Posterior to the oesophagus, the thoracic duct is on the right side inferiorly but crosses to the left more superiorly (at T5).

A blowout fracture is an isolated fracture of the orbital walls without compromise of the orbital rims. The common mechanisms are falls, high-velocity ball-related sports, traffic accidents, and interpersonal violence.

The frontal, ethmoidal, sphenoid, zygomatic, and lacrimal bones form the bony structures of the orbit. Medially, the maxillary and the lacrimal bone form the lacrimal fossa. Together with the lamina papyracea of the ethmoid bone, they form the medial wall. The sphenoid bone forms the posterior wall and houses the orbital canal. Lateral to the orbital canal lies the superior orbital fissure housing cranial nerves III, IV, V, and VI. The zygomatic bone forms the lateral wall. Superior and inferior borders are the frontal and maxillary bones. Located around the globe of the eye and attached to it are 6 extraocular muscles; the 4 rectus muscles and the superior and inferior oblique muscles. The fat and connective tissue around the globe help to reduce the pressure exerted by the extraocular muscles.

The goal of treatment is to restore aesthetics and physiological function. The problem with orbital blowout fractures is that the volume of the orbit can be increased, resulting in enophthalmos and hypoglobus. In addition, the orbital tissue and inferior rectus muscle can become trapped by the bony fragments leading to diplopia, limitation of gaze, and tethering. Finally, the orbital injury can lead to retinal oedema, hyphema, and significant loss of vision.

While some cases may be managed with conservative care, others may require some type of surgical intervention.

C. difficile is normally found in the gut flora but its growth is normally suppressed by more dominant anaerobes. It has exotoxin-mediated effects causing profuse diarrhoea. Oral clindamycin (a broad spectrum antibiotic) is commonly implicated in precipitating C. difficile colitis; first line treatment is with oral metronidazole. Tetanolysin is a toxin produced by Clostridium tetani bacteria.

Thyroid hormones have multiple physiological effects on the body. These include:
1. Heat production (thermogenesis)
2. Increased basal metabolic rate
3. Metabolic effects:
(a) Increase in protein turnover (both synthesis and degradation are increased, although overall effect is catabolic)
(b) Increase in lipolysis
(c)Increase in glycogenolysis and gluconeogenesis
4. Enhanced catecholamine effect – Increase in heart rate, stroke volume and thus cardiac output
5. Important role in growth and development

Antimuscarinic medications may impair the contractility of bladder smooth muscle, resulting in acute urine retention in men with BPH, and should be avoided or used with caution.

Malaria results from infection with single-celled parasites belonging to the Plasmodium genus. Five species of Plasmodium are known to cause disease in humans: P. falciparum, P. vivax, P. ovale, P. malariae, and P. knowlesi.

Chloroquine remains the mainstay of treatment for uncomplicated vivax malaria.

The female Anopheles mosquito serves as the biologic vector and definitive host.

A complication of infection with P. falciparum is blackwater fever, a condition characterized by haemoglobinuria.

Plasmodium ovale has the longest incubation period, which can be up to 40 days. Plasmodium falciparum has a shorter incubation period of 7-14 days.

Multiple investigations may be done to establish a diagnosis of active tuberculosis. In this case, sputum for acid-fast bacilli would be the best option as it can be done immediately, give fast results, and promptly initiate treatment. Three-morning sputum samples are collected and tested for acid-fast bacilli using gram staining.

Blood culture would yield results in tuberculous bacteraemia and would be less sensitive than sputum testing.

A chest X-ray would not differentiate active tuberculosis from an old infection in which the Ghon complex has formed, and the body’s immune reaction contains the Mycobacterium tuberculosis bacteria.

Mantoux test shows the presence of antibodies to tuberculosis and may be positive if the patient has had a previous infection or been vaccinated against tuberculosis.

A CT chest would also be unable to differentiate between an active infection and the findings of old tuberculosis infection.

