Lecture 11- Endocrine System Pathologies Flashcards

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Review Endocrine System

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Responsible for helping maintain homeostasis.
Massage can also be an adjunct to maintaining homeostasis by affecting the actions of the endocrine system. For example, some of the hormones released by endocrine glands are responsible for stress responses in the body. By decreasing stress through relaxation, massage can indirectly lower the levels of these hormones and bring about a sense of well-being in a client.

The endocrine system works with the nervous system to coordinate the functioning of all body systems. The nervous system uses nerve impulses to communicate and the endocrine system uses chemicals called hormones to communicate. Most hormones are released in one part of the body and travel through the bloodstream, affecting cells in other parts of the body. Some hormones do not enter the bloodstream but instead work on neighboring cells.

Functions of endocrine system:
Regulating the activity of smooth muscle, cardiac muscle, and some glands
Altering metabolism
Regulating the chemical composition and volume of body fluids and fluids inside cells
Regulating growth and development
Helping regulate reproductive processes
Participating in circadian rhythms.
The body contains two kinds of glands:
Exocrine glands secrete their products into ducts that empty into body cavities, the hollow center of an organ or onto the surface of the body.

Types:
sudoriferous (secrete perspiration),
sebaceous (secrete oil)
ceruminous (secrete earwax)
digestive glands (secrete digestive enzymes into the gastrointestinal tract)
mucous glands (secrete mucus in a variety of areas of the body)
Endocrine glands secrete their hormones into surrounding interstitial fluids and then into the blood or they may affect nearby cells.
adrenals
pineal
gonads
pituitary
pancreas (islets)
thyroid
parathyroids
Some organs and tissues are not endocrine glands but do contain cells that secrete hormones. These organs and tissues include the hypothalamus, thymus, kidneys, intestinal mucosa, heart, and placenta.

Feedback systems (negative and positive), other hormones and the nervous system regulate hormonal secretions. Negative-feedback systems are the most common method of hormonal regulation by causing a decrease in secretion in response to a stimulus.
An example of a negative-feedback system is hormonal secretion of thyroid hormones by the thyroid gland. Thyroid hormones regulate metabolism. When metabolic needs are low, fewer thyroid hormones are secreted; when metabolic needs are high, more thyroid hormones are released.
An example of hormones themselves controlling the secretion of other hormones is the hypothalamus and the pituitary gland. The anterior pituitary secretes hormones in response to hypothalamic hormones. Some of the hypothalamic hormones cause an increase in the secretion of anterior pituitary hormones; other hypothalamic hormones cause a decrease in the secretion of these hormones.
An example of how the nervous system regulates hormones is demonstrated by how the hypothalamus communicates with the posterior pituitary. The posterior pituitary gland does not synthesize any hormones. Instead, it stores two hormones (antidiuretic hormone and oxytocin) made by the hypothalamus. Nerve impulses from the hypothalamus cause the posterior pituitary gland to release these hormones.

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2
Q

Pancreatitis
Acute & Chronic

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Description: inflammation of the pancreas. The pancreas produces enzymes that aid in digestion and hormones that help regulate glucose metabolism. Pancreatitis occurs when enzymes are activated resulting in autodigestion. This activation of enzymes leads to massive inflammation, bleeding, atrophy, and necrosis of the pancreas and may lead to chronic.
Acute: sudden onset, in 50-60 year, 20% death rates (50% elderly)
Chronic: develops gradually over years, follows acute 20% of the time and carries a risk factor for pancreatic cancer.

Etiology: most commonly gallstones and alcohol abuse (80% of cases) Q. Gallstone obstruction of the pancreatic duct leads to bile reflux to the pancreas. Bile activates pancreatic enzymes normally inactive, leading to autodigestion. Fifteen percent of cases are idiopathic. The other 5% of cases are related to medication use, systemic viral or bacterial infections, injury to the pancreas during surgery or other types of trauma (seat belt injury after a motor-vehicle accident). Leakage of digestive enzymes can cause peritonitis. Damage to islet cells can lead to insulin-dependent diabetes.

