Spironolactone, a potassium sparing diuretic, is the preferred initial treatment for ascites. Ascites triggers the renin-angiotensin-aldosterone system (RAAS), causing sodium retention (Hypernatraemia) and potassium excretion (Hypokalaemia). By blocking aldosterone, spironolactone helps to counteract these effects. Other diuretics can worsen potassium deficiency, so close monitoring of electrolyte levels is necessary if they are used instead.

Further Reading:

Cirrhosis is a condition where the liver undergoes structural changes, resulting in dysfunction of its normal functions. It can be classified as either compensated or decompensated. Compensated cirrhosis refers to a stage where the liver can still function effectively with minimal symptoms, while decompensated cirrhosis is when the liver damage is severe and clinical complications are present.

Cirrhosis develops over a period of several years due to repeated insults to the liver. Risk factors for cirrhosis include alcohol misuse, hepatitis B and C infection, obesity, type 2 diabetes, autoimmune liver disease, genetic conditions, certain medications, and other rare conditions.

The prognosis of cirrhosis can be assessed using the Child-Pugh score, which predicts mortality based on parameters such as bilirubin levels, albumin levels, INR, ascites, and encephalopathy. The score ranges from A to C, with higher scores indicating a poorer prognosis.

Complications of cirrhosis include portal hypertension, ascites, hepatic encephalopathy, variceal hemorrhage, increased infection risk, hepatocellular carcinoma, and cardiovascular complications.

Diagnosis of cirrhosis is typically done through liver function tests, blood tests, viral hepatitis screening, and imaging techniques such as transient elastography or acoustic radiation force impulse imaging. Liver biopsy may also be performed in some cases.

Management of cirrhosis involves treating the underlying cause, controlling risk factors, and monitoring for complications. Complications such as ascites, spontaneous bacterial peritonitis, oesophageal varices, and hepatic encephalopathy require specific management strategies.

Overall, cirrhosis is a progressive condition that requires ongoing monitoring and management to prevent further complications and improve outcomes for patients.

Thyroid storm, also known as thyrotoxic crisis, is a rare and dangerous complication of hyperthyroidism. The initial management of this condition involves the use of specific medications. These medications include a beta blocker, a corticosteroid, an antithyroid drug, and an iodine solution.

The beta blocker used is typically propranolol, which is administered intravenously at a dose of 1 mg over 1 minute. If a beta blocker is contraindicated, a calcium channel blocker such as diltiazem may be used instead, at a dose of 0.25 mg/kg over 2 minutes.

For corticosteroids, hydrocortisone is commonly used and given intravenously at a dose of 200 mg. Alternatively, dexamethasone can be used at a dose of 2 mg intravenously.

The antithyroid drug used is usually propylthiouracil, which is given orally, through a nasogastric tube, or rectally, at a dose of 200 mg.

An iodine solution, specifically Lugol’s iodine, is also part of the initial management. However, it should not be administered until at least 1 hour after the antithyroid drug has been given. This is because iodine can exacerbate thyrotoxicosis by stimulating thyroid hormone synthesis. Propylthiouracil, on the other hand, inhibits the normal interactions of iodine and peroxidase with thyroglobulin, preventing the formation of T4 and T3. Therefore, it is given first and allowed time to take effect before iodine is administered.

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.

TCA toxicity can be identified through specific changes seen on an electrocardiogram (ECG). Sinus tachycardia, which is a faster than normal heart rate, and widening of the QRS complex are key features of TCA toxicity. These ECG changes occur due to the blocking of sodium channels and muscarinic receptors (M1) by the medication. In the case of an amitriptyline overdose, additional ECG changes may include prolongation of the QT interval, an R/S ratio greater than 0.7 in lead aVR, and the presence of ventricular arrhythmias such as torsades de pointes. The severity of the QRS prolongation on the ECG is associated with the likelihood of adverse events. A QRS duration greater than 100 ms is predictive of seizures, while a QRS duration greater than 160 ms is predictive of ventricular arrhythmias like ventricular tachycardia or torsades de pointes.

Further Reading:

Tricyclic antidepressant (TCA) overdose is a common occurrence in emergency departments, with drugs like amitriptyline and dosulepin being particularly dangerous. TCAs work by inhibiting the reuptake of norepinephrine and serotonin in the central nervous system. In cases of toxicity, TCAs block various receptors, including alpha-adrenergic, histaminic, muscarinic, and serotonin receptors. This can lead to symptoms such as hypotension, altered mental state, signs of anticholinergic toxicity, and serotonin receptor effects.

TCAs primarily cause cardiac toxicity by blocking sodium and potassium channels. This can result in a slowing of the action potential, prolongation of the QRS complex, and bradycardia. However, the blockade of muscarinic receptors also leads to tachycardia in TCA overdose. QT prolongation and Torsades de Pointes can occur due to potassium channel blockade. TCAs can also have a toxic effect on the myocardium, causing decreased cardiac contractility and hypotension.

Early symptoms of TCA overdose are related to their anticholinergic properties and may include dry mouth, pyrexia, dilated pupils, agitation, sinus tachycardia, blurred vision, flushed skin, tremor, and confusion. Severe poisoning can lead to arrhythmias, seizures, metabolic acidosis, and coma. ECG changes commonly seen in TCA overdose include sinus tachycardia, widening of the QRS complex, prolongation of the QT interval, and an R/S ratio >0.7 in lead aVR.

