Rüzgar Miroğlu

Medicine


Renal Artery Stenosis

Renal artery stenosis is the narrowing of the renal artery, most often caused by atherosclerosis or fibromuscular dysplasia.Atherosclerosis is the predominant cause of renal artery stenosis in the majority of patients, usually those with a sudden onset of hypertension at age 50 or older. Fibromuscular dysplasia is the predominant cause in young patients, usually females under 40 years of age.

The macula densa of the kidney detects the decreased systemic blood pressure owing to the reduced blood flow through the narrowed artery. The response of the kidney to this perceived decreased blood pressure is activation of the renin-angiotension aldosterone system, which normally counteracts low blood pressure but in this case leads to hypertension.The decreased perfusion pressure leads to decreased blood flow to the kidney and a decrease in the GFR.If the stenosis is longstanding and severe the GFR in the affected kidneys never increases again and renal failure is the result.
Most cases of renal artery stenosis are asymptomatic, and the main problem is high blood pressure that cannot be controlled with medication. Deterioration in renal function may develop if both kidneys are poorly supplied, or when treatment with an ACE inhibitor is initiated. Some patients present with episodes of flash pulmonary edema.
Diagnosis can be made by captopril challenge test and renal artery arteriogram.

 

 

Treatment of Chronic Heart Failure aims to relieve symptoms, to maintain a euvolemic state (normal fluid level in the circulatory system), and to improve prognosis by delaying progression of heart failure and reducing cardiovascular risk. Drugs used include: diuretic agents, vasodilator agents, positive inotropes, ACE inhibitors, beta blockers, and aldosterone antagonists (e.g.spironolactone).
ACE inhibitor therapy is recommended for all patients with systolic heart failure, irrespective of symptomatic severity or blood pressure.ACE inhibitors improve symptoms, decrease mortality and reduce ventricular hypertrophy. Angiotensin II receptor antagonist therapy,particularly using candesartan, is an acceptable alternative if the patient is unable to tolerate ACEI therapy.
Diuretic therapy is indicated for relief of congestive symptoms. Several classes are used, with combinations reserved for severe heart failure:
* Loop diuretics (e.g. furosemide) – most commonly used class in CHF, usually for moderate CHF.
* Thiazide diuretics (e.g. hydrochlorothiazide) – may be useful for mild CHF, but typically used in severe CHF in combination with loop diuretics, resulting in a synergistic effect.
* Potassium-sparing diuretics (e.g.Spironolactone) – used first-line use to correct hypokalaemia.
As with ACEI therapy, the addition of a β-blocker can decrease mortality and improve left ventricular function. Several β-blockers are specifically indicated for CHF including: bisoprolol, carvedilol, nebivolol and extended-release metoprolol.
Digoxin (a mildly positive inotrope and negative chronotrope), once used as first-line therapy, is now reserved when the adequate control is not achieved with an ACEI, a beta blocker and a loop diuretic.There is no evidence that digoxin reduces mortality in CHF, although some studies suggest a decreased rate in hospital admissions.It is contraindicated in cardiac tamponade and restrictive cardiomyopathy.

 

 

Alcoholic liver disease is the major cause of liver disease in Western countries, (in Asian countries, viral hepatitis is the major cause). It arises from the excessive ingestion of alcohol.When alcohol damages the liver, the function of the organ is not immediately compromised as the liver has a tremendous capacity to regenerate and even when 75% of the liver is damaged, it continues to function as normal. When alcohol is consumed for a long time, it eventually results in liver scarring or what is known as cirrhosis or end-stage alcoholic liver disease.

Between 10% to 20% of heavy drinkers will develop Cirrhosis of the liver.Cirrhosis is a late stage of serious liver disease marked by inflammation, fibrosis and damaged membranes preventing detoxification of chemicals in the body, ending in scarring and necrosis. Symptoms include jaundice,liver enlargement, and pain and tenderness from the structural changes in damaged liver architecture. It is progressive and without total abstinence from alcohol use, (80% of alcohol passes through the liver to be detoxified) will eventually lead to liver failure. Late complications of cirrhosis or liver failure include portal hypertension,coagulation disorders blood clotting is impaired, ascites and other complications, including hepatic encephalopathy and the hepatorenal syndrome.Cirrhosis can also result from other causes than alcohol abuse, such as viral hepatitis and heavy exposure to toxins other than alcohol.

