Management of Iron Deficiency Anemia

Iron deficiency anemia is a common condition that can be effectively managed with oral iron supplementation. The haemoglobin concentration should rise by about 20 g/l over 3-4 weeks if there is a response. It is important to check the full blood count at 2-4 months to ensure that the haemoglobin level has returned to normal. Treatment should be continued for a further three months to replenish the iron stores once the haemoglobin is in the reference range.

Epithelial tissue changes such as atrophic glossitis and koilonychia may improve, but the response is often slow. If there is an inadequate response to oral iron, it is important to assess compliance and whether the iron treatment is tolerated. Malabsorption or other complicating factors such as another source of blood loss are also possible and should be considered. Effective management of iron deficiency anemia requires careful monitoring and evaluation to ensure optimal outcomes.

Symptoms and Signs that Require Investigation in Children

Leukaemia can present with symptoms such as pallor, fatigue, unexplained irritability, fever, recurrent infections, lymphadenopathy, bone pain, and unexplained bruising. If any of these symptoms are present, a full blood count and blood film should be conducted to investigate the possibility of leukaemia. If the results indicate leukaemia, an urgent referral should be made.

Generalised lymphadenopathy with the above symptoms also requires further investigation. On the other hand, a healthy 3-year-old may experience two fevers a month due to exposure to new pathogens, especially if they have older siblings or attend nursery. A fever of 39°C makes a bacterial infection more likely, and a thorough history and examination should be carried out to identify the source of the fever.

If a child has a vesicular rash, it is often caused by Chickenpox, which is associated with a prodromal period of being non-specifically unwell. If the rash looks like Chickenpox, no further investigations are required. Erythema in the throat and ears is usually caused by a viral illness, and no further investigations are necessary unless there are other concerning symptoms.

An aplastic crisis, often caused by parvovirus infection, is characterized by a sudden decrease in haemoglobin levels without a corresponding increase in reticulocytes.

Understanding Sickle-Cell Crises

Sickle-cell anaemia is a condition that is characterized by periods of good health with intervening crises. There are different types of crises that are recognized, including thrombotic or painful crises, sequestration, acute chest syndrome, aplastic, and haemolytic. Thrombotic crisis, also known as painful crises or vaso-occlusive crises, are usually triggered by infection, dehydration, or deoxygenation. These crises are diagnosed clinically, and infarcts can occur in various organs, including the bones, lungs, spleen, and brain.

Sequestration crises occur when sickling occurs within organs such as the spleen or lungs, causing pooling of blood and worsening of the anaemia. Acute chest syndrome is another type of crisis that is caused by vaso-occlusion within the pulmonary microvasculature, leading to infarction in the lung parenchyma. This can result in dyspnoea, chest pain, pulmonary infiltrates on chest x-ray, and low pO2. Management of acute chest syndrome includes pain relief, respiratory support, antibiotics, and transfusion.

Aplastic crises are caused by infection with parvovirus, leading to a sudden fall in haemoglobin. Bone marrow suppression causes a reduced reticulocyte count. Haemolytic crises are rare and are characterized by a fall in haemoglobin due to an increased rate of haemolysis. Understanding the different types of sickle-cell crises is important for effective management and treatment of this condition.

Understanding Polycythemia Rubra Vera: Symptoms, Diagnosis, and Treatment

Polycythemia rubra vera is a rare blood disorder that causes the body to produce too many red blood cells. A person with this condition may experience generalized pruritus, splenomegaly, thrombocytosis, and neutrophil leukocytosis. To confirm the diagnosis, a blood test for a specific mutation (JAK2) present in more than 95% of people with polycythemia vera is necessary.

Without treatment, the life expectancy of a person with polycythemia rubra vera is only 6-18 months. This is due to the high risk of thrombosis, which can lead to ischaemic stroke and myocardial infarction. Venous and arterial thrombosis can also cause other complications such as pulmonary emboli, renal failure, intestinal ischaemia, and peripheral arterial emboli. Bleeding is also a common complication, usually resulting from vascular occlusion due to thrombosis or hyperviscosity. Acute leukaemia, myelofibrosis, and peptic ulcer disease are also possible complications.

