Immune globulin IM is indicated for prophylaxis following exposureto hepatitis A, to prevent or modify measles (rubeola) in a susceptible person exposed fewer than 6 days previously,for susceptible household contacts of measles patients,particularly contacts <1 year and pregnant women without evidence of immunity, and to modify rubella in exposed pregnant women who will not consider a therapeutic abortion.

Diazepam boosts GABA’s effects, giving it sedative, hypnotic, anxiolytic, anticonvulsant, and muscle-relaxing properties. It can be administered orally, rectally, or intravenously.With a half-life of 20-100 hours, it is a long-acting benzodiazepine. Midazolam, oxazepam, and alprazolam are examples of short-acting benzodiazepines with a half-life of less than 12 hours (Xanax).If used in the presence of hepatic impairment, benzodiazepines can cause coma. If treatment is necessary, benzodiazepines with shorter half-lives should be used in lower doses. Diazepam is a sedative that crosses into breast milk and should be avoided by breastfeeding mothers.

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.

Insulin is an anabolic hormone. Its actions can be broadly divided into:Lipid metabolismProtein metabolism andCarbohydrate metabolismFor lipid metabolism, insulin:Stimulates lipogenesisInhibits lipolysis by lipaseFor carbohydrate metabolism, insulin:Decreases gluconeogenesisStimulates glycolysisPromotes glucose uptake in muscle and adipose tissuePromotes glycogen storageIncreases glycogenesisDecreases glycogenolysisProtein metabolism:Stimulates protein synthesisAccelerates net formation of proteinStimulates amino acid uptakeInhibits protein degradationInhibits amino acid conversion to glucose

Aspirin (at analgesic doses) is contraindicated in severe heart failure. Aspirin irreversibly inhibits cyclooxygenase (COX) enzymes resulting in decreased production of prostaglandins (which can lead to irritation of the gastric mucosa). The analgesic dose is greater than the antiplatelet dose, and taken orally it has a duration of action of about 4 hours. Clinical features of salicylate toxicity in overdose include hyperventilation, tinnitus, deafness, vasodilatation, and sweating.

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.

Clinical features of hyperkalaemia may include: paraesthesia, muscle weakness or paralysis, cardiac conduction abnormalities and dysrhythmias. Clinical features of hypokalaemia may include: muscle weakness, muscle cramps, rhabdomyolysis and myoglobinuria, ascending paralysis resulting in respiratory failure, constipation, gut ileus with distension, anorexia, nausea and vomiting, impaired ADH action with polyuria and polydipsia, ECG changes and cardiac arrhythmias.

Acute lymphoblastic leukaemia (ALL) is a clonal (malignant) bone marrow disorder in which early lymphoid precursors multiply and replace the marrow’s normal hematopoietic cells. ALL is most common between the ages of 3 and 7, with 75 percent of cases occurring before the age of 6.

Calcium channel blockers inhibit L-type voltage-sensitive calcium channels in arterial smooth muscle, causing relaxation and vasodilation (reduction in peripheral vascular resistance). They also block calcium channels within the myocardium and conducting tissues of the heart which produces a negative inotropic effect by reducing calcium influx during the plateau phase of the action potential. They have a variety of uses, including:HypertensionAnginaAtrial fibrillationMigraineCalcium channel blockers have been found to be moderately useful in the prevention of migraines. The best evidence is for this is with verapamil. This may be due to the prevention of the arteriolar constriction that is associated with migraine. They are commonly used for this elsewhere in the world but are not currently licensed for this use in the UK.The following are common side effects of all calcium-channel blockers:Abdominal painDizzinessDrowsinessFlushingHeadacheNausea and vomitingPalpitationsPeripheral oedemaSkin reactionsTachycardiaVerapamil is highly negatively inotropic and reduces cardiac output, slows the heart rate and may impair atrioventricular conduction. It may precipitate heart failure, exacerbate conduction disorders, and cause hypotension at high doses and should not be used with beta-blockers. Nifedipine has less myocardial effects than verapamil and has no antiarrhythmic properties but has more influence on the vessels. Nimodipine is used solely for the prevention and treatment of vascular spasm following aneurysmal subarachnoid haemorrhage.

Chronic hepatitis B infection is indicated by the persistence of HBsAg for more than 6 months. Hepatitis B has a long incubation period of about 2 – 6 months. Hepatitis B vaccine has recently been introduced to the routine childhood immunisation schedule – given at 2, 3 and 4 months. It is also given to babies born to hepatitis B infected mothers at birth, four weeks and 12 months old. Treatment of acute hepatitis is supportive. Treatment with antivirals should be considered in chronic infection as responders have a reduced risk of liver damage and liver cancer in the long term.

