Loop diuretics are drugs used to manage and treat fluid overload associated with CHF, liver cirrhosis, and renal disease. The drugs commonly used are:

• Furosemide
• Bumetanide
• Torsemide
• Ethacrynic Acid

Loop diuretics inhibit the Na-K-Cl pump in the ascending loop of Henle, resulting in salt-water excretion. This relieves congestion and reduces oedema.

The contra-indications to the use of loop diuretics are:
1. Anuria
2. Comatose and precomatose states associated with liver cirrhosis
3. Renal failure due to nephrotoxic or hepatotoxic drugs
4. Severe hypokalaemia
5. Severe hyponatremia
6. History of hypersensitivity to furosemide, bumetanide, or torsemide (or sulphonamides)

The following conditions or states are not contraindications, but loop diuretics needs to be used cautiously in these conditions:
1. Diabetes (but hyperglycaemia less likely than with thiazides)
2. Gout
3. Hypotension (correct before initiation of treatment)
4. Hypovolaemia (Correct before initiation of treatment)

The commonest implicated organisms in hospital-acquired bacteraemia following cannulation are Staphylococcus aureus and Staphylococcus epidermidis.
The risk is directly proportional to the length of time in-situ. Peripheral cannula should be replaced after 48 hours.

Extensor carpi radialis brevis is a fusiform muscle found in the lateral part of the posterior forearm. Together with anconaeus, brachioradialis, extensor carpi radialis longus, extensor digitorum, extensor digiti minimi and extensor carpi ulnaris, it belongs to the superficial forearm extensor group. Extensor carpi radialis brevis originates from the lateral epicondyle of humerus via the common extensor tendon. This is a common origin that it shares with the extensor digitorum, extensor digiti minimi and extensor carpi ulnaris muscles. Some fibres also originate from the lateral intermuscular septum, a thick aponeurosis that covers the muscle itself, and from the radial collateral ligament.

The muscle courses inferiorly, giving off a long tendon in the middle of the forearm which descends towards the dorsal hand. The tendon passes through a groove on the posterior surface of radius, deep to the extensor retinaculum. After traversing the extensor retinaculum space, the tendon inserts into the posterior aspect of the base of the third metacarpal bone.

Extensor carpi radialis brevis is innervated directly by the radial nerve (C5- C8), or sometimes from its deep branch/posterior interosseous nerve. The radial nerve stems from the posterior cord of the brachial plexus.

The muscle is vascularized by the radial recurrent artery, radial artery and deep brachial artery (via its radial collateral branch).

Extensor carpi radialis brevis works together with extensor carpi ulnaris and extensor carpi radialis longus to extend the hand at the wrist joint. This action is vital in a sequence of muscle contractions needed for clenching a fist or making a grip. When performing these functions, wrist extension blocks the flexor muscles from on acting upon the hand. Instead, flexors act only on the digits, thereby flexing them and producing an effective hand grip, such as that seen in a tennis backhand. When the extensor carpi radialis brevis muscle contracts together with extensor carpi radialis longus and flexor carpi radialis, it contributes to producing hand abduction (radial deviation).

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.

Hepatitis B surface antigen (HBsAg) is a protein on the surface of the hepatitis B virus, that is the first serologic marker to appear in a new acute infection.It can be detected as early as 1 week and as late as 9 weeks. It can be detected in high levels in serum during acute or chronic hepatitis B virus infection. The presence of HBsAg indicates that the person is infectious. The body normally produces antibodies to HBsAg as part of the normal immune response to infection. HBsAg is the antigen used to make hepatitis B vaccine.
Hepatitis B surface antibody (anti-HBs) indicates recovery and immunity from the hepatitis B virus infection. Anti-HBs also develops in a person who has been successfully vaccinated against hepatitis B.
Total hepatitis B core antibody (anti-HBc): Appears at the onset of symptoms in acute hepatitis B and persists for life. The presence of anti-HBc indicates previous or ongoing infection with hepatitis B virus in an undefined time frame. It is not present following hepatitis B vaccination.
IgM antibody to hepatitis B core antigen (IgM anti-HBc) indicates recent infection with hepatitis B virus (<6 months). Its presence indicates acute infection.
The following table summarises the presence of hepatitis B markers according to each situation:
Susceptible to infection:
HBsAg = Negative
Anti-HBc = Negative
Anti-HBs = Negative

