Escherichia coli strain 0157 causes enterohaemorrhagic diarrhoea and can lead to renal failure, haemolytic anaemia and thrombocytopenia.

Norwalk virus is an RNA virus.

Although transmission of rotavirus is primarily through the faeco-oral route, airborne spread has been seen in some cases.

Cryptosporidium are protozoa with acid fast walls and are resistant to both chlorine treatment and conventional filtering methods.

There is no therapy effective in treating cryptosporidium diarrhoea as the protozoa is not susceptible to antibiotics.

Following a myocardial infarction scar tissue formation will take place at the site of the damaged muscle. This places increased load on the rest of the myocardium causing it to hypertrophy. The left ventricle will hypertrophy first as it is pumping blood against a greater afterload as compared to the right ventricle.

There are three types of cells in the body with regards to the cell cycle: 1. permanent
2. labile
3. stable cells

Permanent cells do not re-enter the cell cycle and remain in G0. If there is a pool of stem cells the stem cells will enter the cell cycle to form more cells. Myocardial cells are a type of permanent cell and there is no pool of stem cells in the heart muscle. The anterior wall will not hypertrophy as it is formed by the right atrium and ventricle and both of these hypertrophy after the left ventricle.

Calcium-channel blockers, also known as calcium antagonists, stop calcium from entering cells through the L-type calcium channel. This causes vascular smooth muscle in vessel walls to relax, resulting in a decrease in peripheral vascular resistance.
They can be used for a variety of things, including:
Hypertension
Angina
Atrial fibrillation
Migraine

Calcium-channel blockers can be divided into two categories: dihydropyridines and non-dihydropyridines. The basic chemical structure of these two classes differs, as does their relative selectivity for cardiac versus vascular L-type calcium channels.

Dihydropyridines have a high vascular selectivity and lower systemic vascular resistance and blood pressure. As a result, they’re frequently used to treat hypertension. Modified release formulations are also used to treat angina, but their powerful systemic vasodilator and pressure-lowering effects can cause reflex cardiac stimulation, resulting in increased inotropy and tachycardia, which can counteract the beneficial effects of reduced afterload on myocardial oxygen demand.

The suffix -dpine distinguishes dihydropyridines from other pyridines. Examples of dihydropyridines that are commonly prescribed include:
Amlodipine
Felodipine
Nifedipine
Nimodipine

The phenylalkylamine class and the benzothiazepine class are two subgroups of non-dihydropyridines.

Phenylalkylamines are less effective as systemic vasodilators because they are relatively selective for the myocardium. This group of drugs lowers myocardial oxygen demand and reverses coronary vasospasm, making them useful in the treatment of angina. They are also occasionally used to treat arrhythmias. A phenylalkylamine calcium-channel blocker like verapamil is an example.

In terms of selectivity for vascular calcium channels, benzothiazepines fall somewhere between dihydropyridines and phenylalkylamines. They can lower arterial pressure without producing the same level of reflex cardiac stimulation as dihydropyridines because they have both cardiac depressant and vasodilator effects. Diltiazem is the only benzothiazepine currently in clinical use.

Rubella can be contagious from 7 days before to 7 days after the rash appears.

Patients with measles are contagious from 1-2 days before the onset of symptoms.

A person with chickenpox is considered contagious beginning 1 to 2 days before rash onset until all the chickenpox lesions have crusted (scabbed).

The infectious period of mumps is considered from 2 days before to 5 days after parotitis onset.

Hepatitis A is highly transmissible and has an average incubation period of 28 to 30 days (range 15–50 days). The maximum infectivity is during the second half of the incubation period (i.e. while asymptomatic) and most cases are considered non-infectious after the first week of jaundice.

The NICE guidelines for women with lower UTIs who are not pregnant are:
1. Consider prescribing a different antibiotic if symptoms do not improve within 48 hours or worsen at any time
2. If the urine culture and susceptibility test results are available, review the choice of antibiotic according to the results and change the antibiotic accordingly if symptoms are not improving or bacteria is resistant to the prescribed antibiotic

The first choice of antibiotics for non-pregnant women aged 16 years and over is:
1. Nitrofurantoin
100 mg modified-release PO BD for 3 days – if eGFR >45 ml/minute
2. Trimethoprim
200 mg PO BD for three days

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. Nitrofurantoin
100 mg modified-release PO BD for three days – if eGFR >45 ml/minute
2. Pivmecillinam
400 mg PO initial dose, then 200 mg PO TDS for three days
3. Fosfomycin 3 g single sachet dose

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.