However, with treatment to maintain a normal haematocrit, the life expectancy of a person with polycythemia rubra vera can increase to an average of 20 years. While this is still reduced compared to the general population, it is a significant improvement. It is important for individuals with this condition to receive proper medical care and monitoring to manage their symptoms and reduce the risk of complications.

Urgent Referral for Unexplained Iron Deficiency Anaemia in Men Over 60

According to NICE guidelines, men over 60 with unexplained iron deficiency anaemia and a haemoglobin level of 120 g/L or less should be urgently referred to a lower gastrointestinal specialist for further assessment. In this case, the patient has been confirmed to have iron deficiency anaemia with a haemoglobin level below 120 g/L, despite being otherwise well with no other focal signs or symptoms, including gastrointestinal symptoms. Therefore, based solely on the unexplained nature and level of the iron deficiency anaemia, urgent referral is necessary.

Polycythaemia Rubra Vera: Symptoms and Differential Diagnosis

Polycythaemia rubra vera (PRV) is a myeloproliferative disorder characterized by excessive production of red blood cells, leukocytes, and platelets. This condition arises when a single clone of stem cells gains a proliferative advantage over other stem cells. PRV is often discovered through routine blood tests and may present with nonspecific symptoms such as headache, weakness, and joint pain. However, about one-third of patients may present with thrombosis. Physical examination may reveal ruddy cyanosis, hepatomegaly, splenomegaly, and hypertension. The haemoglobin level is typically elevated in PRV.

Differential diagnosis includes von Willebrand’s disease, which presents with mucosal bleeding, and haemochromatosis, which is characterized by iron accumulation in the liver and other organs. Secondary polycythaemia, on the other hand, is caused by an underlying condition and only affects red blood cells. Thrombotic thrombocytopenic purpura is a rare disorder of the blood-coagulation system that causes extensive microscopic clots to form in small blood vessels throughout the body. It is a medical emergency and presents with symptoms such as purpura, fever, dyspnoea, confusion, and headache.

Indicators of Excessive Alcohol Consumption

Excessive alcohol consumption can be indicated by a combination of elevated MCV, elevated gamma GT, low platelet count, and low folate levels. These indicators are commonly seen in patients with alcoholic hepatitis, which is characterized by raised intracellular enzymes. It is important to monitor these indicators in patients who consume alcohol excessively as it can lead to serious health complications. By identifying these indicators early on, healthcare professionals can provide appropriate interventions and support to help patients reduce their alcohol consumption and improve their overall health.

Glimepiride, a medication used to treat type 2 diabetes and belonging to the sulphonylurea class, can trigger haemolysis in patients with G6PD deficiency. This can be indicated by mild anaemia, elevated bilirubin levels, and the presence of bite cells and blister cells on a blood film, suggesting haemolytic anaemia. Simvastatin, on the other hand, can induce hepatitis and cause jaundice, but this is unlikely if alanine transaminase and alkaline phosphatase levels are normal. Metformin, ramipril, and lansoprazole are not associated with haemolytic anaemia.

Understanding G6PD Deficiency

G6PD deficiency is a common red blood cell enzyme defect that is inherited in an X-linked recessive fashion and is more prevalent in people from the Mediterranean and Africa. The deficiency can be triggered by many drugs, infections, and broad (fava) beans, leading to a crisis. G6PD is the first step in the pentose phosphate pathway, which converts glucose-6-phosphate to 6-phosphogluconolactone and results in the production of nicotinamide adenine dinucleotide phosphate (NADPH). NADPH is essential for converting oxidized glutathione back to its reduced form, which protects red blood cells from oxidative damage by oxidants such as superoxide anion (O2-) and hydrogen peroxide. Reduced G6PD activity leads to decreased reduced glutathione and increased red cell susceptibility to oxidative stress, resulting in neonatal jaundice, intravascular hemolysis, gallstones, splenomegaly, and the presence of Heinz bodies on blood films. Diagnosis is made by using a G6PD enzyme assay, and some drugs are known to cause hemolysis, while others are considered safe.

Compared to hereditary spherocytosis, G6PD deficiency is more common in males of African and Mediterranean descent and is characterized by neonatal jaundice, infection/drug-induced hemolysis, and gallstones. On the other hand, hereditary spherocytosis affects both males and females of Northern European descent and is associated with chronic symptoms, spherocytes on blood films, and the presence of erythrocyte membrane protein band 4.2 (EMA) binding.