Management of TCA overdose involves ensuring a patent airway, administering activated charcoal if ingestion occurred within 1 hour and the airway is intact, and considering gastric lavage for life-threatening cases within 1 hour of ingestion. Serial ECGs and blood gas analysis are important for monitoring. Intravenous fluids and correction of hypoxia are the first-line therapies. IV sodium bicarbonate is used to treat haemodynamic instability caused by TCA overdose, and benzodiazepines are the treatment of choice for seizure control. Other treatments that may be considered include glucagon, magnesium sulfate, and intravenous lipid emulsion.

There are certain things to avoid in TCA overdose, such as anti-arrhythmics like quinidine and flecainide, as they can prolonged depolarization. Amiodarone should

The connection between latex sensitivity and food allergy is commonly known as the latex-fruit syndrome. Foods that have been found to be allergenic in relation to latex are categorized into high, moderate, or low risk groups.

High risk foods include banana, avocado, chestnut, and kiwi fruit.

Moderate risk foods include apple, carrot, celery, melon, papaya, potato, and tomato.

Citrus fruits and pears are considered to have a low risk of causing allergic reactions in individuals with latex sensitivity.

Infantile hypertrophic pyloric stenosis is a condition characterized by the thickening and enlargement of the smooth muscle in the antrum of the stomach, leading to the narrowing of the pyloric canal. This narrowing can easily cause obstruction. It is a relatively common condition, occurring in about 1 in 500 live births, and is more frequently seen in males than females, with a ratio of 4 to 1. It is most commonly observed in first-born male children, although it can rarely occur in adults as well.

The main symptom of infantile hypertrophic pyloric stenosis is vomiting, which typically begins between 2 to 8 weeks of age. The vomit is usually non-bilious and forcefully expelled. It tends to occur around 30 to 60 minutes after feeding, leaving the baby hungry despite the vomiting. In some cases, there may be blood in the vomit. Other clinical features include persistent hunger, dehydration, weight loss, and constipation. An enlarged pylorus, often described as olive-shaped, can be felt in the right upper quadrant or epigastric in approximately 95% of cases. This is most noticeable at the beginning of a feed.

The typical acid-base disturbance seen in this condition is hypochloremic metabolic alkalosis. This occurs due to the loss of hydrogen and chloride ions in the vomit, as well as decreased secretion of pancreatic bicarbonate. The increased bicarbonate ions in the distal tubule of the kidney lead to the production of alkaline urine. Hyponatremia and hypokalemia are also commonly present.

Ultrasound scanning is the preferred diagnostic tool for infantile hypertrophic pyloric stenosis, as it is reliable and easy to perform. It has replaced barium studies as the investigation of choice.

Initial management involves fluid resuscitation, which should be tailored to the weight and degree of dehydration. Any electrolyte imbalances should also be corrected.

The definitive treatment for this condition is surgical intervention, with the Ramstedt pyloromyotomy being the procedure of choice. Laparoscopic pyloromyotomy is also an effective alternative if suitable facilities are available. The prognosis for infants with this condition is excellent, as long as there is no delay in diagnosis and treatment initiation.

Renal colic, also known as ureteric colic, refers to a sudden and intense pain in the loin area caused by a blockage in the ureter, which is the tube that carries urine from the kidney to the bladder. This condition is commonly associated with urinary tract stones. The pain typically starts in the flank or loin and radiates to the labia in women or to the groin or testicle in men.

The pain experienced during renal or ureteric colic is severe and comes in spasms, with periods of no pain or a dull ache in between. It can last for minutes to hours. Nausea, vomiting, and the presence of blood in the urine (haematuria) often accompany the pain. Many individuals describe this pain as the most intense they have ever felt, with some women even comparing it to the pain of childbirth.

People with renal or ureteric colic are restless and unable to find relief by lying still, which helps distinguish this condition from peritonitis. They may have a history of previous episodes and may also present with fever and sweating if there is a concurrent urinary infection. As the stone irritates the detrusor muscle, they may complain of dysuria (painful urination), frequent urination, and straining when the stone reaches the vesicoureteric junction.

To support the diagnosis, it is recommended to perform urine dipstick testing to check for evidence of a urinary tract infection. The presence of blood in the urine can also indicate renal or ureteric colic, although it is not a definitive diagnostic marker. Nitrite and leukocyte esterase in the urine suggest the presence of an infection.

In terms of pain management, non-steroidal anti-inflammatory drugs (NSAIDs) are the first-line treatment for adults, children, and young people with suspected renal colic. Intravenous paracetamol can be offered if NSAIDs are contraindicated or not providing sufficient pain relief. Opioids may be considered if both NSAIDs and intravenous paracetamol are contraindicated or not effective. Antispasmodics should not be given to individuals with suspected renal colic.

For more detailed information, refer to the NICE guidelines on the assessment and management of renal and ureteric stones.

Thought broadcast is one of the primary symptoms of schizophrenia identified by Schneider. This symptom refers to the patient’s belief that their thoughts can be perceived by others.

Acute kidney injury (AKI), previously known as acute renal failure, is a sudden decline in kidney function. This leads to the accumulation of urea and other waste products in the body, as well as disturbances in fluid balance and electrolyte levels. AKI can occur in individuals with previously normal kidney function or those with pre-existing kidney disease, known as acute-on-chronic kidney disease. It is a relatively common condition, with approximately 15% of adults admitted to hospitals in the UK developing AKI.

