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.

A lesion at the optic chiasm will result in a bitemporal hemianopia.
A lesion of the optic nerve will result in ipsilateral monocular visual loss.
A lesion of the optic tract will result in a contralateral homonymous hemianopia.

The most common type of adult leukaemia is chronic lymphocytic leukaemia (CLL). It develops as a result of relatively mature lymphocytes clonally proliferating. The B-cell lineage accounts for approximately 95% of cases. CLL is primarily a disease of adult men, with men over the age of 50 accounting for more than 75% of CLL patients.

It is the most indolent form of chronic leukaemia, and it is frequently discovered by chance when blood counts are taken for other reasons, such as ‘well man’ screening tests. The patient may develop lymphadenopathy, hepatosplenomegaly, anaemia, and infections as the disease progresses.

The following are examples of CLL laboratory findings:
Clonal B cell lymphocytosis (diagnosed at greater than 5 x 109/l, but can reach 300 x 109/l)
In advanced disease, normocytic, normochromic anaemia is present.

Patients with autoimmune-related haemolytic anaemias have a positive direct antiglobulin test (DAT).

Although bone marrow aspiration is not always required, it can aid in the diagnosis of CLL. If there has been rapid lymph node enlargement, a lymph node biopsy is required to rule out Richter’s syndrome. This is the transition from low-grade lymphoma to high-grade lymphoma, which is characterised by fever, weight loss, and pain.

Although there is no cure for CLL, it can be managed with chemotherapy regimens that help patients live longer. Early treatment has no benefit, and the standard treatment for early disease is to watch and wait, with examinations and blood counts every 3 to 12 months. Chemotherapy is usually reserved for patients who have a disease that is active and causing symptoms.

The following is the overall prognosis for CLL:
1/3 will not require treatment and will live a long time.
1/3 will go through an indolent phase before the disease progresses.
1/3 of patients will have an aggressive disease that requires immediate treatment.

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.

The main function of the spinothalamic tract is to carry pain and temperature via the lateral part of the pathway and crude touch via the anterior part. The spinothalamic tract pathway is an imperative sensory pathway in human survival because it enables one to move away from noxious stimuli by carrying pain and temperature information from the skin to the thalamus where it is processed and transmitted to the primary sensory cortex. The primary sensory cortex communicates with the primary motor cortex, which lies close to it, to generate rapid movement in response to potentially harmful stimuli. Furthermore, the spinothalamic tract has a role in responding to pruritogens, causing us to itch. Interestingly, itching suppresses the spinothalamic tract neuron response to the histamine effect.

Lidocaine is a tertiary amide local anaesthetic and also a class IV antiarrhythmic.

Like other local anaesthetics, lidocaine works on the voltage-gated sodium ion channel on the nerve cell membranes. It works in the following steps:
1. diffuses through neural sheaths and the axonal membrane into the axoplasm
2. binds fast voltage-gated Na+ channels in the neuronal cell membrane and inactivates them
3. 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

The same principle applies to Lidocaine’s actions in the heart as it blocks the sodium channels in the conduction system and the myocardium. This raises the threshold for depolarizing, making it less likely for the heart to initiate or conduct any action potential that can cause arrhythmia.

Phenytoin is in the anticonvulsants class of drugs and is used in the management and treatment of the following:
1. epilepsy
2. generalized tonic-clonic seizures
3. complex partial seizures
4. status epilepticus.

It works by inactivating the voltage-gated sodium channels responsible for increasing the action potential. It is non-specific and targets almost all voltage-gated sodium channel subtypes. More specifically, phenytoin prevents seizures by inhibiting the positive feedback loop that results in neuronal propagation of high-frequency action potentials.

The brachial artery can be palpated in the antecubital fossa, medial to the tendon of the biceps brachii muscle.

End-organ damage (e.g. encephalopathy, intracranial haemorrhage, acute myocardial infarction or ischaemia, dissection, pulmonary oedema, nephropathy, eclampsia, papilledema, and/or angiopathic haemolytic anaemia) characterises a hypertensive emergency (also known as ‘accelerated hypertension’ or malignant hypertension’ It’s a life-threatening condition that necessitates rapid blood pressure reduction to avoid end-organ damage and a negative outcome.

Hypertensive encephalopathy is a syndrome that includes headaches, seizures, visual changes, and other neurologic symptoms in people who have high blood pressure. It is reversible if treated quickly, but it can progress to coma and death if not treated properly.

Any patient with suspected hypertensive encephalopathy should have an urgent CT scan to rule out an intracranial haemorrhage, as rapid blood pressure reduction could be dangerous in these circumstances.

