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

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

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

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

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

Ptosis and mydriasis are visible in surgical third nerve palsy, and the eye looks ‘down and out.’ The loss of innervation to all of the major structures supplied by the oculomotor nerve is reflected in these characteristics.

Ptosis is caused by the paralysis of the levator palpebrae superioris in oculomotor nerve palsy. Due to the unopposed actions of the superior oblique and lateral rectus muscles, the eye rotates down and out.

Mydriasis is caused by surgical (compressive) causes of third nerve palsy, which disrupt the parasympathetic pupillomotor fibres on the nerve’s periphery.

Medical (ischaemic) causes of a third nerve palsy, on the other hand, leave the superficial parasympathetic fibres relatively unaffected and the pupil unaffected.

Horner’s syndrome is characterised by ptosis, anhidrosis, and miosis, which are caused by a loss of sympathetic innervation to the tarsal muscle of the upper lid, facial skin, and dilator pupillae, respectively.

Approximately 70% of the heart’s ATP requirement is met by cardiac mitochondria through beta-oxidation of fatty acids at rest. The remaining 30% is supplied by glucose.

Amino acids and ketones, in the presence of ketoacidosis, may supply at most 10% of the ATP requirement. And, when in high levels, lactate may also contribute to the ATP requirement of the heart, particularly during moments of high muscular activity.

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.

Nitric oxide (NO), an endothelial-derived relaxant factor (EDRF), is a powerful vasodilator. Its cell-signalling molecule is calcium-dependant and generated endogenous by nitric oxide synthetases from the precursor L-arginine, oxygen and NADPH. Three main isoforms have been isolated and they are inducible (iNO), neuronal (nNO) and endothelial (eNO).

Endothelial NO stimulates intracellular guanylyl cyclase which generates cyclic GMP (cGMP) from its action on guanylyl tri-phosphate (GTP). The cGMP goes on to activate protein kinase G (PKG). PKG phosphorylates cell membrane proteins that regulate intracellular calcium concentrations and level of calcium sensitisation.

Smooth muscle vasodilatation results from:

1. Light chain phosphatase activation.
2. Inhibition of calcium entry into the cell (reducing Ca2+ concentrations) and
3. Hyperpolarisation of cells by activation of H+ channels.

Whatever the age, the dead space ratio is 0.3. It’s the dead space (Vd) to tidal volume ratio (Vt).

The glottis is the narrowest point of the upper airway in an adult, while the cricoid ring is the narrowest point in a child.

A child’s airway resistance is much higher than an adult’s. The resistance to airflow increases as the diameter of a paediatric airway shrinks. The radius (r) to the power of 4 is inversely proportional to airway resistance (r4). As a result, paediatric patients are more susceptible to changes in airflow caused by a small reduction in airway diameter, such as caused by oedema.

The compliance of a newborn’s lungs is very low (5 mL/cmH2O), but it gradually improves as lung size and elasticity grow. Lung compliance in an adult is 200 mL/cmH2O.

In children, minute ventilation (mL/kg/minute) is much higher.

T cells function as a part of the body’s adaptive immune system. There are different types of T cells, including:

Cytotoxic T cells: Function as killer cells by releasing cytotoxic granules into the membrane of targeted cells.

T-Helper cells: When activated, they function to activate other immune cell types, assist in antibody production with B cells and releasing cytokines including IL-2.

Memory T cells: Function as to provide immune memory against already encountered antigens.

T cells possess specific glycoproteins and receptors on their surface.

T-Helper cells work with HLA class II antigens on the cell surfaces in order to recognise foreign antigens

T cells survive ranges from a few weeks, to a lifetime depending on the subtype in question.

Immunoglobulins are expressed on the surface of, and secreted by B-lymphocytes.

Native antigens are recognised by B cells. T cells only recognise antigens that have been processed by the cells and presented on the surface of the cell.

Haemorrhage, including intracranial bleeding, is a common and potentially fatal side effect of warfarin therapy, and reversing anticoagulation quickly and completely can save lives. When complete and immediate correction of the coagulation defect is required in orally anticoagulated patients with life-threatening haemorrhage, clotting factor concentrates are the only viable option.

For rapid reversal of vitamin K anticoagulants, prothrombin complex concentrates (PCC) are recommended. They contain the vitamin K-dependent clotting factors II, VII, IX, and X and are derived from human plasma. They can be used as an adjunctive therapy in patients with major bleeding because they normalise vitamin K dependent clotting factors and restore haemostasis.

The most common treatments are fresh frozen plasma (FFP) and vitamin K. The efficacy of this approach is questioned due to the variable content of vitamin K-dependent clotting factors in FFP and the effects of dilution. Significant intravascular volume challenge, as well as the possibility of rare complications like transfusion-associated lung injury or blood-borne infection, are all potential issues.

To avoid anaphylactic reactions, vitamin K should be given as a slow intravenous infusion over 30 minutes. Regardless of the route of administration, the reversal of INRs with vitamin K can take up to 24 hours to reach its maximum effect.

Reversal of anticoagulation in patients with warfarin-associated intracranial haemorrhage may be considered with factor VIIa (recombinant), but its use is controversial. There are concerns about thromboembolic events following treatment, as well as questions about assessing efficacy in changes in the INR. If the drug is to be administered, patients should be screened for an increased risk of thrombosis before the drug is given.

The AAGBI and the British Hypertension Society has published guidelines for the measurement of adult blood pressure and management of hypertension before elective surgery.

The objective is to ensure that patients admitted for elective surgery have a known systolic blood pressure below 160 mmHg and diastolic blood pressures below 100 mmHg. The primary health care teams, if possible, should ensure that this is the case and provide evidence to the pre-assessment clinic staff or on admission.

Avoiding cancellation on the day of surgery because of white coat hypertension is a secondary objective.

Patients with blood pressures below 180 mmHg systolic and 110 mmHg diastolic (measured in the preop assessment clinic), who present to pre-operative assessment clinics without documented evidence of primary care blood pressures should proceed to elective surgery.

