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.

Loop diuretics inhibit the Na+/K+/2Cl- symporter on the luminal membrane in the thick ascending limb of the loop of Henle, thus preventing reabsorption of NaCl and water. These agents reduce reabsorption of Cl- and Na+ and increase Ca2+ excretion and loss of K+ and Mg2+.

Overdosing on calcium-channel blockers should always be taken seriously and regarded as potentially fatal. Verapamil and diltiazem are the two most lethal calcium channel blockers in overdose. These work by binding the alpha-1 subunit of L-type calcium channels, preventing calcium from entering the cell. In cardiac myocytes, vascular smooth muscle cells, and islet beta-cells, these channels play an important role.The standard ABC approach should be used to resuscitate all patients as needed. If life-threatening toxicity is expected, intubation and ventilation should be considered early on. If hypotension and shock are developing, early invasive blood pressure monitoring is recommended.The primary goal of specific treatments is to support the cardiovascular system. These are some of them:1. Fluid resuscitation: Give up to 20 mL of crystalloid per kilogramme of body weight.2. Calcium supplementationThis can be a good way to raise blood pressure and heart rate temporarily.via central venous access: 10% calcium gluconate 60 mL IV (0.6-1.0 mL/kg in children) or 10% calcium chloride 20 mL IV (0.2 mL/kg in children)Boluses can be given up to three times in a row.To keep serum calcium >2.0 mEq/L, consider a calcium infusion.3. Atropine: 0.6 mg every 2 minutes up to 1.8 mg is an option, but it is often ineffective.4. HIET (high-dose insulin-euglycemic therapy):The role of HIET in the step-by-step management of cardiovascular toxicity has changed.5. Vasoactive infusions:This was once thought to be a last-ditch measure, but it is now widely recommended that it be used sooner rather than later.Insulin with a short half-life 50 mL of 50 percent glucose IV bolus plus 1 U/kg bolus (unless marked hyperglycaemia present)Short-acting insulin/dextrose infusions should be continued.Glucose should be checked every 20 minutes for the first hour, then hourly after that.Regularly check potassium levels and replace if they fall below 2.5 mmol/L.Titrate catecholamines to effect (inotropy and chronotropy); options include dopamine, adrenaline, and/or noradrenaline infusions.6. Sodium bicarbonate: Use 50-100 mEq sodium bicarbonate (0.5-1.0 mEq/kg in children) in cases where a severe metabolic acidosis develops.7. Cardiac pacing: It can be difficult to achieve electrical capture, and it may not improve overall perfusion.Bypass AV blockade with ventricular pacing, which is usually done at a rate of less than 60 beats per minute.8. Intralipid transportCalcium channel blockers are lipid-soluble agents, so they should be used in refractory cases.

Isoniazid, a first-line agent for the treatment of tuberculosis, has the commonest side effect of peripheral neuropathy. It occurs in up to 20% of patients taking the drug at a dose > 6 mg/kg daily. Isoniazid combines with pyridoxine (vitamin B6) to form hydrazone, which is excreted in the urine. This causes a deficiency of biologically active pyridoxine leading to peripheral neuropathy.Peripheral neuropathy of isoniazid is prevented by the co-administration of pyridoxine at a dose of 10 mg for each 100 mg of isoniazid given.

Each pelvic bone is formed by three elements: the ilium (superiorly), the pubis (anteroinferiorly) and the ischium (posteroinferiorly).

The periurethral portion of the prostate gland increases in size during puberty and after the age of 55 years due to the growth of non-malignant cells in the transition zone of the prostate that surrounds the urethra. Most cancers develop in the posterior lobe, and cancers in this location may be palpated during a digital rectal examination (DRE).

