Terms : Hide Images
| Coronary Artery Disease | ||
| Cerebral Vascular Accident | ||
| Peripheral Vascular Disease | ||
| Lack of insulin (from the start. Pancreas in not secreting enough insulin) or Insensitivity to insulin (even if body is making it, the body is unable to use it as a tool to take in glucose as an energy source. | ||
| helping us know if patients are telling the truth. When the glucose is in a saturated place, circulating in the body, get stuck on the hg molecule, and does not let go, until it regenerates 3-4 months later. Able to tell the trend of blood sugar for last 3 or 4 months. A hemoglobin molecule with glucose attached, live for 4 months.... acts like a poison, causes basement membrane damage. What the average to be below a 6.5. | ||
| Coronary artery disease; Stroke, piece of plaque or a thrombus. (Also - Hypertension - no longer have the elasticity of the vessels, so the amt of hydrostatic pressure that we read within the vescle is higher. Would not be able to stretch for a higher volume or pressure.) | ||
| Retinopathy; Nephropathy; Neuropathy | ||
| Increases glucose transport, involved in glycogen synthesis (the form in which glucose is stored for future use as fuel) Main problem in diabetes is the metabolism of glucose, but isulin also increases lipid and cholesterol synthesis and Increases protein synthesis, involved in amino acid transport. (diabetics when at this level are dealing with no protein synthesis for repairing of vital organs); ONLY hormone to decrease blood glucose circulating in the blood. | ||
| Counter regulatory hormones (increase the levels of glucose in the blood); glucagon (hormone that stimulates the conversion of glycogen in the liver back to glucose); glucocorticoids (a general class of adrenal cortical hormones that gives rise to or directly produces glucose). ***If pt is under stress, an increased level of glucocorticoids (or used as an anti-inflammatory) is in their body and the amt of glucose in the blood is slightly elevated, the pt may need sm amts of insulin to regulate. | ||
| Fasting glucose greater than 125, Random glucose greater than 200, Fasting glucose between 105 and 125 now called glucose intolerance and believed to be developing diabetes | ||
| Pregnant mother is tested using 1 hr post prandial glucose values; caused by high levels of estrogen and circulating growth hormone. Aat risk for Type II later in life | ||
| Results from a severe lack of insulin (beta cells are not making insulin) caused by loss of beta cells. Related to genetic susceptibility, (two types of) autoimmunity , and environmental factors. | ||
| cause unknown, genetic susceptibility very complex, not autoimmunity, more common in certain ethnicities (Africain American and Pacific Islander). Risk for developing increases 10X with (morbid) obesity. | ||
| Counter regulatory issue, secondary to glucocorticoid steroid usage, causing higher circulation of glucose | ||
| (maturity onset diabetes of youth), a subset of type II except normal to underweight, an autosomal dominant disease. (used to only see in young children). | ||
| Formerly called IDDM (insulin dependent DM), juvenile onset; Lack of insulin - destruction of islet cells - believed to be autoimmune; Until recently thought that it developed rapidly - usually rapid symptomatic onset in children - but in some people may be a chronic inflammation that finally reaches symptomatic stage; 80 - 90 % of islet cells destroyed when symptomatic; Increased levels of glucagon (the hormone secreted by alpha cells in the pancreas that increase the concentration of glucose in the blood by stimulating the conversion of glycogen in the liver to glucose) | ||
| Stimulate pancreas to procude more insulin and helps body utilize it. (not usable by Type I) | ||
| Formerly called - adult onset, NIDDM (noninsulin dependent DM). Body is still making insulin, just not enough or body can't utilize it. Combination of insulin insensitivity and weak secretion (need a hypoglycemic pill); Morbid OBESITY (80%); Genetic predisposition 90% concordance in identical twins; Now appearing in children (processed food) | ||