The tonsils are collections of lymphatic tissue located within the pharynx. They collectively form a ringed arrangement, known as Waldeyer’s ring: pharyngeal tonsil, 2 tubal tonsils, 2 palatine tonsils, and the lingual tonsil. Lymphatic fluid from the lingual tonsil drains into the jugulodigastric and deep cervical lymph nodes.Lymphatic fluid from the pharyngeal tonsil drains into the retropharyngeal nodes (which empty into the deep cervical chain), and directly into deep cervical nodes within the parapharyngeal space.The retropharyngeal and the deep cervical lymph nodes drain the tubal tonsils.The palatine tonsils drain to the jugulodigastric node, a node of the deep cervical lymph nodes, located inferior to the angle of the mandible.

An important mechanism that provides protection to the foetus is placental transfer of maternal IgG antibodies while his/her humoral response is inefficient. The only antibody class that significantly crosses the human placenta is IgG.

Phyllocontin continus contains aminophylline (a mixture of theophylline and ethylenediamine), a bronchodilator used in the management of COPD and asthma.This patient is exhibiting symptoms of theophylline toxicity, which may have been triggered by the prescription of the antibiotic. Quinolone antibiotics, such as ciprofloxacin and levofloxacin, and macrolide antibiotics, such as erythromycin, increase the plasma concentration of theophyllines and can lead to toxicity.The drugs that commonly affect the half-life and the plasma concentration of theophylline are summarised in the table below:Drugs increasing plasma concentration of theophyllineDrugs decreasing plasma concentration of theophyllineCalcium channel blockers, e.g. VerapamilCimetidineFluconazoleMacrolides, e.g. erythromycinQuinolones, e.g. ciprofloxacinMethotrexateBarbituratesCarbamazepinePhenobarbitolPhenytoin (and fosphenytoin)RifampicinSt. John’s wort

Weber syndrome is a midbrain stroke characterized by crossed hemiplegia along with oculomotor nerve deficits and it occurs with the occlusion of the median and/or paramedian perforating branches of the basilar artery. Typical clinical findings include ipsilateral CN III palsy, ptosis, and mydriasis (such as damage to parasympathetic fibres of CN III) with contralateral hemiplegia.

Anaphylaxis is an example of a type I hypersensitivity reaction. It is IgE mediated. It requires a prior exposure to the antigen. The initial exposure sensitizes the body to the antigen and a second exposure to that antigen leads to an anaphylactic reaction.Massive calcium influx into the cells leads to mast cell degranulation. The Immunoglobulin antigen complex binds to Fc receptors on the surface of mast cells. The result is mast cell degranulation and release of histamine, proteoglycans and serum proteases from cytoplasmic granules.

Hyperaemia is the process where the body adjusts blood flow to meet the metabolic needs of different tissues in health and disease. Vasoactive mediators that take part in this process include K+, adenosine, CO2, H+, phosphates and H2O2. Although the mechanism is not clear, all these mediators likely contribute to some extent at different points.Specific organs are more sensitive to specific metabolites:K+ and adenosine are the most potent vasodilators in skeletal musclesCO2 and K+ are the most potent vasodilators in cerebral circulation.

At birth, the conus medullaris lies at L3. By the age of 21, it sits at L1/L2.

Extensor pollicis brevis is a short and slender muscle located in the posterior compartment of the forearm, extending from the posterior surface of radius to the proximal phalanx of thumb. It is one of the deep extensors of the forearm, together with supinator, abductor pollicis longus, extensor pollicis longus and extensor indicis muscles.Extensor pollicis brevis is a deep extensor of the thumb that lies deep to extensor digitorum muscle. It sits directly medial to abductor pollicis longus and posterolateral to extensor pollicis longus muscle. Just above the wrist, extensor pollicis brevis obliquely crosses the tendons of extensor carpi radialis brevis and extensor carpi radialis longus muscles.Extensor pollicis brevis is innervated by posterior interosseous nerve which is a continuation of a deep branch of radial nerve (root value C7 and C8).Extensor pollicis brevis receives its blood supply by posterior interosseous artery and perforating branches from the anterior interosseous artery, which are the branches of common interosseous artery. The common interosseous artery arises immediately below the tuberosity of radius from the ulnar artery.Together with extensor pollicis longus, extensor pollicis brevis is in charge of extension of the thumb in the first metacarpophalangeal joint. It also extends the thumb in the carpometacarpal joint of the thumb. This movement is important in the anatomy of the grip, as it enables letting go of an object. As it crosses the wrist, extensor pollicis brevis also participates in the extension and abduction of this joint.

