ICP is significant because it influences cerebral perfusion pressure and cerebral blood flow. The normal ICP ranges from 5 to 13 mmHg.

The components within the skull include the brain (80%/1400 ml), blood (10%/150 ml), and cerebrospinal fluid (CSF) (10%/150 ml).

Because the skull is a rigid box, if one of the three components increases in volume, one or more of the remaining components must decrease in volume to compensate, or the ICP will rise (Monroe-Kellie hypothesis).

Primary brain injury occurs as a result of a head injury and is unavoidable unless precautions are taken to reduce the risk of head injury. A reduction in oxygen delivery due to hypoxemia (low arterial PaO2) or anaemia, a reduction in cerebral blood flow due to hypotension or reduced cardiac output, and factors that cause a raised ICP and reduced CPP are all causes of secondary brain injury. Secondary brain injury can be avoided with proper management.

The most important initial management task is to make certain that:

There is protection of the airway and the cervical spine
There is proper ventilation and oxygenation
Blood pressure and cerebral perfusion pressure are both adequate (CPP).

Following the implementation of these management principles, additional strategies to reduce ICP and preserve cerebral perfusion are required. The volume of one or more of the contents of the skull can be reduced using techniques that can be used to reduce ICP.

Reduce the volume of brain tissue
Blood volume should be reduced.
CSF volume should be reduced.

The following are some methods for reducing the volume of brain tissue:
Abscess removal or tumour resection
Steroids (especially dexamethasone) are used to treat oedema in the brain.
To reduce intracellular volume, use mannitol/furosemide or hypertonic saline.
To increase intracranial volume, a decompressive craniectomy is performed.

The following are some methods for reducing blood volume:

Haematomas must be evacuated.
Barbiturate coma reduces cerebral metabolic rate and oxygen consumption, lowering cerebral blood volume as a result.
Hypoxemia, hypercarbia, hyperthermia, vasodilator drugs, and hypotension should all be avoided in the arterial system.
PEEP/airway obstruction/CVP lines in neck: patient positioning with 30° head up, avoid neck compression with ties/excessive rotation, avoid PEEP/airway obstruction/CVP lines in neck

The following are some methods for reducing CSF volume:

To reduce CSF volume, an external ventricular drain or a ventriculoperitoneal shunt is inserted (although more a long term measure).

The neuroleptic malignant syndrome (NMS) is a rare complication in response to neuroleptic or antipsychotic medication.

The main features are:
– Elevated creatinine kinase
– Hyperthermia and tachycardia
– Altered mental state
– Increased white cell count
– Insidious onset over 1-3 days
– Extrapyramidal dysfunction (muscle rigidity, tremor, dystonia)
– Autonomic dysfunction (Labile blood pressure, sweating, salivation, urinary incontinence)

Management is supportive of ICU care, anticholinergic drugs, increasing dopaminergic activity with Amantadine, L-dopa, and dantrolene, and non- depolarising neuromuscular blockade drugs.

Since Olanzapine is a potential cause of NMS it is not a treatment.

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.

The duodenojejunal flexure is the point where the duodenum becomes the jejunum.

The ligament of Treitz, which arises from the right crus of diaphragm, provides suspension for support.

Between the ileum and the caecum is the ligament of Treves.

The aminosteroid rocuronium is the neuromuscular blocking agent in question.

0.3 mg/kg is the effective dose 95 (ED95) (the dose required to depress the twitch height by 95 percent )
The dose for intubation is 0.6 mg/kg.
75 seconds is the time it takes to reach 95 percent depression of the first twitch of the train of four (ToF) or the onset time.
The clinical duration or time to 25% recovery of the first twitch of the train of four (ToF) is 33 minutes.

A modified cyclodextrin can quickly reverse both rocuronium and vecuronium (sugammadex).

It is more fat-soluble than vecuronium, with the liver absorbing the majority of the drug and excreting it in the bile. The only metabolite found in the blood (17-desacetylrocuronium) is 20 times less potent than the parent drug and is unlikely to cause neuromuscular block.

Despite its quick onset of action (60-90 seconds), suxamethonium arguably is still the neuromuscular blocker of choice for a quick sequence induction. Rocuronium is becoming increasingly popular for this purpose.

The standard error of the mean (SEM) is a measure of the spread expected for the mean of the observations – i.e. how ‘accurate’ the calculated sample mean is from the true population mean. The relationship between the standard error of the mean and the standard deviation is such that, for a given sample size, the standard error of the mean equals the standard deviation divided by the square root of the sample size.

SEM = SD / square root (n)

where SD = standard deviation and n = sample size

Breathing 100% oxygen for three minutes will provide the best reservoir of oxygen during apnoea by oxygenating the functional residual capacity (FRC).

Sitting at 45 degrees might increase the FRC and improve oxygen reserve but not compared with 100% oxygenation.

The following table compares the oxygen reserves in the body following pre-oxygenation with room air and 100% oxygen:

Compartment Factors Room air (mL) 100% O2 (mL)
Lung FAO2, FRC 630 2850
Plasma PaO2, DF, PV 7 45
Red blood cells Hb, TGV, SaO2 788 805
Myoglobin – 200 200
Interstitial space – 25 160

FAO2 = alveolar fraction of oxygen.
FRC = Functional residual capacity.
PaO2 = partial pressure of oxygen dissolved in arterial blood
DF = dissolved form.
PV = plasma volume.
TG = total globular volume .
Hb = haemoglobin concentration.
SaO2 = arterial oxygen saturation

Stopping smoking one month prior to surgery will not be more effective than pre-oxygenation with 100% oxygen though it may reduce postoperative pulmonary complications. Note that both long term and short term abstinence reduces pulse rate and blood pressure thus reducing oxygen consumption and also reduce carboxyhaemoglobin levels.

Blood transfusion will not make a big difference in oxygen reserve, particularly if a blood transfusion is administered within 12-24-hours before surgery.

Heliox (79% helium and 21% oxygen) despite its lower viscosity is unlikely to be more effective than 100% oxygen .

Among the breathing circuits, the Lack circuit is the most efficient for spontaneous breathing.

An outer coaxial tube is present to deliver fresh air; exhaust air is routed to an inner tube, which is then delivered to a scavenging system. An expiratory valve is seen at the patient end, which is an advantage over other circuits. Moreover, the Lack circuit prevents rebreathing slightly greater than the alveolar minute ventilation at 4-5 litres per minute.

The Bain circuit prevents rebreathing at 160-200ml/kg per minute, and is a co-axial version of the Mapleson D circuit.

The Mapleson E circuit prevent rebreathing at a fresh gas flow (FGF) of approximately twice the patient’s normal minute volume. A modification of this, the Mapleson F, has a reservoir bag at the opposite end for the FGF. This circuit is appropriate for paediatric patients with a body weight less than 20 kg.

30 mmol Na+ and 30 mmol Cl- are found in 1 litre of 0.18 percent N. saline with 4% dextrose. Percent (percent) refers to the number of grammes of a compound per 100 mL, so a litre of 4 percent dextrose solution contains 40 grammes.

As a result, a 500 mL bag of 1/5th N. saline and 4% dextrose contains approximately 15 mequivalents of sodium and 20 g of glucose. It is hypotonic due to its osmolarity of 284.

Because of the risk of hyponatraemia, it is no longer considered the crystalloid of choice for fluid maintenance in children.

Because alpha glucosidase inhibitors slow starch digestion in the small intestine, glucose from a meal enters the bloodstream more slowly and can be matched more effectively by an impaired insulin response or sensitivity, glucose from a meal enters the bloodstream more slowly and can be matched more effectively by an impaired insulin response or sensitivity.

Biguanides decrease hepatic glucose output while increasing glucose uptake in peripheral cells.

The meglitinides are secretagogues that act on a different site of the KATP receptors.

Insulin secretion is stimulated by sulphonylureas, which stimulate insulin secretion from pancreatic beta cells. The KATP channels are inhibited by these substances.

Insulin-sensitive genes are influenced by thiazolidinediones, which increase the production of mRNAs for insulin-dependent enzymes. As a result, the cells make better use of glucose.

The patient is rebreathing carbon dioxide that has been exhaled.

Exhaustion of the soda lime and failure of the expiratory valve are the two most likely causes. A leak in the inspiratory limb is a less likely cause. Increased inhaled and exhaled carbon dioxide levels may appear with a normal-looking capnogram if the expiratory valve is ineffective.

The patient will exhale into both the inspiratory and expiratory limbs if the inspiratory valve is inoperable. A slanted downstroke inspiratory phase (as the patient inhales carbon dioxide-containing gas from the inspiratory limb) and increased end-tidal carbon dioxide can be seen on the capnogram.

Even if the soda lime were exhausted, a high fresh gas flow would be enough to prevent rebreathing. The difference in oxygen concentrations in inspired and expired breaths would be less pronounced.

Hypercapnia is caused by respiratory obstruction and malignant hyperthermia, but not by rebreathing.

Loop diuretics act by causing inhibition of Na+ K+ 2Cl– symporter present at the luminal membrane of the ascending limb of the loop of Henle.

Furosemide, torsemide, bumetanide, ethacrynic acid, furosemide, piretanide, tripamide, and mersalyl are the important members of this group

The main use of loop diuretics is to remove the oedema fluid in renal, hepatic, or cardiac diseases. Thus they are useful in the treatment of acute heart failure. These can be administered i.v. for prompt relief of acute pulmonary oedema (due to vasodilatory action).