| Polyurea (urine), polydypsia (thirst), polyphagia (hungry) | ||
| from glucose spilling from blood damaging the glomerulous leading to glucose in the urine and osmotically pulling water with it | ||
| because they lose BV due to polyuria | ||
| Insulin needed to transport glucose into cells except those in brain, kidney and RBC - other cells are starving for this carb; Cells starved of glucose in cells because they can't break it down, metabolize fat instead *hard to do ) ketones are by product of fat metabolism | ||
| metabolic acidosis (byproduct of the breakdown of fat) from ketone production, (glucose levels 300- 750 mg/dl) mostly in Type 1, rare in type 2. First able to catch Type I in this state. Where they metabolize fat to fuel their body, to the point were ketones cause metabolic acidosis (Kuesmal Breathing, expelling CO2, smells like juicy fruit.) Blood sugar get to a chronically high state. | ||
| very high glucose (600- 2000mg/dl) osmotically pulls, still have the ability to burn carbohydrates so eludes fat breakdown; type 2, rare in type 1. Is easy to overlook | ||
| Fluid and Electrolyte loss from osmotic diuresis esp K, Na, PO4. Osmotic pull of glucose, is causing isotonic fluid loss | ||
| low body K (may have normal serum K, but may have dangerously low levels inside the cell); When treated with insulin, K moves back into cells, can become hypokalemic! But for a short period this is ok. | ||
| low body K (may have normal serum K; Fruity breath from acetone odor (results from poorly oxidized fat because fat needs glucose to oxidize properly); Kussmaul breathing metabolic acidosis (blowing off CO2 to compensate!); Hyperglycemia | ||
| Without intervention can enter into a coma. Uncommon but significant complication with high mortality. Occurs most often in compromised individuals; (elderly who have co-morbidities [infections, cardiac or renal diseases]); Osmotic diuresis from increased serum glucose (>600 mg/dl)(Lack of thirst and/or functional inability to obtain H2O) ; Hyperosmolality combined with dehydration creates(Confusion, Lethargy, fever, hypotension, shock); Nonketotic because in Type II diabetes, there is enough insulin to prevent fat and protein catabolism; Carefully rehydrate - can cause cerebral edema if too rapid | ||
| Will alter ability to utilize cholesterol; Hyperlipidemia with damage to basement membrane - atherosclerotic diseases, usually microangiopathy (sm vessels show pathologies first); Retinopathy - microaneuryms & hemorrhages; Atherosclerosis CAD, PVD, CVA; Neuropathy, loss of sensation in extremities; Renal Cells with Basement membrane changes from nephrotic syndrome (protein loss in urine)-eventual renal failure | ||
| Exercise in Type II; Weight loss in Type II (even 10 lbs. can improve glucose control); Diet - foods with low glycemic index can decrease post prandial rise in glucose | ||
| Insulin | ||
| Oral compounds that: Increase insulin secretion; Increase insulin sensitivity in muscle. Insulin - after years, islet cells function is depleted then insulin treatment necessary | ||
| Fever, stress, infection, pregnancy, surgery, and hyperthyroidism | ||
| Liver disease, hypothyroidism, vomiting, and renal disease | ||
| excess insulin | ||
| CNS can only use glucose for metabolism - symptoms include pallor, tremor, anxiety, tachycardia, palpitations, diaphoresis, headache, dizziness, irritability, fatigue, poor judgment, confusion, visual disturbances, hunger, seizures, coma when glucose 45 - 65 mg/dl; Give orange juice, sugar, or IV dextrose, cake icing! | ||
| Cushings diesese is very rare, it happens when there is a disease stte in the adrenal glad; Cushings syndrome is caused by the administration of steriod glucococorticoid hormone. | ||
| glucocorticoids, mineralocorticoids, sex hormones | ||
| Responsible for secondary sex characteristics | ||
| used in conjunction with other hormones. the most potent one is aldosterone | ||
| Control and regulate...stress and anti-inflammatory response; aldosterone renin angiotensin (blood pressure, fl retention + secrestion); Sex hormones and the hypothalamic - pituitary - gland axis with negative feedback (HPA Axis) | ||
