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Endrocrinology lec1
G Carlsons DM lecture part one
| Question | Answer |
|---|---|
| Insulin is produced in which cells of the pancreas | Beta cells, in the islets of Lagerhans |
| Diabetes is a disease in which the body does not produce or properly use what | insulin |
| Glucagon is produced by which cells in the pancreas? | alpha cells |
| The hormone glucagon is synthesized and secreted from the | alpha cells (α-cells) of the islets of Langerhans, which are located in the endocrine portion of the pancreas |
| What is the action of insulin | Insulin stops the use of fat as an energy source by inhibiting the release of glucagon. |
| Insulin is a hormone that | regulates carbohydrate and fat metabolism in the body. |
| Insulin causes cells in the | liver, muscle, and fat tissue to take up glucose from the blood, storing it as glycogen in the liver and muscle. |
| When glucose levels fall, insulin secretion stops and glucagon release is stimulated | glucose is released from the cell |
| Glucagon causes release of | glucose from the liver |
| In what order does glucagon cause release of glucose from the liver | fat cells then muscle |
| Without insulin, glucose builds up in the blood | causing hyperglycemia. |
| Glucose build up in the blood can lead to fluid and electrolyte imbalances, which leads to the classic symptoms of diabetes | polyuria, polydipsia, and polyphagia |
| When is someone diagnosed with pre-diabetes | 3 separate checks of glucose plasma are done |
| Pre-diabetes raises the risk of developing | heart disease and stroke |
| Is progression to diabetes inevitable when diagnosed with pre-diabetes | n |
| Type 1 diabetes | Genetic predisposition,Environmental exposure, Age of onset, Peak incidence(during puberty 10-12 yrs) |
| Abrupt onset of signs/symptoms of hyperglycemia | polyuria, polydipsia, and polyphagia |
| Other characteristics of hyperglycemia | HTN, dislipidemia if untreated will result in ketoacidosis |
| Treatment for DM1 | insulin, exercise, diet |
| Define DMII | Insulin resistance, Decreased insulin secretion, Excess production of glucose from the liver |
| Factors in DMII | Age, Genetics, Weight |
| Signs/symptoms of DMII | slow progression to polyuria, polydipsia, and polyphagia |
| Treatment | diet, exercise, oral hypoglycemics and insulin |
| Stress and illness effects blood sugar because | the body releases counter-regulatory hormones cortisol and epinephrine |
| Glucagon tells the liver | to release insulin |
| Define TYPE 1 DIABETES | • Beta-cell destruction leading to absolute insulin deficiency • Autoimmune • Idiopathic |
| Define TYPE 2 DIABETES | • Ranges from insulin resistance with relative insulin deficiency to secretory deficit with insulin resistance |
| clinical manifestations of diabetes | Polyuria, Polydipsia (thirst), Polyphagia(hunger). Polyuria→↑thirst→more polyruia→dehydration and electrolyte imbalances |
| What is used to diagnose diabetes | Blood glucose ( fasting blood plasma three times to confirm)(FBG or FBS) |
| Oral Glucose Tolerance Test (OGTT) | testing over 2 hrs. If OGTT is between 140-199, considered prediabetic, >200 is diabetic |
| Oral Glucose Tolerance Test (OGTT) | testing over 2 hrs. If OGTT is between 140-199, considered prediabetic, >200 is diabetic |
| Glycosylated Hemoglobin Assay (HbA1c) | <5.5. measures how well you are metabolizing glucose over 120 days |
| What increases red blood cell turnover and reduces HbA1c levels | Hemolysis, blood loss, and pregnancy |
| HbA1c testing is recommended at least | 2 yearly in patients who are meeting treatment goals and have stable blood glucose control. |
| How often is HbA1c recommended for patients whose therapy has changed or who are poorly managed | 4 times a year |
| Urine testing for ketones is important especially for | DM1. means you are using your body for energy instead of your food. |
| Ketones in the urine indicate | acidosis |
| When do you check for ketones | if FSBS is >300, N/V, abd pain, if sick w/cold or flu, fatigued, 3 p’s, fruity breath, brian fog |
| Tests for renal functions look for | microablumin, BUN, creatinine (spec to renal), nitrogen |
| Creatinine norms | 0.5-1.2 most important in renal functions |
| BUN normals | 8-21, more indicative of dehydration (If higher than creatinine) |
| Urine test for glucose measure | sugar & specific gravity, used for pg women |
| DM increases the risk for serious and sometimes life-threatening complications. Most die from | end stage renal disease |
| Macrovascular and microvascular changes occur and may lead to many complications as a result | of poor tissue circulation and cell death. |
| Heart disease and stroke account for about | 65% of deaths in people with diabetes. |
