Hypogonadism is a condition where your sex glands do not function properly. Your sex glands might produce too little or no sex hormones. The sex glands in men are called as testes and in females, they are called ovaries. They can also be named as gonads. The main function of sex hormones is to develop secondary sexual characters such as testicular development in men and breast development in women. These hormones play an important role in menstrual cycles and also the production of sperm.

Hypogonadism- Types, Causes, Symptoms, Diagnosis, Treatment

Hypogonadism is also known as gonads deficiency. In males, it is referred to as low serum testosterone or andropause.

This condition can be treated with appropriate medical treatment.

Types of Hypogonadism

They are two types of hypogonadism. Let’s have a look at both types of hypogonadism:

• Primary Hypogonadism:- It is also known as a primary testicular failure. Because the problem originated from the testicles. The main causes of primary hypogonadism are Klinefelter syndrome- in this condition they are a congenital abnormality of the sex chromosomes, undescended testicles, mumps orchitis, hemochromatosis, injury to the testicles and cancer treatment.
• Secondary Hypogonadism:- In this condition, the problem is with the pituitary glands or hypothalamus which do not function properly. Hypothalamus produces a hormone called gonadotropin-releasing hormones. This hormone signals the brain to produce follicle-stimulating hormone (FSH) and luteinizing hormone (LH). These hormones signal the testes to produce male sex hormone called testosterone. Common causes of secondary hypogonadism are Kallmann’s syndrome, pituitary disorders, inflammatory diseases, HIV/AIDS, certain medications, obesity and the normal ageing process.

Causes of Hypogonadism:-

The following are the causes of primary Hypogonadism:-

• Autoimmune disorders which are addison’s diseases and hypoparathyroidism.
• Severe infections which involve mumps in your testicles as well.
• Kidney and liver diseases
• Exposure to radiations
• Hemochromatosis which due to more absorption of iron in the body
• Sexual organ surgery
• Genetic disorders

Causes of Central or Secondary Hypogonadism

• Genetic disorders which includes kallmann’s syndrome
• Infections
• Pituitary disorders
• Inflammatory diseases
• Obesity
• Frequent Weight fluctuations
• Brain surgery
• Exposure to radiations
• Any injury to pituitary gland

Symptoms of Hypogonadism

The following are the symptoms of hypogonadism seen in women:-

• No menstrual cycle
• No growth of breast or slow growth
• Hot flashes
• Less hair growth in the body
• Low or Absence of sex drive
• Milky discharge from breasts

The Following are the Symptoms of Hypogonadism seen in Men:-

• Muscle loss
• Loss of body hair is seen
• Abnormal growth of the breast
• Reduction in the growth of penis and testicles
• Erectile dysfunction
• Osteoporosis
• Low or Absence of sex drive
• Fatigue
• Infertility
• Hot flashes
• Difficulty in concentration
  
  

  Hypogonadism

How to Diagnose Hypogonadism?

Your doctor will conduct a physical exam in order to assess the growth of secondary sexual characteristics. The doctor will also look for the levels of testosterone in the body. The following are the tests performed to confirm hypogonadism:

• Hormonal testing
• Analysis of the semen
• Pituitary imaging
• Genetics study
• Testicular biopsy

Treatment for Hypogonadism

Treatment options available for females are as follows:-

• Increasing the number of female sex hormones
• Estrogen supplementation is done when hysterectomy is performed.
• But in normal cases, the combination of estrogen and progesterone is given because there is a risk of developing endometrial cancer. If the increased levels of estrogen are alone is given.

Treatment in Male as Follows:-

1. Testosterone replacement therapy is widely used in hypogonadism. You can get
   • Injection
   • Patch
   • Gel
   • Lozenge

Take a Note:-

Hypogonadism is a chronic condition which requires life-long treatment. Your sex hormones may decrease if you stop treatment. You will need support from groups and through therapy which can help you before, during and after the treatment.

References:
https://www.healthline.com/health/hypogonadism#outlook
https://www.mayoclinic.org/diseases-conditions/male-hypogonadism/diagnosis-treatment/drc-20354886

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Cardiac arrhythmias occur because of abnormalities of impulse formation or propagation. Abnormal impulse formation

Abnormal Automaticity

Automaticity is another term for pacemaker activity, a characteristic possessed by all cells of the specialised cardiac conduction system during health and, potentially, by other cardiac myocytes during certain disease states. The rate of firing of a pacemaker cell is largely determined by the duration of the phase 4 diastolic interval This in turn is determined by (i) the maximum diastolic potential following depolarization of the preceding action potential, (ii) the slope of diastolic depolarisation due to pacemaker currents and (iii) the threshold potential for generation of a new action potential. In the healthy state, there is a hierarchy of firing rates within the specialised conduction system with the highest rate in the sinus node followed by the AV node and then the His–Purkinje system.

