Capnography is the non-invasive measurement and pictorial display of inhaled and exhaled carbon dioxide (CO2) partial pressure.

It is depicted graphically as the concentration of CO2 over time.

It is used in disease diagnosis, determining disease severity, assessing response to treatment and is the best method to for indicating when an endotracheal tube is placed in the trachea after intubation.

The wavelength of IR light usually absorbed by nitrous oxide is between 4.4-4.6?m (very close to that of CO2). Its absorption of wavelengths at 3.9 ?m is much weaker. It causes a measurable deficit of 0.1% for every 10% of nitrous oxide. The maximal wavelength of infrared (IR) light absorbed by carbon monoxide is 4.7 ?m. The volatile agents have strong absorption bands at 3.3 ?m and throughout the ranges 8-12 ?m.

IR light is not absorbed by oxygen (O2), but O2 and CO2 molecules are constantly colliding which interrupts the absorption of IR light by CO2. This increases the band of absorption, that is the Collison or pressure broadening). An oxygen percentage of 95 will result in a 0.5 percentage fall in CO2 measure.

IR light is also absorbed by water vapour which will result in an overlap of the absorption band, collision broadening and a dilution of partial pressure. This is why water trap and water permeable tubing is recommended for use as it reduces measurement inaccuracies.

The use of multi-gas analysers of modern gases also help reduce the effects of collision broadening.

Beer’s law is also applied in this system as an increase in the concentrations of CO2 causes a decrease in the amount of IR able to pass through the gas. This IR light is what generated the signal that is analysed for display.

The capnograph can indicate oesophageal intubation, but cannot determine if it is endotracheal or endobronchial. For this, auscultation is used.

The posterior tibial artery originates from the popliteal artery in the popliteal fossa. It passes posterior to the popliteus muscle to pierce the soleus muscle. It descends between the tibialis posterior and flexor digitorum longus muscles.

The posterior tibial artery supplies blood to the posterior compartment of the lower limb. The artery can be palpated posterior to the medial malleolus.

There are 4 main pulse points for the lower limb:

1. Femoral pulse 2-3 cm below the mid-inguinal point
2. Popliteal partially flexed knee to loosen the popliteal fascia
3. Posterior tibial behind and below the medial ankle
4. Dorsal pedis dorsum of the foot over the navicular bone

Cardiac output = stroke volume x heart rate

Left ventricular ejection fraction = (stroke volume / end diastolic LV volume ) x 100%

Stroke volume = end diastolic LV volume – end systolic LV volume

Pulse pressure = Systolic Pressure – Diastolic Pressure

Systemic vascular resistance = mean arterial pressure / cardiac output
Factors that increase pulse pressure include:
-a less compliant aorta (this tends to occur with advancing age)
-increased stroke volume

Flowmeters measure the rate at which a specific gas, that the flowmeter has been calibrated for, passes through. This calibration is done at room temperature and standard atmospheric pressure with an accuracy of +/- 2%.

Reading the flowmeter is done from the top of a bobbin (the midpoint of a ball). Oxygen is the last gas to be added downstream to the mixture delivered to the back bar as a safety feature. This prevents delivery of a hypoxic mixture.

Inaccurate flow measurements occur when the bobbin sticks to the inside wall of the flowmeter. Stannic oxide has been used as a successful antistatic substance thus, reducing the aforementioned risk.

Carbon dioxide being easily delivered is found on some older machines, but those attached flowmeters are limited by a maximum flow of 500 ml /min. Thus avoiding the delivery of a hypercarbic mixture.

Lorazepam is an intermediate-acting benzodiazepine that binds to the GABA-A receptor subunit to increase the frequency of chloride channel opening and cause membrane hyperpolarization.

Lorazepam has emerged as the preferred benzodiazepine for acute management of status epilepticus. Lorazepam differs from diazepam in two important respects. It is less lipid-soluble than diazepam, with a distribution half-life of two to three hours versus 15 minutes for diazepam. Therefore, it should have a longer duration of clinical effect. Lorazepam also binds the GABAergic receptor more tightly than diazepam, resulting in a longer duration of action. The anticonvulsant effects of lorazepam last six to 12 hours, and the typical dose ranges from 4 to 8 mg. This agent also has a broad spectrum of efficacy, terminating seizures in 75-80% of cases. Its adverse effects are identical to those of diazepam. Thus, lorazepam also is an effective choice for acute seizure management, with the added possibility of a longer duration of action than diazepam.