 

 

Hemodialysis is a method for removing waste products such as creatinine and urea, as well as free water from the blood when the kidneys are in renal failure. Hemodialysis is one of three renal replacement therapies (the other two being renal transplant; peritoneal dialysis).In hemodialysis, three primary methods are used to gain access to the blood: an intravenous catheter, an arteriovenous (AV) fistula and a synthetic graft. The type of access is influenced by factors such as the expected time course of a patient’s renal failure and the condition of his or her vasculature.
Hemodialysis often involves fluid removal (through ultrafiltration). Side effects caused by removing too much fluid and/or removing fluid too rapidly include low blood pressure, fatigue, chest pains, leg-cramps, nausea and headaches. These symptoms can occur during the treatment and can persist post treatment; they are sometimes collectively referred to as the dialysis hangover or dialysis washout. The severity of these symptoms is usually proportionate to the amount and speed of fluid removal.
Since hemodialysis requires access to the circulatory system, patients undergoing hemodialysis may expose their circulatory system to microbes, which can lead to sepsis, endocarditis or an osteomyelitis.
Heparin is the most commonly used anticoagulant in hemodialysis, as it is generally well tolerated and can be quickly reversed with protamine sulfate. Heparin allergy can infrequently be a problem and can cause a low platelet count. In such patients, alternative anticoagulants can be used. In patients at high risk of bleeding, dialysis can be done without anticoagulation.
Longterm complications of hemodialysis include amyloidosis, neuropathy and various forms of heart disease. Increasing the frequency and length of treatments have been shown to improve fluid overload and enlargement of the heart that is commonly seen in such patients.

 

 

Urinalysis is an array of tests performed on urine and one of the most common methods of medical diagnosis.
Urine specific gravity – This test detects ion concentration of the urine. Small amounts of protein or ketoacidosis tend to elevate results of the specific gravity.The specific gravity of your urine is measured by using a urinometer.If the specific gravity of your urine is under 1.007, you are hydrated. If your urine is above 1.010, you are dehydrated.
Glucose can be measured with Benedict’s Test.
The numbers and types of cells and/or material such as urinary casts can yield a great detail of information and may suggest a specific diagnosis.
    * Hematuria – associated with kidney stones, infections, tumors and other conditions
    * Pyuria – associated with urinary infections
    * eosinophiluria – associated with allergic interstitial nephritis, atheroembolic disease
    * Red blood cell casts – associated with glomerulonephritis, vasculitis, malignant hypertension
    * White blood cell casts – associated with acute interstitial nephritis, exudative glomerulonephritis, severe pyelonephritis
    * granular casts – associated with acute tubular necrosis
    * crystalluria — associated with acute urate nephropathy

 

 

Chylous ascites is the extravasation of milky chyle into the peritoneal cavity. This can occur de novo as a result of trauma or obstruction of the lymphatic system. Moreover, an existing clear ascitic fluid can turn chylous as a secondary event.Milky ascites is subdivided into 3 groups as follows:

* True chylous ascites – Fluid with high triglyceride content usually higher than 110 mg/dL.
* Chyliform ascites – Fluid with a lecithin-globulin complex due to fatty degeneration of cells
* Pseudochylous ascites – Fluid that is milky in appearance due to the presence of pus
In adults, chylous ascites is associated most frequently with malignant conditions. These conditions particularly include lymphomas and disseminated carcinomas from primaries in the pancreas, breast, colon, prostate, ovary, testes, and kidney. Inflammatory disorders, such as tuberculosis, can infrequently be associated with chylous ascites.In children, the most common causes are congenital abnormalities, such as lymphangiectasia, mesenteric cyst, and idiopathic “leaky lymphatics.” Neoplasia is an uncommon cause of pediatric chylous ascites.
The incidence of spontaneous chylous ascites in patients with chronic liver diseases is estimated to be 0.5%. The lymphatics rupture spontaneously as a result of high portal pressures. Abdominal surgery is a common cause of chylous ascites. The surgical procedures most frequently associated with chylous ascites are resection of abdominal aortic aneurysm and retroperitoneal lymph node dissection.

