Hypothyroidism in Adults

Hypothyroidism, a state of low serum thyroid hormone, results from hypothalamic, pituitary, or thyroid insufficiency. The disorder can progress to life-threatening myxedema coma. Hypothyroidism is more prevalent in women than in men.

Etiology
Hypothyroidism results from inadequate production of thyroid hormone, usually because of dysfunction of the thyroid gland due to surgery (thyroidectomy), radiation therapy (particularly with 131I), inflammation, chronic autoimmune thyroiditis (Hashimoto’s disease) or, rarely, conditions such as amyloidosis and sarcoidosis. It may also result from pituitary failure to produce thyroid-stimulating hormone (TSH), hypothalamic failure to produce thyrotropin-releasing hormone, inborn errors of thyroid hormone synthesis, inability to synthesize thyroid hormone because of iodine deficiency (usually dietary), or the use of antithyroid medications such as propylthiouracil.
In patients with hypothyroidism, infection, exposure to cold, and sedatives may precipitate myxedema coma.

Signs and symptoms:
Typically, the early clinical features of hypothyroidism are vague and may include fatigue, forgetfulness, sensitivity to cold, unexplained weight gain, and constipation. As the disorder progresses, characteristic myxedematous signs and symptoms appear, such as decreasing mental stability; dry, flaky, inelastic skin; puffy face, hands, and feet; hoarseness; periorbital edema; upper eyelid droop; dry, sparse hair; and thick, brittle nails.

Acromegaly and Gigantism

Introduction

Chronic, progressive diseases, acromegaly and gigantism are marked by hormonal dysfunction and startling skeletal overgrowth. Acromegaly occurs after epiphyseal closure, causing bone thickening and transverse growth and visceromegaly. Gigantism begins before epiphyseal closure and causes proportional overgrowth of all body tissues. Although the prognosis depends on the causative factor, these disorders usually reduce life expectancy unless treated in a timely way.

Pathophysiology
Typically, oversecretion of human growth hormone (HGH) produces changes throughout the entire body, resulting in acromegaly and, when oversecretion occurs before puberty, gigantism. Somatotrope adenomas and, rarely, extrapyradimal pituitary lesions or other tumors may cause this oversecretion, but the cause of the tumors themselves remains unclear. Elevated HGH levels in more than one family member suggest a genetic cause.
The earliest sign of acromegaly is soft-tissue swelling of the extremities, which causes coarsening of the facial features. This rare form of hyperpituitarism occurs equally among men and women, usually between ages 30 and 50.

Signs and symptoms
Acromegaly develops slowly, whereas gigantism develops abruptly.

Acromegaly
Acromegaly commonly produces hyperdidrosis, arthropathy, carpal tunnel syndrome, proximal muscle weakness and fatigue, acanthosis nigricans and skin tags, and oily skin.
Hypersecretion of HGH produces cartilaginous and connective tissue overgrowth, resulting in a characteristic hulking appearance, with an enlarged supraorbital ridge and thickened ears and nose. Prognathism, projection of the jaw, becomes marked and may interfere with chewing. Laryngeal hypertrophy, paranasal sinus enlargement, and thickening of the tongue cause the voice to sound deep and hollow. Also, the fingers are thickened.
Coronary artery disease, cardiomyopathy with arrhythmias, left ventricular hypertrophy, decreased diastolic function, and hypertension occur in 30% of patients; upper airway obstruction with sleep apnea, in 60% of patients. Generalized visceromegaly occurs, including cardiomegaly, macroglossia, and thyroid gland enlargement.
Prolonged effects of excessive HGH secretion include barrel chest and kyphosis. Both gigantism and acromegaly may also cause signs of glucose intolerance and diabetes mellitus because of the insulin-antagonistic character of HGH.

Male Infertility

Male infertility may be suspected whenever a couple fails to achieve pregnancy after about 1 year of regular unprotected intercourse. 

Between 40% and 50% of infertility problems in the United States are totally or partially attributed to the male.