Phenobarbitone is a long-acting barbiturate that binds to GABA-A receptor site and increase the duration of chloride channel opening. It also blocks glutamic acid neurotransmission, and, at high doses, can block sodium channels. It is considered as the drug of choice for seizures in infants.

Phenytoin is an anti-seizure drug that blocks voltage-gated sodium channels. It is preferred in prolonged therapy of status epilepticus because it is less sedating.

In cases wherein airway protection is required, thiopentone and propofol are the preferred drugs.

The ASA physical status classification system is a system for assessing the fitness of patients before surgery. It was last updated in October 2014.

ASA I A normal healthy patient
ASA II A patient with mild systemic disease
ASA III A patient with severe systemic disease
ASA IV A patient with severe systemic disease that is a constant threat to life
ASA V A moribund patient who is not expected to survive without the operation
ASA VI A declared brain-dead patient whose organs are being removed for donor purposes

A 20-year old woman who is 39-weeks pregnant with no other medical conditions – ASA II

A 35-year-old man with a BMI of 29 with a good exercise tolerance who smokes-ASA II

A 50-year old man with a BMI of 41 with a reduced exercise tolerance -ASA III

A 65-year old woman with a BMI of 34 with treated hypertension with no functional limitations-ASA II

A 73-year old man who has had a TIA ten-weeks ago but has a good exercise tolerance and is a non-smoker-ASA IV

The sternocleidomastoid muscle divides the neck into anterior and posterior triangles on both sides of the neck.

The posterior triangle has the following boundaries:
anteriorly – sternocleidomastoid muscle
posteriorly – trapezius
roof – investing layer of deep cervical fascia
floor – prevertebral fascia overlying splenius capitis, levator scapulae, and the scalene muscles

The contents of the posterior triangle are:
1. fat
2. lymph nodes (level V)
3. accessory nerve
4. cutaneous branches of the cervical plexus – greater auricular nerve, transverse cervical nerve, lesser occipital nerve, supraclavicular nerve (A major branch of this plexus is the phrenic nerve, which arises from the anterior divisions of spinal nerves C3-C5)
5. inferior belly of omohyoid
6. branches of the thyrocervical trunk (transverse cervical and suprascapular arteries)
7. third part of the subclavian artery
8. external jugular vein

The patient in the case has a fluid volume requirement of 30 mL/kg/day. His basic electrolyte requirement per day is:

Sodium at 2 mmol/kg/day x 110 = 220 mmol/day
Potassium at 1 mmol/kg/day x 110 = 110 mmol/day

His energy requirement per day is:

35 kcal/kg/day x 110 kg = 3850 kcal/day

One gram of glucose in fluid can provide approximately 4 kilocalories.

The following are the electrolyte components of the different intravenous fluids:

Fluid Na (mmol/L) K (mmol/L)
0.9% Normal saline (NSS) 154 0
0.45% NSS + 5% dextrose 77 0
0.18% NSS + 4% dextrose 30 0
Hartmann’s 131 5
5% dextrose 0 0

1000 mL of 5% dextrose has 50 g of glucose

Option B is inadequate for his sodium and caloric requirements (30 mmol of Na+ and 560 kcal). It is adequate for his K+ requirement (120 mmol of K+).

Option C is in excess of his Na+ requirement (462 mmol of Na+). Moreover, it does not provide any K+ replacement.

Option D is inadequate for his caloric requirement (600 kcal) and K+ requirement (60 mmol of K+). Moreover it does not provide any Na+ replacement.

Option E is in excess of his Na+ requirement (393 mmol of Na+), and is inadequate for his potassium requirement (15 mmol of K+)

Option A has adequate amounts for his Na+ (231 mmol of Na+) and K+ (120 mmol of K+) requirements. It is inadequate for his caloric requirement (600 kcal).

The pulse oximeter provides a continuous non-invasive measurement of the arterial oxygen saturation. The light emitting diodes (LEDs) produce beams of red and infrared light at 660 nm and 940 nm respectively (not 640 and 960 nm), which travel through a finger (toe, ear lobe or nose) and are then detected by a sensitive photodetector.

The light absorbed by non-pulsatile tissues is constant (DC), and the non-constant absorption (AC) is the result of arterial blood pulsation. The DC and AC components at 660 and 940 nm are then analysed by the microprocessor and the result is related to the arterial saturation.