The drug of choice is labetalol, which reduces blood pressure steadily and consistently without compromising cerebral blood flow.
An initial reduction of approximately 25% in mean arterial pressure (MAP) over an hour should be aimed for, followed by a further controlled MAP reduction over the next 24 hours. In patients who are unable to take beta-blockers, nicardipine can be used as a substitute.

Ketamine is the only anaesthetic agent available that has analgesic, hypnotic, and amnesic properties. When used correctly it is a very useful and versatile drug.
Ketamine acts by non-competitive antagonism of the NMDA receptor Ca2+ channel pore and also inhibits NMDA receptor activity by interaction with the phencyclidine binding site.
Ketamine can be used intravenously and intramuscularly. The intramuscular dose is 10 mg/kg, and when used by this route, it acts within 2-8 minutes and has a duration of action of 10-20 minutes. The intravenous dose is 1.5-2 mg/kg administered over a period of 60 seconds. When used intravenously, it acts within 30 seconds and has a duration of action of 5-10 minutes. Ketamine is also effective when administered orally, rectally, and nasally.
Ketamine causes tachycardia, an increase in blood pressure, central venous pressure, and cardiac output, secondary to an increase in sympathetic tone. Baroreceptor function is well maintained, and arrhythmias are uncommon.
The main disadvantage to the use of ketamine is the high incidence of hallucinations, nightmares, and other transient psychotic effects. These can be reduced by the co-administration of a benzodiazepine, such as diazepam or midazolam.
The main side effects of ketamine are:
Nausea and vomiting
Hypertension
Nystagmus
Diplopia
Rash

Haemoglobin is a 64.4 kd tetramer consisting of two pairs of globin polypeptide chains: one pair of alpha-like chains, and one pair of non-alpha chains. The chains are designated by Greek letters, which are used to describe the particular haemoglobin (e.g., Hb A is alpha2/beta2).

Two copies of the alpha-globin gene (HBA2, HBA1) are located on chromosome 16 along with the embryonic zeta genes (HBZ). There is no substitute for alpha globin in the formation of any of the normal haemoglobins (Hb) following birth (e.g., Hb A, Hb A2, and Hb F). Thus, absence any alpha globin, as seen when all 4 alpha-globin genes are inactive or deleted is incompatible with extrauterine life, except when extraordinary measures are taken.

A homotetramer of only alpha-globin chains is not thought to occur, but in the absence of alpha chains, beta and gamma homotetramers (HbH and Bart’s haemoglobin, respectively) can be found, although they lack cooperativity and function poorly in oxygen transport. The single beta-globin gene (HBB) resides on chromosome 11, within a gene cluster consisting of an embryonic beta-like gene, the epsilon gene (HBE1), the duplicated and nearly identical fetal, or gamma globin genes (HBG2, HBG1), and the poorly expressed delta-globin gene (HBD). A heme group, consisting of a single molecule of protoporphyrin IX co-ordinately bound to a single ferrous (Fe2+) ion, is linked covalently at a specific site to each globin chain. If the iron is oxidized to the ferric state (Fe3+), the protein is called methaemoglobin.

Alpha globin chains contain 141 amino acids (residues) while the beta-like chains contain 146 amino acids. Approximately 75 percent of haemoglobin is in the form of an alpha helix. The non helical stretches permit folding of the polypeptide upon itself. Individual residues can be assigned to one of eight helices (A-H) or to adjacent non helical stretches.

Heme iron is linked covalently to a histidine at the eighth residue of the F helix (His F8), at residue 87 of the alpha chain and residue 92 of the beta chain. Residues that have charged side groups, such as lysine, arginine, and glutamic acid, lie on the surface of the molecule in contact with the surrounding water solvent. Exposure of the hydrophilic (charged) amino acids to the aqueous milieu is an important determinant of the solubility of haemoglobin within the red blood cell and of the prevention of precipitation.

The haemoglobin tetramer is a globular molecule (5.0 x 5.4 x 6.4 nm) with a single axis of symmetry. The polypeptide chains are folded such that the four heme groups lie in clefts on the surface of the molecule equidistant from one another.

