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PCB 3703 Fall 2018 - Final Clinical Guide – Chapters 15, 16, & 17-Fetal Alcohol Syndrome: The use of drugs and alcohol, and smoking habits during pregnancy can affect fetal central nervous system development, as these noxious substances can cross the placental membrane. Fetal exposure to these substances (especially alcohol) can cause mental disabilities, disordered bone growth, bone and joint deficiencies, congenital heart disease, cardiovascular disorders, speech and learning disabilities, hyperactivity, aggressive behavior, behavioral disorders, misshapen or smaller than average head, small eyes and thin upper lip, large oracles (ears), stunted growth, short stature, and visual disabilities.-Fetal Smoking Syndrome: maternal smoking habits or exposure to second-hand smoke can cause suppression of bone development, congenital anemia, aggressive behavior, short stature, mental disabilities, learning disorders, social behavior issues, and negative affects on organs connected to the CNS (like the eyes (blindness) and ears(deafness))-Common Placental Viral Infection: viruses can pass through the placental membrane, infecting the fetus and causing damage in CNS development of the eyes and ears. -Klinefelter Syndrome: A form of intersexuality where the individual has an XXY trisomy and male external genitalia, but may also have a uterus and fallopian tubes, smaller than average testicles, longer legs, breasts, wide rounded hips and narrow shoulders with little or no hair growth on the face and chest. Patient cannot reproduce normally. This can be caused by active increased female hormones like estrogen, which leads to the formation of female secondary sex characteristics or can be caused by a deficiency of Anti-Müllerian Hormone, which inhibits paramesonephric ducts from becoming the female reproductive organs. Deficiency of testosterone and an extra X chromosome causes feminization of the body, but the genitals are male. -Intersexuality: >In males: can be due to excess estrogen which affects secondary sex characteristics and cause feminization; testosterone can be converted into estrogen via the enzyme Aromatase found in fat tissue, so in obesity or in the presence of excess fat tissue this enzyme is abundant and accelerates testosterone conversion. >In females: can be caused by excess Androgen being produced by the Adrenal Cortex, which becomes active after puberty and normally is responsible for acne and hair growth in the axillary and pubic region. Excess Androgen suppresses female hormones and affects secondary sex characteristics.-Hyperkalemia: High levels of K+ in the blood, which can prolong repolarization of cells (which delays Action Potentials) and cause heart arrythmias, palpitations, and chest pain. Can be caused by kidney disease and Renal failure, Primary Addison’s (because of Adrenal failure and resulting deficiency of its 3 hormones), or due to ACE inhibitors or alcoholism. Other symptoms include weakness and fatigue, shortness of breath, numbness or tingling in limbs, nausea and vomiting.-Thyroiditis: Inflammation of the Thyroid gland, initially causes Hyperthyroidism but resulting swelling impairs the Thyroid and ends up causing Hypothyroidism. Can be caused by a bacterial or viral infection, or by Hashimoto’s. >Symptoms: (may or may not occur) sweating, fatigue, heat intolerance, diarrhea, anxiety, weight gain/loss, puffy or protruding eyes, dry hair and skin, and tender/painful local inflammation. >Treatment: Hormone replacement therapy with synthetic thyroid hormones, Non-steroidal Anti-Inflammatories (NSAIDs), Radioactive Iodine Therapy. Thyroiditis caused by viral infections are treated with antivirals and NSAIDs (Non-steroidal Anti-Inflammatories) like aspirin, while bacterial infections are treated with antibiotics.-Hashimoto’s: an auto-immune disease where anti-bodies attack the Thyroid gland, resulting in inflammation of the tissue; 80% of cases cause Hypothyroidism (“post-Hashimoto’s Hypothyroidism”), while 20% of cases cause Hyperthyroidism. >Symptoms: increased antibodies in blood, Goiter (enlarged and inflamed thyroid gland, usually very prominent) obesity, symmetric an bilateral inflammation of both lobes of the gland, memory and learning disorders, heart issues, Bradycardia, Hypotension (Primary), fatigue, dry skin and hair, tender local inflammation of thyroid that is painful to the touch. Same treatment as Thyroiditis.-Post-Hashimoto’s Hypothyroidism: causes increased blood levels of antibodies, obesity, memory and learning disorders, cardiovascular issues, Bradycardia, Hypotension, and most of the normal symptoms associated with Hypothyroidism.