Among neonates, group B streptococci (GBS) are the most commonly identified causes of bacterial meningitis, implicated in roughly 50% of all cases. Escherichia coli(Gram-negative rods) accounts for another 20%. Thus, the identification and treatment of maternal genitourinary infections is an important prevention strategy.

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).

Naloxone is a specific antagonist of mu(μ)-opioid receptors, the specific antidote for opioid overdose and will reverse respiratory depression and coma if given at sufficient dosage. The initial dose is usually 0.8 mg (2 mL) intravenously (the dose range suggested by BNF is 0.4-2 mg). It can also be given by intramuscular injection if the intravenous route is not feasible.
As naloxone has a shorter duration of action than most opioids, close monitoring and repeated injections are necessary according to the respiratory rate and depth of coma. The dose is generally repeated every 2-3 minutes to a maximum of 10 mg. When repeated doses are needed, naloxone may be given by a continuous infusion adjusted according to the vital signs. Initially, the infusion rate can be set at 60% of the initial resuscitative IV dose per hour.
In opioid addicts, naloxone administration may precipitate a withdrawal syndrome with abdominal cramps, nausea and diarrhoea, but these usually settle within 2 hours.

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 infection (CDI) 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.

CDI is the most severe consequence of antibiotic treatment and is a major cause of morbidity and mortality.
Risk for CDI has been found to be greatest with clindamycin followed by fluoroquinolones Tetracyclines are not associated with risk for CDI.

Opioid receptors are widely distributed throughout the central nervous system. Opioid analgesics mimic endogenous opioid peptides by causing prolonged activation of these receptors, mainly the mu(μ)-receptors which are the most highly concentrated in brain areas involved in nociception.

Ecchymosis are discolouration of the skin or mucous membranes caused by extravasation of blood. They are usually red or purple in colour and measure greater than 1 cm in diameter and do not blanch on applying pressure.

A macule is a flat, well circumscribed area of discoloured skin less than 1 cm in diameter with no changes in the thickness or texture of the skin.

Petechiae are discolouration of the skin measuring less than 3 mm in diameter

Purpura are discolouration of the skin measuring between 0.3 cm and 1 cm in diameter.

Erythema is redness of the skin or mucous membranes caused by hyperaemia of superficial capillaries caused by skin injury, infection or inflammation. Erythema blanches when pressure is applied whereas ecchymosis, purpura and petechiae do not.

Diabetes insipidus is the inability to produce concentrated urine. It is characterised by the presence of excessive thirst, polyuria and polydipsia. There are two distinct types of diabetes insipidus:
Cranial (central) diabetes insipidus and;
Nephrogenic diabetes insipidus
Cranial diabetes insipidus is caused by a deficiency of vasopressin (anti-diuretic hormone). Patients with cranial diabetes insipidus can have a urine output as high as 10-15 litres per 24 hours, but adequate fluid intake allows most patients to maintain normonatraemia. 30% of cases are idiopathic, and a further 30% are secondary to head injuries. Other causes include neurosurgery, brain tumours, meningitis, granulomatous disease (e.g. sarcoidosis) and drugs, such as naloxone and phenytoin. A very rare inherited form also exists that is associated with diabetes mellitus, optic atrophy, nerve deafness and bladder atonia.
Nephrogenic diabetes insipidus is caused by renal resistance to the action of vasopressin. As with cranial diabetes insipidus, urine output is markedly elevated. Serum sodium levels can be maintained by secondary polydipsia or can be elevated. Causes of nephrogenic diabetes insipidus include chronic renal disease, metabolic disorders (e.g. hypercalcaemia and hypokalaemia) and drugs, including long-term lithium usage and demeclocycline.
In view of the history of long-term lithium use, in this case, nephrogenic diabetes insipidus is the most likely diagnosis.

The history of nosebleeds and fatigue, and gingival hyperplasia presents a typical picture of acute myeloid leukaemia. Leukemic infiltrates within the gingiva cause hypertrophy and distinguish this condition from other types of leukaemia. The fatigue is secondary to anaemia, while the nosebleeds are caused by thrombocytopenia secondary to leukemic infiltration of bone marrow. Patients may also report frequent infections secondary to neutropenia and hepatosplenomegaly.

