Klumpke palsy, named after Augusta Dejerine-Klumpke, is a neuropathy involving the lower brachial plexus. In contrast, the more common Erb–Duchenne palsy involves the more cephalic portion of the brachial plexus C5 to C6. The brachial plexus is a bundle of individual nerves that exit between the anterior and middle scalene muscles in the anterior lateral and basal portion of the neck. Although the most common anatomical presentation of the brachial plexus is between the anterior and middle scalene, there are variations, with the most common being penetration of the anterior scalene. The main mechanism of injury to the lower brachial plexus is hyper-abduction traction, and depending on the intensity, it will lead to signs and symptoms consistent with a neurological insult.The most common aetiology resulting in Klumpke palsy is a hyper-abduction trauma to the arm that has enough intensity to traction the lower brachial plexus. Trauma during birth can cause brachial plexus injuries, but again hyper-abduction and traction forces to the upper extremity are usually present.The history presented by the patient usually depicts a long axis hyper-abduction traction injury with high amplitude and velocity. The typical patient presentation is a decrease of sensation along the medial aspect of the distal upper extremity along the C8 and T1 dermatome. The patient might also present myotome findings that can range from decreasing muscular strength to muscular atrophy and positional deformity. For example, if the neurological damage has led to muscular atrophy and tightening, the patient may present with a claw hand. This deformity presents a finger and wrist flexion. The patient may also describe the severe pain that starts at the neck and travels down the medial portion of the arm. One other sign of a lower brachial plexus injury is Horner syndrome; because of its approximation to the T1 nerve root, it may damage the cephalic sympathetic chain. If this happens, the patient will develop ipsilateral ptosis, anhidrosis, and miosis.

In foreign body aspiration, the foreign body is more likely to enter the right main bronchus because it is shorter, wider and more vertical than the left main bronchus. In a patient who is standing or sitting, the foreign body tends to become lodged in the posterobasal segment of the inferior lobe of the right lung.

Factors decreasing FRC:Restrictive ventilatory defects e.g. pulmonary fibrosisPosture – lying supineIncreased intra-abdominal pressure (e.g. obesity, pregnancy, ascites)Reduced muscle tone of diaphragm e.g. muscle relaxants in anaesthesia, neuromuscular disease

Polydipsia is the feeling of extreme thirstiness. It is often linked to polyuria, which is a urinary condition that causes a person to urinate excessively. The cycle of these two processes makes the body feel a constant need to replace the fluids lost in urination. In healthy adults, a 3 liter urinary output per day is considered normal. A person with polyuria can urinate up to 15 liters of urine per day. Both of these conditions are classic signs of diabetes. The other options are also types of diabetes, except for psychogenic polydipsia (PPD), which is the excessive volitional water intake seen in patients with severe mental illness or developmental disability. However, given the patient’s previous head injury, the most likely diagnosis is cranial diabetes insipidus. By definition, cranial diabetes insipidus is caused by damage to the hypothalamus or pituitary gland after an infection, operation, brain tumor, or head injury. And the patient’s history confirms this diagnosis. To define the other choices, nephrogenic diabetes insipidus happens when the structures in the kidneys are damaged and results in an inability to properly respond to antidiuretic hormone. Kidney damage can be caused by an inherited (genetic) disorder or a chronic kidney disorder. As with cranial diabetes insipidus, nephrogenic diabetes insipidus can also cause an elevated urine output. Diabetes mellitus is classified into two types, and the main difference between them is that type 1 diabetes is a genetic disorder, and type 2 diabetes is diet-related and develops over time. Type 1 diabetes is also known as insulin-dependent diabetes, in which the pancreas produces little or no insulin. Type 2 diabetes is termed insulin resistance, as cells don’t respond customarily to insulin.

Flucloxacillin is unique in that it is beta-lactamase stable and it can be used in infections caused by beta-lactamase producing staphylococci e.g. S. aureus. It is acid-stable and can therefore be given by mouth as well as by injection. It is used first line for treatment of widespread impetigo infection, cellulitis, mastitis, osteomyelitis, septic arthritis, severe erysipelas, severe/spreading otitis externa and infective endocarditis caused by staphylococci. The most common adverse effects of flucloxacillin include nausea, vomiting, skin rash, and diarrhoea. Cholestatic jaundice and hepatitis may occur very rarely, up to two months after treatment with flucloxacillin has been stopped. Administration for more than 2 weeks and increasing age are risk factors. First line treatment of animal and human bites is co-amoxiclav.

