Lidocaine is a tertiary amine that is primarily used as a local anaesthetic but can also be used intravenously in the treatment of ventricular dysrhythmias.Lidocaine works as a local anaesthetic by diffusing in its uncharged base form through neural sheaths and the axonal membrane to the internal surface of the cell membrane sodium channels. Here it alters signal conduction by blocking the fast voltage-gated sodium channels. With sufficient blockage, the membrane of the postsynaptic neuron will not depolarise and will be unable to transmit an action potential, thereby preventing the transmission of pain signals.Each 1 ml of plain 1% lidocaine solution contains 10 mg of lidocaine hydrochloride. The maximum safe dose of plain lidocaine is 3 mg/kg. When administered with adrenaline 1:200,000, the maximum safe dose is 7 mg/kg. Because of the risk of vasoconstriction and tissue necrosis, lidocaine should not be used in combination with adrenaline in extremities such as fingers, toes, and the nose.The half-life of lidocaine is 1.5-2 hours. Its onset of action is rapid within a few minutes, and it has a duration of action of 30-60 minutes when used alone. Its duration of action is prolonged by co-administration with adrenaline (about 90 minutes).Lidocaine tends to cause vasodilatation when used locally. This is believed to be due mainly to the inhibition of action potentials via sodium channel blocking in vasoconstrictor sympathetic nerves.

A histogram is used to demonstrate the distribution of continuous quantitative data. It is a very familiar graphical display device for representing the distribution of a single batch of data. The range of the data is divided into class intervals or bins, and the number of values falling into each interval is counted. The histogram then consists of a series of rectangles whose widths are defined by the class limits implied by the binwidths, and whose heights depend on the number of values in each bin. Histograms quickly reveal such attributes of the data distribution as location, spread, and symmetry. If the data are multimodal (i.e., more than one “hump” in the distribution of the data), this is quickly evident as well.

Raised platelet levels have emerged as a cancer risk marker, according to a large population-based study published in 2017(link is external). According to the study, 12 percent of men and 6% of women with thrombocytosis were diagnosed with cancer within a year. These figures increased to 18% in men and 10% in women if a second platelet count was taken within 6 months of the first and showed an increased or stable elevated platelet count.The researchers discovered that thrombocytosis linked to cancer is most common in colorectal and lung cancers, and it is linked to a worse prognosis. Furthermore, one-third of the cancer patients in the study had no other symptoms that would have prompted an immediate cancer referral.The exact mechanism by which these cancers cause thrombocytosis is unknown, but one theory proposes the existence of pathogenic feedback loops between malignant cells and platelets, with a reciprocal interaction between tumour growth and metastasis, as well as thrombocytosis and platelet activation. Another hypothesis is that thrombocytosis occurs independently of cancer but aids in its spread and progression.The findings show that routinely testing for thrombocytosis could cut the time it takes to diagnose colorectal and lung cancer by at least two months. In the UK, this could result in around 5500 earlier cancer diagnoses per year.Because the positive predictive value of thrombocytosis in middle age for cancer (10%) is higher than the positive predictive value for a woman in her 50s presenting with a new breast lump (8.5%), this is clearly an important research paper that should be used to adjust future clinical practise. The current NICE guidelines predate these new research findings, so we’ll have to wait and see how they affect cancer referral guidelines in the UK.Because there are so many possible cancers associated with thrombocytosis, the treating clinician should take a thorough history and perform a thorough clinical examination if a patient is diagnosed with it. Further investigation and the most appropriate referral route should be aided by this information.It’s worth noting that the patients in the study had their blood tests done for a medical reason rather than as a random screening test.If there are no other symptoms to guide investigation and referral (one-third of the patients in the study had no other symptoms), keep in mind that the two most common cancers encountered were colorectal and lung cancer, so a chest X-ray and a faecal immunochemical test (FIT) for faecal blood may be reasonable initial investigations.