Causes
Factors that cause male infertility include:

• varicocele, a mass of dilated and tortuous varicose veins in the spermatic cord
• semen disorders, such as volume or motility disturbances or inadequate sperm density
• proliferation of abnormal or immature sperm, with variations in the size and shape of the head
• systemic disease, such as diabetes mellitus, neoplasms, liver or kidney disease, or viral disturbances, especially mumps orchitis
• genital infection, such as gonorrhea, tuberculosis, or herpes
• disorders of the testes, such as cryptorchidism, Sertoli-cell–only syndrome, varicocele, ductal obstruction (caused by absence or ligation of the vas deferens or infection), hydrocele (collection of fluid in the testes), or infection (orchitis and epididymitis).
• genetic defects, such as Klinefelter’s syndrome (chromosomal pattern XXY, eunuchoidal habitus, gynecomastia, and small testes) or Reifenstein’s syndrome (chromosomal pattern 46XY, reduced testosterone, azoospermia, eunuchoid-ism, gynecomastia, and hypospadias)
• immune disorders, such as autoimmune infertility and allergic orchitis
• endocrine imbalance (rare) that disrupts pituitary gonadotropins, inhibiting spermatogenesis, testosterone production, or both; such imbalances occur with Kallmann’s syndrome, panhypopituitarism, hypothyroidism, and congenital adrenal hyperplasia
• chemicals and drugs that can inhibit gonadotropins or interfere with spermatogenesis, such as arsenic, methotrexate, medroxyprogesterone acetate, nitrofurantoin, monoamine oxidase inhibitors, and some antihypertensives. sexual problems, such as erectile dysfunction, ejaculatory incompetence, and low libido.

Other factors include age, occupation, trauma to the testes, and tight-fitting clothing that constricts the scrotum and affects sperm production.

Special considerations in Patients with Diabetes Mellitus

Special considerations in Patients with Diabetes Mellitus

• Stress that compliance with the prescribed program is essential. Emphasize the effect of blood glucose control on long-term health.
• Watch for acute complications of diabetic therapy, especially hypoglycemia (vagueness, slow cerebration, dizziness, weakness, pallor, tachycardia, diaphoresis, seizures, and coma). Immediately give carbohydrates in the form of fruit juice, hard candy, or honey; if the patient is unconscious, subcutaneous, I.M. or I.V. glucagon or I.V. dextrose may be given.
• Be alert for signs and symptoms of ketoacidosis (acetone breath, dehydration, weak and rapid pulse, Kussmaul’s respirations) and hyperosmolar coma (polyuria, thirst, neurologic abnormalities, stupor). These hyperglycemic crises require I.V. fluids, insulin and, usually, potassium replacement.
• Monitor diabetic control by obtaining blood glucose levels.
• Watch for diabetic effects on the cardiovascular system, such as cerebrovascular, coronary artery, and peripheral vascular impairment, and on the peripheral and autonomic nervous systems.
• Treat all injuries, cuts, and blisters (particularly on the legs or feet) meticulously.
• Be alert for signs of urinary tract infection and renal disease.
• Urge regular ophthalmologic examinations to detect diabetic retinopathy.
• Assess for signs of diabetic neuropathy (numbness or pain in the hands and feet, footdrop, neurogenic bladder). Stress the need for personal safety precautions; explain that decreased sensation can mask injuries. Minimize complications by maintaining strict blood glucose control.

Diabetic In Pregnancy- A Brief Discussion

Pregnancy places special demands on carbohydrate metabolism and causes the insulin requirement to increase, even in a healthy woman. Consequently, pregnancy may lead to a prediabetic state, to the conversion of an asymptomatic subclinical diabetic state to a clinical one (gestational diabetes occurs in about 1% to 2% of all pregnancies), or to complications in a previously stable diabetic state.
Prevalence of diabetes mellitus increases with age. Maternal and fetal prognoses can be equivalent to those in nondiabetic women if maternal blood glucose is well controlled and ketosis and other complications are prevented. Infant morbidity and mortality depend on recognizing and successfully controlling hypoglycemia, which may develop within hours after delivery.

Causes
In diabetes mellitus, glucose is inadequately used either because insulin isn’t synthesized (as in type 1, insulin-dependent diabetes) or because tissues are resistant to the hormonal action of endogenous insulin (as in type 2, non–insulin-dependent diabetes).

