A person remaining at high altitudes for days, weeks, or years becomes more and more acclimatized to the low PO2, so it causes fewer deleterious effects on the body.

After acclimatization, it becomes possible for the person to work harder without hypoxic effects or to ascend to still higher altitudes. The principal means by which acclimatization comes about are (1) a great increase in pulmonary ventilation, (2) increased numbers of red blood cells, (3) diffusing capacity of the lungs, (4) increased vascularity of the peripheral tissues, and (5) increased ability of the tissue cells to use oxygen despite low PO2.

The cardiac output often increases as much as 30% immediately after a person ascends to high altitude but then decreases back toward normal over a period of weeks as the blood haematocrit increases, so the amount of oxygen transported to the peripheral body tissues remains about normal.

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.

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 bispectral index (BIS) monitors works to determine the level of consciousness of a patient by processing electroencephalographic (EEG) signals to obtain a value between 0 and 100, where 0 reflects no brain activity, and 100 reflects a patient is completely awake.

The general meaning of BIS values are:

>95: Patient is in an awake state.
65-85: Patient is in a sedated state.
40-65: Patient is in a state that is optimal for general surgery.
<40: Patient is in a deep hypnotic state It is important in measuring the depths of anaesthesia to prevent haemodynamic changes or patient awareness during surgery. The nature of anaesthetic agent used is a determinant factor in resultant BIS values. Intravenous agents, such as propofol, thiopental and midazolam, result in a deeper hypnotic state, whilst inhalation agents have a lesser hypnotic effect at the same BIS values. Certain agents result in inaccurate BIS values such as ketamine and nitrous oxide (NO). These two agents appear to increase the BIS value, whilst putting the patient in a deeper hypnotic state, and should therefore not be used with BIS monitoring. Hypothermia also affects the BIS value as it causes a 1.12 per °C decrease in body temperature.

Bucks fascia refers to the layer of loose connective tissue, nerves and blood vessels that encapsulates the penile erectile bodies, the corpa cavernosa and the anterior part of the urethra, including the entirety of the spongiose part of the urethra.

It runs with the external spermatic fascia and the penile suspensory ligament.

Cell membrane pore formation, Bacterial DNA damage, Peptidoglycan cross-linking inhibition, and peptidoglycan synthesis inhibitor are always lethal and such mechanisms are possible only in bactericidal drugs. But Protein synthesis inhibition would only prevent cell replication or cell growth and is responsible for bacteriostatic effects of the drug.

The Glasgow Coma Scale (GCS) has been used in outcome models as a measure of physiological derangement and as a tool for assessing head trauma.

Eye opening (E):

4 Spontaneously
3 Responds to voice
2 Responds to painful stimulus
1 No response.

Best verbal response (V):

5 Orientated, converses normally
4 Confused, disoriented conversation, but able to answer basic questions
3 Inappropriate responses, words discernible
2 Incomprehensible speech
1 Makes no sounds.

Best motor response (M):

6 Obeys commands for movement
5 Purposeful movement to painful stimulus
4 Withdraws from pain
3 Abnormal (spastic) flexor response to painful stimuli, decorticate posture
2 Extensor response to painful stimuli, decerebrate posture
1 No response.

In this case, GCS = 2+3+5 = 10.

The formula for calculating air: oxygen entrainment ratio is given as :
100% − FiO2 = air/oxygen entrainment ratio
Since FiO2 − 21% and the entrainment ratio is already known. Substituting the values in the equation: x = FiO2.

100 − x = 9
x − 21
100 − x = 9(x − 21)
100 − x = 9x − 189
10x = 289
x = 289/10
x = 28.9%

Aldosterone is produced in the zona glomerulosa of the adrenal cortex and acts to increase sodium reabsorption via intracellular mineralocorticoid receptors in the distal tubules and collecting ducts of the nephron.

Its release is stimulated by hypovolaemia, blood loss ,and low plasma sodium and is inhibited by hypertension and increased sodium. It is regulated by the renin-angiotensin system.

Approximately 20% of halothane and 0.02% desflurane undergo hepatic biotransformation. Desflurane, halothane, and isoflurane are metabolised in the liver by cytochrome p450 to trifluoroacetate. Through an immunological mechanism involving trifluoroacetyl hapten formation, trifluoroacetate is thought to be responsible for hepatotoxicity.

Potency of inhaled anaesthetic agents is measured using the minimal alveolar concentration (MAC). The MAC of halothane is 0.74% while that of desflurane is 6.3%. The potency can also be compared using the oil: gas partition coefficient (224 and 18.7 for halothane and desflurane respectively).

Onset of action of volatile agents depends on the blood:gas partition coefficient. A lower blood:gas partition coefficient and insolubility in blood means faster onset and offset of action. The blood gas coefficient for halothane is 2.4 while that of desflurane is 0.42. Desflurane is less soluble than halothane in blood. Halothane has a pungent smell that can irritate the airway which limits its use for a gaseous induction especially in paediatric anaesthesia. desflurane is not pungent.

Desfluranes boiling point is only slightly above normal room temperature (22.8°C) making it extremely volatile while the boiling point of halothane is approximately 50.2°C.

The derived SI unit of force is Newton.
F = m·a (where a is acceleration)
F = 1 kg·m/s2

The joule (J) is a converted unit of energy, work, or heat. When a force of one newton (N) is applied over a distance of one metre (Nm), the following amount of energy is expended:

J = 1 kg·m/s2·m =
J = 1 kg·m2/s2 or 1 kg·m2·s-2

The unit of velocity is metres per second (m/s or ms-1).