Immune due to natural infection:
HBsAg = Negative
Anti-HBc = Positive
Anti-HBs = Positive

Immune due to vaccination:
HBsAg = Negative
Anti-HBc = Negative
Anti-HBs = Positive

Acute infection:
HBsAg = Positive
Anti-HBc = Positive
Anti-HBs = Negative
IgM anti-HBc = Positive

Chronic infection:
HBsAg = Positive
Anti-HBc = Positive
Anti-HBs = Negative
IgM anti-HBc = Negative

Preload refers to the initial stretching of the cardiac myocytes before contraction. It is therefore related to muscle sarcomere length. The sarcomere length cannot be determined in the intact heart, and so, other indices of preload are used, like ventricular end-diastolic volume or pressure. The end-diastolic pressure and volume of the ventricles increase when venous return to the heart is increased, and this stretches the sarcomeres, which increase their preload.

Angiotensin I is converted to angiotensin II by the removal of two C-terminal residues by the enzyme angiotensin-converting enzyme (ACE). This primarily occurs in the lungs, although it does also occur to a lesser degree in endothelial cells and renal epithelial cells.
The main actions of angiotensin II are:
Vasoconstriction of vascular smooth muscle (resulting in increased blood pressure)
Vasoconstriction of the efferent arteriole of the glomerulus (resulting in an increased filtration fraction and preserved glomerular filtration rate)
Stimulation of aldosterone release from the zona glomerulosa of the adrenal cortex
Stimulation of anti-diuretic hormone (vasopressin) release from the posterior pituitary
Stimulation of thirst via the hypothalamus
Acts on the Na+/H+ exchanger in the proximal tubule of the kidney to stimulate Na+reabsorption and H+excretion

Overuse of cortisol medication, as seen in the treatment of patients with chronic asthma or rheumatoid arthritis, can cause Cushing’s syndrome.

Weight gain, thin arms and legs, a round face, increased fat around the base of the neck, a fatty hump between the shoulders, easy bruising, wide purple stretch marks primarily on the abdomen, breasts, hips, and under the arms, weak muscles, hirsutism, hypertension, erectile dysfunction, osteoporosis, frontal alopecia, acne, depression, poor wound healing, and polycythaemia are all clinical features of Cushing’s syndrome.

Medial medullary syndrome is a form of stroke that affects the medial medulla of the brain. It is caused by a lesion in the medial part of the medulla, which is due to an infraction of vertebral arteries and/or paramedian branches of the anterior spinal artery.

It is characterized by contralateral paralysis of the upper and lower limb of the body, a contralateral decrease in proprioception, vibration, and/or fine touch sensation, paresthesias or less commonly dysesthesias in the contralateral trunk and lower limb, and loss of position and vibration sense with proprioceptive dysfunction. Ipsilateral deviation of the tongue due to ipsilateral hypoglossal nerve damage can also be seen.

A study should only be undertaken if the power is at least 80%; a study power set at 80% accepts a likelihood of 1 in 5 (20%) of missing a statistically significant difference where one exists.The determinants of power are:the sample size (the power increases with sample size)the variability of the observations (the power increases as the variability decreases)the effect size of interest (the power is greater for a larger expected effect size)and the significance level, α (the power is greater if the significance level is larger); therefore the probability of a type I error increases as the probability of a type II error decreases.

Long-term administration of oxygen, usually at least 15 hours daily, improves survival in COPD patients who have severe hypoxaemia.

Long-term oxygen therapy should be considered in:

A non-smoker with COPD and a PaO2<7.3 kPa when stable

A non-smoker with COPD and PaO27.3–8 kPa when stable and with secondary polycythaemia, peripheral oedema, or evidence of pulmonary hypertension

Severe chronic asthma with PaO2<7.3 kPa or persistent disabling breathlessness

A patient with Interstitial lung disease with PaO2<8 kPa and in patients with PaO2>8 kPa with disabling dyspnoea

A patient with cystic fibrosis when PaO2<7.3 kPa or if PaO27.3–8 kPa in the presence of secondary polycythaemia, nocturnal hypoxaemia, pulmonary hypertension, or peripheral oedema

Pulmonary hypertension, without parenchymal lung involvement when PaO2<8 kPa

Neuromuscular or skeletal disorders, after specialist assessment

Obstructive sleep apnoea despite continuous positive airways pressure therapy, after specialist assessment

Pulmonary malignancy or other terminal disease with disabling dyspnoea

Heart failure with daytime PaO2<7.3 kPa when breathing air or with nocturnal hypoxaemia

Only a very small fraction of the thyroid hormones circulating in the blood are free. The majority is bound to transport proteins. Only the free thyroid hormones are biologically active, and measurement of total thyroid hormone levels can be misleading.

