The occurrence of schizophrenia is consistent across all social classes. It affects individuals from all walks of life without discrimination. The likelihood of developing schizophrenia over one’s lifetime is 1%, and this probability remains the same for both men and women. However, it is worth noting that men tend to experience the onset of symptoms at a younger age compared to women, with the average age of onset falling between 15 and 45 years.

There is a recognized genetic predisposition for schizophrenia, meaning that certain individuals may have a higher likelihood of developing the condition due to their genetic makeup. The risk of schizophrenia affecting first-degree relatives, such as siblings or parents, is approximately 10%. Furthermore, the risk of children being affected by schizophrenia increases to 40%.

When considering the impact of genetics on schizophrenia, it is interesting to note that monozygotic twins, who share identical genetic material, have a concordance rate of around 50%. This suggests that genetic factors play a significant role in the development of the condition.

Tragically, approximately 10% of individuals suffering from schizophrenia ultimately die by suicide, particularly during the early stages of the illness. This highlights the importance of providing appropriate support and intervention to individuals with schizophrenia to prevent such devastating outcomes.

If IV methylene blue is obtained, it is typically used to treat a specific cause. However, if there is no response to methylene blue, alternative treatments such as hyperbaric oxygen or exchange transfusion may be considered. In cases where the cause is NADH-methaemoglobinaemia reductase deficiency, ascorbic acid can be used as a potential treatment.

Further Reading:

Methaemoglobinaemia is a condition where haemoglobin is oxidised from Fe2+ to Fe3+. This process is normally regulated by NADH methaemoglobin reductase, which transfers electrons from NADH to methaemoglobin, converting it back to haemoglobin. In healthy individuals, methaemoglobin levels are typically less than 1% of total haemoglobin. However, an increase in methaemoglobin can lead to tissue hypoxia as Fe3+ cannot bind oxygen effectively.

Methaemoglobinaemia can be congenital or acquired. Congenital causes include haemoglobin chain variants (HbM, HbH) and NADH methaemoglobin reductase deficiency. Acquired causes can be due to exposure to certain drugs or chemicals, such as sulphonamides, local anaesthetics (especially prilocaine), nitrates, chloroquine, dapsone, primaquine, and phenytoin. Aniline dyes are also known to cause methaemoglobinaemia.

Clinical features of methaemoglobinaemia include slate grey cyanosis (blue to grey skin coloration), chocolate blood or chocolate cyanosis (brown color of blood), dyspnoea, low SpO2 on pulse oximetry (which often does not improve with supplemental oxygen), and normal PaO2 on arterial blood gas (ABG) but low SaO2. Patients may tolerate hypoxia better than expected. Severe cases can present with acidosis, arrhythmias, seizures, and coma.

Diagnosis of methaemoglobinaemia is made by directly measuring the level of methaemoglobin using a co-oximeter, which is present in most modern blood gas analysers. Other investigations, such as a full blood count (FBC), electrocardiogram (ECG), chest X-ray (CXR), and beta-human chorionic gonadotropin (bHCG) levels (in pregnancy), may be done to assess the extent of the condition and rule out other contributing factors.

Active treatment is required if the methaemoglobin level is above 30% or if it is below 30% but the patient is symptomatic or shows evidence of tissue hypoxia. Treatment involves maintaining the airway and delivering high-flow oxygen, removing the causative agents, treating toxidromes and consider giving IV dextrose 5%.

If someone with IBS experiences unintentional weight loss or rectal bleeding, it is important to investigate further as these symptoms are not typical of IBS and may indicate a more serious underlying condition. Other alarm symptoms to watch out for include positive faecal immunochemical test (FIT), change in bowel habit after the age of 60, elevated faecal calprotectin levels, iron deficiency anaemia, persistent or frequent bloating in females (especially if over 50), the presence of an abdominal or rectal mass, or a family history of bowel cancer, ovarian cancer, coeliac disease, or inflammatory bowel disease.

Further Reading:

Irritable bowel syndrome (IBS) is a chronic disorder that affects the interaction between the gut and the brain. The exact cause of IBS is not fully understood, but factors such as genetics, drug use, enteric infections, diet, and psychosocial factors are believed to play a role. The main symptoms of IBS include abdominal pain, changes in stool form and/or frequency, and bloating. IBS can be classified into subtypes based on the predominant stool type, including diarrhea-predominant, constipation-predominant, mixed, and unclassified.

