In a patient with severe otitis externa on the left side, it is expected that they will experience conductive deafness on the left side. This means that their ability to hear sound will be impaired due to a problem in the ear canal or middle ear. When conducting a Rinne’s test, a vibrating 512 Hz tuning fork is placed on the mastoid process until the patient can no longer hear the sound. Then, the top of the tuning fork is positioned 2 cm from the external auditory meatus, and the patient is asked where they hear the sound loudest.

In individuals with normal hearing, the sound from the tuning fork should still be audible outside the external auditory canal even after it can no longer be heard on the mastoid. This is because air conduction should be better than bone conduction. However, in cases of conductive hearing loss, the patient will no longer be able to hear the tuning fork once it is removed from the mastoid. This indicates that their bone conduction is greater than their air conduction, suggesting an obstruction in the ear canal that prevents sound waves from reaching the cochlea. This is referred to as a true negative result.

It is important to note that a Rinne’s test may yield a false negative result if the patient has a severe unilateral sensorineural deficit. In this case, they may still sense the sound in the unaffected ear due to the transmission of sound through the base of the skull. In contrast, individuals with sensorineural hearing loss will have diminished ability to hear the tuning fork both on the mastoid and outside the external auditory canal compared to the opposite ear. The sound will disappear earlier on the mastoid and outside the external auditory canal in the affected ear.

When performing Weber’s test, a vibrating 512 Hz tuning fork is placed on the center of the patient’s forehead. The patient is then asked if they perceive the sound in the middle of the forehead or if it lateralizes to one side. If the sound lateralizes to one side, it can indicate either ipsilateral conductive hearing loss or contralateral sensorineural hearing loss.

In the UK, the most commonly used treatment for acute exacerbations of hereditary angioedema (HAE) in emergency departments is C1-Esterase inhibitor. However, there are alternative options available. Icatibant acetate, sold under the brand name Firazyr®, is a bradykinin receptor antagonist that can be used as an alternative treatment. Another alternative is the transfusion of fresh frozen plasma.

Further Reading:

Angioedema and urticaria are related conditions that involve swelling in different layers of tissue. Angioedema refers to swelling in the deeper layers of tissue, such as the lips and eyelids, while urticaria, also known as hives, refers to swelling in the epidermal skin layers, resulting in raised red areas of skin with itching. These conditions often coexist and may have a common underlying cause.

Angioedema can be classified into allergic and non-allergic types. Allergic angioedema is the most common type and is usually triggered by an allergic reaction, such as to certain medications like penicillins and NSAIDs. Non-allergic angioedema has multiple subtypes and can be caused by factors such as certain medications, including ACE inhibitors, or underlying conditions like hereditary angioedema (HAE) or acquired angioedema.

HAE is an autosomal dominant disease characterized by a deficiency of C1 esterase inhibitor. It typically presents in childhood and can be inherited or acquired as a result of certain disorders like lymphoma or systemic lupus erythematosus. Acquired angioedema may have similar clinical features to HAE but is caused by acquired deficiencies of C1 esterase inhibitor due to autoimmune or lymphoproliferative disorders.

The management of urticaria and allergic angioedema focuses on ensuring the airway remains open and addressing any identifiable triggers. In mild cases without airway compromise, patients may be advised that symptoms will resolve without treatment. Non-sedating antihistamines can be used for up to 6 weeks to relieve symptoms. Severe cases of urticaria may require systemic corticosteroids in addition to antihistamines. In moderate to severe attacks of allergic angioedema, intramuscular epinephrine may be considered.

The management of HAE involves treating the underlying deficiency of C1 esterase inhibitor. This can be done through the administration of C1 esterase inhibitor, bradykinin receptor antagonists, or fresh frozen plasma transfusion, which contains C1 inhibitor.

In summary, angioedema and urticaria are related conditions involving swelling in different layers of tissue. They can coexist and may have a common underlying cause. Management involves addressing triggers, using antihistamines, and in severe cases, systemic corticosteroids or other specific treatments for HAE.

Pick’s disease is a rare neurodegenerative disorder that leads to a gradual decline in cognitive function known as frontotemporal dementia. One of the key features of this condition is the accumulation of tau proteins in neurons, forming silver-staining, spherical aggregations called ‘Pick bodies.’

Typically, Pick’s disease manifests between the ages of 40 and 60. Initially, individuals may experience changes in their personality, such as disinhibition, tactlessness, and vulgarity. They may also exhibit alterations in their moral values and attempt to distance themselves from their family. Difficulties with concentration, increased activity levels, pacing, and wandering are also common during this stage.

What sets Pick’s disease apart from Alzheimer’s disease is that the changes in personality occur before memory loss becomes apparent. As the disease progresses, patients will experience deficits in intellect, memory, and language.