Hypokalaemia, hypomagnesemia, hyponatremia, alkalosis, hyperglycaemia, hyperuricemia, and dyslipidaemia are seen with both thiazides as well as loop diuretics

Dopamine (DA) is a dopaminergic (D1 and D2) as well as adrenergic ? and?1 (but not ?2 ) agonist.

The D1 receptors in renal and mesenteric blood vessels are the most sensitive: i.v. infusion of a low dose of DA dilates these vessels (by raising intracellular cAMP). This increases g.f.r. In addition, DA exerts a natriuretic effect by D1 receptors on proximal tubular cells.

Moderately high doses produce a positive inotropic (direct?1 and D1 action + that due to NA release), but the little chronotropic effect on the heart.

Vasoconstriction (?1 action) occurs only when large doses are infused.

At doses normally employed, it raises cardiac output and systolic BP with little effect on diastolic BP. It has practically no effect on nonvascular ? and ? receptors; does not penetrate the blood-brain barrier—no CNS effects.

Dopamine is used in patients with cardiogenic or septic shock and severe CHF wherein it increases BP and urine outflow.

It is administered by i.v. infusion (0.2–1 mg/min) which is regulated by monitoring BP and rate of urine formation

Such a high rise of end-tidal CO2 (EtCO2) in a patient who is spontaneously breathing is often encountered.

Close observation should occur for further rises in EtCO2 and other signs of malignant hyperthermia. If this were to rise even more, it might be wise to ensure that ventilatory support is available.

A lot would depend on whether surgery was almost completed. At this stage of anaesthesia, it would be inappropriate to administer opioid antagonists or respiratory stimulants.

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.

When using dry soda lime for VOCs, very high amounts of carbon monoxide may be produced, regardless of the inhalational anaesthetic agent used. The carbon monoxide produced is sufficient enough to cause cytotoxic and anaemic hypoxia. To prevent this, soda lime canisters are shaken well to even out the packing of granules. This can help to evenly distribute gas flow for proper CO2 absorption and ventilation.

Compound A is formed when dry soda lime, or soda lime in high temperature, reacts with the inhalational anaesthetic Sevoflurane. Animal studies have shown renal toxicity in rats, but renal adverse effects in humans are yet to be observed.

When monitors are not employed with VOCs, deleterious effects are not for certain. However, monitors not employed with vaporiser inside the circuit (VIC) can lead to significant adverse events.

Decreased platelet concentrations with eclampsia were described as early as 1922 by Stancke. The platelet count is routinely measured in women with any form of gestational hypertension. The frequency and intensity of thrombocytopenia vary and are dependent on the severity and duration of the preeclampsia syndrome and the frequency with which platelet counts are performed.

Overt thrombocytopenia defined by a platelet count < 100,000/microliter - indicates severe disease. In general, the lower the platelet count, the higher the rates of maternal and fetal morbidity and mortality. In most cases, delivery is advisable because thrombocytopenia usually continues to worsen. After delivery, the platelet count may continue to decline for the first day or so. It then usually increases progressively to reach a normal level within 3-5 days. In some instances with HELLP syndrome, the platelet count continues to fall after delivery. If these do not reach a nadir until 48 to 72 hours, then preeclampsia syndrome may be incorrectly attributed to one of the thrombotic microangiopathies. The following are other severe features associated with preeclampsia: Proteinuria: >/= 300 mg/24 hours; or urine protein: creatinine ratio >/= 0.3; or dipstick 1+

Renal insufficiency: serum creatinine > 1.1 mg/dL or doubling of creatinine in the absence of other renal disease

Impaired liver function: two times elevated AST/ALT or unexplained right upper quadrant pain or epigastric pain unresponsive to medications

Pulmonary oedema

Cerebral or visual symptoms: headache, visual disturbances

There are different classes of electrical equipment that can be classified in the table below:

Class 1 – provides basic protection only. It must be connected to earth and insulated from the mains supply

Class II – provides double insulation for all equipment. It does not require an earth.

Class III – uses safety extra low voltage (SELV) which does not exceed 24 V AC. There is no risk of gross electrocution but risk of microshock exists.

Type B – All of above with low leakage currents (0.5mA for Class IB, 0.1 mA for Class IIB)

Type BF – Same as with other equipment but has ‘floating circuit’ which means that the equipment applied to patient is isolated from all its other parts.

Type CF – Class I or II equipment with ‘floating circuits’ that is considered to be safe for direct connection with the heart. There are extremely low leakage currents (0.05mA for Class I CF and 0.01mA for Class II CF)

These clinical signs suggest that 15-30% of circulating blood volume has been lost.

Pelvic fractures are associated with significant haemorrhage (>2000 ml) that can be concealed. This may require aggressive fluid resuscitation which is initially with crystalloids and then blood. What is also important is including stabilisation of the fracture(s) and pain relief.

The Advanced Trauma Life Support (ATLS) classification of haemorrhagic shock is as follows:

Class I haemorrhage (blood loss up to 15%):
<750 ml of blood loss
Minimal tachycardia
No changes in blood pressure, RR or pulse pressure
Patients do not normally not require fluid replacement as will be restored in 24 hours, but in trauma, this needs to be correct.

Class II haemorrhage (15-30% blood volume loss):
Uncomplicated haemorrhage requiring crystalloid resuscitation
Represents about 750 – 1500 ml of blood loss
Tachycardia, tachypnoea and a decrease in pulse pressure (due to a rise in diastolic component due action of catecholamines).
There are minimal systolic pressure changes.
There may be associated anxiety, fright or hostility

Class III haemorrhage (30-40% blood volume loss):
Complicated haemorrhagic state – crystalloid and probably blood replacement are required
There are classical signs of inadequate perfusion, marked tachycardia, tachypnoea, significant changes in mental state and measurable fall in systolic pressure.
Almost always require blood transfusion, but decision based on patient initial response to fluid resuscitation.

Class IV haemorrhage (> 40% blood volume loss):
Preterminal event patient will die in minutes
Marked tachycardia, significant depression in systolic pressure and very narrow pulse pressure (or unobtainable diastolic pressure)
Mental state is markedly depressed
Skin cold and pale.
Needs rapid transfusion and immediate surgical intervention.

A blood loss of >50% results in loss of consciousness, pulse and blood pressure.

Fluid resuscitation following trauma is a controversial area.

This clinical scenario points to a 15-30% blood loss. However, further crystalloid and blood replacement may be required after assessing the clinical situation. There is increasing evidence to suggest that transfusion of large volumes of crystalloid in the hospital setting are likely to be deleterious to the patient and hypotensive resuscitation and judicious blood and blood product resuscitation is a more appropriate option. A ratio of 1 unit of plasma to 1 unit of red blood cells is used to replace fluid volume in adults.

This patient does not require immediate transfusion of O negative blood and there is time for a formal crossmatch. The argument about colloids versus crystalloids has existed for decades. However, while they have a role in fluid resuscitation, they are not first line.

There is a risk of anaphylaxis, Hypernatraemia, and acute renal injury with colloidal solutions.

Colligative properties are properties of solutions that depend on the number of dissolved particles in solution. They do not depend on the identities of the solutes.

All of the above have colligative properties with the exception of depression of melting point.

The osmolality from the concentration of a substance in a solution is measured by an osmometer. The freezing point of a solution can determines concentration of a solution and this can be measured by using a freezing point osmometer. This is applicable as depression of freezing point is directly correlated to concentration.

Vapour pressure osmometers, which measure vapour pressure, may miss certain volatiles such as CO2, ammonia and alcohol that are in the solution

The use of a freezing point osmometer provides the most accurate and reliable results for the majority of applications.

Colligative properties does not include melting point depression . Mixtures of substances in which the liquid phase components are insoluble, display a melting point depression and a melting range or interval instead of a fixed melting point.

The magnitude of the melting point depression depends on the mixture composition.

The melting point depression is used to determine the purity and identity of compounds. EMLA (eutectic mixture of local anaesthetics) cream is a mixture of lidocaine and prilocaine and is used as a topical local anaesthetic. The melting point of the combined drugs is lower than that individually and is below room temperature (18°C).

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.

The incidence of a disease is the number of new cases of the disease in a population over a defined time period.

The prevalence of a disease is the number of cases of the disease in a population over a defined time period describes. It is NOT the number of new cases.

The number of new cases of a disease only, has no denominator (time period or population) from which to derive an incidence.

The number of new cases of a disease seeking medical treatment is the incidence of patients seeking medical treatment NOT the incidence of the disease in a population.

The death rate from a disease is the number of patients dying from the disease in a population.

With regards to compensatory response to blood loss, the following sequence of events take place:

1. Decrease in venous return, right atrial pressure and cardiac output
2. Baroreceptor reflexes (carotid sinus and aortic arch) are immediately activated
3. There is decreased afferent input to the cardiovascular centre in medulla. This inhibits parasympathetic reflexes and increases sympathetic response
4. This results in an increased cardiac output and increased SVR by direct sympathetic stimulation. There is increased circulating catecholamines and local tissue mediators (adenosine, potassium, NO2)
5. Fluid moves into the intravascular space as a result of decreased capillary hydrostatic pressure absorbing interstitial fluid.

