Campylobacter jejuni is the primary human pathogen, typically causing dysentery (bloody diarrhoea illness) following ingestion of contaminated meat, especially poultry. Infection is typically self-limiting and does not require antibiotic therapy. Campylobacter gastroenteritis is associated with the immune-mediated complications of Guillain-Barre syndrome, reactive arthritis and Reiter’s syndrome.

High-dose NSAIDs are the first-line treatment for acute gout. In the absence of any contraindications, Naproxen 750 mg as a stat dose followed by 250 mg TDS is commonly used.

Aspirin is contraindicated in gout. It reduces the urinary clearance of urate and also interferes with the action of uricosuric agents.

Colchicine is preferred in patients with heart failure or in those who are intolerant of NSAIDs. It is as effective as NSAIDs in relieving acute attacks.

Colchicine acts on the neutrophils, binding to tubulin to prevent neutrophil migration into the joint. Where Allopurinol is not tolerated, it has a role in prophylactic treatment of gout.

Allopurinol should not be started in the acute phase of gout as it increases the severity and duration of symptoms. It is used as a prophylaxis in preventing future attacks and acts by reducing serum uric acid levels.

Mast cells play a central role in the response to allergen challenges. The activation of mast cells results in both an early and a delayed phase of inflammation. Mast cells have been implicated in both physiologic and pathogenic processes. Mast cells are important in defence against some bacteria and viruses and contribute to defence against parasites. They are key effector cells in both innate and acquired immunity and are capable of inducing and amplifying both types of responses. Specifically, mast cells are capable of detecting microbial products through surface pattern recognition receptors, and they are involved in the recruitment of other leukocytes, containment of bacterial infections, and tissue repair.

The inflammatory phase of healing is sometimes called the lag phase because wound strength does not begin to return immediately. The inflammatory phase is completed within three days except in the presence of infection or other factors associated with impaired wound healing. Mononuclear leukocytes accumulate and are transformed into macrophages. The maturation of blood-derived monocytes into macrophages is heralded by several events, including secretion of vimentin, which is a structural filament protein involved in wound healing.

NSAIDs are associated with serious gastrointestinal irritation and drug-induced ulcers.

Among the NSAIDs included in the choices, ibuprofen has the lowest risk.

Piroxicam, ketoprofen, and ketorolac trometamol are associated with the highest risk of serious upper gastrointestinal side effects.

Indomethacin, diclofenac, and naproxen are associated with an intermediate risk of serious upper gastrointestinal side effects.

HIV mainly infects CD4+ T helper cells. Viral replication results in progressive T-cell depletion and impaired cell-mediated immunity with subsequent secondary opportunistic infections and increased risk of malignancy. B-cell function is also reduced as a result of lack of T-cell stimulation.
HIV is not a notifiable disease.

Fusidic acid is a narrow spectrum antibiotic used for staphylococcal infections, primarily topically for minor staphylococcal skin (impetigo) or eye infection. It is sometimes used orally for penicillin-resistant staphylococcal infection, including osteomyelitis or endocarditis, in combination with other antibacterials.

Central cord syndrome is the most common type of incomplete cord injury and almost always occurs due to a traumatic injury. It results in motor deficits that are worse in the upper extremities as compared to the lower extremities. It may also cause bladder dysfunction (retention) and variable sensory deficits below the level of injury.

The majority of these patients will be older and present with symptoms after a fall with hyperextension of their neck. On examination, patients will have more significant strength impairments in the upper extremities (especially the hands) compared to the lower extremities. Patients often complain of sensory deficits below the level of injury, but this is variable. Pain and temperature sensations are typically affected, but the sensation of light touch can also be impaired. The most common sensory deficits are in a cape-like distribution across their upper back and down their posterior upper extremities. They will often have neck pain at the site of spinal cord impingement.

Bladder dysfunction (most commonly urinary retention) and priapism can also be signs of upper motor neuron dysfunction. The sacral sensation is usually preserved, but the clinician should assess the rectal tone to evaluate the severity of the compression.

Cortisol levels fluctuate throughout the day, with the greatest levels occurring around 0900 hours and the lowest occurring at 2400 hrs during sleep.

The diurnal swing of cortisol levels is lost in Cushing’s syndrome, and levels are greater throughout the 24-hour period. In the morning, levels may be normal, but they may be high at night-time, when they are generally repressed.

HBsAg is the serological hallmark of HBV infection. After an acute exposure to HBV, HBsAg appears in serum within 1 to 10 weeks. Persistence of this marker for more than 6 months implies chronic HBV infection.

Anti-HBs is known as a neutralizing antibody, and confers long-term immunity. In patients with acquired immunity through vaccination, anti-HBs is the only serological marker detected in serum.