Bullous pemphigoid (BP) is a chronic autoimmune disorder that affects the skin, causing blistering. It occurs when the immune system mistakenly attacks the basement membrane of the epidermis. This attack is carried out by immunoglobulins (IgG and sometimes IgE) and activated T lymphocytes. The autoantibodies bind to proteins and release cytokines, leading to complement activation, neutrophil recruitment, and the release of enzymes that destroy the hemidesmosomes. As a result, subepidermal blisters form.

Pemphigus, on the other hand, is a group of autoimmune disorders characterized by blistering of the skin and mucosal surfaces. The most common type, pemphigus vulgaris (PV), accounts for about 70% of cases worldwide. PV is also autoimmune in nature, with autoantibodies targeting cell surface antigens on keratinocytes (desmogleins 1 and 3). This leads to a loss of adhesion between cells and their separation.

Here is a comparison of the key differences between pemphigus vulgaris and bullous pemphigoid:

Pemphigus vulgaris:
– Age: Middle-aged people (average age 50)
– Oral involvement: Common
– Blister type: Large, flaccid, and painful
– Blister content: Fluid-filled, often haemorrhagic
– Areas commonly affected: Initially face and scalp, then spread to the chest and back
– Nikolsky sign: Usually positive
– Pruritus: Rare
– Skin biopsy: Intra-epidermal deposition of IgG between cells throughout the epidermis

Bullous pemphigoid:
– Age: Elderly people (average age 80)
– Oral involvement: Rare
– Blister type: Large and tense
– Blister content: Fluid-filled
– Areas commonly affected: Upper arms, thighs, and skin flexures
– Nikolsky sign: Usually negative
– Pruritus: Common
– Skin biopsy: A band of IgG and/or C3 at the dermo-epidermal junction

Discitis is an infection that affects the space between the intervertebral discs in the spine. This condition can have serious consequences, including the formation of abscesses and sepsis. The most common cause of discitis is usually Staphylococcus aureus, but other organisms like Streptococcus viridans and Pseudomonas aeruginosa may be responsible in intravenous drug users and those with weakened immune systems. Gram-negative organisms such as Escherichia coli and Mycobacterium tuberculosis can also cause discitis.

There are several risk factors that increase the likelihood of developing discitis. These include having undergone spinal surgery (which occurs in 1-2% of cases post-operatively), having an immunodeficiency, being an intravenous drug user, being under the age of eight, having diabetes mellitus, or having a malignancy.

The typical symptoms of discitis include back or neck pain (which occurs in over 90% of cases), pain that often wakes the patient from sleep, fever (present in 60-70% of cases), and neurological deficits (which can occur in up to 50% of cases). In children, refusal to walk may also be a symptom.

When diagnosing discitis, MRI is the preferred imaging modality due to its high sensitivity and specificity. It is important to image the entire spine, as discitis often affects multiple levels. Plain radiographs are not very sensitive to the early changes of discitis and may appear normal for 2-4 weeks. CT scanning is also not very sensitive in detecting discitis.

Treatment for discitis involves admission to the hospital for intravenous antibiotics. Before starting the antibiotics, it is important to send three sets of blood cultures and a full set of blood tests, including a CRP, to the lab. The choice of antibiotics depends on the specific situation. A typical antibiotic regimen for discitis may include IV flucloxacillin as the first-line treatment if there is no penicillin allergy, IV vancomycin if the infection was acquired in the hospital or there is a high risk of MRSA, and possibly IV gentamicin if there is a possibility of a Gram-negative infection. In cases where there is acute kidney injury and Gram-negative cover is required, IV piperacillin-tazobactam alone may be used.

Fluid deficit in children and young people with severe diabetic ketoacidosis (DKA) is determined by measuring their blood pH and bicarbonate levels. If the blood pH is below 7.1 and/or the bicarbonate level is below 5, it indicates a fluid deficit. This simplified explanation uses a cutoff value of 5 to determine the severity of the fluid deficit in DKA.

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.

Thiamine deficiency is linked to episodes of acute confusion, but it is not typically associated with depression. On the other hand, depression is commonly seen in individuals with hypercalcemia. Chronic diseases like Parkinson’s disease and COPD are strongly correlated with depression. Additionally, both psychosis and depression can be associated with the use of steroids.

Anaphylaxis is a prime example of a type I hypersensitivity reaction. It is mediated by IgE antibodies. The complex formed by IgE and the antigen binds to Fc receptors found on the surface of mast cells. This binding triggers the degranulation of mast cells, leading to the release of histamine, proteoglycans, and serum proteases from their granules. It is important to note that anaphylaxis can only occur after prior exposure to the antigen. During the initial exposure, a sensitization reaction takes place, and it is only upon subsequent exposure to the antigen that anaphylaxis is triggered. The degranulation of mast cells is a result of a significant influx of calcium into these cells.

