The drug of choice for the treatment of anaphylaxis is adrenaline. It has an intravenous route of administration. Since the patient already has intravenous access, the intramuscular route is not appropriate.

Second-line pharmacological intervention includes the use of chlorpheniramine 10mg intravenous, Hydrocortisone 200mg.

Staphylococcus aureus infection is the most likely cause.

Surgical site infections (SSI) occur when there is a breach in tissue surfaces and allow normal commensals and other pathogens to initiate infection. They are a major cause of morbidity and mortality.

SSI comprise up to 20% of healthcare associated infections and approximately 5% of patients undergoing surgery will develop an SSI as a result.
The organisms are usually derived from the patient’s own body.

Measures that may increase the risk of SSI include:
-Shaving the wound using a single use electrical razor with a disposable head
-Using a non iodine impregnated surgical drape if one is needed
-Tissue hypoxia
-Delayed prophylactic antibiotics administration in tourniquet surgery, patients with a prosthesis or valve, in clean-contaminated surgery of in contaminated surgery.

Measures that may decrease the risk of SSI include:
1. Intraoperatively
– Prepare the skin with alcoholic chlorhexidine (Lowest incidence of SSI)
-Cover surgical site with dressing

In contrast to previous individual RCT’s, a recent meta analysis has confirmed that administration of supplementary oxygen does not reduce the risk of wound infection and wound edge protectors do not appear to confer benefit.

2. Post operatively
Tissue viability advice for management of surgical wounds healing by secondary intention

Use of diathermy for skin incisions
In the NICE guidelines the use of diathermy for skin incisions is not advocated. Several randomised controlled trials have been undertaken and demonstrated no increase in risk of SSI when diathermy is used.

The external urethral sphincter functions to provide voluntary control of urine flow from the bladder to the urethra.

It receives its innervation from the branches of the pudendal nerve which originate from S2, S3 and S4.

An epidemic is declared when the increase in a give disease is above a certain level in a specific interval of time.

An endemic is the general, usual level of a disease in a population at a particular time.

A pandemic is an epidemic that is spread across many countries and continents.

The umbilical vein closes once the umbilical cord is clamped following birth. This causes a rise in systemic vascular resistance, closing the ductus venosus.

Upon birth, the pulmonary vascular resistance is decreased as the lungs are aerated.

At birth, there is a rise in oxygen tension which causes the corresponding constriction of the ductus arteriosus. This prevents a left to right shunt as it stops aortic blood and blood from the pulmonary artery from mixing. The ventricles do no have an opening connecting them.

The foramen ovale closes soon after birth. It is the septum opening between the left and right atrium.

An adult’s cardiac output is expected to be 5 L/min.

Atrial natriuretic peptide (ANP) is secreted mainly from myocytes of right atrium and ventricle in response to increased blood volume.
It is secreted by both the right and left atria (right >> left).

It is a 28 amino acid peptide hormone, which acts via cGMP
degraded by endopeptidases.

It serves to promote the excretion of sodium, lowers blood pressure, and antagonise the actions of angiotensin II and aldosterone.

The Wolff-Parkinson-White syndrome (WPWS) is linked to an additional electrical conduction pathway between the atria and ventricles. This accessory pathway (bundle of Kent), unlike the atrioventricular (AV) node, is incapable of slowing down a rapid rate of atrial depolarization. In other words, a short circuit bypasses the AV node. Patients with a rapid ventricular response or narrow complex AV re-entry tachycardia are more likely to develop atrial fibrillation or flutter.

Digoxin can promote impulse transmission through this accessory pathway if a patient with WPWS develops atrial fibrillation because it works by blocking the AV node. This can cause ventricular fibrillation and an extremely rapid ventricular rate. As a result, it’s not advised.

Adenosine, beta-blockers, and calcium channel blockers, among other drugs that interfere with AV nodal conduction, are also generally contraindicated.

The class III antiarrhythmic drugs amiodarone and ibutilide (K+ channel block) and procainamide (Na+ channel block) are the drugs of choice.

Prerenal failure has a serum urea: creatinine ratio of >100, while acute kidney injury has a ratio of 40.
In prerenal failure, ADH levels are typically high, resulting in water, urea, and sodium resorption. The fractional sodium excretion is less than 1%, but it is greater than 2% in acute tubular necrosis.
Prerenal azotaemia has higher serum urea nitrogen/serum creatinine ratios (>20), whereas acute tubular necrosis has lower ratios (10-15). The normal range is between 12 and 20.
Urinary sodium is less than 20 in prerenal failure and greater than 40 in acute tubular necrosis.
Prerenal failure has a urine osmolality of >500, while acute tubular necrosis has an osmolality of 350.
Prerenal failure has a urine/serum creatinine ratio of >40, while acute tubular necrosis has a urine/serum creatinine ratio of 20.

