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BIO230 Module 5 Study Guide
Chapter 16 Endocrine System Disorders
- Identify the primary effect of these pituitary gland hormones: a. Growth hormone Stimulates protein synthesis b. ACTH Stimulates adrenal cortex to secrete cortisol c. TSH Stimulates thyroid gland d. FSH Women – stimulates growth of ovarian follicles and estrogen secretion; Men – stimulates sperm production e. ADH Increases reabsorption of water by kidney f. Oxytocin Stimulates contraction of uterus after delivery and stimulates ejection of breast milk during lactation
- Identify the primary effect of these pancreas hormones. a. Insulin Transport of glucose and other substances into cells; lowers blood glucose level b. Glucagon Glyconeolysis in liver; increases blood glucose levels.
- Identify the primary effect of these adrenal hormones. a. Aldosterone Increases sodium and water reabsorption by the kidney b. Cortisol Anti-inflammatory and decreases immune response; catabolic effect on tissues; stress response c. Norepinephrine General vasoconstriction
- Why is it beneficial for more than one hormone to control certain body functions, such as blood pressure? Multiple hormones can provide better control of an activity and if there is impairment of one hormone, others can take over.
- Explain the effect(s) adenomas may have upon hormone levels. An adenoma is a benign tumor, and is often secretory, causing excess hormone to be released. They can also have a destructive effect on the gland, which would cause a hormonal deficit, so there could be either too much, or too little hormone. An adenoma of the pituitary will also
cause increased intracranial pressure and neurological effects, due to the location of the pituitary.
- What can cause target cells to resist or become insensitive to hormones? A lack of response may result from a genetic defect, an autoimmune response, or excessive demand on the target cells.
- What is the effect of insulin deficit on the body? (find this under Pathophysiology under Type 1 and Type 2 Diabetes) Since insulin is an anabolic hormone (builds up or synthesis of complex substances from simple molecules), a deficiency results in abnormal carbohydrate, protein, and fat metabolism because glucose can’t be transported inside of cells for energy. Glucose will then remain high in the blood (serum) because it lacks “transportation” (insulin) to move it into the cell where it can be used for energy. Cells must have energy to function and if they lack glucose they will stimulate breakdown of body lipids (fats) for energy instead. If there is not sufficient fat stores, body protein stores will be used instead. The cells energy-course preference hierarchy is: 1) glucose, then 2) fat, then 3) protein.
- Describe the impact of exercise upon blood glucose. Regular exercise can improve glucose utilization and aid in controlling blood glucose for those who are diabetic. However, excessive exercise can also deplete blood glucose and cause hypoglycemia.
- What is the etiology of Type I diabetes mellitus (DM)? What is the etiology of Type 2 DM? Type I - Autoimmune destruction of the pancreatic beta cells, resulting in a deficit of insulin Type II - Reduced effectiveness of insulin due to reduced production, increased resistance of body cells to insulin, increased production of glucose by the liver, or a combination of these factors
- What are the clinical manifestations of DM? Are there any differences between Type 1 and Type 2? Type I - Hunger and fatigue, thirst, polyuria with frequent urination and excretions of large volumes of urine, dry mouth (dehydrated), itchy skin and blurred vision. Weight loss is common. Type II - Same as with Type 1, plus weight gain or increased abdominal girth is common. The three Ps- polyuria, polydipsia, and polyphagia are hallmark.
- A person with diabetes is at risk for developing ketoacidosis (DKA) because….. they lack sufficient insulin, or their cells resist insulin effects, preventing insulin from transporting glucose into the cell where it can be used for energy. Excess blood glucose spills over into urine and glucosuria exerts osmotic pressure in the urine filtrate, resulting in large volume of urine (polyuria). Fluid loss through urine and high blood glucose levels draw water from the cells, resulting in dehydrated body cells. Dehydration causes thirst (polydipsia) and a lack of nutrients entering cells stimulates appetite (polyphagia). A lack of glucose inside the cells leads to catabolism of stored fats (and proteins), producing excess fatty acids known as ketones. Because the liver is limited in the amount of lipids, fatty acids, or ketones it can
depression of the CNS). As ketoacids accumulate in the blood they bind with available bicarbonate ions; this reduces
levels of serum bicarbonate, which causes decreased serum pH. As pH falls, acidosis worsens and loss of consciousness can occur. Electrolyte imbalances also occur, specifically hyponatremia.