The beta thalassaemias are a group of blood disorders that occur when there is an abnormality in the production of the globin chains. These disorders are inherited in an autosomal recessive manner. In individuals with beta thalassaemia trait, there is a slight decrease in the production of beta-globin chains. This condition is most commonly found in people of Mediterranean and Asian descent.

The presentation of beta thalassaemia trait is characterized by a mild form of microcytic hypochromic anaemia. This type of anaemia can be challenging to differentiate from iron deficiency anaemia. However, it can be distinguished from iron deficiency anaemia by the presence of normal iron levels. Another useful marker for diagnosing beta thalassaemia trait is an elevated HbA2 level. A value greater than 3.5% is considered diagnostic for this condition.

People with chronic mitral regurgitation often experience atrial fibrillation.

Mitral Stenosis:
– Causes: Rheumatic fever, Mucopolysaccharidoses, Carcinoid, Endocardial fibroelastosis
– Features: Mid-late diastolic murmur, loud S1, opening snap, low volume pulse, malar flush, atrial fibrillation, signs of pulmonary edema, tapping apex beat
– Features of severe mitral stenosis: Length of murmur increases, opening snap becomes closer to S2
– Investigation findings: CXR may show left atrial enlargement, echocardiography may show reduced cross-sectional area of the mitral valve

Mitral Regurgitation:
– Causes: Mitral valve prolapse, Myxomatous degeneration, Ischemic heart disease, Rheumatic fever, Connective tissue disorders, Endocarditis, Dilated cardiomyopathy
– Features: pansystolic murmur radiating to left axilla, soft S1, S3, laterally displaced apex beat with heave
– Signs of acute MR: Decompensated congestive heart failure symptoms
– Signs of chronic MR: Leg edema, fatigue, arrhythmia (atrial fibrillation)
– Investigation findings: Doppler echocardiography to detect regurgitant flow and pulmonary hypertension, ECG may show signs of LA enlargement and LV hypertrophy, CXR may show LA and LV enlargement in chronic MR and pulmonary edema in acute MR.

Heat stroke is a condition characterized by a core temperature higher than 40.6°C, accompanied by changes in mental state and varying levels of organ dysfunction. There are two forms of heat stroke: classic non-exertional heat stroke, which occurs during high environmental temperatures and typically affects elderly patients during heat waves, and exertional heat stroke, which occurs during strenuous physical exercise in hot conditions, such as endurance athletes competing in hot weather.

The main treatment for heat stroke involves supportive measures. It is important to rapidly reduce the core temperature to around 39.0°C. Patients with severe heat stroke should be managed in a critical care setting. The ABCDE approach should be followed, with a focus on cooling the patient. This includes obtaining a definitive airway if the patient is unresponsive, providing ventilation if necessary, using haemodynamic monitoring to guide fluid therapy, correcting electrolyte imbalances, managing blood glucose levels, removing clothes, eliminating the cause of hyperthermia, and monitoring core and skin temperatures.

There are various cooling techniques that can be used, although there is limited evidence on which approach is the most effective. Some possible methods include simple measures like cold drinks, fanning, ice water packs, and spraying tepid water. Cold water immersion therapy can be beneficial, but it requires the patient to be stable and cooperative, making it impractical for very sick patients. Advanced cooling techniques, such as cold IV fluids, surface cooling devices, intravascular cooling devices, and extracorporeal circuits, may be used for sicker patients.

Benzodiazepines, like diazepam, can be helpful in managing agitation and shivering in heat stroke patients. They not only reduce excessive heat production but also help to calm the patient. In severe cases of agitation, paralysis may be necessary. Dantrolene is commonly used, although there is currently limited high-level evidence to support its use. Neuroleptics, such as chlorpromazine, which were once commonly used, should be avoided due to their potential adverse effects, including lowering the seizure threshold, interfering with thermoregulation, causing anticholinergic side effects, hypotension, and hepatotoxicity.

Septic arthritis occurs when an infectious agent invades a joint, causing it to become purulent. The main symptoms of septic arthritis include pain in the affected joint, redness, warmth, and swelling of the joint, and difficulty moving the joint. Patients may also experience fever and systemic upset. The most common cause of septic arthritis is Staphylococcus aureus, but other bacteria such as Streptococcus spp., Haemophilus influenzae, Neisseria gonorrhoea, and Escherichia coli can also be responsible.

According to the current recommendations by NICE and the BNF, the initial treatment for septic arthritis is flucloxacillin. However, if a patient is allergic to penicillin, clindamycin can be used instead. If there is a suspicion of MRSA infection, vancomycin is the recommended choice. In cases where gonococcal arthritis or a Gram-negative infection is suspected, cefotaxime is the preferred treatment. The suggested duration of treatment is typically 4-6 weeks, although it may be longer if the infection is complicated.

