A lumbar puncture, also known as a spinal tap, is a procedure that involves inserting a needle into the lower back’s lumbar region.

A needle is inserted into the space between the arachnoid mater and the pia mater, also known as the subarachnoid space, to remove a sample of cerebrospinal fluid.

Dexamethasone and betamethasone have the most potent glucocorticoid (anti-inflammatory) effect.

Throughout the airways, there are irritant receptors which are located between epithelial cells which are made of rapidly adapting afferent myelinated fibres in the vagus nerve. A cough is as a result of receptor stimulation located in the trachea, hyperpnoea is as a result of receptor stimulation in the lower airway. Stimulation may also result in reflex bronchial and laryngeal constriction. Many factors can stimulate irritant receptors. These include irritant gases, smoke and dust, airway deformation, pulmonary congestion, rapid inflation/deflation and inflammation. Deep augmented breaths or sighs seen every 5 – 20 minutes at rest are due to stimulation of these irritant receptors. This reverses the slow lung collapse that occurs in quiet breathing.

Elevation of the mandible is generated by the temporalis, masseter and medial pterygoid muscles.

Flow through airways is described by Darcy’s law which states that flow is directly proportional to the mouth-alveolar pressure gradient and inversely proportional to airway resistance. Airway resistance is primarily determined by the airway radius according to Poiseuille’s law, and whether the flow is laminar or turbulent. Parasympathetic stimulation causes bronchoconstriction and sympathetic stimulation causes bronchodilation, but mediated by beta2-adrenoceptors. Muscarinic antagonists e.g. ipratropium bromide cause bronchodilation.

Phagocytosis is largely responsible for depletion of cells coated with antibodies. Cells opsonized by IgG antibodies are recognized by phagocyte Fc receptors, which are specific for the Fc portions of some IgG subclasses. In addition, when IgM or IgG antibodies are deposited on the surfaces of cells, they may activate the complement system by the classical pathway. Complement activation generates by-products, mainly C3b and C4b, which are deposited on the surfaces of the cells and recognized by phagocytes that express receptors for these proteins. The net result is phagocytosis of the opsonized cells and their destruction.

Osmolality and osmolarity are measurements of the solute concentration of a solution. Although the two terms are often used interchangeably, there are differences in the definitions, how they are calculated and the units of measurement used.

Osmolarity, expressed as mmol/L, is an estimation of the osmolar concentration of plasma. It is proportional to the number of particles per litre of solution.
Measured Na+, K+, urea and glucose concentrations are used to calculate the value indirectly.
It is unreliable in pseudohyponatremia and hyperproteinaemia.

The equations used to calculate osmolarity are:
Osmolarity = 2 (Na+) + 2 (K+) + Glucose + Urea (all in mmol/L)
OR
Osmolarity = 2 (Na+) + Glucose + Urea (all in mmol/L)

Doubling of sodium accounts for the negative ions associated with sodium, and the exclusion of potassium approximately allows for the incomplete dissociation of sodium chloride.

Nimodipine is a smooth muscle relaxant that is related to nifedipine, but the effects preferentially act on cerebral arteries. It is exclusively used for the prevention and treatment of vascular spasm after an aneurysmal subarachnoid haemorrhage.

Typically, granuloma has Langerhan’s cells (large multinucleated cells ) surrounded by epithelioid cell aggregates, T lymphocytes and fibroblasts.

Antigen presenting monocytic cells found in the skin are known as Langerhan’s cells.

The Loop of Henle connects the proximal tubule to the distal convoluted tubule and lies parallel to the collecting ducts. It consists of three major segments, including the descending thin limb, the ascending thin limb, and the ascending thick limb. These segments are differentiated based on structure, anatomic location, and function.

The main function of the loop of Henle is to recover water and sodium chloride from urine. When fluid enters the loop of Henle, it has an osmolality of approximately 300 mOsm, and the main solute is sodium.

The thin descending limb has a high water permeability but a low ion permeability. Because it lacks solute transporters, it cannot reabsorb sodium. Aquaporin 1 (AQP1) channels are used to passively absorb water in this area. The peritubular fluid becomes increasingly concentrated as the loop descends into the medulla, causing water to osmose out of the tubule. The tubular fluid in this area now equalizes to the osmolality of the peritubular fluid, to a maximum of approximately 1200 mOsm in a long medullary loop of Henle and 600 mOsm in a short cortical loop of Henle.

The thin ascending limb is highly permeable to ions and impermeable to water. It allows the passive movement of sodium, chloride, and urea down their concentration gradients, so urea enters the tubule and sodium and chloride leave. Reabsorption occurs paracellularly due to the difference in osmolarity between the tubule and the interstitium.