An isosbestic point is a point at which two substances absorb a wavelength of light to the same degree. In pulse oximetry the different absorption profiles of oxyhaemoglobin and deoxyhaemoglobin are used to quantify the haemoglobin saturation (in %). Isosbestic points occur at 590 and 805 nm (not 490 and 805 nm), where the light absorbed is independent of the degree of saturation, and are used as reference points.

The pulse oximeter is accurate to within +/- 2% in the range of 70% to 100% saturation, and below 70% the readings are extrapolated. Pulse oximeters average their readings every 10 to 20 seconds and thus they cannot detect acute desaturation events. Consequently, they are often referred to as ‘lag’ monitors, due to the time delay in identifying the desaturation episode.

Ambient pressure has no effect on a volatile agent’s saturated vapour pressure (SVP). At a temperature of 20°C, the SVP of sevoflurane is approximately 21 kPa, or 21% of atmospheric pressure (100 kPa).

The SVP of sevoflurane remains the same when the ambient pressure is doubled to 200 kPa, but the output of the vaporiser is halved, now 21 percent of 200 kPa, equalling 10.5 percent. The vaporiser’s output has increased to 1%, but the partial pressure output has remained unchanged. The splitting ratio will not change because it is determined by temperature changes.

Calculations can be made as follows:

Vaporizer output % (ambient pressure) = % volatile (calibrated) x 100 kPa calibrated pressure/ambient pressure
2% = 2% (dialled) × 100/100
2% of 100 = 2 kPa

Altitude, pressure 50 kPa
4% = 2% (dialled) × 100/50
4% of 50 = 2 kPa

High pressure at 200 kPa
1% = 2% (dialled) × 100/200
1% of 200 = 2 kPa

Sevoflurane has a boiling point of 58°C and, unlike desflurane (which has a boiling point of 22.8°C), does not need to be heated and pressurised with a Tec 6 vaporiser.

The inguinal triangle of Hesselbach’s is an important clinical landmark on the posterior wall of the inguinal canal. It has the following relations:
Inferiorly – medial third of the inguinal ligament
Medially – lower lateral border of the rectus abdominis
Laterally – inferior epigastric vessels

Direct inguinal hernia is when the bowel bulges directly through the abdominal wall. These hernias usually protrude through Hesselbach’s triangle

A is correct. Common myeloid progenitor cells are involved in the anaphylaxis reaction.
B is incorrect. The common lymphoid lineage gives rise to T-cells, B-cell and NK cells.
C is incorrect as megakaryocytes give rise to platelets.
D is incorrect – Neural crest cells give rise to various cells throughout the body, including melanocytes, enterochromaffin cells and Schwann cells. However, they do not give rise to mast cells.
E is incorrect. Reticulocytes give rise to erythrocytes.

This is a classic case of anaphylaxis. In this situation, IgE previously raised against antigens (in this case peanut antigen) bind to mast cells, and this causes them to degranulate.
There is release of vasoactive substances like histamine into the blood, and this is responsible for the symptoms seen. Therefore, the main type of cells involved in the pathogenesis of the disease is mast cells.

Sodium-chloride symporter inhibitor.

The thiazide sensitive sodium chloride symporter is inhibited by thiazides at the proximal portion of the distal convoluted tubule leading to increased sodium and water excretion. Increased delivery of sodium to the distal portion of the distal convoluted tubule promotes potassium loss. This is why thiazides are associated with hyponatraemia and hypokalaemia.

Carbonic anhydrase inhibitors are used mainly in the treatment of glaucoma. They act on the proximal convoluted tubule to promote bicarbonate, sodium and potassium loss.

Sodium potassium chloride symporter is inhibited by Loop diuretics.
Epithelial sodium channels are inhibited by Amiloride.
Drugs which lead to nephrogenic diabetes insipidus such as lithium and demeclocycline, are Inhibitors of vasopressin.

Cephalosporin belongs to a family of beta-lactam antibiotics. All ?-lactam antibiotics interfere with the synthesis of the bacterial cell walls. The ?-lactam antibiotics inhibit the transpeptidases so that cross-linking (which maintains the close-knit structure of the cell wall) does not take place i.e. they inhibit bacterial cell wall formation.

The cricoid cartilage is a hyaline cartilage ring surrounding the trachea. It provides support for key phonation muscles.