Protective mechanisms
During pregnancy, the fetus relies on maternal glucose as a primary fuel source. Pregnancy triggers protective mechanisms that have anti-insulin effects: increased hormone production (placental lactogen, estrogen, and progesterone), which antagonizes the effects of insulin; degradation of insulin by the placenta; and prolonged elevation of stress hormones (cortisol, epinephrine, and glucagon), which raise blood glucose levels.
In a normal pregnancy, an increase in anti-insulin factors is counterbalanced by an increase in insulin production to maintain normal blood glucose levels. However, women who are prediabetic or diabetic can’t produce sufficient insulin to overcome the insulin antagonist mechanisms of pregnancy, or their tissues are insulin-resistant.
As insulin requirements rise toward term, the patient who is prediabetic may develop gestational diabetes, necessitating dietary management and, possibly, exogenous insulin to achieve glycemic control. The insulin-dependent patient may need increased insulin dosage.

Introduction to Pituitary Tumors

Constituting 10% of intracranial neoplasms, pituitary tumors typically originate in the anterior pituitary (adenohypophysis). They occur in adults of both sexes, usually during the third and fourth decades of life. The three tissue types of pituitary tumors are chromophobe adenoma (90%), basophil adenoma, and eosinophil adenoma.
The prognosis is fair to good, depending on the extent to which the tumor spreads beyond the sella turcica.

Causes
Although the exact cause is unknown, a predisposition to pituitary tumors may be inherited through an autosomal dominant trait. Some are part of a hereditary disorder called multiple endocrine neoplasia 1. Pituitary tumors aren’t malignant in the strict sense; however, because their growth is invasive, they’re considered a neoplastic disease.
Chromophobe adenoma may be associated with the production of corticotropin, melanocyte-stimulating hormone, growth hormone, and prolactin; basophil adenoma, with evidence of excess corticotropin production and, consequently, with signs of Cushing’s syndrome; and eosinophil adenoma, with excessive growth hormone.

Signs and symptoms
As pituitary adenomas grow, they replace normal glandular tissue and enlarge the sella turcica, which houses the pituitary gland. The resulting pressure on adjacent intracranial structures produces typical clinical features.

Neurologic features

• Frontal headache
• Visual symptoms, beginning with blurring and progressing to field cuts (hemianopias) and then unilateral blindness
• Cranial nerve involvement (III, IV, VI) from lateral extension of the tumor, resulting in strabismus; double vision, with compensating head tilting and dizziness; conjugate deviation of gaze; nystagmus; lid ptosis; and limited eye movements
• Increased intracranial pressure (secondary hydrocephalus)
• Personality changes or dementia, if the tumor breaks through to the frontal lobes
• Seizures
• Rhinorrhea, if the tumor erodes the base of the skull
• Pituitary apoplexy secondary to hemorrhagic infarction of the adenoma. Such hemorrhage may lead to both cardiovascular and adrenocortical collapse.

Adrenal Hypofunction

Introduction

Primary adrenal hypofunction or insufficiency (Addison’s disease) originates within the adrenal gland itself and is characterized by decreased mineralocorticoid, glucocorticoid, and androgen secretion. Secondary adrenal hypofunction is due to impaired pituitary secretion of corticotropin and is characterized by decreased glucocorticoid secretion. Secretion of aldosterone, the major mineralocorticoid, is often unaffected.
Addison’s disease is relatively uncommon, though it can occur at any age, in either sex. Secondary adrenal hypofunction occurs when a patient abruptly stops taking an exogenous steroid after long-term therapy or when the pituitary is injured by a tumor or by infiltrative or autoimmune processes. With an early diagnosis and adequate replacement therapy, the prognosis for the person with adrenal hypofunction is good.
Adrenal crisis (addisonian crisis), a critical deficiency of mineralocorticoids and glucocorticoids, generally follows acute stress, sepsis, trauma, surgery, or omission of steroid therapy in patients who have chronic adrenal insufficiency. A medical emergency, adrenal crisis necessitates immediate, vigorous treatment.