HBcAg is an intracellular presence in infected hepatocyte, thus it is not identified in the serum. During acute infection, anti-HBc IgM and IgG emerges 1–2 weeks after the presence of HBsAg along with raised serum aminotransferase and symptoms. After 6 months of acute infection, anti-HBc IgM wears off. Anti-HBc IgG continues to detect in both patients with resolved HBV infection and chronic hepatitis B.

Hepatitis D virus, also known as the delta hepatitis virus, is a defective ssRNA virus that requires HBV for replication. The infection can occur in one of two clinical forms, co-infection or superinfection. In a co-infection, the patient is simultaneously infected with HBV and HDV. In a superinfection, an HDV infection develops in a patient with a chronic HBV infection.

Non-specific signs of anaemia include:
1. pallor of mucous membranes or nail beds (if Hb < 90 g/L),
2. tachycardia
3. bounding pulse
4. wide pulse pressure
5. flow murmurs
6. cardiomegaly
7. signs of congestive cardiac failure (in severe cases)

Immunosuppressants like corticosteroids may be an important risk factor for developing tuberculosis.

All of the other statements are true.

Endocarditis is infective or non infective inflammation (marantic endocarditis) of the inner layer of the heart and it often involves the heart valves.

Risk factors include:
Prosthetic heart valves
Congenital heart defects
Prior history of endocarditis
Rheumatic fever
Illicit intravenous drug use

In the presentation of endocarditis, the following triad is often quoted:
Persistent fever
Embolic phenomena
New or changing murmur

A combination of vancomycin, rifampicin and gentamicin is advised if the patient has a cardiac prostheses, is penicillin allergic, or if methicillin-resistant Staphylococcus aureus (MRSA) is suspected. In this case the patient has a prosthetic valve making this the most appropriate initial treatment regimen.

Flucloxacillin and gentamicin are current recommended by NICE and the BNF for the initial ‘blind’ therapy in endocarditis. This patient has prostheses and this is not the most appropriate initial treatment regimen.

Other features that may be present include heart failure, splenomegaly, finger clubbing, renal features (haematuria, proteinuria, nephritis), and vasculitic features (splinter haemorrhages, Osler’s nodes, Janeway lesions, Roth’s spots).

An ambulatory blood pressure reading of >150/95 is classified as stage 2 hypertension, according to the NICE care pathway for hypertension, and the patient should be treated with an antihypertensive drug.

A calcium-channel blocker, such as amlodipine, would be the most appropriate medication for a 48-year-old Afro-Caribbean man.

An ACE inhibitor, such as ramipril, or a low-cost angiotensin-II receptor blocker (ARB), such as losartan, would be the most appropriate medication for a 48-year-old Caucasian man.

A deficiency of aldosterone, as seen in adrenal insufficiency, can result in hyponatraemia and hyperkalaemia.

Hepatitis A usually doesn’t pose a special risk to a pregnant woman or her baby. Maternal infection doesn’t result in birth defects, and a mother typically doesn’t transmit the infection to her baby. HAV is almost always transmitted by the faecal-oral route and is usually acquired through close personal contact or via contaminated food.

When a woman has chickenpox in the first 20 weeks of pregnancy, there is a 1 in 50 chance for the baby to develop a set of birth defects. This is called the congenital varicella syndrome. It includes scars, defects of muscle and bone, malformed and paralyzed limbs, small head size, blindness, seizures, and intellectual disability.

TORCH Syndrome refers to infection of a developing foetus or newborn by any of a group of infectious agents. “TORCH” is an acronym meaning (T)toxoplasmosis, (O)ther Agents, (R)ubella (also known as German Measles), (C)ytomegalovirus, and (H)erpes Simplex.
Infection with any of these agents may cause a constellation of similar symptoms in affected newborns. These may include fever; difficulties feeding; small areas of bleeding under the skin, causing the appearance of small reddish or purplish spots; enlargement of the liver and spleen (hepatosplenomegaly); yellowish discoloration of the skin, whites of the eyes, and mucous membranes (jaundice); hearing impairment; abnormalities of the eyes; and other symptoms and findings.

Treatment should be commenced with antibiotics immediately before laboratory confirmation due to the potentially life-threatening nature of the disease.

In a hospital setting, 2g of IV ceftriaxone (80 mg/kg for a child) or IV cefotaxime (2 g adult; 80 mg/kg child) are the drugs of choice.
In the prehospital setting, IM benzylpenicillin can be given as an alternative.

Doxycycline may be used first line for chlamydia, pelvic inflammatory disease (with metronidazole and ceftriaxone), acute bacterial sinusitis, exacerbation of chronic bronchitis, moderate-severity community acquired pneumonia and high-severity community acquired pneumonia (with benzylpenicillin).