If a child under 3 months old has a temperature of 38ºC or higher, it is considered a red flag according to the NICE traffic light system. This indicates that the child may have acute otitis media and it is recommended that they be admitted for further evaluation and treatment.

Further Reading:

Acute otitis media (AOM) is an inflammation in the middle ear accompanied by symptoms and signs of an ear infection. It is commonly seen in young children below 4 years of age, with the highest incidence occurring between 9 to 15 months of age. AOM can be caused by viral or bacterial pathogens, and co-infection with both is common. The most common viral pathogens include respiratory syncytial virus (RSV), rhinovirus, adenovirus, influenza virus, and parainfluenza virus. The most common bacterial pathogens include Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and Streptococcus pyogenes.

Clinical features of AOM include ear pain (otalgia), fever, a red or cloudy tympanic membrane, and a bulging tympanic membrane with loss of anatomical landmarks. In young children, symptoms may also include crying, grabbing or rubbing the affected ear, restlessness, and poor feeding.

Most children with AOM will recover within 3 days without treatment. Serious complications are rare but can include persistent otitis media with effusion, recurrence of infection, temporary hearing loss, tympanic membrane perforation, labyrinthitis, mastoiditis, meningitis, intracranial abscess, sinus thrombosis, and facial nerve paralysis.

Management of AOM involves determining whether admission to the hospital is necessary based on the severity of systemic infection or suspected acute complications. For patients who do not require admission, regular pain relief with paracetamol or ibuprofen is advised. Decongestants or antihistamines are not recommended. Antibiotics may be offered immediately for patients who are systemically unwell, have symptoms and signs of a more serious illness or condition, or have a high risk of complications. For other patients, a decision needs to be made on the antibiotic strategy, considering the rarity of acute complications and the possible adverse effects of antibiotics. Options include no antibiotic prescription with advice to seek medical help if symptoms worsen rapidly or significantly, a back-up antibiotic prescription to be used if symptoms do not improve within 3 days, or an immediate antibiotic prescription with advice to seek medical advice if symptoms worsen rapidly or significantly.

The first-line antibiotic choice for AOM is a 5-7 day course of amoxicillin. For individuals allergic to or intolerant of penicillin, clarithromycin or erythromycin a 5–7 day course of clarithromycin or erythromycin (erythromycin is preferred in pregnant women).

Pericarditis refers to the inflammation of the pericardium, which can be caused by various factors such as infections (typically viral, like coxsackie virus), drug-induced reactions (e.g. isoniazid, cyclosporine), trauma, autoimmune conditions (e.g. SLE), paraneoplastic syndromes, uraemia, post myocardial infarction (known as Dressler’s syndrome), post radiotherapy, and post cardiac surgery.

The clinical presentation of pericarditis often includes retrosternal chest pain that is pleuritic in nature. This pain is typically relieved by sitting forwards and worsened when lying flat. It may also radiate to the shoulders. Other symptoms may include shortness of breath, tachycardia, and the presence of a pericardial friction rub.

The pericardium receives sensory supply from the phrenic nerve, which also provides sensory innervation to the diaphragm, various mediastinal structures, and certain abdominal structures such as the superior peritoneum, liver, and gallbladder. Since the phrenic nerve originates from the 4th cervical nerve, which also provides cutaneous innervation to the front of the shoulder girdle, pain from pericarditis can also radiate to the shoulders.

Depression and dementia are both more prevalent in the elderly population and often coexist. Diagnosing these conditions can be challenging due to the overlapping symptoms they share.

Depression is characterized by a persistent low mood throughout the day, significant unintentional weight changes, sleep disturbances, fatigue, feelings of worthlessness or guilt, difficulty concentrating, loss of interest in activities, and recurrent thoughts of death. It may also manifest as agitation or slowed movements, which can be observed by others.

Dementia, on the other hand, refers to a group of symptoms resulting from a pathological process that leads to significant cognitive impairment. This impairment is more severe than what would be expected for a person’s age. Alzheimer’s disease is the most common form of dementia.

Symptoms of dementia include memory loss, particularly in the short-term, changes in mood that are usually reactive to situations and improve with support and stimulation, infrequent thoughts about death, alterations in personality, difficulty finding the right words, struggles with complex tasks, urinary incontinence, loss of appetite and weight in later stages, and agitation in unfamiliar environments.

By understanding the distinct features of depression and dementia, healthcare professionals can better identify and differentiate between these conditions in the elderly population.

Multiple myeloma is a cancerous growth of plasma cells, a type of white blood cell responsible for producing antibodies. It is more prevalent in men and typically occurs in individuals over the age of 60.

When a patient over 60 presents with an elevated ESR, unexplained anemia, hypercalcemia, renal impairment, and bone pain, the initial diagnosis is usually multiple myeloma until proven otherwise.