Causes
The following are causes of primary and secondary adrenal hypofunction and adrenal crisis.
Primary hypofunction
Addison’s disease occurs when more than 90% of both adrenal glands are destroyed. Such destruction usually results from an autoimmune process (autoimmune adrenalitis) in which circulating antibodies react specifically against the adrenal tissue.
Other causes include tuberculosis (once the chief cause; now responsible for less than 10% of adult cases), bilateral adrenalectomy, hemorrhage into the adrenal gland, neoplasms, and infections (histoplasmosis, cytomegalovirus). Rarely, a family history of autoimmune disease predisposes the patient to Addison’s disease and other endocrinopathies.
Secondary hypofunction
Secondary hypofunction, which results in glucocorticoid deficiency, can stem from hypopituitarism (causing decreased corticotropin secretion), abrupt withdrawal of long-term corticosteroid therapy (long-term exogenous corticosteroid stimulation suppresses pituitary corticotropin secretion and results in adrenal gland atrophy), or the removal of a corticotropin-secreting tumor.
Adrenal crisis
After trauma, surgery, or other physiologic stress, adrenal crisis exhausts the body’s stores of glucocorticoids in a person with adrenal hypofunction.

Examining a Diabetic Patient

Diabetes mellitus is a clinical syndrome characterized by chronic hyperglycemia and disturbances in carbohydrate,lipid and protein metabolism. A patient with diabetes need a complete physical examination to look for any related complications and to manage accordingly.

General Appearance

• Check the weight and look for obesity and measure BMI
• Facial appearance: note any features of cushings disease
• State of hydration

Lower Limbs

• Inspect and look for any ulceration, infection, hair loss, skin atrophy.
• Check injection sites on the thigh and note any skin atrophy due to insulin use.
• Palpate all the peripheral pulses that includes femoral, popliteal, posterior tibial, dorsalis pedis.
• Check pedal edema that can be present due to nephropathy.
• Feel the tempreture as the feet may be cold due to ischemia.
• Do the neurological assessment by checking the sensations including those of dorsal column.
• Reflexes may be diminished due to neuropathy and also look for any signs of proximal muscle wasting.
• Joints for Charcot’s joints ( loss of proprioception )

Upper Limbs

• Nails : for candidiasis
• Feel upper limb injection sites
• Check Blood pressure in supine and standing to detect autonomic neuropathy
• Palpate upper limb pulses .

Diabetes- Patient Monitoring,Care And Education

Diabetes mellitus is a common disease affecting a large number of population. It is characterized by increased blood sugars and abnormalities of carbohydrate and lipid metabolism.Diabetes can be managed by family physicians as effectively as in hospital clinics.

Aims Of Diabetic Care

• Alleviation of symptoms.
• Minimization of complications.
• Reduction of early mortality.
• Quality of life enhancement.
• Education of the patient and family.
• Features of well organized care
• Use of a register and well maintained records.
• Regular review , following a proper protocol and provision of adequate time and open access for patients to review advice.
• Multidisciplinary team covering all aspects of diabetes care- GPs, diabetes nurses/assistants and educators.
• Continuing education for professional staff.

Routine diabetic review
Each diabetic patient requires 6 monthly review or more frequently as necessary. This should include a through annual review of all aspects of disease and care.

Review include

Introduction To Diabetic Neuropathy

Diabetic neuropathy is a complication of diabetes in which the nerves are damaged most commonly in the legs and feet which leads to impaired sensations. It is a common but a serious complication of diabetes mellitus and depending upon the nerves damaged the symptoms may range from pain and numbness in the extremities to problems with digestive system, blood vessels and heart and may even sometimes be fatal.

Clinical features:There are basically four types of diabetic neuropathies with different presenting symptoms. A patient may have symptoms of only type or may have overlapping symptoms.

1. Peripheral Neuropathy: In this type the patient usually have the legs and feet affected first followed by the hands and the arms. The nerve damage in the feet can lead to decreased sensation and increased chances of foot injury. Symptoms include:

• Numbness
• Reduced ability to feel pain or changes in temperature mainly in the feet and the toes.
• Tingling sensation
• Burning sensation
• Pain when walking
• Extreme sensitivity to light touch
• Repeated ulcers, infections in the foot.

Peripheral neuropathy most commonly occurs in patients who have poor;y controlled blood sugar levels and can be prevented by keeping good control on blood sugar, as well as taking good care for the feet and legs to prevent foot injury.

