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)

Specific knowledge of the anatomical relationship is required to address this examination question.

The first rib is small and thick and contains a single facet that articulates at the costovertebral joint. It consist of a head, neck and shaft but a discrete angle is deficit. Along the side the shaft is indented with a groove for the subclavian artery and the lower brachial plexus trunk. Front to the scalene tubercle is a space for the subclavian vein.

The first rib has the scalenus front muscle joined to the scalene tubercle, isolating the subclavian vein (anteriorly) from the subclavian artery (posteriorly). This anatomical relationship is of major significance with respect to subclavian vein cannulation.

The 1st rib has the following relationships:

superior: lower trunk of the brachial plexus, subclavian vessels, clavicle.

inferior: intercostal vessels and nerves

posterior and inferior: pleura

anterior: sympathetic trunk (over neck)

superior intercostal artery, ventral T1 nerve root.

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.

With regards to the autonomic nervous system (ANS)

1. It is not under voluntary control
2. It uses reflex pathways and different to the somatic nervous system.
3. The hypothalamus is the central point of integration of the ANS. However, the gut can coordinate some secretions and information from the baroreceptors which are processed in the medulla.

With regards to the central nervous system (CNS)
1. There are myelinated preganglionic fibres which lead to the
ganglion where the nerve cell bodies of the non-myelinated post ganglionic nerves are organised.
2. From the ganglion, the post ganglionic nerves then lead on to the innervated organ.

Most organs are under control of both systems although one system normally predominates.

The nerves of the sympathetic nervous system (SNS) originate from the lateral horns of the spinal cord, pass into the anterior primary rami and then pass via the white rami communicates into the ganglia from T1-L2.

There are short pre-ganglionic and long post ganglionic fibres.
Pre-ganglionic synapses use acetylcholine (ACh) as a neurotransmitter on nicotinic receptors.
Post ganglionic synapses uses adrenoceptors with norepinephrine / epinephrine as the neurotransmitter.
However, in sweat glands, piloerector muscles and few blood vessels, ACh is still used as a neurotransmitter with nicotinic receptors.

The ganglia form the sympathetic trunk – this is a collection of nerves that begin at the base of the skull and travel 2-3 cm lateral to the vertebrae, extending to the coccyx.

There are cervical, thoracic, lumbar and sacral ganglia and visceral sympathetic innervation is by cardiac, coeliac and hypogastric plexi.

Juxta glomerular apparatus, piloerector muscles and adipose tissue are all organs under sole sympathetic control.

The PNS has a craniosacral outflow. It causes reduced arousal and cardiovascular stimulation and increases visceral activity.

The cranial outflow consists of
1. The oculomotor nerve (CN III) to the eye via the ciliary ganglion,
2. Facial nerve (CN VII) to the submandibular, sublingual and lacrimal glands via the pterygopalatine and submandibular ganglions
3. Glossopharyngeal (CN IX) to lungs, larynx and tracheobronchial tree via otic ganglion
4. The vagus nerve (CN X), the largest contributor and carries ¾ of fibres covering innervation of the heart, lungs, larynx, tracheobronchial tree parotid gland and proximal gut to the splenic flexure, liver and pancreas

The sacral outflow (S2 to S4) innervates the bladder, distal gut and genitalia.

The PNS has long preganglionic and short post ganglionic fibres.
Preganglionic synapses, like in the SNS, use ACh as the neuro transmitter with nicotinic receptors.
Post ganglionic synapses also use ACh as the neurotransmitter but have muscarinic receptors.

Different types of these muscarinic receptors are present in different organs:
There are:
M1 = pupillary constriction, gastric acid secretion stimulation
M2 = inhibition of cardiac stimulation
M3 = visceral vasodilation, coronary artery constriction, increased secretions in salivary, lacrimal glands and pancreas
M4 = brain and adrenal medulla
M5 = brain

The lacrimal glands are solely under parasympathetic control.

Oxygen consumption (VO2) refers to the optimal amount of oxygen used by the body during exercise.