In this question, the history/assessment does not appear to point to obvious end-organ damage so there is no indication for further investigation for secondary causes of hypertension or an echocardiogram at this point. Further review and treatment at this point is not required.

However, you should write to the patient’s GP and encourage serial blood pressure measurements in the primary health care setting.

Bilirubin is formed by metabolizing heme, mostly from haemoglobin in red blood cells.

Bilirubin is conjugated to glucuronic acid in the hepatocytes by the glucuronyl transferase enzyme in order to enable it to become soluble and allow for its secretion across the canalicular membrane and into bile.

The conjugation process is increased by rifampicin and decreased by valproate.

Gilbert’s syndrome is caused by a decrease in glucuronyl transferase in the hepatic system, decreasing the transport of bilirubin into the hepatocyte, causing unconjugated bilirubinaemia.

Crigler-Najjer syndrome is caused by mutations in the genes responsible for hepatic glucuronyl transferase, decreasing the activity of the enzyme, meaning bilirubin cannot be conjugated, causing unconjugated bilirubinaemia.

Dubin-Johnson syndrome does not cause an impairment in the conjugation of bilirubin, but it blocks the transport of bilirubin out of the hepatocyte resulting in conjugated bilirubinaemia.

T3 is produced by peripheral de-iodination of T4. It is more active than T4.

TBG, like most binding proteins, is increased in pregnancy. Because of this, measurement of free thyroid hormone concentration is more important than total.

T4 and T3 concentrations are decreased in Illness and starvation.

L-T4 that is the active molecule while D-T4 is inactive.

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.

During normal tissue metabolism, there is production of CO2 (acid) which is then expired by the lungs. If metabolism switches from aerobic to anaerobic due to a lack of oxygen, the tissues are unable to completely oxidise sugars to CO2. As a consequence, the sugars can only be partially oxidised to lactic acid. Since lactic acid cannot be expired by the lungs, it remains in the circulation leading to metabolic acidosis.

Also, normal tissue metabolism leads to the production of some amount of acid from the breakdown of proteins. These acids are excreted from the body by kidney filtration. Renal failure will therefore results in acidosis after several days.

An increased acidosis stimulates the brain’s respiratory centres to increase the respiratory rate. This lowers the CO2 in the blood, leading to a decrease in its acidity. Renal excretion removes the excess acid, resulting in a normal pH, and a reduced PaCO2 and HCO3.

pH PaCO2 (kPa) HCO3
Compensated respiratory acidosis 7.34 7.2 29
Acute respiratory acidosis 7.25 7.3 22
Compensated metabolic acidosis 7.34 3.6 14
Metabolic acidosis 7.21 5.3 15
Metabolic alkalosis 7.51 5.1 30

Paediatric life support differs from adult life support in that hypoxia is the primary cause of deterioration.

After checking for danger, the child should be given a gentle stimulus (such as holding the head and shaking the arm) and asked, Are you alright? according to current advanced paediatric life support (APLS) guidelines. Safety, Stimulate, Shout is a phrase that is frequently remembered. Any airway assessment should be preceded by these actions.

Although the algorithm includes five rescue breaths, they are performed after the airway assessment.

It is not recommended to ask parents to leave unless they are obstructing the resuscitation. A team member should be with them at all times to explain what is going on and answer any questions they may have.

CPR should not begin until the child has been properly assessed and rescue breaths have been administered.

Organophosphate poisoning occurs most often due to accidental exposure to toxic amounts of pesticides. Signs and symptoms include diarrhoea, urination, miosis, bradycardia, emesis, lacrimation, lethargy and salivation.

Organophosphates are classified as indirect acting cholinomimetics, and their mode of action involves: (1) the inhibition of acetylcholinesterase (AChE) by forming a stable covalent bond on the active site serine; and, (2) amplification of endogenously release acetylcholine (ACh), hence the clinical manifestation.

There are 4 types of bonds or interactions: ionic, covalent, hydrogen bonds, and van der Waals interactions. Ionic and covalent bonds are strong interactions that require a larger energy input to break apart. When an element donates an electron from its outer shell, a positive ion is formed. The element accepting the electron is now negatively charged. Because positive and negative charges attract, these ions stay together and form an ionic bond. Covalent bonds form when an electron is shared between two elements and are the strongest and most common form of chemical bond in living organisms. Covalent bonds form between the elements that make up the biological molecules in our cells. Unlike ionic bonds, covalent bonds do not dissociate in water.

When polar covalent bonds containing a hydrogen atom form, the hydrogen atom in that bond has a slightly positive charge. This is because the shared electron is pulled more strongly toward the other element and away from the hydrogen nucleus. Because the hydrogen atom is slightly positive, it will be attracted to neighbouring negative partial charges. When this happens, a weak interaction occurs between the slightly positive charge of the hydrogen atom of one molecule and the slightly negative charge of the other molecule. This interaction is called a hydrogen bond.

An ankle block is commonly used for anaesthesia and postoperative analgesia when operating on bunions. It results in the selective block of the superficial peroneal, deep peroneal, and posterior tibial nerves.

The deep peroneal nerve supplies sensory input to the web space between the first and second toes (L4-5).

The L2-S1 nerve, often known as the superficial peroneal nerve, is a mixed motor and sensory neuron. It gives sensory supply to the anterolateral region of the leg, the anterior aspect of the 1st, 2nd, 3rd, and 4th toes, and innervates the peroneus longus and brevis muscles (with the exception of the web space between 1st and 2nd toes).

The sensory area of the saphenous nerve (L3-4) in the foot stretches from the proximal portion of the midfoot on the medial side to the proximal part of the midfoot on the lateral side.

The lateral side of the little (fifth) toe is innervated by the sural nerve’s sensory supply (S1-2). The heel, medial (medial plantar nerve), and lateral (lateral plantar nerve) soles of the foot are all served by the posterior tibial nerve.

