Sodium concentration for different fluids
3% N saline 513 mmol/L
5% N saline 856 mmol/L
0.9% N saline 154 mmol/L
Hartmann’s solution 131 mmol/L
0.45% N saline with 5% glucose 77 mmol/L

This means that:

500 mL 5% N saline contains 428 mmol of sodium
1000 mL 3% N saline contains 513 mmol of sodium
3500 mL 0.9% N saline contains 539 mmol of sodium
4000 mL Hartmann’s contains 524 mmol of sodium
6000 mL 0.45% N saline with 5% glucose contains 462 mmol of sodium.

Staphylococcus aureus colonizes the nasopharynx in >20% of the general population.

Methicillin-resistant Staphylococcus aureus (MRSA) is resistant to flucloxacillin.

Trimethoprim binds to dihydrofolate reductase and inhibits the reduction of dihydrofolic acid (DHF) to tetrahydrofolic acid (THF). THF is an essential precursor in the thymidine synthesis pathway and interference with this pathway inhibits bacterial DNA synthesis.

All β-lactam antibiotics like penicillin interfere with the synthesis of the bacterial cell walls. The β-lactam antibiotics inhibit the transpeptidases so that cross-linking (which maintains the close-knit structure of the cell wall) does not take place

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

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

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

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

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

The oesophagus is a muscular tube that connects the pharynx to the stomach. It begins at the lower border of the cricoid cartilage and C6 vertebra. It ends at T11.

The oesophagus has physiological constrictions at the following levels:
1. Cervical constriction: Pharyngo-oesophageal junction (15 cm from the incisor teeth) produced by the cricopharyngeal part of the inferior pharyngeal constrictor muscle
2. Thoracic constrictions:
i. where the oesophagus is first crossed by the arch of the aorta (22.5 cm from the incisor teeth)
ii. where the oesophagus is crossed by the left main bronchus (27.5 cm from the incisor teeth)
3. Diaphragmatic constriction: where the oesophagus passes through the oesophageal hiatus of the diaphragm (40 cm from the incisor teeth)

Awareness of these constrictions is important for clinical purposes when it is required to pass instruments through the oesophagus into the stomach or when viewing radiographs of patients’ oesophagus.

Dabigatran template is a prodrug and its active metabolite is a direct thrombin inhibitor. It is a synthetic, reversible, non-peptide thrombin inhibitor. This inhibition of thrombin results in a decrease of fibrin and reduces platelet aggregation.

Drugs like warfarin act by inhibiting the activation of vitamin K-dependent clotting factors. These factors are synthesized by the liver and activated by gamma-carboxylation of glutamate residues with the help of vitamin K. Hydroquinone form of vitamin K is converted to epoxide form in this reaction and regeneration of hydroquinone form by enzyme vitamin K epoxide reductase (VKOR) is required for this activity. Oral anticoagulants prevent this regeneration by inhibiting VKOR, thus vitamin K-dependent factors are not activated. These factors include clotting factors II, VII, IX, and X as well as anti-clotting proteins, protein C and protein S.

The anterior cerebral artery supplies the midline portion of the frontal lobe and the superior medial parietal lobe of the brain. It also supplies the front four-fifths of the corpus callosum and provides blood to deep structures such as the anterior limb of the internal capsule, part of the caudate nucleus, and the anterior part of the globus pallidus.

The cerebral hemispheres are supplied by arteries that make up the Circle of Willis. The Circle of Willis is formed by the anastomosis of the two internal carotid arteries and two vertebral arteries.

Clinically, the internal carotid arteries and their branches are often referred to as the anterior circulation of the brain. The anterior cerebral arteries are connected by the anterior communicating artery. Near their termination, the internal carotid arteries are joined to the posterior cerebral arteries by the posterior communicating arteries, completing the cerebral arterial circle around the interpeduncular fossa, the deep depression on the inferior surface of the midbrain between the cerebral peduncles.

The middle cerebral artery supplies part of the frontal, temporal and parietal lobes.

The posterior cerebral artery supplies the occipital lobe.

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.

68% of the population will be found in one standard deviation (SD) above plus one SD below the mean. Two SDs above plus two SDs below the mean will include 95% of the population.

The median can be greater or less than the mean as it is simply the mid point of the data after the data is arranged. Half the data are above and half below the median .

The mode is a true score, unlike the mean or the median. It is the most common score or the score obtained from the largest number of subjects in any given data.

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.