- Identify three signs that would help differentiate someone with hypoglycemia from someone with diabetic ketoacidosis. Differences include skin (pale and moist in hypo but warm and dry in hyper), sensorium (impaired concentration in hypo, but clear sensorium, until late, in hyper, and breath (sweet and fruity in hyper and normal in hypo).
- What are the tissue and organ consequences of microangiopathy and macroangiopathy? Elevated blood glucose causes degeneration in both the small and large arteries. Capillary basement membranes become thick and hard, causing obstruction or rupture of capillaries and small arteries. Tissue necrosis and loss of functioning occurs because these vessels are responsible for carrying blood, oxygen and nutrients to the cells. Damage to the eye is retinopathy, and damage to the kidney is nephropathy. Diabetes is a leading cause of blindness and kidney failure. There is also damage to the large vessels, must like atherosclerosis, with increases risks of heart attacks, strokes, and peripheral vascular disease. Obstruction of the arteries in the legs can result in foot and leg ulcerations, which will be slow to heal and vulnerable to infection. Damage to the peripheral vessels leads to peripheral nerve damage, resulting in reduced sensation which increases risks for tissue injury.
- Individuals with diabetes are at greater risk for developing serious tissue trauma and infections because….. …..over time hyperglycemia damages both large and small blood vessels, which reduces perfusion to tissues. Reduced perfusion causes reduced functioning, including neurological functions like sensation. Numbness, tingling, weakness, and muscle wasting is common in peripheral tissue. The diabetic may lose the ability to feel toes, or even feet and without sensation injuries go un-noticed. Un-noticed and un-treated injuries are prone to infection and once infected healing is difficult because circulation is reduced (thus tissues are chronically “under-nourished” and “under-oxygenated”).
- Hyperparathyroidism is associated with what electrolyte imbalance? Knowing that, what effects would you expect to see? Hypercalcemia so you’d expect excessive fatigue, lethargy, muscle weakness, poor tone, arrhythmia, bradycardia, hypertension, polyuria, increased thirst, renal insufficiency, renal calculi, constipation, nausea, osteoporosis and fractures.
- What electrolyte imbalance and effects would you expect in hypoparathyroidism? Hypocalcemia so you’d expect increased neuroexcitability, tingling of fingers and around mouth, muscle spasm, tetany, arrhythmia, hypotension, diarrhea, nausea, cramps.
d. What is the etiology of Hashimoto thyroiditis? Also an autoimmune disorder.
- What is a pheochromocytoma, what does it cause, and how can it be treated? Pheochromocytoma is a benign tumor of the adrenal medulla that secretes epinephrine and norepinephrine. It causes hypertension, headache, heart palpitations, sweating, and intermittent or constant anxiety and can be cured with surgical removal of the tumor.