Pathogenesis: reflux of bile in the pancreas causes the enzymes (normally inactive) to activate, beginning to digest the pancreas (called autodigestion), this causes necrosis, inflammation and damaged tissues and cells.

Causes of Pancreatitis:
Gallstones
Alcoholism
Overeating
Virus
Drugs
Trauma or surgery

Clinical Features:
- acute pancreatitis: severe epigastric or upper
abdominal pain that is referred to the back, pain
intensifies when lying supine and is worse after eating. Fever, loss of appetite, nausea, vomiting, and bloating are also common. In severe cases, the person becomes dehydrated, has hypotension and may go into shock.

  • chronic pancreatitis: epigastric pain or upper abdominal region, nausea and vomiting, weight loss, fatigue and oily smelly stools. 70% will have signs of diabetes caused by loss of islet cells.

Treatment: fasting, analgesics and IV fluids, mild cases recover with little or no treatment, severe cases require emergency medical treatment or surgery to remove any obstruction and antibiotics. Chronic cases are monitored for diabetic symptoms. Oral enzyme replacements are used during meals to address any enzyme imbalances.

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3
Q

Pancreatic Cancer

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Description: malignancy of the pancreas, most commonly
in the cells that carry digestive enzymes out of the pancreas,
peak age of diagnosis is between 40 and 60 years of age and
incidence between men and women is equal. Pancreatic
cancer is often asymptomatic and advanced at the time of diagnosis, with only 20% of cases in which the cancer is confined to the pancreas. Metastasis occurs early and often involves the liver, stomach, lungs, brain and bone. Persons with pancreatic cancer seldom survive a year beyond diagnosis. The following are risk factors; smoking, diet high in fat, chronic pancreatitis (50% of cases), exposure to carcinogenic compounds, family history of pancreatic, breast or colon cancer
Canadian Stats ( 2020) 6000 new cases
5300 deaths
Highest mortality rate: 92% die within 5 years
Canadian Stats (2020)

6000 new cases
5300 deaths

Highest mortality rate: 92% die within 5 years

Etiology: mutations to genes in the cells of the pancreas causes them to grow uncontrollably and never die. These cells accumulate into masses or tumours and then spread throughout the body.

Pathogenesis: uncontrolled cancerous cell growth invades all tissues of the pancreas, making them less productive and efficient for digestion

Clinical Features: abdominal pain and tenderness, vague back pain, loss of appetite, weight loss, nausea, vomiting, fatigue, itchy skin, jaundice, and bulky fatty, clay-colored stools (steatorrhea). An abdominal mass is often palpable. Recent-onset diabetes may be an indicator. Severe skin itching related to elevated levels of bile acids. One third of persons with pancreatic cancer also have abdominal swelling (ascites).

Treatment: no effective treatment, surgical resection is the only potentially curative treatment. However, because of late detection, only 15% to 20% of persons with pancreatic cancer are candidates for surgery. Radiation therapy and chemotherapy are ineffectual in advanced disease, these treatment methods have improved the cure rate when used after complete surgical removal (Whipple procedure) a pancreatoduodenectomy. Treatment also includes pain control (often with opiates) and treatment for depression as the person faces the fear of fatal illness.

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4
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Diabetes Mellitus

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A group of disorders characterized by chronic elevated blood glucose levels and disturbances in protein, fat, and carbohydrate metabolism (mainly carbohydrates). It is caused by insufficient insulin or resistance to insulin by the cells or both. Several types of diabetes mellitus have been identified. Most commonly are: type I, type II, and gestational diabetes. Glucose is the main source of fuel and source of energy for movement, growth, repair, and other functions. It is obtained by ingested foods or from body storage (glycogen). When cells need fuel, glucose can enter the cells only with the help of insulin. When glucose enters the cells, blood glucose levels are lowered. Without insulin, glucose does not enter the cells and blood glucose levels remain high (hyperglycemia). Diabetics maintain their blood sugar within a healthy range. Levels are determined by using a glucose meter. During testing, a drop of blood is extracted and placed on test strip. Once the test strip is attached to the meter, it will indicate a person’s blood glucose level. People diagnosed with diabetes will be well versed in how to monitor their blood sugar, how to interpret this information, and what to do if levels are too high or too low.