It is calculated mathematically by:

VO2 = 3.5 x 50 x 8 = 1400 mL/kg/minute

where,

1 MET = 3.5 mL O2/kg/minute is utilized by the body.

Note:

1 MET Eating
Dressing
Use toilet
Walking slowly on level ground at 2-3 mph
2 METs Playing a musical instrument
Walking indoors around house
Light housework
4 METs Climbing a flight of stairs
Walking up hill
Running a short distance
Heavy housework, scrubbing floors, moving heavy furniture
Walking on level ground at 4 mph
Recreational activity, e.g. golf, bowling, dancing, tennis
6 METs Leisurely swimming
Leisurely cycling along the flat (8-10 mph)
8 METs Cycling along the flat (10-14 mph)
Basketball game
10 METs Moderate to hard swimming
Competitive football
Fast cycling (14-16 mph).

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%.

The axillary nerve arises from spinal roots C5-C6. It has both sensory and motor functions:

Sensory: Provides innervation to the skin over the lower deltoid area

Motor: Provides innervation to the teres minor (responsible for stabilisation of glenohumeral joint and external rotation of shoulder joint) and deltoid muscles (responsible for abduction of arms glenohumeral joint).

Injury to the axillary nerve will result in the patient being unable to abduct the arm beyond 15 degrees and a loss of sensory feeling over lower deltoid area.

These symptoms could also be a result of over-abduction of the arm (>90°) which would cause the head of the humerus to become dislocated.

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

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

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

The 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.

Accumulation of morphine-6-glucuronide is a risk factor for opioid toxicity during morphine treatment. Morphine is metabolized in the liver to morphine-6-glucuronide and morphine-3-glucuronide, both of which are excreted by the kidneys. In the setting of renal failure, these metabolites can accumulate, resulting in a lowering of the seizure threshold. However, it does not occur in all patients with renal insufficiency, which is the most common reason for accumulation of morphine-6-glucuronide; this suggests that other risk factors can contribute to morphine-6-glucuronide toxicity.

The active metabolites of codeine are morphine and the morphine metabolite morphine-6-glucuronide. The enzyme systems responsible for this metabolism are: CYP2D for codeine and UGT2B7 for morphine, codeine-6-gluronide, and morphine-6-glucuronide. Both of these systems are subject to genetic variation. Some patients are ultrarapid metabolizers of codeine and produce higher levels of morphine and active metabolites in a very short period of time after administration. These increased levels will produce increased side effects, especially drowsiness and central nervous system depression.

Ventricular fibrillation (VT) is an arrhythmia caused by a distortion in the organized contraction of the ventricles leading to an inability to pump blood out into the body.

Amiodarone is an anti arrhythmic drug used for the treatment of ventricular and atrial fibrillations. It is the gold standard of treatment for refractory pulseless ventricular tachycardia (VT) and ventricular fibrillation (VF).

Guidelines for emergency treatment state that only the rescuer carrying out chest compressions on the patient may stand near the defibrillator as it charges.

Cardio-pulmonary resuscitation (CPR) during cardiac arrest is required for 2 minute cycles.

Hypovolaemia is as a cause of pulseless electrical activity (PEA) can be reversed using fluid resuscitation, whereas hypotension during cardiac arrest is either persistent or undetectable and is therefore irreversible.

Hyperkalaemia and hypocalcaemia are treated using calcium salts, but calcium chloride is often preferred over calcium gluconate.

During a pulseless VT or VF, a single precordial thump will be effective if administered within the first seconds of the occurrence of a shockable rhythm.

Mivacurium, when administered at doses greater than 0.2 mg/kg,increases the risk for hypotension, tachycardia, and erythema. This is due to the ability of mivacurium to release histamine with increasing dose. Contrary to this fact, anaphylaxis is rare for mivacurium because of the short duration of histamine release.

The effective dose 50 (ED50) of mivacurium is between 0.08-0.15 mg/kg. It is administered slowly to prevent and decrease the risk of developing adverse effects.

Mivacurium has a high potency thus a longer duration of action, however this is not the answer that we are looking for.

Although drug metabolism takes longer for mivacurium than succinylcholine, it has no effect on the dose required for intubation.

