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.

The glossopharyngeal nerve, which is responsible for the afferent pathway of the gag reflex, the vagus nerve, which is responsible for the efferent pathway of the gag reflex, and the spinal accessory nerve all exit the skull through the jugular foramen. These nerves are most frequently affected if the jugular foramen is compressed. As a result, the patient’s gag reflex is impaired. The vestibulocochlear nerve is primarily responsible for hearing. The trigeminal nerve provides sensation in the face. The facial nerve innervates the muscles of face expression (including those responsible for closing the eye). Tongue motions are controlled mostly by the hypoglossal nerve.

Amiodarone has a lot of potential toxic side effects, so it’s important to get a full clinical evaluation before starting treatment with it.The following are some of the most common amiodarone side effects:ArrhythmiasCorneal microdepositsHepatic disordersHyperthyroidismHypothyroidismHepatic disorders and jaundiceNauseaPeripheral neuropathyRespiratory disorders (including lung fibrosis)Sleep disturbanceSkin reactionsQT prolongationAmiodarone can cause optic neuritis, which is a very rare side effect. If this happens, the amiodarone should be stopped right away because it poses a risk of blindness.Most people who take amiodarone develop corneal microdeposits, which go away once the medication is stopped and rarely cause vision problems.Amiodarone has a chemical structure that is similar to that of thyroxine and can bind to the nuclear thyroid receptor. It can cause both hypothyroidism and hyperthyroidism, though hypothyroidism is far more common, with 5-10% of patients suffering from it.

Meta-analysis is a quantitative, formal, epidemiological study design used to systematically assess previous research studies to derive conclusions about that body of research. Outcomes from a meta-analysis may include a more precise estimate of the effect of treatment or risk factor for disease, or other outcomes, than any individual study contributing to the pooled analysis. The examination of variability or heterogeneity in study results is also a critical outcome.The benefits of meta-analysis include a consolidated and quantitative review of a large, and often complex, sometimes apparently conflicting, body of literature. The specification of the outcome and hypotheses that are tested is critical to the conduct of meta-analyses, as is a sensitive literature search.Important medical questions are typically studied more than once, often by different research teams in different locations. In many instances, the results of these multiple small studies of an issue are diverse and conflicting, which makes the clinical decision-making difficult. The need to arrive at decisions affecting clinical practise fostered the momentum toward evidence-based medicine. Evidence-based medicine may be defined as the systematic, quantitative, preferentially experimental approach to obtaining and using medical information. Therefore, meta-analysis, a statistical procedure that integrates the results of several independent studies, plays a central role in evidence-based medicine.

Damage to the femoral nerve results in weakness of hip flexion and knee extension and loss of sensation over the anterior thigh and the anteromedial knee, medial leg and medial foot.

Hepatitis B surface antigen (HBsAg) is a protein on the surface of the hepatitis B virus, that is the first serologic marker to appear in a new acute infection.It can be detected as early as 1 week and as late as 9 weeks. It can be detected in high levels in serum during acute or chronic hepatitis B virus infection. The presence of HBsAg indicates that the person is infectious. The body normally produces antibodies to HBsAg as part of the normal immune response to infection. HBsAg is the antigen used to make hepatitis B vaccine.Hepatitis B surface antibody (anti-HBs) indicates recovery and immunity from the hepatitis B virus infection. Anti-HBs also develops in a person who has been successfully vaccinated against hepatitis B.Total hepatitis B core antibody (anti-HBc): Appears at the onset of symptoms in acute hepatitis B and persists for life. The presence of anti-HBc indicates previous or ongoing infection with hepatitis B virus in an undefined time frame. It is not present following hepatitis B vaccination.IgM antibody to hepatitis B core antigen (IgM anti-HBc) indicates recent infection with hepatitis B virus (<6 months). Its presence indicates acute infection.The following table summarises the presence of hepatitis B markers according to each situation:Susceptible to infection:HBsAg = NegativeAnti-HBc = NegativeAnti-HBs = NegativeImmune due to natural infection:HBsAg = NegativeAnti-HBc = PositiveAnti-HBs = PositiveImmune due to vaccination:HBsAg = NegativeAnti-HBc = NegativeAnti-HBs = PositiveAcute infection:HBsAg = PositiveAnti-HBc = PositiveAnti-HBs = NegativeIgM anti-HBc = PositiveChronic infection:HBsAg = PositiveAnti-HBc = PositiveAnti-HBs = NegativeIgM anti-HBc = Negative

