A posterolateral herniation of the disc at the L4 – L5 level would be most likely to damage the fifth lumbar nerve root, not the fourth lumbar nerve root, due to more oblique descending of the fifth lumbar nerve root within the subarachnoid space.

125 mg PO q6hr for 10 days is indicated for treatment of Clostridium difficile (C. difficile)-associated diarrhoea

Inguinal hernias can present with an array of different symptoms. Most patients present with a bulge in the groin area, or pain in the groin. Some will describe the pain or bulge that gets worse with physical activity or coughing. Symptoms may include a burning or pinching sensation in the groin. These sensations can radiate into the scrotum or down the leg. It is important to perform a thorough physical and history to rule out other causes of groin pain. At times an inguinal hernia can present with severe pain or obstructive symptoms caused by incarceration or strangulation of the hernia sac contents. A proper physical exam is essential in the diagnosis of an inguinal hernia. Physical examination is the best way to diagnose a hernia. The exam is best performed with the patient standing. Visual inspection of the inguinal area is conducted first to rule out obvious bulges or asymmetry in groin or scrotum. Next, the examiner palpates over the groin and scrotum to detect the presence of a hernia. The palpation of the inguinal canal is completed last. The examiner palpates through the scrotum and towards the external inguinal ring. The patient is then instructed to cough or perform a Valsalva manoeuvre. If a hernia is present, the examiner will be able to palpate a bulge that moves in and out as the patient increases intra abdominal pressure through coughing or Valsalva.Groin hernias are categorized into 2 main categories: inguinal and femoral.Inguinal hernias are further subdivided into direct and indirect. An indirect hernia occurs when abdominal contents protrude through the internal inguinal ring and into the inguinal canal. This occurs lateral to the inferior epigastric vessels. The hernia contents may extend into the scrotum, and can be reduced superiorly then superolaterally. A direct inguinal hernia is protrusion of abdominal contents through the transversalis fascia within Hesselbach’s triangle. The borders of Hesselbach’s triangle are the inferior epigastric vessels superolaterally, the rectus sheath medially, and inguinal ligament inferiorly.A femoral hernia is a protrusion into the femoral ring. The borders of the femoral ring are the femoral vein laterally, Cooper’s ligament posteriorly, the iliopubic tract/inguinal ligament anteriorly and lacunar ligament medially.

Complications of mumps include meningitis, post meningitis deafness, encephalitis, pancreatitis, orchitis and oophoritis. Subacute sclerosing panencephalitis is a complication typically associated with measles infection.

Most vasoconstrictors bind to G-protein coupled receptors. These mediate elevation in intracellular [Ca2+] which leads to vascular smooth muscle contraction. Important vasoconstrictors include noradrenaline, endothelin-1 and angiotensin II. Increased intracellular Ca2+ is as a result of the release of Ca2+from the sarcoplasmic reticulum and depolarisation and entry of Ca2+via L-type voltage-gated Ca2+channels. Most types of vascular smooth muscle do not generate action potentials – instead, the depolarisation is graded, which allows graded entry of Ca2+.sequestration by the sarcoplasmic reticulum Ca2+ATPase, removal from the cell by a plasma membrane Ca2+ATPase and Na+/Ca2+exchange decreases intracellular Ca2+, resulting in vasodilation. Relaxation is a result of most endogenous vasodilators when there is an increase in cyclic guanosine monophosphate (cGMP) like nitric oxide) or cyclic adenosine monophosphate (cAMP) like prostacyclin and beta-adrenergic receptor agonists. These activate protein kinases causing substrate level phosphorylation. Clinically effective vasodilators are L-type Ca2+channel blocker drugs.

Abductor pollicis longus is a muscle found in the posterior compartment of the forearm. It is one of the five deep extensors in the forearm, along with the supinator, extensor pollicis brevis, extensor pollicis longus and extensor indicis.Abductor pollicis longus is innervated by the posterior interosseous nerve (C7, C8), which is a continuation of the deep branch of the radial nerve. The radial nerve is a branch of the posterior cord of the brachial plexus.Blood supply to the abductor pollicis longus muscle comes from the interosseous branches of the ulnar artery.Acting alone or with abductor pollicis brevis, abductor pollicis longus pulls the thumb away from the palm. More specifically, it produces (mid-) extension and abduction of the thumb at the first metacarpophalangeal joint. This action is seen in activities such as bowling and shovelling.Working together with the long and short extensors of the thumb, the muscle also helps to fully extend the thumb at the metacarpophalangeal joint. This action is important for loosening the hand grip, for example, when letting go of objects previously being held. Abductor pollicis longus also helps to abduct the hand (radial deviation) at the radiocarpal joint.

