The first line treatment for acute gout includes NSAIDs like diclofenac, indomethacin or naproxen. In patients in whom NSAIDs are contraindicated, not tolerated or ineffective, colchicine is an alternative. In those who cannot tolerate or who are resistant to NSAIDs and colchicine, oral or parenteral corticosteroids are an effective alternative. In acute monoarticular gout, intra-articular injection of a corticosteroid can be used occasionally. In acute gout. allopurinol is not used in the actual treatment, but its use should be continued during an acute attack if the patient is already established on long term therapy.

Parathyroid hormone (PTH) is a polypeptide containing 84 amino acids. It is the principal controller of free calcium in the body.
The main actions of parathyroid hormone are:
Increases plasma calcium concentration
Decreases plasma phosphate concentration
Increases osteoclastic activity (increasing calcium and phosphate resorption from bone)
Increases renal tubular reabsorption of calcium
Decreases renal phosphate reabsorption
Increases renal conversion of 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol (via stimulation of 1-alpha hydroxylase)
Increases calcium and phosphate absorption in the small intestine (indirectly via increased 1,25-dihydroxycholecalciferol)

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

The NICE guidelines for pregnant women with lower UTIs are:
1. Prescribe an antibiotic immediately, taking into account the previous urine culture and susceptibility results or avoiding past antibiotics that may have caused resistance
2. Obtain a midstream urine sample before starting antibiotics and send for urine culture and susceptibility
– Review the choice of antibiotic when the results are available
– change the antibiotic according to susceptibility results if the bacteria are resistant, using a narrow-spectrum antibiotic wherever possible

The first choice of antibiotics for pregnant women aged 12 years and over is:
1. Nitrofurantoin
100 mg modified-release PO BD for 3 days – if eGFR >45 ml/minute

The second-choice (no improvement in lower UTI symptoms on first-choice for at least 48 hours, or when first-choice is not suitable) are:
1. Amoxicillin
500 mg PO TDS for seven days (ONLY if culture results available and susceptible)
2. Cefalexin
500 mg BD for seven days
Alternative second-choices – consult local microbiologist, choose antibiotics based on culture and sensitivity results

Aminophylline has the following properties:
Phosphodiesterase inhibitor that increases intracellular cAMP and relaxes smooth muscle in the bronchial airways and pulmonary blood vessels.
Mast cell stabilization is achieved by using a non-selective adenosine receptor antagonist.

Lidocaine is a class 1B antidysrhythmic; combines with fast Na channels and thereby inhibits recovery after repolarization, resulting in decreasing myocardial excitability and conduction velocity. However, in ischaemic areas, where anoxia causes depolarisation and arrhythmogenic activity, many Na+ channels are inactivated and therefore susceptible to lidocaine.

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)

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.

Grey baby syndrome is a rare but causes significant adverse effect caused by the build-up of chloramphenicol in neonates (particularly preterm babies).

The following are the main characteristics of ‘grey baby syndrome’:

Skin that is ashy grey in colour.
Feeding problems
Vomiting
Cyanosis
Hypotension
Hypothermia
Hypotonia
Collapse of the cardiovascular system
Distension of the abdomen
trouble breathing