Local currents propagate action potentials down the axons of neurons. Following depolarization, this local current flow depolarizes the next axonal membrane, and when this region crosses the threshold, more action potentials are formed, and so on. Due to the refractory period, portions of the membrane that have recently depolarized will not depolarize again, resulting in the action potential only being able to go in one direction.

The square root of axonal diameter determines the velocity of the action potential; the axons with the biggest diameter have the quickest conduction velocities. When a neuron is myelinated, the speed of the action potential rises as well.

The myelin sheath is an insulating coating that surrounds certain neural axons. By increasing membrane resistance and decreasing membrane capacitance, the myelin coating increases conduction. This enables faster electrical signal transmission via a neuron, making them more energy-efficient than non-myelinated neuronal axons.

Nodes of Ranvier are periodic holes in a myelinate axon when there is no myelin and the axonal membrane is exposed. There are no gated ion channels in the portion of the axon covered by the myelin sheath, but there is a high density of ion channels in the Nodes of Ranvier. Action potentials can only arise at the nodes as a result of this.
Electrical impulses are quickly transmitted from one node to the next, causing depolarization of the membrane above the threshold and triggering another action potential, which is then transmitted to the next node. An action potential is rapidly conducted down a neuron in this manner. Saltatory conduction is the term for this.

Glucagon is a peptide hormone that is produced and secreted by alpha cells of the islets of Langerhans, which are located in the endocrine portion of the pancreas. The main physiological role of glucagon is to stimulate hepatic glucose output, thereby leading to increases in glycaemia. It provides the major counter-regulatory mechanism to insulin in maintaining glucose homeostasis.
Hypoglycaemia is the principal stimulus for the secretion of glucagon but may also be used as an antidote in beta-blocker overdose and in anaphylaxis in patients on beta-blockers that fail to respond to adrenaline.
Glucagon then causes:
Glycogenolysis
Gluconeogenesis
Lipolysis in adipose tissue
The secretion of glucagon is also stimulated by:
Adrenaline
Cholecystokinin
Arginine
Alanine
Acetylcholine
The secretion of glucagon is inhibited by:
Insulin
Somatostatin
Increased free fatty acids
Increased urea production

Glycolysis is the metabolic pathway that converts glucose into pyruvate. The free energy released by this process is used to form ATP and NADH. Glycolysis is inhibited by glucagon, and glycolysis and gluconeogenesis are reciprocally regulated so that when one cell pathway is activated, the other is inactive and vice versa.

Glucagon has a minor effect of enhancing lipolysis in adipose tissue. Lipolysis is the breakdown of lipids and involves the hydrolysis of triglycerides into glycerol and free fatty acids. It makes fatty acids available for oxidation.

Fracture of the medial epicondyle is most likely to result in damage to the ulnar nerve.

The three hypothenar muscles, two medial lumbricals, seven interossei, the adductor pollicis, and the deep head of the flexor pollicis brevis are all innervated by the deep branch of the ulnar nerve.

Calcium gluconate is given to antagonise cardiac cell membrane excitability to reduce the risk of arrhythmias. It has no effect on serum potassium levels unlike the alternative drugs listed above.

Angina pectoris is the most common symptom of ischemic heart disease and presents with chest pain relieved by rest and nitro-glycerine.

Nitrates are the first-line treatment to relieve chest pain caused by angina. The commonly used nitrates are:
1. Glyceryl trinitrate
2. Isosorbide dinitrate

The nitrate drugs are metabolized in the following steps:
1. Release Nitrite ions (NO2-), which are then converted to nitric oxide (NO) within cells.
2. NO activates guanylyl cyclase, which causes an increase in the intracellular concentration of cyclic guanosine-monophosphate (cGMP) in vascular smooth muscle cells.
3. Relaxation of vascular smooth muscle.

Although nitrates are potent coronary vasodilators, their principal benefit in the management of angina results from a predominant mechanism of venous dilation:
– Bigger veins hold more blood
– Takes blood away from the left ventricle
– Lowers LVEDV (preload), LA pressure
– Less pulmonary oedema → improved dyspnoea

In the majority of patients the commonest causative organism for osteomyelitis isStaphylococcus aureus.Salmonella spp. are the commonest cause in patients with sickle cell disease.
Other bacteria that can cause osteomyelitis include:
Enterobacter spp.
Group A and B streptococcus
Haemophilus influenzae
The current recommendations by NICE and the BNF on the treatment of osteomyelitis are:
Flucloxacillin first-line
Consider adding fusidic acid or rifampicin for initial 2 weeks
If penicillin allergic use clindamycin
If MRSA is suspected use vancomycin
Suggested duration of treatment is 6 weeks for acute infection

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.