The thick ascending limb is also impermeable to water but actively transports sodium, potassium, and chloride out of the tubular fluid. The osmolality of the tubular fluid is lower compared to the surrounding peritubular fluid. This area is water impermeable. This results in tubular fluid leaving the loop of Henle with an osmolality of approximately 100 mOsm, which is lower than the osmolality of the fluid entering the loop, and urea being the solute.

JVP Waveform in Cardiac Cycle Physiology: a wave Right atrial contraction causes atrial systole (end diastole). the c wave During right isovolumetric ventricular contraction, the tricuspid valve bulges into the right atrium, resulting in isovolumetric contraction (early systole). descent by x Rapid ventricular ejection (mid systole) is caused by a combination of right atrial relaxation, tricuspid valve downward movement during right ventricular contraction, and blood ejection from both ventricles. the v-wave Ventricular ejection and isovolumetric relaxation (late systole) occur as a result of venous return filling the right atrium. y lineage Ventricular filling occurs when the tricuspid valve opens, allowing blood to flow rapidly from the right atrium to the right ventricle.

Activated vitamin D acts to:
GUT:increase calcium and phosphate absorption in the small intestine (the main action)
KIDNEYS:increase renal calcium reabsorption (in the distal tubule via activation of a basolateral Ca2+ATPase pump), increase renal phosphate reabsorption, inhibit 1-alpha-hydroxylase activity in the kidneys (negative feedback)
PARATHYROID GLANDS:inhibit PTH secretion from the parathyroid glands

Angiotensin-converting enzyme (ACE) inhibitors are the most common cause of drug-induced angioedema in the United Kingdom and the United States, owing to their widespread use.

Angioedema is caused by ACE inhibitors in 0.1 to 0.7 percent of patients, with data indicating a persistent and relatively constant risk year after year. People of African descent have a five-fold higher chance of contracting the disease.

Swelling of the lips, tongue, or face is the most common symptom, but another symptom is episodic abdominal pain due to intestinal angioedema. Itching and urticaria are noticeably absent.

The mechanism appears to be activated complement or other pro-inflammatory cytokines like prostaglandins and histamine, which cause rapid vasodilation and oedema.

Other medications that are less frequently linked to angioedema include:
Angiotensin-receptor blockers (ARBs)
Nonsteroidal anti-inflammatory drugs (NSAIDs)
Bupropion (e.g. Zyban and Wellbutrin)
Beta-lactam antibiotics
Statins
Proton pump inhibitors

The majority of these reactions are minor and can be treated by stopping the drug and prescribing antihistamines.

Atracurium is a non-depolarizing neuromuscular blocker that is used to help with intubation and controlled ventilation by causing muscle relaxation and paralysis.

At the neuromuscular junction’s post-synaptic membrane, atracurium competes with acetylcholine for nicotinic (N2) receptor binding sites. This prevents the receptors from being stimulated by acetylcholine.

Muscle paralysis occurs gradually due to the competitive blockade.

A negative feedback mechanism involving the hypothalamic-pituitary-thyroid axis controls the release of T3 and T4 into the bloodstream.

When metabolic rate is low or serum T3 and/or T4 levels are decrease, this triggers the secretion of thyrotropin-releasing hormone (TRH) from the hypothalamus.

TRH goes to the anterior pituitary gland and stimulates secretion of thyroid-stimulating hormone (TSH).

An increased serum level of T3 and T4 inhibits the release of TRH.

Febrile transfusion reactions presents with an unexpected temperature rise (≥ 38ºC or ≥ 1ºC above baseline, if baseline ≥ 37ºC) during or shortly after transfusion. It is usually an isolated finding and the fever is accompanied by chills and malaise occasionally.

Allergic reaction is commonly caused by foreign plasma proteins but may be due to anti-IgA. Allergic type reactions usually present with urticaria, pruritus, hives. Associations include laryngeal oedema or bronchospasm.

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.

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. 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.

Transfusion-related lung injury (TRALI) is a form of acute respiratory distress caused by the donor plasma containing antibodies against the patient’s leukocytes. It is defined as hypoxia and bilateral pulmonary oedema that occurs within 6 hours of a transfusion in the absence of other causes of acute lung injury. Clinical features include Breathlessness, cough, frothy sputum, hypertension or hypotension, hypoxia and fever. Chest X-ray shows multiple perihilar nodules with infiltration of the lower lung fields.

The transmural pressure (pressure across the wall of a flexible tube) can be described by Laplace’s law which states that:
Transmural pressure = (Tw) / r
Where:
T = Wall tension
w = Wall thickness
r = The radius
A small bubble with the same wall tension as a larger bubble will contain higher pressure and will collapse into the larger bubble if the two meet and join.