-Goiter: the abnormal enlargement and inflammation of the Thyroid glands. Can be caused by Thyroiditis, or by an iodine deficiency which inhibits T3 & T4 production, causing the glands to overcompensate with hyperactivity and swelling. Since iodine is necessary for the production of T3 & T4, a deficiency of iodine results in an underactive Thyroid (Hypothyroidism), weight gain, increased heart rate, shortness of breath, heat intolerance. Meds and surgery if needed.-Gestational Thyroiditis: Inflammation and Hyperthyroidism triggered by hormonal changes during Pregnancy; can cause Hypothyroidism instead; is a temporary condition that resolves itself after pregnancy ends (often called “Silent Thyroiditis” for this reason). -Thyroid Cancer: Tumors of the Thyroid gland grow with irregular margins and are usually unilateral (on one gland), though there could be more than one tumor growing on both lobes of the thyroid gland. Tissue is enlarged but tough to the touch when palpated. Depending on what specific cells become cancerous it can result in Hypofunction (hypothyroidism) or Hyperfunction (hyperthyroidism), which can usually be determined by the measuring the hormone levels or considering the patient’s symptoms.-Insulinoma: A tumor on Pancreatic β-cells (which produce insulin), which causes excess production of Insulin. This results in a decrease in blood sugar levels (Hypoglycemia) which can result in Hypoglycemic coma.-Glucagonoma: A tumor on Pancreatic α-cells (which produce glucagon), causing excessive production of Glucagon which increases blood sugar levels (Hyperglycemia) by stimulating the Liver to induce Gluconeogenesis and Glycogenolysis. >Symptoms: Similar to Type I Diabetes, Hypertension and high blood pressure, Renal failure, Nephropathy, Vasculopathy, general tissue damage associated with Hyperglycemia. Some unique symptoms of Glucagonoma includes skin irritation, especially in the axillary and thoracic region, and the patient’s tongue will be dark pink or red.-Hyperglycemia: Normal blood glucose is 70-110mg/dL, symptoms occur above 120 mg/dL, and irreversible damage occurs around 350 mg/dL. Hyperglycemia can increase Insulin production even though it can be caused by an Insulin deficiency/Insulin receptor damage. >Symptoms: -Vasculopathy: destruction of blood vessels which can lead to local bleeding, obstruction of blood vessels, hypertension, and obstructed circulation to organs and tissues. Atherosclerosis can occur, as well as heart disease, Renal failure, and decreased nutrient absorption in GI. -Neuropathy: can damage neuron cells when glucose can’t enter cells, damages the ANS, CNS, and PNS, optic nerves (blindness), Brachial plexus and Lumbosacral plexus damage (motor and sensory disorders in the upper & lower limbs, and difficulties with defecation & urination). -Glucosuria: destroys Nephrons because they can’t reabsorb the excess glucose, resulting in excess glucose in the urine, increased osmotic pressure in filtration tubes (because Nephrons are attempting to dilute the glucose in the urine). This can later result in Polyuria and Proteinuria. -Polyuria: Dehydrates the body in an attempt to dilute the urine, associated with frequent urination, Hypotension, decreased blood volume, decreased Renal filtration (leading to Hypertension), and Renal failure. -Proteinuria: tissue damage in Nephrons caused by glucose results in proteins filtering into the Nephrons and into the urine. -other symptoms: anxiety, nosebleeds, sleep disorders, dehydration, GI and respiratory issues.-Hypoglycemia: blood glucose below 50-60 mg/dL, can cause CNS coma, confusion, heart palpitations, tremors, anxiety, sweating, hunger, nausea, vomiting, blurred vision, headache, irritability, fatigue, dry mouth. >Treatment: Glucagon injection, increased sugar in the diet.-Hypercalcemia: PTH increases blood levels of Ca2+ which causes muscle spasms and random contractions (increased depolarizations, increased heart rate and contractility), vasoconstriction, increased blood pressure (Hypertension). Usually occurs as a symptom of Hyperparathyroidism, but a deficiency in Mg2+ can cause Hypercalcemia as well. Can be treated with Benidipine, a calcium-channel blocker.-Hypocalcemia: Deficiencies of PTH can cause decreases in blood levels of Ca2+, which can result in Osteoporosis, weak bones and muscles, and difficulties with muscle control.-Hyperparathyroidism: excess blood levels of PTH cause Hypercalcemia because PTH binds to bone and removes Ca2+ from them to put into the bloodstream. This can cause Osteoporosis and Hypertension (high blood pressure), weak and brittle bones, headaches, vomiting, and nausea. Can be caused by a tumor on the Parathyroid gland, which may be treatable with surgery to remove the gland (given the cancer hasn’t already metastasized).