The relative percentages of bound and unbound thyroid hormones are:
Bound to thyroid-binding globulin -70%
Bound to albumin -15-20%
Bound to transthyretin -10-15%
Free T3 -0.3%
Free T4 -0.03%

At the optic chiasm, fibres from the medial (nasal) half of each retina crossover, forming the right and left optic tracts.
The left optic tract contains fibres from the left lateral (temporal) retina and the right medial retina.
The right optic tract contains fibres from the right lateral retina and the left medial retina.
Each optic tract travels to its corresponding cerebral hemisphere to reach its lateral geniculate nucleus (LGN) located in the thalamus where the fibres synapse.
A lesion of the optic tract will cause a contralateral homonymous hemianopia.

In the setting of cervical radiculopathy, because the nerve root of a spinal nerve is compressed or otherwise impaired, the pain and symptomatology can spread far from the neck and radiates to arm, neck, chest, upper back and/or shoulders. Often muscle weakness and impaired deep tendon reflexes are noted along the course of the spinal nerve.

Cervical radiculopathy is almost always unilateral, although, in rare cases, both nerves at a given level may be impacted. Those rare presentations can confound physical diagnosis and require acceleration to advanced imaging especially in cases of trauma. If there is nerve impingement, the affected side will be reduced relative to the unaffected side. Reduction in strength of muscles innervated by the affected nerve is also significant physical finding.

For a C4-C5 injury, the following symptoms may present:

Weakness in the deltoid muscle (front and side of the shoulder) and upper arm
Shoulder pain
Numbness along the outside of the upper arm

Brachioradialis is a fusiform muscle located in the lateral part of the posterior forearm. Along with extensor carpi radialis brevis and extensor carpi radialis longus, it comprises the radial group of forearm muscles, which belong to the superficial layer of posterior forearm muscles. Although anatomically part of the posterior forearm muscles, which are known to be forearm extensors, brachioradialis’ fibre orientation enables it to rather flex the forearm, and aids in supination of the forearm at the radioulnar joint.

The brachioradialis muscle originates from the upper two-thirds of the lateral supracondylar ridge of humerus and the anterior surface of the lateral intermuscular septum of the arm. It slides over the lateral surface of the elbow joint, entering the anterolateral cubital area. The muscle fibres course inferiorly down the radial part of the anterior forearm, forming a thick tendon in approximately the middle of the forearm. This tendon then traverses the remainder of the forearm, inserting near the wrist, just proximal to the styloid process of radius.

Brachioradialis is innervated by the radial nerve (from the root values C5-C6) that stems from the posterior cord of the brachial plexus. Blood supply to the brachioradialis muscle comes from branches of the radial artery, radial recurrent artery and the radial collateral branch of the deep brachial artery.

Ciprofloxacin increases plasma concentrations of theophylline. There is an increased risk of convulsions when quinolones are given with NSAIDs or theophylline. There is an increased risk of tendon damage when quinolones are given with corticosteroids. Quinolones are known to increase the QT-interval and should not be taken with concomitantly with other drugs that are known to cause QT-interval prolongation. There is an increased risk of myopathy when erythromycin or clarithromycin are taken with simvastatin or atorvastatin.

Bile functions to eliminate endogenous and exogenous substances from the liver (including bilirubin), to neutralise gastric acid in the small intestine, and to emulsify fats in the small intestine and facilitate their digestion and absorption. Bile salts also act as bactericides, destroying many of the microbes that may be present in the food. Bile doesn’t contain digestive enzymes for digestion of lipids into monoglycerides and fatty acids; this is performed mainly by pancreatic lipase.

About 25% of filtered sodium is reabsorbed in the the loop of Henle.

