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wvc endo lecture
wvc endo lecture winter 2011
| Question | Answer |
|---|---|
| 2010 statistics for DM | Age 20 or older=25.6 million diagnosed; Age 65 or older=10.9 million diagnosed; Men 13.0 million aged 20 or older diagnosed; Women 12.6 million aged 20 or older diagnosed;Estimated diabetes costs in the US, 2007 |
| Diabetes is a disease in which the body does not produce or properly use what? | insulin |
| Insulin is produced in which cells of the pancreas? | Beta cells (islet of Langerhans) |
| Glucagon is produced by which cells in the pancreas? | Alpha cells |
| What is the action of insulin? | allows glucose to enter the cells |
| Type 1 diabetes vs type 2 diabetes | Refer to Table 67-4, Page 1471 |
| Without insulin, glucose builds up in the blood, causing hyperglycemia. | This can lead to fluid and electrolyte imbalances which leads to the classic symptoms of diabetes. |
| Pre Diabetes | glucose level > 100-125 on 3 checks; also increased risk of developing heart disease and stroke |
| Type 1 diabetes | Genetic predisposition; Environmental exposure; Age of onset usually under age 30. (peak occurrence at 10-12 years of age) |
| Abrupt onset of signs/symptoms of hyperglycemia | 3 P’s (Polyuria; Polydipsia; Polyphagia) |
| 3 P’s | (Polyuria; Polydipsia; Polyphagia) |
| Other characteristics of type I DM | hypertension; dislipidemia; if untreated they will end up with DKA |
| Treatment of type 1 dm | insulin; diet and exercise, minimize associated risk factors |
| Type 2 diabetes | Insulin resistance & or Decreased insulin secretion; Excess production of glucose from the liver because of reduced insulin; normally age 30 or above, but is being seen in kids; Genetics can be risk factor; increased Weight is correlated w/ occurrence. |
| Signs/symptoms of type II DM | 3 Ps (Polyuria; Polydipsia; Polyphagia); slower progression because small amount of insulin being produced (this can delay diagnosis). |
| Treatment of type II DM | diet, exercise, oral hypoglycemic, insulin; |
| Indications for testing for type II DM (Refer to Table 67-5, page 1473 for more info) | 45 years of age or older/ BMI > 25/ family history of DM/ inactive/ members of high risk ethnic group/ delivery of a child weighing more 9 lbs/ hypertensive/ HDL < 35/ triglyceride level 250/ ploycystic ovary syndrome/ history of vascular disease. |
| Clinical manifestations of diabetes of type II DM | Polyuria; Polydipsia; Polyphagia |
| Diagnosing diabetes | Blood glucose levels are used to diagnose diabetes. Fasting Plasma Glucose Test (FGT, FBS) x 3 >126; Oral Glucose Tolerance Test (OGTT)@ 2hrs 140-199 (pre-diabetic) @2hrs >200 (diabetes); Glycosylated Hemoglobin Assay (HbA1c) <5.5 (non-diabetic) |
| Urine test for DM and kidney function | Urine testing for ketones ; Tests for renal function; Urine test for glucose |
| Oral Glucose Tolerance Test (OGTT) results | @ 2hrs 140-199 (pre-diabetic) ----\\ @2hrs >200 or higher (diabetes) |
| OGTT for Pre-diabetes diagnosis | @ 2hrs 140-199 (pre-diabetic) |
| OGTT for diabetes diagnosis | @2hrs >200 (diabetes) |
| Frequency of HbA1c testing | 2x year if well controlled and 4x year if poorly controled |
| Normal glucose | 70-99 |
| Fasting Plasma Glucose diagnosis for DM | (FGT, FBS) x 3 >126 |
| Pre diabetes | 100-125 on 3 consecutive FBS checks |
| Normal HbA1c | < 6.0 |
| When should you check for ketones in urine | when the blood glucose is greater than 300, or if N& V, cramping, sick with cold or flu, lethargy, thirsty, dry mouth, fruity breath; decreased LOC; |
| Tests for renal function | testing for microalbumin/ BUN 7-21 (dehydration) / creatinine 0.5-1.2 (renal function) |
| Glucagon cascade | Glucagon acts on the liver to breakdown glycogen into glucose |
| Increased risk for serious and sometimes life-threatening complications associated with DM | Macrovascular & microvascular changes occur & may lead complications as a result of poor tissue circulation & cell death; Cardiovascular & Cereborvascular Disease; |
| Associated complications with DM | heart disease, cerbrovascular disease, peripheral vascular disease |