2. Autonomic Neuropathy: In this type the nerves of the autonomic nervous system that controls the heart, digestive system, bladder, sex organs and eye are damaged secondary to diabetes. Symptoms include:

• Constipation
• Bloating
• Diarrhea
• Lack of awareness when blood sugar levles falls
• Frequent urinary tract infections
• Urinary incontinence
• Heartburn
• Nausea and vomiting
• Loss of appetite
• Feeling of fullness of stomach due to delayed emptying.
• Sexual difficulties
• Sudden abnormal sweating
• Palpitations
• Problems in blood pressure regulation

Management Of Diabetes Mellitus Type 2

Introduction:
Diabetes Mellitus type 2 is condition in which the there is insufficient production of hormone insulin from the pancreas or the body becomes resistant to normal or even high levels of insulin. This leads to high blood sugar (glucose) levels and if not manged properly may cause a number of complications in long term.

Managing Diabetes mellitus:
The goal of the treatment is not only to manage the symptoms but to keep the blood sugar levels in control and prevent related complications.

1. Identifying The Underlying Disease: Early in the course most patients may have no symptoms at all the the disease may go undiagnosed for years. It is important for any family physician to ask patients while taking a general history the risk factors and family history of diabetes and if suspected carry out appropriate test to identify the disease and control it at a early stage before the complications begin to develop.

2. Dietary And Exercise Modifications: Patient should be properly education and encouraged to change their life style and diet modification. Strict adherence to diet and regular exercise should be encouraged by the primary care physician at each visit. Although there is a common perception that there is a specific diabetic diet in reality it is not so. Patients just need to avoid animal fats, refined carbohydrates and sweets, and center on high fiber low fat food like vegetables and whole grains.

Some patients may have good control of their blood sugar only by managing their diet and will not need medicines. Sometimes a nutritionist may help patients educate about the diet that is healthy and protective for them.

Regular physical activity is important for every one and more so for patients with diabetes. Exercise helps to :

• Lower blood sugar levels without the need for medications
• Burns extra calories and fats and helps manage an ideal body weight.
• Improves blood flow and maintains a normal blood pressure
• Increases energy levels
• Improves the body’s ability to handle stress

3. Regular Monitoring of Blood glucose:
The goal of treatment in type 2 Diabetes mellitus is to keep the blood glucose levels at normal or near normal levels. This can be achieved by regular monitoring and adjusting the diet and medicine if needed.
Home blood sugar testing is easy and may be recommended for patients who are on insulin or oral diabetes medicines. A normal fasting blood glucose is usually less than 100 mg/dl.
Measuring HbA1c helps in determining the average blood sugar during the past two to three months. The goal for most patients is Less than 7%.

4. Pharmacological Treatment:
A number of oral medicines are available to treat type 2 diabetes. They are briefly described below:

Cushing Syndrome: Causes, Symptoms, Diagnosis And Treatment.

Introduction: Cushing syndrome is an endocrinological disorder and it describes the signs and symptoms associated with abnormally high levels of the hormone cortisol.  

Cushing syndrome is also known as Hypercortisolism.

Etiology:

1. Use Of Glucocorticosteroid Medicines: The most common cause of Cushing syndrome is the excessive use of corticosteroid medicine. Prednisone, dexamethasone and Prednisolone are the examples of these medicines. The glucocorticosteroid given externally mimic the actions of the body,s normal hormone cortisol. These drugs are mainly used in the treatment of asthma, skin allergies, inflammatory diseases, etc.

2. Excess Production of the hormone Cortisol In The Body: The other cause is the excessive production of the hormone cortisol from the body. This hormone is normally produced from the adrenal glands in response to ACTH (adrenocorticotropic hormone) from the Pituitary gland. This hormone in turn is controlled by CRH (Corticotropic releasing hormone) from the hypothalamus. Some of the causes for excess production of cortisol in the body include:
A pituitary gland tumor that release too much ACTH leading to excess stimulation of adrenal glands to produce cortisol.
Tumors of the adrenal gland that produce excess cortisol.
Tumors elsewhere in the body that may produce ACTH or CRH.