If you have missed one pill, which means it has been 48-72 hours since you took the last pill in your current packet or you started the first pill in a new packet 24-48 hours late, you need to take the missed pill as soon as you remember. Make sure to continue taking the remaining pills at your usual time. Emergency contraception is generally not necessary in this situation, but it may be worth considering if you have missed pills earlier in the packet or during the last week of the previous packet.

Whooping cough, also known as pertussis, is a respiratory infection caused by the bacteria Bordetella pertussis. It is transmitted through respiratory droplets and has an incubation period of about 7-21 days. This highly contagious disease can be passed on to around 90% of close household contacts.

To prevent the spread of whooping cough, Public Health England advises that children with the illness should stay away from school, nursery, or childminders for 48 hours after starting antibiotic treatment. If no antibiotic treatment is given, they should be kept away for 21 days from the onset of the illness. It’s important to note that even after treatment, non-infectious coughing may persist for several weeks.

For more information on how to control infections in schools and other childcare settings, you can refer to the guidance provided by Public Health England.

De Quervain’s tenosynovitis is a condition characterized by inflammation and thickening of the sheath that contains the tendons of the extensor pollicis brevis and abductor pollicis longus. This leads to pain on the radial side of the wrist. It is more commonly observed in women, particularly those aged between 30 and 50 years. The condition is often associated with repetitive activities that involve pinching and grasping.

During examination, swelling and tenderness along the tendon sheath may be observed. The tendon sheath itself may also appear thickened. The most pronounced tenderness is usually felt over the tip of the radial styloid. A positive Finkelstein’s test, which involves flexing the wrist and moving it towards the ulnar side while the thumb is flexed across the palm, can help confirm the diagnosis.

Treatment for De Quervain’s tenosynovitis involves avoiding movements that can trigger symptoms and using a thumb splint to immobilize the thumb. In cases where symptoms persist, a local corticosteroid injection or surgical decompression may be considered.

Immunoglobulin light chains that are present in the urine are commonly known as Bence-Jones proteins (BJP). These proteins are primarily observed in individuals with multiple myeloma, although they can occasionally be detected in Waldenström macroglobulinemia, although this is a rare occurrence. It is important to note that BJP in the urine is not observed in the other conditions mentioned in this question.

The ATLS guidelines categorize chest injuries in trauma into two groups: life-threatening injuries that require immediate identification and treatment in the primary survey, and potentially life-threatening injuries that should be identified and treated in the secondary survey.

During the primary survey, the focus is on identifying and treating life-threatening thoracic injuries. These include airway obstruction, tracheobronchial tree injury, tension pneumothorax, open pneumothorax, massive haemothorax, and cardiac tamponade. Prompt recognition and intervention are crucial in order to prevent further deterioration and potential fatality.

In the secondary survey, attention is given to potentially life-threatening injuries that may not be immediately apparent. These include simple pneumothorax, haemothorax, flail chest, pulmonary contusion, blunt cardiac injury, traumatic aortic disruption, traumatic diaphragmatic injury, and blunt oesophageal rupture. These injuries may not pose an immediate threat to life, but they still require identification and appropriate management to prevent complications and ensure optimal patient outcomes.

By dividing chest injuries into these two categories and addressing them in a systematic manner, healthcare providers can effectively prioritize and manage trauma patients, ultimately improving their chances of survival and recovery.

The Severity of Alcohol Dependence Questionnaire (SADQ) is a brief, self-administered questionnaire consisting of 20 items. It was developed by the World Health Organisation with the aim of assessing the severity of alcohol dependence. Another assessment tool recommended by NICE is the Leeds Dependence Questionnaire (LDQ), which is a self-completion questionnaire comprising of 10 items. The LDQ is designed to measure dependence on various substances. Both the SADQ and LDQ are considered useful in evaluating the severity of alcohol misuse.

NICE suggests the use of specific assessment tools to effectively evaluate the nature and severity of alcohol misuse. The AUDIT is recommended for identification purposes and as a routine outcome measure. For assessing the severity of dependence, the SADQ or LDQ are recommended. To evaluate the severity of withdrawal symptoms, the Clinical Institute Withdrawal Assessment of Alcohol Scale, revised (CIWA-Ar) is recommended. Lastly, the APQ is recommended for assessing the nature and extent of problems arising from alcohol misuse.

to the NICE guidance on the diagnosis, assessment, and management of harmful drinking and alcohol dependence.

