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

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

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

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

T cells possess specific glycoproteins and receptors on their surface.

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

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

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

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

Case control studies in particular are prone to recall bias, people who are suffering from COPD might sometimes relate the ailment to marijuana usage in past and hence contrary to the control group, they are more able to describe to what extent they have been using the drug in the past.

As recommended, all the doctors should make sure that there practice is based on evidence and thus it is paramount that the doctors learn to appraise the paper in a critical manner i.e. ability to detect any potential source of bias.

Detection Bias: Outcomes are more looked for in one group than the other.

Observer Bias: Subjectivity of observers regarding the outcome.

Publication bias: Not publishing the results of a valid study just because they are negative or uninteresting can be termed as publication bias.

Recall bias: Recall bias is specifically appropriate to the case control studies that is when ever the memories retrieved by the participants differ in accuracy.

Response Bias: The participants that filled out the response forms containing information that was going to be used for a trial, don’t represent the target population.

The duodenojejunal flexure is the point where the duodenum becomes the jejunum.

The ligament of Treitz, which arises from the right crus of diaphragm, provides suspension for support.

Between the ileum and the caecum is the ligament of Treves.

The left gastric artery is the smallest branch that originates from the coeliac trunk—the coeliac trunk branches of the abdominal aorta at the vertebral level of T12.

The left gastric artery runs along the superior portion of the lesser curvature of the stomach. A peptic ulcer that is serious enough to erode through the stomach mucosa into a branch of the left gastric artery can cause massive blood loss in the stomach, leading to hematemesis. The patient also takes Naproxen, a non-steroidal anti-inflammatory drug that is a common cause for peptic ulcers in otherwise healthy patients.

The left gastric artery is responsible for 85% of upper GI bleeds. In cases refractory to initial treatment, angiography is sometimes needed to embolise the vessel at its origin and stop bleeding. During an angiogram, the radiologist will enter the aorta via the femoral artery, ascend to the level of the 12th vertebrae and then enter the left gastric artery via the coeliac trunk.

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 action of class 1 anti-arrhythmic is sodium channel blockade. Subclasses of this action reflect effects on the action potential duration (APD) and the kinetics of sodium channel blockade.

Drugs with class 1A prolong the APD and refractory period, and dissociate from the channel with intermediate kinetics.

Drugs with class 1B action shorten the APD in some tissues of the heart, shorten the refractory period, and dissociate from the channel with rapid kinetics.

Drugs with class 1C action have minimal effects on the APD and the refractory period, and dissociate from the channel with slow kinetics.

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.

Charles’ Law states that there is a direct correlation between temperature and volume, where pressure and amount gas are constant. As temperature increases, volume also increases.

Boyle’s Law states that Pressure is inversely proportional to volume, assuming that temperature and amount of gas are constant. As volume increases, pressure decreases. In Dalton’s law of partial pressure, the total pressure exerted by a mixture of gases is equal to the sum of the partial pressure of the gases in mixture.

According to Henry’s Law for concentration of dissolved gases, at a constant temperature, the amount of a given gas that dissolves in a given type and volume of liquid is directly proportional to the partial pressure of that gas in equilibrium with that liquid. An equivalent way of stating the law is that the solubility of a gas in a liquid is directly proportional to the partial pressure of the gas above the liquid.

Gay-Lussac’s Law states that the pressure of a given mass of gas varies directly with the absolute temperature of the gas, when the volume is kept constant. This law is very similar to Charles’ Law, with the only difference being the type of container. Whereas the container in a Charles’ Law experiment is flexible, it is rigid in a Gay-Lussac’s Law experiment.

Nitrous oxide increases cerebral blood flow by direct cerebral stimulation and tends to elevate intracranial pressure (ICP)

It increases the cerebral metabolic rate of oxygen consumption (CMRO2)

It is not an NMDA agonist as it antagonizes NMDA receptors.

Cerebral autoregulation is impaired with the use of nitrous oxide but when used with propofol, it is maintained.

