Theophylline is a medication used to treat severe asthma. It is a bronchodilator that comes in modified-release forms, which can maintain therapeutic levels in the blood for 12 hours. Theophylline works by inhibiting phosphodiesterase and blocking the breakdown of cyclic AMP. It also competes with adenosine on A1 and A2 receptors.

Achieving the right dose of theophylline can be challenging because there is a narrow range between therapeutic and toxic levels. The half-life of theophylline can be influenced by various factors, further complicating dosage adjustments. It is recommended to aim for serum levels of 10-20 mg/l six to eight hours after the last dose.

Unlike many other medications, the specific brand of theophylline can significantly impact its effects. Therefore, it is important to prescribe theophylline by both its brand name and generic name.

Several factors can increase the half-life of theophylline, including heart failure, cirrhosis, viral infections, and certain drugs. Conversely, smoking, heavy drinking, and certain medications can decrease the half-life of theophylline.

There are several drugs that can either increase or decrease the plasma concentration of theophylline. Calcium channel blockers, cimetidine, fluconazole, macrolides, methotrexate, and quinolones can increase the concentration. On the other hand, carbamazepine, phenobarbitol, phenytoin, rifampicin, and St. John’s wort can decrease the concentration.

The clinical symptoms of theophylline toxicity are more closely associated with acute overdose rather than chronic overexposure. Common symptoms include headache, dizziness, nausea, vomiting, abdominal pain, rapid heartbeat, dysrhythmias, seizures, mild metabolic acidosis, low potassium, low magnesium, low phosphates, abnormal calcium levels, and high blood sugar.

Seizures are more prevalent in acute overdose cases, while chronic overdose typically presents with minimal gastrointestinal symptoms. Cardiac dysrhythmias are more common in chronic overdose situations compared to acute overdose.

Enzyme-inducing anticonvulsants have been found to enhance the metabolism of ethinyl estradiol and progestogens. This increased breakdown diminishes the effectiveness of the oral contraceptive pill (OCP) in preventing pregnancy. Some examples of enzyme-inducing anticonvulsants include carbamazepine, phenytoin, phenobarbitol, and topiramate.

On the other hand, non-enzyme-inducing anticonvulsants are unlikely to have an impact on contraception. Some examples of these anticonvulsants are sodium valproate, clonazepam, gabapentin, levetiracetam, and piracetam.

It is important to note that lamotrigine, although classified as a non-enzyme-inducing anticonvulsant, requires special consideration. While there is no evidence suggesting that the OCP directly affects epilepsy, there is evidence indicating that it reduces the levels of lamotrigine in the bloodstream. This reduction in lamotrigine levels could potentially compromise seizure control and increase the likelihood of experiencing seizures.

Hypothyroidism is a condition characterized by an underactive thyroid gland, which leads to a decrease in the production of thyroid hormones. This can result in various clinical features. Some common symptoms include fatigue, lethargy, and cold intolerance. Patients may also experience bradycardia (a slow heart rate) and diastolic hypertension (high blood pressure). Hair loss and weight gain are also commonly seen in individuals with hypothyroidism. Other possible symptoms include constipation, poor appetite, and carpal tunnel syndrome. Skin pigmentation changes, particularly yellow discoloration, may occur due to carotene deposition in the dermis, most notably on the palms and soles.

Further Reading:

The thyroid gland is an endocrine organ located in the anterior neck. It consists of two lobes connected by an isthmus. The gland produces hormones called thyroxine (T4) and triiodothyronine (T3), which regulate energy use, protein synthesis, and the body’s sensitivity to other hormones. The production of T4 and T3 is stimulated by thyroid-stimulating hormone (TSH) secreted by the pituitary gland, which is in turn stimulated by thyrotropin-releasing hormone (TRH) from the hypothalamus.