Dalton’s law states that when two or more gases, which do not react chemically, are present in the same container, the total pressure is the sum of the partial pressures of each gas.

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.

Gastrin secretion is stimulated by:
The presence of small peptides and amino acids in chyme
Gastric distension
Vagal stimulation directly via acetylcholine and indirectly via gastrin-releasing peptide (GRP)
Raised gastric pH

In hypokalaemia, initial potassium replacement therapy should not involve glucose infusions, as glucose may cause a further decrease in the plasma-potassium concentration. Glucose infusions are used for the other indications like diabetic ketoacidosis, hypoglycaemia, routine fluid maintenance in patients who are nil by mouth (very important in children), and in hyperkalaemia.

Pronator teres syndrome (PTS) is caused by a compression of the median nerve (MN) by the pronator teres (PT) muscle in the forearm.

The median nerve, C6 and C7, innervates the pronator teres.

Peripheral nerves are nerves that lie outside the brain and spinal cord. Peripheral nerves readily regenerate, while central nervous system axonal injury does not spontaneously regenerate.
If there is damage to the axons of peripheral nerves, the nerves will regenerate at a slow rate of 1 mm per day. The slow regeneration process may lead to muscle atrophy before regeneration is complete.

Each peripheral nerve has a single cell body that supplies nutrients to the growing nerve fibre. The cell body does not undergo mitosis; only the axon is regenerated.

Schwann cells of the peripheral nervous system provide support for this process, while the analogous oligodendrocytes of the central nervous system do not. Schwann cells themselves do not cause regeneration. Schwann cells provide myelin for myelinated fibres and surround non-myelinated fibres with their cytoplasm.

If an axon is completely severed, as in the case of amputation, the axonal fibres regenerating from the cell body may never find their original route back to the muscle. Instead, they may form a traumatic neuroma, a painful collection of nerve fibres and myelin.

Interleukin-1, which is released by leukocytes and acts on the thermoregulatory centre of the hypothalamus, causes fever. Because prostaglandins mediate this process, antipyretics such as NSAIDs, paracetamol, and aspirin reduce prostaglandin levels by inhibiting cyclooxygenase enzymes. Malignant disease secretes interleukins, which cause the B-symptoms seen in lymphoma, for example. Bacterial toxins can also cause interleukins to be produced.

Pyrexia of unknown origin (PUO) is defined as a fever of greater than 38.3 degrees Celsius that lasts for more than 2-3 weeks with no clear diagnosis despite extensive investigation.

Investigation necessitates a thorough understanding of the conditions that can cause febrile illness, which may be missed during an initial investigation, as well as a thorough history, examination, and investigation centred on that list.

Pyrexia of unknown origin has a wide differential diagnosis, which includes:
Infection
Bacterial
Pyogenic abscess
Tuberculosis
Infective endocarditis
Brucellosis
Lyme disease
Viral
HIV
Epstein Barr Virus
Cytomegalovirus
Parasite
Toxoplasmosis
Malignancy
Leukaemia
Lymphoma
Renal cell carcinoma
Hepatocellular carcinoma
Vasculitides
Still’s disease
Granulomatosis with polyangiitis (formerly Wegener’s)
Systemic lupus erythematosus
Giant cell arteritis
Rheumatoid arthritis
Polymyalgia rheumatica
Miscellaneous
Drug induced fevers
Familial Mediterranean fever
Thyrotoxicosis
Inflammatory bowel disease
Sarcoidosis
Factitious fever
Exaggerated normal circadian fluctuation

The patient might need to be admitted to the hospital for observation and further investigation. Because infection is still a possibility, blood cultures should be repeated on a regular basis, and inflammatory markers should be closely monitored. CT, PET, and MRI imaging have largely replaced diagnostic laparotomy as a diagnostic tool.