The most common symptoms of multiple myeloma include:

1. Anemia: This is caused by the infiltration of the bone marrow and suppression of blood cell production. It is typically normocytic and normochromic, but can also be macrocytic.

2. Bone pain: Approximately 70% of patients experience bone pain, which commonly affects the spine and ribs. Localized pain and tenderness may indicate a pathological fracture, and vertebral fractures can lead to spinal cord compression.

3. Renal failure: Acute or chronic renal failure occurs in about one-third of patients. This is generally due to the effects of light chains on the tubules.

4. Neurological symptoms: Hypercalcemia can cause weakness, lethargy, and confusion, while hyperviscosity can result in headaches and retinopathy. Amyloid infiltration can lead to peripheral neuropathies, with carpal tunnel syndrome being the most common.

5. Infection: The most common infections seen in multiple myeloma patients are pyelonephritis and pneumonia.

In addition to the routine blood tests already conducted, a suspected diagnosis of multiple myeloma should prompt further investigations, including:

– Plasma viscosity measurement
– Urinary protein electrophoresis to detect Bence-Jones proteins
– Serum electrophoresis to identify the type of paraprotein
– Quantitative immunoglobulin level testing
– Skeletal survey to look for lytic lesions
– Bone marrow aspirate and possibly biopsy

A diagnosis of multiple myeloma is confirmed by the presence of a monoclonal protein in the serum or urine, lytic lesions on X-ray, and an increased number of plasma cells in the bone marrow.

The patient presents with a medical history and physical examination findings that are consistent with a diagnosis of Löfgren’s syndrome, which is a specific subtype of sarcoidosis. This syndrome is most commonly observed in women in their 30s and 40s, and it is more prevalent among individuals of Nordic and Irish descent.

Löfgren’s syndrome is typically characterized by a triad of clinical features, including bilateral hilar lymphadenopathy seen on chest X-ray, erythema nodosum, and arthralgia, with a particular emphasis on ankle involvement. Additionally, other symptoms commonly associated with sarcoidosis may also be present, such as a dry cough, breathlessness, fever, night sweats, malaise, weight loss, Achilles tendonitis, and uveitis.

In order to further evaluate this patient’s condition, it is recommended to refer them to a respiratory specialist for additional investigations. These investigations may include measuring the serum calcium level, as it may be elevated, and assessing the serum angiotensin-converting enzyme (ACE) level, which may also be elevated. A high-resolution CT scan can be performed to assess the extent of involvement and identify specific lymph nodes for potential biopsy. If there are any atypical features, a lymph node biopsy may be necessary. Lung function tests can be conducted to evaluate the patient’s vital capacity, and an MRI scan of the ankles may also be considered.

Fortunately, the prognosis for Löfgren’s syndrome is generally very good, and it is considered a self-limiting and benign condition. The patient can expect to recover within a timeframe of six months to two years.

The electrolyte imbalances that are commonly observed in individuals with Addison’s disease are decreased sodium levels, increased potassium levels, increased calcium levels, and decreased glucose levels. In cases of Addisonian crisis, which is a severe form of Addison’s disease, patients may also experience hyponatremia (low sodium levels), hyperkalemia (high potassium levels), hypercalcemia (high calcium levels), and hypoglycemia (low glucose levels). Additionally, these patients may often develop acidosis.

Further Reading:

Addison’s disease, also known as primary adrenal insufficiency or hypoadrenalism, is a rare disorder caused by the destruction of the adrenal cortex. This leads to reduced production of glucocorticoids, mineralocorticoids, and adrenal androgens. The deficiency of cortisol results in increased production of adrenocorticotropic hormone (ACTH) due to reduced negative feedback to the pituitary gland. This condition can cause metabolic disturbances such as hyperkalemia, hyponatremia, hypercalcemia, and hypoglycemia.

The symptoms of Addison’s disease can vary but commonly include fatigue, weight loss, muscle weakness, and low blood pressure. It is more common in women and typically affects individuals between the ages of 30-50. The most common cause of primary hypoadrenalism in developed countries is autoimmune destruction of the adrenal glands. Other causes include tuberculosis, adrenal metastases, meningococcal septicaemia, HIV, and genetic disorders.

The diagnosis of Addison’s disease is often suspected based on low cortisol levels and electrolyte abnormalities. The adrenocorticotropic hormone stimulation test is commonly used for confirmation. Other investigations may include adrenal autoantibodies, imaging scans, and genetic screening.

Addisonian crisis is a potentially life-threatening condition that occurs when there is an acute deficiency of cortisol and aldosterone. It can be the first presentation of undiagnosed Addison’s disease. Precipitating factors of an Addisonian crisis include infection, dehydration, surgery, trauma, physiological stress, pregnancy, hypoglycemia, and acute withdrawal of long-term steroids. Symptoms of an Addisonian crisis include malaise, fatigue, nausea or vomiting, abdominal pain, fever, muscle pains, dehydration, confusion, and loss of consciousness.

