Tuberculosis is an infection caused by the microorganism Mycobacterium tuberculosis. TB can affect any organ system in the body, but it most commonly affects the lungs, followed by the lymph nodes.

Option Tuberculosis is spread by the faecal-oral route: It is spread by inhalation of droplet nuclei.

There are different methods to diagnose a tuberculosis infection.
1) Direct Microscopy: The organisms are visualised using Ziehl-Neelsen or Auramine staining. This is the quickest method to establish a diagnosis and start treatment.
2) Culture: M. tuberculosis can be grown on Lowenstein-Jensen or Ogawa mediums, but it can take up to 8 weeks; therefore, ZN staining is also performed to start treatment immediately.

Option There are several types of vaccine currently available: The BCG vaccine is the only vaccine approved to prevent TB and is administered at birth.

Option Miliary tuberculosis refers to tuberculosis that affects the spine: Miliary tuberculosis refers to a tuberculosis infection disseminated throughout the body’s organ systems via the blood or lymphatics. Pott’s disease is extrapulmonary TB that affects the spine. It usually affects the lower thoracic and upper lumbar regions.

Option A Ghon focus typically appears at the apex of a lung: The Ghon focus is a primary sign of TB that forms in the lung of previously unaffected patients. It typically occurs in the mid or lower zones of the lung.

About half of meningococcal disease occurs in children aged less than five years, and babies are at the highest risk because their immune systems have not yet fully developed. There is a second, smaller increase in risk for older adolescents, mainly for social and behavioural reasons. Infection is most common in winter months. Antibiotics should be given as soon as the diagnosis is suspected (ideally cultures should be performed first but this should not delay treatment), and ceftriaxone/cefuroxime is the first line antibiotic. Only healthcare workers who have been directly exposed to large particle droplets/secretions from the respiratory tract of the index case should receive prophylaxis.

Fenestrated capillaries, found in renal glomeruli, endocrine glands and intestinal villi, are more permeable than continuous capillaries with less tight junctions, and the endothelial cells are also punctured by pores which allow large amounts of fluids or metabolites to pass.

In the thick ascending limb is the part of the loop of Henle in which there is active reabsorption of Na+and Cl- ions from the tubular fluid. This occurs via the Na+/K+/2Cl-symporter on the apical membrane.
This mechanism is by:
1. Na+ions are transported across the basolateral membrane by Na+pumps and the Cl-ions by diffusion.
2. K+leaks back into the tubular fluid via apical ROMK K+channels which creates a positive charge.
3. This positive charge drives the reabsorption of cations (Na+, K+, Ca2+, Mg2+) through paracellular pathways.
4. Due to the thick ascending limb being impermeable to water, the tubular fluid osmolality is reduced by ion reabsorption, the interstitial fluid osmolality is increased, and an osmotic difference is created.

General Practitioners are advised to give a single injection of benzylpenicillin by intravenous or intramuscular injection before transferring the patient urgently to the ED when bacterial meningitis is suspected.

The recommended doses are:
Infants under 1 year: 300 mg
Children ages 1 to 9 years: 600 mg
Children aged 10 years and over: 1.2g
Adults: 1.2g

Nosocomial infections are defined as those occurring within 48 hours of hospital admission, 3 days of discharge or 30 days of an operation. They affect 1 in 10 patients admitted to hospital. Annually, this results in 5000 deaths with a cost to the National Health Service of a billion pounds. On average, a patient with hospital acquired infection spent 2.5-times longer in hospital, incurring additional costs of £3000 more than an uninfected patient. Intensive care units (ICU) have the highest prevalence of hospital-acquired infections in the hospital setting.
The current recommendations by NICE and the BNF on the treatment of hospital acquired pneumonia are:
Early onset infection(less than 5 days after admission to hospital): co-amoxiclav or cefuroxime for 7 days
Late-onset infection(more than 5 days after admission to hospital): an antipseudomonal penicillin (e.g. piperacillin with tazobactam), a broad-spectrum cephalosporin (e.g. ceftazidime), or a quinolone (e.g. ciprofloxacin)
If the patient developed a hospital-acquired pneumonia within 5 days of admission – co-amoxiclav would be the most appropriate choice.
If the patient has developed a hospital-acquired pneumonia > 5 days after admission – ciprofloxacin would be the most appropriate choice from the list of options available.