Peroneus brevis is innervated by the superficial peroneal nerve.
Peroneus longus is innervated by the superficial peroneal nerve.
Peroneus tertius is innervated by the deep peroneal nerve.

An overdose of levothyroxine can happen by accident or on purpose. Intentional overdosing is sometimes done to lose weight, but it can also happen in patients who are suicidal. The development of thyrotoxicosis, which can lead to excited sympathetic activity and high metabolism syndrome, is the main source of concern. The time between ingestion and the emergence of clinical features associated with an overdose is often quite long.

After a levothyroxine overdose, the majority of patients are asymptomatic. Symptoms and signs are usually only seen in patients who have taken more than 10 mg of levothyroxine in total.

The following are the most commonly seen clinical features in patients developing clinical features:
Tremor
Agitation
Sweating
Insomnia
Headache
Increased body temperature
Increased blood pressure
Diarrhoea and vomiting
Less common clinical features associated with levothyroxine overdose include:
Seizures
Acute psychosis
Thyroid storm
Tachycardia
Arrhythmias
Coma

The continued absorption of the ingested levothyroxine causes a progressive rise in both total serum T4 and total serum T3 levels in the first 24 hours after an overdose. However, in some cases, the biochemical picture is completely normal. Thyroid function tests are not always recommended after a thyroxine overdose. Although elevated thyroxine levels are common, they have little clinical significance and have no impact on treatment. Following a levothyroxine overdose, the following biochemical features are common:
T4 and T3 levels in the blood are elevated.
Free T4 and Free T3 levels are higher.
TSH levels in the blood are low.
If the patient is cooperative and more than 10 mg of levothyroxine has been consumed, activated charcoal can be given (i.e., likely to become symptomatic)
Within an hour of ingestion, the patient presents.

The treatment is mostly supportive and aimed at managing the sympathomimetic symptoms that come with levothyroxine overdose. If beta blockers aren’t an option, try propranolol 10-40 mg PO 6 hours or diltiazem 60-180 mg 8 hours.

In the absence of any contra-indications, high-dose NSAIDs are the first-line treatment for acute gout. Naproxen 750 mg as a stat dose followed by 250 mg TDS is a commonly used and effective regime.
Aspirin should not be used in gout as it reduces the urinary clearance of urate and interferes with the action of uricosuric agents. Naproxen, Diclofenac or Indomethacin are more appropriate choices.
Allopurinol is used prophylactically, preventing future attacks by reducing serum uric acid levels. It should not be started in the acute phase as it increases the severity and duration of symptoms.
Colchicine acts on the neutrophils, binding to tubulin to prevent neutrophil migration into the joint. It is as effective as NSAIDs in relieving acute attacks. It also has a role in prophylactic treatment if Allopurinol is not tolerated.
NSAIDs are contra-indicated in heart failure as they can cause fluid retention and congestive cardiac failure. Colchicine is the preferred treatment in patients with heart failure or those who are intolerant of NSAIDs.

Gluteus minimus is the smallest muscle of the glutei. It is located just beneath the gluteus medius muscle. Gluteus minimus predominantly acts as a hip stabilizer and abductor of the hip.
The superior gluteal nerve innervates the gluteus minimus.

If SBP is less than 90 mmHg , 500 mL sodium chloride 0.9 percent should be administered intravenously over 10–15 minutes, and repeated if SBP remains less than 90 mmHg. When SBP is greater than 90 mmHg, sodium chloride infusion must be maintained at a rate that replaces the deficit.

The tidal volume(TV) is the amount of air that moves in and out of the lungs with each respiratory cycle. In a healthy male, the usual volume is 0.5 L (,7 ml/kg body mass).

The vital capacity(VC) is the maximum amount of air that can be exhaled following maximal inspiration. The usual volume in a healthy male is 4.5 L.

The residual volume(RV) is the amount of air remaining in the lungs after maximum expiration. The usual volume in a healthy male is 1.0 L.