There is no fixed consensus on diagnostic criteria for an Addisonian crisis, as symptoms are non-specific. Investigations may include blood tests, blood gas analysis, and septic screens if infection is suspected. Management involves administering hydrocortisone and fluids. Hydrocortisone is given parenterally, and the dosage varies depending on the age of the patient. Fluid resuscitation with saline is necessary to correct any electrolyte disturbances and maintain blood pressure. The underlying cause of the crisis should also be identified and treated. Close monitoring of sodium levels is important to prevent complications such as osmotic demyelination syndrome.

Alteplase (rt-pA) is recommended for the treatment of acute ischaemic stroke in adults if it is administered as soon as possible within 4.5 hours of the onset of stroke symptoms. It is important to exclude intracranial haemorrhage through appropriate imaging techniques before starting the treatment. The initial dose of alteplase is 0.9 mg/kg, with a maximum dose of 90 mg. This dose should be given intravenously over 60 minutes, with the initial 10% administered by intravenous injection and the remainder by intravenous infusion. In the case of a patient weighing 120 kg, the maximum dose of 90 mg should be administered. For more information, please refer to the NICE guidelines on stroke and transient ischaemic attack in individuals over 16 years old.

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 of this bacterium are responsible for causing genitourinary infections.

Chlamydia is the most commonly diagnosed sexually transmitted infection in the United Kingdom and 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 remain asymptomatic. However, if left untreated, chlamydia can lead to complications such as pelvic inflammatory disease, ectopic pregnancy, and tubal infertility in women. In men, it can result in proctitis, epididymitis, and epididymo-orchitis.

The patient is currently taking 20 mg of Atorvastatin once daily. They do not have a history of heart disease, vascular disease, or stroke. Their blood pressure is 148/92 mmHg, pulse rate is 86 bpm, and respiration rate is 1.

Further Reading:

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, affecting around 5% of patients over the age of 70-75 years and 10% of patients aged 80-85 years. While AF can cause palpitations and inefficient cardiac function, the most important aspect of managing patients with AF is reducing the increased risk of stroke.

AF can be classified as first detected episode, paroxysmal, persistent, or permanent. First detected episode refers to the initial occurrence of AF, regardless of symptoms or duration. Paroxysmal AF occurs when a patient has 2 or more self-terminating episodes lasting less than 7 days. Persistent AF refers to episodes lasting more than 7 days that do not self-terminate. Permanent AF is continuous atrial fibrillation that cannot be cardioverted or if attempts to do so are deemed inappropriate. The treatment goals for permanent AF are rate control and anticoagulation if appropriate.

Symptoms of AF include palpitations, dyspnea, and chest pain. The most common sign is an irregularly irregular pulse. An electrocardiogram (ECG) is essential for diagnosing AF, as other conditions can also cause an irregular pulse.

Managing patients with AF involves two key parts: rate/rhythm control and reducing stroke risk. Rate control involves slowing down the irregular pulse to avoid negative effects on cardiac function. This is typically achieved using beta-blockers or rate-limiting calcium channel blockers. If one drug is not effective, combination therapy may be used. Rhythm control aims to restore and maintain normal sinus rhythm through pharmacological or electrical cardioversion. However, the majority of patients are managed with a rate control strategy.

Reducing stroke risk in patients with AF is crucial. Risk stratifying tools, such as the CHA2DS2-VASc score, are used to determine the most appropriate anticoagulation strategy. Anticoagulation is recommended for patients with a score of 2 or more. Clinicians can choose between warfarin and novel oral anticoagulants (NOACs) for anticoagulation.

Before starting anticoagulation, the patient’s bleeding risk should be assessed using tools like the HAS-BLED score or the ORBIT tool. These tools evaluate factors such as hypertension, abnormal renal or liver function, history of bleeding, age, and use of drugs that predispose to bleeding.

Schistosomiasis, also known as bilharzia, is a tropical disease caused by parasitic trematodes (flukes) of the Schistosoma type. The transmission of this disease occurs when water becomes contaminated with faeces or urine containing eggs, and a specific freshwater snail serves as the intermediate host. Human contact with water inhabited by the intermediate host snail is necessary for transmission to occur.

There are five species of Schistosoma that can cause human disease: S. japonicum, S. mansoni, S. haematobium, S. intercalatum, and S. mekongi. Among these, S. japonicum and S. mansoni are the most significant causes of intestinal schistosomiasis, while S. haematobium is the primary cause of urogenital schistosomiasis.

