The superior laryngeal nerve gives off two branches: the sensory branch which is the internal laryngeal nerve, and the motor branch which is the external laryngeal nerve.

The recurrent laryngeal nerve (RLN) rises from the vagus nerve which supplies the intrinsic muscles of the larynx, except the cricothyroid muscles.

Boyle’s law is correctly stated as it states that the volume of a gas of known mass is inversely proportional with absolute pressure, at a constant temperature.

Beer’s law states that radiation absorption by a solution of known thickness and concentration is identical to that of a solution of double thickness and half concentration.

Bougner’s (or Lambert’s) law states that every layer with the same thickness will absorb the same amount of radiation as it passes through.

Graham’s law states that the diffusion rate of a gas is inversely related to the square root of its molecular weight.

Raoult’s law states that the reduction of a solvent’s vapour pressure is directly proportional to the solute’s molar concentration.

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

The Delphi is a group facilitation technique that seeks to obtain consensus on the opinions of `experts’ through a series of structured questionnaires (commonly referred to as rounds). By using successive questionnaires, opinions are considered in a non-adversarial manner, with the current status of the groups’ collective opinion being repeatedly fed back. Studies employing the Delphi make use of individuals who have knowledge of the topic being investigated

The neuroleptic malignant syndrome 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 ICU care, anticholinergic drugs, increasing dopaminergic activity with Amantadine, L-dopa, and dantrolene, and non- depolarising neuromuscular blockade drugs

The vertebral (spinal) column is the skeletal central axis made up of approximately 33 bones called the vertebrae.

Cervical disc herniations occur when some or all of the nucleus pulposus extends through the annulus fibrosus. The most commonly affected discs are the C5-C6 and C6-C7 discs. Each vertebrae has a corresponding nerve root which arises at a level above it. This means that a hernation of the C5-C6 disc will cause a compression of the C6 nerve root.

The foramen transversarium is a part of the transverse process of each cervical vertebrae, however, the vertebral artery only runs through the C1-C6 foramen transversarium.

The costal facets are the point of joint formation between a rib and a vertebrae. As such, they are only present on the transverse processes of T1-T10.

The lumbar vertebrae do not form a joint with the ribs, nor do they possess a foramina in their transverse process.

Intervertebral discs are thickest in the cervical and lumbar regions of the spinal column. However, there are no discs between C1 and C2.

Selegiline is a monoamine oxidase inhibitor. Inhibition of monoamine oxidase leads to increased levels of norepinephrine and serotonin in the central nervous system.

Pethidine, also known as meperidine, is a strong agonist at the mu and kappa receptors. It inhibits pain neurotransmission and blocks muscarinic-specific actions.

Administering opioid analgesic is relatively contraindicated to individuals taking monoamine oxidase inhibitors. This is because of the high incidence of serotonin syndrome, which is characterized by fever, agitation, tremor, clonus, hyperreflexia and diaphoresis. Onset of symptoms is within hours, and the treatment is mainly through sedation, paralysis, intubation and ventilation.

The clinical findings are more consistent with Serotonin syndrome rather than exacerbation of Parkinson’s. Parkinson’s Disease (PD) exacerbations are defined as patient-reported or caregiver-reported episodes of subacute worsening of PD motor function in 1 or more domains (bradykinesia, tremor, rigidity, or PD-related postural instability/gait disturbance) that caused a decline in functional status, developed over a period of < 2 months, did not fluctuate with medication timing, and are not caused by intentional adjustments of PD medications by the treating neurologist.

Malignant hyperthermia usually occurs within minutes of administration of a volatile anaesthetic, such as halothane, or succinylcholine. There is massive release of calcium from the sarcoplasmic reticulum, leading to fever, acidosis, rhabdomyolysis, trismus, clonus, and hypertension.

In sepsis, it more common for patients to present with hypotension rather than hypertension.

Even though aprotinin reduces fibrinolysis and therefore bleeding, there is an associated increased risk of death. It was withdrawn in 2007.
Protein C is dependent upon vitamin K and this may paradoxically increase the risk of thrombosis during the early phases of warfarin treatment.

The coagulation cascade include two pathways which lead to fibrin formation:
1. Intrinsic pathway – these components are already present in the blood
Minor role in clotting
Subendothelial damage e.g. collagen
Formation of the primary complex on collagen by high-molecular-weight kininogen (HMWK), prekallikrein, and Factor 12
Prekallikrein is converted to kallikrein and Factor 12 becomes activated
Factor 12 activates Factor 11
Factor 11 activates Factor 9, which with its co-factor Factor 8a form the tenase complex which activates Factor 10

2. Extrinsic pathway – needs tissue factor that is released by damaged tissue)
In tissue damage:
Factor 7 binds to Tissue factor – this complex activates Factor 9
Activated Factor 9 works with Factor 8 to activate Factor 10

3. Common pathway
Activated Factor 10 causes the conversion of prothrombin to thrombin and this hydrolyses fibrinogen peptide bonds to form fibrin. It also activates factor 8 to form links between fibrin molecules.

