Chemotherapy that is too aggressive weakens your immune system, putting you at risk for a fungal and many other infection. Neutropenia is a condition in which a person’s neutrophil count is abnormally low. Neutrophils are an infection-fighting type of white blood cell. Neutrophils fight infection by killing bacteria and fungi (yeast) that infiltrate the body. Fungal organisms are significant pathogens in the setting of neutropenia.

Heparin works by binding to and activating the enzyme inhibitor antithrombin III. Antithrombin III inactivates thrombin (factor IIa) by forming a 1:1 complex with thrombin. The heparin-antithrombin III complex also inhibits factor Xa and some other proteases involved with clotting. The heparin-ATIII complex can also inactivate IX, XI, XII, and plasmin.Heparin is a polymer of glycosaminoglycan. It occurs naturally and is found in mast cells. Clinically, it is used in two forms:1. Unfractionated: widely varying polymer chain lengths2. Low molecular weight: Smaller polymers only Heparin is not thrombolytic or fibrinolytic. It prevents the progression of existing clots by inhibiting further clotting. The lysis of existing clots relies on endogenous thrombolytics.Heparin is used for:1. Prevention and treatment of venous thromboembolism2. Treatment of disseminated intravascular coagulation3. Treatment of fat embolism4. Priming of haemodialysis and cardiopulmonary bypass machines

The lateral pontine syndrome occurs due to occlusion of perforating branches of the basilar and anterior inferior cerebellar (AICA) arteries. It is also known as Marie-Foix syndrome or Marie-Foix-Alajouanine syndrome. It is considered one of the brainstem stroke syndromes of the lateral aspect of the pons.It is characterized by ipsilateral limb ataxia, loss of pain and temperature sensation of the face, facial weakness, hearing loss, vertigo and nystagmus, hemiplegia/hemiparesis, and loss of pain and temperature sensation.

The facial nerve divides into five terminal branches once in the parotid gland. 1. The temporal branch innervates muscles in the temple, forehead and supraorbital areas.2. The zygomatic branch innervates muscles in the infraorbital area, the lateral nasal area and the upper lip.3. The buccal branch innervates muscles in the cheek, the upper lip and the corner of the mouth. 4. The marginal mandibular branch innervates muscles of the lower lip and chin. 5. The cervical branch innervates the platysma muscle.

Factors increasing compliance:Old ageEmphysemaFactors decreasing compliance:Pulmonary fibrosisPulmonary oedemaAtelectasisExtremes of lung volumes (at higher lung volumes the compliance of the lung becomes less as the lung becomes stiffer)

Of the filtered sodium, about 65% is reabsorbed in the proximal tubule.

Allopurinol should not be started during an acute gout episode because it can both prolong and trigger another acute attack. Allopurinol should be continued in patients who are currently taking it, and acute attacks should be treated as usual with NSAIDs or colchicine, as needed.Non-steroidal anti-inflammatory medications (NSAIDs), such as naproxen, are the first-line treatment for acute gout attacks. Colchicine can be used in situations where NSAIDs are contraindicated, such as in patients with hypertension or those who have had a history of peptic ulcer disease. Because there is no reason for this patient to avoid NSAIDs, naproxen would be the medicine of choice from the list above.It would be reasonable to titrate up the allopurinol dose once the acute episode has subsided, targeting <6 mg/dl (<360 µmol/l) plasma urate levels .Febuxostat (Uloric) is a drug that can be used instead of allopurinol to treat persistent gout.

Absolute risk and relative risk are used to assess the strength of a relationship between a disease and a factor that may affect it.Absolute risk (AR) is the risk of developing a disease over a time period:AR = the number of events that occur in a group / number of people in that groupThe absolute risk reduction (ARR) is the difference between the absolute risk in the control group (ARC) and the absolute risk in the treated group (ART). ARR = ARC – ARTThe control group is the warfarin group, therefore the ARC is 20/500 (0.04). Treatment group is the ticagrelor group and ART = 30/300 (0.1). ARR = 0.04 – 0.1 = -0.06. This shows that treatment with ticagrelor increases risk of developing stroke. This is also termed a relative risk increase.Relative risk, or risk ratio, (RR) is used to compare the risk in the two different groups. It is the ratio of the absolute risks of the disease in the treatment group (ART) to the absolute risk of the disease in the control group (ARC):RR=ART /ARCTherefore RR = 0.1 / 0.04 = 2.5RR < 1 means the intervention reduces the risk of the outcome being studiedRR = 1 means the treatment has no effect on the outcome being studiedRR > 1 means the intervention increased the risk of the outcome being studiedSince RR is 2.5, ticagrelor increases the risk of stroke.SUMMARYAbsolute risk reduction is -0.06Absolute risk in warfarin group = 0.04Relative risk = 2.5Ticagrelor has no effect on stroke is incorrect because RR is not =1

