A study published in the Cochrane Database of Systematic Reviews in 2010 found that a single 1000-mg dose of aspirin is effective in treating acute migraine. It was discovered that 24 percent of aspirin users were pain-free after two hours, compared to 11 percent of placebo users. Because the BNF recommends a maximum dose of 900 mg for analgesia and most non-proprietary aspirin comes in a dose of 300 mg, a dose of 900 mg is frequently prescribed in the UK.

Because aspirin is not recommended for children under the age of 16 due to the risk of Reye’s syndrome, it would be inappropriate to give it to the 12-year-old with the viral URTI.

For uncomplicated dental pain, aspirin is an acceptable option, but not for patients who are taking warfarin. The combination of aspirin’s antiplatelet action and warfarin’s anticoagulation properties puts the patient at high risk of bleeding. Furthermore, aspirin can deplete the therapeutic levels of warfarin by displacing it from plasma proteins. It would be better to use another NSAID or analgesic.

In gout, aspirin should be avoided because it reduces urate clearance in the urine and interferes with the action of uricosuric agents. Naproxen, diclofenac, and indomethacin are better options.

Although aspirin is useful for inflammatory pains, the dose of aspirin required for an adequate analgesic effect in severe pain is associated with significant side effects. Naproxen would be a better first-line treatment option.

Clostridium difficile, a Gram-positive, anaerobic, spore forming bacteria is present in the gut of approximately 3% of healthy adults (2012 UK HPA estimates). Following use of broad spectrum antibiotics, which alter normal gut flora, Clostridium difficile infection (CDI) occurs. About 80% of Clostridium Difficile infections are seen in people over the age of 65 and its main clinical features are:
Abdominal cramps, severe bloody and/or watery diarrhoea, offensive smelling diarrhoea, and fever.

CDI is the most severe consequence of antibiotic treatment and is a major cause of morbidity and mortality.
Risk for CDI has been found to be greatest with clindamycin followed by fluoroquinolones Tetracyclines are not associated with risk for CDI.

Healthcare-associated bacteraemia is most commonly caused by intravenous access. Any intravenous device that is left in place for a long time increases the risk of infection. It allows bacteria like Staphylococcus aureus and Staphylococcus epidermidis to enter the body.

The loop of Henle consists of three functionally distinct segments: the thin descending segment, the thin ascending segment, and the thick ascending segment. About 20 percent of the filtered water is reabsorbed in the loop of Henle and almost all of this occurs in the thin descending limb. Na+ and Cl-ions are actively reabsorbed from the tubular fluid in the thick ascending limb via the Na+/K+/2Cl-symporter on the apical membrane. Because the thick ascending limb is water-impermeable, ion reabsorption lowers tubular fluid osmolality while raising interstitial fluid osmolality, resulting in an osmotic difference. Water moves passively out of the thin descending limb as the interstitial fluid osmolality rises, concentrating the tubular fluid. This concentrated fluid descends in the opposite direction of fluid returning from the deep medulla still higher osmolality areas.

Extensor indicis is a narrow, elongated muscle found in the posterior compartment of the forearm. It belongs to the deep extensors of the forearm, together with supinator, abductor pollicis longus, extensor pollicis longus, and extensor pollicis brevis muscles. It lacks the juncturae tendinum, which connects the extensor digitorum on the dorsal aspect of the hand.

Extensor indicis can be palpated by applying deep pressure over the lower part of the ulna while the index finger is extended. The main function of extensor indicis involves the extension of the index finger at the metacarpophalangeal and interphalangeal joints. As the index finger is one of the few fingers that have their own separate extensor muscle, it is able to extend independently from other fingers. Additionally, extensor indicis muscle produces a weak extension of the wrist.

Extensor indicis receives its nervous supply from posterior interosseous nerve, a branch of the radial nerve derived from spinal roots C7 and C8. The skin overlying the muscle is supplied by the same nerve, with fibres that stem from the spinal roots C6 and C7.

The superficial surface of the extensor indicis receives arterial blood supply from posterior interosseous branch of the ulnar artery, whereas its deep surface receives blood from perforating branches of the anterior interosseous artery.

Autoregulation is the ability to maintain a constant blood flow despite variations in blood pressure (between 50 – 170 mmHg). It is particularly important in the brain, kidney and heart. There are two main methods contributing to autoregulation:
The myogenic mechanism involves arterial constriction in response to stretching of the vessel wall, probably due to activation of smooth muscle stretch-activated Ca2+channels and Ca2+entry. A reduction in pressure and stretch closes these channels, causing vasodilation.
The second mechanism of autoregulation is due to locally produced vasodilating factors; an increase in blood flow dilutes these factors causing vasoconstriction, whereas decreased blood flow has the opposite effect.

At altitude, the oxygen fraction is unaltered but the barometric pressure and thus partial pressure of oxygen is reduced.

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.

Fusidic acid is a narrow spectrum antibiotic used for staphylococcal infections, primarily topically for minor staphylococcal skin (impetigo) or eye infection. It is sometimes used orally for penicillin-resistant staphylococcal infection, including osteomyelitis or endocarditis, in combination with other antibacterials.

The maximum daily dose of paracetamol in an adult is 4 grams. Doses greater than this can lead to hepatotoxicity and, less frequently, acute kidney injury. Early symptoms of paracetamol toxicity include nausea, vomiting, and abdominal pain, and usually settle within 24 hours. Symptoms of liver damage include right subcostal pain and tenderness, and this peaks 3 to 4 days after paracetamol ingestion. Other signs of hepatic toxicity include encephalopathy, bleeding, hypoglycaemia, and cerebral oedema.