Fick’s law describes the rate of diffusion in a solution

Poiseuille’s law is used to calculate volume of flow rate in laminar flow

Darcy’s law describes the flow of a fluid through a porous medium.

Starling’s law describes cardiac haemodynamics as it relates to myocyte contractility and stretch.

Acute bronchiolitis is caused most commonly by respiratory syncytial virus, occurring mostly in children aged 6 months to 2 years. Children with bronchiolitis are febrile and tachypnoeic with a dry cough and difficulty feeding. Examination may reveal chest hyperinflation, respiratory distress, wheezing and fine end-inspiratory crepitations. Chest x-ray may show hyperinflation and increased peribronchial markings (although CXR should only performed if there is diagnostic uncertainty or an atypical course). Treatment is usually supportive, aerosolized ribavirin is reserved for severely ill or immunocompromised patients.

Digoxin is excreted through the kidneys, and impaired renal function can lead to elevated digoxin levels and toxicity.
The patient’s digoxin dose should be reduced in this case, and their digoxin level and electrolytes should be closely monitored.

PTH is synthesised and released from the chief cells of the four parathyroid glands located behind the thyroid gland.
It is a polypeptide containing 84 amino acids and it controls free calcium in the body.

The following stimuli causes release of PTH:
Increased plasma phosphate concentration
Decreased plasma calcium concentration

PTH release is inhibited by:
Normal or increased plasma calcium concentration
Hypomagnesaemia

The main actions of PTH are:
Increases plasma calcium concentration
Decreases plasma phosphate concentration
Increases osteoclastic activity (increasing calcium and phosphate resorption from bone)
Increases renal tubular reabsorption of calcium
Decreases renal phosphate reabsorption
Increases renal conversion of 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol (via stimulation of 1-alpha hydroxylase)
Increases calcium and phosphate absorption in the small intestine (indirectly via increased 1,25-dihydroxycholecalciferol)

Lithium is the drug of choice for recurrent bipolar illness but should be carefully monitored as it has a very low therapeutic index. The normal therapeutic range is 0.4-0.8 mmol/l.

The lower end of the range is usually the target for the elderly and as maintenance therapy. Toxicity is usually seen at levels >1.5 mmol/l. Samples should be taken 12 hours after the dose, and levels should be checked one week after starting therapy and one week after every change in dosage.

Brachioradialis is a fusiform muscle located in the lateral part of the posterior forearm. Along with extensor carpi radialis brevis and extensor carpi radialis longus, it comprises the radial group of forearm muscles, which belong to the superficial layer of posterior forearm muscles. Although anatomically part of the posterior forearm muscles, which are known to be forearm extensors, brachioradialis’ fibre orientation enables it to rather flex the forearm, and aids in supination of the forearm at the radioulnar joint.

The brachioradialis muscle originates from the upper two-thirds of the lateral supracondylar ridge of humerus and the anterior surface of the lateral intermuscular septum of the arm. It slides over the lateral surface of the elbow joint, entering the anterolateral cubital area. The muscle fibres course inferiorly down the radial part of the anterior forearm, forming a thick tendon in approximately the middle of the forearm. This tendon then traverses the remainder of the forearm, inserting near the wrist, just proximal to the styloid process of radius.

Brachioradialis is innervated by the radial nerve (from the root values C5-C6) that stems from the posterior cord of the brachial plexus. Blood supply to the brachioradialis muscle comes from branches of the radial artery, radial recurrent artery and the radial collateral branch of the deep brachial artery.

Glucagon is a peptide hormone that is produced and secreted by alpha cells of the islets of Langerhans, which are located in the endocrine portion of the pancreas. The main physiological role of glucagon is to stimulate hepatic glucose output, thereby leading to increases in glycaemia. It provides the major counter-regulatory mechanism to insulin in maintaining glucose homeostasis.
Hypoglycaemia is the principal stimulus for the secretion of glucagon but may also be used as an antidote in beta-blocker overdose and in anaphylaxis in patients on beta-blockers that fail to respond to adrenaline.
Glucagon then causes:
Glycogenolysis
Gluconeogenesis
Lipolysis in adipose tissue
The secretion of glucagon is also stimulated by:
Adrenaline
Cholecystokinin
Arginine
Alanine
Acetylcholine
The secretion of glucagon is inhibited by:
Insulin
Somatostatin
Increased free fatty acids
Increased urea production

Glycolysis is the metabolic pathway that converts glucose into pyruvate. The free energy released by this process is used to form ATP and NADH. Glycolysis is inhibited by glucagon, and glycolysis and gluconeogenesis are reciprocally regulated so that when one cell pathway is activated, the other is inactive and vice versa.