Legionella pneumophilais a Gram negative bacterium that is found in natural water supplies and in the soil, transmitted predominantly via inhalation of aerosols generated from contaminated water (direct person-to-person spread of infected patients does not occur). It is the cause of Legionnaires’ disease. Outbreaks of Legionnaires’ disease have been linked to poorly maintained air conditioning systems, whirlpool spas and hot tubs.

The clinical features of the pneumonic form of Legionnaires’ disease include:
Mild flu-like prodrome for 1-3 days
Cough (usually non-productive and occurs in approximately 90%)
Pleuritic chest pain
Haemoptysis
Headache
Nausea, vomiting and diarrhoea
Anorexia
Legionella pneumophilainfections can be successfully treated with macrolide antibiotics, such as erythromycin, or quinolones, such as ciprofloxacin. Tetracyclines, such as doxycycline, can also be used.
The syndrome of inappropriate antidiuretic hormone secretion (SIADH) can occur with Legionnaires’ disease and will result in hyponatraemia as is seen in this case.
Legionella pneumophilainfections are resistant to amoxicillin but can be successfully treated with macrolide antibiotics, such as erythromycin, or quinolones, such as ciprofloxacin. Tetracyclines, such as doxycycline, can also be used. The majority of cases of Legionnaires’ disease are caused by Legionella pneumophila, however many other species of Legionella have been identified.
Legionella longbeachae is another less commonly encountered species that has also been implicated in outbreaks. It is predominantly found in soil and potting compost, and has caused outbreaks of Pontiac fever, the non-respiratory and less severe variant of Legionnaires’ disease.

Natural killer (NK) cells are cytotoxic CD8 positive cells that lack the T-cell receptor. They are large cells with cytoplasmic granules. NK cells are designed to kill target cells that have a low level of expression of HLA class I molecules, such as may occur during viral infection or on a malignant cell. NK cells do this by displaying several receptors for HLA molecules on their surface. When HLA is expressed on the target cell these deliver an inhibitory signal into the NK cell. When HLA molecules are absent on the target cell this inhibitory signal is lost and the NK cell can then kill its target. In addition, NK cells display antibody-dependent cell-mediated cytotoxicity. In this, antibody binds to antigen on the surface of the target cell and then NK cells bind to the Fc portion of the bound antibody and kill the target cell.

Glanzmann’s thromboasthenia is a rare platelet disorder in which platelets contain defective or low levels of glycoprotein IIb/IIIa.

A lesion of the parietal optic radiation will result in a contralateral homonymous inferior quadrantanopia.
A lesion of the temporal optic radiation will result in a contralateral homonymous superior quadrantanopia.

Like other non-steroidal anti-inflammatory drugs, Ibuprofen cannot be given with Warfarin as it would increase the bleeding risk of this patient.

The Likelihood Ratio (LR) is the likelihood that a given test result would be expected in a patient with the target disorder compared to the likelihood that that same result would be expected in a patient without the target disorder.

The LR is used to assess how good a diagnostic test is and to help in selecting an appropriate diagnostic tests or sequence of tests. They have advantages over sensitivity and specificity because they are less likely to change with the prevalence of the disorder, they can be calculated for several levels of the symptom/sign or test, they can be used to combine the results of multiple diagnostic test and they can be used to calculate post-test probability for a target disorder.

A LR greater than 1 produces a post-test probability which is higher than the pre-test probability. An LR less than 1 produces a post-test probability which is lower than the pre-test probability. When the pre-test probability lies between 30 and 70 per cent, test results with a very high LR (say, above 10) rule in disease. An LR below 1 produces a post-test probability les than the pre-test probability. A very low LR (say, below 0.1) virtually rules out the chance that the patient has the disease.

Most cells have insulin receptors present on them which can be sequestered into the cell to inactivate them. These receptors consist of two extracellular alpha subunits which contain the insulin-binding site and two transmembrane beta subunits. Because insulin is a polypeptide hormone, it must act via cell surface receptors as it is unable to readily cross the cell membrane. On binding to the receptor, the beta subunit of insulin autophosphorylation, which activates tyrosine kinase. As a result, there is an intracellular cascade of phosphorylation, causing a translocation of the glucose transporter GLUT4 and GLUT-1 to the plasma membrane of the affected cell. This facilitates glucose entry.