Infectious mononucleosis is caused by Epstein-Barr virus (EBV). The incubation period for EBV varies from 2 weeks to 2 months.The usual incubation period for rubella is 14 days; with a range of 12 to 23 days.Gonorrhoea has a short incubation period of approximately 2 to 7 days.The mumps virus can be isolated from infected saliva and swabs rubbed over the Stensen’s duct from 9 days before onset of symptoms until 8 days after parotitis appears.Scarlet fever, which appears within 1 to 2 days after bacterial infection, is characterized by a diffuse red rash that appears on the upper chest and spreads to the trunk and extremities. The rash disappears over the next 5 to7 days and is followed by desquamation.

N. meningitidis, the causative agent of meningococcal meningitis, is considered both a commensal and a pathogen. It can be found in the surfaces of mucous membranes such as the nasopharynx and oropharynx. With this, it can be transmitted from a carrier to a new host via respiratory droplet secretions.

Nitrates are used in the treatment of angina pectoris and the prevention of myocardial ischaemia. Commonly used examples of nitrates are glyceryl trinitrate and isosorbide dinitrate. Unwanted effects, however, are common and can limit therapy, particularly when angina is severe or when patients are unusually sensitive to the effects of nitrates.The following are common or very common side effects of nitratesArrhythmiasAstheniaCerebral ischaemiaDizzinessDrowsinessFlushingHeadacheHypotensionNausea and vomitingDiarrhoea, syncope and cyanosis can occur, but these are rare side effects. Dry eyes, bradycardia and metabolic acidosis have not been reported.

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.

Continuous capillaries, found in the skin, lungs, muscles and CNS, are the most selective with low permeability, as junctions between the endothelial cells are very tight, restricting the flow of molecules with MW > 10,000.

Bence Jones proteins are monoclonal immunoglobulin light chains found in urine (and plasma) of some patients with myeloma. Because of their relatively small size, light chains are readily excreted into the urine. The presence of significant amounts of Bence Jones proteins in urine is indicative of malignant B cell proliferation.

Pectoralis minor is a thin, triangular muscle that is situated in the upper chest. It is thinner and smaller than pectoralis major. It is innervated by the medial pectoral nerve.The origin of pectoralis minor is the 3rdto the 5thribs, near the costal cartilages. It inserts into the medial border and superior surface of the coracoid process of the scapula.The main action of pectoralis minor is to draw the scapula inferiorly and anteriorly against the thoracic wall. This serves to stabilise the scapula.

Diabetes insipidus is the inability to produce concentrated urine. It is characterised by the presence of excessive thirst, polyuria and polydipsia. There are two distinct types of diabetes insipidus:Cranial (central) diabetes insipidus and;Nephrogenic diabetes insipidusCranial diabetes insipidus is caused by a deficiency of vasopressin (anti-diuretic hormone). Patients with cranial diabetes insipidus can have a urine output as high as 10-15 litres per 24 hours, but adequate fluid intake allows most patients to maintain normonatraemia. 30% of cases are idiopathic, and a further 30% are secondary to head injuries. Other causes include neurosurgery, brain tumours, meningitis, granulomatous disease (e.g. sarcoidosis) and drugs, such as naloxone and phenytoin. A very rare inherited form also exists that is associated with diabetes mellitus, optic atrophy, nerve deafness and bladder atonia.Nephrogenic diabetes insipidus is caused by renal resistance to the action of vasopressin. As with cranial diabetes insipidus, urine output is markedly elevated. Serum sodium levels can be maintained by secondary polydipsia or can be elevated. Causes of nephrogenic diabetes insipidus include chronic renal disease, metabolic disorders (e.g. hypercalcaemia and hypokalaemia) and drugs, including long-term lithium usage and demeclocycline.In view of the history of long-term lithium use, in this case, nephrogenic diabetes insipidus is the most likely diagnosis.