Understanding Drug-Induced Thrombocytopenia

Drug-induced thrombocytopenia is a condition where a person’s platelet count drops due to the use of certain medications. This condition is believed to be immune-mediated, meaning that the body’s immune system mistakenly attacks and destroys platelets. Some of the drugs that have been associated with drug-induced thrombocytopenia include quinine, abciximab, NSAIDs, diuretics like furosemide, antibiotics such as penicillins, sulphonamides, and rifampicin, and anticonvulsants like carbamazepine and valproate. Heparin, a commonly used blood thinner, is also known to cause drug-induced thrombocytopenia. It is important to be aware of the potential side effects of medications and to consult with a healthcare provider if any concerning symptoms arise. Proper management and monitoring of drug-induced thrombocytopenia can help prevent serious complications.

Malaria Risk and Prevention

Travellers visiting friends and family are at a higher risk of contracting malaria compared to tourists due to their likelihood of visiting rural areas. To accurately diagnose malaria, repeat blood films should be taken after 12-24 hours and again at 24 hours. The gold standard for diagnosis is the thick and thin blood films, while the antigen test is less sensitive. It is important to note that even with full adherence to prophylaxis, it is still possible to develop malaria. While most cases of P.falciparum present within 6 months of exposure, infection with other species can present months or even years after exposure due to reactivation of the dormant liver stage. By taking preventative measures and seeking prompt medical attention, the risk of contracting and spreading malaria can be greatly reduced.

If an adult presents with unexplained lymphadenopathy, it is recommended to consider referral for Hodgkin’s lymphoma within 2 weeks. The decision to refer should take into account any associated symptoms, such as fever, night sweats, shortness of breath, pruritus, weight loss, or alcohol-induced lymph node pain. This referral is specific to Hodgkin’s lymphoma.

Understanding Hodgkin’s Lymphoma: Symptoms and Risk Factors

Hodgkin’s lymphoma is a type of cancer that affects the lymphocytes and is characterized by the presence of Reed-Sternberg cells. It is most commonly seen in people in their third and seventh decades of life. There are certain risk factors that increase the likelihood of developing Hodgkin’s lymphoma, such as HIV and the Epstein-Barr virus.

The most common symptom of Hodgkin’s lymphoma is lymphadenopathy, which is the enlargement of lymph nodes. This is usually painless, non-tender, and asymmetrical, and is most commonly seen in the neck, followed by the axillary and inguinal regions. In some cases, alcohol-induced lymph node pain may be present, but this is seen in less than 10% of patients. Other symptoms of Hodgkin’s lymphoma include weight loss, pruritus, night sweats, and fever (Pel-Ebstein). A mediastinal mass may also be present, which can cause symptoms such as coughing. In some cases, Hodgkin’s lymphoma may be found incidentally on a chest x-ray.

When investigating Hodgkin’s lymphoma, normocytic anaemia may be present, which can be caused by factors such as hypersplenism, bone marrow replacement by HL, or Coombs-positive haemolytic anaemia. Eosinophilia may also be present, which is caused by the production of cytokines such as IL-5. LDH levels may also be raised.

In summary, Hodgkin’s lymphoma is a type of cancer that affects the lymphocytes and is characterized by the presence of Reed-Sternberg cells. It is most commonly seen in people in their third and seventh decades of life and is associated with risk factors such as HIV and the Epstein-Barr virus. Symptoms of Hodgkin’s lymphoma include lymphadenopathy, weight loss, pruritus, night sweats, and fever. When investigating Hodgkin’s lymphoma, normocytic anaemia, eosinophilia, and raised LDH levels may be present.

The ANA test is commonly used to screen for autoimmune rheumatic diseases in adults, but it is not very accurate without typical clinical features. While tests like anti-dsDNA are more specific for SLE, they are less sensitive, meaning a negative result doesn’t necessarily rule out the condition.

