, erythromelalgia, stroke, myocardial infarction or DVT. The average age for diagnosis of Polycythaemia Vera is 65-74 years. It is a haematological malignancy in which there is overproduction of all three cell lines. Venesection is the treatment of choice as it would cause a decrease in the number of red blood cells within the body.Erythropoietin is given in patients with chronic renal failure as they lack this hormone. Administration of erythropoietin in such patients causes stimulation of the bone marrow to produce red blood cells. Desferrioxamine is a chelating agent for iron and is given to patients with iron overload due to repeated blood transfusions, e.g. in thalassemia patients.Penicillamine is a chelating agent for Copper, given as treatment in Wilson’s disease.

Dobutamine is a synthetic isoprenaline derivative that is used to provide inotropic support to patients with low cardiac output caused by septic shock, myocardial infarction, or other cardiac conditions.Dobutamine is a sympathomimetic drug that stimulates beta-1 adrenergic receptors in the heart to produce its primary effect. As a result, it has inotropic properties that increase cardiac contractility and output. It also has a small amount of alpha1- and beta-2-adrenergic activity.It is infused intravenously after being diluted to a volume of at least 50 ml in a suitable crystalloid solution. The dose is titrated to response and ranges from 0.5 to 40 g/kg/min. Extravasation-induced skin necrosis is uncommon, and dobutamine can be administered through a peripheral line.At doses below 10 g/kg/min, side effects are rare, but at higher doses, they can include:Nausea and vomitingTachycardiaDysrhythmiasAnginaHypertensionHeadache

All vaccines are contraindicated in individuals with: A confirmed anaphylactic reaction to a previous dose of the vaccine or a vaccine containing the same antigens.A confirmed anaphylactic reaction to a component in the vaccine e.g. neomycinThere is no evidence that vaccinating pregnant women with inactivated vaccine or toxoids harms the woman or foetus. The current protocol is that a child with history of egg allergy can be safely vaccinated with Fluenz tetra. However, if they had a previous severe anaphylaxis to egg requiring intensive care, then Flenz tetra is contraindicated. BCG, yellow fever or oral typhoid vaccinations are not safe in HIV positive patients.The normal times recommended for immunization of full-term babies should also be applied to premature infants and correction for gestational age should not be implemented.Concurrent antibiotic therapy is not a contraindication to vaccination.

A supracondylar fracture is a fracture that occurs through the thin section of the distal humerus above the growth plate. A supracondylar fracture is most usually associated with median nerve injury. A medial nerve damage causes paralysis of the thenar muscles, as well as loss of thumb opposition.

Cardiovascular effects such as flushing, tachycardia, hypotension and bronchospasm are associated with significant histamine release; histamine release can be minimised by administering slowly or in divided doses over at least 1 minute. Atracurium undergoes non-enzymatic metabolism which is independent of liver and kidney function, thus allowing its use in patients with hepatic or renal impairment. Atracurium has no sedative or analgesic effects. All non-depolarising drugs should be used with care in patients suspected to be suffering with myasthenia gravis or myasthenic syndrome, as patients with these conditions are extremely sensitive to their effects and may require a reduction in dose.

Muscles of the posterior compartment of the leg, innervated by the tibial nerve, perform plantar flexion of the foot at the ankle joint. The fibularis longus (innervated by the superficial fibular nerve) assists in plantar flexion but is not the most important.

The femoral nerve runs down the front of the leg from the pelvis. It gives the front of the thigh and a portion of the lower leg sensation. Extension of the leg at the knee joint, flexion of the thigh at the hip are produced by muscles that is primarily innervated by the femoral nerve.

Bile is secreted by hepatocytes. It is isotonic and resembles plasma ionically. This fraction of bile is called the bile acid-dependent fraction. As it passes along the bile duct, the bile is modified by epithelial cells lining the duct by the addition of water and bicarbonate ions; this fraction is called the bile acid-independent fraction. Overall, the liver can produce 500 – 1000 mL of bile per day. The bile is either discharged directly into the duodenum or stored in the gallbladder. The bile acid-independent fraction is made at the time it is required i.e. during digestion of chyme. The bile acid-dependent fraction is made when the bile salts are returned from the GI tract to the liver, and is then stored in the gallbladder until needed. The gallbladder not only stores bile but concentrates it by removing non-essential solutes and water, leaving bile acids and pigments, mainly by active transport of Na+into the intercellular spaces of the lining cells which, in turn, draws in water, HCO3-and Cl-from the bile and into the extracellular fluid. Within a few minutes of a meal, particularly when fatty foods have been consumed, the gallbladder contracts and releases bile into the bile duct. The sphincter of Oddi is relaxed, allowing the bile to pass into the duodenum through the ampulla of Vater.

Hospital-acquired pneumonia (HAP), or nosocomial pneumonia, is a lower respiratory infection that was not incubating at the time of hospital admission and that presents clinically 2 or more days after hospitalization. Pneumonia that presents sooner should be regarded as community­ acquired pneumonia. VAP refers to nosocomial pneumonia that develops among patients on ventilators. Ventilator-associated pneumonia (VAP) is defined as pneumonia that presents more than 48 hours after endotracheal intubation.Common bacteria involved in hospital-acquired pneumonia (HAP) include the following [10] :Pseudomonas AeruginosaStaphylococcus aureus, including methicillin-susceptible S aureus (MSSA) and methicillin-resistant S aureus (MRSA)Klebsiella pneumoniaeEscherichia coli

Anti-HCV IgG antibodies indicate exposure to hepatitis C but this could be acute, chronic or resolved infection. If the antibody test is positive, HCV RNA should be tested for, which if positive indicates that a person has current infection with active hepatitis C.