4. Fibrinolysis
Plasminogen is converted to plasmin to facilitate clot resorption

The functional residual capacity (FRC) is the volume in the lungs at the end of passive expiration. It is determined by opposing forces of the expanding chest wall and the elastic recoil of the lung. A normal FRC = 1.7 to 3.5 L. It a marker for lung function, and, during this time, the alveolar pressure is equal to the atmospheric pressure.

FRC cannot be measured by spirometry because it contains the residual volume.

Tidal volume, inspiratory reserve volume, forced expiratory volume in 1 second, and vital capacity can be measured directly.

Linear regression, using a technique called curve fitting, allows us to make predictions regarding a certain variable.

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?

The most important determinant of preoxygenation adequacy is expired fraction of oxygen. Denitrogenating of the functional residual capacity is the purpose of preoxygenation. This is dependent on three vital factors: (1) respiratory rate; (2) inspired volume, and; (3) inspired oxygen concentration (FiO2).

Arterial oxygen saturation does not efficiently determine adequacy of preoxygenation because of its inability to measure tissue reserves. Arterial partial pressure of oxygen is also unsuitable for determining preoxygenation adequacy. Moreover, the absence of central cyanosis is a very crude sign of low tissue oxygenation.

Increasing temperature increases the amount of water vapour contained in air; for example, at 20°C, air contains about 17 g/m3, and at 37°C, air contains about 44 g/m3. The wet and dry bulb hygrometer, like the hair hygrometer, measures relative humidity.

Under normal operating conditions, Heat and moisture exchangers (HMEs) allows relative humidity of up to 70% to be achieved. Mucus can impair their performance, and they should not be used for longer than 24 hours.

Hot water bath humidifiers might cause scalding, condensed water in the tubing can interfere with gas flow, and there is a danger of infection.

The ultrasonic humidifier operates at roughly 2 MHz and may attain relative humidity levels much above 100%.

Elimination of phenytoin from the body follows first-order kinetics. This means that the rate of elimination is proportional to plasma concentration.

The rate of elimination can be described by the equation:

C = C0·e-kt

Where:

C = drug concentration
C0 = drug concentration at time zero (extrapolated)
k = Rate constant
t = Time

Enzyme systems become saturated when phenytoin concentrations exceed the normal range and elimination of the drug becomes zero-order. At this point, the drug is metabolised at a fixed rate and metabolism is independent of plasma concentration.

Aspirin and ethyl alcohol are other drugs that behave this way.

Funnel plot is essentially a scatterplot of the effect of treatment against a particular measure of study precision. Its primal purpose is to serve as a visual aid and help in detection of bias or systematic heterogenity.

Mast cell tryptase is a reliable marker of mast cell degranulation. Tryptase is a protease enzyme that acts via widespread protease-activated receptors (PARs).

The femoral triangle is a wedge-shaped area found within the superomedial aspect of the anterior thigh. It is a passageway for structures to leave and enter the anterior thigh.

Superior: Inguinal ligament
Medial: Adductor longus
Lateral: Sartorius
Floor: Iliopsoas, adductor longus and pectineus

The contents include: (medial to lateral)
Femoral vein
Femoral artery-pulse palpated at the mid inguinal point
Femoral nerve
Deep and superficial inguinal lymph nodes
Lateral cutaneous nerve
Great saphenous vein
Femoral branch of the genitofemoral nerve.

The toxicity of organophosphorus (OP) nerve agents is manifested through irreversible inhibition of acetylcholinesterase (AChE) at the cholinergic synapses, which stops nerve signal transmission, resulting in a cholinergic crisis and eventually death of the poisoned person. Oxime compounds used in nerve agent antidote regimen reactivate nerve agent-inhibited AChE and halt the development of this cholinergic crisis.

Static lung compliance refers to the change in volume within the lung per given change in unit pressure. It is usually measured when air flow is absent, such as during pauses in inhalation and exhalation.

It is a combination of:

Chest wall compliance: normal value is 200 mL/cmH2O
Lung tissue compliance: normal value is 200 mL/ cmH2O

It is represented mathematically as:

1/Crs = 1/Cl + 1/Ccw

Where,

Crs = total compliance of the respiratory system
Cl = compliance of the lung
Ccw = compliance of the chest wall

Therefore in this case:

1/Crs = 1/200 + 1/200

1/Crs = 0.005 + 0.005 = 0.01

1/Ct = 0.01

Rearranging equation gives:

Ct = 1/0.01 = 100 mL/cmH2O.