Glucagon, a peptide hormone, is produced and secreted by alpha cells of the islets of Langerhans, located in the endocrine portion of the pancreas. Its main physiological role is stimulation of hepatic glucose output leading to increase in blood glucose. It is the major counter-regulatory hormone to insulin in maintaining glucose homeostasis.The principal stimulus for the secretion of glucagon is hypoglycaemia. Hypoglycaemia then stimulates:GlycogenolysisGluconeogenesisLipolysis in adipose tissue leading to increased glycaemia.Secretion of glucagon is also stimulated by arginine, alanine, adrenaline, acetylcholine and cholecystokininSecretion of glucagon is inhibited by:InsulinSomatostatinIncreased free fatty acidsIncreased urea production

Flecainide inhibits the transmembrane influx of extracellular Na+ ions via fast channels on cardiac tissues resulting in a decrease in rate of depolarisation of the action potential, prolonging the PR and QRS intervals. At high concentrations, it exerts inhibitory effects on slow Ca2+ channels, accompanied by moderate negative inotropic effect.

Meningitis is defined as the inflammation of the meninges due to an infection caused by a bacteria or a virus. Symptoms usually include stiffness of the neck, headache, and fever. There are 3 meningeal layers that surround the spinal cord and they are the dura mater, arachnoid matter, and pia mater. The dura mater is the outermost and thickest layer out of all the 3 layers. The arachnoid atter is the middle layer, and is very thin.The third and deepest meningeal layer is the pia mater that is bound tightly to the surface of the spinal cord.

Potassium (K+) is the principal intracellular ion; approximately 4 mmol/L is extracellular (3%) and 140 mmol/L intracellular (97%).

Anatomical barriers to infection include:tight junctions between cells of the skin and mucosal membranesthe flushing action of tears, saliva and urinethe mucociliary escalator in the respiratory tract (together with the actions of coughing and sneezing)the acidic pH of gastric and vaginal secretionsthe acidic pH of the skin (maintained by lactic acid and fatty acids in sebum)enzymes such as lysozyme found in saliva, sweat and tearspepsin present in the stomachbiological commensal flora formed on the skin and the respiratory, gastrointestinal and genitourinary tracts which protect the host by competing with pathogenic bacteria for nutrients and attachment sites and by producing antibacterial substances

In facial nerve palsy, LMN damage will involve the forehead and there will be an inability to close the eyes due to paralysis of the orbicularis oculi or raise the eyebrows due to paralysis of the occipitofrontalis muscle.UMN damage causes sparing of the forehead as the occipitofrontalis and orbicularis oculi muscles have bilateral cortical representation.

When there are excessive levels of aldosterone independent of the renin-angiotensin aldosterone axis, primary hyperaldosteronism occurs. Secondary hyperaldosteronism occurs due to high renin levels.Causes of primary hyperaldosteronism include:Conn’s syndromeAdrenal hyperplasiaAdrenal cancerFamilial aldosteronismCauses of secondary hyperaldosteronism include:Renal vasoconstrictionOedematous disordersDrugs – diureticsObstructive renal artery diseaseAlthough patients are usually asymptomatic, when clinical features are present, classically hyperaldosteronism presents with:HypokalaemiaSodium levels can be normal or slightly raisedHypertensionMetabolic alkalosisLess common, clinical features are:LethargyHeadachesIntermittent paraesthesiaPolyuria and polydipsiaMuscle weakness (from persistent hypokalaemia)Tetany and paralysis (rare)

Cardiac muscle is striated, and the sarcomere is the contractile unit, similar to skeletal muscle. Contracture is mediated by the interaction of calcium, troponins, and myofilaments, much as it occurs in skeletal muscle. Cardiac muscle, on the other hand, differs from skeletal muscle in a number of ways.In contrast to skeletal muscle cells, cardiac myocytes have a nucleus in the middle of the cell and sometimes two nuclei. The cells are striated because the thick and thin filaments are arranged in an orderly fashion, although the arrangement is less well-organized than in skeletal muscle.Intercalated discs, which work similarly to the Z band in skeletal muscle in defining where one cardiac muscle cell joins the next, are a very significant component of cardiac muscle.Adherens junctions and desmosomes, which are specialized structures that hold the cardiac myocytes together, are formed by the transverse sections. The lateral sections produce gap junctions, which join the cytoplasm of two cells directly, allowing for rapid action potential conduction. These critical properties allow the heart to contract in a coordinated manner, allowing for more efficient blood pumping.Cardiac myocytes have the ability to create their own action potentials, which is referred to as myogenic’. They can depolarize spontaneously to initiate a cardiac action potential. Pacemaker cells, as well as the sino-atrial (SA) and atrioventricular (AV) nodes, control this.The Purkinje cells and the cells of the bundle of His are likewise capable of spontaneous depolarization. While the bundle of His is made up of specialized myocytes, it’s vital to remember that Purkinje cells are not myocytes and have distinct characteristics. They are larger than myocytes, with fewer filaments and more gap junctions than myocytes. They conduct action potentials more quickly, allowing the ventricles to contract synchronously.Cardiac myocytes contract by excitation-contraction coupling, just like skeletal myocytes. Heart myocytes, on the other hand, utilise a calcium-induced calcium release mechanism that is unique to cardiac muscle (CICR). The influx of calcium ions (Ca2+) into the cell causes a ‘calcium spark,’ which causes more ions to be released into the cytoplasm.An influx of sodium ions induces an initial depolarisation, much as it does in skeletal muscle; however, in cardiac muscle, the inflow of Ca2+ sustains the depolarisation, allowing it to remain longer. Due to potassium ion (K+) inflow, CICR causes a plateau phase in which the cells remain depolarized for a short time before repolarizing. Skeletal muscle, on the other hand, repolarizes almost instantly.Comparison of skeletal and cardiac muscle:Skeletal muscle Cardiac muscleStriation Striated but arrangement less organised Multiple nuclei located peripherally Usually single nucleus (but can be two), located centrallyDiscs None Intercalated discsNo Gap junctions Gap junctions No Pacemaker PacemakerElectrical stimulation: Nervous system (excitation) Pacemaker (excitation)

