Infectious mononucleosis can be diagnosed using specific EBV antibodies and a variety of unrelated non-EBV heterophile antibodies.Heterophile antibodies:About 70-90% of patients with EBV infectious mononucleosis produce antibodies against an antigen produced in one species that react against antigens from other species called heterophile antibodies. False positives can be seen with rubella, hepatitis, SLE, malaria, toxoplasmosis, lymphoma and leukaemia. These antibodies can be detected by two main screening tests:The monospot test uses horse red blood cells. It agglutinates in the presence of heterophile antibodies.Paul-Bunnell test uses sheep red blood cells. The blood agglutinates in the presence of heterophile antibodies.EBV-specific antibodies:Patients can remain heterophile-negative after six weeks and are then considered to be heterophile-negative and should be tested for EBV-specific antibodies. EBV-specific antibodies test are helpful if a false positive heterophile antibody test is suspected.The indirect Coombs test is used to detect in-vitro antibody-antigen reactions. It is typically used in antenatal antibody screening and in preparation for blood transfusion.Heterophile antibody tests are generally not positive in the incubation period of infectious mononucleosis (4-6 weeks) before the onset of symptoms.

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.

Hartmann’s pouch is a diverticulum that can occur at the neck of the gallbladder. It is one of the rarest congenital anomalies of the gallbladder. Hartmann’s gallbladder pouch is a frequent but inconsistent feature of normal and pathologic human gallbladders. It is caused by adhesions between the cystic duct and the neck of the gallbladder. As a result, it is classified as a morphologic rather than an anatomic entity.There is a significant association between the presence of Hartmann’s pouch and gallbladder stones. It is the most common location for gallstones to become lodged and cause cholestasis.

Each lung root contains a pulmonary artery, two pulmonary veins, a main bronchus, bronchial vessels, nerves and lymphatics. Generally the pulmonary artery is superior in the lung root, the pulmonary veins are inferior and the bronchi are somewhat posterior in position. The vagus nerves pass posterior to the lung roots while the phrenic nerves pass anterior to them.

A cricothyrotomy involves making an opening in the median cricothyroid ligament (the medial part of the cricothyroid membrane), between the cricoid cartilage below and the thyroid cartilage above.

Ventricular fibrillation or pulseless ventricular tachycardia (VF/VT) are referred to as shockable rhythm. IV adrenaline 1 mg (10 mL of 1:10,000 solution) should be administered after 3 shocks and every 3 – 5 minutes/after alternate shocks thereafter for a shockable rhythm. For a non-shockable rhythm, 1 mg IV adrenaline should be administered as soon as IV access is obtained, and then every 3 – 5 minutes/after alternate shocks thereafter.

Varicella-zoster immunoglobulin (VZIG) is indicated for post exposure prevention and treatment of varicella. It is recommended as prophylaxis for high-risk patients with no known immunity (i.e. no known previous chickenpox) who have had a significant exposure to varicella-zoster (considered >4 hours close contact).The high-risk groups are:1. Neonates2. Pregnant women3. The immunocompromised (e.g. cancer, immunosuppressive therapies)4. Those on high dose steroids (children on more than 2 mg/kg/day for more than 14 days, or adults on 40 mg/day for more than a week)This patient is at high risk of developing adrenal insufficiency and may need a temporary increase in her steroid dose during infection or stress. It would be inappropriate to stop or wean down her dose of prednisolone and can cause side effects.Since he is on steroids without immunity for chickenpox, he is at risk of developing severe varicella infection, with possible complications including pneumonia, hepatitis and DIC. If he develops a varicella infection, he will need to be admitted and require a specialist review and intravenous Acyclovir.

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.

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.

Klebsiella is a Gram-negative, rod-shaped, non-motile bacteria. The absence of motility distinguishes Klebsiella spp. from most other members of the family Enterobacteriaceae. K. pneumoniae is the most commonly isolated species and has the distinct feature of possessing a large polysaccharide capsule. The capsule offers the organism protection against phagocytosis and antimicrobial absorption,contributing to its virulence. Colonization of gram-negative bacilli in the respiratory tracts of hospitalized patients, particularly by K. pneumoniae, increases with the length of hospital stay. It is a frequent cause of lower respiratory tract infections among hospitalized patients and in immunocompromised hosts such as newborns,elderly patients, and seriously ill patients on respirators.