The inferior border of the cricoid cartilage is attached to the thyroid cartilage and the inferior border is attached to the first tracheal ring through the cricotracheal ligament.

Application of pressure to the cricoid cartilage to reduce risk of aspiration of gastric contents (Sellick manoeuvre) does not stop tracheal aspiration and cannot stop regurgitation into the oesophagus.

A force of 44 newtons to the cricoid cartilage is needed to control regurgitation.

There are two types of defibrillators
AC defibrillator
DC defibrillator

AC defibrillator,
consists of a step-up transformer with primary and secondary winding and two switches. Since secondary coil consists of more turns of wire than the primary coil, it induces larger voltage. A voltage value ranging between 250V to 750V is applied for AC external defibrillator. And used to enable the charging of a capacitor.

DC defibrillator,
consists of auto transformer T1 that acts as primary of the high voltage transformer T2. Is an iron core that transfers energy between 2 circuits by electromagnetic induction. Transformers are used to isolate circuits, change impedance and alter voltage output. transformers do not convert AC to DC.

Diode rectifier composed of 4 diodes made of semiconductor material allows current to flow only in one direction. Alternating current (AC) passing through these diodes produces direct current (DC). Capacitor stores the charge in the form of an electrostatic field.

Capacitor is used to convert the rectified AC voltage to produce DC voltage but capacitors do not directly convert AC to DC.

Inductor induces a counter electromotive force(emf) that reduces the capacitor discharge value.

In step-down transformer primary coils has more turns of wire than secondary coil, so induced voltage is smaller in the secondary coil.

The ventilatory anaerobic threshold (VAT), formerly referred to as the anaerobic threshold, is an index used to estimate exercise capacity. During the initial (aerobic) phase of CPET, which lasts until 50–60% of Vo2max is reached, expired ventilation (VE) increases linearly with Vo2 and reflects aerobically produced CO2 in the muscles. Blood lactate levels do not change substantially during this phase, since muscle lactic acid production is minimal.

During the latter half of exercise, anaerobic metabolism occurs because oxygen supply cannot keep up with the increasing metabolic requirements of exercising muscles. At this time, there is a significant increase in lactic acid production in the muscles and in the blood lactate concentration. The Vo2 at the onset of blood lactate accumulation is called the lactate threshold or the VAT. The VAT is also defined as the point at which minute ventilation increases disproportionately relative to Vo2, a response that is generally seen at 60–70% of Vo2max.

The VAT is a useful measure as work below this level encompasses most daily living activities. The ability to achieve the VAT can help distinguish cardiac and non‐cardiac (pulmonary or musculoskeletal) causes of exercise limitation, since patients who fatigue before reaching VAT are likely to have a non‐cardiac problem.

When VAT is detected, patients with PVo2 of ⩽10 ml/kg/min have a high event rate.

The coronary sinus is large venous structure located on the posterior aspect of the left atrium, coursing within the left atrioventricular groove. The function of the coronary sinus is to drain the venous blood from the majority of the heart. It opens into the right atrium between the opening of inferior vena cava, the fossa ovalis and the right atrioventricular orifice. The coronary sinus is often guarded by a thin, semicircular endocardial fold, also known as the thebesian valve.
Tributaries include: Great cardiac vein, middle cardiac vein, small cardiac vein, posterior vein of left ventricle, oblique vein of left atrium. The great cardiac vein is the largest tributary of the coronary sinus.

Noradrenaline also called norepinephrine belongs to the catecholamine family that functions in the brain and body as both a hormone and neurotransmitter.

They have sympathomimetic effects acting via adrenoceptors (?1, ?2,?1, ?2, ?3) or dopamine receptors (D1, D2).

May cause reflex bradycardia, reduce cardiac output and increase myocardial oxygen consumption

Myoglobin is a haemoglobin-like, iron-containing pigment that is found in muscle fibres. It has a high affinity for oxygen and it consists of a single alpha polypeptide chain. It binds only one oxygen molecule, unlike haemoglobin, which binds 4 oxygen molecules.

The myoglobin ODC is a rectangular hyperbola. There is a very low P50 0.37 kPa (2.75 mmHg). This means that it needs a lower P50 to facilitate oxygen offloading from haemoglobin. It is low enough to be able to offload oxygen onto myoglobin where it is stored. Myoglobin releases its oxygen at the very low PO2 values found inside the mitochondria.