In cases of anaphylaxis, it is important to administer non-sedating antihistamines after adrenaline administration and initial resuscitation. Previous guidelines recommended the use of chlorpheniramine and hydrocortisone as third line treatments, but the 2021 guidelines have removed this recommendation. Corticosteroids are no longer advised. Instead, it is now recommended to use non-sedating antihistamines such as cetirizine, loratadine, and fexofenadine, as alternatives to the sedating antihistamine chlorpheniramine. The top priority treatments for anaphylaxis are adrenaline, oxygen, and fluids. The Resuscitation Council advises that administration of non-sedating antihistamines should occur after the initial resuscitation.

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

Patients typically initiate dialysis when their glomerular filtration rate (GFR) drops to 10 ml/min. However, if the patient has diabetes, dialysis may be recommended when their GFR reaches 15 ml/min. The GFR is a measure of kidney function and indicates how well the kidneys are able to filter waste products from the blood. Dialysis is a medical procedure that helps perform the function of the kidneys by removing waste and excess fluid from the body.

Patients with primary hyperaldosteronism typically present with hypertension and hypokalemia. This is due to the fact that aldosterone encourages the reabsorption of sodium and the excretion of potassium, leading to an imbalance in these electrolytes. Additionally, hypernatremia, or high levels of sodium in the blood, is often observed in these patients.

Further Reading:

Hyperaldosteronism is a condition characterized by excessive production of aldosterone by the adrenal glands. It can be classified into primary and secondary hyperaldosteronism. Primary hyperaldosteronism, also known as Conn’s syndrome, is typically caused by adrenal hyperplasia or adrenal tumors. Secondary hyperaldosteronism, on the other hand, is a result of high renin levels in response to reduced blood flow across the juxtaglomerular apparatus.

Aldosterone is the main mineralocorticoid steroid hormone produced by the adrenal cortex. It acts on the distal renal tubule and collecting duct of the nephron, promoting the reabsorption of sodium ions and water while secreting potassium ions.

The causes of hyperaldosteronism vary depending on whether it is primary or secondary. Primary hyperaldosteronism can be caused by adrenal adenoma, adrenal hyperplasia, adrenal carcinoma, or familial hyperaldosteronism. Secondary hyperaldosteronism can be caused by renal artery stenosis, reninoma, renal tubular acidosis, nutcracker syndrome, ectopic tumors, massive ascites, left ventricular failure, or cor pulmonale.

Clinical features of hyperaldosteronism include hypertension, hypokalemia, metabolic alkalosis, hypernatremia, polyuria, polydipsia, headaches, lethargy, muscle weakness and spasms, and numbness. It is estimated that hyperaldosteronism is present in 5-10% of patients with hypertension, and hypertension in primary hyperaldosteronism is often resistant to drug treatment.

Diagnosis of hyperaldosteronism involves various investigations, including U&Es to assess electrolyte disturbances, aldosterone-to-renin plasma ratio (ARR) as the gold standard diagnostic test, ECG to detect arrhythmia, CT/MRI scans to locate adenoma, fludrocortisone suppression test or oral salt testing to confirm primary hyperaldosteronism, genetic testing to identify familial hyperaldosteronism, and adrenal venous sampling to determine lateralization prior to surgery.

Treatment of primary hyperaldosteronism typically involves surgical adrenalectomy for patients with unilateral primary aldosteronism. Diet modification with sodium restriction and potassium supplementation may also be recommended.

Heat stroke is a condition characterized by a systemic inflammatory response, where the core body temperature exceeds 40.6°C. It is accompanied by changes in mental state and varying levels of organ dysfunction. Heat stroke occurs when the body’s ability to regulate temperature is overwhelmed by a combination of excessive environmental heat, excessive heat production from metabolic processes (usually due to exertion), and inadequate heat loss.

It is important to consider other clinical conditions that can cause an increased core temperature. Sepsis can present similarly and should be ruled out. Neuroleptic malignant syndrome should be excluded in patients taking phenothiazines or other antipsychotics. Serotonin syndrome should be excluded in patients taking serotonergic medications such as SSRIs. Malignant hyperthermia should be considered in patients with a recent history of general anesthesia. Screening for recreational drug use, particularly cocaine, amphetamines, and ecstasy, is also recommended.

In patients with agitation and/or shivering, benzodiazepines (e.g. diazepam) can be beneficial. They help reduce excessive heat production and agitation. In severe cases of agitation, paralysis may be necessary. Dantrolene is commonly used, although there is currently limited high-level evidence supporting its use. Neuroleptics, such as chlorpromazine, which were once commonly used, should be avoided due to potential adverse effects.