 

 

The main goal of alkali therapy is to counteract the extracellular acidaemia with the aim of reversing or avoiding the adverse clinical effects of the acidosis.

Important points about bicarbonate therapy
1. Ventilation must be adequate to eliminate the CO2 produced from bicarbonate
Bicarbonate decreases H+ by reacting with it to to produce CO2 and water. For this reaction to continue the product (CO2) must be removed. So bicarbonate therapy can increase extracellular pH only if ventilation is adequate to remove the CO2. Indeed if hypercapnia occurs then as CO2 crosses cell membranes easily, intracellular pH may decrease even further with further deterioration of cellular function.
2. Bicarbonate may cause clinical deterioration if tissue hypoxia is present
If tissue hypoxia is present, then the use of bicarbonate may be particularly disadvantageous due to increased lactate production and the impairment of tissue oxygen unloading.
3. Bicarbonate is probably not useful in most cases of high anion gap acidosis
Lactic acidosis can get worse if bicarbonate is given. Clinical studies have shown no benefit from bicarbonate in diabetic ketoacidosis. In these cases, the only indication for bicarbonate use is for the emergency management of severe hyperkalaemia.
4. Bicarbonate therapy may be useful for correction of acidaemia due to non-organic acidosis
In non-organic acidosis, there is no organic anion which can be metabolised to regenerate bicarbonate. Once the primary cause is corrected, resolution of the acidaemia occurs more rapidly if bicarbonate therapy is used. Amounts sufficient for only partial correction of the disorder should be given. The aim is to increase arterial pH to above 7.2 to minimise adverse effects of the acidaemia and to avoid the adverse effects of bicarbonate therapy.

Metabolic Acidosis

 

Uremia is a term used to describe the illness accompanying kidney failure,in particular the nitrogenous waste products associated with the failure of this organ.In kidney failure, urea and other waste products, which are normally excreted into the urine, are retained in the blood. Early symptoms include anorexia and lethargy, and late symptoms can include decreased mental acuity and coma. Other symptoms include fatigue, nausea, vomiting, cold, bone pain, itch, shortness of breath, and seizures. It is usually diagnosed in kidney dialysis patients when the glomerular filtration rate, a measure of kidney function, is below 50% of normal.

Hemodialysis is a method for removing waste products such as creatinine and urea, as well as free water from the blood when the kidneys are in renal failure.Side effects caused by removing too much fluid and/or removing fluid too rapidly include low blood pressure, fatigue, chest pains, leg-cramps, nausea and headaches. These symptoms can occur during the treatment and can persist post treatment; they are sometimes collectively referred to as the dialysis washout.Since hemodialysis requires access to the circulatory system, patients undergoing hemodialysis may expose their circulatory system to microbes, which can lead to sepsis,endocarditis or osteomyelitis.Bleeding may also occur, again the risk varies depending on the type of access used.
Long term complications of hemodialysis include amyloidosis, neuropathy and various forms of heart disease. Increasing the frequency and length of treatments have been shown to improve fluid overload and enlargement of the heart that is commonly seen in such patients.

 

 