Patients who have sustained thermal injuries are at high risk of becoming hypercatabolic with larger cardiac outputs and oxygen consumptions.

The hypermetabolic states increase with an increase in the burn severity and surface area of the skin affected. A patient with thermal injuries affecting 60% of the total surface area of the body will have twice the normal metabolic rate.

The optimal temperature for nursing patients with burn injuries is 30°C to conserve the energy usage. The areas affected by the burn injuries should be covered to reduce loss of fluid via evaporation. Resetting hypothalamic thermoregulation will cause a 1-2°C increase in core temperature.

Burn injuries will have an immediate effect on the intestine, destroying the barrier function and allowing for the movement of bacteria and endotoxins within hours.

Enteral nutrition allows for the delivery of nutrients directly to the stomach or intestine. It has correlation with a dampened hypermetabolic response to a thermal and injury, especially when initiated early as it helps to protect the integrity of the mucosal lining and prevents the movement of bacteria into circulation.

Diet changes have been linked to reduced mortality due to burn injuries. Diets high in protein especially (calorie: nitrogen ratio of 100: 1), have the highest correlation with improved survival rates.

Parenteral feeds may be required alongside enteral nutrition, even with the increased risks of infection.

The hormone parathyroid hormone (PTH) and the receptor parathyroid hormone type 1 (PTH1-Rc) are important regulators of blood calcium homeostasis.

PTH can cause a rapid release of calcium from the matrix in bone, but it also affects long-term calcium metabolism by acting directly on bone-forming osteoblasts (by binding to PTH1-Rc) and indirectly on bone-resorbing osteoclasts.

PTH causes changes in the synthesis and/or activity of several proteins, including osteoclast-differentiating factor, also known as TRANCE or RANKL, when it acts on osteoblasts.

RANK receptors are found on the cell surfaces of osteoclast precursors. The osteoclasts are activated when RANKL binds to the RANK receptors. Osteoclasts lack PTH receptors, whereas osteoblasts do. Osteoclasts are activated indirectly when the RANK receptor binds to the RANKL secreted by osteoblasts, resulting in bone resorption. PTH1 receptors are found in osteoclasts, but they are few.

PTH activates G-protein coupled receptors in all target cells via adenylate cyclase.

The PTH2 receptor is most abundant in the nervous system and pancreas, but it is not a calcium metabolism regulator. It is abundant in the septum, midline thalamic nuclei, several hypothalamic nuclei, and the dorsal horn of the spinal cord, as well as the cerebral cortex and basal ganglia. Expression in pancreatic islet somatostatin cells is the most prominent on the periphery.

The distribution of the receptor is being used to test functional hypotheses. It may play a role in pain modulation and hypothalamic releasing-factor secretion control.

The emulsification and absorption of fats requires Bile salts.

Absorption of fats is associated with the activation of lipases in the intestine.

Bile salts are involved in fat soluble vitamin absorption and are reabsorbed in the terminal ileum (B12 is NOT fat soluble).

Although Vitamin B12 is also absorbed in the terminal ileum, it is a water soluble vitamin (as are B1, nicotinic acid, folic acid and vitamin C) .

The gastric parietal cells secretes Intrinsic factor that is essential for the absorption of B12.

Detsky’s Modified cardiac risk classification system in patients undergoing non-cardiac surgery:

Age more than 70: 05 points

History of myocardial infarction:

Less than 6 months: 10 points
More than 6 months: 5 points

Angina Pectoris:

Angina with minimal exertion: 10 points

Angina at any level of exertion: 20 points

Pulmonary Oedema:

Within 7 days: 10 points
At any time: 5 points

Suspected aortic valve stenosis with valve area 30 points = high risk.

In patients with an intact hypothalamic-pituitary axis, serial TSH measurements are used to determine the adequacy of treatment with thyroid hormones . changes in TSH levels becoming apparent after approximately eight weeks of therapy with thyroid hormone replacement. Change in T3/T4 levels are seen before changes in TSH .

In patients taking thyroid replacement therapy, the most frequent reason for persistent elevation of serum TSH is poor compliance. Patients who do not regularly take their L-thyroxine try and catch up just before a visit to a clinician for blood test.

Tissue-level unresponsiveness to thyroid hormone is caused by mutation in the gene controlling a receptor for T3 and is rare.

Reduced responsiveness of target tissues to thyroid hormone aka resistance to thyroid hormones (rTH) occurs when there is a mutation in the thyroid hormone receptor β gene. It is a rare autosomal dominant inherited syndrome of reduced end-organ responsiveness to thyroid hormone and has two types:

Generalised resistance (GrTH)
Pituitary resistance (PrTH)

Patients with rTH have normal or slightly elevated serum thyroid stimulating hormone (TSH) level, elevated serum free thyroxine (FT4) and free triiodothyronine (FT3) concentrations.

Drugs that increase metabolism of thyroxine include:

Warfarin
Rifampin
Phenytoin
Phenobarbital
St John’s Wort
Carbamazepine

These drugs lower circulating thyroid hormones and would be associated with a raised TSH but low T3/T4.

A beta-1 adrenoreceptor agonist is most likely the ligand that causes increased automaticity, increased chronotropy, increased excitability, and increased inotropy on the sino-atrial node. However, alpha-1 adrenoreceptor effects may cause an increase in systemic vascular resistance. Noradrenaline, adrenaline, dopamine, and ephedrine are examples of drugs with mixed alpha and beta effects.

Adrenaline, noradrenaline, dopamine, dopexamine, dobutamine, ephedrine, and isoprenaline are examples of drugs that have some beta-1 activity. The beta-1 receptor is a G protein-coupled metabotropic receptor. When the beta-1 agonist binds to the cell surface membrane, it causes a conformational change in the Gs unit, which triggers a cAMP-dependent pathway and a calcium influx into the cell.

Catecholamines also help to relax the heart muscle (positive lusitropy). Dromotropy is the ability to increase the atrioventricular (AV) node’s conduction velocity.