-Hypoparathyroidism: extreme deficiency in blood serum levels of Magnesium (Mg2+) results in an inhibition in PTH secretion, and PTH deficiency causes vitamin D and calcium deficiencies (Hypocalcemia), which may lead to Osteoporosis and weak bones/muscles.-Hypernatremia: excess Na+ in the blood causes Hypertension (high blood pressure), dehydration, thirst, decreased urination, high heart rate, muscle spasms (increased Action Potential frequency).-Pheochromocytoma: A tumor in the Adrenal Medulla which causes an over-secretion of Catecholamines (Adrenaline/Noradrenaline & Epinephrine/Norepinephrine) >Symptoms: extreme Hypertension, sweating, headaches, heart palpitations, vomiting, nausea, nosebleeds, anxiety, sleep issues, shortness of breath, weight loss and fatigue. >Treatment: surgical removal of cancerous Adrenal gland tissue, Atenolol or Propranolol (β1-blockers), Prazosin (α1-blocker), blood pressure medication and dietary changes, Hormone Replacement Therapy.-Conn’s Disease: “Hyperaldosteronism”, a tumor of specific Aldosterone-producing cells in the Adrenal Cortex that causes an excess in Aldosterone secretion. >Symptoms: Hypertension, headache, vomiting, nausea, sleep issues, nosebleed, Hypernatremia, Hypokalemia, increased bicarbonate (HCO3-), heart palpitations, acidic urine and basic blood. >Treatment: surgical removal of Adrenal gland tissue, Spironolactone (Aldosterone receptor blocker)-Infertility: >Male: causes include sperm structure, hormones present in semen, Testosterone deficiency, excess Estrogen, damage to Leydig cells, deficiency of LH (which causes Testosterone deficiency and decreased sperm production called “Aspermia”), deficiency of FSH, excess Prolactin. >Female: causes include excess Prolactin which suppresses Estrogen and Progesterone into a deficiency, causing irregular menstruation and ovulation, deficiency in FSH affects development of ovum and follicles, and deficiency of LH inhibits ovulation.-Cushing’s Syndrome: a tumor, infection, or auto-immune issue in the Adrenal Cortex, anterior Pituitary gland, or the Hypothalamus (depending on primary or secondary), that leads to an over-secretion of 3 hormones: Aldosterone, Cortisol, and Androgen. This is an Adrenocortical excess of peripheral hormones. -Primary Cushing’s: Typically caused by a tumor in the Adrenal Cortex which causes and increase of these 3 peripheral hormones, which sends feedback to the anterior Pituitary gland and Hypothalamus, causing a decrease in ACTH and CRH central hormone secretion. The tumor is usually able to be removed with surgery. Other causes of Primary Cushing’s include irritation or damage of Adrenal gland tissue as a result of manipulation during surgery, bacterial infection, or an autoimmune condition. >Symptoms associated with excess Cortisol: “Moon face” with localized fat displacement in the face and torso, combined with thin limbs (since Cortisol breaks down muscle proteins), Hyperglycemia, increased systolic/diastolic blood pressure, hypertension, weak immune system. >Symptoms associated with excess Aldosterone: Hypernatremia, Hypokalemia, headache, vomiting, sleep issues, nosebleeds, local bleeding and/or internal hemorrhage (because of excess Na+), inflammation, hypertension, vertigo >Symptoms associated with excess Androgen: facial hair growth in females, infertility in females due to decreased levels of sex hormones like estrogen (which are being suppressed by excess Androgen), increased testosterone as a result of suppressed estrogen, irregular menstruation and ovulation, called “Amenorrhea” (irregular/absent menstruation). -Secondary Cushing’s: Caused by an infection or issue with the anterior Pituitary (or Hypothalamus), which causes an increase in ACTH or CRH (which then increases ACTH), which increases the production of the 3 peripheral hormones from the Adrenal Cortex. Symptoms are the same as Primary.