Carbon dioxide reactivity is not affected by it.

The degree of correlation is summarised by the correlation coefficient (r). This indicates how closely the points lie to a line drawn through the plotted data. In parametric data this is called Pearson’s correlation coefficient and can take any value between -1 to +1. A correlation of -1.0 indicates a perfect negative correlation, and a correlation of 1.0 indicates a perfect positive correlation.

For example

r = 1 – strong positive correlation (e.g. systolic blood pressure always increases with age)

r = 0 – no correlation (e.g. there is no correlation between systolic blood pressure and age)

r = – 1 – strong negative correlation (e.g. systolic blood pressure always decreases with age)

Whilst correlation coefficients give information about how one variable may increase or decrease as another variable increases they do not give information about how much the variable will change. They also do not provide information on cause and effect.

In contrast to the correlation coefficient, linear regression may be used to predict how much one variable changes when a second variable is changed.

The ventilation/perfusion ratio varies in different areas of the lung. In an upright individual, although both ventilation and perfusion increase from the apex to the base of the lung, the increase in ventilation is less than the increase in blood flow. As a result, the normal V̇ /Q̇ ratio at the apex of the lung is much greater than 1 (ventilation exceeds perfusion), whereas the V̇ /Q̇ ratio at the base of the lung is much less than 1 (perfusion exceeds ventilation).

There is more volume in the alveoli found in the apices than in the bases of the lungs. This is due to the weight of the lung stretching the apical alveoli to the maximum size. Also, the weight of the lungs pull themselves away from the chest wall, creating a negative intrapleural pressure. These factors, however, do not directly affect the PAO2.

The ‘ideal’ alveolar PO2 minus arterial PO2 is the alveolar-arterial (A-a) oxygen difference.

The ‘ideal’ alveolar PO2 is derived from the alveolar air equation and is the PO2 that the lung would have if there was no ventilation-perfusion (V/Q) inequality and it was exchanging gas at the same respiratory exchange ratio as real lung.

The amount of oxygen in the blood is measured directly in the arteries.

The A-a oxygen difference (or gradient) is a useful measure of shunt and V/Q mismatch, and it is less than 2 kPa in normal adults breathing air (15 mmHg). Because the shunt component is not corrected, the A-a difference increases when breathing 100 percent oxygen, and it can be up to 15 kPa (115 mmHg).

An abnormally low or abnormally high V/Q ratio within the lung can cause an increased A-a difference, though the former is more common. Atelectasis, which results in a low V/Q ratio, is the most likely cause of an A-a difference in a healthy adult breathing 100 percent oxygen.

Hypoventilation may cause an increase in alveolar (and thus arterial) CO2, lowering alveolar PO2 according to the alveolar air equation.

The alveolar PO2 is also reduced at high altitude.

Healthy people are unlikely to have a right-to-left shunt or an oxygen transport diffusion defect.

Thiopental is a new British Approved Name for thiopentone and is thio-barbiturate.
Methohexitone is an oxy- barbiturate. Both thiopental and methohexitone are intravenous induction agents.

Ketamine cannot cause loss of consciousness in less than 30 seconds. At least 30 seconds is needed to cause loss of consciousness following intravenous administration.

Etomidate is an imidazole but it is not used in the Intensive Care unit for sedation because it has an antidepressant effect on the steroid axis.

The fibrotendinous ring formed by the congregation of the rectus muscles at the apex of the orbit does not include superior oblique. This muscle is completely outside the ring and so it is the most difficult muscle to anaesthetise completely. A good grasp of the anatomy of the area being anaesthetised is important with all regional anaesthetic techniques so that potential problems and complications with a block can be anticipated.

The borders of this pyramid whose apex points upwards and outwards of the bony orbit are as follows:
Floor – Zygoma and Maxilla
Roof – frontal bone
Medial wall – maxilla, ethmoid, sphenoid and lacrimal bones.
Lateral wall – greater wing of the sphenoid and the zygoma.