Inodilators cause an increase in intracellular calcium as a result of phosphodiesterase III (PDIII) inhibition. Milrinone, enoximone, and amrinone are some examples. Positive inotropy is caused by increased calcium entry into the myocytes. Lusitropy is also increased by phosphodiesterase inhibitors. Increased cAMP inhibits myosin light chain kinase, resulting in reduced phosphorylation of vascular smooth muscle myosin, lowering systemic and pulmonary vascular resistance.

The mechanism of action of alpha-1 adrenoreceptor agonists is an increase in intracellular calcium caused by an increase in inositol triphosphate (IP3). IP3 is a second messenger that causes an increase in systemic vascular resistance by stimulating the influx of Ca2+ into smooth muscle cells. Reflex bradycardia can occur as a result of the subsequent increase in blood pressure. Phenylephrine and metaraminol are examples of pure alpha-1 agonists.

Levosimendin is a novel inotrope that makes myocytes more sensitive to intracellular Ca2+. It causes a positive inotropy without changing heart rate or oxygen consumption significantly.

The Na-K-ATPase membrane pump in the myocardium is inhibited by digoxin. This inhibition promotes sodium-calcium exchange, resulting in an increase in intracellular Ca2+ and increased contraction force. The parasympathetic effects of digoxin on the AV node result in bradycardia. Systemic vascular resistance will not be affected by it.

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.

After thyroid surgery, about 10-15% of patients experience a temporary subjective voice change of varying degrees. A frog in the throat or cracking of the voice, or a weak voice, are common descriptions. These modifications are only temporary, lasting a few days to a few weeks.

Swelling of the muscles in the area of the dissection, as well as inflammation and oedema of the larynx due to the dissection, or minor trauma from the tracheal tube, are all suspected causes.

On both sides of the thyroid gland, the superior laryngeal nerve (EBSLN) runs along the upper part. The muscles that fine-tune the vocal cords are innervated by these nerves. The quality of their voice is usually normal if they are injured, but making high-pitched sounds may be difficult. Injury to the EBSLN occurs in about 2% of the population.

Injuries to the recurrent laryngeal nerve (RLN) have been reported to occur in 1 percent to 14 percent of people. Except for the cricothyroid muscle, the RLN supplies all of the laryngeal intrinsic muscles.

This complication is usually unilateral and temporary, but it can also be bilateral and permanent, and it can be intentional or unintentional. The most common complication following thyroid surgery is a permanent lesion of damaged RLN, which manifests as an irreversible phonation dysfunction.

The crico-arytenoid joint dislocation is a relatively uncommon complication of tracheal intubation and blunt neck trauma. The probability is less than one in a thousand.

Vocal cord polyps affect 0.8 percent of people.

Monoamine oxidase (MOA) enzymes are responsible for the catalyses of monoamine oxidative deamination. It assists the degradation of serotonin, norepinephrine (NE) and dopamine.

They are found in the mitochondria of most central and peripheral nerve tissues.

There are 2 different types:

Type A: Whose main function it to inactivate dopamine, tyramine, norepinephrine and 5-hydroxytryptamine. In addition to the nervous system, it is also found in the liver, brain gastrointestinal tract, pulmonary endothelium and placenta
Type B: Whose main function is to inactivate dopamine, tyramine, tryptamine and phenylethylamine. In addition to the nervous system, it is also found in the liver, brain (especially in the basal ganglia) and blood platelets.

The incidence of vertebral canal haematoma following neuraxial blockade was reported (third National Audit Project (NAP3)) as 0.85 per 100 000 (95% CI 0-1.8 per 100 000). The incidence following neuraxial blockade in coagulopathic patients is likely to be higher hence coagulopathy remains a relative contraindication for conducting a spinal or epidural. When indicate, risk and benefits are weighed, and it is only performed by experienced personnel in this case.

Acceptable time to perform a block after the last dose of rivaroxaban in a patient with a creatinine clearance of greater than 30mL/minute is 18 hours.

Acceptable time to perform a block after the last dose of subcutaneous LMWH as prophylaxis is 12 hours.

Acceptable time to perform a block after the last dose of subcutaneous UFH as prophylaxis is 4 hours.

Acceptable time to perform a block after the last dose of thrombolytic therapy (streptokinase or alteplase) is 10 days.

Clopidogrel should be stopped 7 days prior to surgery, particularly if a central neuraxial procedure is considered.

BMR is lower in females than males.

It decreases with increasing age.

There is an increase in BMR with increased muscle (i.e. lean tissue)

BMR is increased in stress and illness. There is also an catabolic state in these conditions.

The option that is most responsible is the progressive decrease in venous return of blood to the right atrium. The heart rate does not usually change with PEEP so the fall in cardiac output is due to a reduction in left ventricular (LV) stroke volume (SV).

Note that the interventricular septum does shift toward the left and there is an increased pulmonary vascular resistance (PVR) from overdistention of alveolar air sacs that contribute to the reduction in cardiac output. Any increase in PVR will be associated with reduced pulmonary vascular capacitance.

Standard wire gauge cannulas for intravenous and intraarterial use are available (SWG or G). The SWG is a former imperial unit (which requires metric conversion). The cross sectional area of wires is becoming more popular as a size measurement.

The number of wires that will fit into a standard hole template is referred to as SWG.

This standard sized hole can accommodate 22 thin wires side by side (each wire the diameter of a 22 gauge cannula)
In the same hole, 14 thicker wires would fit (each wire the diameter of a 14 gauge cannula)

While the diameter and thus radius of a parallel sided tube are the most important determinants of fluid flow rate, they are not commonly used to compare cannula sizes.

The circumference of French gauge (FG) catheters (urinary or chest drains) is measured. Sizes of double lumen tracheal tubes are FG. Internal diameter is used to measure single lumen tubes.