Glucagon has a minor effect of enhancing lipolysis in adipose tissue. Lipolysis is the breakdown of lipids and involves the hydrolysis of triglycerides into glycerol and free fatty acids. It makes fatty acids available for oxidation.

Persons with chronic diseases. Persons with chronic renal disease or undergoing dialysis, and those with hyposplenism or asplenia, may receive BCG vaccine if indicated.

Only 2 absolute contraindications apply to all vaccines:

• anaphylaxis following a previous dose of the relevant vaccine
• anaphylaxis following any component of the relevant vaccine

2 further contraindications apply to live vaccines (both parenteral and oral):

• People who are significantly immunocompromised should not receive live vaccines. This is regardless of whether the immunocompromising condition is caused by disease or treatment.
• Pregnant women should not receive live vaccines, in general. Women should be advised not to become pregnant within 28 days of receiving a live vaccine.

Use of live vaccines in people who are immunocompromised:
People who are immunocomprised are at risk of adverse events or vaccine-related disease if they receive a live vaccine.

Live vaccines include:

BCG (bacille Calmette–Guérin) vaccine
oral cholera vaccine (Vaxchora)
Some Japanese encephalitis virus vaccines
MMR (measles-mumps-rubella) vaccine
rotavirus vaccine
oral typhoid vaccine
varicella vaccine
yellow fever vaccine
zoster vaccine (Zostavax)

The ventilation/perfusion ratio (V/Q ratio) is a ratio used to assess the efficiency and adequacy of the matching ventilation and perfusion.

A pulmonary artery carries deoxygenated blood from the right side of the heart to the lungs. When a large pulmonary embolus completed blocked a pulmonary artery the alveoli were ventilated but not perfused at all, then the V/Q ratio would be infinity.

Clostridium perfringens is an obligate anaerobe and has exotoxin mediated effects. It is the most common cause of gas gangrene. C. perfringens is also implicated in food poisoning, cellulitis, enteritis necrotican (life-threatening infection involving ischaemic necrosis of the jejunum), and rarely, CNS infections such as meningitis and encephalitis.

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.

Nosocomial infections are defined as those occurring within 48 hours of hospital admission, 3 days of discharge or 30 days of an operation. They affect 1 in 10 patients admitted to hospital. Annually, this results in 5000 deaths with a cost to the National Health Service of a billion pounds. On average, a patient with hospital acquired infection spent 2.5-times longer in hospital, incurring additional costs of £3000 more than an uninfected patient. Intensive care units (ICU) have the highest prevalence of hospital-acquired infections in the hospital setting.
The current recommendations by NICE and the BNF on the treatment of hospital acquired pneumonia are:
Early onset infection(less than 5 days after admission to hospital): co-amoxiclav or cefuroxime for 7 days
Late-onset infection(more than 5 days after admission to hospital): an antipseudomonal penicillin (e.g. piperacillin with tazobactam), a broad-spectrum cephalosporin (e.g. ceftazidime), or a quinolone (e.g. ciprofloxacin)
If the patient developed a hospital-acquired pneumonia within 5 days of admission – co-amoxiclav would be the most appropriate choice.
If the patient has developed a hospital-acquired pneumonia > 5 days after admission – ciprofloxacin would be the most appropriate choice from the list of options available.

ADH binds V2 receptors on renal principal cells in the late distal tubule and collecting ducts, raising cAMP levels and causing intracellular vesicles to fuse with the apical membrane. In their membrane these vesicles have water channels called aquaporins, which increase the water permeability allowing greater water reabsorption and concentration of urine. ADH also binds to V1 receptor receptors on vascular smooth muscle, causing vasoconstriction and enhancing the effect of aldosterone on sodium reabsorption in the distal tubule. ADH release is stimulated primarily by raised plasma osmolality detected by osmoreceptors in the anterior hypothalamus. Other factors that increase ADH release include: extracellular fluid volume depletion, angiotensin II, nausea, pain, stress, exercise, emotion, hypoglycaemia. ADH release is inhibited by low plasma osmolality, alcohol, caffeine, glucocorticoids and atrial natriuretic peptide (ANP). ADH deficiency (or an inadequate response to ADH) results in diabetes insipidus. Excess levels of ADH results in syndrome of inappropriate ADH secretion (SIADH).

The O’Donoghue unhappy triad or terrible triad often occurs in contact and non-contact sports, such as basketball, football, or rugby, when there is a lateral force applied to the knee while the foot is fixated on the ground. This produces an abduction-external rotation mechanism of injury.

The O’Donoghue unhappy triad comprises three types of soft tissue injury that frequently tend to occur simultaneously in knee injuries. O’Donoghue described the injuries as: anterior cruciate ligament tear, medial collateral ligament injury, and medial meniscal tear (lateral compartment bone bruise).