>Treatment for both: medication for hypertension/high blood pressure, ACE inhibitor, Aldosterone blockers (Spironolactone), surgical removal of any tumor tissue, antibiotics for infectious causes, immunosuppressants for autoimmune conditions. >To make a Differential Diagnosis between Primary and Secondary: -Primary: there is an INCREASE in the 3 peripheral hormones (Androgen, Cortisol, Aldosterone), and DECREASE in CRH & ACTH -Secondary: INCREASE in the 3 peripheral hormones, CRH & ACTH-Hyperthyroidism: Overproduction of T3 & T4 in the Thyroid. -Primary Hyperthyroidism: cause originates in the Thyroid gland, such as in Grave’s Disease, an autoimmune disorder where IgG antibodies recognize TSH receptors on Thyroid follicle cells and causes them to proliferate abnormally, resulting in overproduction of T3 & T4 and a DECREASE in TSH & TRH. Excessive T3 & T4 causes increased metabolic rates, an increase in sensitivity at α1 and β1 receptors for Norepinephrine binding, increased heart rate, and increased O2 consumption. This can also be caused by a tumor or other condition that irritates the tissue. >Symptoms: Exophthalmia (protruding “bug” eyes) and Periorbital Edema (puffiness around the eyes) both caused by IgG antibody infiltration into the tissues, heart palpitations and tachycardia, Hypertension, anxiety, oily skin and hair, sleep issues, persistent feeling of being warm/hot, excessive sweating, weight loss due to high metabolism (weight loss may be extreme), swollen and enlarged Thyroid glands, easily irritated and/or easily excitable or nervous behavior (due to CNS stimulation). >Treatment: Medication (antithyroid agents or beta-blockers), radioactive iodine, or surgical removal if the condition is extreme or cancerous. -Secondary Hyperthyroidism: cause originates in the anterior Pituitary gland and/or in the Hypothalamus, can be due to a tumor, infection, or autoimmune condition. >Symptoms: same as Primary except for the addition of infertility (due to Prolactin increase), and an irregular menstruation cycle >Treatment: Since cause is different the treatment is different, surgical removal of tumor if cause is cancerous (in Pituitary or Hypothalamus), or antibiotics if the cause is infectious, antithyroid agents and beta-blockers -How to make a Differential Diagnosis: >Primary: blood tests reveal DECREASED TSH and TRH but INCREASED T3 and T4 >Secondary: blood tests reveal INCREASED TSH, TRH, T3, T4, and Prolactin (increased by TSH)-Hypothyroidism: Decreased levels of T3 & T4 and INCREASED TSH & TRH, many symptoms are the extreme opposite of what is seen in Hyperthyroidism. >General Symptoms: slowed speech, impaired memory, decreased mental capability, and somnolence (extreme drowsiness, and prolonged periods of sleep), weight gain & obesity, Hypotension, Bradycardia and other heart conditions that can become severe enough to result in heart failure, persistent feeling of being cold, dry skin and hair-Primary Hypothyroidism: “Adult onset Hypothyroidism” Excess TRH stimulates excess Prolactin secretion, which suppresses sex hormones (especially estrogen in females, leading to irregular menstruation and ovulation, and eventually infertility) >Specific Symptoms: memory issues but no reduced mental capacity but may present with a learning disorder, sleep issues, obesity, Bradycardia and Hypotension, lack of motivation, irregular menstruation/ovulation or reduced sperm production (Aspermia), Testosterone deficiency (due to increased TRH->increased Prolactin->suppression of sex hormones), infertility in male & female patients. -Secondary Hypothyroidism: “Adult onset Hypothyroidism” originates in anterior Pituitary or Hypothalamus, usually caused by a deficiency in TSH and/or TRH.-Congenital Hypothyroidism: develops in newborn babies due to thyroid hormone deficiencies (hypothyroidism) in the mother, causing stunted mental development, stunted bone growth, cardiovascular disorders, obesity, thin & dry skin, hair and nails, and later in life it results in short stature, infertility, and speech and learning disabilities. -Addison’s Disease: “Hypocortisolism”, an Adrenocortical insufficiency of all 3 hormones: Aldosterone, Cortisol, and Androgen, which causes feedback to increase central hormones CRH and ACTH -Primary Addison’s: A deficiency of 3 Adrenal Cortex hormones due to tumor cells in the Adrenal tissue or due to irritation/destruction of Adrenal Cortex tissue. Can also be autoimmune or congenital. >Symptoms: Hypotension (low Aldosterone), Hyponatremia and Hyperkalemia (from low Aldosterone) which both contribute to cardiovascular disorders (arrythmias) and muscular disorders, Hypoglycemia (low Cortisol), loss of body hair (especially in females) due to Androgen deficiency, acidic blood (high [H+] levels), weakened immune system and inflammation (low Cortisol) >symptoms unique to Primary: Hyperpigmentation of lips, face, skin, nails, buccal (inner cheek) tissue, and palmar/dorsal regions of hands due to deficiency of the 3 peripheral hormones in the Adrenal Cortex, which induces feedback to the anterior Pituitary gland to increase CRH and ACTH (central hormones) causing stimulation of the Anterior & Intermediate Pituitary gland to secrete Pro-Opiomelanocortin (POMC), which