Non-Hodgkin’s lymphoma (NHL) refers to a group of lymphoproliferative malignancies (about 85% of B-cell and 15% of T or NK (natural killer) cell origin) with different behavioural patterns and treatment responses. This group of malignancies encompasses all types of lymphoma without Reed-Sternberg cells being present. The Reed-Sternberg cell is classically seen in Hodgkin’s lymphoma.
NHL is five times as common as Hodgkin’s lymphoma. 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 most common clinical features at presentation are:
Lymphadenopathy (typically asymmetrical and painless)
Weight loss
Fatigue
Night sweats
Hepatosplenomegaly
For clinical purposes, NHL is divided into three groups: indolent, high-grade, and lymphoblastic.
Indolent (low-grade) NHL:
The cells are relatively mature
Disease follows an indolent course without treatment
Often acceptable to follow a ‘watch and wait’ strategy
Local radiotherapy often effective
Relatively good prognosis with median survival of 10 years
High-grade NHL:
Cells are immature
Disease progresses rapidly without treatment
Significant number of patients can be cured with intensive combination chemotherapy regimens
Approximately 40% cure rate
Lymphoblastic NHL:
Cells are very immature and have a propensity to involve the CNS
Treatment and progression are similar to that of acute lymphoblastic leukaemia (ALL)

Darcy’s law states that flow through a tube is dependent on the pressure differences across the ends of the tube (P1 – P2) and the resistance to flow provided by the tube (R). Resistance is due to frictional forces and is determined by the length of the tube (L), the radius of the tube (r) and the viscosity of the fluid flowing down that tube (V). The radius of the tube has the largest effect on resistance and therefore flow – this explains why smaller gauge cannulas with larger diameters have a faster rate of flow. Increased viscosity, as seen in polycythemia, will slow the rate of blood flow through a vessel.

Gastric lipase, commonly known as LIPF, is an acidic lipase released by gastric chief cells, which are found deep within the stomach lining’s mucosal layer. It’s an enzymatic protein that’s in charge of fat digestion in the stomach.

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.

Malaria is an infectious disease transmitted by female of theAnophelesgenus of mosquito. It is a parasitic infection caused by the genusPlasmodium. Five species are recognized as causing disease in humans;Plasmodium falciparum,Plasmodium ovale,Plasmodium vivax,Plasmodium malariaeandPlasmodium knowlesi.
The classic symptom of malaria is the malarial paroxysm, a cyclical occurrence of a cold phase, where the patient experiences intense chills, a hot stage, where the patient feels extremely hot and finally a sweating stage, where the fever declines and the patient sweats profusely. On examination the patient may show signs of anaemia, jaundice and have hepatosplenomegaly without evidence of lymphadenopathy.

Plasmodium falciparum is the most serious form and is responsible for most deaths. Severe or complicated malaria is suggested by the presence of impaired consciousness, seizures, hypoglycaemia, anaemia, renal impairment, respiratory distress and spontaneous bleeding.
Plasmodium falciparum is the most likely type in this case in view of the presentation.
Haemoglobinuria and renal failure following treatment is suggestive of blackwater fever, which is caused byPlasmodium falciparum. An autoimmune reaction between the parasite and quinine causes haemolysis, haemoglobinuria, jaundice and renal failure. This can be fatal.
The benign malarias: P.vivax, P. malariae and P.ovale are usually treated with chloroquine. A course of primaquine is also required in P.vivax and P.ovale infection. Artesunate is the drug treatment of choice for Plasmodium falciparum malaria. Quinine can still be used where artesunate is not available. Often combination therapy with drugs such as doxycycline or fansidar is also required.

A risk ratio of 1 indicates no difference in risk between groups.If the risk ratio of an event is > 1, the rate of that event is increased in the exposed group compared to the control group.If the risk ratio is < 1, the rate of that event is reduced in the exposed group compared to the control group.

Acetaminophen is an acetanilide derivative and is a widely used non-prescription analgesic and antipyretic medication for mild-to-moderate pain and fever.

The route of elimination: Paracetamol is metabolised extensively in the liver and excreted in the urine mainly as inactive glucuronide and sulfate conjugates, <5% is excreted as free (unconjugated) acetaminophen, and >90% of the dose administered is excreted within 24 hours.

It is thought to work by selectively inhibiting COX-1 receptors in the brain and spinal cord: It is categorized by the FDA as an NSAID 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.

Toxicity is primarily due to glutathione production: Acetaminophen metabolism by the CYP2E1 pathway releases a toxic metabolite known as N-acetyl-p-benzoquinoneimine (NAPQI). NAPQI primarily contributes to the toxic effects of acetaminophen. NAPQI is an intermediate metabolite that is further metabolized by fast conjugation with glutathione. The conjugated metabolite is then excreted in the urine as mercapturic acid. High doses of acetaminophen (overdoses) can lead to hepatic necrosis due to depleting glutathione and high binding levels of reactive metabolite (NAPQI) to important parts of liver cells.