Cirrhosis is a consequence of chronic liver disease characterized by replacement of liver tissue by fibrosis, scar tissue and regenerative nodules leading to loss of liver function.
Cirrhosis has many possible causes. In the Western World, chronic alcoholism and hepatitis C are the most common causes.
* Alcoholic liver disease . Alcoholic cirrhosis develops for between 10% and 20% of individuals who drink heavily for a decade or more.AST and ALT are both elevated but less than 300 IU/L with a AST:ALT ratio more than 2.0, a value rarely seen in other liver diseases. Liver biopsy may show hepatocyte necrosis, Mallory bodies, neutrophilic infiltration with perivenular inflammation.
* Chronic hepatitis C.Cirrhosis caused by hepatitis C is the most common reason for liver transplant. 
* Chronic hepatitis B. The hepatitis B virus causes liver inflammation and injury that over several decades can lead to cirrhosis. Hepatitis D is dependent on the presence of hepatitis B, but accelerates cirrhosis in co-infection. 
* Non-alcoholic steatohepatitis (NASH). In NASH, fat builds up in the liver and eventually causes scar tissue. This type of hepatitis appears to be associated with diabetes, protein malnutrition, obesity, coronary artery disease, and treatment with corticosteroid medications. 
* Primary biliary cirrhosis. May be asymptomatic or complain of fatigue, pruritus, and non-jaundice skin hyperpigmentation with hepatomegaly. There is prominent alkaline phosphatase elevation as well as elevations in cholesterol and bilirubin. Gold standard diagnosis is antimitochondrial antibodies with liver biopsy as confirmation if showing florid bile duct lesions.
* Primary sclerosing cholangitis. PSC is a progressive cholestatic disorder presenting with pruritus, steatorrhea, fat soluble vitamin deficiencies, and metabolic bone disease. There is a strong association with inflammatory bowel disease (IBD), especially ulcerative colitis.
* Autoimmune hepatitis. This disease is caused by the immunologic damage to the liver causing inflammation and eventually scarring and cirrhosis. Findings 
* Hereditary hemochromatosis. Usually presents with family history of cirrhosis, skin hyperpigmentation, diabetes mellitus, pseudogout, and/or cardiomyopathy, all due to signs of iron overload. 
* Wilson’s disease. Autosomal recessive disorder characterized by low serum ceruloplasmin and increased hepatic copper content on liver biopsy. May also have Kayser-Fleischer rings in the cornea and altered mental status.
* Alpha 1-antitrypsin deficiency (AAT). Autosomal recessive disorder. Patients may also have COPD, especially if they have a history of tobacco smoking. Serum AAT levels are low. Recombinant AAT is used to prevent lung disease due to AAT deficiency.
Others – Cardiac cirrhosis(in Right heart failure),Galactosemia,Glycogen storage disease type IV,Cystic fibrosis,Hepatotoxic drugs or toxins and Certain parasitic infections (such as schistosomiasis)

 

Gynecomastia is the development of abnormally large mammary glands in males resulting in breast enlargement.The condition can occur physiologically in neonates (due to female hormones from the mother), in adolescence, and in the elderly. In adolescent boys the condition is often a source of distress, but for the large majority of boys whose pubescent gynecomastia is not due to obesity, the breast development shrinks or disappears within a couple of years.The causes of common gynecomastia remain uncertain, although it has generally been attributed to an imbalance of sex hormones or the tissue responsiveness to them; a root cause is rarely determined for individual cases. The condition may also be caused due to an imbalance of estrogenic and androgenic effects on the breast, resulting in an increased or unopposed estrogen action on breast tissue. Approximately 4 to 10% cases of gynecomastia are due to drugs. Both Digoxin and Furosemide  are reported to cause the same condition. Although, chances of gynecomastia could be more if these two drugs are coadministered.Breast prominence can result from hypertrophy of breast tissue, chest adipose tissue and skin, and is typically a combination. Breast prominence due solely to excessive adipose is often termed pseudogynecomastia or sometimes lipomastia.

Treating the underlying cause of the gynecomastia may lead to improvement in the condition. Selective estrogen receptor modulator medications, such as tamoxifen  and clomiphene, or androgens  or aromatase inhibitors such as Letrozole  are medical treatment options, although they are not universally approved for the treatment of gynecomastia. Endocrinological attention may help during the first 2–3 years. After that window, however, the breast tissue tends to remain and harden, leaving surgery (either liposuction, gland excision, skin sculpture, reduction mammoplasty, or a combination of these surgical techniques) as the only treatment option.

 

 
Bu web sitesi ücretsiz olarak Bedava-Sitem.com ile oluşturulmuştur. Siz de kendi web sitenizi kurmak ister misiniz?
Ücretsiz kaydol