The inspiratory reserve volume(IRV) is the maximum amount of air that can be breathed in forcibly after normal inspiration. The usual volume in a healthy male is 3.0 L.

The expiratory reserve volume(ERV) is the volume of air that can be breathed out forcibly after normal expiration. The usual volume in a healthy male is 1.0 L.

Total lung capacity(TLC) is the volume of air the lungs can accommodate. TLC = RV+VC. The usual volume in a healthy male is 5.5 L.

Abductor pollicis longus is a muscle found in the posterior compartment of the forearm. It is one of the five deep extensors in the forearm, along with the supinator, extensor pollicis brevis, extensor pollicis longus and extensor indicis.

Abductor pollicis longus is innervated by the posterior interosseous nerve (C7, C8), which is a continuation of the deep branch of the radial nerve. The radial nerve is a branch of the posterior cord of the brachial plexus.

Blood supply to the abductor pollicis longus muscle comes from the interosseous branches of the ulnar artery.

Acting alone or with abductor pollicis brevis, abductor pollicis longus pulls the thumb away from the palm. More specifically, it produces (mid-) extension and abduction of the thumb at the first metacarpophalangeal joint. This action is seen in activities such as bowling and shovelling.

Working together with the long and short extensors of the thumb, the muscle also helps to fully extend the thumb at the metacarpophalangeal joint. This action is important for loosening the hand grip, for example, when letting go of objects previously being held. Abductor pollicis longus also helps to abduct the hand (radial deviation) at the radiocarpal joint.

A pathogen is an organism that is capable of causing disease.

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.

A low pH in the stomach inhibits gastrin secretion, therefore when the stomach is empty or when acid has been secreted for some time after food has entered it, there is inhibition of acid secretion. However, when food first enters the stomach, the pH rises, and this leads to release of the inhibition and causes a maximum secretion of gastrin. Thus gastric acid secretion is self-regulating.

Clinical features of hyperkalaemia may include:
paraesthesia, muscle weakness or paralysis, cardiac conduction abnormalities and dysrhythmias.

Clinical features of hypokalaemia may include:
muscle weakness, muscle cramps, rhabdomyolysis and myoglobinuria, ascending paralysis resulting in respiratory failure, constipation, gut ileus with distension, anorexia, nausea and vomiting, impaired ADH action with polyuria and polydipsia, ECG changes and cardiac arrhythmias.

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.

Pulmonary oedema causes stimulation of the Juxtacapillary receptors (J receptors) leading to a reflex increase in breathing rate. These receptors are also thought to be involved in the sensation of dyspnoea. The J receptors are sensory cells and are located within the alveolar walls in juxtaposition to the pulmonary capillaries.

Aortic baroreceptor are involved in detecting blood pressure

Central chemoreceptors detect changes in CO2 and hydrogen ion within the brain

Atrial volume receptors regulate plasma volume

Hepatitis B vaccine should be stored at 35°-46° F (2°-8° C) and should not be frozen.

There is no association between hepatitis B vaccination and Guillain-Barre syndrome. Infection with the bacterium Campylobacter jejuni is one of the most common risk factors for GBS. People can also develop GBS after having the flu or other infections (such as cytomegalovirus and Epstein Barr virus).

Hepatitis B vaccine is prepared from initial concentration of surface antigen.

To ensure adequate immunity, anti-HBs (HBsAb) titres may be checked 4-8 weeks following the last shot of the hepatitis B vaccine series.

The pressure measured in the right atrium or superior vena cava is known as central venous pressure (CVP). In a spontaneously breathing subject, the usual CVP value is 0-8 cmH2O (0-6 mmHg).

The structure of the CVP waveform is as follows:
The CVP’s components are listed in the table below:
Component of the waveform
The cardiac cycle phase.
mechanical event
mechanical event Diastole 
Atrial contraction
a wave 
C  wave 
v wave
Early systole
The tricuspid valve closes and bulges 
Late Systole 
Filling of the atrium with systolic blood 
x descent
y descent
Mid systole
Relaxation of the atrium 
Early diastole
Filling of the ventricles at an early stage