Various cooling techniques are recommended, but there is currently insufficient evidence to determine the best approach. Simple measures like cold drinks, fanning, ice water packs, and spraying tepid water can be effective. Cold water immersion therapy may be helpful, but it requires patient stability and cooperation and may not be practical for critically ill patients. Advanced cooling techniques, such as cold IV fluids, surface cooling devices (SCD), intravascular cooling devices (ICD), and extracorporeal circuits, may be used for sicker patients.

Primary sclerosing cholangitis (PSC) is a condition that affects the bile ducts, causing inflammation and blockage over time. This leads to recurrent episodes of cholangitis and progressive scarring of the bile ducts. Ultimately, PSC can result in liver cirrhosis, liver failure, and even hepatocellular carcinoma. It is commonly associated with ulcerative colitis, with more than 80% of PSC patients also having ulcerative colitis. However, there is no association between PSC and Crohn’s disease.

On the other hand, Crohn’s disease has its own set of recognized associations. For instance, there is an increased incidence of Crohn’s disease among smokers, with approximately 50-60% of Crohn’s patients being smokers. Other associations include the presence of aphthous ulcers, uveitis and episcleritis (eye inflammation), seronegative spondyloarthropathies (inflammatory joint diseases), erythema nodosum (painful skin nodules), pyoderma gangrenosum (skin ulceration), finger clubbing, autoimmune hemolytic anemia, cholelithiasis (gallstones), and osteoporosis.

It is important to note the distinct associations and characteristics of these two conditions, as they have different implications for diagnosis, treatment, and management.

Malaria is a contagious illness that is spread by female mosquitoes of the Anopheles genus. It is caused by a parasitic infection from the Plasmodium genus. There are five species of Plasmodium that can cause disease in humans: Plasmodium falciparum, Plasmodium ovale, Plasmodium vivax, Plasmodium malariae, and Plasmodium knowlesi.

The main symptom of malaria is the malarial paroxysm, which is a recurring cycle of cold, hot, and sweating stages. During the cold stage, the patient experiences intense chills, followed by an extremely hot stage, and finally a stage of profuse sweating. Upon examination, the patient may show signs of anemia, jaundice, and have an enlarged liver and spleen, but no signs of swollen lymph nodes.

Plasmodium falciparum is the most severe form of malaria and is responsible for the majority of deaths. Severe or complicated malaria is indicated by impaired consciousness, seizures, low blood sugar, anemia, kidney damage, difficulty breathing, and spontaneous bleeding. Given the presentation, it is likely that this case involves Plasmodium falciparum.

Currently, artemisinin-based combination therapy (ACT) is recommended for treating P. falciparum malaria. This involves combining fast-acting artemisinin-based compounds with a drug from a different class. Companion drugs include lumefantrine, mefloquine, amodiaquine, sulfadoxine/pyrimethamine, piperaquine, and chlorproguanil/dapsone. Artemisinin derivatives include dihydroartemisinin, artesunate, and artemether.

If ACT is not available, oral quinine or atovaquone with proguanil hydrochloride can be used. Quinine is highly effective but not well tolerated for long-term treatment, so it should be combined with another drug, usually oral doxycycline (or clindamycin for pregnant women and young children).

Severe or complicated falciparum malaria should be managed in a high dependency unit or intensive care setting. Intravenous artesunate is recommended for all patients with severe or complicated falciparum malaria, or those at high risk of developing severe disease (such as if more than 2% of red blood cells are infected), or

Pelvic inflammatory disease (PID) is a pelvic infection that affects the upper female reproductive tract, including the uterus, fallopian tubes, and ovaries. It is typically caused by an ascending infection from the cervix and is commonly associated with sexually transmitted diseases like chlamydia and gonorrhea. In the UK, genital Chlamydia trachomatis infection is the most common cause of PID seen in genitourinary medicine clinics.

PID can often be asymptomatic, but when symptoms are present, they may include lower abdominal pain and tenderness, fever, painful urination, painful intercourse, purulent vaginal discharge, abnormal vaginal bleeding, and tenderness in the cervix and adnexa. It is important to note that symptoms of ectopic pregnancy can be similar to those of PID, so a pregnancy test should be conducted for all patients with suspicious symptoms.

To investigate a possible case of PID, endocervical swabs should be taken to test for C. trachomatis and N. gonorrhoeae using nucleic acid amplification tests if available. Mild to moderate cases of PID can usually be managed in primary care or outpatient settings, while patients with severe disease should be admitted to the hospital for intravenous antibiotics. Signs of severe disease include a fever above 38°C, signs of a tubo-ovarian abscess, signs of pelvic peritonitis, or concurrent pregnancy.