The cardiac action potential has several phases which have different mechanisms of action as seen below:
Phase 0: Rapid depolarisation – caused by a rapid sodium influx.
These channels automatically deactivate after a few ms

Phase 1: caused by early repolarisation and an efflux of potassium.

Phase 2: Plateau – caused by a slow influx of calcium.

Phase 3 – Final repolarisation – caused by an efflux of potassium.

Phase 4 – Restoration of ionic concentrations – The resting potential is restored by Na+/K+ATPase.
There is slow entry of Na+into the cell which decreases the potential difference until the threshold potential is reached. This then triggers a new action potential

Of note, cardiac muscle remains contracted 10-15 times longer than skeletal muscle.

Different sites have different conduction velocities:
1. Atrial conduction – Spreads along ordinary atrial myocardial fibres at 1 m/sec

2. AV node conduction – 0.05 m/sec

3. Ventricular conduction – Purkinje fibres are of large diameter and achieve velocities of 2-4 m/sec, the fastest conduction in the heart. This allows a rapid and coordinated contraction of the ventricles

There are two types of defibrillators
AC defibrillator
DC defibrillator

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

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

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

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

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

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

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.

Hiatus is an opening in the diaphragm. A hiatal hernia is a protrusion of the upper part of the stomach through an opening in the diaphragm, the oesophageal hiatus, into the thorax. The oesophageal hiatus occurs at the level of T10 in the right crus of the diaphragm.

Other important openings in the diaphragm:
T8: vena cava, terminal branches of the right phrenic nerve
T10: oesophagus, vagal trunks, left anterior phrenic vessels, oesophageal branches of the left gastric vessels
T12: descending aorta, thoracic duct, azygous and hemi-azygous vein

An opening in the diaphragm is called a hiatus. The oesophageal hiatus is at vertebral level T10. A hiatus hernia is where the stomach bulges through the oesophageal hiatus hence the name – hiatus hernia.

Glyceryl trinitrate (GTN) has a significant first pass metabolism. About 90% of a dose of GTN is metabolised in the liver by the enzyme glutathione organic nitrate reductase.

An INSIGNIFICANT amount of metabolism occurs in the intestinal mucosa.

There is approximately 1% bioavailability after oral administration and 38% after sublingual administration.

GTN does NOT cause gastric irritation and it is well absorbed in the gastrointestinal tract.

The volume of distribution of GTN is 2.1 to 4.5 L/kg. This is HIGH.

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

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

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

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

The formula for resistors in series can be defined as:

R(total) = R1+R2

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

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

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

1/ Rtotal = 1/R1 + 1/R2

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

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

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

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

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

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

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

In a parallel circuit, the formula of capacitors is:

Ctotal = C1 + C2

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

V = 100/10
V = 10 volts

In a series circuit, the formula for capacitors is:

1/Ctotal = 1/C1 + 1/C2

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

Ctotal = C1 × C2/C1 + C2

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

V = 100/2.5
V = 40 volts.

This question is asking which structure would lie posterior to the rectus abdominis muscle and not the prosthetic mesh, as only peritoneum lies posterior to mesh during a total extraperitoneal (TEP) hernia repair.

The region of the repair lies below the arcuate line, meaning that the transversalis fascia and peritoneum lie posterior to the rectus abdominis.

The bucks fascia lies within the penis.

Desflurane is a highly fluorinated methyl ethyl ether used for the maintenance of general anaesthesia. It has been identified as a weak triggering anaesthetic of malignant hyperthermia. That, in the absence of succinylcholine, may produce a delayed onset of symptoms.

The elimination of phenytoin follows first order kinetics. Plasma concentrations determine the rate of elimination. The relationship between drug X plasma concentration and time is described by an exponential process in the following equation used to describe the rate of elimination:

C = C0. e-kt

C=drug concentration, C0= drug concentration at time zero (extrapolated), k = rate constant and t=time

As enzyme systems become saturated when phenytoin concentrations are above the usual range, clearance of the medication becomes zero-order. The medication is metabolised at a constant pace, regardless of its plasma levels. Aspirin and ethyl alcohol are two more significant examples of medications that operate in this way.