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.

Signs and symptoms of Sickle cell disease(SCD):Acute and chronic pain: The most common clinical manifestation of SCD is vaso-occlusive crisis; pain crises are the most distinguishing clinical feature of SCDBone pain: Often seen in long bones of extremities, primarily due to bone marrow infarctionAnaemia: Universally present, chronic, and haemolytic in natureAplastic crisis: Serious complication due to infection with parvovirus B19 (B19V)Splenic sequestration: Characterized by the onset of life-threatening anaemia with rapid enlargement of the spleen and high reticulocyte countInfection: Organisms that pose the greatest danger include encapsulated respiratory bacteria, particularly Streptococcus pneumoniae; adult infections are predominantly with gram-negative organisms, especially SalmonellaGrowth retardation, delayed sexual maturation, being underweightHand-foot syndrome: This is a dactylitis presenting as bilateral painful and swollen hands and/or feet in childrenAcute chest syndrome: Young children present with chest pain, fever, cough, tachypnoea, leucocytosis, and pulmonary infiltrates in the upper lobes; adults are usually afebrile, dyspnoeic with severe chest pain, with multilobar/lower lobe diseasePulmonary hypertension: Increasingly recognized as a serious complication of SCDAvascular necrosis of the femoral or humeral head: Due to vascular occlusionCentral nervous system (CNS) involvement: Most severe manifestation is strokeOphthalmologic involvement: Ptosis, retinal vascular changes, proliferative retinitisCardiac involvement: Dilation of both ventricles and the left atriumGastrointestinal involvement: Cholelithiasis is common in children; liver may become involvedGenitourinary involvement: Kidneys lose concentrating capacity; priapism is a well-recognized complication of SCDDermatologic involvement: Leg ulcers are a chronic painful problem

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.

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.

When you take too much aspirin, you have a mix of respiratory alkalosis and metabolic acidosis. Respiratory centre stimulation produces hyperventilation and respiratory alkalosis in the early phases. The direct acid actions of aspirin tend to create a higher anion gap metabolic acidosis in the latter phases.Below summarizes some of the most common reasons of acid-base abnormalities:Respiratory alkalosis: – Hyperventilation (e.g. anxiety, pain, fever)- Pulmonary embolism- Pneumothorax- CNS disorders (e.g. CVA, SAH, encephalitis)- High altitude- Pregnancy- Early stages of aspirin overdoseRespiratory acidosis:- COPD- Life-threatening asthma- Pulmonary oedema- Respiratory depression (e.g. opiates, benzodiazepines)- Neuromuscular disease (e.g. Guillain-Barré syndrome, muscular dystrophy- Incorrect ventilator settings (hypoventilation)- ObesityMetabolic alkalosis:- Vomiting- Cardiac arrest- Multi-organ failure- Cystic fibrosis- Potassium depletion (e.g. diuretic usage)- Cushing’s syndrome- Conn’s syndromeMetabolic acidosis (with raised anion gap):- Lactic acidosis (e.g. hypoxaemia, shock, sepsis, infarction)- Ketoacidosis (e.g. diabetes, starvation, alcohol excess)- Renal failure- Poisoning (e.g. late stages of aspirin overdose, methanol, ethylene glycol)Metabolic acidosis (with normal anion gap):- Renal tubular acidosis- Diarrhoea- Ammonium chloride ingestion- Adrenal insufficiency

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.

Compression of the median nerve in the carpal tunnel will result in weakness and atrophy of the thenar muscles – resulting in weakness of opposition, abduction and flexion of the thumb at the metacarpophalangeal joint and anaesthesia or paraesthesia over the distribution of the palmar digital branch of the median nerve (skin over the palmar surface and fingertips of the lateral three and a half digits). The adductor pollicis muscle is innervated by the ulnar nerve, and abduction of the fingers is produced by the interossei, also innervated by the ulnar nerve. Flexion of the interphalangeal joint of the thumb is produced by the flexor pollicis longus, and flexion of the distal interphalangeal joint of the index finger is produced by the flexor digitorum profundus. Median nerve injury at the wrist will not affect the long flexors of the forearm as these are innervated by the anterior interosseous nerve which arises in the proximal forearm.