Empirical antibiotic treatment should be initiated as soon as a presumptive diagnosis of PID is made clinically, without waiting for swab results. The current recommended outpatient treatment for PID is a single intramuscular dose of ceftriaxone 500 mg, followed by oral doxycycline 100 mg twice daily and oral metronidazole 400 mg twice daily for 14 days. An alternative regimen is oral ofloxacin 400 mg twice daily and oral metronidazole 400 mg twice daily for 14 days.

For severely ill patients in the inpatient setting, initial treatment includes intravenous doxycycline, a single-dose of intravenous ceftriaxone, and intravenous metronidazole. This is then followed by a switch to oral doxycycline and metronidazole to complete a 14-day treatment course. If a patient fails to respond to treatment, laparoscopy is necessary to confirm the diagnosis or consider alternative diagnoses.

The primary cause of roseola is the human herpesvirus 6B (HHV6B), with the human herpesvirus 7 (HHV7) being a less common cause.

Further Reading:

Roseola infantum, also known as roseola, exanthem subitum, or sixth disease, is a common disease that affects infants. It is primarily caused by the human herpesvirus 6B (HHV6B) and less commonly by human herpesvirus 7 (HHV7). Many cases of roseola are asymptomatic, and the disease is typically spread through saliva from an asymptomatic infected individual. The incubation period for roseola is around 10 days.

Roseola is most commonly seen in children between 6 months and 3 years of age, and studies have shown that as many as 85% of children will have had roseola by the age of 1 year. The clinical features of roseola include a high fever lasting for 2-5 days, accompanied by upper respiratory tract infection (URTI) signs such as rhinorrhea, sinus congestion, sore throat, and cough. After the fever subsides, a maculopapular rash appears, characterized by rose-pink papules on the trunk that may spread to the extremities. The rash is non-itchy and painless and can last from a few hours to a few days. Around 2/3 of patients may also have erythematous papules, known as Nagayama spots, on the soft palate and uvula. Febrile convulsions occur in approximately 10-15% of cases, and diarrhea is commonly seen.

Management of roseola is usually conservative, with rest, maintaining adequate fluid intake, and taking paracetamol for fever being the main recommendations. The disease is typically mild and self-limiting. However, complications can arise from HHV6 infection, including febrile convulsions, aseptic meningitis, and hepatitis.

Von Willebrand disease (vWD) is a common hereditary coagulation disorder that affects approximately 1 in 100 people. It occurs due to a deficiency in Von Willebrand factor (vWF), which leads to reduced levels of factor VIII. vWF plays a crucial role in protecting factor VIII from breaking down quickly in the blood. Additionally, it is necessary for proper platelet adhesion, so a deficiency in vWF also results in abnormal platelet function. As a result, both the APTT and bleeding time are prolonged, while the platelet count and thrombin time remain unaffected.

Many individuals with vWD do not experience any symptoms and are diagnosed incidentally during a routine clotting profile check. However, if symptoms do occur, the most common ones include easy bruising, nosebleeds (epistaxis), and heavy menstrual bleeding (menorrhagia). In severe cases, more significant bleeding and joint bleeding (haemarthrosis) can occur.

For mild cases of von Willebrand disease, bleeding can be treated with desmopressin. This medication works by increasing the patient’s own levels of vWF, as it releases vWF stored in the Weibel-Palade bodies found in the endothelial cells. In more severe cases, replacement therapy is necessary, which involves cryoprecipitate infusions or Factor VIII concentrate. Replacement therapy is recommended for patients with severe von Willebrand’s disease who are undergoing moderate or major surgical procedures.

Congenital afibrinogenaemia is a rare coagulation disorder characterized by a deficiency or malfunction of fibrinogen. This condition leads to a prolongation of the prothrombin time, bleeding time, and APTT. However, it does not affect the platelet count.

Aspirin therapy works by inhibiting platelet cyclo-oxygenase, an essential enzyme in the generation of thromboxane A2 (TXA2). By inhibiting TXA2, aspirin reduces platelet activation and aggregation. Consequently, aspirin therapy prolongs the bleeding time but does not have an impact on the platelet count, prothrombin time, or APTT.

Warfarin, on the other hand, inhibits the synthesis of clotting factors II, VII, IX, and X, as well as protein C and protein S, which are all dependent on vitamin K.