A hypertensive emergency is defined as severe hypertension (blood pressure ≥ 180/110 mmHg) with acute damage to the target organs. Prompt treatment with intravenous antihypertensive therapy is generally required; over the first few minutes or within 2 hours, blood pressure should be reduced by 20 – 25%. Severe hypertension without acute target organ damage is defined as hypertensive urgency.; blood pressure should be reduced gradually over 24 – 48 hours with oral antihypertensive therapy. If blood pressure is reduced too quickly in the management of hypertensive crises, there is a risk of reduced organ perfusion leading to cerebral infarction, blindness, deterioration in renal function, and myocardial ischaemia.

10 mg of lidocaine hydrochloride is contained in each 1 mL of plain 1 percent lidocaine solution.

Dopamine is a neurotransmitter and a metabolic precursor of the catecholamines. It acts on beta1-receptors in cardiac muscle increasing cardiac contractility, and increases renal perfusion by stimulating dopamine receptors in the renal vasculature. This is of benefit in cardiogenic shock where deterioration of renal function is common.

B-cells (20% of lymphocytes) mature in the bone marrow and circulate in the peripheral blood until they undergo recognition of antigen. B-cell immunoglobulin molecules synthesised in the cell are exported and bound to the surface membrane to become the B-cell receptor (BCR) which can recognise and bind to a specific antigen (either free or presented by APCs). The BCR is also important for antigen internalisation, processing and presentation to T helper cells. Most antibody responses require help from antigen-specific T helper cells (although some antigens such as polysaccharide can lead to T-cell independent B-cell antibody production). When the B-cell is activated, the receptor itself is secreted as free soluble immunoglobulin and the B-cell matures into a memory B-cell or a plasma cell (a B-cell in its high-rate immunoglobulin secreting state). Plasma cells are non-motile and are found predominantly in the bone marrow or spleen. Most plasma cells are short-lived (1 – 2 weeks) but some may survive much longer. A proportion of B-cells persist as memory cells, whose increased number and rapid response underlies the augmented secondary response of the adaptive immune system.

Calcium channel blockers inhibit L-type voltage-sensitive calcium channels in arterial smooth muscle, causing relaxation and vasodilation (reduction in peripheral vascular resistance). They also block calcium channels within the myocardium and conducting tissues of the heart which produces a negative inotropic effect by reducing calcium influx during the plateau phase of the action potential.
They have a variety of uses, including:
Hypertension
Angina
Atrial fibrillation
Migraine
Calcium channel blockers have been found to be moderately useful in the prevention of migraines. The best evidence is for this is with verapamil. This may be due to the prevention of the arteriolar constriction that is associated with migraine. They are commonly used for this elsewhere in the world but are not currently licensed for this use in the UK.
The following are common side effects of all calcium-channel blockers:
Abdominal pain
Dizziness
Drowsiness
Flushing
Headache
Nausea and vomiting
Palpitations
Peripheral oedema
Skin reactions
Tachycardia
Verapamil is highly negatively inotropic and reduces cardiac output, slows the heart rate and may impair atrioventricular conduction. It may precipitate heart failure, exacerbate conduction disorders, and cause hypotension at high doses and should not be used with beta-blockers. Nifedipine has less myocardial effects than verapamil and has no antiarrhythmic properties but has more influence on the vessels. Nimodipine is used solely for the prevention and treatment of vascular spasm following aneurysmal subarachnoid haemorrhage.

Flexor carpi ulnaris is a fusiform muscle located in the anterior compartment of the forearm. It belongs to the superficial flexors of the forearm, along with pronator teres, palmaris longus, flexor digitorum superficialis and flexor carpi radialis. Flexor carpi ulnaris is the most medial of the superficial flexors.

Innervation of the flexor carpi ulnaris muscle is from the brachial plexus via the ulnar nerve (C7-T1).

Flexor carpi ulnaris receives its arterial blood supply via three different routes. Proximally, a branch of the posterior ulnar recurrent artery supplies the muscle as it passes between the humeral and ulnar heads. Branches of the ulnar artery supply the middle and distal parts of the muscle, with an accessory supply also present distally via the inferior ulnar collateral artery.

Due to its position and direction in the forearm, flexor carpi ulnaris can move the hand sideways as well as flexing it. Contracting with flexor carpi radialis and palmaris longus, flexor carpi ulnaris produces flexion of the hand at the wrist joint. However, when it contracts alongside the extensor carpi ulnaris muscle in the posterior compartment, their counteracting forces produce adduction of the hand at the wrist, otherwise known as ulnar deviation or ulnar flexion

Adverse actions include anticholinergic effects such as drowsiness, dry mouth, and blurred vision, extrapyramidal effects, and postural hypotension. Phenothiazines can all induce acute dystonic reactions such as facial and skeletal muscle spasms and oculogyric crises; children (especially girls, young women, and those under 10 kg) are particularly susceptible.