| High BP= | 130/80 or greater |
| Cardiovascular disease Risk factors associated with DM | hyperglycemia, hyperlipidemia, HTN, clotting abnormalities/ problems with peripheral vasculature |
| Complications from atherosclerosis in clients with diabetes is very common | Diabetics have a higher incidence of heart failure. |
| Cerebrovascular disease Risk factors associated with DM (2-4 time higher in people with DM) | hyperlipidemia, HTN, CAD, PVD, smoking & drinking gives diabetics have a higher risk for stroke…Elevated blood glucose levels at the time of stroke are associated with greater brain injury. |
| Kidney disease associated with DM | DM is the leading cause of kidney failure; In people with type 1 diabetes, therapy that keeps blood glucose levels as close to normal as possible reduces damage to the kidneys by 35-56% |
| Increased pressure from HTN in the kidney vessels causes damage to the kidney in many ways. | blood vessels become leaking in glomerulos; because of the leaking larger particles pass through and form deposits in the kidney tissue. The deposits narrow the vessels, decreasing oxygenation leading to cell death. |
| Why would protein in the urine be indicative of kidney disease? | protein is suppose to remain in filtrate. |
| Nervous system disease Diabetic Neuropathy (60-70% of people w/ diabetes have mild to severe forms of nervous system damage) | Neuropathy: progressive deterioration of nerves, result in loss of function. DM neuropathy can be focal (limited to a single nerve or group. Leads to nerve damage or nerve death) or diffuse neuropathy slow onset, effects both sides, involve motor & sensor |
| Foot assessment for DM (PCP does foot check yearly) | history of ulcers or amputation; assess for dry, cracked skin, ulcers; thickened, long ingrown nails; assess for deformity (corns, toe contractures, bunions); limited ankle & toe ROM; numbness; & 10 point monofilament testing on each foot. |
| Foot care for DM | check feet daily, good fitting shoes; lotion, no bare feet; wash & dry, daily; inspect shoes; clean nails; moisture absorbing powder; monitor gait; monitor hydration of feet; monitor for edema; monitor for arterial insufficiency. |
| Amputations associated with DM | More than 60% of nontraumatic lower-limb amputations occur in people with diabetes; The rate of amputation for people with diabetes is 10x higher than for people without diabetes. |
| Eye and Vision complications | Legal blindness is 25x more common in diabetic patients; After 20 years of diabetes, nearly all clients with type 1 diabetes and 60% of those with type 2 diabetes have some degree of retinopathy. |
| Nonproliferative diabetic retinopathy (NPDR) Characteristics | structural abnormalities of retina vessels, no new growth of blood vessels. Areas of poor circulation, edema, hard fatty deposits in the eye, retinal hemorrhage. Micro aneurism, leaking fluid & blood into retina. Causes more edema & hard exudates. |
| Nonproliferative diabetic retinopathy (onset) | develops slowly over time and rarely causes blindness.; Clients with severe NPDR have a 50% chance of developing proliferative diabetic retinopathy. |
| Proliferative diabetic retinopathy (PDR) Characteristics | Growth of new retinal blood vessels(poor circulation); Retinal cells secrete growth factor; New vessels are thick, fragile, and prone to bleeding; Leads to eye hemorrhage. Fibrous tissue bands develop, along with new blood vessels causing retinal detachme |
| Consideration for the older adult associated with DM | Older client w/ diabetic retinopathy has the additional effect of visual changes that occur with aging. Selfcare deficits may arise & be more seriously affected than those of a younger client w/ DM. Website review |
| Sexual dysfunction associated with DM | Men with diabetes are 2x as likely to experience erectile dysfunction as men without diabetes; Women with type 1 diabetes are twice as likely to experience prevalence of sexual dysfunction compared with women without diabetes. |