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.In the presence of cardiac ischaemia, hypertensive emergencies require immediate treatment to prevent myocardial infarction. Similarly, if myonecrosis occurs in the presence of an existing infarction, prompt treatment is required to prevent further myonecrosis. When thrombolysis is used as the primary reperfusion therapy for acute myocardial infarction, blood pressure control is especially important.An intravenous nitrate is the drug of choice in this situation (e.g. GTN). These have a dual purpose in that they can help patients with ischaemic chest pain manage their symptoms. Because lowering blood pressure with nitrates isn’t always enough to achieve optimal results, intravenous beta-blockers are frequently used as a supplement. For this, intravenous atenolol and metoprolol are commonly used.

Once muscle tissue is damaged, there will be healing via diffuse formation of fibrous tissue, especially due to the widespread ischemia. Callus formation takes place in the healing of bone, not muscle. Organised scar formation occurs when a lacerated wound is approximated by sutures so that primary intention wound healing can occur. Liquefaction degeneration occurs following ischemia in the brain. Volkmann’s ischemic contracture may occur, but it is not the primary type of healing that will take place but rather the effect of the fibrous scar formation.

Urgent referral to ophthalmology is indicated if the patient with conjunctivitis has any of the following:Suspected gonococcal or chlamydial conjunctivitisCorneal involvement associated with soft contact lens useSevere disease indicated by presence of a pseudomembraneConjunctivitis associated with rheumatoid arthritis or in immunocompromised patient. Ophthalmia neonatorum.Possible herpes infection.Had recent intraocular surgery. A red flag indicating a serious cause of red eye.Suspected periorbital or orbital cellulitis.Bilateral conjunctivitis is not an indication for urgent referral to ophthalmology.

A patient suffering from acute ischemic stroke can commonly present with hypertensive emergencies. Thrombolytic therapy is contraindicated in a patient with:1. Systolic blood pressure greater than 185 mmHg2. Diastolic blood pressure greater than 110 mmHgBut delaying thrombolytic therapy is associated with increased morbidity in patients with acute ischemic stroke. Managing high blood pressure in acute ischemic stroke requires a slower and more controlled reduction in BP. In the presence of an ischaemic stroke, rapid reduction of MAP can compromise blood flow, causing further ischemia and worsening of the neurological deficit.Intravenous labetalol is the agent of choice. The dose is 10 mg IV over 1-2 minutes. This dose can be repeated, or an infusion can be set up that runs at 2-8 mg/minute. Thrombolysis can be performed once the blood pressure is brought down to less than 180/105 mmHg.A nitrate infusion (for example, Isoket) can be used as an alternative in patients with contraindications to the use of beta-blockers (e.g., asthma, heart block, cardiac failure).

Diastole is usually twice the length of systole at rest, but decreases with increased heart rate. During systole, contraction of the ventricles compresses the coronary arteries and suppresses blood flow. This is particularly evident in the left ventricle, where during systole the ventricular pressure is the same as or greater than that in the arteries and as a result more than 85% of left ventricular perfusion occurs during diastole. This becomes a problem if the heart rate is increased as the diastolic interval is shorter and can result in ischaemia. The second heart sound, caused by closure of the semilunar valves, marks the end of systole.

Eversion of the foot is primarily produced by the fibularis longus and fibularis brevis, both innervated by the superficial fibular nerve. The fibularis tertius, innervated by the deep fibular nerve, also assists in this action.

A L’Abbé plot is a scatter plot with the risk in the control group on the x-axis and the risk in the experimental group on the y-axis. It can be used to evaluate heterogeneity in meta-analysis. Furthermore, this plot can aid to choose a summary measure (odds ratio, risk ratio, risk difference) that will result in more consistent results.