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5
Q

Diabetes Mellitus Type 1

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Description: 10% of all diabetic cases, was once called juvenile diabetes because it was most often seen in children and also called insulin-dependent, because sufferers are dependent on injected insulin to live. Pancreatic beta-cells are damaged or destroyed creating a lack of insulin. Without insulin, glucose cannot enter cells.

Etiology: autoimmune processes destroy insulin producing cells called islets of langerhans. There is also a strong genetic factor. Some viral infections such as mumps and the Epstein-Barr virus have been implicated.

Pathogenesis: islets of langerhans cells are destroyed causing a reduction of insulin in the bloodstream, needed to uptake glucose into cells.

Clinical Features: three Ps of diabetes mellitus
polyuria (excessive urination
polydipsia (excessive thirst
polyphagia (excessive hunger)
Other symptoms include fatigue, blurred vision, weight loss and increased frequency of infections. Persistent hyperglycemia damages cells and leads to complications
such as vision problems (diabetic retinopathy), reduced sensations (diabetic neuropathy) and kidney and cardiovascular diseases.

Treatment: no cure, monitoring blood sugar, taking insulin, regular exercise and maintaining optimum weight. Because digestive enzymes interfere with the absorption of insulin, it must be administered through the skin by either injection or by an insulin pump or insulin pen.

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6
Q

Diabetes Mellitus Type 2

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Description: 90% of all cases. Pancreatic beta-cells produce insulin, sometimes not enough, but mostly cells throughout the body become resistant to it, this is called insulin resistance. Often preventable, but the condition is on the rise, fuelled largely by the current obesity epidemic. Young people are more likely now than ever to be diagnosed with type II diabetes, and it is the most common chronic disease in children and adolescents.

Etiology: unknown, but truncal or central obesity and sedentary lifestyle are strong contributing factors. A genetic link also exists.

Pathogenesis: beta cells in pancreas are destroyed or dysfunctional leading to a lack of insulin production, insulin is required to transport glucose from the bloodstream into cells for use to make energy.

Clinical Features: the three P’s of diabetes mellitus: polyuria (excessive urination), polydipsia (excessive thirst), and polyphagia (excessive hunger). Obesity, fatigue and lethargy are also common findings. There are many serious long-term complications, mostly peripheral arterial disease and diabetic neuropathy (causing reduced sensations). These may lead to life-threatening infections, gangrene and possible amputation. Other long-term complications are atherosclerosis, hypertension, diabetic retinopathy, cataracts, kidney and heart diseases. Fungi thrive in an environment high in glucose, sufferers often have fungal infections like thrush, jock itch, athlete’s foot and ringworm.

Treatment: regular exercise, good nutrition and maintaining optimum weight. Oral medications, unlike type 1 where insulin must be injected.

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7
Q

Pancreatic Insufficiency

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Description: inability to properly digest food due to a lack of digestive enzymes made by the pancreas. Chronic pancreatitis is the most common cause of this deficiency. It is also found with cystic fibrosis which causes progressive loss of the pancreatic cells that make digestive enzymes. Loss of digestive enzymes leads to maldigestion and malabsorption of nutrients.

Etiology: cystic Fibrosis (a genetic disorder) and chronic pancreatitis destroy pancreatic digestive enzyme producing cells.

Pathogenesis: damage to enzyme producing cells causes inflammation and a deficiency and digestive difficulties causing malabsorption of fats, proteins and carbohydrates.

Clinical Features: may be asymptomatic, oil in the stool (steatorrhea) and pale, foul-smelling bulky stools. Abdominal discomfort, loss of appetite and bloating are also common. Fat soluble vitamin deficiencies.

Treatment: medications like pancreatic enzymes used to aid in digestion with a low fat diet, supplements for fat soluble vitamins (A, D, E, K).

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8
Q

Cystic Fibrosis (CF) Included with respiratory Diseases also.