Primary hyperaldosteronism occurs when there are excessive levels of aldosterone independent of the renin-angiotensin axis. Secondary hyperaldosteronism occurs due to high renin levels.The causes of primary hyperaldosteronism include:Adrenal adenoma (Conn’s syndrome) – the most common cause of hyperaldosteronism (,80% of all cases). These are usually unilateral and solitary and are more common in women.Adrenal hyperplasia – this accounts for ,15% of all cases. Usually, bilateral adrenal hyperplasia (BAH) but can be unilateral rarely. More common in men than women.Adrenal cancer – a rare diagnosis but essential not to missFamilial aldosteronism – a rare group of inherited conditions affecting the adrenal glandsThe causes of secondary hyperaldosteronism include:Drugs – diureticsObstructive renal artery disease – renal artery stenosis and atheromaRenal vasoconstriction – occurs in accelerated hypertensionOedematous disorders – heart failure, cirrhosis and nephrotic syndromePatients are often asymptomatic. When clinical features are present, the classically described presentation of hyperaldosteronism is with:HypertensionHypokalaemiaMetabolic alkalosisSodium levels can be normal or slightly raisedOther, less common, clinical features include:LethargyHeadachesMuscle weakness (from persistent hypokalaemia)Polyuria and polydipsiaIntermittent paraesthesiaTetany and paralysis (rare)Often the earliest sign of hyperaldosteronism is from aberrant urea and electrolytes showing hypokalaemia and mild hypernatraemia. If the patient is taking diuretics, and the diagnosis is suspected, these should be repeated after the patient has taken off diuretics.If the diagnosis is suspected, plasma renin and aldosterone levels should be checked. Low renin and high aldosterone levels (with a raised aldosterone: renin ratio) is suggestive of primary aldosteronism.If the renin: aldosterone ratio is high, then the effect of posture on renin, aldosterone and cortisol can be investigated to provide further information about the underlying cause of primary hyperaldosteronism. Levels should be measured lying at 9 am and standing at noon:If aldosterone and cortisol levels fall on standing, this is suggestive of an ACTH dependent cause, e.g. adrenal adenoma (Conn’s syndrome)If aldosterone levels rise and cortisol levels fall on standing, this is suggestive of an angiotensin-II dependent cause, e.g. BAHOther investigations that can help to distinguish between an adrenal adenoma and adrenal hyperplasia include:CT scanMRI scanSelective adrenal venous sampling

Caput medusae is a condition that consists of collateral veins radiating from the umbilicus and results from recanalization of the umbilical vein.Under normal conditions, the portal venous blood traverses the liver and drains into the inferior vena cava of the systemic venous circulation by way of the hepatic veins. This is the direct route. However, other, smaller communications exist between the portal and systemic systems, and they become important when the direct route becomes blocked. These communications are as follows:At the lower third of the oesophagus, the oesophageal branches of the left gastric vein (portal tributary) anastomose with the oesophageal veins draining the middle third of the oesophagus into the azygos veins (systemic tributary).Halfway down the anal canal, the superior rectal veins (portal tributary) draining the upper half of the anal canal anastomosis with the middle and inferior rectal veins (systemic tributaries), which are tributaries of the internal iliac and internal pudendal veins, respectively.The paraumbilical veins connect the left branch of the portal vein with the superficial veins of the anterior abdominal wall (systemic tributaries). The paraumbilical veins travel in the falciform ligament and accompany the ligamentum teres.The veins of the ascending colon, descending colon, duodenum, pancreas, and liver (portal tributary) anastomose with the renal, lumbar, and phrenic veins (systemic tributaries).

When the concentration of intracellular Ca2+rises, muscle contraction occurs. The pathway of an action potential is down tube-shaped invaginations of the sarcolemma called T-tubules (transverse tubules). These penetrate throughout the muscle fibre and lie adjacent to the terminal cisternae of the sarcoplasmic reticulum. The voltage changes in the T-tubules result in the opening of sarcoplasmic reticulum Ca2+channels and there is there is release of stored Ca2+into the sarcoplasm. Thus muscle contraction occurs via excitation-contraction coupling (ECC) mechanism.