In most cases of atrial flutter, ventricular rate control is used as a stopgap measure until sinus rhythm is restored. A beta-blocker (e.g. bisoprolol), diltiazem, or verapamil can be used to reduce the rate of contractions in the heart.Electrical cardioversion, pharmacological cardioversion, and catheter ablation can all be used to return the heart to a normal rhythm. Cardioversion should not be attempted until the patient has been fully anticoagulated for at least three weeks if the duration of atrial flutter is unknown or it has lasted longer than 48 hours. Emergency electrical cardioversion is the treatment of choice when there is a sudden onset of symptoms and haemodynamic compromise. For recurrent atrial flutter, catheter ablation is preferred.Verapamil is a calcium-channel blocker that is non-dihydropyridine phenylalkylamine and can be used to treat supraventricular arrhythmias. It’s a calcium channel blocker with a high negative inotropic effect that lowers cardiac output, slows the heart rate, and may impair atrioventricular conduction. At high doses, it can cause heart failure, exacerbate conduction disorders, and cause hypotension.Adults should take 240-480 mg of verapamil in 2-3 divided doses. 5-10 mg IV over 30 seconds is the corresponding intravenous (IV) dose. After an IV injection, the peak effect lasts 3-5 minutes, and the action lasts 10-20 minutes.Verapamil should not be taken with beta-blockers like atenolol or quinidine because the combination of their negatively inotropic and negatively chronotropic effects can result in severe hypotension, bradycardia, impaired atrioventricular conduction, heart failure (due to impaired cardiac contractility), and sinus arrest.The use of verapamil is contraindicated in the following situations:Acute porphyrias are a type of porphyria that occurs suddenly.Accessory conducting pathways are linked to atrial flutter or fibrillation (e.g. Wolff-Parkinson-White-syndrome)BradycardiaShock caused by the heartInsufficiency of the heart (with reduced ejection fraction)Left ventricular function has been significantly harmed in the past (even if controlled by therapy)Hypotension (blood pressure less than 90 mmHg)AV block in the second and third degreesSinusitis is a condition in which the sinuses becomeSino-atrial occlusion

Antibiotics that are bactericidal kill bacteria, while antibiotics that are bacteriostatic limit their growth or reproduction. The antibiotics grouped into these two classes are summarized in the table below:Bactericidal antibioticsBacteriostatic antibioticsVancomycinMetronidazoleFluoroquinolone, such as ciprofloxacinPenicillins, such as benzylpenicillinCephalosporin, such as ceftriaxoneCo-trimoxazoleTetracyclines, such as doxycyclineMacrolides, such as erythromycinSulphonamides, such as sulfamethoxazoleClindamycinTrimethoprimChloramphenicol

Epstein-Barr virus causes infectious mononucleosis which is a clinical entity characterized by sore throat, cervical lymph node enlargement, fatigue and fever. It is accompanied by atypical large peripheral blood lymphocytes. These atypical lymphocytes, also known as Downey cells, are actually activated CD8 T lymphocytes, most of which are responding to EBV-infected cells.

Hyperkalaemia causes a rapid reduction in resting membrane potential leading to increased cardiac depolarisation and muscle excitability. This in turn results in ECG changes which can rapidly progress to ventricular fibrillation or asystole. Very distinctive ECG changes that progressively change as the K+level increases:K+>5.5 mmol/l – peaked T waves (usually earliest sign of hyperkalaemia), repolarisation abnormalitiesK+>6.5 mmol/l – P waves widen and flatten, PR segment lengthens, P waves eventually disappearK+>7.0 mmol/l – Prolonged QRS interval and bizarre QRS morphology, conduction blocks (bundle branch blocks, fascicular blocks), sinus bradycardia or slow AF, development of a sine wave appearance (a pre-terminal rhythm)K+>9.0 mmol/l – Cardiac arrest due to asystole, VF or PEA with a bizarre, wide complex rhythm.

Conjunctivitis is the most common neonatal manifestation of Chlamydia trachomatis infection. The second commonest neonatal manifestation is pneumoniaOphthalmia neonatorum refers to any conjunctivitis in the newborn period, irrespective of causative organism. Presently, chlamydia is the single most common cause, accounting for up to 40% of cases. Ophthalmia neonatorum caused by chlamydia typically presents 5 to 14 days after birth with unilateral or bilateral watery discharge that progressively becomes more copious and purulent. There is no associated risk of ulceration and perforation, and the eyes are less inflamed.

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.

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