Thyroid disorders can occur when there is an imbalance in the production or regulation of thyroid hormones. Hypothyroidism is characterized by a deficiency of thyroid hormones, while hyperthyroidism is characterized by an excess. The most common cause of hypothyroidism is autoimmune thyroiditis, also known as Hashimoto’s thyroiditis. It is more common in women and is often associated with goiter. Other causes include subacute thyroiditis, atrophic thyroiditis, and iodine deficiency. On the other hand, the most common cause of hyperthyroidism is Graves’ disease, which is also an autoimmune disorder. Other causes include toxic multinodular goiter and subacute thyroiditis.

The symptoms and signs of thyroid disorders can vary depending on whether the thyroid gland is underactive or overactive. In hypothyroidism, common symptoms include weight gain, lethargy, cold intolerance, and dry skin. In hyperthyroidism, common symptoms include weight loss, restlessness, heat intolerance, and increased sweating. Both hypothyroidism and hyperthyroidism can also affect other systems in the body, such as the cardiovascular, gastrointestinal, and neurological systems.

Complications of thyroid disorders can include dyslipidemia, metabolic syndrome, coronary heart disease, heart failure, subfertility and infertility, impaired special senses, and myxedema coma in severe cases of hypothyroidism. In hyperthyroidism, complications can include Graves’ orbitopathy, compression of the esophagus or trachea by goiter, thyrotoxic periodic paralysis, arrhythmias, osteoporosis, mood disorders, and increased obstetric complications.

Myxedema coma is a rare and life-threatening complication of severe hypothyroidism. It can be triggered by factors such as infection or physiological insult and presents with lethargy, bradycardia, hypothermia, hypotension, hypoventilation, altered mental state, seizures and/or coma.

A significant proportion of the population experiences a difference of 10 mmHg or more in blood pressure between their upper limbs. Pericarditis can be identified by the presence of saddle-shaped ST elevation and pain in the trapezius ridge. Aortic dissection is characterized by a diastolic murmur with a decrescendo pattern, which indicates aortic incompetence.

Further Reading:

Aortic dissection is a life-threatening condition in which blood flows through a tear in the innermost layer of the aorta, creating a false lumen. Prompt treatment is necessary as the mortality rate increases by 1-2% per hour. There are different classifications of aortic dissection, with the majority of cases being proximal. Risk factors for aortic dissection include hypertension, atherosclerosis, connective tissue disorders, family history, and certain medical procedures.

The presentation of aortic dissection typically includes sudden onset sharp chest pain, often described as tearing or ripping. Back pain and abdominal pain are also common, and the pain may radiate to the neck and arms. The clinical picture can vary depending on which aortic branches are affected, and complications such as organ ischemia, limb ischemia, stroke, myocardial infarction, and cardiac tamponade may occur. Common signs and symptoms include a blood pressure differential between limbs, pulse deficit, and a diastolic murmur.

Various investigations can be done to diagnose aortic dissection, including ECG, CXR, and CT with arterial contrast enhancement (CTA). CT is the investigation of choice due to its accuracy in diagnosis and classification. Other imaging techniques such as transoesophageal echocardiography (TOE), magnetic resonance imaging/angiography (MRI/MRA), and digital subtraction angiography (DSA) are less commonly used.

Management of aortic dissection involves pain relief, resuscitation measures, blood pressure control, and referral to a vascular or cardiothoracic team. Opioid analgesia should be given for pain relief, and resuscitation measures such as high flow oxygen and large bore IV access should be performed. Blood pressure control is crucial, and medications such as labetalol may be used to reduce systolic blood pressure. Hypotension carries a poor prognosis and may require careful fluid resuscitation. Treatment options depend on the type of dissection, with type A dissections typically requiring urgent surgery and type B dissections managed by thoracic endovascular aortic repair (TEVAR) and blood pressure control optimization.

In cases of human bite wounds where the skin is broken but no blood is drawn, it is recommended to consider antibiotic prophylaxis, especially if the bite occurs in a high-risk area like the hands. According to NICE guidelines, a 3-day course of antibiotics is usually sufficient for prophylaxis in bite wounds. However, if the bite wound becomes infected, a 5-day course of antibiotics is advised for treatment.