Systemic lupus erythematosus (SLE) can be investigated through various tests, including antibody tests. ANA testing is highly sensitive and useful for ruling out SLE, but it has low specificity. About 99% of SLE patients are ANA positive. Rheumatoid factor testing is positive in 20% of SLE patients. Anti-dsDNA testing is highly specific (>99%) but less sensitive (70%). Anti-Smith testing is also highly specific (>99%) but has a lower sensitivity (30%). Other antibody tests that can be used include anti-U1 RNP, SS-A (anti-Ro), and SS-B (anti-La).

Monitoring of SLE can be done through various markers, including inflammatory markers such as ESR. During active disease, CRP levels may be normal, and a raised CRP may indicate an underlying infection. Complement levels (C3, C4) are low during active disease due to the formation of complexes that lead to the consumption of complement. Anti-dsDNA titres can also be used for disease monitoring, but it is important to note that they are not present in all SLE patients. Overall, these investigations can help diagnose and monitor SLE, allowing for appropriate management and treatment.

Polycythaemia is a condition that can be classified as relative, primary (polycythaemia rubra vera), or secondary. Relative polycythaemia can be caused by dehydration or stress, such as in Gaisbock syndrome. Primary polycythaemia rubra vera is a rare blood disorder that causes the bone marrow to produce too many red blood cells. Secondary polycythaemia can be caused by conditions such as COPD, altitude, obstructive sleep apnoea, or excessive erythropoietin production due to certain tumors or growths. To distinguish between true polycythaemia and relative polycythaemia, red cell mass studies may be used. In true polycythaemia, the total red cell mass in males is greater than 35 ml/kg and in women is greater than 32 ml/kg. Uterine fibroids may also cause polycythaemia indirectly by causing menorrhagia, but this is rarely a clinical problem.

If there is no bleeding and the INR falls between 5.0-8.0, it is recommended by the BNF to hold back 1-2 doses of warfarin and decrease the following maintenance dose.

Managing High INR Levels in Patients Taking Warfarin

When a patient taking warfarin experiences high INR levels, the management approach depends on the severity of the situation. In cases of major bleeding, warfarin should be stopped immediately and intravenous vitamin K should be administered along with prothrombin complex concentrate or fresh frozen plasma if available. For minor bleeding, warfarin should also be stopped and a lower dose of intravenous vitamin K (1-3 mg) should be given. If the INR remains high after 24 hours, another dose of vitamin K can be administered. Warfarin can be restarted once the INR drops below 5.0.

In cases where there is no bleeding but the INR is above 8.0, warfarin should be stopped and vitamin K (1-5mg) can be given orally using the intravenous preparation. If the INR remains high after 24 hours, another dose of vitamin K can be given. Warfarin can be restarted once the INR drops below 5.0.

If the INR is between 5.0-8.0 and there is minor bleeding, warfarin should be stopped and a lower dose of intravenous vitamin K (1-3 mg) should be given. Warfarin can be restarted once the INR drops below 5.0. If there is no bleeding, warfarin can be withheld for 1 or 2 doses and the subsequent maintenance dose can be reduced.

It is important to note that in cases of intracranial hemorrhage, prothrombin complex concentrate should be considered instead of fresh frozen plasma as it can take time to defrost. These guidelines are based on the recommendations of the British Committee for Standards in Haematology and the British National Formulary.

Understanding Von Willebrand’s Disease

Von Willebrand’s disease is a genetic bleeding disorder that is inherited in an autosomal dominant or recessive manner. It is the most common inherited bleeding disorder, and it behaves like a platelet disorder. Patients with this condition often experience epistaxis and menorrhagia, while haemoarthroses and muscle haematomas are rare.

The disease is caused by a deficiency or abnormality in von Willebrand factor, a large glycoprotein that promotes platelet adhesion to damaged endothelium and serves as a carrier molecule for factor VIII. There are three types of von Willebrand’s disease: type 1, which involves a partial reduction in vWF and accounts for 80% of cases; type 2, which is characterized by an abnormal form of vWF; and type 3, which involves a total lack of vWF and is inherited in an autosomal recessive manner.