Arrhythmias

Abnormal Impulse Propagation

Re-entry

Many clinically important arrhythmias are due to reentry, in which an activation wavefront rotates continuously around a circuit. Re-entry depends upon a trigger in the form of a premature beat, and a substrate, that is, the reentry circuit itself.

Signs And Symptoms of Arrhythmias

Patients with a cardiac arrhythmia may present with a number of symptoms:

The most common symptom is palpitation, an awareness of an abnormal heartbeat, although some patients with clearly documented arrhythmia have no palpitation. Arrhythmias start suddenly and, therefore, if the patient clearly describes palpitation of sudden onset (‘like flicking a switch’), this is a useful pointer to an arrhythmia rather than heightened awareness of sinus tachycardia, which has a less sudden onset.

The heart is designed to work most efficiently in sinus rhythm. Any arrhythmia compromises cardiac function. Classical symptoms that arise due to reduced cardiac output include reduced exercise capacity, breathlessness and fatigue.

Angina may accompany tachycardia, even in the absence of coronary artery disease. Tachycardia increases the metabolic rate of cardiac muscle and hence its demand for blood flow. Myocardial perfusion occurs predominantly during diastole and during tachycardia proportionately less time is spent in diastole and so myocardial demand for blood can exceed supply, resulting in angina.

A sudden drop in cardiac output may accompany either bradycardia or tachycardia, causing episodes of dizziness (presyncope), loss of consciousness (syncope) or, in extreme cases, sudden death from cardiac arrest.

Atrial tachyarrhythmias such as atrial flutter and atrial fibrillation may be complicated by the development of intracardiac thrombus, usually within the left atrial appendage. This thrombus may embolize to any part of the body but the most common clinical presentation is with a transient ischaemic attack or stroke. Arrhythmias may aggravate heart failure in two ways: (i) the haemodynamic effect of the arrhythmia may precipitate heart failure or aggravate existing heart failure and (ii) prolonged tachycardia of any type may lead to tachycardia-induced cardiomyopathy

Diagnosis of Arrhythmias

It includes a 12-lead ECG and an echocardiogram to detect structural heart disease. Other investigations for structural and ischaemic heart disease may be indicated at this stage with the aim of detecting any underlying structural heart disease. If the history does not include sinister features such as syncope or a family history of sudden unexpected death at a young age, and the resting 12-lead ECG and echocardiogram are normal, then the patient can be reassured that they are extremely unlikely to have a serious heart rhythm disturbance. The extent of further investigation will be dictated by how troublesome the symptoms are.

Treatment for Arrhythmias

Management

Cardiac arrhythmias associated with unstable angina, heart failure or hypotension requires emergency treatment. In most cases, the treatment of choice is d.c. cardioversion.

Concerns about thromboembolism as the heart returns to sinus rhythm are valid but should not delay emergency treatment. Immediate d.c. cardioversion is appropriate when the onset of arrhythmias is clearly identified as within 48 h of presentation or when the patient is already taking warfarin and has had a therapeutic INR for at least 4 weeks.

If facilities permit, a transesophageal echocardiogram may be performed in patients not already on warfarin in order to exclude intracardiac thrombus. Heparin should then be given immediately and continued until the INR is within the therapeutic range.

Anticoagulant therapy should be continued for at least 3 months following cardioversion. Long-term stroke prophylaxis is guided thereafter by the CHADS2 score.

If d.c. cardioversion is deemed inappropriate, rapid ventricular rate control may be achieved with intravenous ß-blockers, verapamil or digoxin.

Drug Therapy for Arrhythmias

Antiarrhythmic drug therapy is used to control the frequency and severity of arrhythmias, with the aim of maintaining sinus rhythm where possible. Although antiarrhythmic drug treatment has been the mainstay of arrhythmia treatment, many of these drugs have limited efficacy and important toxicity. Many arrhythmias are now curable by catheter ablation. Implantable devices such as permanent pacemakers and ICDs have assumed an increasingly important role in the treatment of arrhythmias and, in many cases, antiarrhythmic drugs have an adjunctive role.