Aspirin contraindications include: hypersensitivity to NSAIDs; asthma, rhinitis, and nasal polyps; and usage in children or teens.There is little evidence of allergic cross-reactivity for salicylates. However, due to similarities in chemical structure and/or pharmacologic activities, the possibility of cross-sensitivity cannot be completely ruled out.

The main factor in determining whether a substance is filtered or not is molecular weight. Molecules < 7 kDa in molecular weight e.g. glucose, amino acids, urea, ions are filtered freely, but larger molecules are increasingly restricted up to 70 kDa, and there is very little filtration for anything above this. There is further restriction of negatively charged molecules because they are repelled by negative charges, particularly in the basement membrane. Albumin, which has a molecular weight of 69 kDa and is negatively charged, is filtered but only in very small amounts. All of the filtered albumin is reabsorbed in the proximal tubule. Small molecules such as ions, glucose, amino acids and urea pass the filter without hindrance. Other than the ultrafiltrate being essentially protein free, it has an otherwise identical composition of plasma. Bowman's capsule consists of:- an epithelial lining which consists of a single layer of cells called podocytes- endothelium which is perforated by pores or fenestrations – this allows plasma components with a molecular weight of < 70 kDa to pass freely.

r = 0 if there is no correlation between two variables. The closer that r is to 0, the weaker the correlation.

Aluminium hydroxide is a common antacid that is used to treat ulcer dyspepsia and non-erosive gastro-oesophageal reflux disease.When antacids containing aluminium salts are given to patients with renal impairment, there is a risk of accumulation and aluminium toxicity. If renal function is normal, aluminium accumulation does not appear to be a risk.Because it reduces gastrointestinal phosphate absorption, aluminium hydroxide can also be used to treat hyperphosphatemia in patients with renal failure.Magnesium-based antacids are generally laxative, whereas aluminium-based antacids can be constipating. Renal impairment, angioedema, and anaphylaxis are not significantly increased.

The femoral nerve runs down the front of the leg from the pelvis. It gives the front of the thigh and a portion of the lower leg sensation. Extension of the leg at the knee joint, flexion of the thigh at the hip are produced by muscles that is primarily innervated by the femoral nerve.

Short vessels called arteriovenous anastomoses (AVAs) link tiny arteries and veins. They have a large lumen diameter. The strong and muscular walls allow AVAs to completely clog the vascular lumen, preventing blood flow from artery to vein (acting like a sphincter). When the AVAs open, they create a low-resistance connection between arteries and veins, allowing blood to flow into the limbs’ superficial venous plexuses. There is no diffusion of solutes or fluid into the interstitium due to their strong muscle walls.AVAs are densely innervated by adrenergic fibres from the hypothalamic temperature-regulation centre. High sympathetic output occurs at normal core temperatures, inducing vasoconstriction of the AVAs and blood flow through the capillary networks and deep plexuses. When the temperature rises, sympathetic output decreases, producing AVA vasodilation and blood shunting from the artery to the superficial venous plexus. Heat is lost to the environment as hot blood rushes near to the skin’s surface.AVAs are a specialized anatomical adaptation that can only be found in large quantities in the fingers, palms, soles, lips, and pinna of the ear.

Amoxicillin is used first line for low to moderate severity community acquired pneumonia, exacerbations of chronic bronchitis, for acute otitis media, for acute sinusitis, for oral infections/dental abscess, for Listeria meningitis (in combination with another antibiotic), for infective endocarditis (in combination with another antibiotic) and for H. Pylori eradication (in combination with metronidazole/clarithromycin and a PPI). Flucloxacillin is used first line for acute cellulitis.

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

Legionella pneumophilais a Gram negative bacterium that is found in natural water supplies and in the soil, transmitted predominantly via inhalation of aerosols generated from contaminated water (direct person-to-person spread of infected patients does not occur). It is the cause of Legionnaires’ disease. Outbreaks of Legionnaires’ disease have been linked to poorly maintained air conditioning systems, whirlpool spas and hot tubs.The clinical features of the pneumonic form of Legionnaires’ disease include:Mild flu-like prodrome for 1-3 daysCough (usually non-productive and occurs in approximately 90%)Pleuritic chest painHaemoptysisHeadacheNausea, vomiting and diarrhoeaAnorexiaLegionella pneumophilainfections can be successfully treated with macrolide antibiotics, such as erythromycin, or quinolones, such as ciprofloxacin. Tetracyclines, such as doxycycline, can also be used.The syndrome of inappropriate antidiuretic hormone secretion (SIADH) can occur with Legionnaires’ disease and will result in hyponatraemia as is seen in this case.Legionella pneumophilainfections are resistant to amoxicillin but can be successfully treated with macrolide antibiotics, such as erythromycin, or quinolones, such as ciprofloxacin. Tetracyclines, such as doxycycline, can also be used. The majority of cases of Legionnaires’ disease are caused by Legionella pneumophila, however many other species of Legionella have been identified.Legionella longbeachae is another less commonly encountered species that has also been implicated in outbreaks. It is predominantly found in soil and potting compost, and has caused outbreaks of Pontiac fever, the non-respiratory and less severe variant of Legionnaires’ disease.