To diagnose von Willebrand’s disease, doctors may perform a bleeding time test, measure APTT, and check factor VIII levels. Defective platelet aggregation with ristocetin is also a common finding. Treatment options include tranexamic acid for mild bleeding, desmopressin to raise levels of vWF, and factor VIII concentrate. The type of von Willebrand’s disease a patient has doesn’t necessarily correlate with their symptoms, but common themes include excessive mucocutaneous bleeding, bruising without trauma, and menorrhagia in females.

Interpretation of FBC Results

When analyzing a full blood count (FBC), it is important to consider all the parameters to determine the underlying cause of any abnormalities. In this case, the FBC shows microcytosis, which is a low mean corpuscular volume (MCV), and anaemia, indicated by low hemoglobin levels. These findings are typical of iron deficiency anaemia.

To confirm iron deficiency, a ferritin test should be requested. If the test confirms iron deficiency, the next step is to identify the source of blood loss. If the faecal occult blood test is positive, an endoscopy may be necessary.

It is important to note that folate and B12 deficiencies cause macrocytic anaemia, which is characterized by elevated MCV. Hypothyroidism is also associated with elevated MCV. However, in this case, the low MCV indicates iron deficiency anaemia.

While a bone marrow biopsy can confirm iron deficiency, it is an invasive procedure and is not necessary at this stage, particularly in a primary care setting.

It is important to keep a close watch on the levels of full blood count, urea and electrolytes, as well as liver function tests while using methotrexate.

Methotrexate is an antimetabolite that hinders the activity of dihydrofolate reductase, an enzyme that is crucial for the synthesis of purines and pyrimidines. It is a significant drug that can effectively control diseases, but its side-effects can be life-threatening. Therefore, careful prescribing and close monitoring are essential. Methotrexate is commonly used to treat inflammatory arthritis, especially rheumatoid arthritis, psoriasis, and acute lymphoblastic leukaemia. However, it can cause adverse effects such as mucositis, myelosuppression, pneumonitis, pulmonary fibrosis, and liver fibrosis.

Women should avoid pregnancy for at least six months after stopping methotrexate treatment, and men using methotrexate should use effective contraception for at least six months after treatment. Prescribing methotrexate requires familiarity with guidelines relating to its use. It is taken weekly, and FBC, U&E, and LFTs need to be regularly monitored. Folic acid 5mg once weekly should be co-prescribed, taken more than 24 hours after methotrexate dose. The starting dose of methotrexate is 7.5 mg weekly, and only one strength of methotrexate tablet should be prescribed.

It is important to avoid prescribing trimethoprim or co-trimoxazole concurrently as it increases the risk of marrow aplasia. High-dose aspirin also increases the risk of methotrexate toxicity due to reduced excretion. In case of methotrexate toxicity, the treatment of choice is folinic acid. Overall, methotrexate is a potent drug that requires careful prescribing and monitoring to ensure its effectiveness and safety.

Understanding the Diagnosis and Treatment of Vitamin B12 Deficiency

Vitamin B12 deficiency can be a challenging condition to diagnose due to the lack of a gold standard test. While the most common test is serum B12, it may not accurately reflect what is happening at the cellular level, as it records both active and inactive B12. Additionally, some patients with clinical features of vitamin B12 deficiency may have false normal vitamin B12 levels. This can be due to antibody interference or inaccuracies in the test.

People with vitamin B12 levels below 100 nanograms/l usually have clinical or metabolic evidence of deficiency, while levels below 200 nanograms/l are common in most people with deficiency. Diagnosis is supported by macrocytosis, reduced white cell count, platelet count, and reticulocyte count, as well as the blood film.

Treatment options vary depending on the cause of the deficiency. Erythropoietin is used to treat anaemia due to renal failure, while folic acid is used for folate deficiency. However, in cases where folate levels are normal, folic acid treatment will not improve the anaemia. Iron treatment is also unlikely to be effective if ferritin levels are normal and the anaemia is macrocytic. Prednisolone may be useful in cases of haemolysis, but the pancytopenia seen in vitamin B12 deficiency points away from this as the cause of anaemia.

Overall, a thorough understanding of the diagnostic challenges and treatment options for vitamin B12 deficiency is crucial for effective management of this condition.