- Use the table to compare Cushing Syndrome and Addison’s Disease. Cushing Syndrome Addison’s Disease Etiology Caused by an excess of glucocorticoids, possibly from an adenoma, of the adrenal or pituitary gland, an ectopic carcinoma, or iatrogenic conditions, such as large intake of glucocorticoids Caused by a deficiency of adrenocortical secretions, glucocorticoids, mineralocorticoids, and androgens due to an autoimmune reaction. The gland may be destroyed by hemorrhage, meningococcal infection, viral tubercular, or histoplasmosis infection, or a destructive tumor. Pathophysiology Glucocorticoids are essential for the stress response and perform important functions in the body, but in excess they produce multiple, undesirable effects Damage from autoimmune destruction results in low glucocorticoid levels and high ACTH and CRH levels Manifestations, Signs & Symptoms Mood face, heavy trunk with fat accumulation at the back of the neck (buffao hump), while extremities appear thin and wasting), fragile skin that may have red streaks, increased hair growth (hirsutism), increased gluconeogenesis and insulin resistance, which may lead to glucose intolerance Retention of sodium and water, leading to HTN, edema, and possible hyperkalemia Suppressed immune and inflammatory responses, with atrophy of lymphoid tissue, predisposing them to infection Stimulation of erythrocyte production Emotional lability and euphoria Decreased blood glucose levels, poor stress response, fatigue, weight loss, anorexia, nausea, diarrhea, frequent infections, low serum sodium, decreased blood volume (from mineralocorticoid/aldosterone deficit), decreased body hair (lack of androgens) and hyperpigmentation of the extremities, skin creases, buccal mucosa and tongue (due to increased ACTH resulting from low cortisol secretion) Potential Complications Catabolic effects such as osteoporosis and decreased protein synthesis, which will delay healing Diabetes mellitus Risks for infections Reduced ability to respond to stress Cardiac arrhythmias and heart failure Treatment(s) Identify and treat the underlying cause Replacement therapy with necessary
hormones; increased doses may be needed in times of stress Chapter 8
- Define these key terms (on a separate sheet of paper)– abscess, acne, atopic, denuded, eosinophilia, excoriations, fissure, keloid, keratin, lichenification, macules, nodule, papule, plaque, pustule, prurutis, ulcer, and vesicle.
- Complete the table to describe common skin conditions.
- Description of Condition Etiology Treatment(s) Acne Vulgaris Common in adolescence, consisting of comedones, which can become inflamed, ranging from mild to severe. Increased sebaceous gland activity results in plugged pores and infection Frequent cleansing with mild soaps, improving nutrition, avoiding oils and lotions, antibacterial meds (topical and oral). Avoid harsh soaps and scrubbing Contact dermatitis A pruritic rash, often with erythema and swelling, at the site/location of exposure/irritation that appears within a few minutes to hours of exposure. An allergic response to direct exposure to a substance that triggers cell-mediated hypersensitivity Identification and removal of the irritant. If severe, topical glucocorticoids may be needed. Urticaria Hard, raised erythematous, and often pruritic lesions, often scattered over the body Due to histamine release of a type I hypersensitivity reaction, triggered by an allergen such as a specific drug, food, or shellfish. Identification and avoidance of the allergen; OTC antihistamines. If severe, oral corticosteroids may be needed. Atopic Dermatitis In babies and children- moist, erythematous, vesicular, pruritic lesions, often involving the face, neck, arms and legs. May also be in the “diaper” area. In adults- pruritus, dry, scaling skin with thick, leathery patches; skin folds may be moist and red, often on the surfaces of arms, hands, legs, and feet Inherited tendency toward allergic skin response with chronic skin inflammation due to exposure to allergens Identification and elimination of the allergen(s) (as much as is possible); use of topical glucorticoids; antihistamines; avoiding any potential skin irritants such as strong detergents and perfumes; hypoallergenic diet; and adequate skin moisture. In severe cases topical glucocorticoids may be needed Psoriasis Chronic inflammatory skin disorder with remissions and exacerbations. Presence of silvery plaques with a erythematous base, dry, cracked skin that may bleed, often on the face, scalp, elbows and knees, as Genetic abnormal activation of T cells and an associated increase in cytokines in affected tissues. Immunologic changes lead to excessive proliferation of Glucocorticoids and ultraviolet light treatments, to reduce cell proliferation. Currently the best response/remission rates are achieved with immunologic medications