Further Reading:

Bite wounds from animals and humans can cause significant injury and infection. It is important to properly assess and manage these wounds to prevent complications. In human bites, both the biter and the injured person are at risk of infection transmission, although the risk is generally low.

Bite wounds can take various forms, including lacerations, abrasions, puncture wounds, avulsions, and crush or degloving injuries. The most common mammalian bites are associated with dogs, cats, and humans.

When assessing a human bite, it is important to gather information about how and when the bite occurred, who was involved, whether the skin was broken or blood was involved, and the nature of the bite. The examination should include vital sign monitoring if the bite is particularly traumatic or sepsis is suspected. The location, size, and depth of the wound should be documented, along with any functional loss or signs of infection. It is also important to check for the presence of foreign bodies in the wound.

Factors that increase the risk of infection in bite wounds include the nature of the bite, high-risk sites of injury (such as the hands, feet, face, genitals, or areas of poor perfusion), wounds penetrating bone or joints, delayed presentation, immunocompromised patients, and extremes of age.

The management of bite wounds involves wound care, assessment and administration of prophylactic antibiotics if indicated, assessment and administration of tetanus prophylaxis if indicated, and assessment and administration of antiviral prophylaxis if indicated. For initial wound management, any foreign bodies should be removed, the wound should be encouraged to bleed if fresh, and thorough irrigation with warm, running water or normal saline should be performed. Debridement of necrotic tissue may be necessary. Bite wounds are usually not appropriate for primary closure.

Prophylactic antibiotics should be considered for human bites that have broken the skin and drawn blood, especially if they involve high-risk areas or the patient is immunocompromised. Co-amoxiclav is the first-line choice for prophylaxis, but alternative antibiotics may be used in penicillin-allergic patients. Antibiotics for wound infection should be based on wound swab culture and sensitivities.

Tetanus prophylaxis should be administered based on the cleanliness and risk level of the wound, as well as the patient’s vaccination status. Blood-borne virus risk should also be assessed, and testing for hepatitis B, hepatitis C, and HIV should be done.

Chlamydia trachomatis is a type of Gram-negative bacteria that is responsible for causing the sexually transmitted infection known as chlamydia. This bacterium is typically either coccoid or rod-shaped in its appearance.

There are various serological variants of C. trachomatis, and each variant is associated with different patterns of disease. Specifically, types D-K are responsible for causing genitourinary infections.

In the United Kingdom, chlamydia is the most commonly diagnosed sexually transmitted infection (STI). It is also the leading preventable cause of infertility worldwide. Interestingly, around 50% of men infected with chlamydia do not experience any symptoms, while at least 70% of infected women are asymptomatic.

If left untreated, chlamydia can lead to various complications. In women, these complications may include pelvic inflammatory disease (PID), ectopic pregnancy, and tubal infertility. Men, on the other hand, may experience complications such as proctitis, epididymitis, and epididymo-orchitis.

This patient has presented with an Addisonian crisis, which is a rare but potentially catastrophic condition if not diagnosed promptly. It is more commonly seen in women than men and typically occurs between the ages of 30 and 50.

Addison’s disease is caused by insufficient production of steroid hormones by the adrenal glands, affecting the production of glucocorticoids, mineralocorticoids, and sex steroids. The main causes of Addison’s disease include autoimmune adrenalitis (accounting for 80% of cases), bilateral adrenalectomy, Waterhouse-Friderichsen syndrome (hemorrhage into the adrenal glands), and tuberculosis.

The most common trigger for an Addisonian crisis in patients with Addison’s disease is the intentional or accidental withdrawal of steroid therapy. Other factors that can precipitate a crisis include infection, trauma, myocardial infarction, cerebral infarction, asthma, hypothermia, and alcohol abuse.