AKI is categorized into three stages based on specific criteria. In stage 1, there is a rise in creatinine levels of 26 micromol/L or more within 48 hours, or a rise of 50-99% from baseline within 7 days (1.5-1.99 times the baseline). Additionally, a urine output of less than 0.5 mL/kg/hour for more than 6 hours is indicative of stage 1 AKI.

Stage 2 AKI is characterized by a creatinine rise of 100-199% from baseline within 7 days (2.0-2.99 times the baseline), or a urine output of less than 0.5 mL/kg/hour for more than 12 hours.

In stage 3 AKI, there is a creatinine rise of 200% or more from baseline within 7 days (3.0 or more times the baseline). Alternatively, a creatinine rise to 354 micromol/L or more with an acute rise of 26 micromol/L or more within 48 hours, or a rise of 50% or more within 7 days, is indicative of stage 3 AKI. Additionally, a urine output of less than 0.3 mL/kg/hour for 24 hours or anuria (no urine output) for 12 hours also falls under stage 3 AKI.

Anterior uveitis refers to the inflammation of the middle layer of the eye, which includes the iris and the ciliary body. If left untreated, it can lead to permanent damage and vision loss due to the development of conditions like glaucoma, cataract, or retinal edema.

There are various causes of anterior uveitis, including eye trauma from being hit or having a foreign object in the eye. It can also be associated with inflammatory disorders such as ankylosing spondylitis.

The clinical features of anterior uveitis are characterized by a red and sore eye, accompanied by pain that worsens when the ciliary muscles contract. Other symptoms include watering of the eye, blurred vision, sensitivity to light (photophobia), and a constricted or distorted pupil. The visual acuity may be normal or reduced.

Overall, anterior uveitis is a condition that requires prompt attention and treatment to prevent further complications and preserve vision.

All of the mentioned medications are antiemetics that can be used to treat nausea. However, cyclizine would be the most appropriate choice as it also possesses anti-histamine properties, which can help alleviate symptoms of vertigo. Ondansetron is a specific 5HT3 antagonist that is particularly effective for patients undergoing cytotoxic treatment. Domperidone acts on the chemoreceptor trigger zone and is also highly beneficial for patients receiving cytotoxic treatment. Metoclopramide directly affects the gastrointestinal tract and is a useful anti-emetic for individuals with gastro-duodenal, hepatic, and biliary diseases. Haloperidol may be considered in end-of-life care situations where other medications have not yielded successful results.

In a young patient who has been experiencing diarrhea and abdominal pain for more than 6 weeks, it is important to consider inflammatory bowel disease as a possible diagnosis. The challenge lies in distinguishing between ulcerative colitis and Crohn’s disease. In this case, a biopsy was performed and the results showed transmural inflammation with the presence of non-caseating granulomas, which strongly suggests a diagnosis of Crohn’s disease.

To differentiate between ulcerative colitis and Crohn’s disease, it is helpful to consider the following characteristics. Ulcerative colitis typically only affects the rectum and colon, although the terminal ileum may be affected in some cases known as backwash ileitis. On the other hand, Crohn’s disease can affect any part of the gastrointestinal tract from the mouth to the anus, and there may be areas of normal mucosa between the affected areas, known as skip lesions.

There are also differences in the associations and systemic manifestations of these two conditions. Ulcerative colitis has a decreased incidence in smokers and is associated with liver conditions such as primary biliary cirrhosis, chronic active hepatitis, and primary sclerosing cholangitis. Crohn’s disease, on the other hand, has an increased incidence in smokers and is more commonly associated with systemic manifestations such as erythema nodosum, pyoderma gangrenosum, iritis/uveitis, cholelithiasis, and joint pain/arthropathy.

Pathologically, ulcerative colitis primarily affects the mucosa and submucosa, with the presence of mucosal ulcers, inflammatory cell infiltrate, and crypt abscesses. In contrast, Crohn’s disease is characterized by transmural inflammation, lymphoid aggregates, and neutrophil infiltrates. Non-caseating granulomas are seen in approximately 30% of cases, which is a distinguishing feature of Crohn’s disease.

When it comes to clinical features, abdominal pain is less prominent in ulcerative colitis, while bloody diarrhea is present in 90% of cases. The passage of mucus is also common, and fever may be present. Symptoms such as urgency, tenesmus (a feeling of incomplete bowel movement), and pre-defecation pain that is relieved by passing stools are frequently reported. In Crohn’s disease, abdominal pain is more prominent, and diarrhea is common, with the possibility of it being bloody.

Individuals who have gastroenteritis should be instructed to refrain from going to work or participating in social activities until at least 48 hours have passed since their last episode of diarrhea or vomiting.

Further Reading:

Gastroenteritis is a transient disorder characterized by the sudden onset of diarrhea, with or without vomiting. It is caused by enteric infections with viruses, bacteria, or parasites. The most common viral causes of gastroenteritis in adults include norovirus, rotavirus, and adenovirus. Bacterial pathogens such as Campylobacter jejuni and coli, Escherichia coli, Clostridium perfringens, Bacillus cereus, Staphylococcus aureus, Salmonella typhi and paratyphi, and Shigella dysenteriae, flexneri, boydii, and sonnei can also cause gastroenteritis. Parasites such as Cryptosporidium, Entamoeba histolytica, and Giardia intestinalis or Giardia lamblia can also lead to diarrhea.

Diagnosis of gastroenteritis is usually based on clinical symptoms, and investigations are not required in many cases. However, stool culture may be indicated in certain situations, such as when the patient is systemically unwell or immunocompromised, has acute painful diarrhea or blood in the stool suggesting dysentery, has recently taken antibiotics or acid-suppressing medications, or has not resolved diarrhea by day 7 or has recurrent diarrhea.

