Diabetes and Endocrine System Flashcards
Definition of Diabetes
A chronic metabolic condition characterized by elevated circulating glucose concentrations resulting fro the insufficient supply or action of the hormone insulin
Insulin
Stimulates glucose uptake by peripheral tissues (mainly skeletal),
Suppresses endogenous glucose production (by hepatic glycogenolysis and gluconeogensis)
Suppresses lipolysis in adipocytes and proteolysis in muscle.
Different Types of Diabetes
Type 1
Type 2
Latent Autoimuune Diabetes of Aging (LADA)
Maturity Onset Diabetes of Youth (MODY)
LADA
Type 1.5 is one of several names now applied to adults diagnosed with diabetes who not immediately require insulin treatment, are not often overweight, and have little or no resistance to insulin. They are found to have anitbodies that attack their beta cells.
Pre-Diabetes
refers to a person with BG fasting 100-125 mg/dl or 5.5-6.875mm. You do not have diabetes yet and without lifestyle changes you will develop T2DM. (IGT or IFG)
Type 1 Diabetes
5-10% of diagnosed cases
Immune mediated- autoimmune destruction of beta cells
Need EXOGENOUS insulin
Idiopathic (arrives spontatenously)
usually not obese; often recent weight loss
First sign in children/adolescented (KDA)
Type 2 Diabetes
Insulin resistance Pancreases increases production Pancreas stops producing insulin Insulin def Glucose intolerance Develops in obese who lack capacity to step up production of insulin Hyperglycemia develops
Hormones
Chemical messengers that are secreted by glands in to the blood and give out numerous interactions between various glands.
Endocrine
Ductless glands that secrete hormones:
Hypothalamus, Posterior Pituitary, Anterior pituitary, Thyroid gland, adrenal gland, PTH,
Exocrine glands
Have ducts that secrete products like saliva, sweat, digestive.
What are the secretions of the pancreas?
Alpha cells secrete glucagon, beta cells secrete insulin, and delta cells secrete somatostatin, F cells secrete pancreatic polypeptide.
Too little hormone activity
Not enough secretion by endocrine gland
Increased removal of the hormone from blood
Abnormal tissue responds to hormone
Lack of target cell responsiveness to hormone
Lack of an enzyme essential to the target cell response
Too much hormone activity
A lot of secretion of hormone by gland
Reduced plasma-protein binding of hormone (too much free biologically active hormone)
Decreased removal of the hormone from the blood
Decreased inactivation
Decreased excretion
How many are projected to have DM by the year 2030?
592 million
What is the 7th leading cause of death in US
DM
Criteria for Diagnosing DM
1) A1C >6.5% using stand lab measures
OR
2) Fasting BG >126mg/dl
OR
3) Symptom of DM plus random BG concentration >200mg/dl
OR
4) 2 hour post prandial glucose >200 mg/dl during an oral glucose tolerance test (OGTT)
Pathophysiology of Hyperglycermia
Increase in gluconeogenesis in liver
Stimulation of glycogenlysis
Excess glucose lost in urine to compensate
Glycosuria and polyuria are present which then leads to polydipsia
Insulin resistance?
Polygenic b/c several factors contribute to its development. Obesity, poor nutrition, and physical inactivity.
Central adiposity seems to increase the degree of insulin resistance
Why do Beta Cells fail?
Over secretion of insulin to compensate for insulin resistance
High circulating free fatty acids
Hyperglycemia
Metabolic syndrome?
Shares characteristics with T2DM
Central obesity and insulin resistance significant contributors
With atheroscelortic risk factors (HTN and dyslipidemia)
Places people at risk for CAD.
