Common Kidney Diseases and Their Clinical Features

Immunoglobulin A (IgA) Nephropathy, Kimmelstiel Wilson Lesions, Cast Nephropathy, Minimal Change Disease, and Thin Basement Membranes are some of the common kidney diseases that affect people. Each of these diseases has unique clinical features that help in their diagnosis.

IgA Nephropathy, also known as Berger’s disease, is the most common cause of glomerulonephritis worldwide. It is characterized by predominant IgA deposition in the glomerular mesangium. Clinical features range from asymptomatic haematuria to rapidly progressive glomerulonephritis.

Kimmelstiel–Wilson Lesions, also known as nodular glomerulosclerosis, is a complication of diabetes mellitus. It is characterized by the formation of nodules of hyaline material in regions of glomerular capillary loops in the glomerulus.

Cast Nephropathy, also known as myeloma cast nephropathy, is the formation of urinary casts in the renal tubules from free immunoglobulin light chains, causing intratubular obstruction and damage, which leads to renal failure in the context of multiple myeloma.

Minimal Change Disease, also known as lipoid nephrosis or nil disease, arises from a histopathologic lesion in the glomerulus and is characterized by intense proteinuria leading to oedema and intravascular volume depletion.

Thin Basement Membranes is a group of inherited heterogeneous disorders involving the basement membranes of the kidney and frequently affecting the cochlea and eye as well. It is characterized by splitting and lamellation of the glomerular basement membrane.

In conclusion, understanding the clinical features of these common kidney diseases is crucial in their diagnosis and management.

Understanding Nephrotic Syndrome in Children

Nephrotic syndrome is a medical condition that is characterized by three main symptoms: proteinuria, hypoalbuminaemia, and oedema. This condition is most commonly seen in children between the ages of 2 and 5 years old. In fact, around 80% of cases in children are caused by a condition called minimal change glomerulonephritis. Fortunately, this condition has a good prognosis, with approximately 90% of cases responding well to high-dose oral steroids.

Aside from the main symptoms, children with nephrotic syndrome may also experience hyperlipidaemia, a hypercoagulable state, and a higher risk of infection. These additional features are caused by the loss of antithrombin III and immunoglobulins in the body.

Overall, understanding nephrotic syndrome in children is important for parents and healthcare professionals alike. With proper treatment and management, most children with this condition can recover and lead healthy lives.

A finding of Auer rods on a blood film strongly indicates the presence of acute promyelocytic leukemia.

The correct answer is ‘Auer rods’. This patient has been diagnosed with APML, and the most common finding on a blood film associated with this is Auer rods. These are needle-like structures that are large, pink or red stained and can be seen within the cytoplasm of myeloid blast cells.

‘Tear-drop’ poikilocytes are typically found in myelofibrosis, which is characterized by flat, elongated red blood cells that resemble a tear-drop in shape. This occurs due to the squeezing of cells through fibrotic tissue in bone marrow in myelofibrotic disorders.

Smear cells are usually seen in chronic lymphocytic leukemia (CLL), which are remnants of cells that lack identifiable plasma membrane or nuclear structure.

Spherocytes are generally found in hereditary spherocytosis or autoimmune hemolytic anemia, which are red blood cells that are sphere-shaped and more fragile than normal red blood cells due to abnormalities in the red cell membrane.

Acute myeloid leukaemia is a common form of acute leukaemia in adults that may occur as a primary disease or following a myeloproliferative disorder. Symptoms are related to bone marrow failure and include anaemia, neutropenia, thrombocytopenia, splenomegaly, and bone pain. Poor prognostic features include age over 60, >20% blasts after first course of chemo, and deletions of chromosome 5 or 7. Acute promyelocytic leukaemia M3 is associated with t(15;17) and has a good prognosis. The French-American-British classification system includes seven subtypes.

The presence of calcitonin in the blood can indicate the presence of medullary thyroid cancer, as this type of cancer originates from the parafollicular cells that produce calcitonin. Therefore, calcitonin is considered a tumor marker for medullary thyroid cancer.

Understanding Tumour Markers

Tumour markers are substances that can be found in the blood, urine, or tissues of people with cancer. They are often used to help diagnose and monitor cancer, as well as to determine the effectiveness of treatment. Tumour markers can be divided into different categories, including monoclonal antibodies against carbohydrate or glycoprotein tumour antigens, tumour antigens, enzymes, and hormones.

Monoclonal antibodies are used to target specific tumour antigens, which are proteins or other molecules that are found on the surface of cancer cells. Some common tumour markers include CA 125 for ovarian cancer, CA 19-9 for pancreatic cancer, and CA 15-3 for breast cancer. However, it is important to note that tumour markers usually have a low specificity, meaning that they can also be found in people without cancer.

Tumour antigens are proteins that are produced by cancer cells and can be detected in the blood or tissues of people with cancer. Some examples of tumour antigens include prostate specific antigen (PSA) for prostatic carcinoma, alpha-feto protein (AFP) for hepatocellular carcinoma and teratoma, and carcinoembryonic antigen (CEA) for colorectal cancer.