The pituitary gland plays a crucial role in the neuro-endocrine axis. It is located at the base of the skull in the sella turcica of the sphenoid bone. It is connected superiorly to the hypothalamus, third ventricle, and visual pathways, and laterally to the cavernous sinuses, internal carotid arteries, and cranial nerves III, IV, V, and VI.

Pituitary tumours make up about 10-15% of all intracranial tumours. The majority of adenomas are benign. Over-secretion of pituitary hormones (most commonly prolactin, growth hormone, or ACTH), under-secretion of hormones, or localised or generalised pressure effects can all cause symptoms.

Compression of the optic chiasm can result in visual field defects, the most common of which is bitemporal hemianopia. This is caused by compression of the nasal retinal fibres, which carry visual impulses from temporal vision across the optic chiasm to the contralateral sides before continuing to the optic tracts.

The interruption of the visual pathways distal to the optic chiasm causes a homonymous visual field defect. The loss of the right or left halves of each eye’s visual field is referred to as homonymous hemianopia. It’s usually caused by a middle or posterior cerebral artery territory stroke that affects the occipital lobe’s optic radiation or visual cortex.

Binasal hemianopia is a condition in which vision is lost in the inner half of both eyes (nasal or medial). It’s caused by compression of the temporal visual pathways, which don’t cross at the optic chiasm and instead continue to the ipsilateral optic tracts. Binasal hemianopia is a rare complication caused by the internal carotid artery impinging on the temporal (lateral) visual fibres.

A monocular visual loss (that is, loss of vision in only one eye) can be caused by a variety of factors, but if caused by nerve damage, the damage would be proximal to the optic chiasm on the ipsilateral side.

A central scotoma is another name for central visual field loss. Every normal mammalian eye has a scotoma, also known as a blind spot, in its field of vision. The optic disc is a region of the retina that lacks photoreceptor cells and is where the retinal ganglion cell axons that make up the optic nerve exit the retina. When both eyes are open, visual signals that are absent in one eye’s blind spot are provided for the other eye by the opposite visual cortex, even if the other eye is closed.

Scotomata can be caused by a variety of factors, including demyelinating disease such as multiple sclerosis, damage to nerve fibre layer in the retina, methyl alcohol, ethambutol, quinine, nutritional deficiencies, and vascular blockages either in the retina or in the optic nerve.

Bilateral scotoma can occur when a pituitary tumour compresses the optic chiasm, causing a bitemporal paracentral scotoma, which then spreads out to the periphery, causing bitemporal hemianopsia. A central scotoma in a pregnant woman could be a sign of severe pre-eclampsia.

Based on the laboratory reports, the patient is suffering from significant hyponatremia. The symptoms of hyponatremia are mainly neurological and depend on the severity and rapidity of onset of hyponatremia.

Patient symptom according to the hyponatremia level is correlated below:

125 – 130mmol/L – Nausea and malaise
115 – 125mmol/L – Headache, lethargy, seizures, and coma
<120mmol/L – Up to 11% present with coma.

Magnesium is a very important cation due to its various physiological roles in the body. This includes:
– playing the role of a cofactor in many enzymatic reactions
– influencing hormone receptor binding
– affecting calcium channels
– impact on cardiac, vascular and neural cells

Magnesium sulphate is used as first line in the treatment of eclampsia. Moreover, it has some preventive role in patients with severe pre-eclampsia. All the clinical effects of magnesium are in line with its plasma concentration.

The first sign of magnesium toxicity in obstetric patients is the loss of patellar reflex, which is regularly monitored during treatment. The other options are all late signs of magnesium toxicity.

Whenever there is a doubt, serum magnesium levels should always be monitored.

The table below correlates the effects of increased levels of magnesium on the body:

Plasma Concentration
(mmol/L) Effect
0.7-1.2 Normal
4-8 Decreased deep tendon reflexes, nausea, headache, weakness, malaise, lethargy and facial flushing
5-10 ECG changes (prolonged PR, prolonged QT, and widened QRS)
10 Muscle weakness, loss of deep tendon reflexes, hypotension
15 SA/AV nodal block, respiratory paralysis and depression
20 Cardiac arrest.

The area described in the question is supplied by the intercostobrachial nerve, which provides sensory innervation to the portions of the axilla, tail of the breast, lateral chest wall and medial side of the arm.

It is a common for it to be ‘missed’ during administration of local anaesthesia because of its very superficial anatomic course. It may be anesthetized by giving an analgesia from the upper border of the biceps at the anterior axillary fold, to the margin of the triceps by the axillary floor.

Pituitary tumours that compress the optic chiasma primarily affect the neurones that decussate at this location. Bitemporal hemianopia is caused by neurones that emerge from the nasal half of the retina and transmit the temporal half of the visual field.

The axons of ganglion cells in the retina form the optic nerve.

It exits the orbit through the optic foramen and projects to the thalamic lateral geniculate body. The optic chiasma forms above the sella turcica as the nasal fibres decussate along the way. The optic radiation travels from the lateral geniculate body to the occipital cortex.

Lesions at various points along this pathway cause the following visual field defects:

Scotoma implies partial retinal or optic nerve damage.
Monocular vision loss occurs when the optic nerve is completely damaged.
Pathology at the optic chiasma causes bitemporal hemianopia.
Cortical blindness with occipital cortex pathology and homonymous hemianopia with lesions compromising the optic radiation.

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.

This patient’s limited haematological profile includes mild normocytic anaemia and a normal platelet count.

Iron deficiency is the most common cause of anaemia during pregnancy. It affects 75 to 95 percent of patients. A haemoglobin level of less than 110 g/L in the first trimester and less than 105 g/L in the second and third trimesters is considered anaemia. There will usually be a low mean cell volume (MCV), mean cell haemoglobin (MCH), and mean cell haemoglobin concentration in addition to a low haemoglobin (MCHC). The MCV may be normal in mild cases of iron deficiency or coexisting vitamin B12 and folate deficiency.

To determine whether you have an iron deficiency, you’ll need to take more tests. Low serum ferritin (15 g/L) and less reliable indices like serum iron and total iron binding capacity are among them.