Criteria to diagnosis MetS
1) Elevated waist circumference: Men >40in. Women >35in 2) Elevated TG >150mg/dl 3) Reduced HDL (good) cholesterol Men <40 Women <50 4) Elevated BP >130/85 mm Hg 5) Elevated Fasting BG >100mg/dL
Criteria for Testing for DM
Habitually Physically Inactive First degree relative with DM Members of high risk ethnic population Delivered a baby weight >9lbs or been diagnosed with GDM Hypertensive Have HDL chol <35 mg/dl Have PCOS Had IGT or IFG on previous testing Other clinical conditions assoc with insulin resistance History of vascular disease
What is HbA1c?
Glycated Hemoglobin (A1C)
Hemoglobin in RBC’s binds glucose irreversibly
Amount of glucose bound to HGB indicated hyperglycemia b/c past 2-3 months of data
It is measured every 3 months since lifespan of RBC is 120 days
Higher amount of glucose the higher amount of glycated HGB
Normal HbA1c?
<5.7%
What is fructosamine?
The carbonyl group of glucose reacts with amino group of Albumin –> glycated serum albumin
glucose attached to plasma albumin protein resembles fructose molecule but no relationship with fructose sugar.
This is not HgbA1c.
Advantage of this test is to show serum glucose control over 2-3 weeks.
Shorter period compared to HgbA1c.
Warning signs of T1DM
Drowsiness, lethargy, blurred vision Extreme thirst Frequent urination Fruity, sweet, wine like odor on breath Glucose or ketones in urine Heavy labored breating increased appetite suddent weight loss stupor
T1DM Pathophysiology
Hyperglycemia and cells starve Excess glucose in urine and polyuria Thirst Hunger Lipolysis FA transformed to Ketones and so pH falls
Management of T1DM
Intensive therapy to achieve near normal glucose levels
Prevent hypoglycemia
BG measured 3-8x daily
Eating at consistent times and synchronized with insulin dose
Teach client CHO counting
Type/Amount of carb influence BG levels
Gestational DM
Glucose intolerance during pregnancy 14-25% of all pregnancies
Alterations in insulin secretion, affecting glucose, a.a., and fat metabolism
Similar to T2DM
Effects fetus, induces fetal hyperglycemia (abnormally large infants)
Clinical manifestations of GDM
Hypertension (preclampsia) Polyhydraminos (excess accumulate of amniotic fluid) Difficult birth Preterm delivery High rate of C section
Medical treatment of GM
Nutrition counseling individualized with focus on energy and nutrient needs
Insulin therapy if needed
Oral meds not recommended.
Nutrition Intervention for GDM
Adequate energy for weight gain First Tri: 0.5-1kg Second and Third Tri: 0.2-0.5kg/week Increase PRO in 2/3 trimester Vit/Min status Use CC Meal plan to provide adequate energy/nutrients. Typicaly diet may have 30-35kcal/kg 20% protein 40-45%CHO 35-40%fat Glycemic stat at 6 weeks after delivery
Acute complications of DM
SE of insulin therapy: hypoglycemia
Dawn phenomenon: Hyperglycemia between 5am -9am because cortisol and growth hormone stimulate gluceoneogensis
DKA: life threatening situation include: nausea/vomitting/ stomach pain, fruity acetone breath, Kussmaul respirations, and mental status change
HHS
Short term illness
Long term complications of DM
Microvascular and macrovascular complications that increase morbidity. Typically occur 15-20 yrs after onset of DM. CVD Nephropathy (CKD) Retinopathy Nervous System Diseases
Macrovascular Complications of DM
Cardiovascular diseases
Microvascular Complications of DM
Nephropathy: Decreased filtering ability of kidneys from persistent albumin in urine.
Retinopathy
Gastroparesis
delayed gastric emptying results from damage to vagus nerve which controls peristalsis.
Diabetic Ketoacidosis
severe form of hyperglycemia
When adequate insulin not available, glucose production via gluconeogenesis and lipolysis are stimulated by counter-regulatory hormones in an effort to avoid starvation. One by product of lipolysis is ketones. As glucose and ketones accumulate in blood stream, osmotic diuresis occurs, resulting in dehydration and electrolyte imbalances. As fluid is lost the blood becomes concentrated further contributing to hyperglycemia.