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 ventilation/perfusion ratio (V/Q ratio) is a ratio used to assess the efficiency and adequacy of the matching ventilation and perfusion. The ideal V/Q ratio is 1.Any mismatch between ventilation and perfusion will be evident in the V/Q ratio. If perfusion is normal but ventilation is reduced, the V/Q ratio will be less than 1, whereas if ventilation is normal, but perfusion is reduced, the V/Q ratio will be greater than 1. If the alveoli were ventilated but not perfused at all, then the V/Q ratio would be infinity. The V/Q ratio is also affected by location. The various areas of the lungs have a different V/Q ratio since ventilation and perfusion increase from the apex to the base of the lungs. The apex of the lungs has a V/Q ratio of approximately 3.3.

AKI is diagnosed based on an acutely rising serum creatinine and/or reduction in urine output.

AKI can often be non-oliguric.

AKI is present if any one or more of the following criteria is met:

• A rise in serum creatinine of ≥26 micromol/L (≥0.3 mg/dL) within 48 hours
• A rise in serum creatinine to ≥1.5 times baseline, which is known or presumed to have occurred within the past 7 days (in practice you can use the lowest value from the past 3 months as the baseline for the patient)
• Urine volume <0.5 ml/kg/hour for at least 6 hours.

Dynamic compression occurs because as the expiratory muscles contract during forced expiration, all the structures within the lungs, including the airways, are compressed by the positive intrapleural pressure. Consequently the smaller airways collapse before the alveoli empty completely and some air remains within the lungs (the residual volume). Physiologically this is important as a completely deflated lung with collapsed alveoli requires significantly more energy to inflate. Dynamic compression does not occur in normal expiration because the intrapleural pressure is negative throughout the whole cycle.

Malaria is an infectious disease transmitted by female of theAnophelesgenus of mosquito. It is a parasitic infection caused by the genusPlasmodium. Five species are recognized as causing disease in humans;Plasmodium falciparum,Plasmodium ovale,Plasmodium vivax,Plasmodium malariaeandPlasmodium knowlesi.The classic symptom of malaria is the malarial paroxysm, a cyclical occurrence of a cold phase, where the patient experiences intense chills, a hot stage, where the patient feels extremely hot and finally a sweating stage, where the fever declines and the patient sweats profusely. On examination the patient may show signs of anaemia, jaundice and have hepatosplenomegaly without evidence of lymphadenopathy.Plasmodium falciparum is the most serious form and is responsible for most deaths. Severe or complicated malaria is suggested by the presence of impaired consciousness, seizures, hypoglycaemia, anaemia, renal impairment, respiratory distress and spontaneous bleeding.Plasmodium falciparum is the most likely type in this case in view of the presentation.Haemoglobinuria and renal failure following treatment is suggestive of blackwater fever, which is caused byPlasmodium falciparum. An autoimmune reaction between the parasite and quinine causes haemolysis, haemoglobinuria, jaundice and renal failure. This can be fatal.The benign malarias: P.vivax, P. malariae and P.ovale are usually treated with chloroquine. A course of primaquine is also required in P.vivax and P.ovale infection. Artesunate is the drug treatment of choice for Plasmodium falciparum malaria. Quinine can still be used where artesunate is not available. Often combination therapy with drugs such as doxycycline or fansidar is also required.

Insulin, a peptide hormone, is produced in the pancreas by the beta-cells of the islets of Langerhans.The beta-cells first synthesise an inactive precursor called preproinsulin which is converted to proinsulin by signal peptidases, which remove a signal peptide from the N-terminus. Proinsulin is converted to insulin by the removal of the C-peptide.Insulin has a short half-life in the circulation of about 5-10 minutes.Glucagon and parasympathetic stimulation stimulates insulin release.

Obstructive lung disorders are characterised by airway obstruction. Many obstructive diseases of the lung result from narrowing of the smaller bronchi and larger bronchioles, often because of excessive contraction of the smooth muscle itself.In obstructive lung disease, FEV1is reduced to <80% of normal and FVC is usually reduced but to a lesser extent than FEV1. The FEV1/FVC ratio is reduced to 80% in the presence of symptomsModerate airflow obstruction = FEV1of 50-79%Severe airflow obstruction = FEV1of 30-49%Very severe airflow obstruction = FEV1<30%.