During the AP plateau, Ca2+enters the cell and activates Ca2+sensitive Ca2+release channels in the sarcoplasmic reticulum allowing stored Ca2+to flood into the cytosol; this is called Ca2+-induced Ca2+release. In relaxation, about 80% of Ca2+is rapidly pumped back into the SR (sequestered) by Ca2+ATPase pumps. The Ca2+that entered the cell during the AP is transported out of the cell primarily by the Na+/Ca2+exchanger in the membrane which pumps one Ca2+ion out in exchange for three Na+ions in, using the Na+electrochemical gradient as an energy source. Increased heart rate increases the force of contraction in a stepwise fashion as intracellular [Ca2+] increases cumulatively over several beats; this is the Treppe effect. Factors that affect intracellular [Ca2+] and hence cardiac contractility are called inotropes.

Extensor carpi ulnaris is a fusiform muscle in the posterior forearm. It spans between the elbow and base of the little finger. This muscle belongs to the superficial forearm extensor group, along with anconaeus, brachioradialis, extensor carpi radialis longus, extensor carpi radialis brevis, extensor digitorum and extensor digiti minimi muscles.

Like all the muscles of this compartment, extensor carpi ulnaris works as an extensor of the wrist. Moreover, due to its specific course, this muscle also acts to adduct the hand.

Extensor carpi ulnaris is innervated by the posterior interosseous nerve (C7, C8), a branch of the deep division of the radial nerve. The radial nerve stems from the posterior cord of the brachial plexus.

Blood supply to the extensor carpi ulnaris muscle is provided by branches of the radial recurrent and posterior interosseous arteries, which stem from the radial and ulnar arteries, respectively.

Glucagon is a peptide hormone that is produced and secreted by alpha cells of the islets of Langerhans, which are located in the endocrine portion of the pancreas. The main physiological role of glucagon is to stimulate hepatic glucose output, thereby leading to increases in glycaemia. It provides the major counter-regulatory mechanism to insulin in maintaining glucose homeostasis.
Hypoglycaemia is the principal stimulus for the secretion of glucagon but may also be used as an antidote in beta-blocker overdose and in anaphylaxis in patients on beta-blockers that fail to respond to adrenaline.
Glucagon then causes:
Glycogenolysis
Gluconeogenesis
Lipolysis in adipose tissue
The secretion of glucagon is also stimulated by:
Adrenaline
Cholecystokinin
Arginine
Alanine
Acetylcholine
The secretion of glucagon is inhibited by:
Insulin
Somatostatin
Increased free fatty acids
Increased urea production

Glycolysis is the metabolic pathway that converts glucose into pyruvate. The free energy released by this process is used to form ATP and NADH. Glycolysis is inhibited by glucagon, and glycolysis and gluconeogenesis are reciprocally regulated so that when one cell pathway is activated, the other is inactive and vice versa.

Glucagon has a minor effect of enhancing lipolysis in adipose tissue. Lipolysis is the breakdown of lipids and involves the hydrolysis of triglycerides into glycerol and free fatty acids. It makes fatty acids available for oxidation.

Acute lymphoblastic leukaemia (ALL) is caused by an accumulation of lymphoblasts in the bone marrow and is the most common malignancy of childhood. The incidence of ALL is highest at 3 – 7 years, with 75% of cases occurring before the age of 6. There is a secondary rise after the age of 40 years. 85% of cases are of B-cell lineage and have an equal sex incidence; there is a male predominance for the 15% of T-cell lineage.

The RAS pathway begins with renin cleaving its substrate, angiotensinogen (AGT), to produce the inactive peptide, angiotensin I, which is then converted to angiotensin II by endothelial angiotensin-converting enzyme (ACE). ACE activation of angiotensin II occurs most extensively in the lung. Angiotensin II mediates vasoconstriction as well as aldosterone release from the adrenal gland, resulting in sodium retention and increased blood pressure.