| HTN is defined as | 130/80 or above |
| Macrovascular is defined as | heart disease, cerebrovascular & PVD |
| Risk factors for macrovascular disease are | clotting abn, blood vessel problems, hyperlipidemia, HTN, DM, athleroscerosis |
| Risk factors for microvasculare disease are | clotting abn, blood vessel problems, hyperlipidemia, HTN, DM, athleroscerosis |
| Complications from atherosclerosis in clients with diabetes is | very common. |
| Diabetics have a higher incidence of heart failure because it leads to | MI, heart grows →inefficiency→cell death |
| Risk factors cerebrovascular disease are | hyperlipidemia, athleroscerosis, HTN, CAD, PVD, alcohol & cigarrettes↑chance for stroke |
| Higher blood glucose levels at the time of stroke | greater brain injury. |
| If BG is >148=doubles the risk of death from stroke | |
| Hyperglycemia may also worsen | cerebral damage after a stroke. |
| Diabetes 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 causes damage to the kidney, how | the glomerlius becomes leaky, larger particles leak & form deposits in the kidney & in tissues, deposits narrow vessels, ↓oxygenation, →to hypoxia and cell death |
| Why would protein in the urine be indicative of kidney disease | should be filtered not put through |
| Neuropathy is | a progressive deterioration of the nerves that result in loss of nerve function. |
| Diabetic neuropathy can be | focal or diffuse. |
| Focal is | limited to single nerve or nerve group, leads to nerve damage or nerve death, acute in onset |
| Diffuse neuropathies | is generalized, slow onset, effect both sides of body, involves motor and sensory nerves, irreversible |
| Late complications of diffuse | foot ulcers and deformities and is why care is so important |
| Peripheral Sensation Management is | Prevention or minimization of injury or discomfort in the patient with altered sensation |
| Nursing considerations for foot care are to monitor | sharp/dull and/or hot/cold discrimination, paresthesia: numbness, tingling, hyperesthesia, and hypoesthesia & fit of bracing devices, prostheses, shoes, and clothing. |
| Nursing considerations for foot care are to encourage | patient to use the unaffected body part to determine temperatures or use thermometer & to use protective clothing over affected body part |
| The nurse will instruct the patient with foot problems to | monitor position of body parts while bathing, sitting, lying, or changing position; examine skin daily for alteration in skin integrity. |
| The nurse will instruct the patient with foot problems to | monitor position of body parts while bathing, sitting, lying, or changing position; examine skin daily for alteration in skin integrity. |
| Teaching for a DM patient with altered sensations | monitor/protect use of heat or cold; wear well-fitting, low-heeled, soft shoes; √ for objects in clothing/shoes; identify causes of abnormal sensation or sensation changes |
| Foot tests for sensory | filament and tuning fork |
| The rate of amputation for people with diabetes is | 10x higher than for people without diabetes. |
| 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. |
| Characteristics of non-proliferative diabetic retinopathy (NPDR) | structural abn of retinal blood vessels, no new growth of blood vessels, areas of poor retinal circulation, edema, hard fatty deposits & retinal hemorrhage, |
| Microannurisms | burst open and leak fluid into retina, causing more edema & hard excites |
| NPDR retinopathy develops | slowly over time and rarely causes blindness. |
| Clients with severe NPDR have a 50% chance of developing | proliferative diabetic retinopathy. |
| Characteristics of PDR | new retinal BV (cells secrete “growth factor”) New vessels are thick, fragile, and prone to bleeding→eye hemorrhage. Fibrous tissue bands develop, w/new BV →retinal detachment/irreversible vision loss |
| The ability to discriminate between blues, greens, and violets decreases with normal aging. This deterioration of color perception makes | performing visual blood glucose monitoring more difficult. |
| Men with DM1are 2x as likely to experience erectile dysfunction as men without diabetes. Due to | microvascular changes (HTN) |
| Women with type 1 diabetes are twice as likely to experience prevalence of sexual dysfunction compared with women | without diabetes.(HTN or obesity) |
| DKA occurs in DM 1 with blood sugar of | 300 or greater. Call doctor |
| DKA puts the body into | metabolic acidosis, puts the body into kussmaul respirations. Medical emergency |
| Insulin & fluids does what to K | pushes it pack into cells |
| Pathophysiology DKA | glucagon to glycogen to glucose to fats to muscle to acidosis to kussmaul to system failure |