Enzymes and hormones can also be used as tumour markers. For example, alkaline phosphatase and neurone specific enolase are enzymes that can be elevated in people with cancer, while hormones such as calcitonin and ADH can be used to detect certain types of cancer.

In summary, tumour markers are an important tool in the diagnosis and monitoring of cancer. However, they should be used in conjunction with other diagnostic tests and imaging studies, as they are not always specific to cancer and can also be elevated in people without cancer.

Understanding the Interaction of Juices with Medications: A Focus on Cytochrome P450 Enzymes

Certain juices can interact with medications, potentially leading to adverse effects if dosage is not adjusted. Grapefruit juice, for example, can inhibit the CYP3A4 enzyme responsible for metabolizing 90% of drugs, leading to subtherapeutic drug levels. On the other hand, tomato, apple, lemon, and pineapple juices are not known to interact with any medications.

To understand these interactions better, it is important to look at the role of cytochrome P450 enzymes in drug metabolism. These enzymes play a crucial role in metabolizing a wide variety of endogenous and exogenous chemicals, including drugs. Changes in CYP enzyme activity can affect the metabolism and clearance of various drugs, leading to adverse drug interactions.

It is also important to note that certain drugs can either induce or inhibit the activity of various CYP isoenzymes, further affecting drug metabolism. For example, carbamazepine and rifampin can induce the biosynthesis of CYP2C9, while fluconazole and ritonavir can inhibit its activity.

In summary, understanding the interaction of juices with medications requires a deeper understanding of the role of cytochrome P450 enzymes in drug metabolism and the potential effects of drug-induced changes in enzyme activity.

The patient is exhibiting typical signs of polymyalgia rheumatica, which can be effectively treated with steroids. While ibuprofen and codeine may offer some relief, hydroxychloroquine is primarily used to treat systemic lupus erythematosus, and sulfasalazine is a DMARD used for rheumatoid arthritis and psoriasis.

Polymyalgia Rheumatica: A Condition of Muscle Stiffness in Older People

Polymyalgia rheumatica (PMR) is a common condition that affects older people. It is characterized by muscle stiffness and elevated inflammatory markers. Although it is closely related to temporal arteritis, the underlying cause is not fully understood, and it does not appear to be a vasculitic process. PMR typically affects patients over the age of 60 and has a rapid onset, usually within a month. Patients experience aching and morning stiffness in proximal limb muscles, along with mild polyarthralgia, lethargy, depression, low-grade fever, anorexia, and night sweats.

To diagnose PMR, doctors look for raised inflammatory markers, such as an ESR of over 40 mm/hr. Creatine kinase and EMG are normal. Treatment for PMR involves prednisolone, usually at a dose of 15mg/od. Patients typically respond dramatically to steroids, and failure to do so should prompt consideration of an alternative diagnosis.

Breastfeeding has some contraindications that are important to know, especially when it comes to drugs. Antibiotics like penicillins, cephalosporins, and trimethoprim are safe for breastfeeding mothers, as are endocrine drugs like glucocorticoids (in low doses) and levothyroxine. Epilepsy drugs like sodium valproate and carbamazepine, asthma drugs like salbutamol and theophyllines, and hypertension drugs like beta-blockers and hydralazine are also safe. Anticoagulants like warfarin and heparin, as well as digoxin, are also safe. However, some drugs should be avoided, such as antibiotics like ciprofloxacin, tetracycline, chloramphenicol, and sulphonamides, psychiatric drugs like lithium and benzodiazepines, aspirin, carbimazole, methotrexate, sulfonylureas, cytotoxic drugs, and amiodarone. Other contraindications include galactosaemia and viral infections, although the latter is controversial in the developing world due to the increased risk of infant mortality and morbidity associated with bottle feeding.

The use of GnRH agonists (such as goserelin) for treating prostate cancer can lead to the development of gynaecomastia. This medication can also cause loss of libido and erectile dysfunction due to its mode of action. Bisoprolol does not have any known association with gynaecomastia. While metoclopramide can cause nipple discharge and hyperprolactinaemia, it is not linked to gynaecomastia. On the other hand, cimetidine (not omeprazole) is known to cause gynaecomastia.

Understanding Gynaecomastia: Causes and Drug Triggers

Gynaecomastia is a medical condition that occurs when males develop an abnormal amount of breast tissue. This condition is usually caused by an increased ratio of oestrogen to androgen. It is important to differentiate the causes of galactorrhoea, which is due to the actions of prolactin on breast tissue, from those of gynaecomastia.

There are several causes of gynaecomastia, including physiological changes that occur during puberty, syndromes with androgen deficiency such as Kallman’s and Klinefelter’s, testicular failure, liver disease, testicular cancer, ectopic tumour secretion, hyperthyroidism, and haemodialysis. Additionally, certain drugs can trigger gynaecomastia, with spironolactone being the most common drug cause. Other drugs that can cause gynaecomastia include cimetidine, digoxin, cannabis, finasteride, GnRH agonists like goserelin and buserelin, oestrogens, and anabolic steroids.

