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.

Transfusion-associated circulatory overload (TACO) presents as acute or worsening respiratory distress within 6 hours of transfusion of a large volume of blood. It is common in patients with diminished cardiac reserve or chronic anaemia. Elderly patients, infants and severely anaemic patients are particularly susceptible. Typical clinical features of TACO include: Acute respiratory distress, Tachycardia, Hypertension, Acute/worsening pulmonary oedema on chest X-ray. The BNP is usually raised to at least 1.5 times the pre-transfusion baseline.Febrile transfusion reaction presents with a 1 degree rise in temperature from baseline during transfusion. Patient may have chills and malaise. It is the most common transfusion reaction (1 in 8 transfusions) and is usually caused by cytokines released from leukocytes in transfused red cell or platelet components. TRALI (Transfusion Related Acute Lung Injury) is a clinical syndrome with abrupt onset of non-cardiogenic pulmonary oedema within 6 hours of transfusion not explained by another risk factor. Associated with the presence of antibodies in the donor blood to recipient leukocyte antigens. patients present with dyspnoea, hypertension, hypotension, acute leukopenia. Graft versus host disease(GVHD) is an immune mediated condition that arises from a complex interaction between donor and recipients adaptive immunity. It presents as dermatitis, hepatitis and enteritis developing within 100 days after stem cell or bone marrow transplant.Acute haemolytic reaction aka immediate haemolytic transfusion reaction presents with fever, chills, pain at transfusion site, nausea, vomiting, dark urine and feeling of ‘impending doom’. Often, it occurs due to ABO incompatibility.

The nephron’s blood flow is as follows:Afferent arteriole – Glomerular capillary – Efferent arteriole – Peritubular capillary – Vasa recta – Afferent arteriole – Glomerular capillary – Efferent arteriole – Peritubular capillary – Vasa rectaThe kidney is the only vascular network in the body with two capillary beds. With arterioles supplying and draining the glomerular capillaries, higher hydrostatic pressures at the glomerulus are maintained, allowing for better filtration. A second capillary network at the tubules enables for secretion and absorption in the tubules, as well as concentrating urine.

Penicillins and the other ß-lactam antibiotics are bactericidal. They produce their antimicrobial action by preventing cross-linkage between the linear peptidoglycan polymer chains that make up the bacterial cell wall. They, therefore, inhibit cell wall synthesis.An overview of the different mechanisms of action of the various types of antimicrobial agents is shown below:Mechanism of actionExamplesInhibition of cell wall synthesisPenicillinsCephalosporinsVancomycinDisruption of cell membrane functionPolymyxinsNystatinAmphotericin BInhibition of protein synthesisMacrolidesAminoglycosidesTetracyclinesChloramphenicolInhibition of nucleic acid synthesisQuinolonesTrimethoprim5-nitroimidazolesRifampicinAnti-metabolic activitySulfonamidesIsoniazid

Insulin is used mainly in type 1 diabetes, where the pancreas makes no insulin and can sometimes be prescribed in type 1 diabetes. There are different types of insulin categorized by their onset of action:1. Intermediate-acting insulins (isophane insulin NPH): – intermediate duration of action, designed to mimic the effect of endogenous basal insulin- starts their action in 1 to 4 hours- peaks in 4 to 8 hours – dosing is usually twice a day and helps maintain blood sugar throughout the day- Isophane insulin is a suspension of insulin with protamine2. Short-acting insulins (regular insulin)- starts the action in 30 to 40 minutes- peaks in 90 to 120 minutes- duration of action is 6 to 8 hours- taken before meals, and food is necessary within 30 minutes after its administration to avoid hypoglycaemia3. Long-acting insulins (glargine, detemir, degludec)- start action in 1 to 2 hours- plateau effect over 12 to 24 hours- Dosing is usually during the night-time after meals. Their long duration of action helps in reducing the frequency of dosing throughout the day. 4. Rapid-acting insulins (lispro, aspart, glulisine) – start their action in 5 to 15 minutes- peak in 30 minutes- The duration of action is 3 to 5 hours- generally used before meals and always used along with short-acting or long-acting insulins to control sugar levels throughout the day.

Arm oedema is one of the sequelae after breast cancer surgery and radiation therapy. Arm oedema in the breast cancer patient is caused by interruption of the axillary lymphatic system by surgery or radiation therapy, which results in the accumulation of fluid in subcutaneous tissue in the arm, with decreased distensibility of tissue around the joints and increased weight of the extremity. Chronic inflammatory changes result in both subcutaneous and lymph vessel fibrosis.

At rest, most saliva is produced by the submandibular gland (65%). When stimulated by the autonomic nervous system, about 50% of saliva is produced by the parotid gland with only 30% produced by the submandibular gland.

Gentamicin is the aminoglycoside of choice in the UK and is used widely for the treatment of serious infections. It has a broad spectrum but is inactive against anaerobes and has poor activity against haemolytic streptococci and pneumococci. When used for the blind therapy of undiagnosed serious infections it is usually given in conjunction with a penicillin or metronidazole (or both). The main toxic effects are nephrotoxicity and ototoxicity due to damage to the vestibulocochlear nerve (CN VIII).Gentamicin is contraindicated in myasthenia gravis and should be used with caution in renal disease which may result in accumulation and a greater risk of toxic side effects.

Adverse effects of loop diuretics include:Mild gastrointestinal disturbances, pancreatitis and hepatic encephalopathyHyperglycaemiaAcute urinary retentionWater and electrolyte imbalanceHyponatraemia, hypocalcaemia, hypokalaemia, hypomagnesaemia, hypochloraemiaHypotension, hypovolaemia, dehydration, and venous thromboembolismMetabolic alkalosisHyperuricaemiaBlood disorders (bone marrow suppression, thrombocytopenia, and leucopenia)Visual disturbance, tinnitus and deafnessHypersensitivity reactions

The commonest cause of hypercalcaemia in the UK is primary hyperparathyroidism, which accounts for around 70-80% of cases. It is commoner in younger patients and in community setting.