| Illness, surgery or extreme stress elevates | hormones including glucagon. |
| Glucose is moved out of the | muscle to help meet the demand of starving cells. |
| Glucagon converts | glycogen to glucose in the liver r/t an increase demand by the cells. |
| After the glycogen is depleted, the liver converts fatty acids to | glucose and sends the glucose into the bloodstream. |
| Sign/symptoms of DKA include: | hyperglycemia,polyuria, polydipsia, weak, lethargy, abdm cramping, N/V, blurred vision and HA, low BP, hypoTN (tackycardia, confusion, weak pulse) FSBS>300 |
| Sign/symptoms of DKA include: | hyperglycemia,polyuria, polydipsia, weak, lethargy, abdm cramping, N/V, blurred vision and HA, low BP, hypoTN (tackycardia, confusion, weak pulse) FSBS>300 |
| HHNS is | hyperglycemic, hyperosmolar, (non-ketotic)Syndrome. It’s a complication of DMII |
| Same pathophysiology as DKA except there will be no acidosis because | the patient has just enough insulin to handle it. No fruity smell |
| Patients with HHS have extreme | Na loss, dehydration, mental status changes, FSBS of patients with HHNS |
| Onset of HHS is | gradual |
| Signs/symptoms include of HHS:hyperglycemia, polyuria, polydipsia, extreme dehydration, hypovolemia, decreased electrolytes, mental status changes that resemble a stroke | |
| At what glucose level would you expect a client to exhibit s/s of hypoglycemia | usually <60, BUT assess the pt because bases differ |
| Teaching for hypoglycemia | eat protein and complex carbs every 3 hours |
| Mild Hypoglycemia S/Ssudden tremors, palpitations, diaphoresis, hunger | |
| Moderate Hypoglycemia S/S | HA, change in mood, irritability, inability to concentrate, drowsiness, impaired judgment, slurred speech, sweating |
| Severe Hypoglycemia S/S | unresponsive and possible seizure |
| What do you think the front line treatment for someone experiencing s/s of hypoglycemia | rule of 15; 4-6 oz of some juice, wait 15 min and restick for BS, ask how they feel, repeat and check BS til above 70 then give protein and complex carbs |
| You administer insulin in pt with hypoglycemia | when the patients FSBS is above 70 and depends if rapid or fast acting |
| If a pt is NPO, do you withhold insulin | NO |
| What would the intervention be for someone who is unresponsive | IV dextrose or glucagon (IM or SQ) |
| Considerations for glucagon | N/V..so make sure they are on their side. |
| Greatest risk associated with glucagon | RISK for aspirations |
| Diabetics need to have a sick day plan because | during illness, blood glucose levels will rise. |
| During illness DM needs to check | FSBS & urine for ketones q4 |
| Food and drink during sick days. Pt should stay on | a normal meal plan if possible. |
| (Sick Days) Increased N/V implement | push non-caloric liquids first then easy on the stomach foods |
| (Sick Days)Take in the normal amount of calories by eating easy-on-the-stomach foods (BRAT). | |
| What is the goal for DM sick day nutrition | aim for 50 grams of carbohydrate every 3-4 hours. |
| Before beginning exercise | check FSBS (above 250), urine for ketones (DM1). Should not exercise |
| If FSBS < 250 and no ketones then | have a CHO snack before exercise |
| Low insulin levels during exercise stimulate | glucose activity in the liver, pushing more glucose into the blood |
| Fluids during exercise | plenty; before ,during and after |
| Important self-care for DM who exercises | good fitting shoes and inspection of feet |
| Among American children ages 6-11, using the 95th percentile or higher of BMI values on the CDC 2000 growth chart: | indicate a risk of obesity |
| Strongest risk factor for obesity is | obesity of two parents.Dietary intake.Overweight during pregnancy.Rapid weight gain in first 4-6 months of life |
| Prevention/treatment of obesity in children | reduce caloric intake (balanced),become more active,create an environment that fosters physical activity,include (model) parents in the dietary treatment program |
| Obese is defined as | BMI (85-95% kids) >25 for adults |
| ADA standard care for DM | HgA1c (q 3mos not in control) (q2 per year in control) |
| LDL/HDL | yearly |
| Dilated eye exam | yearly. Opthamologists q2 |
| B/P monitoring | q 6 mos, if in good control. |
| Foot exam | daily self exam. Q 6mos to year by doctor doing a filament or tuning fork. If there are problems, foot needs to be checked more often. |
| Risk factors for metabolic syndrome | Age, race, obesity, history diabetes, other diseases |
| S/S of metabolic syndrome | Obesity, elevated triglycerides, reduced HDL, elevated B/P, elevated blood glucose |
| Treatment for metabolic syndrome | Exercise, lose weight, eat healthy, stop smoking |
Created by:
Jillzs
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