Some potential symptoms of frontal lobe damage can include loss of movement, either partial or complete, on the opposite side of the body. In the patient’s case, it is a result of motor cortex damage on the right side since her left side of the body is affected. The conjugate eye deviation symptom towards the side of the lesion is a result of damage to the frontal eye field.

Bias is the term used to describe an error at any stage of the study that was not due to chance. Bias leads to the systematic difference between the results from a study and the true states of affair. Bias may be introduced at all stages of the research process, from study design, through to analysis and publication. Bias can create a spurious association or mask a real association.Good research design can reduce the effect of bias (e.g. blinding, randomisation) but they cannot eliminate it completely. Increasing the sample size does not reduce bias.

Hyoscine butylbromide is an antispasmodic drug that blocks muscarinic receptors and reduces intestinal motility. It is used for gastrointestinal and genitourinary smooth muscle spasms and symptomatic relief of IBS.It has the following side-effects:1. Constipation2. Dizziness3. Drowsiness4. Dry mouth5. Dyspepsia6. Flushing7. Headache8. Nausea and vomiting9. Palpitations10. Skin reactions11. Tachycardia12. Urinary disorders13. Disorders of vision

The hookworm life cycle begins with the passage of eggs from an adult host into the stool. Hookworm eggs hatch in the soil to release larvae that mature into infective larvae. Infection is usually transmitted by larval penetration into human skin (duodenal infection may also be transmitted by the oral route). From the skin, larvae migrate into the blood vessels and are carried to the lungs, where they penetrate the pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed.

Pericardiocentesis is a procedure done to remove fluid build-up in the sac around the heart known as the pericardium. The pericardium can be tapped from almost any reasonable location on the chest wall. However, for the usual blind pericardiocentesis, the subxiphoid approach is preferred. Ideally, 2-D echocardiography is used to guide needle insertion and the subsequent path of the needle/catheter.In the subxiphoid approach, the needle is inserted 1 cm inferior to the left xiphocostal angle with an angle of 30 degrees from the patient’s chest with a direction towards the left mid-clavicle. The fingers may sense a distinct give when the needle penetrates the parietal pericardium. Successful removal of fluid confirms the needle’s position.

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.

Insulin is produced by beta cells, located centrally within the islets of Langerhans, in the endocrine tissues of the pancreas. Insulin is a polypeptide hormone consisting of two short chains (A and B) linked by disulphide bonds. Proinsulin is synthesised as a single-chain peptide. Within storage granules, a connecting peptide (C peptide) is removed by proteases to yield insulin. Insulin release is stimulated initially during eating by the parasympathetic nervous system and gut hormones such as secretin, but most output is driven by the rise in plasma glucose concentration that occurs after a meal. The effects of insulin are mediated by the receptor tyrosine kinase.

The anterior triangle is the triangular area of the neck found anteriorly to the sternocleidomastoid muscle. It is formed by the anterior border of sternocleidomastoid laterally, the median line of the neck medially and by the inferior border of the mandible superiorly. The apex of the anterior triangle extends towards the manubrium sterni. The anterior triangle contains:Muscles: thyrohyoid, sternothyroid, sternohyoid musclesOrgans: thyroid gland, parathyroid glands, larynx, trachea, esophagus, submandibular gland, caudal part of the parotid glandArteries: superior and inferior thyroid, common carotid, external carotid, internal carotid artery (and sinus), facial, submental, lingual arteriesVeins: anterior jugular veins, internal jugular, common facial, lingual, superior thyroid, middle thyroid veins, facial vein, submental vein, lingual veinsNerves: vagus nerve (CN X), hypoglossal nerve (CN XII), part of sympathetic trunk, mylohyoid nerveThe posterior triangle is a triangular area found posteriorly to the sternocleidomastoid muscle. It has three borders; anterior, posterior and inferior borders. The anterior border is the posterior margin of the sternocleidomastoid muscle. The posterior border is the anterior margin of the trapezius muscle, while the inferior border is the middle one-third of the clavicle. The investing layer of deep cervical fascia and integument forms the roof of the space, while the floor is covered with the prevertebral fascia along with levator scapulae, splenius capitis and the scalene muscles. The inferior belly of omohyoid subdivides the posterior triangle into a small supraclavicular, and a large occipital, triangle.Contents:Vessels: the third part of the subclavian artery, suprascapular and transverse cervical branches of the thyrocervical trunk, external jugular vein, lymph nodesNerves: accessory nerve (CN XI), the trunks of the brachial plexus, fibers of the cervical plexus