Clinical features of Addison’s disease include weakness, lethargy, hypotension (especially orthostatic hypotension), nausea, vomiting, weight loss, reduced axillary and pubic hair, depression, and hyperpigmentation (particularly in palmar creases, buccal mucosa, and exposed areas). In an Addisonian crisis, the main symptoms are usually hypoglycemia and shock, characterized by tachycardia, peripheral vasoconstriction, hypotension, altered consciousness, and even coma.

Biochemical markers of Addison’s disease typically include increased ACTH levels (as a compensatory response to stimulate the adrenal glands), elevated serum renin levels, hyponatremia, hyperkalemia, hypercalcemia, hypoglycemia, and metabolic acidosis. Confirmatory investigations may involve the Synacthen test, plasma ACTH level measurement, plasma renin level measurement, and testing for adrenocortical antibodies.

Management of Addison’s disease should be overseen by an Endocrinologist. Treatment usually involves the administration of hydrocortisone, fludrocortisone, and dehydroepiandrosterone. Some patients may also require thyroxine if there is concurrent hypothalamic-pituitary disease. Treatment is lifelong, and patients should carry a steroid card and MedicAlert bracelet to alert healthcare professionals about their condition and the potential for an Addisonian crisis.

To diagnose diabetic ketoacidosis (DKA), all three of the following criteria must be present: ketonaemia (≥3 mmol/L) or ketonuria (> 2+ on urine dipstick), blood glucose > 11 mmol/L or known diabetes mellitus, and blood pH <7.3 or bicarbonate < 15 mmol/L. It is important to note that plasma osmolality and anion gap, although typically elevated in DKA, are not included in the diagnostic criteria. Further Reading: Diabetic ketoacidosis (DKA) is a serious complication of diabetes that occurs due to a lack of insulin in the body. It is most commonly seen in individuals with type 1 diabetes but can also occur in type 2 diabetes. DKA is characterized by hyperglycemia, acidosis, and ketonaemia. The pathophysiology of DKA involves insulin deficiency, which leads to increased glucose production and decreased glucose uptake by cells. This results in hyperglycemia and osmotic diuresis, leading to dehydration. Insulin deficiency also leads to increased lipolysis and the production of ketone bodies, which are acidic. The body attempts to buffer the pH change through metabolic and respiratory compensation, resulting in metabolic acidosis. DKA can be precipitated by factors such as infection, physiological stress, non-compliance with insulin therapy, acute medical conditions, and certain medications. The clinical features of DKA include polydipsia, polyuria, signs of dehydration, ketotic breath smell, tachypnea, confusion, headache, nausea, vomiting, lethargy, and abdominal pain. The diagnosis of DKA is based on the presence of ketonaemia or ketonuria, blood glucose levels above 11 mmol/L or known diabetes mellitus, and a blood pH below 7.3 or bicarbonate levels below 15 mmol/L. Initial investigations include blood gas analysis, urine dipstick for glucose and ketones, blood glucose measurement, and electrolyte levels. Management of DKA involves fluid replacement, electrolyte correction, insulin therapy, and treatment of any underlying cause. Fluid replacement is typically done with isotonic saline, and potassium may need to be added depending on the patient’s levels. Insulin therapy is initiated with an intravenous infusion, and the rate is adjusted based on blood glucose levels. Monitoring of blood glucose, ketones, bicarbonate, and electrolytes is essential, and the insulin infusion is discontinued once ketones are below 0.3 mmol/L, pH is above 7.3, and bicarbonate is above 18 mmol/L. Complications of DKA and its treatment include gastric stasis, thromboembolism, electrolyte disturbances, cerebral edema, hypoglycemia, acute respiratory distress syndrome, and acute kidney injury. Prompt medical intervention is crucial in managing DKA to prevent potentially fatal outcomes.