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Description: a genetic disorder that causes progressive hypersecretion of the cells that produce mucus, saliva, sweat and digestive juices. Normally these secretions are thin and slippery but the gene mutations causes these secretions to be sticky and thick. They plug up, obstruct and narrow respiratory and digestive passageways damaging the lungs, the digestive tract and many other organs. CF is the most common fatal genetic disease and it affects boys and girls equally. Average life expectancy is 38 years, death results from respiratory failure.

Etiology: defective gene must be inherited by both parents is located on the seventh chromosome. It causes a faulty transport of salt in and out of cells. This causes the mucus secretions to be thick and sticky.

Pathogenesis: because of less salt in the process of producing the mucus, it causes dehydration in the mucus, making it thicker and stickier. Q

Clinical Feature: overproduction of thick mucus that causes chronic obstruction, inflammation, and infection of the respiratory tract with associated coughing, wheezing, shortness of breath, a barrel chest, and clubbing of fingernails and toenails. Because of digestive tract involvement, these individuals often have bulky, foul-smelling stools, poor nutrition, and small stature.

Treatment: no cure, symptom management, prevention, and medications. Antibiotics are prescribed for lung infections, mucus-thinning drugs, anti inflammatories, stool softeners and bronchodilators. Postural drainage techniques are employed to loosen and help expel phlegm. Oxygen therapy is also used. Enzyme replacements are used to help with digestion; vitamin supplement and a high-protein diet are advised to improve nutrition.

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9
Q

Hyper pituitary Disorders

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Description: overproduction and secretion of pituitary hormones, causing overstimulation of target endocrine glands. Although the pituitary produces and secretes many hormones, this discussion will consider the overproduction of two hormones:

adrenocorticotropic hormone (ACTH): Cushing’s disease, overproduction causes hyperfunctioning of the adrenal cortex.
growth hormone (GH): overproduction causes Giantism (if before puberty) & Acromegaly (if in adulthood), additionally, excessive levels of GH lead to diabetes mellitus and high blood pressure (hypertension).

Etiology: pituitary or hypothalamic tumour. A genetic link may be involved as well.

Pathogenesis: tumour causes overproduction of pituitary hormones affecting target endocrine glands.

Clinical Features: accelerated growth of body tissues and a tall stature.

Treatment: if tumour, surgery and radiation therapy.

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10
Q

Cushing’s Syndrome

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Description: excessive amounts of cortisol in the blood (hypercortisolism) caused by either hyperpituitarism in Cushing’s disease or from the use of corticosteroids in Cushing’s syndrome. Cushing’s disease is rare, most commonly seen in adults 25 to 40 years of age. Women account for over 70% of all cases. Cushing’s syndrome is more common than Cushing’s disease because of the use of corticosteroids as treatment for many autoimmune diseases.

Etiology: pituitary tumour that stimulates excessive production of adrenocorticotropic hormone (ACTH), resulting in hypercortisolism. Adrenal tumor is another cause. Cushing’s syndrome is most often the result of prolonged and excessive use of high-dose cortisone drugs like prednisone.

Pathogenesis: tumour or medication causes hyper secretions of adrenocorticotropic hormone causing hypercortisolism from the adrenals

Clinical Features: round face (called moon face), acne, puffy eyes, ruddy complexion, thinning scalp hair, and growth of facial hair in women. Central (truncal) obesity is noted with accumulation of fluids and fat on the neck and upper back (called buffalo hump) accompanied by red stretch marks. Typically, the arms and legs remain thin. Conditions such as cardiomyopathy, hypertension, osteoporosis, hyperglycemia (leading to diabetes mellitus in 20% of cases) and adrenal tumor formation often coexist. Fatigue, muscle weakness, and mental and emotional changes are often noted. The skin becomes thin and fragile and is easily bruised. Wound healing is poor, and the person is prone to infection.

Treatment: Treatment involves reducing corticosteroid use (if this is the cause). Other means are surgical removal of an adrenal tumour or pituitary tumour with or without radiation therapy.