Urogenital schistosomiasis occurs when adult worms migrate from their initial site in the liver to the vesical plexus. The presence of blood in the urine, known as haematuria, is a characteristic sign of urogenital schistosomiasis. In women, this condition may manifest with genital and vaginal lesions, as well as dyspareunia. pathology in the seminal vesicles and prostate. Advanced cases of urogenital schistosomiasis can result in fibrosis of the ureter and bladder, as well as kidney damage. Complications such as bladder cancer and infertility are also recognized in association with this disease.

Rapid tranquillisation involves the administration of medication through injection when oral medication is not feasible or appropriate and immediate sedation is necessary. The current guidelines from NICE recommend two options for rapid tranquillisation in adults: intramuscular lorazepam alone or a combination of intramuscular haloperidol and intramuscular promethazine. The choice of medication depends on various factors such as advanced statements, potential intoxication, previous responses to these medications, interactions with other drugs, and existing physical health conditions or pregnancy.

If there is insufficient information to determine the appropriate medication or if the individual has not taken antipsychotic medication before, intramuscular lorazepam is recommended. However, if there is evidence of cardiovascular disease or a prolonged QT interval, or if an electrocardiogram has not been conducted, the combination of intramuscular haloperidol and intramuscular promethazine should be avoided, and intramuscular lorazepam should be used instead.

If there is a partial response to intramuscular lorazepam, a second dose should be considered. If there is no response to intramuscular lorazepam, then intramuscular haloperidol combined with intramuscular promethazine should be considered. If there is a partial response to this combination, a further dose should be considered.

If there is no response to intramuscular haloperidol combined with intramuscular promethazine and intramuscular lorazepam has not been used yet, it should be considered. However, if intramuscular lorazepam has already been administered, it is recommended to arrange an urgent team meeting to review the situation and seek a second opinion if necessary.

After rapid tranquillisation, the patient should be closely monitored for any side effects, and their vital signs should be regularly checked, including heart rate, blood pressure, respiratory rate, temperature, hydration level, and level of consciousness. These observations should be conducted at least hourly until there are no further concerns about the patient’s physical health.

For more information, refer to the NICE guidance on violence and aggression: short-term management in mental health, health, and community settings.

An elevated pH (normal range 7.34-7.45) suggests alkalosis. A low pCO2 (normal range 4.4-6.0 Kpa) indicates that the respiratory system is causing the alkalosis. The metabolic system, on the other hand, is not contributing to either alkalosis or acidosis as both the bicarbonate and base excess levels are within the normal ranges.

Further Reading:

Salicylate poisoning, particularly from aspirin overdose, is a common cause of poisoning in the UK. One important concept to understand is that salicylate overdose leads to a combination of respiratory alkalosis and metabolic acidosis. Initially, the overdose stimulates the respiratory center, leading to hyperventilation and respiratory alkalosis. However, as the effects of salicylate on lactic acid production, breakdown into acidic metabolites, and acute renal injury occur, it can result in high anion gap metabolic acidosis.

The clinical features of salicylate poisoning include hyperventilation, tinnitus, lethargy, sweating, pyrexia (fever), nausea/vomiting, hyperglycemia and hypoglycemia, seizures, and coma.

When investigating salicylate poisoning, it is important to measure salicylate levels in the blood. The sample should be taken at least 2 hours after ingestion for symptomatic patients or 4 hours for asymptomatic patients. The measurement should be repeated every 2-3 hours until the levels start to decrease. Other investigations include arterial blood gas analysis, electrolyte levels (U&Es), complete blood count (FBC), coagulation studies (raised INR/PTR), urinary pH, and blood glucose levels.

To manage salicylate poisoning, an ABC approach should be followed to ensure a patent airway and adequate ventilation. Activated charcoal can be administered if the patient presents within 1 hour of ingestion. Oral or intravenous fluids should be given to optimize intravascular volume. Hypokalemia and hypoglycemia should be corrected. Urinary alkalinization with intravenous sodium bicarbonate can enhance the elimination of aspirin in the urine. In severe cases, hemodialysis may be necessary.

Urinary alkalinization involves targeting a urinary pH of 7.5-8.5 and checking it hourly. It is important to monitor for hypokalemia as alkalinization can cause potassium to shift from plasma into cells. Potassium levels should be checked every 1-2 hours.

In cases where the salicylate concentration is high (above 500 mg/L in adults or 350 mg/L in children), sodium bicarbonate can be administered intravenously. Hemodialysis is the treatment of choice for severe poisoning and may be indicated in cases of high salicylate levels, resistant metabolic acidosis, acute kidney injury, pulmonary edema, seizures and coma.

This patient is displaying symptoms consistent with a malabsorption syndrome, which is supported by the findings of subtotal villous atrophy in his small bowel biopsy. Based on this information, the possible causes can be narrowed down to tropical sprue, coeliac disease, and giardiasis.