A slower response is mounted by the hypothalamus-pituitary-adrenal axis.
6. Reduced renal blood flow is sensed by the intra renal baroreceptors and this stimulates release of renin by the juxta-glomerular apparatus.
7. There is cleavage of circulating Angiotensinogen to Angiotensin I, which is converted to Angiotensin II in the lungs (by Angiotensin Converting Enzyme ACE)

Angiotensin II is a powerful vasoconstrictor that sets off other endocrine pathways.
8. The adrenal cortex releases Aldosterone
9. There is antidiuretic hormone release from posterior pituitary (also in response to hypovolaemia being sensed by atrial stretch receptors)
10. This leads to sodium and water retention in the distal convoluted renal tubule to conserve fluid
Fluid conservation is also aided by an increased amount of cortisol which is secreted in response to the increase in circulating catecholamines and sympathetic stimulation.

The pectinate muscles (musculi pectinati) are parallel muscular ridges that extend anterolaterally on the right atrial walls. The most prominent pectinate muscle, which forms the bridge of the sulcus terminalis internally, is the taenia sagittalis (second crest or septum spurium).

In the left atrium, the pectinate muscles are confined to the inner surface of its atrial appendage. They tend to be fewer and smaller than in the right atrium. This is due to the embryological origin of the auricles, which are the true atria.

Pectinate muscles of the atria are different from the trabeculae carneae, which are found on the inner walls of both ventricles.

The interior of the right atrium has five distinct features:
1. Sinus venarum – smooth, thin-walled posterior part of the right atrium where the SVC, IVC, and coronary sinus open
2. Musculi pectinati – a rough anterior wall of pectinate muscles
3. Tricuspid valve orifice – the opening through which the right atrium empties blood into the right ventricle
4. Crista terminalis – separates the rough (musculi pectinati) from the smooth (sinus venarum) internally
5. Fossa ovalis – a thumbprint size depression in the interatrial septum, which is a remnant of the oval foramen and its valve in the foetus

Penicillinase is a narrow spectrum ?-lactamase that opens the ?-lactam ring and inactivates Penicillin G and some closely related congeners. The majority of Staphylococci and some strains of gonococci, B. subtilis, E. coli, and a few other bacteria produce penicillinase.

N. meningitidis is sensitive to penicillin and less than 20% resistance is found in pseudomonas.

Sugammadex is used for immediate reversal of rocuronium-induced neuromuscular blockade.
It is used at a dose of 16 mg/kg.

Since the patient in the question is 70 kg, the required dose of sugammadex can be calculated as:
16×70 = 1120 mg.

Sugammadex selectively binds rocuronium or vecuronium, thereby reversing their neuromuscular blocking action. Due to its 1:1 binding of rocuronium or vecuronium, it can reverse any depth of neuromuscular block.

Endotoxins are the lipopolysaccharides found in the outer cell wall of Gram-negative bacteria. They are responsible for providing the structure and stability of the cell wall.

They cannot be destroyed by normal sterilisation as they are heat stable molecules. They require the use of certain sterilant such as superoxide, peroxide and hypochlorite to be neutralised.

They stimulate strong immune responses, but can only be destroyed partially by specific antibodies. Repeat infections occur as memory T cells cannot be formed.

It can cause septicaemia and associated symptoms such as fever, shock, hypotension and nausea.

It activates the alternative complement pathway and the coagulation pathway using secreted cytokines.

It is not involved in botulism as clostridium botulinum, the responsible organism, secretes a neurotoxic exotoxin.

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.

The internal jugular vein is found on both sides of the neck and collects blood from the brain, superficial regions of the face, and neck. It drains into the right atrium.

It is a continuation of the sigmoid sinus and begins in the posterior cranial fossa and exits the skull via the jugular foramen.
It runs within the carotid sheath as it descends in the neck and is accompanied by the vagus nerve posteriorly and the common carotid anteromedially.

The hypoglossal nerve emerges from the hypoglossal canal medial to the internal carotid artery and the internal jugular vein and ninth, tenth, and eleventh cranial nerves.

The internal jugular vein crosses anterior to the thoracic duct on the left side.

External carotid artery originates at the upper border of the thyroid cartilage. It ascends and lies anterior to the internal carotid arteries and posterior to the posterior belly of the digastric muscle and stylohyoid muscle.

The external carotid artery has eight important branches:
Anterior surface:
1. Superior thyroid artery (first branch)
2. Lingual artery
3. Facial artery
Medial branch
4. Ascending pharyngeal artery
Posterior branches
5. Occipital artery
6. Posterior auricular artery
Terminal branches
7. Maxillary artery
8. Superficial temporal artery

The Purkinje system, as well as the action potentials of ventricular and atrial myocytes, have the same ionic changes. It lasts about 200 milliseconds and has a resting membrane potential, as well as fast depolarisation and plateau phases.

There are five stages to the process:

Increased Na+ and decreased K+ conductance in Phase 0 (rapid depolarisation).
1st phase (initial repolarisation) : Na+ conductance decreased, while K+ conductance increased.
Phase two (plateau phase) : Ca2+ conductance increased
Phase three (repolarisation phase) : Lower Ca2+ conductance and higher K+ conductance
4th Phase (resting membrane potential) : K+ conductance increased, Na+ conductance decreased, and Ca2+ conductance decreased.

The dose-response curve plots the graph of the dose (drug concentration) versus the response. As doses increase, the response increment diminishes; finally, doses may be reached at which no further increase in response can be achieved. This relation between drug concentration and effect is traditionally described by a hyperbolic curve. When the x-axis is plotted in log scale, the graph yields a sigmoid curve.

Efficacy (Emax) and potency (EC50) can be derived from this curve. Emax is the maximal effect achievable, with increasing concentration of a drug. EC50 is the concentration of the drug, wherein half of the maximal effect is achieved.

When the graph is plotted using a log [response/1-response] against log dose, the sigmoid curve becomes a straight line (Hill plot). A graph that transforms from a straight line to exponential curve is mathematically incorrect. A graph that transforms from either a wash-in or wash-out exponential curve to a straight line comes from an initial set of data plotted against time, to a logarithmic transformation of the initial data set against time.

Structural isomers have a similar molecular formula, but they have a different structural formula as their atoms are arranged in a different manner. Such small changes lead to the differential pharmacological activity. Enflurane and isoflurane are two prime examples of structural isomers.

Stereoisomers are those substances that have a similar molecular and structural formula, but the arrangement spatially of atoms are different and have optical activity.

Enantiomers are a pair of stereoisomers, which are non-superimposable mirror images of each other. They also have chiral centres of molecular symmetry. Ketamine is considered as an example of racemic mixture (contain 50% R and 50% S enantiomers)

Geometric isomers contain a carbon-carbon double bond (i.e. C=C) or a rigid carbon-carbon single bond in a heterocyclic ring. Cis-atracurium is one example.

Dynamic isomers or Tautomers are a pait of unstable structural isomers, which are present in equilibrium. One isomer can easily change after the change in pH. Midazolam and thiopentone are their examples.

Correlation doesn’t justify causality. Correlation coefficient gives us an idea whether or not the two parameters provide have any relation of some sort or not i.e. does change in one prompt any change in other? It has nothing to do with predictions. For that purpose linear regression is used.

This may be the classical case of blood transfusion reaction due to ABO incompatibility.

Here red cells are destroyed in the bloodstream with the release of haemoglobin in circulation (causing haemoglobinuria). Here, IgM or IgG anti-A or anti-B antibody can cause rapid activation of complement cascade usually the classical pathway. This is called intravascular haemolysis.

There may be extravascular haemolysis by cells of the mononuclear phagocyte system situated in the liver and spleen. Extravascular red cell destruction can increase breakdown products of haemoglobin, such as bilirubin and urobilinogen.

The oesophagus has four layers namely; 1. the mucosal layer, 2. the submucosal layer, 3. the muscular layer and 4. the layer of loose connective tissue which binds to the outer mucosal layer. The oesophagus lacks the serosal layer and therefore holds sutures poorly.

The mucosal layer consists of muscularis mucosa and the lamina propria and is made up of non keratinised stratified squamous epithelium. The mucosal layer is the innermost layer of the oesophagus.

The submucosal layer being the strongest layer of all has mucous glands which are called as the tuboalveolar mucous glands.

The outer muscular layer has two types of muscle layers of which one is the circular layer and the other the longitudinal layer. The Auerbach’s and Meissner’s nerve plexuses lie in between the longitudinal and circular muscle layers and submucosally. The muscle fibres present in the upper 1/3rd part of the oesophagus are skeletal muscle fibres, the middle 1/3rd layer has both smooth and skeletal muscle fibres, but the lower 1/3rd only has smooth muscle fibres.

The loose connective tissue layer or the adventitious layer has dense fibrous tissue.

The degree of correlation is summarised by the correlation coefficient (r). This indicates how closely the points lie to a line drawn through the plotted data. In parametric data this is called Pearson’s correlation coefficient and can take any value between -1 to +1. A correlation of -1.0 indicates a perfect negative correlation, and a correlation of 1.0 indicates a perfect positive correlation.

For example

r = 1 – strong positive correlation (e.g. systolic blood pressure always increases with age)

r = 0 – no correlation (e.g. there is no correlation between systolic blood pressure and age)

r = – 1 – strong negative correlation (e.g. systolic blood pressure always decreases with age)

Whilst correlation coefficients give information about how one variable may increase or decrease as another variable increases they do not give information about how much the variable will change. They also do not provide information on cause and effect.

In contrast to the correlation coefficient, linear regression may be used to predict how much one variable changes when a second variable is changed.