Diagnosing IBS involves using the Rome IV criteria, which includes recurrent abdominal pain associated with changes in stool frequency and form. It is important to rule out other more serious conditions that may mimic IBS through a thorough history, physical examination, and appropriate investigations. Treatment for IBS primarily involves diet and lifestyle modifications. Patients are advised to eat regular meals with a healthy, balanced diet and adjust their fiber intake based on symptoms. A low FODMAP diet may be trialed, and a dietician may be consulted for guidance. Regular physical activity and weight management are also recommended.

Psychosocial factors, such as stress, anxiety, and depression, should be addressed and managed appropriately. If constipation is a predominant symptom, soluble fiber supplements or foods high in soluble fiber may be recommended. Laxatives can be considered if constipation persists, and linaclotide may be tried if optimal doses of previous laxatives have not been effective. Antimotility drugs like loperamide can be used for diarrhea, and antispasmodic drugs or low-dose tricyclic antidepressants may be prescribed for abdominal pain. If symptoms persist or are refractory to treatment, alternative diagnoses should be considered, and referral to a specialist may be necessary.

Overall, the management of IBS should be individualized based on the patient’s symptoms and psychosocial situation. Clear explanation of the condition and providing resources for patient education, such as the NHS patient information leaflet and support from organizations like The IBS Network, can also be beneficial.

Central retinal vein occlusion (CRVO) typically results in painless, one-sided vision loss. On fundoscopic examination, the retina displays a distinct appearance resembling a ‘pizza thrown against a wall’. This includes engorged retinal veins, swelling of the optic disc, multiple flame-shaped hemorrhages, and cotton wool spots. Hypertension is present in about 65% of CRVO patients, and it is more common in individuals over 65 years old.

In contrast, central retinal artery occlusion (CRAO) also causes sudden, painless, one-sided vision loss. However, the retina’s appearance in CRAO is different from CRVO. It appears pale, with narrowed blood vessels. A notable feature is the presence of a ‘cherry-red spot’ at the center of the macula, which is supplied by the underlying choroid. Examination often reveals an afferent pupillary defect.

Vitreous hemorrhage occurs when there is bleeding into the middle chamber of the eye, known as the vitreous. This can be caused by conditions such as proliferative diabetic retinopathy, trauma, or retinal detachment. The appearance of vitreous hemorrhage is described as ‘blood within a bloodless gel’, resulting in a diffuse red appearance of the retina. Unlike CRVO, there are no focal flame-shaped hemorrhages.

Diabetic maculopathy refers to the presence of diabetic eye disease within a one-disc diameter of the macula.

Wet age-related macular degeneration (ARMD) causes vision loss due to choroidal neovascularization, which leads to leakage of blood and protein beneath the macula. While there may be hemorrhages visible on the retina, the overall appearance does not match the description provided in the question.

The most common symptom of infective endocarditis is fever, which occurs in the majority of cases and is consistently present throughout the course of the disease. Cardiac murmurs are also frequently detected, although they may only be present in one third of patients at the initial presentation. Individuals who use intravenous drugs often develop right-sided disease affecting the tricuspid and pulmonary valves, making it challenging to detect cardiac murmurs in these cases. Splinter hemorrhages and other symptoms may also be observed.

Further Reading:

Infective endocarditis (IE) is an infection that affects the innermost layer of the heart, known as the endocardium. It is most commonly caused by bacteria, although it can also be caused by fungi or viruses. IE can be classified as acute, subacute, or chronic depending on the duration of illness. Risk factors for IE include IV drug use, valvular heart disease, prosthetic valves, structural congenital heart disease, previous episodes of IE, hypertrophic cardiomyopathy, immune suppression, chronic inflammatory conditions, and poor dental hygiene.

The epidemiology of IE has changed in recent years, with Staphylococcus aureus now being the most common causative organism in most industrialized countries. Other common organisms include coagulase-negative staphylococci, streptococci, and enterococci. The distribution of causative organisms varies depending on whether the patient has a native valve, prosthetic valve, or is an IV drug user.

Clinical features of IE include fever, heart murmurs (most commonly aortic regurgitation), non-specific constitutional symptoms, petechiae, splinter hemorrhages, Osler’s nodes, Janeway’s lesions, Roth’s spots, arthritis, splenomegaly, meningism/meningitis, stroke symptoms, and pleuritic pain.

The diagnosis of IE is based on the modified Duke criteria, which require the presence of certain major and minor criteria. Major criteria include positive blood cultures with typical microorganisms and positive echocardiogram findings. Minor criteria include fever, vascular phenomena, immunological phenomena, and microbiological phenomena. Blood culture and echocardiography are key tests for diagnosing IE.