The watt (W), or number of joules expended per second, is the SI unit of power:

J/s = kg·m2·s-2/s
J/s = kg·m2·s-3

Pressure is measured in pascal (Pa) and is defined as force (N) per unit area (m2):
Pa = kg·m·s-2/m2
Pa = kg·m-1·s-2

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

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

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

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

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.

PaCO2 is one of the most important factors that regulate cerebral vascular tone. CO2 induces cerebral vasodilatation and as a result, it increases CBF. Between 20 mmHg (2.7 kPa) and 80 mmHg (10.7 kPa), there is a linear increase of PaCO2.

Sometimes, there are areas where auto regulation has failed locally but not globally. Similarly, local vs. systemic acidosis will have similar effects. When the PaO2 falls below 50 mmHg (6.5 kPa), the CBF progressively increases.

An increase in the cerebral metabolic rate for oxygen (CMRO2) and therefore CBF can be caused by hyperthermia.
A late feature of cerebral injury is hyperthermia secondary to hypothalamic injury. Therefore this is not the most likely cause of an increased CBF in this scenario.

The important landmarks of vessels arising from the abdominal aorta at different levels of vertebrae are:

T12 – Coeliac trunk

L1 – Left renal artery

L2 – Testicular or ovarian arteries

L3 – Inferior mesenteric artery

L4 – Bifurcation of the abdominal aorta

The amount of oxygen carried by 100 ml of blood is called the arterial oxygen content (CaO2)and is normally 17-24 ml/dL and can be determined by this equation:

CaO2 = oxygen bound to haemoglobin + oxygen dissolved in plasma

CaO2 = (1.34 × Hgb × SaO2 × 0.01) + (0.003 × PaO2)

where:

1.34 = Huffner’s constant (D) – Huffner’s constant does not change and its magnitude relatively small.
Hgb is the haemoglobin level in g/dL and SaO2 is the percent oxyhaemoglobin saturation of arterial blood
PaO2 is (0.0225 = ml of O2 dissolved per 100 ml plasma per kPa, or 0.003 ml per mmHg).

Quantitatively, the amount of oxygen dissolved in plasma is 0.3 mL/dL.

Henry’s law states that at constant temperature, the amount of gas dissolved at equilibrium in a given quantity of a liquid is proportional to the pressure of the gas in contact with the liquid.

Given a haemoglobin concentration of 15 g/dL and a SaO2 of 100% and a PaO2 of 13.3 kPa, the amount of oxygen bound to haemoglobin is 20.4 mL/100mL.

Cardiac output is an important determinant of oxygen delivery but does not influence the oxygen content of blood.

Hydrochloric acid is lost when you vomit for a long time (HCl). As a result, the following can be expected, in varying degrees of severity:

Hypokalaemia
Hypochloraemia
Increased bicarbonate to compensate for chloride loss and metabolic alkalosis

The alkalosis causes potassium to move from the intracellular to the extracellular compartment at first. Long-term vomiting and dehydration cause potassium to be excreted by the kidneys in order to conserve sodium. Dehydration can cause urea and creatinine levels to rise.

The actual base excess is always greater than the standard base excess.

The actual base excess (BE) is a measurement of a base’s contribution to a blood gas picture’s metabolic component. It’s the amount of base that needs to be added to a blood sample to bring the pH back to 7.4 after the respiratory component of a blood gas picture has been corrected (PaCO2 of 40 mmHg or 5.3 kPa). The BE has a normal range of +2 to 2. A large positive BE indicates a severe metabolic alkalosis, while a large negative BE indicates a severe metabolic acidosis. As a result, the actual BE in vitro is unaffected by CO2.

In vivo, however, standard BE is not independent of pCO2 because blood with haemoglobin acts as a better buffer than total ECF.

As a result, it is impossible to tell the difference between compensating for a respiratory disorder and compensating for the presence of a primary metabolic disorder.

The differences between in vitro and in vivo behaviour can be mostly eliminated if the BE is calculated for a haemoglobin concentration of 50 g/L (the ‘effective’ or virtual value of Hb if it was distributed throughout the extracellular space) rather than the actual haemoglobin. Because haemoglobin has a lower buffering capacity, the standard BE is higher than the actual BE. It reflects the BE better in the extracellular space rather than just the intravascular compartment.

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.

The ureter starts from the hilum of the kidney and has different relations with structures along its journey to the bladder.
It runs anterior to the psoas major muscle.
The testicular vessels (males) or the ovarian vessels (females) cross in front of the ureter.
The ureter passes in front of the common iliac artery where it bifurcates into the internal and external iliac arteries.
The ureter passes medial to the branches of the internal iliac vessel downwards and forwards to towards the bladder.
In males, the ductus deferens crosses the pelvic ureter medially.
In females. the ureter passes through the base of the broad ligament
In females, the pelvic part initially has the same relations as in males but, anterior to the internal iliac artery, it is immediately behind the ovary, forming the posterior boundary of the ovarian fossa. It is in extraperitoneal connective tissue in the inferomedial part of the broad ligament of the uterus. In the broad ligament, the uterine artery is anterosuperior to the ureter for approximately 2.5 cm and then crosses to its medial side to ascend alongside the uterus. The ureter turns forwards slightly above the lateral vaginal fornix and is, generally, 2 cm lateral to the supravaginal part of the uterine cervix in this location. It then inclines medially to reach the bladder.

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%.