Pupil size is reduced by the pupillary light reflex and during accommodation for near vision. In the pupillary light reflex, light that strikes the retina is processed by retinal circuits that excite W-type retinal ganglion cells. These cells respond to diffuse illumination. The axons of some of the W-type cells project through the optic nerve and tract to the pretectal area, where they synapse in the olivary pretectal nucleus. This nucleus contains neurons that also respond to diffuse illumination. Activity of neurons of the olivary pretectal nucleus causes pupillary constriction by means of bilateral connections with parasympathetic preganglionic neurons in the Edinger-Westphal nuclei. The reflex results in contraction of the pupillary sphincter muscles in both eyes, even when light is shone into only one eye.

The structures that pass through the foramen magnum are:

Meningeal lymphatics
Spinal cord
Spinal meninges
Sympathetic plexus of vertebral arteries
Vertebral arteries
Vertebral artery spinal branches
The spinal roots of the accessory nerve.

The jugular foramen contains the vagus nerve, the accessory nerve and glossopharyngeal nerve.

The vertebral veins does not pass into the skull.

Only 1 percent of the calcium in the human body is found in the plasma where it performs the most critical functions.

Out of this 1 percent, approximately 15% is complexed calcium bound to organic and inorganic anions, 40% is bound to albumin, and the remaining 45% circulates as free ionized calcium.

The Chvostek sign is a clinical finding associated with hypocalcaemia, or low levels of calcium in the blood. This clinical sign refers to a twitch of the facial muscles that occurs when gently tapping an individual’s cheek, in front of the ear.

Prolonged QT interval are associated with hypocalcaemia as reported in multiple studies.

Krebs’ cycle (tricarboxylic acid cycle or citric acid cycle) is a sequence of reactions to release stored energy through oxidation of acetyl coenzyme A (acetyl-CoA). Some of the products are carbon dioxide and hydrogen atoms.

The sequence of reactions, known collectively as oxidative phosphorylation, only occurs in the mitochondria (not cytoplasm).

The Krebs cycle can only take place when oxygen is present, though it does not require oxygen directly, because it relies on the by-products from the electron transport chain, which requires oxygen. It is therefore considered an aerobic process. It is the common pathway for the oxidation of carbohydrate, fat and some amino acids, required for the formation of adenosine triphosphate (ATP).

Pyruvate enters the mitochondria and is converted into acetyl-CoA. Acetyl-CoA is then condensed with oxaloacetate, to form citrate which is a six carbon molecule. Citrate is subsequently converted into isocitrate, alpha-ketoglutarate, succinyl-CoA, succinate, fumarate, malate and finally oxaloacetate.

The only five carbon molecule in the cycle is Alpha-ketoglutarate.

A passive leg raise can lead to transient increases in blood pressure and stroke volume as it increased the amount of venous return to the heart. Venous return increases in this situation as it transfers a larger volume of blood from the lower limbs to the right heart. It therefore mimics a fluid challenge. However its effects are short lasting and often lead to minimal increases in blood pressure. It therefore should not be used to treat shock in isolation. The passive leg raise is useful in determining the likelihood that a patient with shock will respond to fluid resuscitation.

Stroke volume (via a cardiac monitor) and/or pulse pressure (via an arterial line) should be measured to assess the effects of a passive leg raise. An increase in stroke volume by 9% or in pulse pressure by 10% are considered indicative of fluid responsiveness.

Blood that enters the ventricles during diastole causes stretching of sarcomeres within cardiac muscle. The extent to which they stretch is proportional to the strength of ventricular muscle contraction. Therefore, the venous return (amount of blood returned to the heart) is proportional to stroke volume. The end diastolic volume is determined by venous return and is also proportional to stroke volume.

Cardiac muscle contraction strength is dependent on the action of adrenaline and noradrenaline, but these hormones contribute to cardiac contractility, not to stroke volume.

The surface marking for locating the femoral artery is the mid-inguinal point, which is the halfway point between the anterior superior iliac spine (ASIS) and the pubic symphysis.

The other mentioned options are not specific for any landmark.

However, it is important to note the difference between the mid inguinal point and the midpoint of the inguinal ligament, which is travels from the ASIS to the pubic tubercle.

From superior to inferior, the following structures enter the orbit through the superior orbital fissure:
1. Lacrimal nerve
2. Frontal nerve
3. Superior ophthalmic vein
4. Trochlear nerve
5. Superior division of the oculomotor nerve*
6. Nasociliary nerve*
7. Inferior division of the oculomotor nerve*
8. Abducent nerve*
9. Inferior ophthalmic vein.

The superior and inferior division of the oculomotor nerve, nasociliary nerve, and abducent nerve are within the tendinous ring.

The common origin of the four rectus muscles is the tendinous ring (also known as the annulus of Zinn). The tendinous ring’s lateral portion straddles the superior orbital fissure, while the medial portion encloses the optic foramen, through which the optic nerve and ophthalmic artery pass.

The porta hepatis is a fissure in the inferior surface of the liver. All the neurovascular structures that enter and leave the porta hepatis are:
1. hepatic portal vein
2. hepatic artery
3. hepatic ducts
4. hepatic nerve plexus (It contains the sympathetic branch to the liver and gallbladder and the parasympathetic, hepatic branch of the vagus nerve.)

These structures supply and drain the liver. Only the hepatic vein is not part of the porta hepatis.
The porta hepatis is also surrounded by lymph nodes, that may enlarge to produce obstructive jaundice.
These structures divide immediately after or within the porta hepatis to supply the functional left and right lobes of the liver.

The cystic duct lies outside the porta hepatis and is an important landmark in laparoscopic cholecystectomy.

There are 4 different types of globin chains which surround 4 heme molecules in haemoglobin (Hb) – α (alpha), β (beta), γ (gamma), and δ (delta)
α chains are essential.
δ2β2 and β2γ2 are not found in a healthy adult.
97% of the Hb in a healthy adult is made of α2β2 (2 α chains and 2 β chains).
α2δ2 accounts for around 1.5-3% of the adult Hb.
α2γ2 accounts for less than 1%.

With respect to oxygen transport in cells, almost all oxygen is transported within erythrocytes. There is limited solubility and only 1% is carried as solution. Thus, the amount of oxygen transported depends upon haemoglobin concentration and its degree of saturation.

Haemoglobin is a globular protein composed of 4 subunits. Haem is made up of a protoporphyrin ring surrounding an iron atom in its ferrous state. The iron can form two additional bonds – one is with oxygen and the other with a polypeptide chain. There are two alpha and two beta subunits to this polypeptide chain in an adult and together these form globin. Globin cannot bind oxygen but can bind to CO2 and hydrogen ions. The beta chains are able to bind to 2,3 diphosphoglycerate. The oxygenation of haemoglobin is a reversible reaction. The molecular shape of haemoglobin is such that binding of one oxygen molecule facilitates the binding of subsequent molecules.

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

Awareness during general anaesthesia is a frightening experience, which may result in serious emotional injury and post-traumatic stress disorder.

The incidence of awareness during general anaesthesia with current anaesthetic agents and techniques has been reported as 0.2-0.4% in nonobstetric and noncardiac surgery, as 0.4% during caesarean section, and as 1.5% in cardiac surgery.

The incidence during major trauma surgery is higher. Incidence of recall has been reported to be as high as 11-43% in major trauma cases.

Dopamine (DA) is a dopaminergic (D1 and D2) as well as adrenergic ? and ?1 (but not ?2 )agonist.

The D1 receptors in renal and mesenteric blood vessels are the most sensitive: i.v. infusion of a low dose of DA dilates these vessels (by raising intracellular cyclic adenosine monophosphate).

Moderately high doses produce a positive inotropic (direct ?1 and D1 action + that due to NA release), but the little chronotropic effect on the heart.

Vasoconstriction (?1 action) occurs only when large doses are infused.

At doses normally employed, it raises cardiac output and systolic BP with little effect on diastolic BP. It has practically no effect on nonvascular ? and ? receptors; does not penetrate the blood-brain barrier – no Central nervous system effects.

Dopamine is less arrhythmogenic than adrenaline

Regarding dopamine part of the dose is converted to Noradrenaline in sympathetic nerve terminals.

Ketamine is a phencyclidine (hallucinogenic) derivative that is administered in a dose of 2 mg/kg and acts by blocking NMDA (N-methyl-D-aspartate) receptors of glutamate.

It is a powerful bronchodilator agent and is, therefore, an intravenous anaesthetic of choice in bronchial asthma (halothane is an inhalational anaesthetic agent of choice for bronchial asthma). It is also used in the management of refractory status epilepticus.

It is an acid solution with an elimination half-life of three hours.

It has S (+) enantiomer and R (-) enantiomer. the S(+) enantiomer is two to four times more potent than the R(-) and is less likely to produce hallucinations.

Its use is contraindicated in patients with ischaemic heart disease because it increased sympathetic outflow leading to tachycardia and increased cardiac output which in turn increases the myocardial oxygen demand.

Nonsteroidal anti-inflammatory drugs (NSAIDs) cause bronchospasm, rhinorrhoea, and nasal obstruction in some asthma patients.

The inhibition of cyclooxygenase-1 (Cox-1) appears to be the cause of NSAID-induced reactions. This activates the lipoxygenase pathway, which increases the release of cysteinyl leukotrienes (Cys-LTs), which causes bronchospasm and nasal obstruction.

The following changes in arachidonic acid (AA) metabolism have been observed in NSAID-intolerant asthmatic patients:

Prostaglandin E2 production is low, possibly due to a lack of Cox-2 regulation.
An increase in leukotriene-C4 synthase expression and
A decrease in the production of metabolites (lipoxins) released by AA’s transcellular metabolism.

Phospholipase A produces membrane phospholipids, which are converted to arachidonic acid.

TXA2 causes vasoconstriction as well as platelet aggregation and adhesion.