The four recti muscles (superior, medial, lateral and inferior) originate from a tendinous ring (the annulus of Zinn) and extend anteriorly to insert beyond the equator of the globe. Bands of connective tissue are present between the rectus muscles forming a conical structure and hinder the passage of local anaesthetic.

The superior oblique muscle is situated outside this ring and is the most difficult muscle to anaesthetise completely, particularly with a single inferotemporal peribulbar injection. An additional medial injection may help to prevent this.

The cranial nerve supply to the extraocular muscles are:
3rd (inferior oblique, inferior recti, medial and superior)
4th (superior oblique), and
6th (lateral rectus).

The long and short ciliary nerves provide the sensory supply to the globe and these are branches of the nasociliary nerve, (which is itself a branch of the ophthalmic division of the trigeminal nerve).

To achieve anaesthesia for the eye, these nerves which enter the fibrotendinous ring need to be fully blocked to anaesthetise the eye for surgery.

The laryngeal folds are comprised of two types of folds; the vestibular fold and the vocal fold. The vocal folds are mobile, and concerned with voice production. They are formed by the mucous membrane covering the vocal ligament. They are avascular, hence, are white in colour.

The internal branch of the superior laryngeal nerve provides sensation above the vocal cords. Lesions to this nerve may lead to loss of sensation above the vocal cords and loss of taste on the epiglottis.

The recurrent laryngeal nerve supplies the lateral and posterior cricoarytenoid, the thyroarytenoid. It also provides sensation below the vocal cords. Lesions to this nerve may cause respiratory obstruction, hoarseness, inability to speak and loss of sensation below the vocal cords.

The external branch of the superior laryngeal nerve supplies the cricothyroid muscle.

The glossopharyngeal nerve contains both sensory and motor components, and provides somatic innervation to the stylopharyngeus muscle, visceral motor innervation to the parotid gland, and carries afferent sensory fibres from the posterior third of the tongue, pharynx and tympanic cavity.

Each kidney is composed of about 1.2 million uriniferous tubules. Each tubule consists of two parts that are embryologically distinct from each other. They are as follows:
a) Excretory part, called the nephron, which elaborates urine
b) Collecting part which begins as a junctional tubule from the distal convoluted tubule.

There are two types of nephrons in the kidney:
The cortical nephron comprises 80% of the total nephron and its major function is the excretion of waste products in urine whereas the juxtamedullary nephron comprises 20% of the total nephron and its major function is the concentration of urine by counter current mechanism.
In the superficial (cortical) nephrons, peritubular capillaries branch off the efferent arterioles and deliver nutrients to epithelial cells as well as serve as a blood supply for reabsorption and secretion. In juxtamedullary nephrons, the peritubular capillaries have a specialization called the vasa recta, which are long, hairpin-shaped blood vessels that follow the same course as a loop of Henle. The vasa recta serve as osmotic exchangers for the production of concentrated urine.

The kidney receives about 25% of cardiac output and about 20% of this is filtered at the glomeruli of the kidney. Thus, renal blood flow is 1200 ml/minute and renal plasma flow is 650 ml/minute

A nominal volume of 2 litres is contained in a CD cylinder. It has a pressure of 230 bar when full and contains litres 460 L of useable oxygen at STP.

For every 1000 mL 100% oxygen there will be an entrainment of 1000 mL or air (20% oxygen) in an air/oxygen mix.

The average concentration is, therefore, 120/2=60% or 0.6.

A tonsillar sinus or fossa is a space that is bordered by the triangular fold of the palatoglossal and palatopharyngeal arches in the lateral wall of the oral cavity. The palatine tonsils are in these sinuses.

The glossopharyngeal nerve is the main sensory nerve for the tonsillar fossa. The tonsillar branches of the glossopharyngeal nerve supply the palatine tonsils forming a plexus around it. Filaments from this plexus are distributed to the soft palate and fauces where they communicate with the palatine nerves. A lesser contribution is made by the lesser palatine nerve. Because of this otalgia may occur following tonsillectomy.

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

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 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.