Features of toxicity include:
Increasing gastrointestinal disturbances (vomiting, diarrhoea, anorexia)
Visual disturbances
Polyuria and incontinence
Muscle weakness and tremor
Tinnitus
CNS disturbances (dizziness, confusion and drowsiness increasing to lack of coordination, restlessness, stupor)
Abnormal reflexes and myoclonus
Hypernatraemia
With severe overdosage (serum-lithium concentration > 2 mmol/L) seizures, cardiac arrhythmias (including sinoatrial block, bradycardia and first-degree heart block), blood pressure changes, electrolyte imbalance, circulatory failure, renal failure, coma and sudden death may occur.

Non-Hodgkin’s Lymphoma (NHL) causes neoplastic transformation of both B cell (85%) and T cell (15%) lines.

The most common presentation is with enlarged, rubbery, painless lymph nodes. The patient may also have B symptoms which consist of night sweats, weight loss and fevers. Multiple myeloma most commonly presents with bone pain, especially in the back and ribs.

The presence of Reed-Sternberg cells characterises Hodgkin’s lymphoma. Acute lymphoblastic leukaemia will present with features of anaemia, thrombocytopenia and leukopenia. The most common symptoms of chronic lymphocytic leukaemia are fatigue, night sweats and low-grade fever.

The peak incidence of NHL is in the 50-70 years age group, it affects men and women equally, but affects the Caucasian population more commonly than black and Asian ethnic groups.
The following are recognised risk factors for NHL:
Chromosomal translocations and molecular rearrangements
Epstein-Barr virus infection
Human T-cell leukaemia virus type-1 (HTLV-1)
Hepatitis C
Congenital and acquired immunodeficiency states
Autoimmune disorders, e.g. Sjogren’s syndrome and Hashimoto’s thyroiditis

The FDA categorizes Paracetamol as an NSAID (nonsteroidal anti-inflammatory drug) as it is believed to selectively inhibit cyclo-oxygenase 3 (COX-3) receptors in the brain and spinal cord.

COX-3 is a unique variant of the more known COX-1 and COX-2. It is responsible for the production of prostaglandins in central areas, which sensitizes free nerve endings to the chemical mediators of pain. Therefore, by selectively inhibiting COX-3, paracetamol effectively reduces pain sensation by increasing the pain threshold.
Acetaminophen does not inhibit cyclooxygenase in peripheral tissues and, therefore, has no peripheral anti-inflammatory effects.
The antipyretic actions of acetaminophen are likely attributed to direct action on heat-regulating centres in the brain, resulting in peripheral vasodilation, sweating, and loss of body heat.

Bumetanide is primarily used in patients with heart failure who have failed to respond to high doses of furosemide. Bumetanide and furosemide differ primarily in terms of bioavailability and pharmacodynamic potency. In the intestine, furosemide is only partially absorbed, with a bioavailability of 40-50 percent. Bumetanide, on the other hand, is almost completely absorbed in the intestine and has a bioavailability of about 80%. As a result, when it has a better bioavailability than furosemide, it is commonly used in patients with gut oedema.

When taken alone, Bendroflumethiazide is a moderately potent diuretic that is unlikely to control her oedema.

Mannitol is a type of osmotic diuretic used to treat cerebral oedema and high intracranial pressure.

Acetazolamide is a weak diuretic that inhibits carbonic anhydrase. It’s a rare occurrence.

Blood transfusion can be a life-saving treatment with significant clinical benefits, but it also comes with a number of risks and potential complications, including:
Immunological side effects
Errors in administration (episodes of ‘wrong blood’)
Viruses and Infections (bacterial, viral, possibly prion)
Immunodilution

A culture of better safety procedures as well as steps to reduce the use of transfusion has emerged as a result of growing awareness of avoidable risk and improved reporting systems. Transfusion errors, on the other hand, continue to occur, and some serious adverse reactions go unreported.