The concentrations of serum urea or creatinine change in inverse proportion to glomerular filtration. Changes in serum creatinine concentrations are more reliable than changes in serum urea concentrations in predicting GFR. Creatinine is produced at a constant rate from creatine, and blood concentrations are almost entirely determined by GFR.

A number of factors influence urea formation, including liver function, protein intake, and protein catabolism rate. Urea excretion is also influenced by hydration status, the amount of water reabsorption, and GFR.

A high serum creatinine level, as well as a urine output of less than 10 mL/hour and the production of concentrated looking urine, do not necessarily indicate a specific cause of oliguria.

According to the Ohm’s law, the potential difference is defined as

V(potential difference) = I(current) x (R) resistance

So, for one resistor of 5 ohms, a 10 ampere current will generate:

V = I x R
V = 10 x 5
V = 50 volts

The formula for resistors in series can be defined as:

R(total) = R1+R2

Hence, when a current of 10 amperes passes through two 5 ohms resistors that are connected in series, the potential difference is:

V = I x (R1+R2)
V = 10 x (5+5)
V = 10 x 10
V = 100 volts

The formula for resistors that are connected in a parallel circuit is:

1/ Rtotal = 1/R1 + 1/R2

Hence, when a current of 10 amperes passes through two 5 Ω resistors that are connected in a parallel circuit, the potential difference is:

Rtotal = R1 × R2/ R1 + R2
Rtotal = 25/10
Rtotal = 2.5
V = I x R
V = 10 x (R1xR2 / R1 + R2)
V = 10 x (25/10)
V = 10 x 2.5
V = 25 volts

Capacitors are electronic components that have the ability to store energy and charge (Q). The derived SI unit of capacitance (C) is the farad (F), which is equivalent to one coulomb per volt (V). The typical capacitors usually have a very small capacitance range, that ranges from pico to microfarads. On the contrary, supercapacitors can have a capacitance of up to 1-5000 F.

There are a number of factors that eventually determine the capacitance (C). They are as follows:

– Larger plate area (A)
– Closer plate spacing (d)
– Permittivity (ε) of the material (dielectric) between the plates (vacuum<<<glass), – C = ε × A/d

The units of stored charge are coulombs (Q), which is equal to the pathway of one ampere of current per second.
Stored charge, capacitance and voltage can be defined by the following equation:

V (potential difference across capacitor) = Q(charge) / C (capacitance)

In a parallel circuit, the formula of capacitors is:

Ctotal = C1 + C2

Hence, two 5 farad capacitors in a parallel circuit arrangement with a charge of 100 coulomb and capacitance 10 F will give a potential difference of::

V = 100/10
V = 10 volts

In a series circuit, the formula for capacitors is:

1/Ctotal = 1/C1 + 1/C2

Hence, two 5 farad capacitors with a charge of 100 coulomb will give:

Ctotal = C1 × C2/C1 + C2

In the example total capacitance = 25/10 = 2.5 F

V = 100/2.5
V = 40 volts.

Tracheal tubes are made of either disposable plastic or reusable red rubber.

The tube size refers to the internal diameter (ID) in mm which is marked on the outside of the tube (some manufacturers mark the external diameter on the outside).

Plastic tubes have a radiopaque line spanning the entire length of the tube, which allows their position to be identified on x-rays. The bevel located at the end of the tube is left-facing and oval in shape, which improves the view of the vocal cords during intubation.

Oxford tubes are L-shaped and have a bevel that faces posteriorly. They have thick walls that increase the external diameter, making for a wider internal diameter.

RAE (Ring, Adair, and Elwyn) tubes are preformed and can either be north or south facing and cuffed or uncuffed. The cuffed RAE tubes have one Murphy eye, whereas the uncuffed has two Murphy eyes. Uncuffed tubes are primarily used in paediatric anaesthesia and the two Murphy eyes ensure adequate ventilation- should the tube be too long.

Every surgical procedure is associated with a stress response which comprises a number of endocrine, metabolic, and immunological changes triggered by neuronal activation of the hypothalamic-pituitary-adrenal axis. The overall metabolic effect of the stress response to surgery includes an increase in secretion of catabolic hormones, such as cortisol and catecholamine, and a decrease in secretion of anabolic hormones, such as insulin and testosterone. The increase in levels of catabolic hormones in plasma stimulates glucose production, and there is a relative lack of insulin together with impaired tissue insulin sensitivity and glucose utilization, which is called insulin resistance. Consequently, blood glucose concentrations will increase, even in the absence of pre-existing diabetes.