Features of sickle cell disease include:Anaemia (symptoms are usually mild because the O2 dissociation curve of Hb S is shifted to the right)Vaso-occlusive crisisVisceral sequestration crisisAplastic crisisIncreased susceptibility to infectionOther clinical features: Pigment gallstones with cholecystitisChronic leg ulcersAvascular necrosis of the femoral and humeral heads or other bonesCardiomyopathyPulmonary hypertensionProliferative retinopathyPriapismRenal papillary necrosisStroke

25-year-old receives immunoglobulin and vaccination after cutting her hand on a drinking glass and not knowing her vaccination history.Because this is not a tetanus-prone wound, immunoglobulin is not recommended. Because you can’t be sure about her vaccination history, now is the best time to start a tetanus vaccination course to ensure coverage later in life. The first vaccination should be administered at the time of presentation; the patient’s own GP should then review the patient’s vaccination history and schedule the rest of the course as needed.8-year-old whose hand was cut with a kitchen knife, received her first round of vaccinations as a baby and a booster at the age of four – receives vaccination:The tetanus vaccinations for this child are up to date, and the next booster should not be given too soon. Immunoglobulin is not required because this is not a tetanus-prone wound.80-year-old diabetic, a rusty nail went through his shoe and into his foot while walking in the woods, and he was uncertain of his vaccination history – he received vaccination and immunoglobulin:A tetanus vaccination course may not have been completed by an 80-year-old UK resident (the vaccination was introduced in 1961). The vaccination should be given at a walk-in clinic, and the patient’s own GP should be contacted to confirm vaccination history and to schedule the rest of the course as needed. Because this is a tetanus-prone wound (puncture wound and potential soil contact), immunoglobulin would be recommended in a patient with incomplete tetanus vaccinations.A 28-year-old Polish man cuts his leg while working in the garden, the wound is heavily contaminated with soil, and his vaccination history is unknown – he receives vaccination:In a patient with an unknown vaccination history, this is a tetanus-prone wound. In this case, the best course of action would be to administer both the vaccination and immunoglobulin at the walk-in clinic, then contact the patient’s own GP to check his or her vaccination history and schedule the rest of the course as needed.30-year-old with a large amount of devitalized tissue in the torso from an electrical burn – has had all vaccinations, so no need for vaccination or immunoglobulin:Because this is a high-risk tetanus wound (with a lot of devitalized tissue), even if the patient has had a full course of vaccinations in the past, immunoglobulin is recommended. There is no need for any additional vaccinations.

Cushing’s syndrome is a group of symptoms and signs brought on by long-term exposure to high amounts of endogenous or exogenous glucocorticoids. Cushing’s syndrome affects about 10-15 persons per million, and it is more common in those who have had a history of obesity, hypertension, or diabetes.Cushing’s syndrome has a wide range of clinical manifestations that are dependent on the degree of cortisol overproduction. The appearance might be vague and the diagnosis difficult to detect when cortisol levels are just somewhat elevated. On the other hand, in long-term cases of severely increased cortisol levels, the presentation might be colourful and the diagnosis simple.Cushing’s syndrome has the following clinical features:Obesity and weight growth in the true senseSupraclavicular fat pads are fat pads that are located above the clavicle.Buffalo humpFullness and plethora of the face (‘moon facies’)Muscle atrophy and weakening at the proximal levelDiabetes mellitus, also known as impaired glucose toleranceHypertensionSkin thinning and bruisingDepressionHirsutismAcneOsteoporosisAmenorrhoea or oligomenorrhoeaCortisol levels fluctuate throughout the day, with the greatest levels occurring around 0900 hours and the lowest occurring at 2400 hrs during sleep. The diurnal swing of cortisol levels is lost in Cushing’s syndrome, and levels are greater during the whole 24-hour period. In the morning, levels may be normal, but they may be high at night-time, when they are generally repressed. As a result, random cortisol testing is not an effective screening technique and is not advised.The following are the two most common first-line screening tests:Cortisol levels in the urine are measured every 24 hours.A diagnosis of Cushing’s syndrome can be made if more than two collections measure cortisol excretion more than three times the upper limit of normal.Physical stress (e.g., excessive exercise, trauma), mental stress (e.g., sadness), alcohol or drug misuse, complex diabetes, and pregnancy can all cause false positives.Renal dysfunction, inadequate collection, and cyclical Cushing’s disease can all cause false negatives.The overnight low-dose dexamethasone suppression test (LDDST) involves giving 1 mg of dexamethasone at 11 p.m. and measuring blood cortisol levels at 8 a.m. the next day.Cushing’s syndrome is diagnosed when cortisol is not suppressed to less than 50 nmol/L.It might be difficult to tell the difference between mild Cushing’s disease and normal cortisol production.False positives can occur as a result of depression, severe systemic sickness, renal failure, prolonged alcohol misuse, old age, and the use of hepatic enzyme-inducing medicines, among other things.False negatives are extremely uncommon in Cushing’s disease patients.A characteristic biochemical picture might also be helpful in confirming the diagnosis of Cushing’s syndrome. The following are the primary characteristics:HypokalaemiaAlkalosis metabolique