Transfusion-associated graft-vs-host disease (TA-GVHD) is a rare blood transfusion complication that causes fever, rash, and diarrhoea 1-4 weeks after the transfusion. Pancytopenia and liver function abnormalities are common laboratory findings.

TA-GVHD, unlike GVHD following allogeneic marrow transplantation, causes profound marrow aplasia with a mortality rate of >90%. Survival is uncommon, with death occurring within 1-3 weeks of the onset of symptoms.

Because of immunodeficiency, severe immunosuppression, or shared HLA antigens, viable T lymphocytes in blood components are transfused, engraft, and react against the recipient’s tissues, and the recipient is unable to reject the donor lymphocytes.
The following is a list of the most common transfusion reactions and complications:

1) Reaction to a febrile transfusion
The temperature rises by one degree from the baseline. Chills and malaise are also possible symptoms.
The most common response (1 in 8 transfusions).
Cytokines from leukocytes in transfused red cell or platelet components are usually to blame.
Only supportive. The use of paracetamol is beneficial.

2) Acute haemolytic reaction is a type of haemolytic reaction that occurs when the
Fever, chills, pain at the transfusion site, nausea, vomiting, and dark urine are all symptoms of a transfusion reaction.
Early on, many people report a sense of ‘impending doom.’
The most serious reaction. ABO incompatibility is frequently caused by a clerical error.
STOP THE TRANSFUSION OF INFORMATION. IV fluids should be given. It’s possible that diuretics will be required.

3) Haemolytic reaction that is delayed
It usually happens 4 to 8 days after a blood transfusion.
Fever, anaemia, jaundice, and haemoglobinuria are all symptoms that the patient has.
Positive Coombs test for direct antiglobulin.
Because of the low titre antibody, it is difficult to detect in a cross-match, and it is unable to cause lysis at the time of transfusion.
The majority of delayed haemolytic reactions are harmless and do not require treatment.
Anaemia and renal function should be monitored and treated as needed.

4) Reaction to allergens
Foreign plasma proteins are usually to blame, but anti-IgA could also be to blame.
Urticaria, pruritus, and hives are typical allergic reactions. It’s possible that it’s linked to laryngeal oedema or bronchospasm.
Anaphylaxis is a rare occurrence.
Antihistamines can be used to treat allergic reactions symptomatically. It is not necessary to stop transfusions.
If the patient develops anaphylaxis, the transfusion should be stopped and the patient should be given adrenaline and treated according to the ALS protocol.

5) TRALI (Transfusion Related Acute Lung Injury)
Within 6 hours of transfusion, there was a sudden onset of non-cardiogenic pulmonary oedema.
It’s linked to the presence of antibodies to recipient leukocyte antigens in the donor blood.
The most common cause of death from transfusion reactions is this.
STOP THE TRANSFUSION OF INFORMATION. Oxygen should be given to the patient. Around 75% of patients will require aggressive respiratory support.
The use of diuretics should be avoided.

6) TACO (Transfusion Associated Circulatory Overload)
Acute or worsening respiratory distress within 6 hours of a large blood transfusion. Fluid overload and pulmonary and peripheral oedema can be seen. Rapid blood pressure rises are common. BNP is usually 1.5 times higher than it was before the transfusion. It is most common in the elderly and those who have chronic anaemia.

Blood transfusions should be given slowly, over the course of 3-4 hours.

Glucagon is a peptide hormone that is produced and secreted by alpha cells of the islets of Langerhans, which are located in the endocrine portion of the pancreas. The main physiological role of glucagon is to stimulate hepatic glucose output, thereby leading to increases in glycaemia. It provides the major counter-regulatory mechanism to insulin in maintaining glucose homeostasis.
Hypoglycaemia is the principal stimulus for the secretion of glucagon but may also be used as an antidote in beta-blocker overdose and in anaphylaxis in patients on beta-blockers that fail to respond to adrenaline.
Glucagon then causes:
Glycogenolysis
Gluconeogenesis
Lipolysis in adipose tissue
The secretion of glucagon is also stimulated by:
Adrenaline
Cholecystokinin
Arginine
Alanine
Acetylcholine
The secretion of glucagon is inhibited by:
Insulin
Somatostatin
Increased free fatty acids
Increased urea production

Glycolysis is the metabolic pathway that converts glucose into pyruvate. The free energy released by this process is used to form ATP and NADH. Glycolysis is inhibited by glucagon, and glycolysis and gluconeogenesis are reciprocally regulated so that when one cell pathway is activated, the other is inactive and vice versa.