To control epistaxis, it is recommended to have the patient sit upright with their upper body tilted forward and their mouth open. Firmly pinch the cartilaginous part of the nose, specifically in front of the bony septum, and maintain pressure for 10-15 minutes without releasing it.

Further Reading:

Epistaxis, or nosebleed, is a common condition that can occur in both children and older adults. It is classified as either anterior or posterior, depending on the location of the bleeding. Anterior epistaxis usually occurs in younger individuals and arises from the nostril, most commonly from an area called Little’s area. These bleeds are usually not severe and account for the majority of nosebleeds seen in hospitals. Posterior nosebleeds, on the other hand, occur in older patients with conditions such as hypertension and atherosclerosis. The bleeding in posterior nosebleeds is likely to come from both nostrils and originates from the superior or posterior parts of the nasal cavity or nasopharynx.

The management of epistaxis involves assessing the patient for signs of instability and implementing measures to control the bleeding. Initial measures include sitting the patient upright with their upper body tilted forward and their mouth open. Firmly pinching the cartilaginous part of the nose for 10-15 minutes without releasing the pressure can also help stop the bleeding. If these measures are successful, a cream called Naseptin or mupirocin nasal ointment can be prescribed for further treatment.

If bleeding persists after the initial measures, nasal cautery or nasal packing may be necessary. Nasal cautery involves using a silver nitrate stick to cauterize the bleeding point, while nasal packing involves inserting nasal tampons or inflatable nasal packs to stop the bleeding. In cases of posterior bleeding, posterior nasal packing or surgery to tie off the bleeding vessel may be considered.

Complications of epistaxis can include nasal bleeding, hypovolemia, anemia, aspiration, and even death. Complications specific to nasal packing include sinusitis, septal hematoma or abscess, pressure necrosis, toxic shock syndrome, and apneic episodes. Nasal cautery can lead to complications such as septal perforation and caustic injury to the surrounding skin.

In children under the age of 2 presenting with epistaxis, it is important to refer them for further investigation as an underlying cause is more likely in this age group.

Bartter’s syndrome is a rare genetic defect that affects the ascending limb of the loop of Henle. This condition is characterized by low blood pressure and a hypokalemic alkalosis, which means there is a decrease in potassium levels in the blood.

Hyperkalemia, on the other hand, is defined as having a plasma potassium level greater than 5.5 mmol/L. There are various non-drug factors that can cause hyperkalemia, such as renal failure, excessive potassium supplementation, Addison’s disease (adrenal insufficiency), congenital adrenal hyperplasia, renal tubular acidosis (type 4), rhabdomyolysis, burns and trauma, and tumor lysis syndrome. Additionally, acidosis can also contribute to the development of hyperkalemia.

In addition to these non-drug causes, certain medications can also lead to hyperkalemia. These include ACE inhibitors, angiotensin receptor blockers, NSAIDs, beta-blockers, digoxin, and suxamethonium. It is important to be aware of these potential causes and to monitor potassium levels in order to prevent and manage hyperkalemia effectively.

Hand-foot-and-mouth disease is a viral syndrome characterized by a unique rash and sores. The main culprit behind this condition is typically the Coxsackie A16 virus. After being exposed to the virus, it takes about 3-5 days for symptoms to appear. The disease spreads through droplets in the air. Before the rash and sores develop, individuals may experience a pre-illness phase with symptoms like a sore throat and mouth ulcers. This condition primarily affects children under the age of ten. In addition to the rash, most children will also develop spots on their hands and feet.

When it comes to treatment, the focus is mainly on providing support. This involves using antipyretics to reduce fever and ensuring that the affected individual stays well-hydrated. Due to the mouth ulcers, loss of appetite is common, so it’s important to encourage adequate fluid intake.

One commonly used risk assessment tool for acute upper gastrointestinal bleeding is the Glasgow-Blatchford score. This score takes into account various factors such as blood pressure, heart rate, blood urea nitrogen levels, hemoglobin levels, and the presence of melena or syncope. By assigning points to each of these factors, the Glasgow-Blatchford score helps to stratify patients into low or high-risk categories.

Further Reading:

Upper gastrointestinal bleeding (UGIB) refers to the loss of blood from the gastrointestinal tract, occurring in the upper part of the digestive system. It can present as haematemesis (vomiting blood), coffee-ground emesis, bright red blood in the nasogastric tube, or melaena (black, tarry stools). UGIB can lead to significant hemodynamic compromise and is a major health burden, accounting for approximately 70,000 hospital admissions each year in the UK with a mortality rate of 10%.

