Metab/Obesity2 Flashcards
Is the process of biochemical reactions occuring in the body’s cells that are necessary to produce energy, repair cells and maintain life.
-through the release of hormones, such as insulin, the endocrine system controls the cellular activity that regulates growth and body metabolism.
- Concepts of Metabolism
a disorder of hyperglycemia resulting from defects in insulin secretion, insulin action, or both, leading to abnormalities in carbohydrate, protein and fat metabolism.
Type 1
Type 2
- Concepts of Metabolism (DM)
Destruction of beta cells, usually leading to absolute deficiency of insulin.
- Concepts of Metabolism
Type 1 Diabetes
A range from predominantly insulin resistance with relative insulin deficiency to predominantly secretory defect with insulin resistance
- Concepts of Metabolism
Type 2 Diabetes
Storage of excess calorie fats, resulting from excess energy intake, decreased energy expenditure, or a combo of both. Several hormones are involved in regulating obesity, including thyroid hormone, insulin and leptin. Genetic play a role as well
1 Concepts of Metabolism
Obesity
**Genetics; Type 1 DM
**Type 2 DM; Hx of diabetic parents or siblings
(child 15% chance of developing, 30% developing glucose intolerance)[inability to metabolize carbs normally]
**Obesity; which is 20% over the desired body weight or BMI at least 27 kg/m2.
-Peripheral insulin resistance~decrease the # of available insulin receptor sites in cells of skeletal muscles and adipose tissues.
-obesity also impairs the ability of the beta cells to release insulin in response to increasing glucose levels.
**Physical inactivty
**Race/Ethnicity
**Women-hx of gestational diabetes, polycystic ovary syndrome; or delivering more than 9 lb. baby
**HTN; more than 130/85, decrease HDL, cholesterol levels more than 35 mg/dl and/or triglycerides more than 250 mg/dl
**Metabolic Syndrome; HTN, abd. obesity, dyslipidemia, increase in C-reactive protein, and a fasting blood glucose greater than 100 mg/dl, increase risk of DM2, coronary HD, and Stroke
2.Risk Factors r/t DM & Obesity
prescription for weight loss and increased activity levels
Treatment/preventative measures for DM & Obesity
Type 2: Condition of fasting hyperglycemia that occurs despite the availability of endogenous insulin (produced by ones own body) despite amount produced; available its functioning is impaired by insulin resistance.
-Insulin resistance exceeds the ability of the pancreas to compensate, overtime the pancreas fails to produce enough insulin to meet body needs.
-there is enough to break down fats with resultant ketosis; (an accumulation of ketone bodies produced during oxidation of fatty acids)
(Thus making Type 2; nonketotic form of diabetes)
- Pathophysiology of obesity and DM
- Hx in family
- obesity; BMI more than 27 kg/m2 or greater~peripheral insulin resistance
- physical inactivity
- race/ethnicity
- women, hx of gestational diabetes, big babies more than 9 lbs.
- HTN; more than 130/85 mmHg, decrease HDL, increase cholesterol, and triglycerides more than 250 mg/dL
- Metabolic Syndrome; a disorder characterized by the presence of 3 or more of the following: increase waist circumference, HTN, increase blood triglycerides, and fasting blood sugar, low HDL, cholesterol more than 35 mg/dL
- Risk Factors of DM2
A disorder of hyperglycemia resulting from defects in insulin secretion, insulin action, or both, leading to abnormalities in carbohydrate, protein, and fat metabolism.
- Diabetes Mellitus
Slow onset, often unaware of the disease until healthcare is sought for other issue.
-Hyperglycemia increase gradually
-1/2 of diagnosed (newly) already have complications. (DM2)
-DM2 hyperglycemia not as severe as DM1, but similar symptoms. ie. polyuria and polydipsia, blurred vision, fatigue, paresthesias, and skin infections.
-If available, insulin decrease in times of stress (physical or emotional) may develop diabetic ketoacidosis; but uncommon.
~Hypoglycemic meds begun when lifestyle changes are insufficient.
-usually a combo of insulin and hypoglycemic meds used to achieve best glycemic control.
- Manifestations of DM2 & Obesity
Alterations in blood glucose levels Alterations in cardiovascular system Neuropathies Increase susceptibility to infection Periodontal disease
4. Complications of Diabetes
Hyperglycemia and hypoglycemia, diabetic ketoacidosis (DKA), hyperosmolar hyperglycemic state (HHS),
4 Acute complications of Diabetes
increase glucose levels
hyperglycemia
a form of metabolic acidosis that develops when there is an absolute deficiency of insulin and an increase in the insulin counterregulatory hormones. It may also be induced by stress in an indiv. with type 1 DM
DKA Diabetic Ketoacidosis
Blood glucose between 4 & 8 am. Not a response to hypoglycemia (type 1 and type 2). [teenagers; growth hormone] decrease peripheral uptake of glucose.
#4. Complications of Diabetes Dawn Phenomenon
Combo of hypoglycemia during the night with a rebound morning rise in blood glucose to hyperglycemic levels. (counterregulatory hormones stimulated)
*gluconeogenesis & glycogenolysis inhibits peripheral glucose use: insulin resistance for 12-48 hrs.