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11
Q

Hyperpituitary Disorders

Giantism

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Description: excess production and secretion of growth hormone (GH) from the pituitary gland during childhood years or before the onset of puberty. Giantism is extremely rare

Etiology: pituitary tumour causes overproduction of growth hormone (GH). Genetics are a factor also.

Pathogenesis: increased growth hormone causes excessive growth.

Clinical Features: abnormal and accelerated growth, mainly in long bones. May also have an arched palate, slanted eyes and hypertension.

Treatment: if a tumour, surgery and radiation therapy, is caused by medications, cease.

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12
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Acromegaly

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Description: overproduction and secretion of growth hormone (GH) by the pituitary gland during adult years, causing excessive growth of connective tissues including bones. Most often affecting bones of hands, feet and face. Acromegaly is rare and has a decreased life expectancy. Acromegaly is seen more often in women than in men.

Etiology: overproduction of growth hormone (GH) most often caused by a pituitary tumour.

Pathogenesis: overstimulation of normal growth patterns due to excessive amounts of growth hormone

Clinical Features: epiphyseal plates have already closed so excessive growth is noted in hands, feet, and face. All bones become heavier and thicker and the rib cage elongates. Protrusion of the jaw and an enlarged tongue are also common. Number and size of skin glands are higher and larger than normal, leading to thick, coarse skin and increased body odor. Generalized pain, fatigue and weakness because of the stress of larger, heavier structures on the body. Headaches are seen in 65% of all cases. May lead to other conditions such as carpal tunnel syndrome, Cushing disease, diabetes mellitus, arthritis, hypertension and cardiomyopathy.

Treatment: if tumour: surgery and radiation, medications to lower growth hormone (GH) or other hormone levels.

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13
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Hypopituitary Disorders

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Description: decrease in the production and secretion of pituitary hormones. This factor causes a lack of stimulation of target endocrine glands. Because the pituitary is responsible for many major hormones, the syndrome can be complex and involve many important metabolic processes.

Etiology: mostly by pituitary or hypothalamic tumour. Other causes are head injury, radiation treatment to the head, infections, medications and genetics.

Pathogenesis: tumour disrupts pituitary secretions

Clinical Features: directly related to the particular hormone shortage.
Adrenocorticotropic Hormone (ACTH) deficiency: most dangerous, begins as nausea, vomiting, weight loss, and severe fatigue and ultimately leads to vascular collapse with lowered blood pressure and shock, which can be fatal.
Thyroid Stimulating Hormone (TSH) deficiency: hypothyroidism, fatigue, weight gain, dry skin, constipation and sensitivity to cold
Luteinizing Hormone (LH) deficiency:
Follicle Stimulating Hormone (FSH): both lead to ovarian suppression with irregular periods or absence of periods (amenorrhea), infertility, and osteoporosis. Men develop testicular suppression, erectile dysfunction, loss of body and facial hair and fatigue.
Growth Hormone (GH) deficiency: not serious in adults but leads to delayed puberty and dwarfism in children
Antidiuretic Hormone (ADH) deficiency: causes diabetes insipidus with excessive urination, thirst with electrolyte imbalances

Treatment: if tumour: surgery and radiation, medications for hormone deficiencies.

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14
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Pituitary Tumours

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Description: abnormal growths that develop in the pituitary gland. Some pituitary tumors cause excessive production of hormones, others can restrict normal functions of the pituitary gland causing it to produce lower levels of hormones. The vast majority of pituitary tumors are noncancerous or benign growths called adenomas. Adenomas remain confined to your pituitary gland or surrounding tissues and don’t spread to other parts of the body.

Etiology: unknown, genetic alterations

Pathogenesis: uncontrolled cell growth (benign) disrupts pituitary gland secretions

Clinical Features: may be asymptomatic, from pressure from a pituitary tumour: headaches, vision loss (peripheral), nausea and vomiting, weakness, less frequent or absent menstrual periods, body hair loss, sexual dysfunction, increased frequency and amount of urination, unintended weight loss or gain. Symptoms of pituitary hormone changes, functioning tumours produce hormones, generally causing an overproduction of hormones. Different types of functioning tumours can develop in your pituitary gland, each causing specific signs and symptoms. Others decrease the level of hormones.