It’s crucial that thrombin’s impact is restricted to the injured site. Tissue factor pathway inhibitor (TFPI), which is produced by endothelial cells and found in plasma and platelets, is the first inhibitor to function. It accumulates near the site of harm induced by local platelet activation. Xa and VIIa, as well as tissue factor, are inhibited by TFPI. Other circulating inhibitors, the most potent of which is antithrombin, can also inactivate thrombin and other protease factors directly. Coagulation cofactors V and VIII are inhibited by protein C and protein S. Tissue plasminogen activator (TPA) from endothelial cells facilitates fibrinolysis by promoting the conversion of plasminogen to plasmin.

Pectoralis major is a thick, fan-shaped muscle situated in the chest. It makes up the bulk of the chest musculature in the male and lies underneath the breast in the female. It overlies the thinner pectoralis minor muscle.
Superficial muscles of the chest and arm showing pectoralis major (from Gray’s Anatomy)
Pectoralis major has two heads; the clavicular head and the sternocostal head. The clavicular head originates from the anterior border and medial half of the clavicle. The sternocostal head originates from the anterior surface of the sternum, the superior six costal cartilages and the aponeurosis of the external oblique muscle. It inserts into the lateral lip of the bicipital groove of the humerus.
Pectoralis major receives dual innervation from the medial pectoral nerve and the lateral pectoral nerve.
Its main actions are as follows:
Flexes humerus (clavicular head)
Extends humerus (sternocostal head)
Adducts and medially rotates the humerus
Draws scapula anteriorly and inferiorly

When the vagus nerve is damaged, the soft palate is paralyzed and the uvula is shifted away from the affected side. The vagus nerve innervates the uvulae muscle, which forms the uvula’s core. If only one side is innervated, contraction of the active muscle will draw the uvula towards it.

A history of stroke and poor nutritional status points towards a nutritional deficiency as the most likely cause of her symptoms. The examination would differentiate between Vitamin B12 and Folic acid deficiency as in the former. The patient has a beefy red tongue and symptoms indicating peripheral nervous system involvement or subacute combined spinal cord degeneration. The patient may also have a lemon-yellow skin colour, loss of proprioception and vibratory sense and oral ulceration.

Investigations in B12 deficiency can reveal the following:
1. Macrocytic anaemia
2. Neutropoenia
3. Thrombocytopaenia
4. Blood film: anisocytosis, poikilocytosis
5. Low serum B12
6. Raised serum bilirubin (haemolysis)
7. Intrinsic factor antibodies
8. Positive Schilling test

Angiotensin-converting enzyme (ACE) inhibitors are the most common cause of drug-induced angioedema in the United Kingdom and the United States, owing to their widespread use.

Angioedema is caused by ACE inhibitors in 0.1 to 0.7 percent of patients, with data indicating a persistent and relatively constant risk year after year. People of African descent have a five-fold higher chance of contracting the disease.

Swelling of the lips, tongue, or face is the most common symptom, but another symptom is episodic abdominal pain due to intestinal angioedema. Itching and urticaria are noticeably absent.

The mechanism appears to be activated complement or other pro-inflammatory cytokines like prostaglandins and histamine, which cause rapid vasodilation and oedema.

Other medications that are less frequently linked to angioedema include:
Angiotensin-receptor blockers (ARBs)
Nonsteroidal anti-inflammatory drugs (NSAIDs)
Bupropion (e.g. Zyban and Wellbutrin)
Beta-lactam antibiotics
Statins
Proton pump inhibitors

The majority of these reactions are minor and can be treated by stopping the drug and prescribing antihistamines.

Osteoclasts are a type of bone cell that breaks down bone tissue. This is a critical function in the maintenance, repair and remodelling of bones. The osteoclast disassembles and digests the composite of hydrated protein and minerals at a molecular level by secreting acid and collagenase. This process is known as bone resorption and also helps to regulate the plasma calcium concentration.
Osteoclastic activity is controlled by a number of hormones:
1,25-dihydroxycholecalciferol increases osteoclastic activity
Parathyroid hormone increases osteoclastic activity
Calcitonin inhibits osteoclastic activity
Bisphosphonates are a class of drug that slow down and prevent bone damage. They are osteoclast inhibitors.