Understanding Macrocytosis and its Differential Diagnosis

Macrocytosis is a condition characterized by the presence of abnormally large red blood cells in the bloodstream. While there are several possible causes of macrocytosis, one of the most common is vitamin B12 deficiency. This deficiency can lead to anaemia and macrocytosis, with a mean corpuscular volume (MCV) of 130 femtolitres or more being a strong indicator of B12 deficiency.

Other potential causes of macrocytosis include drug-induced effects, excessive alcohol intake, and human immunodeficiency virus infection. However, these conditions may not necessarily lead to anaemia unless poor nutrition is also a factor.

Myelodysplasia and aplastic anaemia are also in the differential diagnosis of vitamin B12 deficiency, but the MCV level can help differentiate between these conditions. If the MCV is between 100-110 femtolitres, other causes of macrocytosis should be considered.

Overall, understanding the potential causes of macrocytosis and their differential diagnosis is crucial for accurate diagnosis and effective treatment.

Hodgkin’s lymphoma can be cured in the majority of patients, especially those who respond well to treatment. A prompt and complete response to chemotherapy and/or radiotherapy is the most important factor in predicting a patient’s prognosis. Residual masses may not always indicate persisting disease, as fibrosis can persist after effective therapy. Patients who relapse after initial successful treatment can sometimes be treated with further chemotherapy, stem cell transplantation, and/or radiotherapy. The duration of initial remission is a factor in the success of retreatment. Bulky disease, a high ESR, male gender, and stage IV disease are associated with a poorer prognosis. Other adverse prognostic factors include age ≥ 45 years, low haemoglobin, low lymphocyte count, low albumin, high WCC, mixed-cellularity or lymphocyte-depleted histology, and B symptoms.

Monitoring Response to Vitamin B12 Treatment in Pernicious Anaemia

Pernicious anaemia is a condition caused by vitamin B12 deficiency, which can lead to a range of symptoms including fatigue, weakness, and neurological problems. Treatment involves intramuscular injections of hydroxocobalamin, with the frequency and duration of treatment depending on the severity of the deficiency.

To monitor the response to treatment, several indicators can be measured. A rise in the reticulocyte count and haemoglobin level within 7-10 days indicates a positive effect. The mean cell volume (MCV) may initially increase due to the increased reticulocyte count, but should return to normal within 25-78 days. Intrinsic factor antibodies may remain present despite treatment. Measuring cobalamin levels is not always necessary, but can be done 1-2 months after starting treatment if there is no response.

Overall, monitoring these indicators can help confirm a diagnosis of pernicious anaemia and ensure that treatment is effective in addressing the deficiency.

Sickle cell disease can cause priapism, a painful and persistent erection that occurs without sexual stimulation. This is due to vaso-occlusive obstruction of the venous drainage of the penis and is most common in males with sickle cell disease under the age of 20. Priapism can be classified as prolonged or stuttering, with prolonged episodes requiring urgent medical intervention and both types potentially leading to impotence. Sickle cell disease also increases susceptibility to infection, particularly from Streptococcus pneumoniae, and can cause hand-foot syndrome in infants due to vaso-occlusion. Acute stroke is a serious complication of sickle cell disease, with a prevalence of 10% by age 50, and regular blood transfusions may be necessary for those with abnormal findings on transcranial Doppler ultrasonography.

Understanding Neutrophilia: Causes and Differential Diagnosis

Neutrophilia, an increase in absolute neutrophil count, can be acute or chronic and is often seen as an accompanying feature of various medical conditions. Acute bacterial infections, inflammatory response to shock, gout, vasculitis, and malignancies are some of the common causes of neutrophilia. Additionally, certain drugs, activities, pregnancy, myeloproliferative states, and splenectomy can also increase the neutrophil count.

However, it is important to note that neutrophilia alone cannot provide a definitive diagnosis. A thorough evaluation of the patient’s medical history, symptoms, and other laboratory tests is necessary to determine the underlying cause. For instance, in the case of a sore throat, acute bacterial infection is a likely cause of neutrophilia.

On the other hand, conditions such as cytomegalovirus infection, chronic myeloid leukaemia, pregnancy, and tuberculosis are unlikely to cause neutrophilia as a primary symptom. Instead, they may present with other characteristic features such as atypical lymphocytosis, raised WCC with granulocytes, elevated IgM antibodies, or normocytic anaemia and lymphopenia.