Treatment: if symptomatic, surgery with radiation to remove tumour and hormone medication for deficiencies

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15
Q

Empty Sella Syndrome (ESS)

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Description: enlargement or malformation of the sella turcica causing a buildup of cerebrospinal fluid that squishes the pituitary gland in the sella turcica which makes it appear to be empty or only partially filled on Xray. Normally the pituitary gland sits and fills in the sella turcica. It is a bony structure at the base of the brain that surrounds and protects it. The pituitary gland shrinks or becomes flattened.

Etiology: Primary ESS: unknown cause or a defect in sella turcica increasing pressure and squishing the gland causing it to flatten out. Secondary ESS: pituitary gland regresses within the cavity caused by injury, surgery, idiopathic intracranial hypertension or radiation therapy.

Pathogenesis: function of pituitary gland not usually affected

Clinical Features: often asymptomatic, headaches, hypertension, low libido, erectile dysfunction and obesity in women.

Treatment: treatment of symptoms if any, hormone replacement therapy, possible surgery.

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16
Q

Endocrine System Pathologies
Primary Adrenal Insufficiency

Addison’s Disease

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Description: adrenal gland does not produce enough cortisol (also aldosterone), also called adrenal insufficiency. Occurs at 30-50 years old and is rare but may be life threatening.

Etiology: autoimmune disease, local or general infections, adrenal cancer or adrenal hemorrhage.

Pathogenesis: antibodies are produced that attack the adrenal cortex destroying cortisol producing cells
Clinical Features: general weakness, extreme fatigue, GI disturbances like nausea, vomiting, abdominal pain, diarrhea, decreased appetite (anorexia) and weight loss. Other symptoms are decreased cardiac output, general hypotension and orthostatic hypotension with fainting, hyperpigmentation of the skin and mucous membranes (called bronzing), cold intolerance, dramatic behavior and mood changes.

Treatment: hormone replacement therapy, corticosteroids and dietary modifications.

17
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Primary Aldosteronism
Conn’s Syndrome

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Description: a tumour in the adrenal cortex of the adrenal glands that produces aldosterone. Aldosterone is a hormone that is normally involved in regulating the amount of salt and potassium in the blood. In patients who have overproduction of this hormone, excessive amount of salt is retained in their body and potassium is lost, leading to high blood pressure and low potassium levels.

Etiology: adrenal hyperplasia, adrenal carcinoma or genetics.

Pathogenesis: cellular changes in adrenal glands affect their production of aldosterone (too much) causing imbalances in salt and potassium levels in the blood.

Clinical Features: sodium retention leads to high blood pressure, as well as weakness, chronic headaches, frequent urination, increased thirst, vision problems muscle cramps and skeletal muscle weakness (low blood potassium).

Treatment: surgical removal, medications that block aldosterone.

18
Q

Hyperthyroidism

Graves Disease

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Description: an autoimmune disorder causing hyperactivity of the thyroid gland or hyperthyroidism with a resultant goiter (enlargement of the thyroid gland). Excessive thyroid hormone secretions increase the body’s metabolic rate 60% to 100%. Graves disease is more common in women than in men and manifestations occur after age 20 years. Thyroid hormones act to increase the basal metabolic rate, affect protein synthesis, help regulate long bone growth, neuronal maturation and increase the body’s sensitivity to catecholamines. The thyroid hormones are essential to proper development and differentiation of all cells of the human body. They also regulate protein, fat, and carbohydrate metabolism, affecting how human cells use energy and they also stimulate vitamin metabolism. Thyroid hormone leads to heat generation.

Etiology: autoimmune disorder, genetics

Pathogenesis: antibodies are produced in reaction to thyroid hormones and attack regulatory thyroid hormones causing overproduction

Clinical Features: anxiety, hand tremors, weight loss (despite normal or increased food intake), diarrhea, fatigue, insomnia, tachycardia, flushed and warm skin with profuse sweating, heat intolerance, erectile dysfunction, brittle or loss of hair, goiter, joints are often hypermobile, protrusion of the eyeballs (exophthalmos) and Graves dermopathy (pretibial myxedema). The latter is reddening and swelling seen on the shins and tops of the feet.