by infection, sun exposure, or stress. Tinea A fungal, superficial infection which can affect multiple areas of the body. Tinea capitis is a scalp infection, Tinea corporis is commonly called “ringworm” and can occur anywhere on the body, Tinea pedis is commonly called “athlete’s foot” and Tinea unguium affects the nails, usually of the toes. Appearance varies based upon location. On scalp, a bald patch, with erythema and scaling is common. On the skin, pruritis is common as is a round, erythematous ring of vesicles or papules with a clear center. On the feet, the skin between the toes becomes inflamed, pruritic, and painful and there may be a foul odor. In the nails, the nail becomes thick, dark and cracks easily. Fungi live off of dead, keratinized cells of the epidermis. Antifungal medications, usually designed for the specific area affected. Scabies Appears as light brown lines, often with small vesicles, surrounded by erythema, most often in the areas between fingers, the wrists, inner surfaces of the elbow, and waistline area. Inflammation and pruritis occurs. Skin invasion by a mite, the female burrows into the epidermis, lays eggs, and the larvae emerge and migrate to the skin’s surface, and then burrow back into the skin in search of nutrients. Spread by close contact. Antifungal medication. Pediculosis Appears as a macule of papule that is highly pruritic, which leads to scratching and skin excoriations. May occur anywhere on the body or be limited to hair. Small parasites feed off of human blood and attach themselves to hair, skin, or pubic area. Female ice lay eggs on hair shafts, cementing their eggs firmly to the hair close to the scalp. The egg (nit) appears as a small, whitish shell attached to the hair. After hatching the baby louse bites the human to obtain blood for survival. Topical medications, which can usually be obtained OTC. Hair infestation requires meticulous removal of eggs with a fine- toothed comb. All clothing, linen, other items in close contact (stuffed animals, etc) must also be treated to avoid re-infestation. Squamous Slow-growing and painless, Squamous cell is a Surgical removal of the tumor,
Cell Carcinoma tumor with scaly, slightly elevated, red lesions that have an irregular border and central ulceration appearance. malignant tumor of the epidermis, usually due to sun exposure, and most often found on the face and neck. Prognosis is excellent if treated early, before metastasis occurs and any surrounded affected tissue. Malignant Melanoma Nevi that grow, change shape, color, size, texture, or bleed. Melanomas grow quickly and extend downward into tissues and metastasize quickly to regional lymph nodes and then to other organs. The “ABCD” acronym is used to aid detection (see #34). Develops from melanocytes in the basal layer of the epidermis or from a nevus (a collection of melanocytes) and is most often due to genetics, ultraviolet radiation, and hormonal factors. Surgical removal, along with the affected surrounding tissue. Radiation and chemotherapy are also usually required to limit metastasis. Survival is often tied to when the growth is detected with earlier detection being correlated with greater survival chances.
- Explain the “ABCD” signs of melanoma. A = shape is asymmetrical; B = border is irregular; C = more than one color; and D = size is larger than an pencil eraser (>0.5cm). Chapter 15
- Define these key terms (on a separate sheet of paper) - astigmatism, chemoreceptors, conjunctivitis, diplopia, hyperopia, intraocular pressure, mechanoreceptors, myopia, nystagmus, otosclerosis, ototoxic, photophobia, photoreceptors, proprioceptors, presbycusis, presbyopia, ptosis, strabismus, tinnitus, visual acuity.
- Use the table to compare narrow angle and chronic glaucoma. Narrow-angle Glaucoma Chronic Glaucoma Etiology Increased intraocular pressure caused by an excessive accumulation of aqueous humor due to a decrease in the angle between the cornea and iris in the anterior chamber. Angle narrowing can result from an abnormal anterior insertion of the iris. May be caused by a developmental abnormality, aging, or scar tissue in the eye from trauma or infection. Increased intraocular pressure caused by degeneration, usually beginning after age 50. Pathophysiology As the lens enlarges with age, it pushes the iris more forward and to the side. This anatomic position change may block the outflow of aqueous humor when the pupil is dilated and the thickened iris fills the narrow angle. Pressure inside the eyeball The trabecular network and canal of Schlemm become obstructed, gradually diminishing the outflow of aqueous humor, thereby slowly increasing intraocular pressures. The increased pressure compresses blood supply to the retinal
infection.