The first line of defence against acid-base disorder is buffering. The blood mainly utilizes bicarbonate ion (HCO3-) for its buffering capacity (total of 53%, plasma and red blood cells combined).

Strong acids, when acted upon by a buffer, release H+, which then combines to HCO3- and forms carbonic acid (H2CO3). When acted upon by the enzyme carbonic anhydrase, H2CO3 dissociates into H2O and CO.

The rest are the percentage of utilization for the following buffers:
Haemoglobin (by RBCs) – 35%
Plasma proteins (by plasma) – 7%
Organic phosphates (by RBCs) – 3%
Inorganic phosphates (by plasma) – 2%

Tramadol is a centrally acting analgesic with a multimode of action. It acts on serotonergic and noradrenergic nociception, while its metabolite O-desmethyltramadol acts on the mu opioid receptor. Its analgesic potency is claimed to be about one tenth that of morphine. Tramadol is used to treat both acute and chronic pain of moderate to (moderately) severe intensity.

Tramadol exists as the racemic (1:1) mixture of the (+) and (-)-enantiomer. It has a multimodal mechanism of action as on the one hand the (+) and (-)-enantiomer act on the serotonin and noradrenaline reuptake, and on the other hand the O-desmethyl metabolite of tramadol (called M1 or ODT) acts on the µ-opioid receptor. This implies that the analgesic mechanism of action of tramadol includes both non-opioid components, i.e., noradrenergic and serotonergic components, and opioid components. The (+)-enantiomer of tramadol contributes to analgesia by inhibiting the reuptake of serotonin, the (-)-enantiomer by inhibiting the reuptake of
noradrenaline, and the O-desmethyl metabolite by binding with relative high affinity (compared to tramadol) to the µ-opioid receptor.

(+/-)-Tramadol binds with low affinity to the human µ-opioid receptor with an affinity constant (Ki) of 2.4 µM.42 This affinity is approximately 4000-fold less than that of morphine (Ki = 0.34 nM). The affinity of tramadol for the δ- and κ-opioid receptors is even less. The (+/-)-O-desmethyl metabolite (M1) of tramadol, on the other hand, shows about 400-fold higher affinity for the µ-opioid receptor (Ki = 5.4 nM) than the parent compound, but still with much lower affinity than morphine. The affinity of M1 for the µ-opioid receptor is due to the (R) (+)-enantiomer (Ki = 3.4 nM) and not the (S) (-)-enantiomer (Ki = 240 nM). The affinity of the (R) (+)-enantiomer of M1 is one-tenth that of morphine for the µ-opioid receptor, and about 700 times that of (+/-)-tramadol. The metabolite (+/-)-M5 also has a higher affinity than (+/-)-tramadol for the µopioid receptor (Ki = 100 nM). However, animal studies indicate that M5 does not cross
the blood-brain barrier and does not contribute to the anti-nociceptive effect of tramadol. The metabolites M2, M3, and M4 of tramadol have negligible affinity for the human µ-opioid receptor.

Phase I metabolites of tramadol:

Mono-O-desmethyl-tramadol (M1)
Mono-N-desmethyl-tramadol (M2)
Di-N-desmethyl-tramadol (M3)
Tri-N,O-desmethyl-tramadol (M4)
Di-N,O-desmethyl-tramadol (M5)

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.

Osmolarity refers to the osmotic pressure generated by the dissolved solute molecules in 1 L of solvent. Measurements of osmolarity are temperature dependent because the volume of the solvent varies with temperature. The higher the osmolarity of a solution, the more it attracts water from an opposite compartment.

Osmolarity can be computed using the following formulas:

Osmolarity = Concentration x number of dissociable particles; OR
Plasma osmolarity (Posm) = 2([Na+]) + (glucose in mmol/L) + (BUN in mmol/L)

Posm = 2 (144) + 3.5 + 9.5 = 301 mOsm/L

Suppose there is electrical neutrality, the formula will double the cation activity to account for the anions.

Plasma osmolarity (Posm) = 2([Na+] + [K+]) + (glucose in mmol/L) + (BUN in mmol/L)

Posm = 2 (144 + 6) + 3.5 + 9.5 = 313 mOsm/L

Direct laryngoscopy are performed using laryngoscopes and they can be classed according to the shape of the blade as curved or straight.

Miller, Soper, Wisconsin and Seward are examples of straight blade laryngoscopes. Straight blades are commonly used for intubating neonates and infants but can be used in adults too.