Compliance changes at different lung volumes. Initially at lower lung volumes the compliance of the lung is poor and greater pressure change is required to cause a change in volume. This occurs if the lungs become collapsed for a period of time. At functional residual capacity (FRC) compliance is optimal since the elastic recoil of the lung tending towards collapse is balanced by the tendency of the chest wall to spring outwards. At higher lung volumes the compliance of the lung again becomes less as the lung becomes stiffer. At all volumes, the base of the lung has a greater compliance than the apex. Patients with emphysema have increased compliance. Compliance is affected by a person’s age, sex and height.

Ketamine is a dissociative anaesthetic with analgesic, amnesic, and hypnotic effects. It is the only anaesthetic agent which causes all three of these effects.Ketamine exerts its action by non-competitive antagonism at the NMDA (N-methyl-D-aspartate) receptor. Due to its analgesic property, Ketamine is given so that patients do not retain memories of short term procedures. Ketamine is used for the induction and maintenance of anaesthesia in general surgery and for treating burn wounds, battlefield injuries, and children who cannot tolerate other anaesthetic or analgesic agents.It can be given by both intravenous and intramuscular routes. Ketamine causes cardiac stimulation by increasing the sympathetic tone. The major side effect is increased intracranial pressure as an increase in the sympathetic tone causes vasoconstriction and an increase in the MAP.

Gastrin secretion is stimulated by: The presence of small peptides and amino acids in chymeGastric distensionVagal stimulation directly via acetylcholine and indirectly via gastrin-releasing peptide (GRP)Raised gastric pH

A positive correlation coefficient means that the two variables are directly proportional e.g. height and weight in healthy growing children.

Fick’s law tells us that the rate of diffusion of a gas increases: the larger the surface area involved in gas exchangethe greater the partial pressure gradient across the membranethe thinner the membranethe more soluble the gas in the membranethe lower the molecular weight of the gas

Magnesium carbonate is an over the counter antacid commonly used to relieve symptoms in ulcer dyspepsia and non-erosive gastro-oesophageal reflux.Antacids containing magnesium also tend to work as a laxative, while the antacids with aluminium may cause constipation. There is no significant increased risk of anaphylaxis, hepatotoxicity or renal impairment.

Infective causes of bloody diarrhoea include:Salmonella sppCampylobacter sppSchistosomiasisEntamoeba histolytica (Amoebiasis )Shigella sppClostridium difficileYersinia sppEnteroinvasive Escherichia coliEnterotoxigenic Escherichia coli is non-invasive and does not cause inflammation of the gut and bloody diarrhoea. It presents with copious watery diarrhoea and usually are not associated with abdominal cramping.