Management of gastroenteritis in adults typically involves advice on oral rehydration. Intravenous rehydration and more intensive treatment may be necessary for patients who are systemically unwell, exhibit severe dehydration, or have intractable vomiting or high-output diarrhea. Antibiotics are not routinely required unless a specific organism is identified that requires treatment. Antidiarrheal drugs, antiemetics, and probiotics are not routinely recommended.

Complications of gastroenteritis can occur, particularly in young children, the elderly, pregnant women, and immunocompromised individuals. These complications include dehydration, electrolyte disturbance, acute kidney injury, haemorrhagic colitis, haemolytic uraemic syndrome, reactive arthritis, Reiter’s syndrome, aortitis, osteomyelitis, sepsis, toxic megacolon, pancreatitis, sclerosing cholangitis, liver cirrhosis, weight loss, chronic diarrhea, irritable bowel syndrome, inflammatory bowel disease, acquired lactose intolerance, Guillain-Barré syndrome, meningitis, invasive entamoeba infection, and liver abscesses.

Croup, also known as laryngotracheobronchitis, is a respiratory infection that primarily affects infants and toddlers. It is characterized by a barking cough and can cause stridor (a high-pitched sound during breathing) and respiratory distress due to swelling of the larynx and excessive secretions. The majority of cases are caused by parainfluenza viruses 1 and 3. Croup is most common in children between 6 months and 3 years of age and tends to occur more frequently in the autumn.

The clinical features of croup include a barking cough that is worse at night, preceded by symptoms of an upper respiratory tract infection such as cough, runny nose, and congestion. Stridor, respiratory distress, and fever may also be present. The severity of croup can be graded using the NICE system, which categorizes it as mild, moderate, severe, or impending respiratory failure based on the presence of symptoms such as cough, stridor, sternal/intercostal recession, agitation, lethargy, and decreased level of consciousness. The Westley croup score is another commonly used tool to assess the severity of croup based on the presence of stridor, retractions, air entry, oxygen saturation levels, and level of consciousness.

In cases of severe croup with significant airway obstruction and impending respiratory failure, symptoms may include a minimal barking cough, harder-to-hear stridor, chest wall recession, fatigue, pallor or cyanosis, decreased level of consciousness, and tachycardia. A respiratory rate over 70 breaths per minute is also indicative of severe respiratory distress.

Children with moderate or severe croup, as well as those with certain risk factors such as chronic lung disease, congenital heart disease, neuromuscular disorders, immunodeficiency, age under 3 months, inadequate fluid intake, concerns about care at home, or high fever or a toxic appearance, should be admitted to the hospital. The mainstay of treatment for croup is corticosteroids, which are typically given orally. If the child is too unwell to take oral medication, inhaled budesonide or intramuscular dexamethasone may be used as alternatives. Severe cases may require high-flow oxygen and nebulized adrenaline.

When considering the differential diagnosis for acute stridor and breathing difficulty, non-infective causes such as inhaled foreign bodies

Vestibular neuronitis is characterized by the sudden and prolonged onset of rotational vertigo. This vertigo can occur spontaneously, upon waking up, or gradually worsen throughout the day. It is particularly aggravated by changes in head position, although it remains constant even when the head is still. Unlike other conditions, vestibular neuronitis does not cause hearing loss, tinnitus, or focal neurological deficits. On the other hand, in BPPV, episodes of vertigo are usually brief, lasting less than 20 seconds, and only occur when there is a change in head position.

Further Reading:

Vestibular neuritis, also known as vestibular neuronitis, is a condition characterized by sudden and prolonged vertigo of peripheral origin. It is believed to be caused by inflammation of the vestibular nerve, often following a viral infection. It is important to note that vestibular neuritis and labyrinthitis are not the same condition, as labyrinthitis involves inflammation of the labyrinth. Vestibular neuritis typically affects individuals between the ages of 30 and 60, with a 1:1 ratio of males to females. The annual incidence is approximately 3.5 per 100,000 people, making it one of the most commonly diagnosed causes of vertigo.

Clinical features of vestibular neuritis include nystagmus, which is a rapid, involuntary eye movement, typically in a horizontal or horizontal-torsional direction away from the affected ear. The head impulse test may also be positive. Other symptoms include spontaneous onset of rotational vertigo, which is worsened by changes in head position, as well as nausea, vomiting, and unsteadiness. These severe symptoms usually last for 2-3 days, followed by a gradual recovery over a few weeks. It is important to note that hearing is not affected in vestibular neuritis, and symptoms such as tinnitus and focal neurological deficits are not present.

Differential diagnosis for vestibular neuritis includes benign paroxysmal positional vertigo (BPPV), labyrinthitis, Meniere’s disease, migraine, stroke, and cerebellar lesions. Management of vestibular neuritis involves drug treatment for nausea and vomiting associated with vertigo, typically through short courses of medication such as prochlorperazine or cyclizine. If symptoms are severe and fluids cannot be tolerated, admission and administration of IV fluids may be necessary. General advice should also be given, including avoiding driving while symptomatic, considering the suitability to work based on occupation and duties, and the increased risk of falls. Follow-up is required, and referral is necessary if there are atypical symptoms, symptoms do not improve after a week of treatment, or symptoms persist for more than 6 weeks.