The causes of UGIB vary, with peptic ulcer disease being the most common cause, followed by gastritis/erosions, esophagitis, and other less common causes such as varices, Mallory Weiss tears, and malignancy. Swift assessment, hemodynamic resuscitation, and appropriate interventions are essential for the management of UGIB.

Assessment of patients with UGIB should follow an ABCDE approach, and scoring systems such as the Glasgow-Blatchford bleeding score (GBS) and the Rockall score are recommended to risk stratify patients and determine the urgency of endoscopy. Transfusion may be necessary for patients with massive hemorrhage, and platelet transfusion, fresh frozen plasma (FFP), and prothrombin complex concentrate may be offered based on specific criteria.

Endoscopy plays a crucial role in the management of UGIB. Unstable patients with severe acute UGIB should undergo endoscopy immediately after resuscitation, while all other patients should undergo endoscopy within 24 hours of admission. Endoscopic treatment of non-variceal bleeding may involve mechanical methods of hemostasis, thermal coagulation, or the use of fibrin or thrombin with adrenaline. Proton pump inhibitors should only be used after endoscopy.

Variceal bleeding requires specific management, including the use of terlipressin and prophylactic antibiotics. Oesophageal varices can be treated with band ligation or transjugular intrahepatic portosystemic shunts (TIPS), while gastric varices may be treated with endoscopic injection of N-butyl-2-cyanoacrylate or TIPS if bleeding is not controlled.

For patients taking NSAIDs, aspirin, or clopidogrel, low-dose aspirin can be continued once hemostasis is achieved, NSAIDs should be stopped in patients presenting with UGIB

Lidocaine is commonly chosen because it offers some local anesthesia. Alternatively, mineral oil can be used. Cold water irrigation can often cause nausea and vomiting, so it is recommended to use warm water for irrigation. An ENT clinician should be able to remove an insect from the ear canal. However, if removal attempts are unsuccessful or complications arise, a referral may be necessary.

Further Reading:

Foreign bodies in the ear or nose are a common occurrence, especially in children between the ages of 2 and 8. Foreign bodies in the ear are more common than those in the nose. Symptoms of foreign bodies in the ear may include ear pain, a feeling of fullness, impaired hearing, discharge, tinnitus, and vertigo. It is important to consider referral to an ENT specialist for the removal of potentially harmful foreign bodies such as glass, sharp objects, button batteries, and tightly wedged items. ENT involvement is also necessary if there is a perforation of the eardrum or if the foreign body is embedded in the eardrum.

When preparing a patient for removal, it is important to establish rapport and keep the patient relaxed, especially if they are a young child. The patient should be positioned comfortably and securely, and ear drops may be used to anesthetize the ear. Removal methods for foreign bodies in the ear include the use of forceps or a hook, irrigation (except for batteries, perforations, or organic material), suction, and magnets for ferrous metal foreign bodies. If there is an insect in the ear, it should be killed with alcohol, lignocaine, or mineral oil before removal.

After the foreign body is removed, it is important to check for any residual foreign bodies and to discharge the patient with appropriate safety net advice. Prophylactic antibiotic drops may be considered if there has been an abrasion of the skin.

Foreign bodies in the nose are less common but should be dealt with promptly due to the risk of posterior dislodgement into the airway. Symptoms of foreign bodies in the nose may include nasal discharge, sinusitis, nasal pain, epistaxis, or blood-stained discharge. Most nasal foreign bodies are found on the anterior or middle third of the nose and may not show up on x-rays.

Methods for removing foreign bodies from the nose include the mother’s kiss technique, suction, forceps, Jobson horne probe, and foley catheter. The mother’s kiss technique involves occluding the patent nostril and having a parent blow into the patient’s mouth. A foley catheter can be used by inserting it past the foreign body and inflating the balloon to gently push the foreign body out. ENT referral may be necessary if the foreign body cannot be visualized but there is a high suspicion, if attempts to remove the foreign body have failed, if the patient requires sed

This patient is displaying symptoms and signs that are in line with community-acquired pneumonia (CAP). The most frequent cause of CAP in an adult patient who is otherwise in good health is Streptococcus pneumoniae.

This man is experiencing an acute episode of asthma. His initial peak flow measurement is 46% of his best, indicating a severe exacerbation. According to the BTS guidelines, acute asthma can be classified as moderate, acute severe, life-threatening, or near-fatal.

Moderate asthma is characterized by increasing symptoms and a peak expiratory flow rate (PEFR) between 50-75% of the individual’s best or predicted value. There are no signs of acute severe asthma in this case.