Opioids should be avoided in people who have: A risk of paralytic ileus (opioids reduce gastric motility)Acute respiratory depressionAn acute exacerbation of asthma (opioids can aggravate bronchoconstriction as a result of histamine release)Conditions associated with increased intracranial pressure including head injury (opioids can interfere with pupillary response making neurological assessment difficult and may cause retention of carbon dioxide aggravating the increased intracranial pressure)

IgA is the major Ig in secretions, particularly from the gastrointestinal tract (but also in saliva, tears, sweat and breast milk).IgE is important for mast cell degranulation in allergic and antiparasitic response. In the allergic response, the plasma cell produces IgE-antibodies, which, like antibodies of other immunoglobulin isotypes, are capable of binding a specific allergen via its Fab portion.IgG is the most abundant in plasma (comprising 80% of normal serum immunoglobulin) and the main circulatory Ig for the secondary immune response.

A posterior cerebral stroke will most likely result in a contralateral homonymous hemianopia with macular sparing.

Hyperacusis is increased acuity of hearing with hypersensitivity to low tones resulting from paralysis of the stapedius muscle, innervated by the facial nerve. General sensation to the face and to the anterior two-thirds of the tongue is carried by the divisions of the trigeminal nerve (although taste to the anterior two-thirds of the tongue is supplied by the facial nerve). Eye movements are mediated by the oculomotor, trochlear and abducens nerve. Ptosis results from paralysis of the levator palpebrae superioris, innervated by the oculomotor nerve, or the superior tarsal muscle, innervated by the sympathetic chain.

Even if there is no evidence of infection, prophylactic antibiotics should be administered for all human bite wounds that are less than 72 hours old. The first-line therapy is 7 days of co-amoxiclav. In penicillin-allergic people, metronidazole + doxycycline is an option. Streptococcus spp., Staphylococcus aureus, Haemophilus spp., Eikenella corrodens, Bacteroides spp., and other anaerobes are the most prevalent organisms found in human bites.

A history of stroke and poor nutritional status points towards a nutritional deficiency as the most likely cause of her symptoms. The examination would differentiate between Vitamin B12 and Folic acid deficiency as in the former. The patient has a beefy red tongue and symptoms indicating peripheral nervous system involvement or subacute combined spinal cord degeneration. The patient may also have a lemon-yellow skin colour, loss of proprioception and vibratory sense and oral ulceration. Investigations in B12 deficiency can reveal the following:1. Macrocytic anaemia2. Neutropoenia3. Thrombocytopaenia4. Blood film: anisocytosis, poikilocytosis5. Low serum B126. Raised serum bilirubin (haemolysis)7. Intrinsic factor antibodies8. Positive Schilling test

Patients with hypertension are only eligible for the seasonal influenza vaccination if they have co-existent cardiac complications.The UK national policy is that the seasonal influenza vaccine should be offered to the following groups:All those aged 65 years and olderChildren aged 2 to 15 yearsResidents of nursing and residential homes for the elderly (and other long-stay facilities)Carers of persons whose welfare may be at risk if the carer falls illAll those aged 6 months or older in a clinical risk groupThe following table outlines the clinical risk groups that are considered eligible for the vaccine:CategoryExamples of eligible groupsRespiratory diseaseCOPDInterstitial lung diseaseCystic fibrosisAsthma (requiring oral or inhaled steroids)Heart diseaseCongenital heart diseaseChronic heart failureCoronary heart disease (requiring medication and/or follow-up)Hypertension with cardiac complicationsKidney diseaseChronic kidney diseaseNephrotic syndromeRenal transplant patientsLiver diseaseLiver cirrhosisChronic hepatitisBiliary atresiaNeurological diseaseCerebrovascular accidentTransient ischaemic attackEndocrine diseaseType 1 and 2 diabetesImmunosuppressionPatients undergoing chemotherapyPatients taking immunosuppressive drug therapy (including systemic steroids)Asplenia or splenic dysfunctionHIV infectionPregnancyAll pregnant women