Metabolism: Diabetes Mellitus, Obesity Flashcards
Is the process of biochemical reactions occurring in the body’s cells that are necessary to produce energy, repair cells and maintain life
Metabolism
Through the release of hormones, such as insulin, the endocrine system controls the cellular activity that regulates growth and body metabolism.
How metabolism works
- Affects 20.8 million people in the US
- Affects 200 million world-wide.
- Is two and a half times more common in African-Americans and Hispanic Americans
- Is 5x more common in Native Americans.
- Is the 7th Leading cause of death in the US.
- The CDC estimates that a child born in 2000 has a 1 in 3 chances of developing DM in their lifetime.
Statistics on Diabetes Mellitus
kills more quickly
hypoglycemia
kills slowly overtime
hyperglycemia
People live longer.
Obesity has increased in the general population
The use of insulin and other anti-diabetic agents.
Reasons why more people have Diabetes than ever before..
- 25x more likely to develop blindness.
- 17x more likely to develop kidney failure.
- 20x more likely to develop gangrene.
- 15x more likely to require amputation.
- 2x as likely to have an MI or CVA.
People with Diabetes
- All body tissues and organs require a constant supply of glucose.
- Not all tissues require insulin for glucose uptake
- The brain, the liver, the intestines and the renal tubules DO NOT require insulin.
- Skeletal muscle and adipose tissue DO require insulin for glucose movement into the cells.
Blood glucose homeostasis is maintained through the action of insulin and glucagon.
- increased plasma glucose levels
- increased plasma levels of amino acids.
- increased plasma levels of fatty acids.
- incretin hormones-GLP-1 and amylin
How does the pancreas know to secrete insulin?
70-100 mg/dl
Normal blood glucose level is between.
- Includes a group of hormones that will increase glucose in times of hypoglycemia, stress, growth or increased metabolic demands.
- These hormones include: Glycagon, Epinephrine, Norepinephrine, Growth Hormone, and Cortisol.
- Diabetes Mellitus is a Comples disorder of carbohydrate, fat and protein metabolism that is primarily a result of a deficiency or complete lack of insulin secretion.
Counterregulatory System
Complex disorder of carbohydrate, fat and protein metabolism that is primarily a result of a deficiency or complete lack of insulin secretion.
Diabetes Mellitus
- Type I
- Type II
- Gestational
- Pre-diabetes;
- impaired fasting glucose (blood glucose level of 100-125 when fasting)
- impaired glucose tolerance (blood glucose between 140-199 when undergoing a 2 hr. GTT)
- Other Specific Conditions resulting in hyperglycemia such as genetic defects. Disease of the pancreas, drug induced.
Classifications of Diabetes Mellitus
- Age of Onset: can appear at any age, usually young, less than 30 years of age.
- Characterized by a sudden onset
- Etiology: Environmental and Autoimmunity response, may have been inherited (gene coding for HLA-DR and HLA-DQ), or may be the result of a viral infection
- Risk for general population is 1 in 400 and the risk for those who have at least one parent with diabetes is 1 in 20.
Type I Diabetes Mellitus
- Age of onset: may occur at any age, but occurs most commonly in people over 40 years of age.
- Common in the obese (esp. in the upper body)
- Onset is slow (over years)
- Heredity plays dominant role, offspring of pts. with type 2 DM have a 15% chance of developing DM and a 30% risk of having IGT
- Metabolic Syndrome called syndrome X plays a role.
- Common in Hispanic Americans, Native Americans and African Americans.
- Increasing chance with Aging, esp. after age 65.
- Often follows gestational deabetes.
- Obesity is common.
Type 2 Diabetes Mellitus
- decrease in the sensitivity of the cells to insulin (insulin resistance)
- decreased insulin production
- defect at the receptor site. both in and outside cells.
- decrease in the # of receptor sites at the cell level.
- poor control of liver glucose output
Possible causes of Diabetes Mellitus; Type 2
*90% beta cells in pancreas phase out than 10% beta cells start feeling symptoms..
-losing protein; losing weight.
-poor wound healing
-increase urinating
-dehydrated
-diabetic ketoacidosis
Cells starving. glucose not getting to cells; fat break down; forms increasing triglycerides and cholesterol.