Hepatitis B vaccination is included in the routine childhood immunisation schedule to provide long-term protection against hepatitis for children under 1 year of age. For these children, the vaccination consists of a primary course that includes the diphtheria with tetanus, pertussis, hepatitis B, poliomyelitis, and Haemophilus influenza type B vaccine. This primary course is given at 4 weekly intervals.

The Hepatitis B vaccine is a conjugate vaccine that contains a surface antigen of the hepatitis virus (HBsAg) and is combined with an aluminium adjuvant to enhance its effectiveness. It is produced using a recombinant DNA technique.

When administering the vaccine to adults and older children, the preferred injection site is the deltoid muscle. However, in younger children, the anterolateral thigh is the preferred site. It is not recommended to inject the vaccine in the gluteal area as it has been found to have reduced efficacy.

The standard vaccination regime for Hepatitis B consists of three primary doses. The initial dose is followed by further doses at one and six months later. A booster dose is recommended at five years if the individual is still at risk.

In cases of post-exposure prophylaxis, an accelerated vaccination regime is used. This involves administering a vaccination at the time of exposure, followed by repeat doses at one and two months later.

In high-risk situations, Hepatitis B immunoglobulin can be given up to 7 days after exposure. Ideally, it should be administered within 12 hours, but according to the BNF, it can still be effective if given within 7 days after exposure.

During CPR of a hypothermic patient, it is important to follow specific guidelines. If the patient’s core temperature is below 30ºC, resuscitation drugs, such as adrenaline, should be withheld. Once the core temperature rises above 30ºC, cardiac arrest drugs can be administered. However, if the patient’s temperature is between 30-35ºC, the interval for administering cardiac arrest drugs should be doubled. For example, adrenaline should be given every 6-10 minutes instead of the usual 3-5 minutes for a normothermic patient.

Further Reading:

Hypothermic cardiac arrest is a rare situation that requires a tailored approach. Resuscitation is typically prolonged, but the prognosis for young, previously healthy individuals can be good. Hypothermic cardiac arrest may be associated with drowning. Hypothermia is defined as a core temperature below 35ºC and can be graded as mild, moderate, severe, or profound based on the core temperature. When the core temperature drops, basal metabolic rate falls and cell signaling between neurons decreases, leading to reduced tissue perfusion. Signs and symptoms of hypothermia progress as the core temperature drops, initially presenting as compensatory increases in heart rate and shivering, but eventually ceasing as the temperature drops into moderate hypothermia territory.

ECG changes associated with hypothermia include bradyarrhythmias, Osborn waves, prolonged PR, QRS, and QT intervals, shivering artifact, ventricular ectopics, and cardiac arrest. When managing hypothermic cardiac arrest, ALS should be initiated as per the standard ALS algorithm, but with modifications. It is important to check for signs of life, re-warm the patient, consider mechanical ventilation due to chest wall stiffness, adjust dosing or withhold drugs due to slowed drug metabolism, and correct electrolyte disturbances. The resuscitation of hypothermic patients is often prolonged and may continue for a number of hours.

Pulse checks during CPR may be difficult due to low blood pressure, and the pulse check is prolonged to 1 minute for this reason. Drug metabolism is slowed in hypothermic patients, leading to a build-up of potentially toxic plasma concentrations of administered drugs. Current guidance advises withholding drugs if the core temperature is below 30ºC and doubling the drug interval at core temperatures between 30 and 35ºC. Electrolyte disturbances are common in hypothermic patients, and it is important to interpret results keeping the setting in mind. Hypoglycemia should be treated, hypokalemia will often correct as the patient re-warms, ABG analyzers may not reflect the reality of the hypothermic patient, and severe hyperkalemia is a poor prognostic indicator.

Different warming measures can be used to increase the core body temperature, including external passive measures such as removal of wet clothes and insulation with blankets, external active measures such as forced heated air or hot-water immersion, and internal active measures such as inhalation of warm air, warmed intravenous fluids, gastric, bladder, peritoneal and/or pleural lavage and high volume renal haemofilter.