Free movement of the tendons in the carpal tunnel is facilitated by synovial sheaths, which surround the tendons. All of the tendons of the FDP and FDS are contained within a single synovial sheath with a separate sheath enclosing the tendon of the FPL.

In full optic nerve palsy, the afferent pupillary light reflex is lost. Because the afferent optic nerve does not sense light flashed in the afflicted eye, the ipsilateral direct and contralateral consensual reflexes are gone. However, the contralateral direct and ipsilateral consensual reflexes are intact because the efferent oculomotor nerve is normal.

Doxycycline and other tetracycline antibiotics attach to the 30S subunit of the bacterial ribosome, preventing aminoacyl-tRNA binding and so protein synthesis beginning.

The inability to produce concentrated urine is a symptom of diabetes insipidus. Excessive thirst, polyuria, and polydipsia are all symptoms of this condition. There are two forms of diabetes insipidus: Nephrogenic diabetes insipidus and cranial (central) diabetes insipidus.A lack of ADH causes cranial diabetic insipidus. Patients with cranial diabetes insipidus can have a urine output of up to 10-15 litres per 24 hours, however most patients can maintain normonatraemia with proper fluid consumption. Thirty percent of cases are idiopathic, while another thirty percent are caused by head injuries. Neurosurgery, brain tumours, meningitis, granulomatous disease (e.g. sarcoidosis), and medicines like naloxone and phenytoin are among the other reasons. There is also a very rare hereditary type that is linked to diabetes, optic atrophy, nerve deafness, and bladder atonia.Renal resistance to the action of ADH causes nephrogenic diabetes insipidus. Urine output is significantly increased, as it is in cranial diabetes insipidus. Secondary polydipsia can keep serum sodium levels stable or raise them. Chronic renal dysfunction, metabolic diseases (e.g., hypercalcaemia and hypokalaemia), and medications, such as long-term lithium use and demeclocycline, are all causes of nephrogenic diabetes insipidus.The best test to establish if a patient has diabetes insipidus vs another cause of polydipsia is the water deprivation test, commonly known as the fluid deprivation test. It also aids in the distinction between cranial and nephrogenic diabetes insipidus. Weight, urine volume, urine osmolality, and serum osmolality are all measured after patients are denied water for up to 8 hours. At the end of the 8-hour period, 2 micrograms of IM desmopressin is given, and measures are taken again at 16 hours.The following are the way results are interpreted:Urine osmolality after fluid deprivation : Urine osmolality after IM desmopressinCranial diabetes insipidus800 mosmol/kgNephrogenic diabetes insipidus<300 mosmol/kg : 800 mosmol/kg : >800 mosmol/kg

Heparin-induced thrombocytopenia (HIT) is a prothrombotic disorder caused by antibodies that recognize complexes of platelet factor 4 (PF4) and heparin. HIT is frequently considered in the differential diagnosis of thrombocytopenia occurring in patients on heparin therapy. HIT is a challenging diagnosis because of routine heparin use in hospitalized patients, the common occurrence of thrombocytopenia. The process of heparin dependent IgG antibodies binding to heparin/platelet factor 4 complexes activates platelets and produces a hypercoagulable state. This syndrome typically develops 5-10 days (range 4-15 days) after heparin is commenced. It can occur with unfractionated heparin, low molecular weight heparin, or, rarely, fondaparinux. The diagnosis of HIT requires the combination of a compatible clinical picture and laboratory confirmation of the presence of heparin dependent platelet activating HIT antibodies. Discontinuation of heparin alone or initiation of a vitamin K antagonist alone like warfarin, is not sufficient to stop the development of thrombosis in patients with acute HIT. If there is moderate clinical suspicion for HIT, all sources of heparin must be discontinued and there must be consideration of anticoagulant treatment with a non-heparin drug.