Haemoglobin is composed of four polypeptide globin chains each with its own iron containing haem molecule. Haem synthesis occurs largely in the mitochondria by a series of biochemical reactions commencing with the condensation of glycine and succinyl coenzyme A under the action of the key rate-limiting enzyme delta-aminolevulinic acid (ALA) synthase. The globin chains are synthesised by ribosomes in the cytosol. Haemoglobin synthesis only occurs in immature red blood cells.
There are three types of haemoglobin in normal adult blood: haemoglobin A, A2 and F:
– Normal adult haemoglobin (HbA) makes up about 96 – 98 % of total adult haemoglobin, and consists of two alpha (α) and two beta (β) globin chains. 
– Haemoglobin A2 (HbA2), a normal variant of adult haemoglobin, makes up about 1.5 – 3.5 % of total adult haemoglobin and consists of two α and two delta (δ) globin chains.
– Foetal haemoglobin is the main Hb in the later two-thirds of foetal life and in the newborn until approximately 12 weeks of age. Foetal haemoglobin has a higher affinity for oxygen than adult haemoglobin. 
Red cells are destroyed by macrophages in the liver and spleen after , 120 days. The haem group is split from the haemoglobin and converted to biliverdin and then bilirubin. The iron is conserved and recycled to plasma via transferrin or stored in macrophages as ferritin and haemosiderin. An increased rate of haemoglobin breakdown results in excess bilirubin and jaundice.

Atropine 500 mcg IV bolus should be administered if there are any adverse features or risk of asystole. If the reaction is not adequate, repeat the steps every 3 to 5 minutes up to a maximum dose of 3 mg. In the case of acute myocardial ischemia or myocardial infarction, atropine should be taken with caution since the increased heart rate may aggravate the ischemia or increase the size of the infarct.

The hookworm life cycle begins with the passage of eggs from an adult host into the stool. Hookworm eggs hatch in the soil to release larvae that mature into infective larvae. Infection is usually transmitted by larval penetration into human skin (duodenal infection may also be transmitted by the oral route). From the skin, larvae migrate into the blood vessels and are carried to the lungs, where they penetrate the pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed.

Delayed haemolytic transfusion reactions (DHTRs) commonly occurs 4-8 days after blood transfusion, but can occur up to a month after. Signs and symptoms include jaundice, fever, an inadequate rise in PCV, reticulocytosis, a positive antibody screen and a positive Direct Antiglobulin Test (Coombs test). DHTRs usually have a benign course and require no treatment but sometimes, life-threatening haemolysis with severe anaemia and renal failure can occur so haemoglobin levels and renal function should be monitored.

Acute haemolytic reaction aka immediate haemolytic transfusion reaction presents with fever, chills, pain at transfusion site, nausea, vomiting, dark urine and feeling of ‘impending doom’. Often, it occurs due to ABO incompatibility.

Febrile transfusion reaction presents with a 1 degree rise in temperature from baseline during transfusion. Patient may have chills and malaise. It is the most common transfusion reaction (1 in 8 transfusions) and is usually caused by cytokines released from leukocytes in transfused red cell or platelet components.

Transfusion-associated circulatory overload (TACO) presents as acute or worsening respiratory distress within 6 hours of transfusion of a large volume of blood. It is common in patients with diminished cardiac reserve or chronic anaemia. Elderly patients, infants and severely anaemic patients are particularly susceptible. Clinical features of TACO include: Acute respiratory distress, Tachycardia, Hypertension, Acute/worsening pulmonary oedema on chest X-ray. The BNP is usually raised to at least 1.5 times the pre-transfusion baseline.

Graft versus host disease(GVHD) is an immune mediated condition that arises from a complex interaction between donor and recipients adaptive immunity. It presents as dermatitis, hepatitis and enteritis developing within 100 days after stem cell or bone marrow transplant.

Adverse effects include:
Antimuscarinic effects: Dry mouth, Blurred vision, Constipation, Urinary retention, Sedation, Confusion
Cardiovascular effects: Heart block, Arrhythmias, Tachycardia, Postural hypotension, QT-interval prolongation, Hepatic impairment, Narrow-angle glaucoma

Multiple myeloma is a clonal abnormality affecting plasma cells in which there is an overproduction of functionless immunoglobulins. The most common patient complaint is bone pain, especially in the back and ribs. Anaemia and renal failure are common, along with hypercalcemia. Hypercalcemia may lead to an altered mental status, as in this case.