Major Actions of Insulin:↑ Glucose uptake into cells↑ Glycogenesis↓ Glycogenolysis↓ Gluconeogenesis↑ Protein synthesis↓ Protein degradation↑ Fat deposition↓ Lipolysis↓ Ketoacid production↑ K+ uptake into cellsMajor Actions of Glucagon:↓ Glycogenesis↑ Glycogenolysis↑ Gluconeogenesis↓ Fatty acid synthesis↑ Lipolysis↑ Ketoacid production

Parainfluenza virus is the most commonly implicated infectious agent in croup.

Carbohydrate digestion begins in the mouth, by alpha-amylase produced in saliva.

The radial nerve and brachial artery are most likely to be damaged in humerus fractures. They are tethered together to the bone and cannot withstand the forces applied to it as a result of the displacement.

Causes of intravascular haemolysis:Haemolytic transfusion reactionsG6PD deficiencyRed cell fragmentation syndromesSome severe autoimmune haemolytic anaemiasSome drug-and infection-induced haemolytic anaemiasParoxysmal nocturnal haemoglobinuria

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

Action potentials are transmitted to adjacent myocytes via gap junctions.

C. diphtheriae, which is the causative agent of diphtheria, is carried in the upper respiratory tract and spread by droplet infection or hand-to-mouth contact. The incubation period averages 2 to 5 days.Infectious mononucleosis is caused by Epstein-Barr virus (EBV). The incubation period for EBV varies from 2 weeks to 2 months.The incubation for Hepatitis A virus is approximately 1 month.The incubation period for Hepatitis C ranges from 2 weeks to 6 months.The period from infection to development of anti-HIV antibodies is usually less than 1 month but may be up to 3 months.

The purine nucleoside adenosine is used to diagnose and treat paroxysmal supraventricular tachycardia. Adenosine works by stimulating A1-adenosine receptors and opening potassium channels that are sensitive to acetylcholine. This causes the atrioventricular (AV) node’s cell membrane to become hyperpolarized, slowing conduction by inhibiting calcium channels.Patients who have had a heart transplant are extremely sensitive to the effects of adenosine and should start with a lower dose of 3 mg, then 6 mg, and finally 12 mg. Dipyridamole potentiates the effects of adenosine, so it should be used with caution in patients who are taking it.The use of adenosine is contraindicated in the following situations:AsthmaCOPD (chronic obstructive pulmonary disease)Decompensated heart failure Long QT syndromeAV block in the second or third degreeSinusitis is a condition in which the sinuses become (unless pacemaker fitted)Hypotension that is severeIt has a half-life of less than 10 seconds and acts quickly within that time frame. The actions last between 10 and 20 seconds. Because of the short half-life of the drug, any side effects are usually only temporary. These are some of them:a feeling of impending doomFlushing of the faceDyspnoeaUncomfortable chestTastes metallic

Theophylline and Ethylenediamine are combined in a 2:1 ratio to form Aminophylline. Its solubility is improved by the addition of Ethylenediamine. It has a lower potency and a shorter duration of action than Theophylline.It is used to treat the following conditions: Heart failureIt is used to treat the following conditions: COPDBradycardiasAminophylline has the following properties:Phosphodiesterase inhibitor that increases intracellular cAMP and relaxes smooth muscle in the bronchial airways and pulmonary blood vessels.Mast cell stabilization is achieved by using a non-selective adenosine receptor antagonist.It has slight positive inotropic and chronotropic effects, increasing cardiac output and decreasing systemic vascular resistance, lowering arterial blood pressure. It has been used historically in the treatment of refractory heart failure and is indicated by the current ALS guidelines as a substitute treatment for bradycardia. The daily oral dose for adults is 900 mg, divided into 2-3 doses. For severe asthma or COPD, a loading dosage of 5 mg/kg over 10-20 minutes is given, followed by a continuous infusion of 0.5 mg/kg/hour. The therapeutic range is small (10-20 microgram/ml), hence assessments of aminophylline plasma concentrations are useful during long-term treatment.