Glucagon has a minor effect of enhancing lipolysis in adipose tissue. Lipolysis is the breakdown of lipids and involves the hydrolysis of triglycerides into glycerol and free fatty acids. It makes fatty acids available for oxidation.

Lidocaine is a tertiary amine that is primarily used as a local anaesthetic but can also be used intravenously in the treatment of ventricular dysrhythmias.
Lidocaine works as a local anaesthetic by diffusing in its uncharged base form through neural sheaths and the axonal membrane to the internal surface of the cell membrane sodium channels. Here it alters signal conduction by blocking the fast voltage-gated sodium channels. With sufficient blockage, the membrane of the postsynaptic neuron will not depolarise and will be unable to transmit an action potential, thereby preventing the transmission of pain signals.
Each 1 ml of plain 1% lidocaine solution contains 10 mg of lidocaine hydrochloride. The maximum safe dose of plain lidocaine is 3 mg/kg. When administered with adrenaline 1:200,000, the maximum safe dose is 7 mg/kg. Because of the risk of vasoconstriction and tissue necrosis, lidocaine should not be used in combination with adrenaline in extremities such as fingers, toes, and the nose.
The half-life of lidocaine is 1.5-2 hours. Its onset of action is rapid within a few minutes, and it has a duration of action of 30-60 minutes when used alone. Its duration of action is prolonged by co-administration with adrenaline (about 90 minutes).
Lidocaine tends to cause vasodilatation when used locally. This is believed to be due mainly to the inhibition of action potentials via sodium channel blocking in vasoconstrictor sympathetic nerves.

Chickenpox is not a notifiable disease.

The anticoagulant effect of warfarin is enhanced by metronidazole. If use of both cannot be avoided, one must consider appropriately reducing the warfarin dosage. With alcohol, metronidazole can cause a disulfiram-like reaction, with symptoms like flushing, headaches, dizziness, tachypnoea and tachycardia, nausea and vomiting. The common side effects of metronidazole include a metallic taste and gastrointestinal irritation, in particular nausea and vomiting. These side effects are more common at higher doses. This drug has high activity against anaerobic bacteria and protozoa, and is well absorbed orally. For severe infections, the intravenous route is normally reserved.

Insulin is an anabolic hormone. Its actions can be broadly divided into:
Lipid metabolism
Protein metabolism and
Carbohydrate metabolism

For lipid metabolism, insulin:
Stimulates lipogenesis
Inhibits lipolysis by lipase

For carbohydrate metabolism, insulin:
Decreases gluconeogenesis
Stimulates glycolysis
Promotes glucose uptake in muscle and adipose tissue
Promotes glycogen storage
Increases glycogenesis
Decreases glycogenolysis

Protein metabolism:
Stimulates protein synthesis
Accelerates net formation of protein
Stimulates amino acid uptake
Inhibits protein degradation
Inhibits amino acid conversion to glucose

A daily calcium intake of 1,000 to 1,300 mg is advised for adults. Women have a slightly higher calcium need than men and are at a higher risk of developing osteoporosis as they age.

Calcium-rich foods include the following:
Milk, cheese, and butter as dairy products.
Broccoli, spinach, and green beans as green veggies.
Bread, rice, and cereals as whole grain foods.
Sardines, salmon, and other bony fish
Eggs
Nuts
The following foods have the least calcium:
Carrot
Fruits such as kiwis, raspberries, oranges, and papaya
Chicken and pork in meats.