Treatment: decrease thyroid hormone production and control symptoms, especially tachycardia. Medications include beta-blockers and anti-thyroidal drugs. Surgery (thyroidectomy) or irradiated to kill some of it.

19
Q

Hypothyroidism

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Description: underactive thyroid gland leading to deficiency of thyroid hormone secretion (T3 and T4). It develops slowly over many months or years so symptoms appear gradually. May cause joint pain, obesity, infertility and heart disease.

Etiology: autoimmune, also sufferers of Hashimoto’s thyroiditis. Other causes include over-response to treatment for hyperthyroidism, thyroid surgery, radiation therapy for cancers of the head and neck, and medications such as lithium (psychiatric medication), less often: congenital, pituitary disorder, pregnancy, iodine deficiency.

Pathogenesis: immune response creates antibodies that attack the gland causing damage and dysfunction

Clinical Features: fatigue, lethargy, muscle weakness, slowed metabolic rate, bradycardia, cold intolerance, depression, impaired memory, constipation, weight gain, slowed mental processes, cool dry and scaly skin, loss of or thinning hair. Less common symptoms are excessive edema of the face, hands, and feet. Edema is non-pitting and distinctive facial changes such as a bulbous nose and swollen lips are seen as well as hoarseness and slurred speech.

Treatment: medication: synthetic thyroid hormone levothyroxine. This oral medication restores adequate hormone levels, reversing the signs and symptoms of hypothyroidism.

20
Q

Hypothyroidism

Hashimoto’s Disease

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Description: autoimmune disease where the thyroid gland is attacked by a variety of cell and antibody-mediated immune processes causing inflammation and damage (often producing a goiter). It was the first disease to be recognized as an autoimmune disease.

Etiology: genetics, preventable environmental factors, including high iodine intake, selenium deficiency, pollutants such as tobacco smoke, infectious diseases and certain drugs.

Pathogenesis: gene mutations cause an immune response that attacks the thyroid gland cells, killing them and causing destruction of the thyroid and decreasing secretions.

Clinical Features: hypothyroidism with bouts of hyperthyroidism. Symptoms include psychosis, weight gain, depression, goiter, mania, sensitivity to heat and cold, paresthesia, fatigue, panic attacks, bradycardia, tachycardia, high cholesterol, reactive hypoglycemia, constipation, migraines, muscle weakness, stiffness in joints, cramps, memory loss, vision problems, infertility and hair loss.

Treatment: medication: synthetic thyroid hormone levothyroxine. This oral medication restores adequate hormone levels, reversing the signs and symptoms of hypothyroidism.

21
Q

Hyperparathyroidism

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Description: Overproduction of parathyroid hormone from parathyroid gland. This hormone helps maintain appropriate levels of calcium in the bloodstream and in tissues. May be primary or secondary (caused by other disease). A common disease, affecting approximately 1 in 1000 people. Occurrences rise sharply after 40 years of age and are twice as common in women as in men.

Etiology: cancer, non cancerous growth-adenoma (85%), hyperplasia all causing primary. Injury, congenital malformation, severe calcium deficiency, severe Vitamin D deficiency, chronic kidney failure all causing secondary.

Pathogenesis: overproduction of parathyroid hormone causes imbalance of calcium metabolism in the body.

Clinical Features: elevated blood calcium levels, muscle weakness, fatigue, hypertension, mental confusion, abdominal pain, loss of appetite, nausea, and vomiting. Peristalsis is also decreased with accompanying constipation. May also result in spontaneous fractures, osteoporosis, renal damage, urinary tract infections, excessive urination and kidney stones.

Treatment: Hormone replacement therapy and dietary supplements are frequently used. Other treatments include surgery. If a tumor is the cause, it is surgically removed. If the condition is hypertrophy of the parathyroid glands, they are surgically removed.