- Describe the etiology, manifestations, and treatment of Keratitis. Keratitis is an inflammation of the cornea typically caused by infection or injury. Infectious- Herpes simplex virus infection (from the lip or mouth) can be easily transferred to the eye via touch, and will result in corneal inflammation and ulceration. Manifestations typically severe pain and photophobia but corneal ulcerations can occur, and lead to scar tissue and vision loss. Due to the risk of vision loss, ophthalmologist care should be sought. Inflammations- Keratitis can also be caused by trauma to the cornea, such as abrasions from a foreign body caught under the eyelid, a damaged contact lens, object directly scratching the cornea, or exposure to chemicals, splashes or fumes. Wearing protective glasses, avoiding touching the eye, and cleansing contact lenses appropriately can reduce risks. Prompt and prolonged flushing of the eye with cool, clean, running water (sterile saline is best) will help remove irritants, but care from a health care professional should be sought to be sure there is not any damage to the conjunctiva or sclera, which would require prompt treatment.
- Use the table to compare cataracts, detached retina, and macular degeneration. Cataracts Detached Retina Macular Degeneration Etiology Lens becomes cloudy (opaque) and interferes with light transmission. Causes can be congenital, degeneration related to aging, excessive exposure to sunlight or metabolic abnormalities such as diabetes. Trauma to the eye may also cause a cataract to develop. An acute condition of the retina tearing away from underlying choroid due to marked myopia, degeneration of aging, or scar tissue that creates tension on the retina. Age-related vision loss due to a combination of genetic factors and environmental exposures (ultraviolet rays and certain drugs). Predisposing Factors Not wearing protective eye equipment during sports, carpentry, or other activity in which the eye could be injured. Pathophysiology As the retina tears away from the choroid, vitreous humor leaks behind the loosened retina. As increased vitreous humor seeps behind the retina, more of the retina is lifted away from the choroid. Retinal cells cease to function because they are deprived of nutrients from the choroid blood supply, resulting in the Degeneration of the fovea centralis in the macula lutea (high density cone area that provides the most acute vision) at the central point of the retina. It may be: a) dry, or atrophic, in which deposits form in the retinal cells, gradually destroying them; or b) wet
Etiology Inflammation due to allergies, or an An inner ear or labyrinth disorder, usually infection, of the middle ear cavity. affecting only one ear and occurring in 30-50 year olds Predisposing Factors Infants and young children are more prone because their auditory canal is shorter, wider, and at a right angle to the nasopharynx where respiratory secretions can easily flow. Infants also spend more time lying down, which permit reflux of fluid into the ear. Changes in barometric pressure, stress, or other condition that increases blood flow to the ear may trigger an attack. Pathophysiology Upper respiratory infections often spread to the ear, where inflammatory exudate becomes trapped. Gastric reflux can also easily enter the ear of infants who are fed while in a supine position Excessive endolymph develops intermittently, as an “attack” which stretches the membranes and interferes with functioning of the hair cells in the cochlea and vestibule. Rupture of the labyrinth membrane can permit perilymph to mix with endolymph, and increase fluid volume for a period of time (minutes to hours). Manifestations, Signs & Symptoms It may be asymptomatic, but is often painful (otalgia). The tympanic membrane appears red and bulging. Infants and young children may tug at their ear. Mild hearing loss and a sense of fullness/congestion is common. If infected, fever and nausea may be present. If pressure builds the tympanic membrane may rupture, in which case purulent drainage may be seen in the external ear canal. Membrane rupture often relieves the pain that was caused by tympanic membrane pressure. During an attack, severe vertigo, tinnitus, unilateral hearing loss, nausea, sweating, feeling of pressure in the ear, and nystagmus, which also causes an inability to focus. Potential Complications Recurrent infections may cause hearing loss, development of scar tissue on the tympanic membrane, adhesions or damage to the ossicles, mastoiditis, and/or cholesteatoma (mass of epithelial cells in the middle ear that can erode the ossicles). Repeated attacks can cause permanent damage to the hair cells, resulting in permanent hearing loss and vertigo. Diagnosis is Made by Otoscopic exam Electronystagmography, electrocochleography, fluid and balance testing
Treatment(s) OTC ibuprofen or acetaminophen will help relieve pain. If infected, antibiotics may be administered. Surgical implantation of drainage tubes can relieve persistent congestion. Administration of medications, exercise programs, or if severe, surgical shunt placement to remove excess endolymph or resect the vestibular nerve