A number of factors contribute to iron deficiency in pregnancy, including:

Insufficient dietary iron to meet the mother’s and foetus’ nutritional needs
Multiple pregnancies
Blood loss, as well as
Absorption of iron from the gut is reduced.

The volume of plasma increases by about 50% during pregnancy, but the mass of red blood cells (RBCs) increases by only 30%. Dilutional anaemia is the result of this situation. From the first trimester to delivery, the RBC mass increases linearly, while the plasma volume plateaus, stabilises, or falls slightly near term. As a result, between 28 and 34 weeks of pregnancy, haemoglobin concentrations are at their lowest. The effects of haemodilution will be negated in this patient because she is 37 weeks pregnant.

Vitamin B12 and folate deficiency are less common causes of anaemia in pregnancy. The diagnosis could be ruled out if the MVC is normal.

During pregnancy, the platelet count drops, especially in the third trimester. Gestational thrombocytopenia is the medical term for this condition. It’s due to a combination of factors, including haemodilution and increased platelet activation and clearance. Pre-eclampsia and HELLP syndrome are common causes of thrombocytopenia. Pre-eclampsia isn’t the only cause of anaemia during pregnancy.

A typical blood picture of a haemoglobinopathy like sickle cell disease shows quantitative and qualitative defects, with the former leading to a severe anaemia exacerbated by haemodilution and other factors that contribute to iron deficiency. Microcytic cells are the most common type.

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.

The most likely diagnosis is a spinal epidural haematoma, a neurological emergency. A full examination must be carried out to determine the nature of the neurological problem before conducting any investigations or imaging.

The effects of spinal anaesthesia should have worn off by this time point, and the severe back pain is a red flag.

The patient will also require an urgent neurological team referral as a spinal epidural haematoma requires immediate evacuation for spinal decompression. Analgesics may be prescribed for pain management.

Heparin would have been fully metabolised and so a reversal is unnecessary.

A spinal epidural haematoma is a pooling of blood in the epidural space, which can cause compression of the spinal cord. Its presenting symptoms are:

Usually begins with severe backpain and percussion tenderness
Cauda equina syndrome
Paralysis of the lower extremities.
If infected, a fever occurs in 66% of cases
Lower limb weakness developing after stopping an epidural infusion or weakness of the lower limbs which does not resolve within four hours of cessation of infusion of epidural local anaesthetic
Meningism.

An acetylcholinesterase inhibitor or anticholinesterase is a chemical that inhibits the cholinesterase enzyme from breaking down acetylcholine (ACh) therefore increasing the level and duration of action of the neurotransmitter acetylcholine(ACh).

ACh stimulates postganglionic receptors to produce the following effects:

Salivation
Lacrimation
Defecation
Micturition
Sweating
Miosis
Bradycardia, and
Bronchospasm.

Since these effects are produced by muscarine, they are referred to as muscarinic effects, and the postganglionic receptors are called muscarine receptors.

SLUD (Salivation, Lacrimation, Urination, Defecation – and emesis) is usually encountered only in cases of drug overdose or exposure to nerve gases. It is a syndrome of pathological effects indicating massive discharge of the parasympathetic nervous system.

Serum specific IgE assays against allergen sources/molecules are the most commonly used in vitro diagnostic approach. The measurement of specific IgE recognizing allergenic epitopes can be achieved both through the usage of single reagents (singleplex) or with a pre-defined panel of a number of molecules to be tested simultaneously (multiplex).

Several clinical entities have been described and those occurring immediately after drug exposure are immunoglobulin E (IgE)-mediated and explored by skin testing and by the in vitro measurement of serum-specific IgE. The sensitivity of these tests is not 100% and even for patients with a clear positive history, a drug provocation test may be required in order to confirm the diagnosis. The advantages of the in vitro determination of specific IgE antibodies when compared with in vivo testing are that the former poses no direct risk to the patient and does not require personnel with expertise. Even though in vitro tests are recommended in immediate hypersensitivity reactions, their exact place in the diagnostic procedure is not clear and certain authors do not use this method in daily practice. In one study, in terms of sensitivity, 11 of 26 patients (42%) with negative skin tests and a positive drug provocation challenge (or repeated clinical history) had specific IgE to benzylpenicilloyl or amoxicilloyl (4). The specificity of the test was 95€“100%. Therefore, IgE measurements can avoid a potentially harmful drug provocation test.

An elevated serum tryptase does not differentiate between type 1 and type 2 hypersensitivity reaction. It indicates mast cell degranulation.

RAST is a useful aid to improve the overall diagnosis of drug allergies by using radioactive detection. This, however, is now rarely used.

Quantification of basophil activation by CD63 expression can be done by flow cytometry, which forms the basis of experimental drug-induced basophil stimulation tests.

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 (Iˆ’) 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.

Acute pulmonary embolism occurs when a blood clot becomes embedded in a pulmonary artery and restricts lung blood flow.

Thrombolysis is recommended in patients with extremely compromised circulation rather than reduced oxygen in the blood. It is effective when administered via a peripheral vein or a pulmonary artery catheter.

Anticoagulant therapy (heparin use) decreases the risk of further embolic evens and decreases constriction of pulmonary vessels.

An ECG may be normal in patients with an acute pulmonary embolism.

Taste sensation from the anterior two-thirds of the tongue is carried by chorda tympani, a branch of the facial nerve.

The general somatic sensation of the anterior two-third of the tongue is supplied by the lingual nerve, a branch of the mandibular nerve.

Both general somatic sensation and taste from the posterior third of the tongue are carried by the glossopharyngeal nerve.

All the muscles of the tongue except palatoglossus are supplied by the hypoglossal nerve whereas palatoglossus is supplied by the vagus nerve. (This is because palatoglossus is the only tongue muscle derived from the fourth branchial arch)

Asthma is a lung condition that causes reversible narrowing and swelling of airway passages. It is classified by the frequency and severity of symptoms.