Diazepam boosts GABA’s effects, giving it sedative, hypnotic, anxiolytic, anticonvulsant, and muscle-relaxing properties. It can be administered orally, rectally, or intravenously.

With a half-life of 20-100 hours, it is a long-acting benzodiazepine. Midazolam, oxazepam, and alprazolam are examples of short-acting benzodiazepines with a half-life of less than 12 hours (Xanax).

If used in the presence of hepatic impairment, benzodiazepines can cause coma. If treatment is necessary, benzodiazepines with shorter half-lives should be used in lower doses. Diazepam is a sedative that crosses into breast milk and should be avoided by breastfeeding mothers.

Cardiac myocyte contraction is not dependent on an external nerve supply but instead the heart generates its own rhythm, demonstrating inherent rhythmicity. The heartbeat is initiated by spontaneous depolarisation of the sinoatrial node (SAN), a region of specialised myocytes in the right atrium close to the coronary sinus, at a rate of 100-110 beats/min. This intrinsic rhythm is primarily influenced by autonomic nerves, with vagal influences being dominant over sympathetic influences at rest. This vagal tone reduces the resting heart rate down to 60-80 beats/min. To increase heart rate, the autonomic nervous system increases sympathetic outflow to the SAN, with concurrent inhibition of vagal tone. These changes mean the pacemaker potential more rapidly reaches the threshold for action potential generation.

CLL (chronic lymphocytic leukaemia) is the most common type of chronic lymphoid leukaemia, with a peak incidence between the ages of 60 and 80. It is the most common type of leukaemia in Europe and the United States, but it is less common elsewhere.

The CLL tumour cell is a mature B-cell with low immunoglobulin surface expression (IgM or IgD). The average age at diagnosis is 72 years, with only 15% of cases occurring before the age of 50.

The male-to-female ratio is about 2:1. Over 80% of cases are identified by the results of a routine blood test, which is usually performed for another reason.

Lymphocytic anaemia, thrombocytopenia, and normochromic normocytic anaemia are common laboratory findings. Aspiration of bone marrow reveals up to 95% lymphocytic replacement of normal marrow elements.

Newborn babies have a higher concentration of red blood cells with shorter lifespan leading to higher bilirubin levels than in adults. This condition is short-lived and harmless but with potential serious causes that need to be assessed for if present.

The most obvious physical sign of jaundice is a yellow discolouration of the sclera, skin and mucous membranes. At a bilirubin level of 35 μmol/L or higher, the eye is affected. The bilirubin level will need to be higher than 255 μmol/L for the feet and extremities to be affected.

Mannitol is an osmotic diuretic that can be used to treat cerebral oedema and raised intraocular pressure. Mannitol is a low molecular weight compound and is, therefore, freely filtered at the glomerulus and is not reabsorbed. It, therefore, increases the osmolality of the glomerular filtrate and tubular fluid, increasing urinary volume by an osmotic effect. It also does not cross the blood-brain-barrier (BBB).

The primary functions of the Broca area are both language production and comprehension. While the exact role in the production is still unclear, many believe that it directly impacts the motor movements to allow for speech. Although originally thought to only aid in speech production, lesions in the area can rarely be related to impairments in the comprehension of language. Different regions of the Broca area specialize in various aspects of comprehension. The anterior portion helps with semantics, or word meaning, while the posterior is associated with phonology, or how words sound. The Broca area is also necessary for language repetition, gesture production, sentence grammar and fluidity, and the interpretation of others’ actions.

Broca’s aphasia is a non-fluent aphasia in which the output of spontaneous speech is markedly diminished and there is a loss of normal grammatical structure. Specifically, small linking words, conjunctions, such as and, or, and but, and the use of prepositions are lost. Patients may exhibit interjectional speech where there is a long latency, and the words that are expressed are produced as if under pressure. The ability to repeat phrases is also impaired in patients with Broca’s aphasia. Despite these impairments, the words that are produced are often intelligible and contextually correct. In pure Broca’s aphasia, comprehension is intact.

Damage to the C5 and C6 nerve roots causes Erb’s palsy.

The spinal accessory nerve (CN XI) innervates the trapezius muscle, thus you would not expect this muscle to be impacted.

The trapezius is a muscle that runs from the base of the neck across the shoulders and into the centre of the back.

The lateral pontine syndrome occurs due to occlusion of perforating branches of the basilar and anterior inferior cerebellar (AICA) arteries. It is also known as Marie-Foix syndrome or Marie-Foix-Alajouanine syndrome. It is considered one of the brainstem stroke syndromes of the lateral aspect of the pons.

It is characterized by ipsilateral limb ataxia, loss of pain and temperature sensation of the face, facial weakness, hearing loss, vertigo and nystagmus, hemiplegia/hemiparesis, and loss of pain and temperature sensation.