Chronic lymphocytic leukaemia occurs due to the overproduction of lymphocytes, usually B cells. CLL may present with an asymptomatic elevation of B cells. Patients are generally more than 50 years old and present with non-specific fatigue and weight loss symptoms.

There is no history of alcohol abuse in this case. Furthermore, patients with a history of alcohol abuse may have signs of liver failure, which are not present here.

Metastatic prostate cancer would most often cause lower backache as it metastasises first to the lumbar spine via the vertebral venous plexus.

A patient with Vitamin B12 deficiency would have anaemia, megaloblastic, hypersegmented neutrophils, and signs of peripheral neuropathy.

Conjunctivitis is the most common neonatal manifestation of Chlamydia trachomatis infection. The second commonest neonatal manifestation is pneumonia

Ophthalmia neonatorum refers to any conjunctivitis in the newborn period, irrespective of causative organism. Presently, chlamydia is the single most common cause, accounting for up to 40% of cases. Ophthalmia neonatorum caused by chlamydia typically presents 5 to 14 days after birth with unilateral or bilateral watery discharge that progressively becomes more copious and purulent. There is no associated risk of ulceration and perforation, and the eyes are less inflamed.

DIC is characterised by a widespread inappropriate intravascular deposition of fibrin with consumption of coagulation factors and platelets. This may occur as a consequence of many disorders that release procoagulant material into the circulation or cause widespread endothelial damage or platelet aggregation. Increased activity of thrombin in the circulation overwhelms its normal rate of removal by natural anticoagulants. In addition to causing increased deposition of fibrin in the microcirculation and widespread platelet aggregation to the vessels, intravascular thrombin formation interferes with fibrin polymerisation. Intense fibrinolysis is stimulated by thrombi on vascular walls and the release of fibrin degradation products again interferes with fibrin polymerisation. The combined action of thrombin and plasmin causes depletion of fibrinogen and all coagulation factors, compounded by thrombocytopaenia caused by platelet consumption.

The meningococcus is solely a human pathogen, and up to 50% of the population may carry meningococci in the nasopharynx. Factors that lead to invasion and production of disease include complex inter-relationships of genetic predisposition, host status, environmental conditions, and virulence of the organism.

Meningococcal disease is the most common infectious cause of death in childhood in developed countries. It presents as septicaemia, meningitis, or a combination. Septicaemia is the more dangerous presentation, especially with septic shock; meningitis is more likely to lead to neurodevelopmental sequelae. Classic features of septicaemia are a non-blanching rash in a feverish, ill child.

It is very seldom that potassium supplements are required with the small doses of diuretics given to treat hypertension. Potassium-sparing diuretics like spironolactone (rather than potassium supplements), are recommended for hypokalaemia prevention when diuretics are given to eliminate oedema, such as furosemide or the thiazides.

The causes of AKI can be divided into pre-renal, intrinsic renal and post-renal causes. Majority of AKI developing in the community is due to a pre-renal causes (90% of cases).

Pre-renal causes: Haemorrhage, severe vomiting or diarrhoea, burns, cardiac failure, liver cirrhosis, nephrotic syndrome, hypotension, severe cardiac failure, NSAIDs, COX-2 inhibitors, ACE inhibitors or ARBs, Abdominal aortic aneurysm, renal artery stenosis, hepatorenal syndrome,

Intrinsic (renal) causes:
Eclampsia, glomerulonephritis, thrombosis, haemolytic-uraemic syndrome, acute tubular necrosis (ATN), acute interstitial nephritis, drugs ( NSAIDs), infection or autoimmune diseases, vasculitis, polyarteritis nodosa, thrombotic microangiopathy, cholesterol emboli, renal vein thrombosis, malignant hypertension

Post-renal causes: Renal stones, Blood clot, Papillary necrosis, Urethral stricture, Prostatic hypertrophy or malignancy, Bladder tumour, Radiation fibrosis, Pelvic malignancy, Retroperitoneal fibrosis

The femoral nerve runs down the front of the leg from the pelvis. It gives the front of the thigh and a portion of the lower leg sensation.

Extension of the leg at the knee joint, flexion of the thigh at the hip are produced by muscles that is primarily innervated by the femoral nerve.