The stages of wound healing are: haemostasis, inflammatory, proliferative and remodelling (maturation) phases in that order. The first stage in the healing process of a laceration is haemostasis. Haemostasis is the process of the wound being closed by clotting. The inflammatory phase occurs just after and up to 48 hours after injury– Blood vessels dilate to allow white blood cells, antibodies, growth factors, enzymes and nutrients to reach the wounded area leading to the characteristic signs of inflammation seen. Epithelialisation and angiogenesis are not phases of wound healing but occur during the proliferative phase. This ia after haemolysis and inflammation phases have occurred.The maturation phase is the final phase and occurs when the wound has closed. It involves remodelling of collagen from type III to type I. Apoptosis remove unwanted cells, cellular activity reduces and the number of blood vessels in the wounded area regresses and decreases. This can continues for up to 1 year after injury.

Prevention of spread of measles is extremely important and infected patients should be isolated. The infectious stage is from 3 days before the rash emerges and patients are advised to stay away from school/nursery/work for 4 days from onset of the rash.

Pathogenicity is the ability to cause disease.

The composition of immunoglobulin molecules is two identical heavy and two identical light chains. These chains are linked by disulphide bridges and are each have highly variable regions which give the immunoglobulin its specificity. In addition, they have constant regions and there is virtual complete correspondence in amino acid sequence in all antibodies of a given isotype. Five isotypes of immunoglobulin exist – these are IgG, IgA, IgM, IgE and IgD. They are determined by the heavy chain (gamma, alpha, mu, epsilon or delta respectively). The light chains are either kappa or lambda.

The pectoralis minor, in comparison to the pectoralis major, is much thinner and triangular in shape and resides below the major. It originates from the margins of the third to fifth ribs adjacent to the costochondral junction. The fibres consequently pass upward and laterally to insert into the medial border and superior surface of the coracoid process. It is crucial in the stabilization of the scapula by pulling it downward and anteriorly against the thoracic wall.Arterial supply to the pectoralis minor also derives from the pectoral branch of the thoracoacromial trunk. Nerve supply of the pectoralis minor is a function of the lateral pectoral nerve and the medial pectoral nerve.

Bumetanide is primarily used in patients with heart failure who have failed to respond to high doses of furosemide. Bumetanide and furosemide differ primarily in terms of bioavailability and pharmacodynamic potency. In the intestine, furosemide is only partially absorbed, with a bioavailability of 40-50 percent. Bumetanide, on the other hand, is almost completely absorbed in the intestine and has a bioavailability of about 80%. As a result, when it has a better bioavailability than furosemide, it is commonly used in patients with gut oedema.When taken alone, Bendroflumethiazide is a moderately potent diuretic that is unlikely to control her oedema.Mannitol is a type of osmotic diuretic used to treat cerebral oedema and high intracranial pressure.Acetazolamide is a weak diuretic that inhibits carbonic anhydrase. It’s a rare occurrence.

The following are organisms that are capable of producing acute, bloody diarrhoea:- Campylobacter jejuni- Escherichia coli O157:H7- Salmonella species- Shigella species- Yersinia species- Entamoeba histolyticaOther E. coli strains, Giardia, Vibrio, and other parasites are associated with watery, but not bloody, diarrhoea.

Oxygen saturation should be 94 – 98% in most acutely ill patients with a normal or low arterial carbon dioxide (PaCO2). In some clinical situations, however, like cardiac arrest and carbon monoxide poisoning, it is more appropriate to aim for the highest possible oxygen saturation until the patient is stable.