Plasma potassium greater than 5.5 mmol/L is hyperkalaemia or elevated plasma potassium level. Among the causes of hyperkalaemia include congenital adrenal hyperplasia.

Congenital adrenal hyperplasia is a general term referring to autosomal recessive disorders involving a deficiency of an enzyme needed in cortisol and/or aldosterone synthesis. The level of cortisol and/or aldosterone deficiency affects the clinical manifestations of congenital adrenal hyperplasia. When it involves hypoaldosteronism, it can result in hyponatremia and hyperkalaemia. While hypercortisolism can cause hypoglycaemia.

The other causes of hyperkalaemia may include renal failure, excess potassium supplementation, Addison’s disease (adrenal insufficiency), renal tubular acidosis (type 4), rhabdomyolysis, burns, trauma, Tumour lysis syndrome, acidosis, and medications such as ACE inhibitors, angiotensin receptor blockers, NSAIDs, beta-blockers, digoxin, and suxamethonium.

Bartter’s syndrome is characterized by hypokalaemic alkalosis with normal to low blood pressure.

Type 1 and 2 renal tubular acidosis both cause hypokalaemia.

Gitelman’s syndrome is a defect of the distal convoluted tubule of the kidney. It causes metabolic alkalosis with hypokalaemia and hypomagnesemia.

And excessive liquorice ingestion causes hypermineralocorticoidism and hypokalaemia as well. Thus, among the choices, only congenital adrenal hyperplasia can cause hyperkalaemia

.

Eosinophils comprise 1 – 3% of circulating white cells. Eosinophils are similar to neutrophils, except that the cytoplasmic granules are coarser and more deeply red staining, and there are rarely more than three nuclear lobes. They are less motile, but longer lived. They enter inflammatory exudates and have a special role in allergic responses, defence against parasites and removal of fibrin formed during inflammation. Thus they play a role in local immunity and tissue repair.

Klebsiella is a Gram-negative, rod-shaped, non-motile bacteria. The absence of motility distinguishes Klebsiella spp. from most other members of the family Enterobacteriaceae.

K. pneumoniae is the most commonly isolated species and has the distinct feature of possessing a large polysaccharide capsule. The capsule offers the organism protection against phagocytosis and antimicrobial absorption,
contributing to its virulence.

Colonization of gram-negative bacilli in the respiratory tracts of hospitalized patients, particularly by K. pneumoniae, increases with the length of hospital stay. It is a frequent cause of lower respiratory tract infections among hospitalized patients and in immunocompromised hosts such as newborns,
elderly patients, and seriously ill patients on respirators.

Chloramphenicol is a broad-spectrum antibiotic that inhibits bacterial protein synthesis by blocking the 50S subunit of the bacterial ribosome’s peptidyl transferase activity. When administered systemically, it has limited usage due to the potential of significant side effects such as aplastic anaemia, peripheral neuropathy, and optic neuritis. It’s only used to treat typhoid fever and Haemophilus influenzae meningitis, but it’s usually better to use a broad-spectrum cephalosporin.

Features of cell damage that tend to be reversible include: swelling of endoplasmic reticulum and some mitochondrialoss of ribosomescell stress response
Features of cell damage that tend to be irreversible include: loss of nucleolus, no ribosomes, swelling of all mitochondria, nuclear condensation, membrane blebs and holes, lysosome rupture, fragmentation of all inner membranes, nuclear breakup

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.

Flow through a tube is dependent upon:
The pressure difference across the ends of the tube (P1– P2)
The resistance to flow provided by the tube (R)
This is Darcy’s law, which is analogous to Ohm’s law in electronics:
Flow = (P1– P2) / R
Resistance in the tube is defined by Poiseuille’s law, which is determined by the diameter of the tube and the viscosity of the fluid. Poiseuille’s law is as follows:
Resistance = (8VL) / (πR4)
Where:
V = The viscosity of the fluid
L = The length of the tube
R = The radius of the tube
Therefore, in simple terms, resistance is directly proportional to the viscosity of the fluid and the length of the tube and inversely proportional to the radius of the tube. Of these three factors, the most important quantitatively and physiologically is vessel radius.
It can be seen that small changes in the radius can have a dramatic effect on the flow of the fluid. For example, the constriction of an artery by 20% will decrease the flow by approximately 60%.
Another important and frequently quoted example of this inverse relationship is that of the radius of an intravenous cannula. Doubling the diameter of a cannula increases the flow rate by 16-fold (r4). This is the reason the diameter of an intravenous cannula in resuscitation scenarios is so important.
*Please note that knowledge of the detail of Poiseuille’s law is not a requirement of the RCEM Basic Sciences Curriculum.