A plot of drug concentration with time is a washout exponential curve.

A graph of concentration with time is a straight line i.e. Zero-order kinetics

The amount eliminated per unit time is constant defines the point at which zero order kinetics commences.

Elimination involves a rate-limiting reaction operating at its maximal velocity is incorrect.

The half life of the drug is proportional to the drug concentration in the plasma corresponds to a definition of first-order kinetics.

Oxygen is formed by a molecule of oxygen and two molecules of hydrogen with a molecular formula of H2O

The critical temperature is defined as a temperature above which the substance cannot be liquefied, no matter how much pressure is applied.
Water has a critical temperature of -118.6oC. So, it cannot be liquified at room temperature.

Medical oxygen cylinder is stored in a cylinder with a white shoulder and black body. Meanwhile, medial air is stored in cylinders with a white and black shoulder and a French grey body.

The partial pressure of air at a high altitude is less but the relative concentration remains constant.

The extrinsic pathway is best assessed by the PT time.

D-dimer is a fibrin degradation product which is raised in the presence of blood clots.

A 50:50 mixing study is used to assess if a prolonged PT or aPTT is due to factor deficiency or a factor inhibitor.

The thrombin time is a test used to assess fibrin formation from fibrinogen in plasma. Factors that prolong the thrombin time include heparin, fibrin degradation products, and fibrinogen deficiency.

Intrinsic pathway – Best assessed by APTT. Factors 8,9,11,12 are involved. Prolonged aPTT can be seen in haemophilia and use of heparin.

Extrinsic pathway – Best assessed by Increased PT. Factor 7 involved.

Common pathway – Best assessed by APTT & PT. Factors 2,5,10 involved.

Vitamin K dependent factors are factors 2,7,9,10

The abdominal aorta begins at the level of the body of T12 near the midline, as a continuation of the thoracic aorta. It descends and bifurcates at the level of L4 into the common iliac arteries.

An abdominal aortic aneurysm is a swelling in the abdominal aorta. It most commonly occurs in men over 65 years old of age. Smoking, diabetes, hypertension, and hypercholesterolemia are other risk factors contributing to the disease.

The NHS screening program for abdominal aortic aneurysms involves an ultrasound test for men aged 65 or over if they have not undergone screening for a one-off screening test.

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.

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.

The bifurcation of the abdominal aorta into common iliac arteries occurs at the level of L4. The bifurcation is a common site for atherosclerotic plaques as it is an area of high turbulence.

Leriche Syndrome is an aortoiliac occlusive disease and affects the distal abdominal aorta, iliac arteries, and femoropopliteal vessels. It has a triad of symptoms:
1. Claudication (cramping lower extremities pain that is reproducible by exercise)
2. Impotence (reduced penile arterial flow)
3. Absent/weak femoral pulses (hallmark)

T12 – aorta enters the diaphragm with the thoracic duct and azygous veins

L2 – testicular or ovarian arteries branch off the aorta

L3 – inferior mesenteric artery.

Observers may subconsciously measure or report data in a way that favours the expected study outcome. Therefore, by blinding the study we can eliminate expectation bias.

Recall bias is a systematic error that occurs when the study participants omit details or do not remember previous events or experiences accurately.

Verification can occur during investigations when there is a difference in testing strategy between groups of individuals, which might lead to biasness due to differing ways of verifying the disease of interest.

Nonresponse bias is the bias that occurs when the people who respond to a survey differ significantly from the people who do not respond to the survey.

A distortion that modifies an association between an exposure and an outcome because a factor is independently associated with the exposure and the outcome. Randomization is the best way to reduce the risk of confounding.

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

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

The thyroid gland is a gland shaped like a butterfly which lies at the base of the anterior neck. It controls metabolism using hormone secretion.

Iodine is extremely important for the synthesis of hormones within the thyroid. It is internalised into the thyroid follicular cells via the sodium/iodide symporter (NIS).

The parathyroid glands are found posterior to the thyroid gland, with the recurrent laryngeal nerves running posteromedially.

The expected weight of a normal thyroid gland is about 30 grams.