PGI2 causes vasodilation and a reduction in platelet adhesion.

PGE2 is involved in parturition initiation and maintenance, as well as thermoregulation.

Due to an increased tidal volume with little change or slight increase in respiratory rate, Minute ventilation at term is increased by about 50%. Hypothalamic function are thought to influence by Progesterone, oestradiol and prostaglandins. This causes a mild compensated respiratory alkalosis.

Maternal PaCO2 is usually decreased to about 32 mmHg (4.27 kPa) as a result of this increased alveolar ventilation at term . A compensatory decrease in serum bicarbonate from 27 to 21 mmol/L by renal excretion lessens the impact of maternal alkalosis.

Krebs’ cycle (tricarboxylic acid cycle or citric acid cycle) is a sequence of reactions in which acetyl coenzyme A (acetyl-CoA) is metabolised and this results in carbon dioxide and hydrogen atoms production.

This series of reactions occur in the mitochondria of eukaryotic cells, not the cytoplasm. The cycle requires oxygen and so, cannot function under anaerobic conditions.

It is the common pathway for carbohydrate, fat and some amino acids oxidation and is required for high energy phosphate bond formation in adenosine triphosphate (ATP).

When pyruvate enters the mitochondria, it is converted into acetyl-CoA. This represents the formation of a 2 carbon molecule from a 3 carbon molecule. There is loss of one CO2 but formation of one NADH molecule. Acetyl-CoA is condensed with oxaloacetate, the anion of a 4 carbon acid, to form citrate which is a 6 carbon molecule.

Citrate is then converted into isocitrate, alpha-ketoglutarate, succinyl-CoA, succinate, fumarate, malate and finally oxaloacetate.

The only 5 carbon molecule in the cycle is alpha-ketoglutarate.

The basilic vein is one of the primary veins that drain the upper limb, like the cephalic vein. It begins as the dorsal venous arch. The basilic vein originates from the ulnar side of the dorsal arch of the upper limb passes along the posteromedial aspect of the forearm, moving towards the anterior surface of the elbow.

The basilic vein pierces the deep fascia at the elbow and joins the venae commitantes of the brachial vein to form the axillary vein.

The basilic vein passes deep under the muscles as it moves midway up the humerus. At the lower border of the teres major muscle, the anterior and posterior circumflex humeral veins feed into it.

Doxazosin is selective alpha 1 blocker (it causes less tachycardia than a non-selective alpha-blocker) and is the drug of choice for a patient with hypertension and benign hyperplasia of the prostate (BHP).

The major adverse effect of an alpha-blocker is first-dose hypotension.

Atenolol and Labetalol are beta blockers. It works by relaxing blood vessels and slowing heart rate to improve blood flow and decrease blood pressure.

Clonidine is an α2A-adrenergic agonist used to treat high blood pressure, ADHD, drug withdrawal (alcohol, opioids, or nicotine), menopausal flushing, diarrhea, spasticity, and certain pain conditions.

Methyldopa is a centrally-acting alpha-2 adrenergic agonist used to manage hypertension alone or in combination with hydrochlorothiazide, and to treat hypertensive crises.

The statement Epinephrine is formulated as 1 in 1000 solution means 1 gm epinephrine is present in 1000 ml of solution.

Propofol is considered a safe drug to use in porphyria because even if causes mild elevation of porphyrins inpatient, it does not cause any symptoms.

Since barbiturates are inducers of ALA synthetase, they are contraindicated in porphyria patients. So, thiopentone most not be used.

Etomidate is a potent inhibitor of adrenal 11 beta-hydroxylase and 17 alpha-hydroxylase reducing cortisol and aldosterone synthesis in the adrenal cortex and has been associated with exacerbations of porphyria in animal studies and it is advisable not to use it in this condition.

Ketamine should be reserved for the hemodynamically unstable patient, however, it is a safe drug.

Diazepam is safe in porphyria but is not usually used for a rapid sequence induction.

Chest compressions are an essential part of cardiopulmonary resuscitation (CPR) which helps restore spontaneous circulation (ROSC).

Sodium bicarbonate is only prescribed in patients with cardiac arrests as a result of an overdose of tricyclic antidepressants or hyperkalaemia. Its use causes the body to produce more CO2 which causes:

Exacerbation of intracellular acidosis
Negative inotropy to ischaemic myocardium
Increased osmotic load of sodium into failing brain and body
Shift of oxygen dissociation curve to the left.

THAM is often used to treat metabolic acidosis as a result of cardiac bypass surgery and also cardiac arrest, when other standard methods have failed.

Carbicarb (Na2CO3 0.33 molar NaHCO3 0.33 molar) has only mild effects on acidosis. It also causes an increase in arterial CO2 pressure and lactate concentration.

The total body water content of a 70kg man is (70 × 0.6) = 42 litres. For a woman, the calculation is (70 × 0.55) = 38.5 litres.

For a man, it is subdivided into:

Extracellular fluid (ECF) = 14L (1/3)
Intracellular fluid (ICF) = 28L (2/3).

The ECF volume is further divided into:

Interstitial fluid = 10.5 litres
Plasma = 3 litres
Transcellular fluid (CSF/synovial fluid) = 0.5 litres.

Directly measured fluid compartments:

Heavy water (deuterium) can be used to measure total body water content, which is freely distributed.
Albumin labelled with a radioactive isotope or using a dye called Evans blue can be used to measure Plasma volume . They do not diffuse into red blood cells.
Radiolabelled (Cr-51) red blood cells can be used to measure total erythrocyte volume.
Inulin as the tracer can be used to measure ECF volume as it circulate freely in the interstitial and plasma volumes.

Indirectly measured fluid compartments:

Total blood volume can be calculated with the level of haematocrit and the volume of total circulating red blood cells.
ICF volume can be calculated by subtracting ECF volume from total blood volume.

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 oxygen content of arterial blood can be calculated by the following equation:
(10 x haemoglobin x SaO2 x 1.34) + (PaO2 x 0.0225).
This is the sum of the oxygen bound to haemoglobin and the oxygen dissolved in the plasma.

Oxygen content x cardiac output = The amount of oxygen delivered to the tissues in unit time which is known as the oxygen flux.

Any factor that increases the metabolic demand will encourage oxygen offloading from the haemoglobin in the tissues and this causes the oxygen dissociation curve (ODC) to shift to the right. This subsequently reduced the oxygen content of arterial blood.

Conditions like fever, metabolic or respiratory acidosis lowers the oxygen content and shifts the ODC to the right.
A low level of 2,3 diphosphoglycerate (2,3-DPG) is usually related to an increased oxygen content as there is less offloading, and so the ODC is shifted to the left.

So for a given PaO2, a high blood oxygen content is related to any factors that can shift the ODC to the left and not to the right.

A low haematocrit usually means that there is a decreased haemoglobin concentration, and therefore is associated with decreased oxygen binding to haemoglobin.

The arterial cannula inserted should have parallel walls in order to reduce the risk of interruption of blood flow to distal limbs.

It is essential that the monitor used to display the arterial pressure waves has a frequency capacity of 0.5-40Hz. This is because the pressure waves are a combination of different sine waves of varying frequencies and amplitudes.

The diameter of the catheter is directly proportional to the natural frequency which is the frequency at which the system responsible for monitoring the waves resonates and amplifies the signals. This should be at least ten fold in comparison to the fundamental frequency. The diameter of the catheter is also inversely proportional to the square root of the system compliance, the tubing length and the fluid density within the system.

The presence of an air bubble, a clot or an easily malleable diaphragm and tube can result in wave damping. Increased damping will cause a reduction in the systolic pressure, and an increase in diastolic pressure. The maximum damping value of an appropriate monitoring system would be 0.64.

A rigid, non-malleable diaphragm and tubing can cause a resonance within the system. This resonance will result in an increase in the systolic pressure and a reduction in the diastolic pressure

Electrocautery, also known as diathermy, is a technique for coagulation, tissue cutting, and fulguration that uses a high-frequency current to generate heat (cell destruction from dehydration).

The two electrodes in bipolar diathermy are the tips of forceps, and current passes between the tips rather than through the patient. Bipolar diathermy’s power output (40-140 W) is lower than unipolar diathermy’s typical output (400 W). There is no earthing in the bipolar circuit.

A cutting electrode and a indifferent electrode in the form of a metal plate are used in unipolar diathermy. The high-frequency current completes a circuit by passing through the patient from the active electrode to the metal plate. When used correctly, the current density at the indifferent electrode is low, and the patient is unlikely to be burned. Between the patient plate and the earth is placed an isolating capacitor. This has a low impedance to a high frequency current, such as diathermy current, and is used in modern diathermy machines. The capacitor has a high impedance to current at 50 Hz, which protects the patient from electrical shock.

High frequency currents (500 KHz – 1 MHz) are used in both unipolar and bipolar diathermy, which can cause tissue damage and interfere with pacemaker function (less so with bipolar diathermy).

The effect of diathermy is determined by the current density and waveform employed. The current is a pulsed square wave pattern in coagulation mode and a continuous square wave pattern in cutting mode.

Glucose transport is a highly regulated process accomplished mostly by facilitated diffusion using carrier proteins to cross cell membranes.

There are many transporters, but the most important are known as glucose transporters (GLUTs).

Stresses in various form of acute and chronic forms affect the activity of glucose transporters.
They are responsive to many types of metabolic stress, including hypoxia, injury, hypoglycaemia, numerous metabolic inhibitors, stress hormones, and other influences such as growth factors.