| Diabetic ketoacidosis (DKA) Occurs in type 1 diabetics | Illness, surgery, extreme stress elevates hormones (glucagon); Glucose moves from muscle to help meet demand of starving cells; Glucagon converts glycogen to glucose in liver r/t increased demand by cells; After glycogen is depleted, the liver converts |
| Signs/symptoms of DKA | blood glucose greater than 300; polyuria; polydipsia; weak & lethargic; abdominal cramping nausea and vomiting, blurred vision, low bp, tachycardia. |
| It is imperative that the s/s of DKA be recognized early | as this condition can lead to death quickly. |
| Hyperglycemic, Hyperosmolar, (Non-ketotic) Syndrome (HHS) | Complication of type 2 diabetics; Same pathophysiology as DKA except there will be no acidosis; FSBS WILL OFTEN BE GREATER THAN 800. (There is enough insulin to prevent ketones from building, glucose levels continue to rise) |
| Signs/symptoms of HHS | Onset for HHNS is gradual; Hyperglycemia, extreme dehydration;. polyuria, polydipsia; hypovolemia; decreased electrolytes, mental status changes looks like a stroke. no acidosis/ no fruity breath |
| At what glucose level would you expect a client to exhibit s/s of hypoglycemia? | 60 or below (depends on the patient) |
| Signs/symptoms Mild Hypoglycemia | sudden tremors, palpations, diaphoresis, hunger |
| Signs/symptoms Moderate Hypoglycemia | HA, change in mood, irritability, inability to concentrate, drowsiness, may have impaired judgment, slurred speech |
| Severe Hypoglycemia | unresponsive and possible seizure |
| Treatment of hypoglycemia | Rules of 15….4-6 oz of juice and wait 15 min; do another finger stick, assess… 4-6 oz of juice wait 15 min…. check FSBS & give complex carb and protein. |
| What would the intervention be for someone who is unresponsive? | glucagon injection or IV dextrose |
| Sick days with DM | During illness FBS levels rise; eat Food & drink; Pt should stay on normal meal plan; Push non-caloric liquids; Take in normal amount of cal. by eating easy-on-the-stomach foods; Aim for 50g carbs/ 3-4 hours. Check for ketones & FSBS every 3-4 hours. |
| Guidelines for exercise for DM patient | Check FSBS before exercise (if > 250 or ketones don’t exercise); Check urine for ketones (type 1); complex carb snack before exercise; drink lots of fluid before, during & after exercise. Carry ID, wear properly fitting footwear. see chart pp 1497 |
| Strongest risk factor associated with obesity | obesity of two parents. |
| Low insulin will stimulate | hepatic glucose production |
| ADA clinical practice guidelines | HgA1c (good control 2x year/ poor control 4x year);LDL/HDL; Dilated eye exam(yearly); B/P monitoring (every 6 months); Foot exam (every 6-12 months) |
| Metabolic Syndrome | A cluster of conditions that occur together. HTN; elevated blood sugar (100 or greater) elevated cholesterol, triglyerdyes, low HDL, high LDL, |
| Metabolic syndrome Risk factors | Age; Race; Obesity (BMI>5) (> 40 in waist circumference in men/ > 35 in. women) History of DM (type 2 or gestational DM); Other diseases (HTN or CAD or polycystic ovarian syndrome) (use of anti-psychotics drugs/ especially atypical seraquil/ zyprexa ) |
| Signs/Symptoms/ Diagnosing of metabolic syndrome | HTN (>130/80); elevated blood sugar (over 100), elevated cholesterol, triglyerdyes > 150, low HDL (<40 men< 50 women) , high LDL |
| Treatment of metabolic syndrome | Exercise (30-60 min of moderate exercise/ check with doctor) ; Lose weight (losing as little as 5-10% of body weight will reduce risk for diabetes); at healthy (low glycemic diet); Stop smoking (increases insulin resistance) |
| Minimum days per week for exercise for diabetics | 3 days per week |
| Onset | length of time when in begins to effect blood sugar |
| Peak | when is the insulin is at maximum strength |
| Duration | how long it will last. |
| Rapid acting | begins in 15 min (lispro) |
| Regular or short acting | onset is about 30 min (R) |
| Intermediate-acting | onset is about 2-4 (NPH) |
| Long-acting | onset is 2-4 hours (Lantus) |
| Syringes | use U-100 insulin with U-100 syringes/ 100 units syringes = 1ml / 30 unit syringes = .3ml 50units syringes = .5 ml (match the U-100 on bottle with U-100 on bottle regardless of syringe size) |