P50 is defined as the affinity of haemoglobin for oxygen: It is the PO2 at which the haemoglobin becomes 50% saturated with oxygen. Normally, the P50 of adult haemoglobin is 3.47 kPa(26 mmHg).

Foetal haemoglobin has 2 ? and 2 ?chains. The ODC is left shifted – this means that P50 lies between 2.34-2.67 kPa [18-20 mmHg]) compared with the adult curve and it has a higher affinity for oxygen. Foetal haemoglobin has no ? chains so this means that there is less binding of 2.3 diphosphoglycerate (2,3 DPG).

Carbon monoxide binds to haemoglobin with an affinity more than 200-fold higher than that of oxygen. This therefore decreases the amount of haemoglobin that is available for oxygen transport. Carbon monoxide binding also increases the affinity of haemoglobin for oxygen, which shifts the oxygen-haemoglobin dissociation curve to the left and thus impedes oxygen unloading in the tissues.

In sickle cell disease, (HbSS) has a P50 of 4.53 kPa(34 mmHg).

Midazolam is the benzodiazepine in question. It’s the only benzodiazepine that undergoes tautomeric transformation (dynamic isomerism). The molecule is ionised and water soluble at pH 3.5, but when injected into the body at pH 7.4, it becomes unionised and lipid soluble, allowing it to easily pass through the blood brain barrier.

The half-life of midazolam is only 2-4 hours.

It is a GABAA receptor agonist because it is a benzodiazepine. GABAA receptors are found in abundance throughout the central nervous system, particularly in the cerebral cortex, hippocampus, thalamus, basal ganglia, and limbic system. GABAA receptors are ligand-gated ion channels, with the inhibitory neurotransmitter gamma-aminobutyric acid as the endogenous agonist. It is a pentameric protein (2, 2 and one subunit) that spans the cell membrane, and when the agonist interacts with the alpha subunit, a conformational change occurs, allowing chloride ions to enter the cell, resulting in neuronal hyperpolarization.

For status epilepticus, midazolam is not the drug of choice. Lorazepam is the benzodiazepine of choice for status epilepticus.

The guidelines for the management of cardiac arrest in hypothermic patients published by the UK Resuscitation Council differ slightly from the standard algorithm.

In a patient with a core temperature of less than 30°C, do the following:

If you’re on the shockable side of the algorithm (VF/VT), you should give three DC shocks.
Further shocks are not recommended until the patient has been rewarmed to a temperature of more than 30°C because the rhythm is refractory and unlikely to change.
There should be no drugs given because they will be ineffective.

In a patient with a core temperature of 30°C to 35°C, do the following:

DC shocks are used as usual.
Because they are metabolised much more slowly, the time between drug doses should be doubled.

Active rewarming and protection against hyperthermia should be given to the patient.

Option e is false because there is insufficient information to determine whether resuscitation should be stopped.

The level of statistical significance required influences the sample size used. This is because sample size is used in the calculation of SD/SE.

Sample size does not affect

The level of acceptance
The alternative hypothesis with a general level set at p<0.05
The test to be used.

Experience of the investigator and the type of patient recruited should have no bearing on the required sample size.

The vagus nerve is a mixed nerve with both autonomic and somatic effects. Its most important somatic effect is the motor supply to the larynx via recurrent laryngeal nerves. If one vagus nerve is damaged, the result will be the same as damage to a single recurrent laryngeal nerve, leading to hoarseness of voice.

The vagus exits the skull via the jugular foramen, accompanied by the accessory nerve.

Anal tone, erections, and urination are all controlled by the sacral parasympathetic and would not be affected by the loss of the vagus. Parasympathetic controlled pupillary constriction is via the oculomotor nerve and would not be affected by the loss of the vagus.

According to European Group protocol for the investigation of MH susceptibility, muscle biopsy should be performed on quadriceps muscle (either vastus medialis or vastus lateralis), using regional anaesthesia (avoiding local anaesthetic infiltration) or general anaesthetic techniques. Local anaesthetic solution within muscle fibres may affect in vitro contraction testing.

Desflurane is a weak triggering anaesthetic of malignant hyperthermia so is avoided in MH susceptible patients. This includes all volatile inhalational agents and suxamethonium.

General anaesthetic with the volatile free anaesthetic machine may be considered but spinal anaesthesia is a better choice due to the possibility of airway problems.