Number needed to treat is a measure of the impact of a treatment or intervention that is often used to communicate results to patients, clinicians, the public and policymakers. It states how many patients need to be treated for one additional patient to experience an adverse outcome (e.g. a death).

It is calculated as the inverse of the absolute risk reduction and is rounded to the next highest whole number.

The absolute risk reduction is 8% (16% – 8%). 100/8 = 12.5, so rounding up the next integer this gives at NNT of 13. i.e. you would need to give the new drug to 13 people to ensure that you prevented one death.

The prostate gland is primarily supplied by the inferior vesical artery, which branches off from the anterior division of the internal iliac artery. The inferior vesical artery supplies the base of the bladder, the distal ureters, and the prostate. The branches to the prostate communicate with the corresponding vessels of the opposite side.

The inferior vesical artery branches into two main arteries:
1. Urethral artery – supplies the transition zone and is the main arterial supply for the adenomas in BPH
2. Capsular artery – supplies the glandular tissue

The venous drainage of the prostate is from the prostatic venous plexus, which drains into the paravertebral veins.

Bupivacaine is used to decrease feeling in a specific area. It is injected around a nerve that supplies the area, or into the spinal canal’s epidural space.

The maximum volume of 0.5% bupivacaine that should be administered to a 10kg child is 5 ml

Arrhythmias and/or hypotension are the most common causes of death from tricyclic antidepressant (TCA) overdose.

The quinidine-like actions of tricyclic antidepressants on cardiac tissues are primarily responsible for their toxicity. Conduction through the His-Purkinje system and the myocardium slows as phase 0 depolarisation of the action potential slows. QRS prolongation and atrioventricular block are caused by slowed impulse conduction, which also contributes to ventricular arrhythmias and hypotension.

Arrhythmias can also be caused by abnormal repolarization, impaired automaticity, cholinergic blockade, and inhibition of neuronal catecholamine uptake, among other things.

Acidaemia, hypotension, and hyperthermia can all exacerbate toxicity.

The anticholinergic effects of tricyclic antidepressants, as well as the blockade of neuronal catecholamine reuptake, cause sinus tachycardia. Sinus tachycardia is usually well tolerated and does not require treatment. It can be difficult to tell the difference between sinus tachycardia and ventricular tachycardia with QRS prolongation.

A QRS duration of more than 100 milliseconds indicates a higher risk of arrhythmia and should be treated with systemic sodium bicarbonate.

The tricyclic is dissociated from myocardial sodium channels by serum alkalinization, and the extracellular sodium load improves sodium channel function.

The arch of aorta gives rise to three main branches:
1. Brachiocephalic artery
2. Left common carotid artery
3. Left subclavian artery

The brachiocephalic artery then gives rise to the right subclavian artery and the right common carotid artery.

The right common carotid artery arises from the brachiocephalic trunk posterior to the sternoclavicular joint.

The coeliac trunk is a branch of the abdominal aorta.
The ascending aorta supplies the coronary arteries.

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)

Sevoflurane is highly fluorinated methyl isopropyl ether widely used as an inhalational anaesthetic. It is suggested that sevoflurane preconditioning occurs via the opening of mitochondrial Potassium ATP dependent channel similar to that of Ischemic Preconditioning protection.

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

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

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

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).

This data is in a 2 × 2 contingency table so a chi square test can be used. There is a special chi squared formula that gives a value that can be looked up in a table giving the p value.

Since we are comparing proportions not means, the Student’s t test CANNOT be used.

There is no linear regression to plot so Pearson’s co-efficient cannot be calculated.

Nothing is so obvious that no statistical analysis is needed.

The tracheobronchial tree is subdivided into the conducting and the respiratory zones.

The zones from proximal to distal are:

Trachea
Bronchi
Bronchioles
Terminal bronchioles
Respiratory bronchioles
Alveolar ducts
Alveolar sacs

from the trachea to terminal bronchioles are the conducting zone while the respiratory zone is from the respiratory bronchioles to the alveola sacs.

The apex of an equilateral triangle completed by the posterior superior iliac spines is where the sacral hiatus or sacrococcygeal membrane can normally located. The failure of posterior fusion of the laminae of the fourth and fifth sacral vertebrae allows the sacral canal to be accessible via the membrane.

In adults, the spine of L4 usually lies on a line drawn between the highest points of the iliac crests (Tuffier’s line). A line connecting each anterior iliac spine, approximates to the L3/4 interspace in the sitting position. Both of these options are incorrect.

A line connecting the greater trochanters is also incorrect.