Acetaminophen can be administered orally, rectally, or intravenously. It is predominantly metabolized in the liver, and the elimination half-life is 1-3 hours after a therapeutic dose. But maybe greater than 12 hours after an overdose.

It is primarily metabolized via the cytochrome p450 enzyme system: It is predominantly metabolized in the liver by three main metabolic pathways:
1. Glucuronidation (45-55%)
2. Sulphate conjugation (30-35%)
3. N-hydroxylation via the hepatic cytochrome p450 enzyme system (10-15%)

Acute mastoiditis is a complication (rare) of acute otitis media (AOM) and the commonest causative organism is Streptococcus pneumoniae.

Generally, acute mastoiditis presents with:
Pyrexia
Recent history of AOM
Mastoid swelling and erythema
Otalgia
Otorrhoea and perforation of tympanic membrane
Post-auricular pain
Protrusion of the ears

CML is a myeloproliferative disorder characterised by an abnormal pluripotent haemopoietic stem cell. A cytogenetic abnormality known as the Philadelphia chromosome, which results from a reciprocal translocation between the long arms of chromosomes 9 and 22, causes more than 80% of cases of CML.

CML is a disease that develops slowly over several years. This is known as the ‘chronic stage.’ This stage is usually asymptomatic, and 90 percent of patients are diagnosed at this point, with the disease being discovered frequently as a result of a routine blood test. During this stage, the bone marrow contains less than 10% immature white cells (blasts).

When CML cells expand, symptoms typically begin to appear. The ‘accelerated stage’ is what it’s called. Approximately 10% of people are diagnosed at this point. During this stage, between 10% and 30% of blood cells in the bone marrow are blasts. During this stage, common clinical features include:
Fatigue and exhaustion
Night sweats and fever
Distension of the abdomen
Pain in the left upper quadrant (splenic infarction)
Splenomegaly (commonest examination finding)
Hepatomegaly
Bruising is simple.
Gout is a type of arthritis that affects (rapid cell turnover)
Hyperviscosity is a condition in which the viscosity of (CVA, priapism)
A small percentage of patients experience a ‘blast crisis’ (blast stage). More than 30% of the blood cells in the bone marrow are immature blast cells at this stage. Patients with severe constitutional symptoms (fever, weight loss, bone pain), infections, and bleeding diathesis typically present at this stage.

In CML, laboratory findings include:
White cell count is abnormally high (often greater than 100 x 109/l).
Increased number of immature leukocytes causes a left shift.
Anaemia that is mild to moderately normochromic and normocytic.
Platelets can be low, normal, or elevated, and the Philadelphia chromosome can be found in > 80% of patients.
Serum uric acid and ALP levels are frequently elevated.
Tyrosine kinase inhibitors (TKIs), such as imatinib and dasatinib, are the current mainstay of CML treatment.
Allogenic bone marrow transplantation is now only used in cases where TKIs have failed to work.

This patient has Nephrotic Syndrome confirmed by the presence of 1. Heavy proteinuria (greater than 3-3.5 g/24 hours)
2. Hypoalbuminemia (serum albumin < 25 g/L)
3. Generalised oedema (often with periorbital involvement)
4. Severe hyperlipidaemia (total cholesterol is often > 10 mmol/L).

Focal Segmental Glomerulosclerosis will be the most likely answer as it is the most common cause of Nephrotic Syndrome in African American adults.

Minimal change disease is the most common cause of nephrotic syndrome in children.

Membranous glomerulonephritis is the most common cause of Nephrotic Syndrome in Caucasian adults.

In IgA nephropathy, patients will complain of cola-coloured urine.

Mesangiocapillary glomerulonephritis presents with features of Nephritic Syndrome.

Etomidate causes the least cardiovascular depression of the intravenous induction agents, with only a small reduction in the cardiac output and blood pressure. In the past, etomidate was widely used to induce anaesthesia in the shocked, elderly or cardiovascularly unstable patient. However, more recently it has become less popular as a single induction dose blocks the normal stress-induced increase in adrenal cortisol production for 4 – 8 hours, and up to 24 hours in elderly and debilitated patients. Although no increase in mortality has been identified following a single dose during induction of anaesthesia, the use of etomidate has declined due to a perceived potential morbidity.

Some potential symptoms of frontal lobe damage can include loss of movement, either partial or complete, on the opposite side of the body.

In the patient’s case, it is a result of motor cortex damage on the right side since her left side of the body is affected. The conjugate eye deviation symptom towards the side of the lesion is a result of damage to the frontal eye field.