| Basal insulin | insulin that we are secreting all day long, to keep glucose balance (keeps us even throughout day..normally NPH or Lantus) |
| Prandial insulin | the insulin that covers the meal, given after the meal and the carb count is completed (normally lispro) |
| Compensatory insulin | compensates for a high blood sugar (often regular insulin or lispro is used ) |
| Insulin Strength | Most commonly used strength in the U.S. is U-100 |
| FBS | fasting blood sugar |
| FSBS | finger stick blood sugar |
| Check blood sugar record before | giving oral hypoglycemic or insulin |
| Injection sites need to be | assessed and rotated |
| Lipoatrophy | loss of fat tissue around injection sites. |
| Lipohypertrophy | increased swelling of subq tissue at injection site |
| A1c target | < 6.0 |
| How many lobes does the thyroid gland have? | 2 |
| Function of the thyroid gland | Thyroid hormones are involved in the metabolism of every cell in the body. Takes iodine and converts it to thyroid homones |
| Two thyroid hormones, what are they? | T3 |
| Thyroid cells are the only cells in the body which can absorb | iodine. |
| The normal thyroid gland produces about | 80% T-4 and about 20% T-3. |
| Thyroid hormone strength | T-3 possesses about 4x the hormone strength as T-4. |
| Thyroid hormone production cascade | (from hypothalamus) TRH> (from anterior pituitary TSH> (from thyroid gland) T3 & T4 |
| The thyroid gland will become enlarged under the influence of high TSH – What is this called? | goiter (part of hypothyroidism) |
| In Grave’s disease, goiter is caused by | a unique antibody called “thyroid stimulating antibody” which stimulates the thyroid cells to grow larger and produce excessive amounts of thyroid hormone. |
| In hypothyroidism, goiter is related to | the high levels of TSH secretion. TSH binds to thyroid cells causing the gland to enlarge. |
| Serum TSH Levels | 0.4-4.2 |
| Free T-4 | 0.8-2.8 |
| Free T-3 | 260-480 |
| Non-blood test for thyroid disorders —radioactive iodine uptake test | high uptake hyperthyroidism / low uptake hypothyroidism |
| Euthyroidism | normal thyroid function |
| Hyperthyroidism | A state in which too much thyroid hormone is produced; Diagnosed most often in puberty, during pregnancy, or between ages 30-50; 7-10 times more common in women. |
| Signs/Symptoms hyperthyroidism | heat intolerance, weight loss for no reason; frequent bowel movements/ diarrhea; change in vision (Grave’s); fatigue & muscle weakness; changes in menses; may have problem w/ fertility; insomnia; anxiety; fine tremors; may or may not have goiter. |
| Grave’s disease | Autoimmune disorder; The autoantibodies stimulate thyroid growth (antibodies similar in action to TSH except they have a stronger and longer effect) increasing vascularity and hyper-secretion of thyroid hormones. |
| Signs and symptoms of Grave’s disease | Hypermetabolic state; ½ of patients develop exophthalmos. Visual changes will be noted first with exophthalmos, agitation, nervousness, tachycardia & palpitations, you may feel a thrill or auscultate a bruit over the thyroid. |
| Treatment for Hyperthyroidism/Grave’s Disease | Primary goal: to suppress the secretion of thyroid hormones; Antithyroid medication suppress production of T4 (PTU); OR destruction or removal of part of the thyroid gland. |
| Iodine Therapy in hyperthyroidism | excessive amounts of iodine blocks the release and decrease vascualrtiy and size of gland (use prior to surgery to get them back to euthyroid… 10-14 day usage) |
| Radioactive iodine therapy | post surgically to albate/ kill the thyroid cell to reduce thyroid production. Thyroid gland picks up the radioactive iodine & iodine kills off the cells that produce thyroid hormones. Improvements in thyroid levels are seen in 2-4 weeks. |
| Subtotal Thyroidectomy | partial removal of thyroid gland (assess voice for swelling in vocal cords, stridor or constriction of airways, hemorrhage) |
| Total thyroidectomy | total removal of thyroid gland (assess voice for swelling in vocal cords, stridor or constriction of airways, hemorrhage) |