Action potentials are transmitted to adjacent myocytes via gap junctions.

The nerves that supply the adductor magnus muscle have an embryologic origin from the anterior divisions of the lumbosacral plexus and include the obturator nerve, posterior division (L2-4), and the tibial portion of the sciatic nerve (L4). It is innervated by the posterior division of the obturator nerve.

The mean incubation period for P. falciparum is 12 days.

WHO World Malaria Report 2019 states that an estimated 228 million cases of malaria occurred worldwide in 2018, and reports steadily decreasing the number of cases since 2010. In 2018, nineteen sub-Saharan African countries and India carried approximately 85% of the global malaria burden. The most prevalent and pathogenic malaria parasite, most commonly associated with severe illness and death, especially in the WHO African region, accounting for 99.7% malaria cases, is P. falciparum.

The vector for Plasmodium spp. is a female Anopheles mosquito that inoculates sporozoites contained in her salivary glands into the puncture wound when feeding. Sporozoites enter peripheral bloodstream and are uptake by hepatocytes, where they undergo an asexual pre-erythrocytic liver-stage as liver schizonts lasting up to 2 weeks before the onset of the blood stage.

Intravenous or intramuscular artesunate is the first-line treatment in all patients worldwide and should be used for at least 24 hours and until the oral medication is tolerated.

A diagnosis of AIDS can be made in a patient infected with HIV if the patient has a CD4 count < 200 cells/uL, or an AIDS-defining illness. Antiretroviral treatment should be considered in patients with CD4 counts < 350 cells/uL.

Oral candidiasis is not an AIDS defining illness – candidiasis of the bronchi, trachea, lungs or of the oesophagus is an AIDS defining illness.

A positive p24 antigen test seen in early HIV infection and does not indicate the development of AIDS.

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.

Infrahyoid muscles are also known as “strap muscles” which connect the hyoid, sternum, clavicle and scapula. They are located below the hyoid bone on the anterolateral surface of the thyroid gland and are involved in movements of the hyoid bone and thyroid cartilage during vocalization, swallowing and mastication. They are composed of four paired muscles, organized into two layers.

Superficial layer consists of the sternohyoid and omohyoid
Deep layer consists of the sternothyroid and thyrohyoid.

A negative correlation coefficient means that the two variables are inversely related e.g. socio-economic class and mortality.

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.

The periurethral portion of the prostate gland increases in size during puberty and after the age of 55 years due to the growth of non-malignant cells in the transition zone of the prostate that surrounds the urethra. Most cancers develop in the posterior lobe, and cancers in this location may be palpated during a digital rectal examination (DRE).

Lactic acidosis is defined as a pH <7.35 and a lactate >5 mmol/L. It is a common finding in critically ill patients and is often associated with other serious underlying pathologies. The anion gap is raised in lactic acidosis.
There are major adverse consequences of severe acidaemia, which affect all body systems, and there is an associated increase in mortality of critically ill patients with a raised lactate. The mortality associated with lactic acidosis despite full supportive treatment remains at 60-90%.
Acquired lactic acidosis is classified into two subtypes:
Type A is due to tissue hypoxia
Type B is due to non-hypoxic processes affecting the production and elimination of lactate
Lactic acidosis can be extreme after a seizure but usually resolves spontaneously within a few hours.
Left ventricular failure typically results in tissue hypoperfusion and a type A lactic acidosis.
Some causes of type A and type B lactic acidosis are shown below:
Type A lactic acidosis
Type B lactic acidosis
Shock (including septic shock)
Left ventricular failure
Severe anaemia
Asphyxia
Cardiac arrest
CO poisoning
Respiratory failure
Severe asthma and COPD
Regional hypoperfusion
Renal failure
Liver failure
Sepsis (non-hypoxic sepsis)
Thiamine deficiency
Alcoholic ketoacidosis
Diabetic ketoacidosis
Cyanide poisoning
Methanol poisoning
Biguanide poisoning

About one third of patients with allergy to natural latex rubber (NRL) have an associated allergy to some plant-derived foods. It is known as the latex-fruit syndrome and occurs commonly with consumption of fresh fruits. Banana and avocado are the most implicated fruits but it can also be seen with tomato, kiwi and chestnut.