stimulates secretion of Melanocyte Stimulating Hormone (MSH) that then stimulates excessive production of pigment cells (melanocytes) in the skin and areas not exposed to sunlight, and also increases ACTH and Endorphins. >Treatment: Hormone Replace Therapy, surgical removal of tumor if cancerous, antibiotics if cause is infectious, immunosuppressants if cause is autoimmune -Secondary Addison’s: Origin of disease is found in the anterior Pituitary gland or in the Hypothalamus, and can be caused by an autoimmune condition, a tumor, infection, and/or tissue inflammation/damage. Results in decreased CRH and ACTH, which causes a decrease in all 3 peripheral Adrenal Cortex hormones. >Symptoms: Because of the decrease in CRH and ACTH, NO HYPERPIGMENTATION occurs here, but other symptoms of Primary are the same.>Treatment: same as in Primary Addison’s-Type I Diabetes: An autoimmune disease where antibodies destroy Pancreatic β-cells (which produce insulin) which results in the insulin deficiency characteristic of Type I Diabetes. Since Insulin is important for intracellular uptake of glucose, the Insulin deficiency leads to Hyperglycemia (given there is no issue with glucose reabsorption from GI). Over time, Hyperglycemia destroys blood vessel walls (vasculopathy), resulting in tissue damage, Atherosclerosis, and local bleeding in any affected areas: >in Cardiac tissue it can cause Heart disease, which can lead to myocardial infarction >in Renal tissue it can lead to Nephropathy, hypertension, and Renal failure >in nervous tissue it can lead to Neuropathy/Polyneuropathy in the central (CNS), peripheral (PNS), and autonomic (ANS) nervous systems. Neurons starve because they can’t uptake/utilize glucose, which causes nervous tissue destruction. This can lead to Optic Nerve (CN II) damage which leaves the patient at risk for blindness, and peripheral nerve damage in the Lumbosacral Plexus or Brachial Plexus may lead to motor or sensory disorders. -If blood glucose levels rise above 300 mg/dl, patient can also develop Glucosuria (glucose in urine). Glucose in the urine increases osmotic pressure in nephron filtration tubes, causing the tubes to absorb more H2O, leading to Polyuria (frequent urination). Polyuria can decrease blood pressure and blood volume as it dehydrates the patient, causing extreme thirst (Polydipsia). Over time the glucose destroys tissue (Nephropathy) and leads to decreased Renal Filtration Rates, Hypertension, and Edema.-Ketoacidosis can also develop in patients as the body breaks down fatty acids into acidic ketone bodies as alternative fuel generation (in the absence of intracellular glucose), resulting in decreased pH in the blood (acidic blood). This can cause ketonuria (ketone bodies in the urine) and a CNS coma. >Treatment: periodic insulin injection (intravenous or subdermal), no oral insulin supplementation because insulin protein is degraded in the GI. Insulin introduced into the bloodstream allows cells to uptake glucose for consumption, and as a result blood pH should increase back to neutral pH (as the cells stop generating ketone bodies in favor of glucose). Weight loos and dietary changes are recommended to relieve symptoms.-Type II Diabetes: cause is genetic, a defect in the cell-surface Insulin receptor structure that makes it resistant to Insulin binding, meaning its ability to uptake glucose is compromised. Symptoms are similar, but the treatment is different. >Treatment: Exercise and dietary changes are recommended (avoidance of carbohydrates & sugars). Metformin medication decreases blood glucose levels by prolonging Insulin receptor’s exposure to Insulin hormone, which increases the chance Insulin with bind to any remaining functional receptors (facilitates cellular glucose absorption this way).-Steroid Diabetes: NOT caused by Insulin, but instead caused by excess Cortisol, which normally maintains and increases blood glucose levels, so an excessive amount causes Hyperglycemia. -Insipidus Diabetes (Type III): A deficiency in ADH causes disordered salt and water metabolism, resulting in Polyuria (frequent urination) and Polydipsia (extreme thirst) and dehydration, not associated with glucose.-Gestational Diabetes: Occurs as a result of Pregnancy and is normally temporary. This condition mimics Type II, where Insulin receptors become resistant to binding insulin, but it’s not as severe. Light exercise and dietary changes are recommended for the duration of the pregnancy. More frequent check-ups for both mother and fetus with a physician and temporary blood glucose monitor is also recommended. ................
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