It is important to note that while drug-induced gynaecomastia is rare, there are still some drugs that can trigger this condition. Some of the very rare drug causes of gynaecomastia include tricyclics, isoniazid, calcium channel blockers, heroin, busulfan, and methyldopa. Understanding the causes and drug triggers of gynaecomastia can help individuals seek appropriate medical attention and treatment.

After a myocardial infarction, Sertraline is the preferred SSRI due to its extensive research in this patient population compared to other SSRIs. It is important to note that the patient may also be taking antiplatelets and should be cautioned about the potential for dyspepsia and gastrointestinal bleeding. Co-prescribing a proton pump inhibitor should be considered.

Selective serotonin reuptake inhibitors (SSRIs) are commonly used as the first-line treatment for depression. Citalopram and fluoxetine are the preferred SSRIs, while sertraline is recommended for patients who have had a myocardial infarction. However, caution should be exercised when prescribing SSRIs to children and adolescents. Gastrointestinal symptoms are the most common side-effect, and patients taking SSRIs are at an increased risk of gastrointestinal bleeding. Patients should also be aware of the possibility of increased anxiety and agitation after starting a SSRI. Fluoxetine and paroxetine have a higher propensity for drug interactions.

The Medicines and Healthcare products Regulatory Agency (MHRA) has issued a warning regarding the use of citalopram due to its association with dose-dependent QT interval prolongation. As a result, citalopram and escitalopram should not be used in patients with congenital long QT syndrome, known pre-existing QT interval prolongation, or in combination with other medicines that prolong the QT interval. The maximum daily dose of citalopram is now 40 mg for adults, 20 mg for patients older than 65 years, and 20 mg for those with hepatic impairment.

When initiating antidepressant therapy, patients should be reviewed by a doctor after 2 weeks. Patients under the age of 25 years or at an increased risk of suicide should be reviewed after 1 week. If a patient responds well to antidepressant therapy, they should continue treatment for at least 6 months after remission to reduce the risk of relapse. When stopping a SSRI, the dose should be gradually reduced over a 4 week period, except for fluoxetine. Paroxetine has a higher incidence of discontinuation symptoms, including mood changes, restlessness, difficulty sleeping, unsteadiness, sweating, gastrointestinal symptoms, and paraesthesia.

When considering the use of SSRIs during pregnancy, the benefits and risks should be weighed. Use during the first trimester may increase the risk of congenital heart defects, while use during the third trimester can result in persistent pulmonary hypertension of the newborn. Paroxetine has an increased risk of congenital malformations, particularly in the first trimester.

The use of allopurinol in combination with azathioprine can increase the risk of myelosuppression and neutropenic sepsis. This is because azathioprine is metabolized to its active form, 6-mercaptopurine, which is then metabolized by xanthine oxidase. Allopurinol inhibits xanthine oxidase, leading to an accumulation of 6-mercaptopurine and an increased risk of myelosuppression. Chronic alcohol use and omeprazole use do not significantly increase the risk of myelosuppression when used with azathioprine or allopurinol.

Allopurinol is a medication used to prevent gout by inhibiting xanthine oxidase. Traditionally, it was believed that urate-lowering therapy (ULT) should not be started until two weeks after an acute attack to avoid further attacks. However, the evidence supporting this is weak, and the British Society of Rheumatology (BSR) now recommends delaying ULT until inflammation has settled to make long-term drug decisions while the patient is not in pain. The initial dose of allopurinol is 100 mg once daily, with the dose titrated every few weeks to aim for a serum uric acid level of less than 300 µmol/l. Colchicine cover should be considered when starting allopurinol, and NSAIDs can be used if colchicine cannot be tolerated. ULT is recommended for patients with two or more attacks in 12 months, tophi, renal disease, uric acid renal stones, prophylaxis if on cytotoxics or diuretics, and Lesch-Nyhan syndrome.

The most significant adverse effects of allopurinol are dermatological, and patients should stop taking the medication immediately if they develop a rash. Severe cutaneous adverse reaction (SCAR), drug reaction with eosinophilia and systemic symptoms (DRESS), and Stevens-Johnson syndrome are potential risks. Certain ethnic groups, such as the Chinese, Korean, and Thai people, are at an increased risk of these dermatological reactions. Patients at high risk of severe cutaneous adverse reaction should be screened for the HLA-B *5801 allele. Allopurinol can interact with other medications, such as azathioprine, cyclophosphamide, and theophylline. Azathioprine is metabolized to the active compound 6-mercaptopurine, which is oxidized to 6-thiouric acid by xanthine oxidase. Allopurinol can lead to high levels of 6-mercaptopurine, so a much-reduced dose must be used if the combination cannot be avoided. Allopurinol also reduces renal clearance of cyclophosphamide, which may cause marrow toxicity. Additionally, allopurinol causes an increase in plasma concentration of theophylline by inhibiting its breakdown.