Calcium deficiency (low Ca2+ diet or hypocalcemia) activates 1-alpha-hydroxylase in the cells of the renal proximal tubule which catalyses the conversion of vitamin D to its active form, 1,25-dihydroxycholecalciferol. Increased parathyroid hormone (PTH) and hypophosphatemia also stimulate the enzyme. Chronic renal failure is associated with a constellation of bone diseases, including osteomalacia caused by failure of the diseased renal tissue to produce the active form of vitamin D.

Pronator quadratus is a deep-seated, short, flat, and quadrilateral muscle with fibres running in a parallel direction.

It arises from the oblique ridge on the anterior surface of the distal fourth of the Ulna. It is inserted in lateral border and anterior surface of the distal fourth of the radius. It is innervated by the anterior interosseous nerve, a branch of the median nerve (C8-T1). It is vascularized by the anterior interosseous artery.

The action of the pronator quadratus muscle along with the pronator teres result in the pronation of the radioulnar joint. Contraction of this muscle pulls the distal end of the radius over the ulna, resulting in the pronation of the radioulnar joint

There is no evidence to support the use of nebulized magnesium sulphate in the treatment of adults at this time.

In adults with acute asthma, the following medication dosages are recommended:
By using an oxygen-driven nebuliser, you can get 5 milligrams of salbutamol.
500 mcg ipratropium bromide in an oxygen-driven nebuliser
Oral prednisolone 40-50 mg
100 mg hydrocortisone intravenous
1.2-2 g magnesium sulphate IV over 20 minutes
When inhaled treatment is ineffective, intravenous salbutamol (250 mcg IV slowly) may be explored (e.g. a patient receiving bag-mask ventilation).

Following senior counsel, current ALS recommendations propose that IV aminophylline be explored in severe or life-threatening asthma. If utilized, a loading dose of 5 mg/kg should be administered over 20 minutes, then a 500-700 mcg/kg/hour infusion should be given. To avoid toxicity, serum theophylline levels should be kept below 20 mcg/ml.

Digestion of dietary protein begins in the stomach where pepsin hydrolyses protein to polypeptides, and continues in the duodenum where pancreatic proteases (trypsin and chymotrypsin) continue the process of hydrolysis forming oligopeptides. These are further broken down into small peptides and amino acids by pancreatic carboxypeptidases and aminopeptidases located on luminal membrane epithelial cells. Free amino acids are absorbed across the apical membrane by secondary active transport coupled with Na+transport into the cell. Amino acids cross the basal membrane into the capillaries by facilitated diffusion.

Throughout the airways, there are irritant receptors which are located between epithelial cells which are made of rapidly adapting afferent myelinated fibres in the vagus nerve. A cough is as a result of receptor stimulation located in the trachea, hyperpnoea is as a result of receptor stimulation in the lower airway. Stimulation may also result in reflex bronchial and laryngeal constriction. Many factors can stimulate irritant receptors. These include irritant gases, smoke and dust, airway deformation, pulmonary congestion, rapid inflation/deflation and inflammation. Deep augmented breaths or sighs seen every 5 – 20 minutes at rest are due to stimulation of these irritant receptors. This reverses the slow lung collapse that occurs in quiet breathing.

Clostridium difficile, a Gram-positive, anaerobic, spore forming bacteria is present in the gut of approximately 3% of healthy adults (2012 UK HPA estimates). Following use of broad spectrum antibiotics, which alter normal gut flora, Clostridium difficile associated diarrhoea (CDAD) occurs.

About 80% of Clostridium difficile infections are seen in people over the age of 65 and its main clinical features are:
Abdominal cramps, severe bloody and/or watery diarrhoea, offensive smelling diarrhoea, and fever.

Antibiotics with aminoglycosides, such as gentamicin, bind to the 30S subunit of the bacterial ribosome and prevent aminoacyl-tRNA from binding, preventing protein synthesis.

They also cause mRNA misreading, resulting in the production of non-functional proteins. This last mechanism is unique to aminoglycosides, and it may explain why they are bactericidal rather than bacteriostatic, as other protein synthesis inhibitors are.

Patients with myasthenia gravis should avoid aminoglycosides since they can disrupt neuromuscular transmission. They cross the placenta and are linked to poisoning of the 8th cranial nerve in the foetus, as well as permanent bilateral deafness.

It is possible that they will cause deafness, although this is not a contraindication. In individuals with renal impairment, serum aminoglycoside concentrations should be closely monitored, but this is still not considered a contraindication.