Numerous signalling pathways appear to be involved in transporter regulation.

New evidence suggests that stresses regulating GLUTs are not only acute biological stresses. In addition, chronic low-grade inflammation, and their associated chronic diseases also lead to altered glucose transport. These include obesity, type 2 diabetes, cardiovascular disease, and the growth and spread of many tumours that are affected by altered glucose transporters. Some of these glucose transport effects are compensatory, while others are pathogenic.

Ultimately, deliberate manipulation of GLUTs could be used as treatment for some of these chronic diseases.

Professor Mapleson classified non-rebreathing circuits based on the position of the APL valve, which controls fresh gas flow.

The Mapleson A (Magill) circuit is most effective in spontaneous breathing, requiring only 70-100 ml/kg (the patient’s minute volume) of fresh gas flow. The patient inhales fresh gas from the reservoir bag and tubing during inspiration. During expiration, the patient adds dead space gas (gas that hasn’t been exchanged) to the tubing and reservoir bag in addition to the fresh gas flow. At the patient’s end, alveolar gas is vented through the APL valve. During the expiratory pause, the fresh gas flow causes more gas to be released.

The Mapleson A is inefficient during controlled ventilation. Venting occurs during inspiration rather than during the expiratory phase, as it does during spontaneous ventilation. As a result, unless a high fresh gas flow of >20 L/minute is used, alveolar gas is rebreathed.

During spontaneous ventilation, the Mapleson D circuit is inefficient.

The oxygen concentration in a Hudson mask is insufficient to allow for adequate pre-oxygenation.

If the afterload and myocardiac contractility remains unchanged, an increase in the preload can be attributed to an increase in end-diastolic volume.

Preload can be defined as the initial stretching of the cardiac myocytes prior to contraction. Preload, therefore, is related to muscle sarcomere length. Because sarcomere length cannot be determined in the intact heart, other indices of preload are used such as ventricular end-diastolic volume or pressure. When venous return to the heart is increased, the end-diastolic pressure and volume of the ventricles are increased, which stretches the sarcomeres, thereby increasing their preload.

The correct answer is the clotting cascade, which occurs via a positive feedback mechanism. As clotting factors are attracted to a site, their presence attracts further clotting factors. This continues until a functioning clot is formed.

This patient has presented with symptoms of hypothyroidism and symptoms include weight gain, lethargy, cold intolerance, dry skin, coarse hair and constipation. It can be treated by replacing the missing thyroid hormone with levothyroxine which is a synthetic version of thyroxine (T4).

Serum carbon dioxide (CO2) is controlled via a negative feedback mechanism as well. Chemoreceptors can detect when the serum CO2 is high, and send an impulse to the respiratory centre of the brain to increase the respiratory rate. As a result, more CO2 is exhaled which lowers the serum concentration.

Cortisol is also released according to a negative feedback mechanism. Cortisol acts on both the hypothalamus and the anterior pituitary. Its action serve to decrease the formation of corticotrophin releasing hormone (CRH) and adrenocorticotropic hormone (ACTH), respectively. CRH acts on the anterior pituitary to release ACTH. This then acts on the adrenal gland to cause the release of cortisol. Thus, inhibition of CRH and ACTH formation results in high levels of cortisol which inhibit its further release.

Blood pressure (BP) is controlled via a negative feedback mechanism. Low BP results in renin-angiotensin-aldosterone system (RAAS) activation. This leads to vasoconstriction and retention of salt and water which increased BP.
Blood sugar is controlled via a negative feedback mechanism. A rise in blood sugar causes insulin to be released. Insulin acts to transport glucose into the cell which lowers blood sugar.

Gabapentin is an amino acid-like molecules that was originally synthesized as an analogue of GABA but is now known not to act through GABA mechanisms. It is used in the treatment of focal seizures and various nonepilepsy indications, such as neuropathic pain, restless legs syndrome, and anxiety disorders.

Despite its close structural resemblance to GABA, gabapentin does not act through effects on GABA receptors or any other mechanism related to GABA-mediated neurotransmission. Rather gabapentin binds avidly to ?2?, a protein that serves as an auxiliary subunit of voltage-gated calcium channels. Moreover, it binds to NMDA receptor to modulate its transmission.

The autonomic nervous system is divided into the sympathetic and parasympathetic nervous system. They are anatomically and physiologically different.

The sympathetic nervous system arises from the thoracolumbar outflow (T1-L5 ) at the lateral horns of grey matter of the spinal cord. Their preganglionic neurones are usually short myelinated and synapse in ganglia lateral to the vertebral column and have acetyl choline (Ach) as the neurotransmitter. Their postganglionic neurones are longer and unmyelinated and synapse with effector organ where the neurotransmitter is either adrenaline or noradrenaline.

The outflow of the parasympathetic nervous system is craniosacral. The cranial part originates from the midbrain and medulla (cranial nerves III, VII, IX and X) and the sacral outflow is from S2, S3 and S4. Their preganglionic neurones are usually long myelinated and synapse in ganglia close to the target organ and has Ach as its neurotransmitter. The unmyelinated postganglionic neurones is shorter and they synapse with effector organ. The neurotransmitter here is also Ach.

Both sympathetic and parasympathetic preganglionic neurons are cholinergic. Only the postganglionic parasympathetic neurons are cholinergic.

The null hypothesis states that there is no significant difference between two groups.

The alternative hypothesis states that there is a significant difference between two groups.

A type I error (false positive) occurs when a null hypothesis is rejected when it should be accepted.

A type II error (false negative) occurs when the alternative hypothesis is rejected when it should be accepted.

The probability determines the rejection of a null hypothesis.

The level of significance is set at p <0.05.

Number needed to treat (NNT) is a time specific epidemiological measure that indicates how many patients would be require for an intervention to prevent one additional bad outcome. A perfect NNT would be 1, where everyone improves with treatment, thus the higher the NNT, the less effective the treatment.

Thus if you treat 1000 patients then you will expect to have 50 fewer strokes.

Caudal analgesia using bupivacaine is a widely employed technique for achieving both intraoperative and early postoperative pain relief. 0.5 ml/kg of 0.25% plain bupivacaine is favoured by many practitioners who employ this fixed scheme for procedures involving sacral dermatomes (circumcision, hypospadias repair) as well as lower thoracic dermatomes (orchidopexy). However, there are other dosing regimens for caudal blocks with variable analgesic success rates: These include 0.75 ml/kg, 1.0 ml/kg and 1.25 ml/kg.

A study indicated that plain bupivacaine 0.25% at a dose of 0.75 ml/kg compared to a dose of 0.5 ml/kg when administered for herniotomies provided improved quality of caudal analgesia with a low side effects profile. There were consistently more patients with favourable objective pain scale (OPS) scores at all timelines, increased the time to the analgesic request with similar postoperative consumption of paracetamol in the group of patients who received 0.75 ml/kg of 0.25% bupivacaine.

Iliacus, and Psoas major are the most important muscles that produce flexion at the hip.

They are collectively called the iliopsoas muscle. The iliacus muscle originates from the ilium while the psoas major muscle takes its origin from the lumbar vertebrae and sacrum. Their insertion is the lesser trochanter of the femur. They work together to produce flexion and external rotation of the hip. The nerve supply is from branches of the lumbar plexus (L1, 2, 3) femoral nerve (L2, 3, 4) and short direct muscular branches (T12, L1, L2, L3 and L4).

Sartorius, Rectus femoris, Tensor fasciae latae, and Pectineus muscles are two-joint muscles acting at the knee and having less influence on hip flexion:

Rectus femoris and sartorius are involved in extension of the knee. They are supplied by branches of the femoral nerve.

Myotomes associated with key movement of the lower limb are:

L1/L2 – Hip flexion
L2/L3/L4 – Hip adduction, quadriceps (knee extension)
L4/L5 – Hip abduction
L5 – Great toe dorsiflexion.

Since knee extension is not affected, L2, L3 and L4 are still intact.

The major action of ADH is to increase reabsorption of osmotically unencumbered water from the glomerular filtrate and decreases the volume of urine passed. The osmolarity of urine is increased to a maximum of four times that of plasma (approx. 1200 mOsm/kg) by Increasing water reabsorption.

Chronic water loading, Lithium, potassium deficiency, cortisol and calcium excess, all blunt the action of ADH. This leads to nephrogenic diabetes insipidus.

ADH’s primary site of action is the distal tubule and collecting duct.

The Mapleson A (Magill) and coaxial version of the Mapleson A system (Lack circuit) are more efficient for spontaneous breathing than any of the other Mapleson circuits. The fresh gas flow (FGF) required to prevent rebreathing is slightly greater than the alveolar minute ventilation (4-5 litres/minute). This is delivered to the patient through the outer coaxial tube and exhaust gases are moved to the scavenging system through the inner tube. In the Lack circuit, the expiratory valve is located close to the common gas outlet away from the patient end. This is the main advantage of the Lack circuit over the Mapleson A circuit.

The Mapleson E circuit is a modification of the Ayres T piece and the FGF required to prevent rebreathing is 1.5-2 times the patient’s minute volume.

The Bain circuit is the coaxial version of the Mapleson D circuit.

The FGF for spontaneous respiration to avoid rebreathing is 160-200 ml/kg/minute.

The FGF for controlled ventilation to avoid rebreathing is 70-100 ml/kg/min.

The clinical signs suggest a class II haemorrhage – 15-30% of circulating blood volume has been lost.

Pelvic fractures are associated with significant concealed haemorrhage (>2000 ml) and may require aggressive fluid resuscitation. Other priorities include stabilisation of the fracture(s) and pain relief.