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

Cardiac glycosides (e.g. digoxin) slow the removal of Ca2+from the cell by inhibiting the membrane Na+pump (Na+/K+ATPase) which generates the Na+gradient required for driving the export of Ca2+by Na+/Ca2+exchange; consequently the removal of Ca2+from the myocyte is slowed and more Ca2+is available for the next contraction.

Examples of enzyme-inhibiting drugs (raise plasma theophylline level):ErythromycinClarithromycinCiprofloxacinFluconazoleVerapamilAllopurinolCimetidineExamples of enzyme-inducing drugs (lower plasma theophylline level):PrimidonePhenobarbitalCarbamazepinePhenytoinRitonavirRifampicinSt John’s Wort

The following are the lesions of the cranial nerves:1. Olfactory nerve (I)Reduced taste and smell, but not to ammonia which stimulates the pain fibres carried in the trigeminal nerve2. Optic nerve (II)Manifested by visual field defects, pupillary abnormalities, optic neuritis, optic atrophy, papilledema3. Oculomotor nerve (III)A fixed, dilated pupil which doesn’t accommodate, ptosis, complete internal ophthalmoplegia (masked by ptosis), unopposed lateral rectus causes outward deviation of the eye. If the ocular sympathetic fibres are also affected behind the orbit, the pupil will be fixed but not dilated.4. Trochlear nerve (IV)Diplopia due to weakness of downward and inward eye movement. The most common cause of a pure vertical diplopia. The patient tends to compensate by tilting the head away from the affected side.5. Trigeminal nerve (V)Reduced sensation or dysesthesia over the affected area. Weakness of jaw clenching and side-to-side movement. If there is a lower motor neuron (LMN) lesion, the jaw deviates to the weak side when the mouth is opened. There may be fasciculation of temporalis and masseter.6. Abducens nerve (VI)Inability to look laterally. The eye is deviated medially because of unopposed action of the medial rectus muscle.7. Facial nerve (VII)Facial weakness. In an LMN lesion the forehead is paralysed – the final common pathway to the muscles is destroyed; whereas the upper facial muscles are partially spared in an upper motor neurone (UMN) lesion because of alternative pathways in the brainstem. There appear to be different pathways for voluntary and emotional movement. CVAs usually weaken voluntary movement, often sparing involuntary movements (e.g., spontaneous smiling). The much rarer selective loss of emotional movement is called mimic paralysis and is usually due to a frontal or thalamic lesion.8. Vestibulocochlear nerve (VIII)Unilateral sensorineural deafness, tinnitus. Slow-growing lesions seldom present with vestibular symptoms as compensation has time to occur.9. Glossopharyngeal nerve (IX)Unilateral lesions do not cause any deficit because of bilateral corticobulbar connections. Bilateral lesions result in pseudobulbar palsy. These nerves are closely interlinked.10. Vagus nerve (X)Palatal weakness can cause ‘nasal speech’ and nasal regurgitation of food. The palate moves asymmetrically when the patient says ‘ahh’. Recurrent nerve palsy results in hoarseness, loss of volume and ‘bovine cough’.11. Accessory nerve (XI)Weakness and wasting of sternocleidomastoid and trapezius muscles12.Hypoglossal nerve (XII)An LMN lesion produces wasting of the ipsilateral side of the tongue, with fasciculation; and on attempted protrusion the tongue deviates towards the affected side, but the tongue deviates away from the side of a central lesion.

Serious hypokalaemia can occur in severe asthma and the effect can be potentiated by concomitant treatment with theophyllines like aminophylline, corticosteroids, thiazide and loop diuretics, and hypoxia. Plasma-potassium concentration should be monitored in severe asthma.Spironolactone, a potassium-sparing diuretic, is not likely to have contributed to patients hypokalaemia.

Hartmann’s solution (compound sodium lactate) contains: Na+131 mmol/L, K+5 mmol/L, HCO3-29 mmol/L (as lactate), Cl-111 mmol/L, Ca2+2 mmol/L. It can be used instead of isotonic sodium chloride solution during or after surgery, or in the initial management of the injured or wounded; it may reduce the risk of hyperchloraemic acidosis.