In summary, infective endocarditis is an infection of the innermost layer of the heart that is most commonly caused by bacteria. It can be classified as acute, subacute, or chronic and can be caused by a variety of risk factors. Staphylococcus aureus is now the most common causative organism in most industrialized countries. Clinical features include fever, heart murmurs, and various other symptoms. The diagnosis is based on the modified Duke criteria, which require the presence of certain major and minor criteria. Blood culture and echocardiography are important tests for diagnosing IE.

In some cases, the signs of skin or mucosal involvement may be difficult to detect or may not be present at all. The Royal College of Emergency Medicine (RCEM) states that anaphylaxis is likely when three specific criteria are met: the illness has a sudden and rapid onset, there are noticeable changes in the skin or mucosal areas such as flushing, hives, or swelling, and there are severe problems with the airway, breathing, or circulation that pose a life-threatening risk.

Further Reading:

Anaphylaxis is a severe and life-threatening hypersensitivity reaction that can have sudden onset and progression. It is characterized by skin or mucosal changes and can lead to life-threatening airway, breathing, or circulatory problems. Anaphylaxis can be allergic or non-allergic in nature.

In allergic anaphylaxis, there is an immediate hypersensitivity reaction where an antigen stimulates the production of IgE antibodies. These antibodies bind to mast cells and basophils. Upon re-exposure to the antigen, the IgE-covered cells release histamine and other inflammatory mediators, causing smooth muscle contraction and vasodilation.

Non-allergic anaphylaxis occurs when mast cells degrade due to a non-immune mediator. The clinical outcome is the same as in allergic anaphylaxis.

The management of anaphylaxis is the same regardless of the cause. Adrenaline is the most important drug and should be administered as soon as possible. The recommended doses for adrenaline vary based on age. Other treatments include high flow oxygen and an IV fluid challenge. Corticosteroids and chlorpheniramine are no longer recommended, while non-sedating antihistamines may be considered as third-line treatment after initial stabilization of airway, breathing, and circulation.

Common causes of anaphylaxis include food (such as nuts, which is the most common cause in children), drugs, and venom (such as wasp stings). Sometimes it can be challenging to determine if a patient had a true episode of anaphylaxis. In such cases, serum tryptase levels may be measured, as they remain elevated for up to 12 hours following an acute episode of anaphylaxis.

The Resuscitation Council (UK) provides guidelines for the management of anaphylaxis, including a visual algorithm that outlines the recommended steps for treatment.
https://www.resus.org.uk/sites/default/files/2021-05/Emergency%20Treatment%20of%20Anaphylaxis%20May%202021_0.pdf

The mini-mental state examination (MMSE) is a tool consisting of 11 questions that is utilized to evaluate cognitive function. With a maximum score of 30, a score below 24 generally indicates impaired cognitive function. This assessment can be employed to categorize the severity of cognitive impairment in dementia. Mild dementia is typically associated with an MMSE score ranging from 20 to 24, while moderate dementia falls within the MMSE score range of 13 to 20. Severe dementia is characterized by an MMSE score below 12. For more information on testing and assessment for dementia, you can visit the Alzheimer’s Association website. Additionally, the RCEM syllabus references EIP9 for memory loss and EIC4 for dementia and cognitive impairment.

For the treatment of women with lower urinary tract infections (UTIs) who are not pregnant, it is recommended to consider either a back-up antibiotic prescription or an immediate antibiotic prescription. This decision should take into account the severity of symptoms and the risk of developing complications, which is higher in individuals with known or suspected abnormalities of the genitourinary tract or weakened immune systems. The evidence for back-up antibiotic prescriptions is limited to non-pregnant women with lower UTIs where immediate antibiotic treatment is not deemed necessary. It is also important to consider previous urine culture and susceptibility results, as well as any history of antibiotic use that may have led to the development of resistant bacteria. Ultimately, the preferences of the woman regarding antibiotic use should be taken into account.

If a urine sample has been sent for culture and susceptibility testing and an antibiotic prescription has been given, it is crucial to review the choice of antibiotic once the microbiological results are available. If the bacteria are found to be resistant and symptoms are not improving, it is recommended to switch to a narrow-spectrum antibiotic whenever possible.