Acute severe asthma is identified by any one of the following criteria: a PEFR between 33-50% of the best or predicted value, a respiratory rate exceeding 25 breaths per minute, a heart rate over 110 beats per minute, or the inability to complete sentences in one breath.

Life-threatening asthma is indicated by any one of the following: a PEFR below 33% of the best or predicted value, oxygen saturation (SpO2) below 92%, arterial oxygen pressure (PaO2) below 8 kPa, normal arterial carbon dioxide pressure (PaCO2) between 4.6-6.0 kPa, a silent chest, cyanosis, poor respiratory effort, arrhythmia, exhaustion, altered conscious level, or hypotension.

Near-fatal asthma is characterized by elevated PaCO2 levels and/or the need for mechanical ventilation with increased inflation pressures.

Spontaneous bacterial peritonitis (SBP) is a condition where bacteria infect the fluid in the abdomen, known as ascites. It is commonly seen in patients with ascites. Symptoms of SBP include fever, chills, nausea, vomiting, abdominal pain, and mental confusion. To diagnose SBP, a procedure called paracentesis is done to analyze the fluid in the abdomen. If the neutrophil count in the fluid is higher than 250 cells/mm³, it confirms the diagnosis of SBP, regardless of whether bacteria are found in the culture. The initial treatment for acute community-acquired SBP is usually a 3rd generation cephalosporin antibiotic like cefotaxime or ceftriaxone. However, hospital-acquired SBP may require different antibiotics based on local resistance patterns. Patients who have had SBP in the past are at a high risk of recurrence and may need long-term antibiotic prophylaxis.

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.

Here are some suggestions for managing breathlessness in the final days of life, as provided by NICE:

1. It is important to identify and treat any reversible causes of breathlessness in the dying person, such as pulmonary edema or pleural effusion.

2. Non-pharmacological methods can be considered for managing breathlessness in someone nearing the end of life. It is not recommended to start oxygen therapy as a routine measure. Oxygen should only be offered to individuals who are known or suspected to have symptomatic hypoxemia.

3. Breathlessness can be managed using different medications, including opioids, benzodiazepines, or a combination of both.

For more detailed information, you can refer to the NICE guidance on the care of dying adults in the last days of life. https://www.nice.org.uk/guidance/ng31

Phaeochromocytoma is characterized by certain clinical features, including paroxysmal hypertension, palpitations, headache, tremor, and profuse sweating. This patient exhibits paroxysmal symptoms that align with phaeochromocytoma, such as high blood pressure (systolic readings exceeding 220 mmHg are common), headache, sweating, and feelings of anxiety and fear. It is important to note that individuals with conditions like congenital adrenal hyperplasia, diabetes insipidus, and Addisonian crisis typically experience low blood pressure.

Further Reading:

Phaeochromocytoma is a rare neuroendocrine tumor that secretes catecholamines. It typically arises from chromaffin tissue in the adrenal medulla, but can also occur in extra-adrenal chromaffin tissue. The majority of cases are spontaneous and occur in individuals aged 40-50 years. However, up to 30% of cases are hereditary and associated with genetic mutations. About 10% of phaeochromocytomas are metastatic, with extra-adrenal tumors more likely to be metastatic.

The clinical features of phaeochromocytoma are a result of excessive catecholamine production. Symptoms are typically paroxysmal and include hypertension, headaches, palpitations, sweating, anxiety, tremor, abdominal and flank pain, and nausea. Catecholamines have various metabolic effects, including glycogenolysis, mobilization of free fatty acids, increased serum lactate, increased metabolic rate, increased myocardial force and rate of contraction, and decreased systemic vascular resistance.

Diagnosis of phaeochromocytoma involves measuring plasma and urine levels of metanephrines, catecholamines, and urine vanillylmandelic acid. Imaging studies such as abdominal CT or MRI are used to determine the location of the tumor. If these fail to find the site, a scan with metaiodobenzylguanidine (MIBG) labeled with radioactive iodine is performed. The highest sensitivity and specificity for diagnosis is achieved with plasma metanephrine assay.

The definitive treatment for phaeochromocytoma is surgery. However, before surgery, the patient must be stabilized with medical management. This typically involves alpha-blockade with medications such as phenoxybenzamine or phentolamine, followed by beta-blockade with medications like propranolol. Alpha blockade is started before beta blockade to allow for expansion of blood volume and to prevent a hypertensive crisis.