Lymph is the fluid that flows through the lymphatic system. Axillary lymph nodes are near the breasts. They are often the first location to which breast cancer spreads if it moves beyond the breast tissue. They receive approximately 75% of lymph drainage from the breast via lymphatic vessels, laterally and superiorly. The lymph usually first drains to the anterior axillary nodes, and from here, through the central axillary, apical, and supraclavicular nodes in sequence.

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.

Sensory innervation to the external ear is supplied by both cranial and spinal nerves. Branches of the trigeminal, facial, and vagus nerves (CN V, VII, X) are the cranial nerve components, while the lesser occipital (C2, C3) and greater auricular (C2, C3) nerves are the spinal nerve components involved. The lateral surface of the tympanic membrane, the external auditory canal, and the external acoustic meatus are all innervated by nervus intermedius (a branch of CN VII), the auriculotemporal nerve (CN V3), and the auricular branch of the vagus nerve. The concha receives split innervation from nervus intermedius, the auricular branch of the vagus nerve, and the greater auricular (spinal) nerve. Beyond the concha, the anteromedial and anterosuperior parts of the pinna are innervated by the auriculotemporal nerve, and a portion of the lateral helix by the lesser occipital nerve. The greater auricular nerve provides innervation to the area of the pinna inferolateral to the lobule.

Insulin is used mainly in type 1 diabetes, where the pancreas makes no insulin and can sometimes be prescribed in type 1 diabetes. There are different types of insulin categorized by their onset of action:1. Intermediate-acting insulins (isophane insulin NPH): – intermediate duration of action, designed to mimic the effect of endogenous basal insulin- starts their action in 1 to 4 hours- peaks in 4 to 8 hours – dosing is usually twice a day and helps maintain blood sugar throughout the day- Isophane insulin is a suspension of insulin with protamine2. Short-acting insulins (regular insulin)- starts the action in 30 to 40 minutes- peaks in 90 to 120 minutes- duration of action is 6 to 8 hours- taken before meals, and food is necessary within 30 minutes after its administration to avoid hypoglycaemia3. Long-acting insulins (glargine, detemir, degludec)- start action in 1 to 2 hours- plateau effect over 12 to 24 hours- Dosing is usually during the night-time after meals. Their long duration of action helps in reducing the frequency of dosing throughout the day. 4. Rapid-acting insulins (lispro, aspart, glulisine) – start their action in 5 to 15 minutes- peak in 30 minutes- The duration of action is 3 to 5 hours- generally used before meals and always used along with short-acting or long-acting insulins to control sugar levels throughout the day.

Amoxicillin is a derivative of ampicillin and has a similar antibacterial spectrum. It is better absorbed than ampicillin when given orally, producing higher plasma and tissue concentrations; unlike ampicillin, absorption is not affected by the presence of food in the stomach. The adverse effects of amoxicillin are mainly gastrointestinal and mild and include nausea, vomiting and diarrhoea. Amoxicillin is used first line for low to moderate severity community acquired pneumonia, exacerbations of chronic bronchitis, for acute otitis media, for acute sinusitis, for oral infections/dental abscess, for Listeria meningitis (in combination with another antibiotic), for infective endocarditis (in combination with another antibiotic) and for H. Pylori eradication (in combination with metronidazole/clarithromycin and a PPI). Penicillin V is used first line for bacterial tonsillitis; amoxicillin should be avoided in blind treatment of a sore throat as there is a high risk of a rash if glandular fever is present.

Cardiac output (CO) = Stroke volume (SV) x Heart rate (HR). Therefore SV = CO/HR = 4.8/80 = 0.06 L = 60 mL.

Plasma theophylline concentration is usually measured five days after starting oral treatment and three days after each dose adjustment. A blood sample to check theophylline concentration should usually be taken after 4-6 hours if an IV dose of aminophylline was given.