Considering that the patient was previously healthy before his trip to Nepal, it is unlikely that he has coeliac disease. Additionally, tropical sprue is rare outside of the regions around the equator and is uncommon in Nepal. On the other hand, giardiasis is prevalent in Nepal and is the most probable cause of the patient’s symptoms.

Giardiasis is a chronic diarrheal illness caused by a parasite called Giardia lamblia. Infection occurs when individuals ingest cysts present in contaminated food or water. Common symptoms associated with giardiasis include chronic diarrhea, weakness, abdominal cramps, flatulence, smelly and greasy stools, nausea, vomiting, and weight loss.

Stool culture often yields negative results, so the preferred diagnostic test is a stool ova and parasite (O&P) examination. This test should be repeated three times for accuracy. Additionally, the small bowel biopsy should be re-evaluated to check for the presence of Giardia lamblia.

The standard treatment for giardiasis involves antibiotic therapy with a nitroimidazole antibiotic, such as metronidazole.

Septic arthritis occurs when an infectious agent invades a joint, causing it to become purulent. The main symptoms of septic arthritis include pain in the affected joint, redness, warmth, and swelling of the joint, and difficulty moving the joint. Patients may also experience fever and systemic upset. The most common cause of septic arthritis is Staphylococcus aureus, but other bacteria such as Streptococcus spp., Haemophilus influenzae, Neisseria gonorrhoea, and Escherichia coli can also be responsible.

According to the current recommendations by NICE and the BNF, the initial treatment for septic arthritis is flucloxacillin. However, if a patient is allergic to penicillin, clindamycin can be used instead. If there is a suspicion of MRSA infection, vancomycin is the recommended choice. In cases where gonococcal arthritis or a Gram-negative infection is suspected, cefotaxime is the preferred treatment. The suggested duration of treatment is typically 4-6 weeks, although it may be longer if the infection is complicated.

Epidemic keratoconjunctivitis is a type of viral conjunctivitis that is primarily caused by adenoviruses. This highly contagious condition tends to occur in outbreaks. It is a common cause of acute conjunctivitis and has distinct clinical features. These include the sudden onset of acute follicular conjunctivitis, severe pain in the affected eye, a significant amount of watery discharge, the presence of subconjunctival hemorrhages, potential visual changes, hyperemia and chemosis, and the possibility of membranes and pseudomembranes forming. Additionally, ipsilateral preauricular lymphadenopathy may be observed.

Small cell lung cancer (SCLC) that originates from neuroendocrine tissue can lead to the development of paraneoplastic endocrine syndromes, such as Cushing syndrome. This occurs due to the inappropriate secretion of ectopic adrenocorticotropic hormone (ACTH). In this case, it is highly likely that the patient has a neuroendocrine tumor within the lung that is secreting ACTH.

The signs and symptoms of Cushing syndrome may be minimal in cases of ectopic ACTH-secreting tumors, and the onset of symptoms may be sudden, especially in rapidly growing SCLCs. The typical biochemical profile observed in these cases includes elevated sodium levels, low potassium levels, and a metabolic alkalosis.

The tumors associated with the production of ectopic ACTH are as follows:
– Small cell lung cancer (SCLC) – 50%
– Bronchial carcinoid tumors – 10%
– Thymic carcinoma – 10%
– Pancreatic islet cell tumors – 5%
– Phaeochromocytoma – 5%
– Medullary thyroid carcinoma – 5%

Low-velocity gunshot wounds to the abdomen result in tissue damage through laceration and cutting. On the other hand, high-velocity gunshot wounds transfer a greater amount of kinetic energy to the abdominal viscera. These types of wounds can cause more extensive damage in the surrounding area of the missile’s path due to temporary cavitation.

When patients experience penetrating abdominal trauma as a result of gunshot wounds, certain organs are more commonly injured. The small bowel is affected in approximately 50% of cases, followed by the colon in 40% of cases. The liver is injured in around 30% of cases, while abdominal vascular structures are affected in about 25% of cases.

Please note that these statistics have been obtained from the most recent edition of the ATLS manual.

Patients who have suffered burns should receive high-flow oxygen (15 L) through a reservoir bag while their breathing is being evaluated. If intubation is necessary, it is crucial to use an appropriately sized endotracheal tube (ETT). Using a tube that is too small can make it difficult or even impossible to ventilate the patient, clear secretions, or perform bronchoscopy.

According to the ATLS guidelines, adults should be intubated using an ETT with an internal diameter (ID) of at least 7.5 mm or larger. Children, on the other hand, should have an ETT with an ID of at least 4.5 mm. Once a patient has been intubated, it is important to continue administering 100% oxygen until their carboxyhemoglobin levels drop to less than 5%.

To protect the lungs, it is recommended to use lung protective ventilation techniques. This involves using low tidal volumes (4-8 mL/kg) and ensuring that peak inspiratory pressures do not exceed 30 cmH2O.