The following are symptoms of moderate asthma:

Symptoms include cough, wheezing, chest tightness, or difficulty breathing which occurs daily
Decreased activity levels due to flare-ups
Night-time symptoms 5 or more times a month
Lung function test FEV1 is 60-80% of predicted normal values
Peak flow has more than 30% variability

With moderate asthma attacks, the arterial pCO2 levels may decrease, but as severity increases, so does the pCO2, reaching normal levels, and then exceeding them in severe asthma attacks.

Airway obstruction increases the functional residual capacity.

Concentration of serum bicarbonate would not increase in moderate asthma, but it could possibly increase in life-threatening asthma via the same mechanism as what increases arterial PCO2.

FEV1 is a good measure of airway obstruction. and is reduced in acute asthma attacks.

In the case of a pneumothorax, a decrease in arterial PO2 is higher.

This sudden change in pulse rate is due to the oculocardiac reflex. It is a >20% reduction in pulse rate as a result of placing pressure directly on the eyeball. The reflex arc has an afferent and efferent arm:

The afferent (sensory) arm: The trigeminal nerve (CN V)

The efferent arm: The vagus nerve (CN X)

The most appropriate action is to ask the surgeon to stop retraction of the extraocular muscles, Assess for hypoxia, and give 100% oxygen if indicated.

Atropine of glycopyrrolate can be administered to counteract the reflex, and also prevent any further vagal reflexes.

Administration of fentanyl may increase patient’s risk of bradycardia and sinus arrest in this case.

Adrenaline is not indicated here as other treatment options will provide sufficient relief from arrhythmia.

Chronic obstructive pulmonary disease (COPD) is an obstructive, inflammatory lung condition. It encompasses symptoms of emphysema, chronic bronchitis and asthma.

Inhaling high dose steroids are prescribed to treat COPD. They are effective at reducing symptoms and improving lung function. They also work to reduce the number of hospitalisations by decreasing the number of acute exacerbation events. Despite providing effective symptom relief, it cannot slow down the decline of FEV1 as COPD is an irreversible condition.

COPD reduces the FEV1 measurements, as well as the FEV1/FVC ratio.

Breathlessness is a major COPD symptom and can occur at any point in the disease progression, including at an FEV1 >50%.

FEV1 is used in COPD staging, and it is classed as follows:
>80%: Mild or stage I
50 – 79%: Moderate or stage II
30 – 49%: Severe or stage III
<30%: Very severe or stage IV
Patients with mild COPD are usually able to manage their condition on their own, however once the disease progresses to moderate, more GP visits are required, with those in the severe category requiring frequent hospitalisation.

Asthma is correlated to an increase in transfer factor. COPD (emphysema) is correlated to a decreased transfer factor.

COPD predisposes to eventual pulmonary hypertension as a result of an increase in pulmonary vascular resistance.

Normally, at rest vagal influence is dominant producing the heart rate of 60-80 beats per minute even if the intrinsic automaticity of Sinoatrial Node is 100-110 beats per minute.

The transplanted heart has no autonomic nervous supply. So, it will respond to endogenous and exogenous catecholamine. This loss of parasympathetic innervation is responsible for the tachycardia in this patient.

Hypokalaemia can cause myocardial excitability and potential for ventricular ectopic and supraventricular arrhythmias. Hypothyroidism is also unlikely to cause tachycardia in this patient.

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

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

The gag reflex is a protective mechanism that prevents any foreign material to enter the aerodigestive tract.

This reflex has afferent (sensory) and effect (motor) components.
– Glossopharyngeal nerve form the afferent limb
– Vagus nerve form the efferent limb.

Oxygen delivery is related to blood flow as most of the oxygen binds to haemoglobin in red blood cells, although a small amount is dissolved in the plasma. Blood flow per 100 g of tissue is greatest in the kidneys.

The following is the oxygen consumption rate of different organs in ml/minute/100g

Hepatoportal = 2.2
Kidney = 6.8
Brain = 3.7
Skin = 0.38
Skeletal muscle = 0.18
Heart = 11.

The perfect glomerular filtration marker is:

The human body is not harmed by it.
Chemical or physical methods are used to accurately measure
Extracellular fluid (ECF) compartment is freely and evenly diffusible.
Inability to access the intracellular fluid (ICF) compartment
Filtration in the kidney is the only way to remove it from the blood.

The ideal marker should not be reabsorbed into the bloodstream by the renal tubules or other urinary system components.

Creatinine is an endogenous substance that is filtered freely by the glomerulus and secreted by the proximal tubule. As a result, creatinine clearance consistently underestimates GFR. In healthy people, this overestimation ranges from 10% to 40%, but it is higher and more unpredictable in patients with chronic kidney disease.

The gold standard method of inulin clearance necessitates an intravenous infusion and several hours of timed urine collection, making it costly and time-consuming. Inulin is hard to come by and is difficult to mix and keep as a solution.

Exogenous filtration markers include the following:

Although plasma clearance of 51chromium EDTA is a widely used method in Europe, tubular reabsorption can occur.
Because 125I-iothalamate can be excreted by renal tubules in the urine, it cannot be used in patients who have an iodine assay.

Radioactive substances must be stored, administered, and disposed of according to these methods.

The glomerulus filters para-aminohippuric acid (PAH) freely, and any that remains in the peritubular capillaries is secreted into the proximal convoluted tubules. This marker is used to determine the amount of blood flowing through the kidneys.

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.

Endothelin-1 is considered as a powerful coronary vasoconstrictor, produced by the endothelium. It acts to counter the effects of Nitric oxide (NO).
Neuropeptide-Y, angiotensin1, cocaine, vasopressin, and nicotine are some other coronary vasoconstrictors.

Chronotrophy and inotrophy occur after the activation of sympathetic nerve fibres, which in turn results in increasing the myocardial oxygen consumption, leading to increased coronary blood flow via local metabolic processes.