The tip of the miller blade is advanced over the epiglottis to the tracheal entrance then lifted in order to view the vocal cords.

The RIGHT-SIDED Macintosh blade is used in adults while the left-sided blade may be used in conditions that make intubation with standard blade difficult e.g. facial deformities.

The McCoy laryngoscope is based on the STANDARD MACINTOSH blade not Robertshaw’s. It has a lever operated hinged tip, which improves the view during laryngoscopy.

Polio blade is mounted at an angle of 120-135 degrees to the handle. Originally designed for use during the polio epidemic €‹in intubation patients within iron lung ventilators, it is now useful in patients with conditions like breast hypertrophy, barrel chest, and restricted neck mobility.

Phase I and phase II metabolism are used by the liver to break down paracetamol.

1st Phase:

Prostaglandin synthetase and cytochrome P450 (CYP1A2, CYP2E2, CYP3A4 and CYP2D6) to N-acetyl-p-benzoquinoneimine (NAPQI) and N-acetylbenzo-semiquinoneimine. NAPQI is a toxic metabolite that binds to the sulfhydryl groups of cellular proteins in hepatocytes, making it toxic. This can result in centrilobular necrosis.

Glutathione and glutathione transferases prevent NAPQI from binding to hepatocytes at low paracetamol doses by preferentially binding to these toxic metabolites. The cysteine and mercapturic acid conjugates are then excreted in the urine. Depletion of glutathione occurs at higher doses of paracetamol, resulting in high levels of NAPQI and the risk of hepatocellular damage. Hepatotoxicity would not be an issue if the body’s glutathione stores were sufficient.

N-acetylcysteine is a precursor for glutathione synthesis and is the drug of choice for the treatment of paracetamol overdose.

Phase II:

Conjugation with glucuronic acid to paracetamol glucuronide is the most common method of metabolism and excretion, accounting for 60% of renally excreted metabolites. Paracetamol sulphate (35%), unchanged paracetamol (5%), and mercapturic acid are among the other renally excreted metabolites (3 percent ). The capacity of conjugation pathways is limited. The capacity of the sulphate conjugation pathway is lower than that of the glucuronidation pathway.

Because of the low pH in the stomach, paracetamol absorption is minimal (pKa value is 9.5). Paracetamol is absorbed quickly and completely in the alkaline environment of the small intestine. Oral bioavailability is extremely high, approaching 100%.

As a result, measuring paracetamol levels in plasma after an injury is important. Peak plasma concentrations are reached after 30-60 minutes, with a volume of distribution of 0.95 L/kg. It binds to plasma proteins at a rate of 10% to 25%.

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.

The measure of drug potency or therapeutic response is the ED95. This is defined as the dose of a neuromuscular blocking drug required to produce a 95% depression of muscle twitch height. The ED50 and ED90 describe a depression of twitch height by 50% and 90% respectively.

The ED95 (mg/kg) of the commonly used neuromuscular blocking agents are:

suxamethonium: 0.27
rocuronium: 0.31
vecuronium: 0.04
pancuronium: 0.07
cisatracurium: 0.04
mivacurium: 0.08

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)

The amount of energy required to change the temperature of 1 kg of a substance by 1°C is its specific heat capacity.

Energy required to increase the temperature of any object is given by the equation:

E = m × c × θ

Where:
E = energy required to heat an object
m = mass of object
c = specific heat capacity of the substance
θ = temperature change

The specific heat capacity of water is 4181 J/(kg°C)

Therefore the energy required to raise 1kg of water by 10°C is:

1 kg × 4181 J/(kg°C) × 10°C = 41810 J

A 1 kW or 1000 W heater would be expected to supply 1000 J/s.

The approximate time it would take the 1 kW heater to raise the temperature of one Litre of water by 10°C is:

41810/1000 = 41.8 seconds.

Adenosine receptors are expressed on the surface of most cells.
Four subtypes are known to exist which are A1, A2A, A2B and A3.

Of these, the A1 and A2 receptors are present peripherally and centrally. There are agonists at the A1 receptors which are antinociceptive, which reduce the sensitivity to a painful stimuli for the individual. There are also agonists at the A2 receptors which are algogenic and activation of these results in pain.

The role of adenosine and other A1 receptor agonists is currently under investigation for use in acute and chronic pain states.

The adrenal medulla comprises chromaffin cells (pheochromocytes), which are functionally equivalent to postganglionic sympathetic neurons. They synthesize, store and release the catecholamines noradrenaline (norepinephrine) and adrenaline (epinephrine) into the venous sinusoids.
The majority of the chromaffin cells synthesize adrenaline.