Cardinal Signs DM1
180 mg/dl glucose in blood starts to pee it out.
glucose in urine; DKA (total lack of insulin)
thick blood
hemoconcentration
hyperosmolarity
- Assess the airway, LOC, hydration (isotonic 0.9%), electrolytes and blood glucose levels
- Returning Serum pH to normal
- Correcting fluid and electrolyte imbalances (in the presence of mild, moderate, or severe dehydration; decreased HCO3, increased K (mild), decreased K (severe), decreased Na (moderate to severe), decreased Ca, Mg, PO4, pH
- Lowering hyperglycemia (usually above 250 mg/dl) Reg 70-100; increase b/c don’t want to cont. going down. IV stays in body for a couple of hours. If below 250 would have to give dextrose; hypoglycemia worse than hyperglycemia.
- Blood sugar @ 180 mg/dl causes you to urinate.
Treatment for DKA Type I DM
Called Maturity onset diabetes of the young (MODY)
Children Type 2 Diabetes Mellitus
Regular insulin only kind given in an IV!!
Need to know DM
- Administration of Insulin
- Symptoms of hyper/hypoglycemia
- serum glucose monitoring
- Diet
- Long term complications**
- Prudent Living
- Sick day rule
Pt teaching for type I diabetes
- Polyuria
- polydipsia
- polyphagia
- blurred vision
- weightloss
- fatigue
- poor wound healing
If CHF patient: 0.045% NS for dehydration.
S & S Diabetes Mellitus
Cardinal signs
Keep an eye on kidney function because don’t want too much K; kill them
Watch urine output 30 ml/hr; no more
0.1 unit per kg/hr of insulin;
To determine IV drip of insulin
-Explore factors leading to DKA
-Monitor blood glucose every 4-6 hrs.
-Check urine ketones when blood glucose exceeds 300 mg./dl hyperglycemia
-teach pt. to reduce risk for dehydration
See Endocrinologist
Prevention of Diabetes I
*Formally known as hyperglycemia-hyperosmolar nonketotic syndrome (HHNS)
*HHS is life-threatening and clients are often admitted to the ICU, because increased levels of glucose, sicker than one with DkA.
-Typical blood glucose levels are over 700 mg/dl
-Serum osmolarity is increased
-Present with altered levels of consciousness or are having seizures
-Dehydration is profound-fluid loss near 8 liters
(Children can develop cerebral edema is too quickly hydrated; 0.045%)
Acute Complications of Type 2 DM; hyperglycemic-hyperosmolar state (HHS)
*Formally known as hyperglycemia-hyperosmolar nonketotic syndrome (HHNS)
*HHS is life-threatening and clients are often admitted to the ICU, because increased levels of glucose, sicker than one with DkA.
-Typical blood glucose levels are over 700 mg/dl
-Serum osmolarity is increased
-Present with altered levels of consciousness or are having seizures
-Dehydration is profound-fluid loss near 8 liters
(Children can develop cerebral edema is too quickly hydrated; 0.045%)
Diabetes II; still making insulin; making enough to break down fats; no increase ketone levels
Acute Complications of Type 2 DM; hyperglycemic-hyperosmolar state (HHS)
Symptoms slow to appear until health care is sought for some other problems.
-Polyuria and polydipsia is common.
HHS Manifestation;
Sufficient insulin which usually prevents ketosis. (breakdown of fat)
-Occurs most frequently in elderly clients whose fluid intake is poor.
-Occurs with patients with renal insufficiency
-Precipitated by an acute illness or infection.
body increase glucose
Metabolic increase, body would need more glucose.
***Need insulin to bring glucose into cells.
Hyperglycemic-hyperosmolar state
- Establishing and maintaining adequate ventilation.
- Correcting shock with adequate intravenous fluids.
- Maintaining fluid volume. NSS 0.9% or 0.045% (CHF, kids)
- Administering potassium
- Administering insulin
Treatment for HHS
Importance of Weight loss; obesity; if you lose weight maybe able to come off Diabetic meds
- Serum glucose monitoring
- Diet
- Oral hypoglycemic agents &/or insulin
- Prudent living/prevention of complications
Patient Teaching for type 2 Diabetes
Causes;
- overdose of insulin or oral hypoglycemic agents.