The Advanced Trauma Life Support (ATLS) classification of haemorrhagic shock is as follows:

Class I haemorrhage (blood loss up to 15%):
<750 ml of blood loss
Minimal tachycardia
No changes in blood pressure, RR or pulse pressure
Normally not require fluid replacement as will be restored in 24 hours, but in trauma correct.

Class II haemorrhage (15-30% blood volume loss):
Uncomplicated haemorrhage requiring crystalloid resuscitation
Represents about 750 – 1500 ml of blood loss
Tachycardia, tachypnoea and a decrease in pulse pressure (due to a rise in diastolic component due action of catecholamines)
Minimal systolic pressure changes
Anxiety, fright or hostility
Can usually be stabilised by crystalloid, but may later require a blood transfusion.

Class III haemorrhage (30-40% blood volume loss):
Complicated haemorrhagic state in which at least crystalloid and probably blood replacement are required
Classical signs of inadequate perfusion, marked tachycardia, tachypnoea, significant changes in mental state and measurable fall in systolic pressure
Almost always require blood transfusion, but decision based on patient initial response to fluid resuscitation.

Class IV haemorrhage (> 40% blood volume loss):
Preterminal event patient will die in minutes
Marked tachycardia, significant depression in systolic pressure and very narrow pulse pressure (or unobtainable diastolic pressure)
Mental state is markedly depressed
Skin cold and pale
Need rapid transfusion and immediate surgical intervention.

Loss of >50% results in loss of consciousness, pulse and blood pressure.

The route of choice is an arm vein (cephalic) with one or two large bore cannula. This will enable initial aggressive fluid resuscitation. A central line can be inserted at a later stage if central venous monitoring is deemed necessary. If a suitable peripheral vein cannot be cannulated with a large bore cannula then the internal jugular vein could be accessed rapidly (preferably ultrasound guided).

Intravenous access below the diaphragm in this case is inadvisable when other routes are available.

The spinous process is the part of a vertebrae that is directed posteriorly.

Typical cervical vertebra have spinous processes that are small and bifid, except for C7, which has a long and prominent spinous process.

Ligamentum venosum is an anterior relation of the liver: The ligamentum venosum, the fibrous remnant of the ductus venosus of the fetal circulation, lies posterior to the liver. It lies in the fossa for ductus venosus that separates the caudate lobe and the left lobe of the liver.

The portal triad contains three important tubes: 1. Proper hepatic artery 2. Hepatic portal vein 3. Bile ductules It also contains lymphatic vessels and a branch of the vagus nerve.

The bare area of the liver is a large triangular area that is devoid of any peritoneal covering. The bare area is attached directly to the diaphragm by loose connective tissue. This nonperitoneal area is created by a wide separation between the coronary ligaments.

The porta hepatis is a fissure in the inferior surface of the liver. All the neurovascular structures (except the hepatic veins) and hepatic ducts enter or leave the liver via the porta hepatis. It contains the sympathetic branch to the liver and gallbladder and the parasympathetic, hepatic branch of the vagus nerve. The caudate lobe (segment I) lies in the lesser sac on the inferior surface of the liver between the IVC on the right, the ligamentum venosum on the left, and the porta hepatis in front

Laminar flow can be defined as the motion of a fluid where every particle in the fluid follows the same path of its previous particles. The following are properties of laminar flow of gas or fluids:

1. Smooth unobstructed flow of gas through a tube of relatively uniform diameter
2. Few directional changes
3. Slow, steady flow through straight smooth, rigid, large calibre, cylindrical tube
4. Outer layer flow slower than the centre due to friction, results in discrete cylindrical layers, or streamlines
5. Double flow by doubling pressure as long as the flow pattern remains laminar

Poiseuille’s Law relates the factors that determine laminar flow. It indicates the degree of resistance to fluid flow through a tube. The resistance to fluid flow through a tube is directly related to the length, flow and viscosity; and inversely related to the radius of the tube to the fourth power. This means that, when the radius is doubled, there is increase in flow by a factor of 16.

For establishing a cause effect relationship, following criteria must be met:

1. Coherence & Consistency

2. Temporal Precedence

3. Specificity

As can be seen, sensitivity (The probability of a positive test) is not among these deciding factors..

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.

An echocardiogram provides real-time visualisation of cardiac structures. The ejection fraction (EF) is normally measured using this system.

The ejection fraction (EF) can be deduced mathematically if the patient’s end-diastolic volume (EDV), end-systolic volume (ESV) and stroke volume (SV) are known, as:

SV = EDV – ESV, and

EF = SV/EDV x 100

The normal range for EF is >55-70%.

For this patient,

SV= 40 – 30 = 10 mL, therefore

EF = 10/40 x 100 = 25%

Randomisation can be used to provide control over the confounding variables during the design stage of a study however during analytical stage a technique called stratification is used for controlling confounding variables. Since the question asks for the information that is factually incorrect.

With respect to oxygen transport in cells, almost all oxygen is transported within erythrocytes. There is limited solubility and only 1% is carried as solution. Thus, the amount of oxygen transported depends upon haemoglobin concentration and its degree of saturation.

Haemoglobin is a globular protein composed of 4 subunits. Haem is made up of a protoporphyrin ring surrounding an iron atom in its ferrous state. The iron can form two additional bonds – one is with oxygen and the other with a polypeptide chain.
There are two alpha and two beta subunits to this polypeptide chain in an adult and together these form globin. Globin cannot bind oxygen but can bind to CO2 and hydrogen ions.
The beta chains are able to bind to 2,3 diphosphoglycerate. The oxygenation of haemoglobin is a reversible reaction. The molecular shape of haemoglobin is such that binding of one oxygen molecule facilitates the binding of subsequent molecules.

The oxygen dissociation curve (ODC) describes the relationship between the percentage of saturated haemoglobin and partial pressure of oxygen in the blood.
Of note, it is not affected by haemoglobin concentration.

Chronic anaemia causes 2, 3 DPG levels to increase, hence shifting the curve to the right

Haldane effect – Causes the ODC to shift to the left. For a given oxygen tension there is increased saturation of Hb with oxygen i.e. Decreased oxygen delivery to tissues.
This can be caused by:
-HbF, methaemoglobin, carboxyhaemoglobin
-low [H+] (alkali)
-low pCO2
-ow 2,3-DPG
-ow temperature

Bohr effect – causes the ODC to shifts to the right = for given oxygen tension there is reduced saturation of Hb with oxygen i.e. Enhanced oxygen delivery to tissues. This can be caused by:
– raised [H+] (acidic)
– raised pCO2
-raised 2,3-DPG
-raised temperature

The question mentions a quantitative, ratio scale data set. The use of mean would be ideal under normal circumstances, however, in this situation median is preferred as it is less sensitive to the skewness of data. The median is usually preferred to other measures of central tendency when your data set is skewed (i.e., forms a skewed distribution)

Each kidney is composed of about 1.2 million uriniferous tubules. Each tubule consists of two parts that are embryologically distinct from each other. They are as follows:
a) Excretory part, called the nephron, which elaborates urine
b) Collecting part which begins as a junctional tubule from the distal convoluted tubule.

There are two types of nephrons in the kidney:
The cortical nephron comprises 80% of the total nephron and its major function is the excretion of waste products in urine whereas the juxtamedullary nephron comprises 20% of the total nephron and its major function is the concentration of urine by counter current mechanism.
In the superficial (cortical) nephrons, peritubular capillaries branch off the efferent arterioles and deliver nutrients to epithelial cells as well as serve as a blood supply for reabsorption and secretion. In juxtamedullary nephrons, the peritubular capillaries have a specialization called the vasa recta, which are long, hairpin-shaped blood vessels that follow the same course as a loop of Henle. The vasa recta serve as osmotic exchangers for the production of concentrated urine.

The kidney receives about 25% of cardiac output and about 20% of this is filtered at the glomeruli of the kidney. Thus, renal blood flow is 1200 ml/minute and renal plasma flow is 650 ml/minute

Primary FRCA is concerned with two issues. The first is a working knowledge of the Henderson-Hasselbalch equation, and the second is a working knowledge of logarithms and antilogarithms.

The pH at which the drug exists in 50 percent ionised and 50 percent unionised forms is known as the pKa.

To calculate the proportion of ionised to unionised form of a drug, use the Henderson-Hasselbalch equation.

pH = pKa + log ([A-]/[HA])

or

pH = pKa + log [(salt)/(acid)]
pH = pKa + log ([ionised]/[unionised])

Hence, if the pKa − pH = 0, then 50% of drug is ionised and 50% is unionised.

In this example:
7.4 = 8.4 + log ([ionised]/[unionised])
7.4 − 8.4 = log ([ionised]/[unionised])
log −1 = log ([ionised]/[unionised])

Simply put, the antilog is the inverse log calculation. In other words, if you know the logarithm of a number, you can use the antilog to find the value of the number. The antilogarithm’s definition is as follows:

y = antilog x = 10x

Antilog to the base 10 of 0 = 1, −1 = 0.1, −2 = 0.01, −3 = 0.001 and, −4 = 0.0001.

[A-]/[HA] = 0.1

Assuming that we can apply the approximation [A-] << [HA} then this means the acid is 0.1 x 100% = 10% ionised so the percentage of (non-ionized) acid will be 100% – 10% = 90%

The ECG changes seen in hypomagnesaemia include:

Prolonged PR interval
Prolonged QT interval
Flattening of T waves
ST segment depression
Prominent U waves

These changes are almost the same as those of hypokalaemia.