Cardiac glycosides (e.g. digoxin) slow the removal of Ca2+from the cell by inhibiting the membrane Na+pump (Na+/K+ATPase) which generates the Na+gradient required for driving the export of Ca2+by Na+/Ca2+exchange; consequently the removal of Ca2+from the myocyte is slowed and more Ca2+is available for the next contraction.

One of the results of Klebsiella pneumoniae is pneumonia that is usually a very severe infection. It is characterised by thick, bloody sputum (red currant jelly sputum), and is associated with complications like lung abscess, cavitation, necrosis, empyema and pleural effusions.

Chickenpox is not a notifiable disease.

Acute bronchiolitis is caused most commonly by respiratory syncytial virus, occurring mostly in children aged 6 months to 2 years. Children with bronchiolitis are febrile and tachypnoeic with a dry cough and difficulty feeding. Examination may reveal chest hyperinflation, respiratory distress, wheezing and fine end-inspiratory crepitations. Chest x-ray may show hyperinflation and increased peribronchial markings (although CXR should only performed if there is diagnostic uncertainty or an atypical course). Treatment is usually supportive, aerosolized ribavirin is reserved for severely ill or immunocompromised patients.

A low anion gap is frequently caused by hypoalbuminemia. Albumin is a negatively charged protein and its loss from the serum results in the retention of other negatively charged ions such as chloride and bicarbonate. As bicarbonate and chloride anions are used to calculate the anion gap, there is a subsequent decrease in the gap. The anion gap is sometimes reduced in multiple myeloma, where there is an increase in plasma IgG (paraproteinaemia).

Actions of adrenaline:
Cardiovascular system
– Increased rate and force of cardiac contraction
– Vasoconstriction of vessels in skin, mucous membranes and splanchnic bed
– Vasodilation of skeletal muscle vessels
– Increased cardiac output and blood pressure
Respiratory system
– Bronchodilation
– Increased ventilation rate
Gastrointestinal system
– Smooth muscle relaxation
– Contraction of sphincters
– Metabolism
– Decreased insulin release
– Increased glucagon release
– Increased thermogenesis
– Increased glycolysis
– Increased lipolysis
Eye
– Pupillary dilation

JVP Waveform in Cardiac Cycle Physiology: a wave Right atrial contraction causes atrial systole (end diastole). the c wave During right isovolumetric ventricular contraction, the tricuspid valve bulges into the right atrium, resulting in isovolumetric contraction (early systole). descent by x Rapid ventricular ejection (mid systole) is caused by a combination of right atrial relaxation, tricuspid valve downward movement during right ventricular contraction, and blood ejection from both ventricles. the v-wave Ventricular ejection and isovolumetric relaxation (late systole) occur as a result of venous return filling the right atrium. y lineage Ventricular filling occurs when the tricuspid valve opens, allowing blood to flow rapidly from the right atrium to the right ventricle.

Anaphylaxis is an example of a type I hypersensitivity reaction.

It is IgE mediated.

It requires a prior exposure to the antigen. The initial exposure sensitizes the body to the antigen and a second exposure to that antigen leads to an anaphylactic reaction.

Massive calcium influx into the cells leads to mast cell degranulation.

The Immunoglobulin antigen complex binds to Fc receptors on the surface of mast cells. The result is mast cell degranulation and release of histamine, proteoglycans and serum proteases from cytoplasmic granules.

Platelets are produced in the bone marrow by fragmentation of the cytoplasm of megakaryocytes, derived from the common myeloid progenitor cell. The time interval from differentiation of the human stem cell to the production of platelets averages 10 days. Thrombopoietin is the major regulator of platelet formation and 95% of this is produced by the liver. The normal platelet count is approximately 150 – 450 x 109/L and the normal platelet lifespan is 10 days. Under normal circumstances, about one-third of the marrow output of platelets may be trapped at any one time in the normal spleen.

Inferior medial pontine syndrome, also known as Foville syndrome, is one of the brainstem stroke syndromes which occurs when there is infarction of the medial inferior aspect of the pons due to occlusion of the paramedian branches of the basilar artery.

It is characterized by ipsilateral sixth nerve palsy, facial palsy, contralateral hemiparesis, contralateral loss of proprioception and vibration, ipsilateral ataxia, ipsilateral facial weakness, and lateral gaze paralysis and diplopia.