| Permissive Actions -ADH, Epi, estrogen; Increase hepatic gluconeogenesis and glycogen breakdown; Increase protein catabolism (break down protein); Increase lipolysis; **Suppresses Inflammation and immune system (why we use it as a drug Cushings Syndrom; Critical for stress response (not meant to be present at all times); Can cause insomnia, even psychosis; Inhibits osteoblasts (causes bone resorption) | ||
| A hormone that increases the reabsorption of sodium ions and water and the release (secretion) of potassium ions in the collecting ducts and distal convoluted tubule of the kidneys' functional unit, the nephron. This increases blood volume and, therefore, increases blood pressure. | ||
| is the process by which osteoclasts break down bone[1] and release the minerals, resulting in a transfer of calcium from bone fluid to the blood | ||
| ACTH excess (Pituitary adenomas); Adrenal neoplasms; **Administration of Glucocorticoids (80%) | ||
| Due to increased protein catabolism, thin skin, big trunk, atrophy of limb muscles, increased bruising, purple straie (stretch marks); Due to lipid deposition, pendulous abdomen, moon face, buffalo hump | ||
| Poor wound healing (L-shaped wounds); Glucose intolerance or diabetes; Hypertension; Osteoporosis due to bone breakdown. Psychiatric Disturbances | ||
| aimed at radiologic or surgical removal of ACTH secreting tissue (adrenals may be totally removed, then there is need for pharmacologic replacements); lowiiering the amt of glucocorticoid drugs | ||
| Glucocorticoid Deficit; Causes -autoimmune or disruption of feedback regulation; (there is also mineralocorticoid loss), less secondary sex characteristics. | ||
| Hyperkalemia (K is saturating inside of the cells and spilling into the blood stream), hyponatremia ( battle for positive charge in the bloods stream is won by K+); Hypotension and shock (any stressor can cause because no flight of flight response); Nausea, vomiting, abdominal tenderness; Weakness, anorexia, weight loss; Fever; androgenic hormone loss (male hormones) | ||
| Characterized by increased bronze pigmentation; Decreased tolerance to physical and emotional stress (don' have stress response); Weakness, decreased endurance, anorexia, dehydration, weight loss, GI disturbances, salt cravings (hyponatremia), anxiety, depression | ||
| Long term Glucocorticoid and mineralocorticoids; Adequate fluid intake; Control of electrolyte balance; Diet high in complex carbs and protein (normalize blood sugar) | ||
| process that produces heat or energy or that increases the consumption of oxygen | ||
| Calorigenic (Increase basal metabolic rate); Normal development of CNS; Normal growth & development; Controlled by hypothalamic pituitary axis, TRF(Thyroid Releasing Factor), TSH | ||
| Lack of CNS development... severe limitation of mental functioning; Congenital hypothyroidism - cretinism | ||
| (due to lack of iodine) - if there is a disconnect of endocrine feedback mechanism, the thyroid would actually grow. If the body doesn't feel like it is having enough thyroid hormone, it would make the gland bigger. If a person has a lack of iodine in their diet, which is important in the development of regular levels of thyroid hormone. | ||
| Child - severe limitation of mental functioning at birth- cretinism; Adult - myxedema (look puffy) - causes: autoimmune, lack of iodine (goiters), radiation to chest, aging | ||
| Slow reflexes, mentation, decreased motor activity; Cold intolerance; Weight gain; thick puffy skin...Myxedema (literally means mucous swelling; - Constipation (decreased GI motility); Thyroid Nodules | ||
| thyroid hormone and use iodized salt | ||
| Hyperthyroid | ||
| autoimmune - antibody stimulates TSH receptor | ||
| Graves Disease (autoimmune - antibody stimulates TSH receptor); Thyroid adenoma | ||
| Weight loss, tachycardia (atrial arrhythmias), heat insensitivity, diarrhea (not enough time for absorption, sweating, nervousness, insomnia; Unique to Graves - exopthalmos | ||
| Abnormal protrusion of the eyeball or eyeballs | ||
| Treat with antithyroid drugs or subtotal thyroidectomy |