A line connecting the posterior superior iliac spines is correct, but in adults the presence of a sacral fat pad can still make identification of this landmark less straightforward.

The processes of S5 are remnants only and form the sacral cornua, which are also used to help identify the sacral hiatus.

The occlusion of the left anterior descending (LAD) coronary artery causes anterior ST elevation myocardial infarction (STEMI). It has the worst prognosis of all the infarct locations due to its larger infarct size. It has a higher rate of total mortality (27 percent versus 11 percent), heart failure (41 percent versus 15 percent), and a lower ejection fraction on admission than an inferior myocardial infarction (38 percent versus 55 percent ).

The LAD artery supplies the majority of the interventricular septum, as well as the anterior, lateral, and apical walls of the left ventricle, as well as the majority of the right and left bundle branches and the bicuspid valve’s anterior papillary muscle (left ventricle).

The left or right ventricle’s end-diastolic volume (EDV) is the volume of blood in each chamber at the end of diastole before systole. Preload is synonymous with the EDV.

120 mL is a typical left ventricular EDV (range 65-240 mL). The EDV of the right ventricle in a typical range is (100-160 mL).

With an ejection fraction (EF) of less than 45 percent, the patient is most likely suffering from systolic dysfunction. Increases in right and left ventricular end-diastolic pressures and volumes are likely with a reduced EF because the ventricles are not adequately emptied. The left atrium and the pulmonary vasculature are affected by the increased pressures on the left side of the heart.

By causing an imbalance of the Starling forces acting across the capillaries, increased hydrostatic pressure in the pulmonary circulation favours the development of pulmonary oedema. With cardiogenic pulmonary oedema, capillary permeability is likely to remain unchanged.

Biventricular failure will result as a result of the pressure changes being transmitted to the right side of the circulation. The patient’s systemic vascular resistance is likely to be elevated as well, but it is not the most likely cause of his symptoms. The patient is suffering from cardiogenic shock as a result of biventricular failure. The patient has low cardiac output and is hypotensive. Right ventricular filling pressures are elevated, indicating right ventricular dysfunction.

Eye damage is the most common potential hazard associated with laser energy. Everyone in the laser treatment room has the risk of eye exposure when working with a Class 3b or Class 4 healthcare laser system, and damage to various structures in the eye depending on wavelength of the laser if they are unprotected.

Red and near-infrared light (400-1400 nm) has very high penetration power. The light causes painless burns on the retina after it is absorbed by melanin in the pigment epithelium just behind the photoreceptors.

Infrared radiation (IR), or infrared light (>1060 nm), is a type of radiant energy that’s invisible to human eyes and hence won’t elicit the protective blink.

Ultraviolet light (<400 nm) is also a form of electromagnetic radiation which is can penetrate the cornea and be absorbed by the iris or the pupil and cause burn injuries or cataract occur due to irreversible photochemical retinal damage.

Safety eyewear is the best method of providing eye protection and are designed to absorb light specific to the laser being used. Laser protective eyewear (LPE) includes glasses or goggles of proper optical density (OD). The lenses should not be glass or plastic. The LPE should withstand direct and diffuse scattered laser beams.

The laser protection supervisor (LPS) or LSO is an individual who is responsible for any clinical area in which lasers are used. They are expected to have a certain level of equipment and determine what control measures are appropriate, for each individual system, but their presence does not guarantee the chances of having an eye injury.

Class 1 lasers are generally safe under every conceivable condition and is not likely to cause any eye damage. Class 3b or Class 4 medical laser systems are utilized in healthcare which have their own safety precautions.

Polarized spectacles can make your eyes more comfortable by eliminated glare, however, they will not be able to offer any protection against wavelengths at which laser act.
Using short bursts to reduce energy is also not correct as it would still be harmful to eye.

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

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

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

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

The right atrium receives blood supply from the SVC, IVC, and coronary sinus. It forms the right border of the heart.

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

The trabeculae carneae are irregular muscular elevations that form the interior of the right ventricle.

The oxygen consumption rate (VO2) at rest is 3.5 ml/kg/minute (one metabolic equivalent or 1 MET).
3.86 ml/kg/minute thyrotoxicosis

Young children consume a lot of oxygen: around 7 ml/kg/min when they are born. The metabolic cost of breathing is higher in children than in adults, and it can account for up to 15% of total oxygen consumption. Similarly, an infant’s metabolic rate is nearly twice that of an adult, resulting in a larger alveolar minute volume and a lower FRC.