#4. Complications of Diabetes Somogyi Phenomenon
Untreated type1 DM continues, the insulin deficit causes fat stores to break down; the result is continued hyperglycemia and mobilization of fatty acids with a subsequent ketosis
Diabetic Ketoacidosis
When an individual is sick, who has an infection or decreases or omits insulin doses is @ greater risk of
DKA
- HYperosmolarity from hyperglycemia and dehydration
- Metabolic acidosis is from an accumulation of ketoacids
- Extracellular volume depletion from osmotic diuresis
- Electrolyte imbalances (loss of K and Na) from osmotic diuresis.
Diabetic Ketoacidosis
Severe dehydration and acidosis & DKA need immediate medical attention
-blood glucose levels greater than 250 mg/dL, decrease in pH, and ketone in urine.
Manifestations of DKA
Regular insulin is used in the treatment of DKA
-mild ketosis; sub q insulin
-severe ketosis; iv insulin
Regular insulin only insulin giving IV!
Treatment of DKA
Occurs in individuals who have type 2 DM and is characterized by a plasma osmolarity of 340 mOsm/L or greater (normal range 280-300 mOsm/L. Increase blood glucose levels and altered LOC
Onset is slow; 24 hrs to 2 weeks
Life-threatening medical emergency;
**precipitating factors; infection, therapeutic agents, therapeutic procedures, acute illness and chronic illness
**MOST common; infection
Hyperosmolar Hyperglycemic State HHS
Treatment is correcting fluid and electrolyte imbalances, decrease blood glucose levels and give insulin.
Treatment of HHS
decrease blood glucose levels; common in ind. with type 1 DM, occasionally DM2
Hypoglycemia
Insulin Shock; insulin reaction “the lows” in type 1 DM
;results primarily from a mismatch between insulin intake (error of insulin dose), physical activity, and carb availability (omitting a meal)
-intake of alcohol and drugs, such as
-chloramphenicol (Chloromycetin)
-sodium warfarin (Coumadin)
-monoamine oxidase inhibitors
-probenecid (Benemid)
-Salicylates
-Sulfonamides; all can cause hypoglycemia
Hypoglycemia causes
Compensatory ANS response:
-impaired cerebral function; decrease glucose availability to brain
-onset SUDDEN, and blood glucose decrease of 45-60 mg/dL
**Severe hypoglycemia may cause death
Hypoglycemia Awareness; counterregulatory system stops working
15/15 Rule! 15 g. of rapid acting sugar; Apple juice. 1 tsp honey, Wait 15 mins, monitor blood glucose again, then if still low eat another 15 g. of carbs.
Manifestations Hypoglycemia
Alterations in cardiovascular system
- the peripheral & ANS
- mood as well as increase susceptibility to infection
- periodontal disease
- complication involving the feet
Chronic Complications of DM
Changes in lg blood vessels resulting in atherosclerosis Abnormalities in platelets RBC's clotting factors Changes in arterial walls
Chronic Complications
Cardiovascular System changes with DM
major risk factor for developing of an MI.
***MOST common cause of death in an indiv with DM
Chronic Complications
Coronary Artery Disease with DM
more than 140/80 mmHg common comorbidity of DM. Affects 20-60% with diabetes
Complications;
-retinopathy
-nephropathy
-HTN; reduced by weight loss, exercise, and decrease in Na intake and alcohol comsumption.
-plus meds to lower
Chronic Complications
HTN with Diabetes
with diabetes 2-6x more likely to have a stroke.
HTN; risk factor
~atherosclerosis of cerebral vessels develop @ an earlier age and is more extensive with ind. with diabetes.
Manifestations of impaired cerebral circulation are similar-hypoglycemia or HHS, blurred vision, slurred speech, weakness, and dizziness.
Chronic Complications
Stroke with Diabetes
lower extremities accompany both types of diabetes, but greater in ind. with type 2 DM.
Chronic Complications
Peripheral Vascular Disease
refers to the changes in the retina that occur in the ind. with diabetes.
- retinal capillary structure undergoes alterations in blood flow, then retinal ischemia and breakdown in the blood; retinal barrier.
- *Leading cause of blindness in individuals between 20 & 74 years of age.
- Stage I: nonproliferative retinopathy; dilated veins, microaneuryms, edema of the macula; exudates
- Stage II; Retinal ischemia infarcts of nerve fibers “cotton wool”
- Stage III; proliferative retinopathy; traction on the vitreous humor, may cause hemorrhage or retinal detachment.
Chronic complications DM
Diabetic Retinopathy
disease of the kidneys characterized by the presence of albumin in the urine, HTN, edema, and progressive renal insufficiency.
- occurs in 20-40%
- **Single leading cause of end-stage renal disease.
1st indication of nephropathy is microalbuminuria; (a low but abnormal level of albumin in the urine)
*****Aggressive antihypertensive management!!
B/c HTN accelerates the progress of diabetic nephropathy.
Glomerulosclerosis thickens the basement membrane and simultaneously makes it functionally leaky, allowing large molecules (ie. protein) to be lost in the urine.
Chronic complications
Diabetic Nephropathy
fibrosis of the glomerular tissue
Glomerulosclerosis