Infectious mononucleosis can be diagnosed using specific EBV antibodies and a variety of unrelated non-EBV heterophile antibodies.

Heterophile antibodies:
About 70-90% of patients with EBV infectious mononucleosis produce antibodies against an antigen produced in one species that react against antigens from other species called heterophile antibodies. False positives can be seen with rubella, hepatitis, SLE, malaria, toxoplasmosis, lymphoma and leukaemia.

These antibodies can be detected by two main screening tests:
The monospot test uses horse red blood cells. It agglutinates in the presence of heterophile antibodies.
Paul-Bunnell test uses sheep red blood cells. The blood agglutinates in the presence of heterophile antibodies.

EBV-specific antibodies:
Patients can remain heterophile-negative after six weeks and are then considered to be heterophile-negative and should be tested for EBV-specific antibodies. EBV-specific antibodies test are helpful if a false positive heterophile antibody test is suspected.
The indirect Coombs test is used to detect in-vitro antibody-antigen reactions. It is typically used in antenatal antibody screening and in preparation for blood transfusion.
Heterophile antibody tests are generally not positive in the incubation period of infectious mononucleosis (4-6 weeks) before the onset of symptoms.

PTH is synthesised and released from the chief cells of the four parathyroid glands located behind the thyroid gland.
It is a polypeptide containing 84 amino acids and it controls free calcium in the body.

The following stimuli causes release of PTH:
Increased plasma phosphate concentration
Decreased plasma calcium concentration

PTH release is inhibited by:
Normal or increased plasma calcium concentration
Hypomagnesaemia

The main actions of PTH 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 DVLA sends a detailed information sheet about their licence and driving to all drivers with diabetes mellitus. The primary danger of driving while diabetic is hypoglycaemia.

The DVLA must be notified of the following diabetic patients:
All of the drivers are on insulin. (Licenses are being reviewed more frequently.)
Those who are at high risk of hypoglycaemia and have had more than one episode of severe hypoglycaemia in the previous year. (Severe hypoglycaemia is defined as requiring the assistance of another person to manage.)
Those who are unaware of their hypoglycaemia
Anyone who has ever been in a car accident due to hypoglycaemia
Anyone with diabetic retinopathy who needs laser treatment (to both eyes or to a second eye if sight only in one eye)
Patients with diabetes complications that impair their ability to drive.

To drive, drivers with insulin-treated diabetes must meet the following requirements:
They need to be aware of hypoglycaemia.
They must not have had more than one episode of hypoglycaemia in the previous 12 months that necessitated the assistance of another person.
They must check their blood glucose levels no later than 2 hours before the first journey.
While driving, they must check their blood glucose levels every two hours.
The visual acuity and visual field standards must be met.

Any significant changes in their condition must be reported to the DVLA. Furthermore, on days when they are not driving, group 2 licence holders must test their blood glucose twice daily using a metre that can store three months’ worth of readings.

In addition to this advice, the DVLA also offers the following advice to diabetic patients:
When taking tablets that have the potential to cause hypoglycaemia (such as sulfonylureas and glinides), monitoring may be necessary if there has been more than one episode of severe hypoglycaemia.
Drivers must show good control and be able to recognise hypoglycaemia.
Verify that your vision meets the required standard.

If a patient feels hypoglycaemic or has a blood glucose level of less than 4.0 mmol/L, they should not drive. Driving should not be resumed until blood glucose levels have returned to normal, which should take 45 minutes.

If there are any warning signs, patients should carry rapidly absorbed sugar in their vehicle and stop, turn off the ignition, and eat it.

If resuscitation is required, a card stating which medications they are taking should be carried.

If hypoglycaemia causes an accident, a diabetic driver may be charged with driving under the influence of drugs.

The following are the NICE guidelines on the management of bacterial conjunctivitis:
– Infective conjunctivitis is a self-limiting illness that usually settles without treatment within 1-2 weeks. If symptoms persist for longer than two weeks they should return for review.
– Seek medical attention urgently if marked eye pain or photophobia, loss of visual acuity, or marked redness of the eye develop.
– Remove contact lenses, if worn, until all symptoms and signs of infection have completely resolved and any treatment has been completed for 24 hours.
– Lubricant eye drops may reduce eye discomfort; these are available over the counter, as well as on prescription.
– Clean away infected secretions from eyelids and lashes with cotton wool soaked in water.
– Wash hands regularly, particularly after touching the eyes.
– Avoid sharing pillows and towels.
– It is not necessary to exclude a child from school or childcare if they have infective conjunctivitis, as mild infectious illnesses should not interrupt school attendance. An exception would be if there is an outbreak of infective conjunctivitis, when advice should be sought from the Health Protection Agency by the school.
– Adults who work in close contact with others, or with vulnerable patients, should avoid such contact until the discharge has settled.