Cholera is caused by Vibrio cholerae, a motile, Gram-negative, curved bacillus. It is transmitted through water and food (especially seafood) and is primarily a disease seen in developing countries where there is poor sanitation and lack of safe water supplies.The cholera toxin leads to stimulation of adenyl cyclase, ADP-ribosylation of the G regulatory protein, inactivation of GTPase leading to active outpouring of NaCl. The cholera toxin consists of an A (the toxin) and B subunit. The B subunit attaches to the gut mucosa and presents the A subunit to the cell. The toxin stimulates adenyl cyclase by irreversible ADP-ribosylation of the GTP binding domain of adenyl cyclase leading to the opening of chloride channels resulting in an outpouring of NaCl and water into the lumen of the gut and causing secretory diarrhoea.Incubation period is between 2 and 5 days, but can be as short as just a few hours.

Anti-D is an IgG antibody that targets the antigen Rhesus D (RhD). Plasma from rhesus-negative donors who have been immunised against the anti-D-antigen is used to make anti-D immunoglobulin.Only RhD negative women are given Anti-D Ig. Women who are RhD negative do not have the RhD antigen on their RBC. If a foetus has the RhD antigen (i.e. is RhD positive) and the mother is exposed to foetal blood, she may develop antibodies to RhD that pass through the placenta and attack foetal red cells (resulting in newborn haemolytic disease). Anti-D is given to bind and neutralise foetal red cells in the maternal circulation before an immune response is triggered. In the event of a sensitising event, 500 IU Anti-D Ig should be administered intramuscularly. The following are examples of potentially sensitising events:BirthHaemorrhage during pregnancyMiscarriageEctopic pregnancyDeath within the wombAmniocentesisChorionic villus samplingTrauma to the abdomenThe sooner anti-D is given in the event of a sensitising event, the better; however, it is most effective within 72 hours, and the BNF states that it is still likely to have some benefit if given outside of this time frame.At 28 and 34 weeks, RhD negative women should receive routine antenatal prophylaxis. This is regardless of whether they have previously received Anti-D for a sensitising event during the same pregnancy.Prophylactic anti-D is not necessary before 12 weeks gestation, as confirmed by scan, in uncomplicated miscarriage (where the uterus is not instrumented), or mild, painless vaginal bleeding, as the risk of foeto-maternal haemorrhage (FMH) is negligible. In cases of therapeutic termination of pregnancy, whether by surgical or medical means, 250 IU of prophylactic anti-D immunoglobulin should be given to confirmed RhD negative women who are not known to be RhD sensitised.

The common carotid artery runs through the neck and divides into internal and external carotid arteries on both sides near the upper thyroid cartilage. In emergency situations, carotid sinus massage is also used to diagnose or treat paroxysmal supraventricular tachycardia. During the procedure, to maximize access to the carotid artery, the patient is put in a supine position with the neck extended (i.e. elevating the chin away from the chest). The carotid sinus is normally positioned inferior to the angle of the jaw, near the arterial impulse, at the level of the thyroid cartilage. For 5 to 10 seconds, pressure is administered to one carotid sinus. Although pulsatile pressure applied in a vigorous circular motion may be more effective, continuous pressure is preferred since it is more reproducible. If the predicted reaction is not obtained, the operation is repeated on the opposite side after a one- to two-minute wait.

Action potentials are transmitted to adjacent myocytes via gap junctions.