Glanzmann’s thrombasthenia is an uncommon condition affecting platelets, where they have a deficiency or abnormality in glycoprotein IIb/IIIa. This disorder leads to platelet dysfunction and can result in various complications.

Standard pain relievers are generally not effective in treating cluster headaches. They take too long to work, and by the time they start to relieve the pain, the headache has usually already gone away. It is not recommended to use opioids for cluster headaches as they may actually make the headaches worse, and using them for a long time can lead to dependency.

However, there are other options that can be effective in treating cluster headaches. One option is to use subcutaneous sumatriptan, which is a medication that works by stimulating a specific receptor in the brain. This can help reduce the inflammation in the blood vessels that is associated with migraines and cluster headaches. Most people find that subcutaneous sumatriptan starts to work within 10-15 minutes of being administered.

Another option is to use zolmitriptan nasal spray, which is also a medication that works in a similar way to sumatriptan. However, it may take a bit longer for the nasal spray to start working compared to the subcutaneous injection.

In addition to medication, high-flow oxygen can also be used as an alternative therapy for cluster headaches. This involves breathing in oxygen at a high flow rate, which can help relieve the pain and other symptoms of a cluster headache.

Lastly, octreotide can be administered subcutaneously and has been shown to be more effective than a placebo in treating acute cluster headache attacks.

Gout and pseudogout are both characterized by the presence of crystal deposits in the joints that are affected. Gout occurs when urate crystals are deposited, while pseudogout occurs when calcium pyrophosphate crystals are deposited. Under a microscope, these crystals can be distinguished by their appearance. Urate crystals are needle-shaped and negatively birefringent, while calcium pyrophosphate crystals are brick-shaped and positively birefringent.

Gout can affect any joint in the body, but it most commonly manifests in the hallux metatarsophalangeal joint, which is the joint at the base of the big toe. This joint is affected in approximately 50% of gout cases. On the other hand, pseudogout primarily affects the larger joints, such as the knee.

Peri-orbital cellulitis, also known as preseptal cellulitis, is an infection that affects the eyelid and the skin surrounding the eye in front of the orbital septal. On the other hand, orbital cellulitis is a medical emergency that occurs when there is an infection in the tissues of the eye located behind the orbital septum.

The most common organisms that cause these infections include Streptococcus pneumoniae, Staphylococcus aureus, Streptococcus pyogenes, and Haemophilus influenzae.

Peri-orbital cellulitis may present with various symptoms, such as swelling of the eyelid, redness around the eye, discharge, difficulty closing the eye, conjunctival injection, mild fever, teary eyes, and discomfort.

To distinguish orbital cellulitis from peri-orbital cellulitis, it is important to look out for additional symptoms, including pain when moving the eye, protrusion of the eye (proptosis), redness of the eye (red desaturation), vision loss, eye muscle paralysis (ophthalmoplegia), double vision (diplopia), and optic nerve damage (optic neuropathy). These symptoms indicate a more severe condition that requires immediate medical attention.

Phaeochromocytoma is a rare neuroendocrine tumor that secretes catecholamines. It typically arises from chromaffin tissue in the adrenal medulla, but can also occur in extra-adrenal chromaffin tissue. The majority of cases are spontaneous and occur in individuals aged 40-50 years. However, up to 30% of cases are hereditary and associated with genetic mutations. About 10% of phaeochromocytomas are metastatic, with extra-adrenal tumors more likely to be metastatic.

The clinical features of phaeochromocytoma are a result of excessive catecholamine production. Symptoms are typically paroxysmal and include hypertension, headaches, palpitations, sweating, anxiety, tremor, abdominal and flank pain, and nausea. Catecholamines have various metabolic effects, including glycogenolysis, mobilization of free fatty acids, increased serum lactate, increased metabolic rate, increased myocardial force and rate of contraction, and decreased systemic vascular resistance.

Diagnosis of phaeochromocytoma involves measuring plasma and urine levels of metanephrines, catecholamines, and urine vanillylmandelic acid. Imaging studies such as abdominal CT or MRI are used to determine the location of the tumor. If these fail to find the site, a scan with metaiodobenzylguanidine (MIBG) labeled with radioactive iodine is performed. The highest sensitivity and specificity for diagnosis is achieved with plasma metanephrine assay.

The definitive treatment for phaeochromocytoma is surgery. However, before surgery, the patient must be stabilized with medical management. This typically involves alpha-blockade with medications such as phenoxybenzamine or phentolamine, followed by beta-blockade with medications like propranolol. Alpha blockade is started before beta blockade to allow for expansion of blood volume and to prevent a hypertensive crisis.