Intrinsic factor is essential for the absorption of the small amounts of vitamin B12 normally present in the diet from the terminal ileum. The parietal cells of the stomach produce intrinsic factor, and following a gastrectomy, the absorption of vitamin B12 will be markedly reduced, and a deficiency state will exist.

Passive expiration is produced primarily by relaxation of the inspiratory muscles (diaphragm and external intercostal muscles) in addition to the elastic recoil of the lungs. In expiration, several movements occur. There are:1. depression of the sternal ends of the ribs (‘pump handle’ movement), 2. depression of the lateral shafts of the ribs (‘bucket handle’ movement) and 3. elevation of the diaphragm. These result in a reduction of the thorax in an anteroposterior, transverse and vertical direction respectively. There is then a decreased intrathoracic volume and increased intrathoracic pressure and air is forced out of the lungs.

Inflammation can be divided intoacute inflammation, which occurs over seconds, minutes, hours, and days, andchronic inflammation, which occurs over longer periods.Acute inflammationcommences within seconds or minutes following the injury of tissues. There are numerous potential stimuli for an acute inflammatory response including infections (bacterial, viral, fungal, parasitic), tissue necrosis, foreign bodies, and Immune reactions (hypersensitivity reactions). The chief cell type of acute inflammation is the neutrophil.There are three main processesthat occur in the acute inflammatory response:Increased blood flowIncreased capillary permeabilityNeutrophil migration1. Increased blood flow:Vasoactive mediators are released, such as nitric oxide, histamine, bradykinins, and prostaglandin E2. These mediators cause vasodilatation and increased blood flow to the area (causing redness and heat).2. Increased capillary permeability:The vasoactive mediators also cause increased capillary permeability by causing endothelial cell contraction that widens the intercellular gaps of venules. This allows an outpouring of protein-rich fluid (exudate) into the extracellular tissues that results in a reduction of intravascular osmotic pressure and an increase in extravascular/interstitial pressure. The increased interstitial osmotic pressure leads to oedema.3. Neutrophil migration:Neutrophils leave the vasculature through the following sequence of events:Margination and rolling: neutrophils flow nearer the vessel wall, rather than in the axial stream, which is referred to as margination. Following margination the neutrophils begin rolling along the surface of the vascular endothelium.Activation and adhesion: then as a result of interaction with endothelial cell adhesion molecules (CAMs) that is mediated by selectins, the neutrophils are activated and adhere to the endothelium.Transmigration: once bound to the endothelium, neutrophils squeeze through gaps between adjacent endothelial cells into the interstitial fluid, in a process calleddiapedesis.

The management of bleeding in a patient receiving heparin depends upon the location and severity of bleeding, the underlying thromboembolic risk, and the current aPTT (for heparin) or anti-factor Xa activity (for LMW heparin). As an example, a patient with minor skin bleeding in the setting of a mechanical heart valve (high thromboembolic risk) and a therapeutic aPTT may continue heparin therapy, whereas a patient with major intracerebral bleeding in the setting of venous thromboembolism several months prior who is receiving heparin bridging perioperatively may require immediate heparin discontinuation and reversal with protamine sulphate. If haemorrhage occurs it is usually sufficient to withdraw unfractionated or low molecular weight heparin, but if rapid reversal of the effects of the heparin is required, protamine sulphate is a specific antidote (but only partially reverses the effects of low molecular weight heparins). Clinician judgment and early involvement of the appropriate consulting specialists is advised.