A study compared the effects of spinal and general anaesthesia on changes in blood glucose concentrations during surgery in nondiabetic patients. Although mean blood glucose concentrations showed a significant proportional increase during surgery in both groups, this effect was much more significant with general anaesthesia than with spinal anaesthesia. These results indicate that spinal anaesthesia is more effective than general anaesthesia in attenuating the hyperglycaemic response to surgery.

To begin, one must determine the child’s approximate weight. There are a variety of formulas to choose from. It is acceptable to use the advanced paediatric life support formula:

(age + 4) 2 = weight

A 5-year-old child will weigh around 18 kilogrammes.

The following are the appropriate doses of the drugs listed above:

Gentamicin (once daily) – 5-7 mg/kg = 90-126 mg and subsequent dose modified according to plasma levels
Ondansetron – 0.1 mg/kg, but a maximum of 4 mg as a single dose = 1.8 mg
Codeine should be administered orally at a dose of 1 mg/kg rather than intravenously, as the latter can cause ‘dangerous’ hypotension due to histamine release.
15 mg/kg paracetamol = 270 mg orally or intravenously (a loading dose of 20 mg/kg, or 360 mg, is sometimes recommended, which is not far short of the doses listed above).
Cefuroxime – the initial intravenous dose is 20 mg/kg (360 mg) depending on the indication (again, similar to the dose given in the answer options above).

The National Institute for Health and Care Excellence (NICE) has published guidelines on infective endocarditis prophylaxis (IE). The goal was to create clear guidelines for antibiotic prophylaxis in patients undergoing dental procedures as well as certain non-dental interventional procedures. A number of studies have found an inconsistent link between recent interventional procedures and the development of infective endocarditis in both dental and non-dental procedures.

Antibiotic prophylaxis against infective endocarditis is not advised or required in the following situations:

Dental patients undergoing procedures
Patients undergoing procedures involving the upper and lower gastrointestinal tracts, the genitourinary tract (including urological, gynaecological, and obstetric procedures, as well as childbirth), and the upper and lower respiratory tract (including ear, nose and throat procedures and bronchoscopy).

Antibiotic resistance can be exacerbated by the indiscriminate use of prophylactic antibiotics, but this is not the primary reason for avoiding their use in these situations.

To reduce the risk of endocarditis, any patient who is at risk of developing IE should be investigated and treated as soon as possible. Patients with the following conditions are at risk of developing IE:
acquired valvular heart disease with regurgitation or stenosis
previous valve replacement
structural congenital heart disease
past history of IE, or
hypertrophic cardiomyopathy (HOCM)

It would also be appropriate for high-risk dental procedures and those with severe gingival disease.

Although this patient may not have structural heart disease, ABs should be administered on a case-by-case basis.

It is well known that atropine will cross the placenta and that maternal administration results in an increase in fetal heart rate.

Atropine is highly selective for muscarinic receptors. Its potency at nicotinic receptors is much lower, and actions at non-muscarinic receptors are generally undetectable clinically. Atropine does not distinguish among the M1, M2, and M3 subgroups of muscarinic receptors. In contrast, other antimuscarinic drugs are moderately selective for one or another of these subgroups. Most synthetic antimuscarinic drugs are considerably less selective than atropine in interactions with nonmuscarinic receptors.

A study on glycopyrrolate, a quaternary ammonium salt, was found to have a fetal: maternal serum concentration ratio of 0.4 indicating partial transfer.

Heparin, suxamethonium, and vecuronium do not cross the placenta.

Intra-arterial blood pressure monitoring is a common place procedure in the ICU. It is used to provide accurate beat-to-beat information using a pressure wave displayed on a monitor.

It involves catheter insertion in a peripheral artery (most commonly the radial, brachial and dorsalis pedis arteries). Each subsequent contraction of cardiac muscles results in pressure wave which induces a mechanical motion of flow in the catheter. This mechanical motion is then passed on to a transducer through a rigid fluid-filled tubing. The transducer is the able to process this mechanical motion into electrical signals which are displayed as arterial waves and pressure represented numerically on the monitor.

The transducer should be placed at the same level as the heart on the phlebostatic axis, and at the level of the atria (the 4th intercostal space, in the mid-axillary line).

Air bubbles and catheter tubing with longer lengths result in wave dampening (rounding of the resulting pressure waves). This dampening causes a decrease in systolic pressure, and an increase in diastolic pressure.

An elevated arterial blood lactate level and an increase anion gap ([Na + K] – [Cl + HCO3]) of >20mmol gives rise to lactic acidosis. It can also be a result of overproduction and/or reduced metabolism of lactic acid.