The prognosis for vestibular neuritis is generally good, with the majority of individuals fully recovering within 6 weeks. Recurrence is thought to occur in 2-11% of cases, and approximately 10% of individuals may develop BPPV following an episode of vestibular neuritis. A very rare complication of vestibular neuritis is ph

Korsakoff syndrome is a form of dementia that occurs due to a lack of thiamine (vitamin B1) in the body. This condition is most commonly observed in individuals who have a long history of alcoholism. The main features of Korsakoff syndrome include anterograde amnesia, patchy retrograde amnesia, and confabulation. Additionally, many patients also experience difficulties with language (aphasia), movement (apraxia), recognition (agnosia), or executive functioning. It is important to note that Korsakoff syndrome often coexists with Wernicke’s encephalopathy, which is characterized by a triad of symptoms including ophthalmoplegia, altered mental state, and gait disturbance (ataxia). When both conditions are present, it is referred to as Wernicke-Korsakoff syndrome (WKS).

Narrow QRS complex tachycardia is a term used to describe a fast heart rhythm with a pulse rate over 100 bpm and a QRS duration shorter than 120 ms.

Further Reading:

Supraventricular tachycardia (SVT) is a type of tachyarrhythmia that originates from the atria or above the bundle of His in the heart. It includes all atrial and junctional tachycardias, although atrial fibrillation is often considered separately. SVT typically produces a narrow QRS complex tachycardia on an electrocardiogram (ECG), unless there is an underlying conduction abnormality below the atrioventricular (AV) node. Narrow complex tachycardias are considered SVTs, while some broad complex tachycardias can also be SVTs with co-existent conduction delays.

SVT can be classified into three main subtypes based on where it arises: re-entrant accessory circuits (the most common type), atrial tachycardias, and junctional tachycardias. The most common SVTs are AVNRT (AV nodal re-entry tachycardia) and AVRT (AV re-entry tachycardia), which arise from accessory circuits within the heart. AVNRT involves an accessory circuit within the AV node itself, while AVRT involves an accessory pathway between the atria and ventricles that allows additional electrical signals to trigger the AV node.

Atrial tachycardias originate from abnormal foci within the atria, except for the SA node, AV node, or accessory pathway. Junctional tachycardias arise in the AV junction. The ECG features of SVTs vary depending on the type. Atrial tachycardias may have abnormal P wave morphology, an isoelectric baseline between P waves (in atrial flutter), and inverted P waves in certain leads. AVNRT may show pseudo R waves in V1 or pseudo S waves in certain leads, with an RP interval shorter than the PR interval. AVRT (WPW) may exhibit a delta wave on a resting ECG and retrograde P waves in the ST segment, with an RP interval shorter than the PR interval. Junctional tachycardias may have retrograde P waves before, during, or after the QRS complex, with inverted P waves in certain leads and upright P waves in others.

Treatment of SVT follows the 2021 resuscitation council algorithm for tachycardia with a pulse. The algorithm provides guidelines for managing stable patients with SVT.

One of the clinical features of mitral stenosis is malar flush, which refers to a reddening or flushing of the cheeks. Other clinical features include a mid-late diastolic murmur that is best heard during expiration, a loud S1 heart sound with an opening snap, a low volume pulse, atrial fibrillation, and signs of pulmonary edema such as crepitations or the presence of white or pink frothy sputum.

Further Reading:

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.

Clang associations refer to the grouping of words, typically rhyming words, that share similar sounds but lack any logical connection. These associations are commonly observed in individuals diagnosed with schizophrenia and bipolar disorder.

The most frequently encountered virus transmitted through blood transfusion is parvovirus B19. This particular occurrence happens in roughly 1 out of every 10,000 transfusions.

On the other hand, the transmission of other viruses is extremely uncommon. The likelihood of contracting Hepatitis B through a blood transfusion is estimated to be around 1 in 100,000 to 200,000. Similarly, the chances of acquiring Hepatitis C or HIV through a blood transfusion are even rarer, with the odds being approximately 1 in 1 million for both viruses.

Le Fort III fractures can be distinguished from Le Fort II fractures by the presence of damage to the zygomatic arch.

Further Reading:

The Le Fort fracture classification describes three fracture patterns seen in midface fractures, all involving the maxilla and pterygoid plate disruption. As the classification grading increases, the anatomic level of the maxillary fracture ascends from inferior to superior.

Le Fort I fractures, also known as floating palate fractures, typically result from a downward blow struck above the upper dental row. Signs include swelling of the upper lip, bruising to the upper buccal sulcus, malocclusion, and mobile upper teeth.

Le Fort II fractures, also known as floating maxilla fractures, are typically the result of a forceful blow to the midaxillary area. Signs include a step deformity at the infraorbital margin, oedema over the middle third of the face, sensory disturbance of the cheek, and bilateral circumorbital ecchymosis.

Le Fort III fractures, also known as craniofacial dislocation or floating face fractures, are typically the result of high force blows to the nasal bridge or upper maxilla. These fractures involve the zygomatic arch and extend through various structures in the face. Signs include tenderness at the frontozygomatic suture, lengthening of the face, enophthalmos, and bilateral circumorbital ecchymosis.

Management of Le Fort fractures involves securing the airway as a priority, following the ABCDE approach, and identifying and managing other injuries, especially cervical spine injuries. Severe bleeding may occur and should be addressed appropriately. Surgery is almost always required, and patients should be referred to maxillofacial surgeons. Other specialties, such as neurosurgery and ophthalmology, may need to be involved depending on the specific case.