A daily calcium intake of 1,000 to 1,300 mg is advised for adults. Women have a slightly higher calcium need than men and are at a higher risk of developing osteoporosis as they age.Calcium-rich foods include the following:Milk, cheese, and butter as dairy products.Broccoli, spinach, and green beans as green veggies.Bread, rice, and cereals as whole grain foods.Sardines, salmon, and other bony fishEggsNutsThe following foods have the least calcium:CarrotFruits such as kiwis, raspberries, oranges, and papayaChicken and pork in meats.

Glucagon, secreted from the pancreatic islet alpha cells, is considered to be the main catabolic hormone of the body. It raises the concentration of glucose and fat in the bloodstreamThere are five different pancreatic islet cells:Alpha cells (20%) – produce glucagonBeta cells (70%) – produce insulin and amylinDelta cells (<10%) – produce somatostatinGamma cells (<5%) – produce pancreatic polypeptideEpsilon cells (<1%) – produce ghrelin

Many medications, including warfarin, require cytochrome P450 enzymes for their metabolism. When co-prescribing cytochrome p450 enzyme inducers and inhibitors with warfarin, it’s critical to be cautious.Inhibitors of the cytochrome p450 enzyme potentiate the effects of warfarin, resulting in a higher INR. To remember the most commonly encountered cytochrome p450 enzyme inhibitors, use the mnemonic O DEVICES:O– OmeprazoleD– DisulfiramE– Erythromycin (And other macrolide antibiotics)V– Valproate (sodium valproate)I– IsoniazidC– CiprofloxacinE– Ethanol (acute ingestion)S- Sulphonamides

With hepatitis B, about 90% of people will develop lifelong immunity after clearing the infection. Chronic hepatitis develops in about 10% of patients and this may be complicated by cirrhosis or hepatocellular carcinoma. There is a very high risk of chronic infection and hepatocellular carcinoma when there is congenital infection. The risk of this in healthy adults is only about 5%.

Depression of the mandible is generated by the digastric, geniohyoid, mylohyoid and lateral pterygoid muscles on both side, assisted by gravity. The lateral pterygoid muscles are also involved as this movement also involves protraction of the mandible. The masseter muscle is a powerful elevator of the mandible.

Inflammation of the appendix is a significant public health problem with a lifetime incidence of 8.6% in men and 6.7% in women, with the highest incidence occurring in the second and third decade of life. While the rate of appendectomy in developed countries has decreased over the last several decades, it remains one of the most frequent emergent abdominal operations. Appendicitis can often result in anorexia, nausea, vomiting, and fever.McBurney’s point, which is found one-third of the distance between the anterior superior iliac spine and the umbilicus, is often the point of maximal tenderness in a patient with an anatomically normal appendix. A McBurney’s incision is chiefly used for cecostomy and appendectomy. It gives a limited exposure only, and should any doubt arise about the diagnosis, an infraumbilical right paramedian incision should be used instead.

Antidiuretic hormone (ADH) is produced in the hypothalamus’s supraoptic nucleus and then released into the blood via axonal projections from the hypothalamus to the posterior pituitary.It is carried down axonal extensions from the hypothalamus (the neurohypophysial capillaries) to the posterior pituitary, where it is kept until it is released, after being synthesized in the hypothalamus.The secretion of ADH from the posterior pituitary is regulated by numerous mechanisms:Increased plasma osmolality: Osmoreceptors in the hypothalamus detect an increase in osmolality and trigger ADH release.Hypovolaemia causes a drop in atrial pressure, which stretch receptors in the atrial walls and big veins detect (cardiopulmonary baroreceptors). ADH release is generally inhibited by atrial receptor firing, but when the atrial receptors are stretched, the firing reduces and ADH release is promoted.Hypotension causes baroreceptor firing to diminish, resulting in increased sympathetic activity and ADH release.An increase in angiotensin II stimulates angiotensin II receptors in the hypothalamus, causing ADH production to increase.Nicotine, Sleep, Fright, and Exercise are some of the other elements that might cause ADH to be released.Alcohol (which partly explains the diuretic impact of alcohol) and elevated levels of ANP/BNP limit ADH release.