The fibrotendinous ring formed by the congregation of the rectus muscles at the apex of the orbit does not include superior oblique. This muscle is completely outside the ring and so it is the most difficult muscle to anaesthetise completely. A good grasp of the anatomy of the area being anaesthetised is important with all regional anaesthetic techniques so that potential problems and complications with a block can be anticipated.

The borders of this pyramid whose apex points upwards and outwards of the bony orbit are as follows:
Floor – Zygoma and Maxilla
Roof – frontal bone
Medial wall – maxilla, ethmoid, sphenoid and lacrimal bones.
Lateral wall – greater wing of the sphenoid and the zygoma.

The four recti muscles (superior, medial, lateral and inferior) originate from a tendinous ring (the annulus of Zinn) and extend anteriorly to insert beyond the equator of the globe. Bands of connective tissue are present between the rectus muscles forming a conical structure and hinder the passage of local anaesthetic.

The superior oblique muscle is situated outside this ring and is the most difficult muscle to anaesthetise completely, particularly with a single inferotemporal peribulbar injection. An additional medial injection may help to prevent this.

The cranial nerve supply to the extraocular muscles are:
3rd (inferior oblique, inferior recti, medial and superior)
4th (superior oblique), and
6th (lateral rectus).

The long and short ciliary nerves provide the sensory supply to the globe and these are branches of the nasociliary nerve, (which is itself a branch of the ophthalmic division of the trigeminal nerve).

To achieve anaesthesia for the eye, these nerves which enter the fibrotendinous ring need to be fully blocked to anaesthetise the eye for surgery.

Malignant hyperthermia (MH) is a autosomal dominant inherited medical condition which predisposes affected individuals to a clinical syndrome of hypermetabolism which involves abnormal ryanodine receptors in skeletal muscle causing a deregulation of calcium in muscle.

It is a life threatening condition requiring immediate medical intervention. It often lies dormant until triggered in susceptible individuals mostly by volatile inhaled anaesthetic agents and succinylcholine which is a muscle relaxant.

The signs and symptoms of MH are related to this hypermetabolism, which includes an increase in carbon dioxide production, metabolic and respiratory acidosis, accelerated oxygen consumption, heat production, activation of the sympathetic nervous system, hyperkalaemia, disseminated intravascular coagulation (DIC), and multiple organ dysfunction and failure.

Early signs of MH to look out for in patients includes an uptick in end-tidal carbon dioxide (even with increasing minute ventilation), tachycardia, muscle rigidity, tachypnoea, and hyperkalaemia. Later signs include fever, myoglobinuria, and multiple organ failure.

In vitro muscle contracture test (IVCT) is the standard for determining individual susceptibility to MH. It is conducted by measuring the force of muscle contraction after exposing the patient’s muscle sample to halothane and caffeine., the sample is normally taken from the vastus medialis or lateralis under regional anaesthesia.

The patient likely suffers from pulmonary embolism due to her history of frequent international travels. A filter is placed in the inferior vena cava to decrease the risk of future episodes of pulmonary embolism. The IVC filter is a small, wiry device that can catch blood clots and stop them from going into the heart and lungs. Your IVC is a major vessel that brings deoxygenated blood from the lower body to the heart, from where it is pumped into the lungs.

The filter is placed via a thin catheter inserted into the femoral vein in the groin. The catheter is gently moved up into your IVC, and a filter is introduced.

The IVC is a retroperitoneal organ.

Insulin is the primary anabolic hormone that dominates regulation of metabolism during digestive phase. It promotes glucose uptake in skeletal myocytes and adipocytes, and other insulin-target cells. It promotes glycogenesis and inhibits gluconeogenesis.

Glucagon is the primary counterregulatory hormone that increases blood glucose levels, primarily through its effects on liver glucose output.

Similar to glucagon, growth hormone, catecholamines and corticosteroids are also counterregulatory factors released in response to decreased glucose concentrations. Growth hormone promotes glycogenolysis and inhibits gluconeogenesis; catecholamines stimulate glycogenolysis and gluconeogenesis; while corticosteroids stimulate glycogenesis and gluconeogenesis.

The process used in the study is Delphi method. This method kicks off with an open ended questionnaire and uses its responses as a survey instrument for the next round in which each of the participants is asked to rate the items that the investigators have summarized on the basis of the data collected in the first round.

Any disagreement is further discussed in phases to come on the basis of information obtained from previous phases.