The two-level PE Wells score has been simplified to determine the likelihood of a pulmonary embolism (PE) into two outcomes: likely or unlikely. A score of over 4 indicates that a PE is likely, while a score of 4 points or less indicates that a PE is unlikely.

The allocation of points is as follows:

– Clinical symptoms and signs of deep vein thrombosis (DVT) = 3 points
– An alternative diagnosis that is less likely than a PE = 3 points
– Heart rate greater than 100 = 1.5 points
– Immobilization for more than 3 days or recent surgery within 4 weeks = 1.5 points
– Previous history of DVT or PE = 1.5 points
– Presence of haemoptysis = 1 point
– Malignancy (currently on treatment, treated in the last 6 months, or palliative care) = 1 point.

The symptoms and signs of strokes can vary depending on which blood vessel is affected. Here is a summary of the main symptoms based on the territory affected:

Anterior cerebral artery: This can cause weakness on the opposite side of the body, with the leg and shoulder being more affected than the arm, hand, and face. There may also be minimal loss of sensation on the opposite side of the body. Other symptoms can include difficulty speaking (dysarthria), language problems (aphasia), apraxia (difficulty with limb movements), urinary incontinence, and changes in behavior and personality.

Middle cerebral artery: This can lead to weakness on the opposite side of the body, with the face and arm being more affected than the leg. There may also be a loss of sensation on the opposite side of the body. Depending on the dominant hemisphere of the brain, there may be difficulties with expressive or receptive language (dysphasia). In the non-dominant hemisphere, there may be neglect of the opposite side of the body.

Posterior cerebral artery: This can cause a loss of vision on the opposite side of both eyes (homonymous hemianopia). There may also be defects in a specific quadrant of the visual field. In some cases, there may be a syndrome affecting the thalamus on the opposite side of the body.

It’s important to note that these are just general summaries and individual cases may vary. If you suspect a stroke, it’s crucial to seek immediate medical attention.

When suxamethonium is administered for neuromuscular blockade during rapid sequence induction, one of the clinical observations typically seen is muscle fasciculations. However, when rocuronium is used instead, muscle fasciculations are not present.

Further Reading:

Rapid sequence induction (RSI) is a method used to place an endotracheal tube (ETT) in the trachea while minimizing the risk of aspiration. It involves inducing loss of consciousness while applying cricoid pressure, followed by intubation without face mask ventilation. The steps of RSI can be remembered using the 7 P’s: preparation, pre-oxygenation, pre-treatment, paralysis and induction, protection and positioning, placement with proof, and post-intubation management.

Preparation involves preparing the patient, equipment, team, and anticipating any difficulties that may arise during the procedure. Pre-oxygenation is important to ensure the patient has an adequate oxygen reserve and prolongs the time before desaturation. This is typically done by breathing 100% oxygen for 3 minutes. Pre-treatment involves administering drugs to counter expected side effects of the procedure and anesthesia agents used.

Paralysis and induction involve administering a rapid-acting induction agent followed by a neuromuscular blocking agent. Commonly used induction agents include propofol, ketamine, thiopentone, and etomidate. The neuromuscular blocking agents can be depolarizing (such as suxamethonium) or non-depolarizing (such as rocuronium). Depolarizing agents bind to acetylcholine receptors and generate an action potential, while non-depolarizing agents act as competitive antagonists.

Protection and positioning involve applying cricoid pressure to prevent regurgitation of gastric contents and positioning the patient’s neck appropriately. Tube placement is confirmed by visualizing the tube passing between the vocal cords, auscultation of the chest and stomach, end-tidal CO2 measurement, and visualizing misting of the tube. Post-intubation management includes standard care such as monitoring ECG, SpO2, NIBP, capnography, and maintaining sedation and neuromuscular blockade.

Overall, RSI is a technique used to quickly and safely secure the airway in patients who may be at risk of aspiration. It involves a series of steps to ensure proper preparation, oxygenation, drug administration, and tube placement. Monitoring and post-intubation care are also important aspects of RSI.

The British Society of Gastroenterology (BSG) has developed guidelines for healthcare professionals who are assessing cases of acute lower intestinal bleeding in a hospital setting. These guidelines are particularly useful when determining which patients should be referred for further evaluation.

When patients present with lower gastrointestinal bleeding (LGIB), they should be categorized as either unstable or stable. Unstable patients are defined as those with a shock index greater than 1, which is calculated by dividing the heart rate by the systolic blood pressure (HR/SBP).

For stable patients, the next step is to determine whether their bleed is major (requiring hospitalization) or minor (suitable for outpatient management). This can be determined using a risk assessment tool called the Oakland risk score, which takes into account factors such as age, hemoglobin level, and findings from a digital rectal examination.

Patients with a minor self-limiting bleed (e.g., an Oakland score of less than 8 points) and no other indications for hospital admission can be discharged with urgent follow-up for further investigation as an outpatient.

Patients with a major bleed should be admitted to the hospital and scheduled for a colonoscopy as soon as possible.

If a patient is hemodynamically unstable or has a shock index greater than 1 even after initial resuscitation, and there is suspicion of active bleeding, a CT angiography (CTA) should be considered. This can be followed by endoscopic or radiological therapy.

If no bleeding source is identified by the initial CTA and the patient remains stable after resuscitation, an upper endoscopy should be performed immediately, as LGIB associated with hemodynamic instability may indicate an upper gastrointestinal bleeding source. Gastroscopy may be the first investigation if the patient stabilizes after initial resuscitation.