In summary, understanding the various causes and differential diagnosis of neutrophilia is crucial in providing accurate and timely medical care to patients.

Thrombocytopenia can be caused by heparin, including the low molecular weight heparin enoxaparin. Prosthetic joints are not a common cause of thrombocytopenia, while the other drugs listed are not typically associated with this condition. If heparin-induced thrombocytopenia is suspected or confirmed, it is important to discontinue heparin and switch to an alternative anticoagulant like danaparoid. Platelet counts should be monitored and normalized before administering warfarin.

Understanding Drug-Induced Thrombocytopenia

Drug-induced thrombocytopenia is a condition where a person’s platelet count drops due to the use of certain medications. This condition is believed to be immune-mediated, meaning that the body’s immune system mistakenly attacks and destroys platelets. Some of the drugs that have been associated with drug-induced thrombocytopenia include quinine, abciximab, NSAIDs, diuretics like furosemide, antibiotics such as penicillins, sulphonamides, and rifampicin, and anticonvulsants like carbamazepine and valproate. Heparin, a commonly used blood thinner, is also known to cause drug-induced thrombocytopenia. It is important to be aware of the potential side effects of medications and to consult with a healthcare provider if any concerning symptoms arise. Proper management and monitoring of drug-induced thrombocytopenia can help prevent serious complications.

Temporal arteritis is a well-known historical condition. Immediate treatment with high doses of steroids, such as prednisolone at 1 mg/kg/day, is crucial to minimize the risk of vision loss.

Temporal arteritis is a type of large vessel vasculitis that often occurs in patients over the age of 60 and is commonly associated with polymyalgia rheumatica. This condition is characterized by changes in the affected artery that skip certain sections while damaging others. Symptoms of temporal arteritis include headache, jaw claudication, and visual disturbances, with anterior ischemic optic neuropathy being the most common ocular complication. A tender, palpable temporal artery is also often present, and around 50% of patients may experience symptoms of PMR, such as muscle aches and morning stiffness.

To diagnose temporal arteritis, doctors will typically look for elevated inflammatory markers, such as an ESR greater than 50 mm/hr or elevated CRP levels. A temporal artery biopsy may also be performed to confirm the diagnosis, with skip lesions often being present. Treatment for temporal arteritis involves urgent high-dose glucocorticoids, which should be given as soon as the diagnosis is suspected and before the temporal artery biopsy. If there is no visual loss, high-dose prednisolone is typically used, while IV methylprednisolone is usually given if there is evolving visual loss. Patients with visual symptoms should be seen by an ophthalmologist on the same day, as visual damage is often irreversible. Other treatments may include bone protection with bisphosphonates and low-dose aspirin, although the evidence supporting the latter is weak.

In cases of iron-deficiency anemia, it is common for both the total iron-binding capacity (TIBC) and transferrin levels to be elevated. However, it should be noted that the transferrin saturation level is typically decreased.

Iron deficiency anaemia is a prevalent condition worldwide, with preschool-age children being the most affected. The lack of iron in the body leads to a decrease in red blood cells and haemoglobin, resulting in anaemia. The primary causes of iron deficiency anaemia are excessive blood loss, inadequate dietary intake, poor intestinal absorption, and increased iron requirements. Menorrhagia is the most common cause of blood loss in pre-menopausal women, while gastrointestinal bleeding is the most common cause in men and postmenopausal women. Vegans and vegetarians are more likely to develop iron deficiency anaemia due to the lack of meat in their diet. Coeliac disease and other conditions affecting the small intestine can prevent sufficient iron absorption. Children and pregnant women have increased iron demands, and the latter may experience dilution due to an increase in plasma volume.

The symptoms of iron deficiency anaemia include fatigue, shortness of breath on exertion, palpitations, pallor, nail changes, hair loss, atrophic glossitis, post-cricoid webs, and angular stomatitis. To diagnose iron deficiency anaemia, a full blood count, serum ferritin, total iron-binding capacity, transferrin, and blood film tests are performed. Endoscopy may be necessary to rule out malignancy, especially in males and postmenopausal females with unexplained iron-deficiency anaemia.