At term, oxygen consumption at rest can increase by as much as 40% (5 ml/kg/minute) and can rise to 60% during labour.

When compared to normal basal metabolism, sepsis syndrome increases VO2 and resting metabolic rate by 30% (4.55 ml/kg/minute). In septicaemic shock, VO2 decreases.

Dobutamine hydrochloride was infused into 12 healthy male volunteers at a rate of 2 micrograms per minute per kilogramme, gradually increasing to 4 and 6 micrograms per minute per kilogramme. Dobutamine was infused for 20 minutes for each dose. VO2 increased by 10% to 15%. (3.85-4.0 ml/kg/min).

The clinical picture best describes a probable drug interaction with pethidine.

Phenelzine, a monoamine oxidase (MAO) inhibitor, when given with pethidine, an opioid analgesic, may lead to episodes of hypertension, rigidity, excitation, hyperpyrexia, seizures, coma and death. Studies have shown that pethidine reacts more significantly with MAO inhibitors than morphine.

When pethidine is metabolised to normeperidine, it acts as a serotonin reuptake inhibitor and cause an increase in serotonin levels in the brain. MAO inhibitors can also lead to elevated levels of serotonin because of its mechanism of action by inhibiting the enzyme monoamine oxidase that degrades serotonin.

The excess serotonin levels may lead to serotonin syndrome, of which some of the common precipitating drugs are selective serotonin reuptake inhibitors, MAO inhibitors, tricyclic antidepressants, meperidine, and St. John’s Wort. Onset of symptoms is within hours, which includes fever, agitation, tremor, clonus, hyperreflexia and diaphoresis.

Drug interaction between phenelzine and paracetamol do not commonly precipitate serotonin syndrome.

Neuroleptic malignant syndrome is due to dopamine antagonism, precipitated commonly by antipsychotics. Its onset of symptoms occur in 1 to 3 days, and is characterized by fever, encephalopathy, unstable vitals signs, elevated CPK, and rigidity.

Altered mental status is the most common manifestation of sepsis-associated encephalopathy. Patient also exhibit confusional states and inappropriate behaviour. In some cases, this may lead to coma and death.

The following is the Advanced Trauma Life Support (ATLS) classification of haemorrhagic shock:

Class I haemorrhage:
It has blood loss up to 15%. There is very less tachycardia, and no changes in blood pressure, RR or pulse pressure. Usually, fluid replacement is not required.

Class II haemorrhage:
It has 15-30% blood loss, equivalent to 750 – 1500 ml. There is tachycardia, tachypnoea and a decrease in pulse pressure. Patient may be frightened, hostile and anxious. It can be stabilised by crystalloid and blood transfusion.

Class III haemorrhage:
There is 30-40% blood loss. It portrays inadequate perfusion, marked tachycardia, tachypnoea, altered mental state and fall in systolic pressure. It requires blood transfusion.

Class IV haemorrhage:
There is > 40% blood volume loss. It is a preterminal event, and the patient will die in minutes. It portrays tachycardia, significant depression in systolic pressure and pulse pressure, altered mental state, and cold clammy skin. There is need for rapid transfusion and surgical intervention.

After a paediatric case, you’ll frequently have to calculate and prescribe maintenance fluids. The ‘4-2-1 rule’ should be used as a guideline:

1st 10 kg – 4 ml/kg/hr
2nd 10 kg – 2 ml/kg/hr
Subsequent kg – 1 ml/kg/hr

Hence

1st 10 kg = 4 × 10 = 40 ml
2nd 10 kg = 2 × 10 = 20 ml
Subsequent kg = 1 × 1 = 1 ml
Total = 61 ml/hr

61 × 12 = 732 ml over 12 hrs.

The external iliac artery is the larger of the two branches of the common iliac artery. It forms the main blood supply to the lower limbs. The common iliac bifurcates into the internal and external iliac artery anterior to the sacroiliac joint.

The external iliac artery courses on the medial border of the psoas major muscles and exits the pelvic girdle posterior to the inguinal ligament. Here, midway between the anterior superior iliac spine and the pubic symphysis, the external iliac artery becomes the femoral artery and descends along the anteromedial part of the thigh in the femoral triangle.

The pectineus forms the posterior border of the femoral canal.
The femoral vein forms the lateral border of the femoral canal.
The medial border of the adductor longus muscle forms the medial wall of the femoral triangle.
The medial border of the sartorius muscle forms the lateral wall of the femoral triangle.