If indicated, catheter angiography with the possibility of embolization should be performed as soon as possible after a positive CTA to increase the chances of success. In centers with a 24/7 interventional radiology service, this procedure should be available within 60 minutes for hemodynamically unstable patients.

Emergency laparotomy should only be considered if all efforts to locate the bleeding using radiological and/or endoscopic methods have been exhausted, except in exceptional circumstances.

In some cases, red blood cell transfusion may be necessary. It is recommended to use restrictive blood transfusion thresholds, such as a hemoglobin trigger of 7 g/dL and a target of 7-9 g/d

The recommended first-line diagnostic test for TMJ dislocation is an OPG. The Royal College of Emergency Medicine suggests that an OPG is the most effective initial imaging technique for diagnosing TMJ dislocation. However, mandibular series X-ray views and CT scans can also be used as alternative imaging methods.

Further Reading:

TMJ dislocation occurs when the mandibular condyle is displaced from its normal position in the mandibular fossa of the temporal bone. The most common type of dislocation is bilateral anterior dislocation. This occurs when the mandible is dislocated forward and the masseter and pterygoid muscles spasm, locking the condyle in place.

The temporomandibular joint is unique because it has an articular disc that separates the joint into upper and lower compartments. Dislocation can be caused by trauma, such as a direct blow to the open mouth, or by traumatic events like excessive mouth opening during yawning, laughing, shouting, or eating. It can also occur during dental work.

Signs and symptoms of TMJ dislocation include difficulty fully opening or closing the mouth, pain or tenderness in the TMJ region, jaw pain, ear pain, difficulty chewing, and facial pain. Connective tissue disorders like Marfan’s and Ehlers-Danlos syndrome can increase the likelihood of dislocation.

If TMJ dislocation is suspected, X-rays may be done to confirm the diagnosis. The best initial imaging technique is an orthopantomogram (OPG) or a standard mandibular series.

Management of anterior dislocations involves reducing the dislocated mandible, which is usually done in the emergency department. Dislocations to the posterior, medial, or lateral side are usually associated with a mandibular fracture and should be referred to a maxillofacial surgeon.

Reduction of an anterior dislocation involves applying distraction forces to the mandible. This can be done by gripping the mandible externally or intra-orally. In some cases, procedural sedation or local anesthesia may be used, and in rare cases, reduction may be done under general anesthesia.

After reduction, a post-reduction X-ray is done to confirm adequate reduction and rule out any fractures caused by the procedure. Discharge advice includes following a soft diet for at least 48 hours, avoiding wide mouth opening for at least 2 weeks, and supporting the mouth with the hand during yawning or laughing. A Barton bandage may be used to support the mandible if the patient is unable to comply with the discharge advice. Referral to a maxillofacial surgeon as an outpatient is also recommended.

The Blatchford score, also known as the Glasgow-Blatchford Bleeding Score, is a commonly used tool to evaluate individuals who present with an acute upper gastrointestinal bleed. It is recommended by NICE (National Institute for Health and Care Excellence) that healthcare professionals use specific risk assessment scores for patients with this condition. The Blatchford score is used for initial assessment, while the full Rockall score is used after endoscopy.

The Blatchford score consists of 9 criteria, including gender, urea levels, hemoglobin levels, systolic blood pressure, pulse rate, presence of melena (black, tarry stools) at presentation, syncope (fainting) at presentation, presence of hepatic disease, and presence of cardiac failure. These criteria are used to determine the patient’s risk level. A calculator for the Blatchford score can be found in the links section.

Further Reading:

Peptic ulcer disease (PUD) is a condition characterized by a break in the mucosal lining of the stomach or duodenum. It is caused by an imbalance between factors that promote mucosal damage, such as gastric acid, pepsin, Helicobacter pylori infection, and NSAID drug use, and factors that maintain mucosal integrity, such as prostaglandins, mucus lining, bicarbonate, and mucosal blood flow.

The most common causes of peptic ulcers are H. pylori infection and NSAID use. Other factors that can contribute to the development of ulcers include smoking, alcohol consumption, certain medications (such as steroids), stress, autoimmune conditions, and tumors.

Diagnosis of peptic ulcers involves screening for H. pylori infection through breath or stool antigen tests, as well as upper gastrointestinal endoscopy. Complications of PUD include bleeding, perforation, and obstruction. Acute massive hemorrhage has a case fatality rate of 5-10%, while perforation can lead to peritonitis with a mortality rate of up to 20%.

The symptoms of peptic ulcers vary depending on their location. Duodenal ulcers typically cause pain that is relieved by eating, occurs 2-3 hours after eating and at night, and may be accompanied by nausea and vomiting. Gastric ulcers, on the other hand, cause pain that occurs 30 minutes after eating and may be associated with nausea and vomiting.

Management of peptic ulcers depends on the underlying cause and presentation. Patients with active gastrointestinal bleeding require risk stratification, volume resuscitation, endoscopy, and proton pump inhibitor (PPI) therapy. Those with perforated ulcers require resuscitation, antibiotic treatment, analgesia, PPI therapy, and urgent surgical review.

For stable patients with peptic ulcers, lifestyle modifications such as weight loss, avoiding trigger foods, eating smaller meals, quitting smoking, reducing alcohol consumption, and managing stress and anxiety are recommended. Medication review should be done to stop causative drugs if possible. PPI therapy, with or without H. pylori eradication therapy, is also prescribed. H. pylori testing is typically done using a carbon-13 urea breath test or stool antigen test, and eradication therapy involves a 7-day triple therapy regimen of antibiotics and PPI.