The liver and kidney are the main sites of lactate metabolism, not skeletal muscle.

The two types of lactic acidosis that are known are:

Type A – due to tissue hypoxia, inadequate tissue perfusion and anaerobic glycolysis. These may be seen in cardiac arrest, shock, hypoxaemia and anaemia. The management of type A lactic acidosis involves reversing the underlying cause of the tissue hypoxia.

Type B – occurs in the absence of tissue hypoxia. Some of the causes of this include hepatic failure, renal failure, diabetes mellitus, pancreatitis and infection. Some drugs can also cause this lie aspirin, ethanol, methanol, biguanides and intravenous fructose.

The mainstay of treatment involves:
1. Optimising tissue oxygen delivery
2. Correcting the cause
3. Intravenous sodium bicarbonate

In resistant cases, peritoneal dialysis can be performed.

A compound that contains an asymmetric centre (chiral atom or chiral centre) and thus can occur in two non-superimposable mirror-image forms (enantiomers) are called chiral compounds.

Desflurane, Halothane, and isoflurane are chiral compounds but Sevoflurane is not a chiral compound.

The adrenal (suprarenal) gland is composed of two main parts: the adrenal cortex, which is the largest and outer part of the gland, and the adrenal medulla. The adrenal cortex consists of three zones: 1. Zona glomerulosa (outermost layer) is responsible for the production of mineralocorticoids, mainly aldosterone, which regulates blood pressure and electrolyte balance. 2. Zona fasciculata (middle layer) is responsible for the production of glucocorticoids, predominantly cortisol, which increases blood sugar levels via gluconeogenesis, suppresses the immune system, and aids in metabolism. It also produces 11-deoxycorticosterone and corticosterone in addition to cortisol. 3. Zona reticularis (innermost layer) is responsible for the production of gonadocorticoids, mainly dehydroepiandrosterone (DHEA), which serves as the starting material for many other important hormones produced by the adrenal gland, such as oestrogen, progesterone, testosterone, and cortisol. It is also responsible for administering these hormones to the reproductive regions of the body.

The adrenal medulla majorly secretes epinephrine (adrenaline), and norepinephrine in small quantity. Both hormones have similar functions and initiate the flight or fight response.

Catecholamine is mediated by cholinergic nicotinic transmission through changes in sympathetic nervous system (T5 – T11), being increased during stress and hypoglycaemia.

Blood supply to the adrenal gland is by these three arteries: superior suprarenal arteries, middle suprarenal artery and inferior suprarenal artery. Venous drainage is via the suprarenal vein to the left renal vein or directly to the inferior vena cava on the right side. There is no portal (venous) system between cortex and medulla.

Staphylococcus aureus infection is the most likely cause.

Surgical site infections (SSI) occur when there is a breach in tissue surfaces and allow normal commensals and other pathogens to initiate infection. They are a major cause of morbidity and mortality.

SSI comprise up to 20% of healthcare associated infections and approximately 5% of patients undergoing surgery will develop an SSI as a result.
The organisms are usually derived from the patient’s own body.

Measures that may increase the risk of SSI include:
-Shaving the wound using a single use electrical razor with a disposable head
-Using a non iodine impregnated surgical drape if one is needed
-Tissue hypoxia
-Delayed prophylactic antibiotics administration in tourniquet surgery, patients with a prosthesis or valve, in clean-contaminated surgery of in contaminated surgery.

Measures that may decrease the risk of SSI include:
1. Intraoperatively
– Prepare the skin with alcoholic chlorhexidine (Lowest incidence of SSI)
-Cover surgical site with dressing

In contrast to previous individual RCT’s, a recent meta analysis has confirmed that administration of supplementary oxygen does not reduce the risk of wound infection and wound edge protectors do not appear to confer benefit.

2. Post operatively
Tissue viability advice for management of surgical wounds healing by secondary intention

Use of diathermy for skin incisions
In the NICE guidelines the use of diathermy for skin incisions is not advocated. Several randomised controlled trials have been undertaken and demonstrated no increase in risk of SSI when diathermy is used.

Erythromycin binds to the 50s subunit of bacterial rRNA complex and inhibits protein synthesis.

Vancomycin binds to the acyl-D-ala-D-ala portion of the growing cell wall in a susceptible gram-positive bacterium. After binding, it prevents the cell wall from forming the cross-linking.

Trimethoprim binds to dihydrofolate reductase and inhibits the reduction of dihydrofolic acid to tetrahydrofolic acid. Tetrahydrofolic acid is an essential precursor in the thymidine synthesis pathway and interference with this pathway inhibits bacterial DNA synthesis.