There is an increased risk of digoxin toxicity and a risk of atrial and ventricular ectopic and ventricular arrhythmias.

There is impaired synthesis and release of parathyroid hormone (PTH) in chronic hypomagnesaemia leading to impaired target organ response to PTH. This produces secondary hypocalcaemia.

The use of potassium ‘wasting’ diuretics (e.g. loop diuretics like furosemide) may lead to Hypomagnesaemia.

A tall T wave is seen in hypermagnesemia.

Propranolol is a nonselective beta-blocker with a half-life of 3 to 6 hours.

Since it is lipid-soluble it crosses the blood-brain barrier and causes Central Nervous System side effects like sedation, nightmares, and depression.

They are contraindicated in asthma, Congestive heart failure, and diabetes.

It has a large volume of distribution with no intrinsic sympathomimetic action.

Giardiasis is known to have a longer incubation time and doesn’t cause bloody diarrhoea.

Cholera usually doesn’t cause bloody diarrhoea.

Generally, most of the E.coli strains do not cause bloody diarrhoea.

Diverticulitis can be a cause of bloody stool but the history here points out to an infectious cause.

Campylobacter infection is the most probable cause as it is characterized by a prodrome, abdominal pain and bloody diarrhoea

Epinephrine is used for the treatment of cardiac arrest because it causes vasoconstriction via the alpha-adrenergic (?1) receptor. This vasoconstriction increases cerebral and coronary blood flow by increasing mean arterial, aortic diastolic, and cerebral pressures. Furthermore, epinephrine is also a?1 and ?2 adrenoreceptor agonist which shows inotrope, chronotrope, and bronchodilator effects.
– Adrenaline is also used to prolong the duration of action and decrease the systemic toxicity of local anaesthetics.
– Preferred route of adrenaline in patients with cardiac arrest is i.v. followed by intra-osseous and endotracheal

The following are some basic assumptions:

Extracellular fluid (ECF) makes up one-third of total body water (TBW), while intracellular fluid makes up the other two-thirds (ICF).
One-quarter of ECF is plasma, and three-quarters is interstitial fluid (ISF).
The volume receptors have a 7-10% blood volume change threshold. The osmoreceptors are sensitive to changes in osmolality of 1-2 percent.
Prior to the transfusion, the plasma osmolality is normal (between 287 and 290 mOsm/kg).
[Na+] in 0.9 percent N. saline is 154 mmol/L, which is similar to that of extracellular fluid. When given intravenously, this limits its distribution within the extracellular space, resulting in a plasma compartment:ISF volume ratio of 1:3.
In this time frame, one litre of 0.9 percent N. saline will increase plasma volume by about 250 mL, which could be the threshold for activation of the volume receptors in the atria, resulting in the release of atrial natriuretic peptide (ANP).

Because 0.9 percent N. saline is isosmotic, after a 1 L infusion, plasma osmolality will not change. No changes in antidiuretic hormone secretion will be detected by the hypothalamic osmoreceptors.

Because normal saline is protein-free, the oncotic pressure in the blood is slightly reduced after the saline infusion. As a result, fluid movement into the ISF is favoured (Starling’s hypothesis), and the lower oncotic pressure causes an immediate increase in the glomerular filtration rate (GFR) and a reduction in water reabsorption in the proximal tubule.

The flow of urine increases. There is no hormonal intermediary in this effect, so it is strictly local. Urine flow immediately increases. The fluid returns to the intravascular compartment, and urine flow continues until all of the transfused fluid has been excreted.

Blood pressure changes associated with a 1 L fluid infusion are unlikely to affect high-pressure baroreceptors in the carotid sinus.

The juxta-glomerular cells of the afferent arteriole are adjacent to the specialised cells (macula densa) of distal tubules. The sodium and chloride ions in the tubular fluid are detected by the macula densa. Renin release is inhibited when the tubular fluid contains too much sodium chloride. Hormonal changes take longer to manifest than physical changes that control glomerulotubular balance.
Hypertonic saline, not 0.9 percent N saline, is an osmotic diuretic.

A paediatric 19G Tuohy catheter is available that is 5cm in length and has 0.5cm markings

18G Tuohy catheters are generally 9 to 10cm to hub

Distal end of catheter is angled (15 to 30 degrees) and closed to avoid puncturing the dura

Epidural mesh are usually 0.2 microns and are used to filter bacteria and viruses to ensure sterility of procedure

Transparent catheters are 90cm long with diameters depending on gauge size. It has 1cm graduations from 5 to 20cm to ensure they have been inserted amply and removed completely. Distal end is smooth which can be open or closed (with lateral openings)

The follicle is the functional unit of the thyroid gland. The follicular cells surround the follicle which is filled with colloid. Suspended within the colloid is the is a pro-hormone complex thyroglobulin.

The synthesis and storage of thyroid hormones is done by follicular cells and the thyroglobulin within the colloid.

Iodide ions (I−) are actively transported against a concentration gradient into the follicular cell under the influence of thyroid stimulating hormone (TSH). It then undergoes oxidation to active iodine catalysed by thyroid peroxidase (TPO). The synthesis of thyroglobulin is in the follicular cells and it contains up to 140 tyrosine residues. The tyrosine residues of thyroglobulin and active iodine are merged to form mono- and di-iodotyrosines (MIT and DIT). The iodinated thyroglobulin is then taken up into the colloid where it is stored and dimerised. Two DIT molecules are joined to produce thyroxine (T4) while one MIT and one DIT molecule are joined to produce tri-iodotyrosine (T3) by a process catalysed by TPO.

Thyroglobulin droplets are taken up as vesicles into follicular cells by pinocytosis. This process is stimulated by TSH. When these vesicles fuse with lysosomes, hydrolysis of the thyroglobulin molecules and subsequent release of T4 and T3 into the circulation occurs.

Platelets are fragments of megakaryocytes and they are encapsulated by membrane.

They have no nucleus but are metabolically active and are able to express membrane receptors and release stored substances when triggered. adenosine diphosphate and serotonin are 2 of its content.

Because they have no nucleus, they are not able to produce new proteins. This is why aspirin and other drugs affect function for their entire lifespan after exposure. Its lifespan is approximately 9-10 days in normal individuals.

Platelets does NOT PRODUCE prostacyclin but are able to produce nitric oxide, prostaglandins and thromboxane.

The attributable risk is the rate of a disease in an exposed group to that of a group that has not been exposed to it. It involves the measure of association that is pertinent to making decisions for the individuals.

Dopamine (DA) is a dopaminergic (D1 and D2) as well as adrenergic ? and?1 (but not ?2 ) agonist.

The D1 receptors in renal and mesenteric blood vessels are the most sensitive: i.v. infusion of a low dose of DA dilates these vessels (by raising intracellular cAMP). This increases g.f.r. In addition, DA exerts a natriuretic effect by D1 receptors on proximal tubular cells.

Moderately high doses produce a positive inotropic (direct?1 and D1 action + that due to NA release), but the little chronotropic effect on the heart.

Vasoconstriction (?1 action) occurs only when large doses are infused.

At doses normally employed, it raises cardiac output and systolic BP with little effect on diastolic BP. It has practically no effect on nonvascular ? and ? receptors; does not penetrate the blood-brain barrier—no CNS effects.

Dopamine is used in patients with cardiogenic or septic shock and severe CHF wherein it increases BP and urine outflow.

It is administered by i.v. infusion (0.2–1 mg/min) which is regulated by monitoring BP and rate of urine formation

When a person forcefully expires against a closed glottis, changes occur in intrathoracic pressure that dramatically affect venous return, cardiac output, arterial pressure, and heart rate. This forced expiratory effort is called a Valsalva maneuver.

Initially during a Valsalva, intrathoracic (intrapleural) pressure becomes very positive due to compression of the thoracic organs by the contracting rib cage. This increased external pressure on the heart and thoracic blood vessels compresses the vessels and cardiac chambers by decreasing the transmural pressure across their walls. Venous compression, and the accompanying large increase in right atrial pressure, impedes venous return into the thorax. This reduced venous return, and along with compression of the cardiac chambers, reduces cardiac filling and preload despite a large increase in intrachamber pressures. Reduced filling and preload leads to a fall in cardiac output by the Frank-Starling mechanism. At the same time, compression of the thoracic aorta transiently increases aortic pressure (phase I); however, aortic pressure begins to fall (phase II) after a few seconds because cardiac output falls. Changes in heart rate are reciprocal to the changes in aortic pressure due to the operation of the baroreceptor reflex. During phase I, heart rate decreases because aortic pressure is elevated; during phase II, heart rate increases as the aortic pressure falls.

When the person starts to breathe normally again, the intrathoracic pressure declines to normal levels, the aortic pressure briefly decreases as the external compression on the aorta is removed, and heart rate briefly increases reflexively (phase III). This is followed by an increase in aortic pressure (and reflex decrease in heart rate) as the cardiac output suddenly increases in response to a rapid increase in cardiac filling (phase IV). Aortic pressure also rises above normal because of a baroreceptor, sympathetic-mediated increase in systemic vascular resistance that occurred during the Valsava.

Standard error can be calculated by the following formula:

Standard Error= (Standard Deviation)/√(Sample Size)
= (12) / √(64)
= 12 / 8
= 1.5

As there is no brachiocephalic artery on the left side, the artery is entered by the catheter on the right side.

The brachiocephalic artery branches into the common carotid and the right subclavian artery, so the catheter is most likely to enter the right subclavian artery, or also possibly the right carotid.