Migraine without aura typically needs to meet the specific criteria set by the International Headache Society. These criteria include experiencing at least five attacks that meet the requirements outlined in criteria 2-4. The duration of these headache attacks should last between 4 to 72 hours. Additionally, the headache should exhibit at least two of the following characteristics: unilateral location, pulsating quality, moderate or severe pain intensity, and aggravation or avoidance of routine physical activity. Furthermore, during the headache, individuals should experience at least one of the following symptoms: nausea and/or vomiting, photophobia, and phonophobia. For more detailed information, you can refer to the guidelines provided by The British Association for the Study of Headache.

The NICE guidelines for suspected deep vein thrombosis (DVT) suggest considering the possibility of DVT if typical symptoms and signs are present, particularly if the person has risk factors like previous venous thromboembolism and immobility.

Typical signs and symptoms of DVT include unilateral localized pain (often throbbing) that occurs during walking or bearing weight, as well as calf swelling (or, less commonly, swelling of the entire leg). Other signs to look out for are tenderness, skin changes such as edema, redness, and warmth, and vein distension.

To rule out other potential causes for the symptoms and signs, it is important to conduct a physical examination and review the person’s general medical history.

When assessing leg and thigh swelling, it is recommended to measure the circumference of the leg 10 cm below the tibial tuberosity and compare it with the unaffected leg. A difference of more than 3 cm between the two legs increases the likelihood of DVT.

Additionally, it is important to check for edema and dilated collateral superficial veins on the affected side.

To assess the likelihood of DVT and guide further management, the two-level DVT Wells score can be used.

For more information, you can refer to the NICE Clinical Knowledge Summary on deep vein thrombosis.

This patient is currently experiencing moderate shock, classified as class III. This level of shock corresponds to a loss of 30-40% of their circulatory volume, which is equivalent to a blood loss of 1500-2000 mL.

Hemorrhage can be categorized into four different classes based on physiological parameters and clinical signs. These classes are classified as class I, class II, class III, and class IV.

In class I hemorrhage, the blood loss is up to 750 mL or up to 15% of the blood volume. The pulse rate is less than 100 beats per minute, and the systolic blood pressure is normal. The pulse pressure may be normal or increased, and the respiratory rate is within the range of 14-20 breaths per minute. The urine output is greater than 30 mL per hour, and the patient’s CNS/mental status is slightly anxious.

In class II hemorrhage, the blood loss ranges from 750-1500 mL or 15-30% of the blood volume. The pulse rate is between 100-120 beats per minute, and the systolic blood pressure remains normal. The pulse pressure is decreased, and the respiratory rate increases to 20-30 breaths per minute. The urine output decreases to 20-30 mL per hour, and the patient may experience mild anxiety.

The patient in this case is in class III hemorrhage, with a blood loss of 1500-2000 mL or 30-40% of the blood volume. The pulse rate is elevated, ranging from 120-140 beats per minute, and the systolic blood pressure is decreased. The pulse pressure is also decreased, and the respiratory rate is elevated to 30-40 breaths per minute. The urine output decreases significantly to 5-15 mL per hour, and the patient may experience anxiety and confusion.

Class IV hemorrhage represents the most severe level of blood loss, with a loss of over 40% of the blood volume. The pulse rate is greater than 140 beats per minute, and the systolic blood pressure is significantly decreased. The pulse pressure is decreased, and the respiratory rate is over 40 breaths per minute. The urine output becomes negligible, and the patient may become confused and lethargic.

The leads V3 and V4 represent the anterior myocardial area.

Acute Coronary Syndromes (ACS) is a term used to describe a group of conditions that involve the sudden reduction or blockage of blood flow to the heart. This can lead to a heart attack or unstable angina. ACS includes ST segment elevation myocardial infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI), and unstable angina (UA).

The development of ACS is usually seen in patients who already have underlying coronary heart disease. This disease is characterized by the buildup of fatty plaques in the walls of the coronary arteries, which can gradually narrow the arteries and reduce blood flow to the heart. This can cause chest pain, known as angina, during physical exertion. In some cases, the fatty plaques can rupture, leading to a complete blockage of the artery and a heart attack.

There are both non modifiable and modifiable risk factors for ACS. non modifiable risk factors include increasing age, male gender, and family history. Modifiable risk factors include smoking, diabetes mellitus, hypertension, hypercholesterolemia, and obesity.

The symptoms of ACS typically include chest pain, which is often described as a heavy or constricting sensation in the central or left side of the chest. The pain may also radiate to the jaw or left arm. Other symptoms can include shortness of breath, sweating, and nausea/vomiting. However, it’s important to note that some patients, especially diabetics or the elderly, may not experience chest pain.

The diagnosis of ACS is typically made based on the patient’s history, electrocardiogram (ECG), and blood tests for cardiac enzymes, specifically troponin. The ECG can show changes consistent with a heart attack, such as ST segment elevation or depression, T wave inversion, or the presence of a new left bundle branch block. Elevated troponin levels confirm the diagnosis of a heart attack.

The management of ACS depends on the specific condition and the patient’s risk factors. For STEMI, immediate coronary reperfusion therapy, either through primary percutaneous coronary intervention (PCI) or fibrinolysis, is recommended. In addition to aspirin, a second antiplatelet agent is usually given. For NSTEMI or unstable angina, the treatment approach may involve reperfusion therapy or medical management, depending on the patient’s risk of future cardiovascular events.