The primary hip extensors are the gluteus maximus and the hamstrings such as the long head of the biceps femoris, the semitendinosus, and the semimembranosus. The extensor head of the adductor magnus is also considered a primary hip extensor.The hip abductor muscle group is located on the lateral thigh. The primary hip abductor muscles include the gluteus medius, gluteus minimus, and tensor fasciae latae.The secondary hip abductors include the piriformis, sartorius, and superior fibres of the gluteus maximus.

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

Dietary fat is chiefly composed of triglycerides (esters of free fatty acids and glycerol which may be saturated or unsaturated). The essential fatty acids are linoleic acid and alpha-linoleic acid, which cannot be manufactured in the body. Dietary fat provides 37 kJ (9 kcal) of energy per gram. Fats are digested almost entirely in the small intestine and are only released from the stomach into the duodenum at the rate at which they can be digested.Pancreatic lipase is the most significant enzyme for fat digestion. In the duodenum fat is emulsified by bile acids, a process where larger lipid droplets are broken down into much smaller droplets providing a greater surface area for enzymatic digestion. Micelles are arranged so that hydrophobic lipid molecules lie in the centre, surrounded by bile acids arranged such the outer region is hydrophilic. Dietary and synthesised lipids are incorporated into chylomicrons in the Golgi body, which are exocytosed from the basolateral membrane to enter lacteals and thus the lymphatic system.

Features of toxicity include:Increasing gastrointestinal disturbances (vomiting, diarrhoea, anorexia)Visual disturbancesPolyuria and incontinenceMuscle weakness and tremorTinnitusCNS disturbances (dizziness, confusion and drowsiness increasing to lack of coordination, restlessness, stupor)Abnormal reflexes and myoclonusHypernatraemiaWith severe overdosage (serum-lithium concentration > 2 mmol/L) seizures, cardiac arrhythmias (including sinoatrial block, bradycardia and first-degree heart block), blood pressure changes, electrolyte imbalance, circulatory failure, renal failure, coma and sudden death may occur.

The principal enzyme involved in lipid digestion is pancreatic lipase. It breaks down triglycerides into free fatty acids and monoglycerides. Pancreatic lipase works with the help of emulsifying agents secreted by the liver and the gallbladder. The main emulsifying agents are the bile acids, cholic acid and chenodeoxycholic acid. These are conjugated with the amino acids glycine and taurine to form bile salts. Bile salts are more soluble than bile acids and act as detergents to emulsify lipids. The free fatty acids and monoglycerides form tiny particles with these bile salts called micelles. The outer region of the micelle is water-attracting (hydrophilic), whereas the inner core is water-repelling (hydrophobic). This arrangement allows the micelles to enter the aqueous layers surrounding the microvilli and free fatty acids and monoglycerides to diffuse passively into the small intestinal cells.Pancreatic amylase breaks down some carbohydrates (notably starch) into oligosaccharides. Chymotrypsin is a proteolytic enzyme that aids in digestion of proteinCarboxypeptidase hydrolyses the first peptide or amide bond at the carboxyl or C-terminal end of proteins and peptides

Metoclopramide is a dopamine-receptor antagonist. Blockade of inhibitory dopamine receptors in the GI tract may allow stimulatory actions of ACh at muscarinic synapses to predominate. Metoclopramide also blocks dopamine D2-receptors within the chemoreceptor trigger zone (CTZ). At high doses, it is also thought to have some 5-HT3antagonist activity.

All nephrons have their renal corpuscles in the renal cortex. Cortical nephrons have their renal corpuscles in the outer part of the cortex and relatively short loops of Henle. Juxtamedullary nephrons have their corpuscles in the inner third of the cortex, close to the corticomedullary junction, with long loops of Henle extending into the renal medulla.

Overuse of cortisol medication, as seen in the treatment of patients with chronic asthma or rheumatoid arthritis, can cause Cushing’s syndrome. Weight gain, thin arms and legs, a round face, increased fat around the base of the neck, a fatty hump between the shoulders, easy bruising, wide purple stretch marks primarily on the abdomen, breasts, hips, and under the arms, weak muscles, hirsutism, hypertension, erectile dysfunction, osteoporosis, frontal alopecia, acne, depression, poor wound healing, and polycythaemia are all clinical features of Cushing’s syndrome.