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The liver weighs up to 1500g in adults and as such is one of the largest organs in the body. The main functions of the liver include protein synthesis, storage, and metabolism of fats and carbohydrates, detoxification of drugs and other toxins, excretion of bilirubin and metabolism of hormones,

Liver Disease

Acute Liver Disease

It is a self-limiting episode of hepatocyte damage which in most cases resolves spontaneously without clinical sequelae. This is a rare condition in which there is a rapid deterioration in liver function with associated encephalopathy (altered mentation) and coagulopathy. It may result in Acute liver failure which carries a significant morbidity and mortality and may require emergency liver transplantation.

The Chronic Liver Disease

It occurs when permanent structural changes within the liver develop secondary to long-standing cell damage, with the consequent loss of normal liver architecture. In many cases, this progresses to cirrhosis, where fibrous scars divide the liver cells into areas of regenerative tissue called nodules. The conventional wisdom is that this process is irreversible, but therapeutic intervention in hepatitis B and hemochromatosis has now repeatedly documented cases of reversal of cirrhosis. Once the patient reaches this stage they are at risk of developing liver failure, portal hypertension or hepatocellular carcinoma.

Symptoms of Liver Disease

The common symptoms of liver disease are the weakness, increased fatigue, and general malaise. Weight loss and anorexia are more commonly seen in chronic liver disease and loss of muscle bulk is a characteristic of the very advanced disease. Abdominal discomfort may be seen in patients with an enlarged liver or spleen while distension with ascites is usually the cause of more advanced disease. Abdominal pain is common in hepatobiliary disease, frequently localized to the right upper quadrant. This mostly results in rapid or gross enlargement of the liver when the pain is thought to be a consequence of capsular stretching. There is Tenderness over the liver in case of acute hepatitis, hepatic abscess or hepatic malignancy.

liver

Causes of Liver Disease

Viral Infections

Viruses are the common causative agents which the affect liver, resulting in a transient and innocuous hepatitis.Five human viruses have been well described to date, including hepatitis A (HAV), B (HBV), C (HCV), D (HDV) and E (HEV). Each type of viral hepatitis causes similar symptoms with acute inflammation of the liver.

Alcohol:

Alcohol is the single most significant cause of liver disease throughout the Western world accounting for between 40% and 60% of cases of cirrhosis in different countries. About 20% of alcohol abusers develop progressive liver fibrosis, which can eventually lead to alcoholic cirrhosis, typically after a period of 10–20 years of heavy indulgence

Non-Alcohol Related Fatty Liver Disease:

Liver pathology that is very similar to alcohol-induced disease is now well recognized in a number of settings including obesity, diabetes mellitus, and the metabolic syndrome.

Immune Disorder:

Autoimmune disease can affect the hepatocyte or bile duct and is characterized by the presence of autoantibodies and raised immunoglobulin levels. It includes Autoimmune Hepatitis (AIH), Primary biliary cirrhosis (PBC), Primary sclerosing cholangitis (PSC).

Vascular Abnormalities:

The Budd–Chiari syndrome (BCS) is a rare, heterogeneous and potentially fatal condition related to the obstruction of the hepatic venous outflow tract.

Metabolic and Genetic Disorders:

There are various inherited metabolic disorders that can affect the functioning of the liver. Hemochromatosis, Wilson’s disease, α1-Antitrypsin deficiency, Glycogen storage disease, Gilbert’s syndrome.

Drugs:

Drugs are an important cause of abnormal liver function tests and acute liver injury, including ALF (DILI drug induced liver injury).

Diagnosis of Liver Disease

All patients with liver disease must undergo a comprehensive and thorough assessment to ascertain the underlying etiology. Although causes of acute and chronic liver disease may differ, a similar approach is used to investigate both patient groups to ensure no primary cause or cofactor is overlooked.

• Biochemical tests
• Imaging Techniques
• Liver Biopsy
• Lab Investigation Of Aetiology

Treatment for Liver Disease

Several pharmacological agents are available for the emergency control of variceal bleeding. Most act by lowering portal venous pressure. They are generally used to control bleeding in addition to balloon tamponade and emergency endoscopic techniques.

• Vasopressin was the first vasoconstrictor used to reduce portal pressure in patients with actively bleeding varices. However, its associated systemic vasoconstrictive adverse effects limited its use.
• The synthetic vasopressin analog, terlipressin, is highly effective in controlling bleeding and in reducing mortality. It can be administered in bolus doses every 4–6h and has a longer biological activity and a more favorable side effect profile.
• Once a diagnosis of variceal bleeding has been established, a vasoactive drug infusion (usually terlipressin) should be started without further delay and continued for 2–5 days. Somatostatin and the somatostatin analog, octreotide, are reported to cause selective splanchnic vasoconstriction and reduce portal pressure.
• Although they are reported to cause less adverse effects on the systemic circulation, terlipressin remains the agent of choice.

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