An alpha-receptor mediated coronary vasoconstrictor effect is also initiated that usually competes with vasodilation, resulting in decreased coronary vascular resistance. Some of the other dilators include hydrogen ions, CO2, potassium, and lactic acid. The action of endothelial NO synthase (eNOS) on L-arginine results in the formation of NO. This messenger also plays a vital role in the regulation of coronary blood flow via vasodilation, inhibition of platelet aggression, and decreasing vascular resistance.
Adenosine is considered as purine nucleoside that forms after the breakdown of adenosine triphosphate (ATP). Adenosine binds to adenosine type 2A (A2A) receptors in coronary vascular smooth muscles. These are coupled to the Gs protein. This mechanism leads to hyperpolarisation of muscle cells, resulting in relaxation and increased coronary blood flow.

GTN is an veno and arteriolar dilator, which behaves as pro-drug with NO.

Tonic-clonic (Grand mal) epilepsy is characterised by a general loss of consciousness with violent involuntary muscle contractions.

The NICE guidelines for treatment indicates the use of sodium valproate and lamotrigine, but sodium valproate unsuitable in this case and she is a woman of reproductive age and it is known to have teratogenic effects. Lamotrigine is a more suitable choice, prescribed as 800mg daily.

NICE guidelines also advice an additional prescription of 5mg of folic acid daily for women on anticonvulsant therapy looking to get pregnant. It also warns of the need for extra contraceptive precaution as there is a possibly that the anticonvulsant agent can reduce levels of contraceptive agents.

Stimulation of the vagal nerve stimulation is only necessary in patients who are refractory to medical treatment and not candidates for surgical resection.

Trigeminal neuralgia is characterized by excruciating paroxysms of pain in the lips, gums, cheek, or chin and, very rarely, in the distribution of the fifth nerve. The pain seldom lasts more than a few seconds or a minute or two but may be so intense that the patient winces, hence the term tic. The paroxysms, experienced as single jabs or clusters, tend to recur frequently, both day and night, for several weeks at a time. They may occur spontaneously or with movements of affected areas evoked by speaking, chewing, or smiling. Another characteristic feature is the presence of trigger zones, typically on the face, lips, or tongue, that provoke attacks; patients may report that tactile stimuli – e.g., washing the face, brushing the teeth, or exposure to a draft of air – generate excruciating pain. An essential feature of trigeminal neuralgia is that objective signs of sensory loss cannot be demonstrated on examination.

Trigeminal neuralgia is relatively common, with an estimated annual incidence of 4€“8 per 100,000 individuals. Middle-aged and elderly persons are affected primarily, and ,60% of cases occur in women. Onset is typically sudden, and bouts tend to persist for weeks or months before remitting spontaneously. Remissions may be long-lasting, but in most patients, the disorder ultimately recurs.

An ESR or CRP is indicated if temporal arteritis is suspected. In typical cases of trigeminal neuralgia, neuroimaging studies are usually unnecessary but may be valuable if MS is a consideration or in assessing overlying vascular lesions in order to plan for decompression surgery.

Type I – immediate hypersensitivity reaction

Examples are: Atopy, urticaria, Anaphylaxis, Asthma( IgE mediated).

Type II – Antibody mediated cytotoxic reaction

Examples are: Autoimmune haemolytic anaemia, Thrombocytopenia( IgM or IgG mediated).

Type III – Immune complex mediated reaction

Examples are: Serum sickness,SLE – IgG., Farmers lungs, rheumatoid arthritis

Type IV – Delayed hypersensitivity reaction

Examples are: Contact dermatitis, drug allergies.

Type V – Autoimmune

Graves’
Myasthenia – IgM or IgG.

Nitric oxide is generated from L-arginine by nitric oxide synthase. It is produced in response to haemodynamic stress by the vascular endothelium, and it produces both smooth muscle relaxation and reduced vascular resistance.

Nitric oxide may be inactivated through interaction with other oxygen free radicals, (e.g. oxidised low-density lipoprotein (LDL)).

Nitric oxide causes the production of the second messenger, cyclic guanosine monophosphate (cGMP).

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 .

The incidence of Pulmonary aspiration in children is about 0.07%€�0.1%.

The Association of Paediatric Anaesthetists of Great Britain and Ireland, The European Society of Paediatric Anaesthetists and L’Association Des Anesthésistes€�Réanimateurs Pédiatriques d’Expression Française produced a consensus statement in April 2018 with revised starvation times in children prior to elective surgery.

The preoperative fasting for elective procedures for children aged 0-16 years of age are:

Solid food/formula milk – 6 hours
Breast milk – 4 hours
Clear fluid – 1 hour

A liberal clear fluid fasting regime does not affect the incidence of pulmonary aspiration in children as long as there are no specific contraindications (e.g. gastro-oesophageal reflux, cerebral palsy). Prolonged periods of fasting in children are associated with increase thirst and irritability and can lead to other adverse physiological and metabolic effects.

Clear fluids are defined as water, clear (nonopaque) fruit juice or squash/cordial, ready diluted drinks, and non-fizzy sports drinks.

The central venous pressure (CVP) waveform depicts changes of pressure within the right atrium. Different parts of the waveform are:

A wave: which represents atrial contraction. It is synonymous with the P wave seen during an ECG. It is often eliminated in the presence of atrial fibrillation, and increased tricuspid stenosis, pulmonary stenosis and pulmonary hypertension.

C wave: which represents right ventricle contraction at the point where the tricuspid valve bulges into the right atrium. It is synonymous with the QRS complex seen on ECG.

X descent: which represents relaxation of the atrial diastole and a decrease in atrial pressure, due to the downward movement of the right ventricle as it contracts. It is synonymous with the point before the T wave on ECG.

V wave: which represents an increase in atrial pressure just before the opening of the tricuspid valve. It is synonymous with the point after the T wave on ECG. It is increased in the background of a tricuspid regurgitation.

Y descent: which represents the emptying of the atrium as the tricuspid valve opens to allow for blood flow into the ventricle in early diastole.