| Post thyroid surgery | assess airway.. (assess voice for swelling in vocal cords, stridor or constriction of airways, hemorrhage) |
| Thyroid storm | Rare, but potentially fatal hypermetabolic state; Characterized by exaggerated clinical manifestations of hyperthyroidism. |
| Thyroid storm S/S include: | high fever 106’; tachy(150-200 bpm); diaphoresis;A-fib; abdominal pain; N&V, diarrhea; extreme vaso-dilation leading to hypotension (shock); psychosis may be seen; if not treated can lead to cardiac collapse & death can occur within 48 hours. |
| Hypothyroidism | Defect in the thyroid gland. TSH elveted—T3/ T4 low…Unable to produce or release enough thyroid hormone. |
| Most common hypothyroidism s/s include: | fatigue, weight gain, constipation, sensitivity to cold … other S/S are: decreased CO, RR deceased, anemia, |
| Treatment for hypothyroidism | Life-long thyroid replacement medication (T3/T4) levothyroxine is most common thyroid hormone replacement. |
| What would patient teaching for these medications include? | If you feel signs of hyperthyroidism check in with doctor. Do not share hormone replacement therapies. |
| Myxedema Coma | Very low thyroid levels…Rare, but has a high mortality rate; Myxedema coma may cause death; MEDICAL EMERGENCY! |
| Myxedema Coma S/S | low thyroid level, Marked by decreased CO, decreased perfusion, multi organ failure; leads to multi organ failure; bradycardic, reduced LOC. |
| PTH | 10-65 |
| What is the function of calcium? | muscle contraction and bone density |
| Who gets parathyroid disease? | 50,000 people in the US develop parathyroid disease |
| Ca level | 9.0-10.5 (10.2) |
| Phosphorous | 3.0 -4.5 |
| Hyperparathyroidism | An excess of parathyroid hormone (PTH)…calcium level is elevated/ decreased phosphorus |
| Hyperparathyroidism signs/symptoms of this disorder? | Depression weakness, fatigue, muscle cramps, osteoporosis; kidney stones. |
| How is osteoporosis caused by hyperparathyroidism? | pulling Ca from the bone. |
| Surgery: a new technique known as “minimally invasive radioguided parathyroidectomy.” | using a radio-isotope scan to locate tumor, then a probe to remove tumor and gland. |
| Lasix is used in | hyperparathyrodisim (lasix and IV saline increase kidney excreation of calcium) |
| Calctonin | decreases releases of Ca from the bone and increases kidney excretion |
| Hypoparathyroidism | A condition in which the body produces too little parathyroid hormone. Injury to parathyroid gland in surgery is a common cause. |
| Signs/symptoms of hypoparathyroidism | bands or pits around crown of tooth because loss of Ca, spasms, muscle cramps, spasms, trousueas sign, tingling, abdominal pain, chechtovs sign, tetny. |
| Diagnosis and Treatment of hypoparathyroidism | oral calcium and vitamin D for rest of life…high Ca and low phosphrous diet for rest of their life. If there is tentey or life thereating symptoms give Ca via IV. |
| What lab results might you expect for hypoparathyroidism this disorder? | Ca low/ Phosphrous high/ PTH low/ may see change in heart rhythm on ECG |
| Treatment goal in hypoparathyroidism: | To restore the calcium and mineral balance in the body. Oral calciumcarbonate and vit D for the rest of their lives. High calcium, low phosphorus for rest of life. Monitor blood Ca levels. |
| Calcitonin: | Secreted by the parafollicular cells of the thyroid in response to elevated Ca levels. Antagonizes the effects of PTH & Vit D so that Ca continues to be laid down in the bones rather than reabsorbed into the blood. males<19 pg/mL Female: <14 pg/mL |
| Phosphorus: | Approximately 85% of the body’s phosphorus is stored in bones. Serum phosphorus is increased when serum calcium is decreased. ADULTS: 3.0-4.5 mg/dL |
| Calcium: | Calcium concentration is largely regulated by the parathyroid glands. Calcium values should be interpreted in conjunction with results of other tests. ADULTS: 9.0-10.2 mg/dL |
| Parathyroid Hormone (PTH): | Secreted by the parathyroid glands in response to decreased levels of circulating calcium. PTH assists in the mobilization of calcium from bone into the bloodstream. ADULTS: 10-65 pg/mL |
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