Angiotensin-converting enzyme (ACE) inhibitors prevent angiotensin I from being converted to angiotensin II. Angiotensin II has a variety of effects:Sympathetic activity has increased.Vasoconstriction in the arteriesSecretion of VasopressinSecretion of aldosteroneThe increase in systemic blood pressure is caused by arteriolar vasoconstriction. Vasopressin stimulates water reabsorption in the kidneys as well as the thirst sensation. In the distal convoluted tubules and collecting ducts, aldosterone causes the reabsorption of sodium and water from the urine in exchange for potassium secretion. As a result, ACE inhibitors lower systemic blood pressure while also causing hyperkalaemia.Angiotensin-converting enzyme inhibitors (ACE inhibitors) are used in a variety of clinical settings, including heart failure. According to a meta-analysis, ACE inhibitors reduce death, MI, and overall admission in patients with heart failure by 28%.ACE inhibitors are also used in the following clinical settings:HypertensionChronic kidney diseaseDiabetic nephropathy Following a myocardial infarctionIn the presence of renal artery stenosis, ACE inhibitors are contraindicated because they can cause or exacerbate renal failure.The most common side effect of ACE inhibitors is a dry cough caused by increased bradykinin production. There is, however, no known link to fibrosis of the lungs.

Typically, granuloma has Langerhan’s cells (large multinucleated cells ) surrounded by epithelioid cell aggregates, T lymphocytes and fibroblasts.Antigen presenting monocytic cells found in the skin are known as Langerhan’s cells.

End-organ damage (e.g. encephalopathy, intracranial haemorrhage, acute myocardial infarction or ischaemia, dissection, pulmonary oedema, nephropathy, eclampsia, papilledema, and/or angiopathic haemolytic anaemia) characterises a hypertensive emergency (also known as ‘accelerated hypertension’ or malignant hypertension’ It’s a life-threatening condition that necessitates rapid blood pressure reduction to avoid end-organ damage and a negative outcome.Hypertensive encephalopathy is a syndrome that includes headaches, seizures, visual changes, and other neurologic symptoms in people who have high blood pressure. It is reversible if treated quickly, but it can progress to coma and death if not treated properly.Any patient with suspected hypertensive encephalopathy should have an urgent CT scan to rule out an intracranial haemorrhage, as rapid blood pressure reduction could be dangerous in these circumstances.The drug of choice is labetalol, which reduces blood pressure steadily and consistently without compromising cerebral blood flow.An initial reduction of approximately 25% in mean arterial pressure (MAP) over an hour should be aimed for, followed by a further controlled MAP reduction over the next 24 hours. In patients who are unable to take beta-blockers, nicardipine can be used as a substitute.

Cholera has an incubation period of 12 hours to 6 days.Other infectious disease that have an incubation period of less than 1 week include:Staphylococcal enteritis (1-6 hours)Salmonella enteritis (12-24 hours)Botulism (18-36 hours)Gas gangrene (6 hours to 4 days)Scarlet fever (1-4 days)Diphtheria (2-5 days)Gonorrhoea (3-5 days)Yellow fever (3-6 days)Meningococcaemia (1-7 days)Brucellosis has an incubation period of 7-21 days.Measles has an incubation period of 14-18 days.Falciparum malaria usually has an incubation period of 7-14 days. The other forms of malaria have a longer incubation period of 12-40 days.Rubella has an incubation period of 14-21 days.

Cardiac myocyte contraction is not dependent on an external nerve supply but instead the heart generates its own rhythm, demonstrating inherent rhythmicity. The heartbeat is initiated by spontaneous depolarisation of the sinoatrial node (SAN), a region of specialised myocytes in the right atrium close to the coronary sinus, at a rate of 100-110 beats/min. This intrinsic rhythm is primarily influenced by autonomic nerves, with vagal influences being dominant over sympathetic influences at rest. This vagal tone reduces the resting heart rate down to 60-80 beats/min. To increase heart rate, the autonomic nervous system increases sympathetic outflow to the SAN, with concurrent inhibition of vagal tone. These changes mean the pacemaker potential more rapidly reaches the threshold for action potential generation.

IgA is the predominant antibody class in secretions and tremendous quantities are secreted into various body spaces and onto mucosal surfaces (the gut lumen, the pharynx and sinuses, the larger airways, although not the alveoli). Because of its size, the majority of IgM is found in the circulation.Along with IgM, IgD is predominant among the surface receptors of mature B cells, where it plays a key role in B cells activation.IgE has the lowest concentration in normal human serum. It plays a prominent role in immune responses to helminth parasites, and in allergic reactions.IgG is the most abundant immunoglobulin and constitutes 75 percent of serum immunoglobulin in an adult human

Gluteus minimus is the smallest muscle of the glutei. It is located just beneath the gluteus medius muscle. Gluteus minimus predominantly acts as a hip stabilizer and abductor of the hip. The superior gluteal nerve innervates the gluteus minimus.

An intention tremor is characteristic of cerebellar dysfunction. Resting tremor may be seen in Parkinsonism.