An acute focal or diffuse suppurative inflammation of the prostate gland is called acute bacterial prostatitis.According to the National Institute for Health and Care Excellence (NICE), acute prostatitis should be suspected in a man presenting with:A feverish illness of sudden onset which may be associated with rigors, arthralgia, or myalgia; Irritative urinary voiding symptoms; acute urinary retention; perineal or suprapubic pain and an exquisitely tender prostate on rectal examination.Treatment of acute prostatitis as recommended by NICE and the BNFare:Ciprofloxacin or ofloxacin for 14 daysAlternatively, trimethoprim can be used. Duration of treatment is still 14 days

Tombstoning ST elevation myocardial infarction can be described as a STEMI characterized by tombstoning ST-segment elevation. This myocardial infarction is associated with extensive myocardial damage, reduced left ventricle function, serious hospital complications and poor prognosis. Tombstoning ECG pattern is a notion beyond morphological difference and is associated with more serious clinical results.Studies have shown that tombstoning is more commonly found in anterior than non-anterior STEMI, thus, higher rates of left anterior descending artery disease are observed in patients with tombstoning pattern.The following ECG leads determine the location and vessels involved in myocardial infarction:ECG Leads Location Vessel involvedV1-V2 Septal wall Left anterior descendingV3-V4 Anterior wall Left anterior descendingV5-V6 Lateral wall Left circumflex arteryII, III, aVF Inferior wall Right coronary artery (80%) or Left circumflex artery (20%)I, aVL High lateral wall Left circumflex arteryV1, V4R Right ventricle Right coronary arteryV7-V9 Posterior wall Right coronary artery

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.

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

In hypokalaemia, initial potassium replacement therapy should not involve glucose infusions, as glucose may cause a further decrease in the plasma-potassium concentration. Glucose infusions are used for the other indications like diabetic ketoacidosis, hypoglycaemia, routine fluid maintenance in patients who are nil by mouth (very important in children), and in hyperkalaemia.

Hepatitis B vaccine should be stored at 35°-46° F (2°-8° C) and should not be frozen.There is no association between hepatitis B vaccination and Guillain-Barre syndrome. Infection with the bacterium Campylobacter jejuni is one of the most common risk factors for GBS. People can also develop GBS after having the flu or other infections (such as cytomegalovirus and Epstein Barr virus).Hepatitis B vaccine is prepared from initial concentration of surface antigen.To ensure adequate immunity, anti-HBs (HBsAb) titres may be checked 4-8 weeks following the last shot of the hepatitis B vaccine series.

General Practitioners are advised to give a single injection of benzylpenicillin by intravenous or intramuscular injection before transferring the patient urgently to the ED when bacterial meningitis is suspected.The recommended doses are:Infants under 1 year: 300 mgChildren ages 1 to 9 years: 600 mgChildren aged 10 years and over: 1.2gAdults: 1.2g

Predisposing factors for digoxin toxicity include hypoxia, hypercalcaemia, hypokalaemia and hypomagnesaemia There should also be care taken in the elderly who are particularly susceptible to digoxin toxicity. Hypokalaemia may be precipitated by use of diuretics. Hyponatremia can result in the development of other pathological disturbances, but it does not make digoxin toxicity worse.

Measles belongs to the paramyxoviridae group of viruses. The incubation period is 7-18 days (average 10) and it is spread by airborne or droplet transmission. The classical presentation is of a high fever with coryzal symptoms and photophobia with conjunctivitis often being present. The rash that is associated is a widespread erythematous maculopapular rash. Koplik spots are pathognomonic for measles, and are the presence of white lesions on the buccal mucosa.Differential diagnoses would include:RubellaRoseola infantum (exanthem subitom)Scarlet feverKawasaki diseaseErythema infectiosum (5thdisease)EnterovirusInfectious mononucleosisDiagnosis can be confirmed by the following means:Salivary swab for measles specific IgMSerum sample for measles specific IgMSalivary swab for RNA detectionPossible complications include:Otitis mediaFebrile convulsionsPneumoniaBronchiectasisDiarrhoeaMeningitisEncephalitisImmunosuppressionSubacute sclerosing panencephalitisDeath

Bone pain, pathologic fractures, weakness, anaemia, infection, hypercalcemia, spinal cord compression, and renal failure are all signs and symptoms of multiple myeloma (MM). The patient’s condition matched the signs and symptoms of myeloma.