The management of iron deficiency anaemia involves identifying and treating the underlying cause. Oral ferrous sulfate is commonly prescribed, and patients should continue taking iron supplements for three months after the iron deficiency has been corrected to replenish iron stores. Iron-rich foods such as dark-green leafy vegetables, meat, and iron-fortified bread can also help. It is crucial to exclude malignancy by taking an adequate history and appropriate investigations if warranted.

Managing High INR Levels in Patients on Warfarin: Choosing the Right Course of Action

When a patient on warfarin presents with a high international normalised ratio (INR), prompt management is crucial to prevent haemorrhage. The appropriate course of action depends on the severity of the INR elevation and whether the patient is bleeding.

If the patient has no active bleeding and their INR is between 5-8, warfarin should be withheld for 24-48 hours and restarted at a reduced dose. The INR should be rechecked 2-3 days later, and the cause investigated.

If the patient is bleeding, warfarin should be stopped and intravenous vitamin K administered. It can be restarted once the INR is below 5.

For an INR greater than 8 in a patient with no bleeding, the correct management is to stop warfarin, give vitamin K orally, and repeat the INR in 24 hours.

Dose reduction alone is not sufficient for an INR greater than 5, and warfarin should also be withheld for 1-2 days, with rechecking sooner (3-4 days).

While a confirmatory laboratory sample may be reasonable, it should not delay action being taken. Point-of-care testing is comparable in accuracy to laboratory samples, and management should reflect this.

In summary, managing high INR levels in patients on warfarin requires careful consideration of the severity of the INR elevation and whether the patient is bleeding. Prompt action and appropriate monitoring can prevent haemorrhage and ensure optimal patient outcomes.

Delayed Grief Reaction and Elevated MCV in a Patient

This patient is exhibiting signs of a delayed grief reaction following the recent death of her husband. Her FBC shows a normal picture, except for an elevated MCV, which suggests alcohol excess. Macrocytosis caused by folate or B12 deficiency would typically result in anemia alongside the macrocytosis. Hypothyroidism can also cause macrocytosis, but the patient’s weight loss contradicts this diagnosis.

Alcohol-Associated Pain in Hodgkin’s Lymphoma

Pain during or after drinking alcohol has been linked to Hodgkin’s lymphoma since the 1950s. This pain typically occurs in affected lymph nodes and can be sharp or dull, with a radiating distribution. While it only occurs in 2-3% of people with HL, it is considered pathognomonic due to its high specificity. Alcohol-associated pain has also been noted in other conditions such as TB lymphadenitis, cervical carcinoma, and bronchial adenocarcinoma. In some cases, HL may present with nonspecific back pain. If a patient reports alcohol-associated pain, a full history and examination should be conducted to look for other symptoms of HL, including lymphadenopathy and hepatosplenomegaly.

The elevated ferritin level can be attributed to the patient’s excessive alcohol consumption, as the typical transferrin saturation rules out iron overload as a potential cause.

Understanding Ferritin Levels in the Body

Ferritin is a protein found inside cells that binds to iron and stores it for later use. When ferritin levels are increased, it is usually defined as being above 300 µg/L in men and postmenopausal women, and above 200 µg/L in premenopausal women. However, it is important to note that ferritin is an acute phase protein, meaning that it can be synthesized in larger quantities during times of inflammation. This can lead to falsely elevated results, which must be interpreted in the context of the patient’s clinical picture and other blood test results.

There are two main categories of causes for increased ferritin levels: those without iron overload (which account for around 90% of patients) and those with iron overload (which account for around 10% of patients). Causes of increased ferritin levels without iron overload include inflammation, alcohol excess, liver disease, chronic kidney disease, and malignancy. Causes of increased ferritin levels with iron overload include primary iron overload (hereditary hemochromatosis) and secondary iron overload (which can occur after repeated transfusions).

On the other hand, reduced ferritin levels can be an indication of iron deficiency anemia. Since iron and ferritin are bound together, a decrease in ferritin levels can suggest a decrease in iron levels as well. Measuring serum ferritin levels can be helpful in determining whether a low hemoglobin level and microcytosis are truly caused by an iron deficiency state. It is important to note that the best test for determining iron overload is transferrin saturation, with normal values being less than 45% in females and less than 50% in males.