The following antibiotics are recommended for non-pregnant women aged 16 years and older:

First-choice:
– Nitrofurantoin 100 mg modified-release taken orally twice daily for 3 days (if eGFR >45 ml/minute)
– Trimethoprim 200 mg taken orally twice daily for 3 days (if low risk of resistance*)

Second-choice (if there is no improvement in lower UTI symptoms on first-choice treatment for at least 48 hours, or if first-choice treatment is not suitable):
– Nitrofurantoin 100 mg modified-release taken orally twice daily for 3 days (if eGFR >45 ml/minute)
– Pivmecillinam 400 mg initial dose taken orally, followed by 200 mg taken orally three times daily for 3 days
– Fosfomycin 3 g single sachet dose

*The risk of resistance may be lower if the antibiotic has not been used in the past 3 months, previous urine culture suggests susceptibility (although this was not used), and in younger individuals in areas where local epidemiology data indicate low resistance rates. Conversely, the risk of resistance may be higher with recent antibiotic use and in older individuals in residential facilities.

Thyroid storm is a rare condition that affects only 1-2% of patients with hyperthyroidism. However, it is crucial to diagnose it promptly because it has a high mortality rate of approximately 10%. Thyroid storm is often triggered by a physiological stressor, such as stopping antithyroid therapy prematurely, recent surgery or radio-iodine treatment, infections (especially chest infections), trauma, diabetic ketoacidosis or hyperosmolar diabetic crisis, thyroid hormone overdose, pre-eclampsia. It typically occurs in patients with Graves’ disease or toxic multinodular goitre and presents with sudden and severe hyperthyroidism. Symptoms include high fever (over 41°C), dehydration, rapid heart rate (greater than 140 beats per minute) with or without irregular heart rhythms, low blood pressure, congestive heart failure, nausea, jaundice, vomiting, diarrhea, abdominal pain, confusion, agitation, delirium, psychosis, seizures, or coma.

To diagnose thyroid storm, various blood tests should be conducted, including a full blood count, urea and electrolytes, blood glucose, coagulation screen, CRP, and thyroid profile (T4/T3 and TSH). A bone profile/calcium test should also be done as 10% of patients develop hypocalcemia. Blood cultures should be taken as well. Other important investigations include a urine dipstick/MC&S, chest X-ray, and ECG.

The management of thyroid storm involves several steps. Intravenous fluids, such as 1-2 liters of 0.9% saline, should be administered. Airway support and management should be provided as necessary. A nasogastric tube should be inserted if the patient is vomiting. Urgent referral for inpatient management is essential. Paracetamol (1 g PO/IV) can be given to reduce fever. Benzodiazepines, such as diazepam (5-20 mg PO/IV), can be used for sedation. Steroids, like hydrocortisone (100 mg IV), may be necessary if there is co-existing adrenal suppression. Antibiotics should be prescribed if there is an intercurrent infection. Beta-blockers, such as propranolol (80 mg PO), can help control heart rate. High-dose carbimazole (45-60 mg/day) is recommended.

Typhoid fever is a bacterial infection caused by Salmonella typhi. Paratyphoid fever, on the other hand, is a similar illness caused by Salmonella paratyphi. Together, these two conditions are collectively known as the enteric fevers.

Typhoid fever is prevalent in India and many other parts of Asia, Africa, Central America, and South America. It is primarily transmitted through the consumption of contaminated food or water that has been infected by the feces of an acutely infected or recovering person, or a chronic carrier. About 1-6% of individuals infected with S. typhi become chronic carriers. The incubation period for this illness ranges from 7 to 21 days.

During the first week of the illness, patients experience weakness and lethargy, accompanied by a gradually increasing fever. The onset of the illness is usually subtle, and constipation is more common than diarrhea in the early stages. Other early symptoms include headaches, abdominal pain, and nosebleeds. In cases of typhoid fever, the fever can occur with a relatively slow heart rate, known as Faget’s sign.

As the illness progresses into the second week, patients often become too fatigued to get out of bed. Diarrhea becomes more prominent, the fever intensifies, and patients may become agitated and delirious. The abdomen may become tender and swollen, and approximately 75% of patients develop an enlarged spleen. In up to a third of patients, red macules known as Rose spots may appear.

In the third week, the illness can lead to various complications. Intestinal bleeding may occur due to bleeding in congested Peyer’s patches. Other potential complications include intestinal perforation, secondary pneumonia, encephalitis, myocarditis, metastatic abscesses, and septic shock.

After the third week, surviving patients begin to show signs of improvement, with the fever and symptoms gradually subsiding over the course of 7-14 days. Untreated patients have a mortality rate of 15-30%. Traditionally, drugs like ampicillin and trimethoprim have been used for treatment. However, due to the emergence of multidrug resistant cases, azithromycin or fluoroquinolones are now the primary treatment options.