- omitting or delaying a meal
- overexertion without compensation with additional CHO
- Nutritional and fluid imbalances due to vomiting
- Erratic or altered absorption of insulin
- Changing to a different insulin
- counterregulatory Hormone deficiencies
- severe sepsis
Forget to eat took too much insulin need to eat; energize cells Ran marathon; not enough carbs Change 1 type or manufacturer to another
Hypoglycemia; blood glucose less than 60 mg/dl
Kills Fast
- Blood glucose level less than or equal to 60 mg/dl
- Neurogenic symptoms (Adrenergic) results from autonomic nervous activity triggered by a rapid decline in blood glucose; can happen to anyone (counterregulatory kicks in; glucose rises)
- Neuroglycopenic Symptoms occur when brain glucose gradually declines to a low level.
- *brain gradually loses blood glucose.
- Adrenergic symptoms; treatment; give 15 to 20 grams of rapid-acting CHO; use the 15/15 rule
(After 5-10 years for Type 2 Diabetics; they lose Adrenergic response)
Classifications of Hypoglycemia
Can give: 6 life savors 1 tsp honey Applejuice; no OJ b/c of K+; cardiac patients 4-6 oz soda
Keep checking q 15 mins for raising of glucose levels to normal
15/15 rule
- disorientation (seems drunk)
- seizures
- somnolence (difficulty arousing from sleep)
- loss of consciousness
- **death
Neuroglycopenic symptoms; Life Threatening
TIRED tremors and tachycardia irritability restlessness excessive hunger diaphoresis and depression
Treatment
parenteral glucagon and/or IV 50% dextrose (usually instantly) Book will say 20mins
Neuroglycopenic symptoms
beta blockers: which block receptors; can become hypoglycemic in diabetes
Avoid beta blockers in Diabetics
characterized by morning hyperglycemia from the counterregulatory response to nighttime hypoglycemia. bad HA, horrible nightmares, increase blood glucose keeps getting higher every night sleeping, decrease blood glucose; counterregulatory system kicks in
**treat: less insulin @ dinner; have a bedtime snack
Smogyi Phenomenon (Fasting hyperglycemia)
results from a night time release of growth hormone that causes blood glucose elevations at about 5 to 6 am.
-Teenagers growing; Not becoming hypoglycemic. increase in glucose bc of growth hormone;
Treatment: would give insulin before bed time
Dawn Phenomenon (Fasting hyperglycemia)
Metabolic Syndrome (Syndrome X)
Degenerative Vascular Changes including:
-alternations in the macrocirculation.
-alterations in the microcirculation including;
*Diabetic Retinopathy
*Diabetic Neuropathy
*Diabetic Nephropathy
Fasting hyperglycemia; Long term effects of hyperglycemia
The Retina
Diabetic Retinopathy
-related to problems that block retinal blood vessels and cause them to leak, leading to retinal hypoxia..
Microvascular complications theories: Diabetic Retinopathy
Cluster of metabolic factors that occur together increasing the risk of developing type 2 DM, heart disease, and stroke;
- Encompasses varying degrees of:
- hyperglycemia
- hypertension
- high triglyceridemia
- low levels of high density lipoprotein (HDL)
- abdominal obesity
Metabolic Syndrome (AKA syndrome X)
- Coronary Artery Disease; increases chance of stroke
- Cerebral Vascular Disease
- Peripheral Vascular Disease (higher incidence in Type 2 Diabetics)
Macrocirculation; Atherosclerotic changes lead to
- Coronary Artery Disease; increases chance of stroke
- Cerebral Vascular Disease
- Peripheral Vascular Disease (higher incidence in Type 2 Diabetics)
Macrocirculation; Atherosclerotic changes lead to
causes thickening of the basement membrane of the small blood vessels and organ damage.
-a weakening of the capillary membrane, increase capillary permeability and capillary perfusion.
Glucose toxicity directly effects functional cell integrity
Chronic hyperglycemia
is the nerve layer that lines the inside of the eye and converts light into nerve signals that the brain can interpret.
The Retina
is an alteration in the blood flow within the retinal capillary structure which leads to retinal ischemia and breakdown in the retinal barrier. blindness
Diabetic Retinpathy
The Retina
Diabetic Retinopathy is an alteration
Related to problems that block retinal blood vessels and cause them to leak, leading to retinal hypoxia.
Microvascular complication theories: Diabetic Retinopathy
- **Nonproliferative diabetic retinopathy; new blood vessels grow bc of occlusions. they go nowhere; don’t help with perfusion. Fatty tissue. aneurysms in eye
- **Proliferative retinopathy (Neovascular disease); blood vessels; no blood perfusion; more form and crowd eye *cotton wooly; increases pressure in eyes itself, detached retina. Blindness. leaking blood vessels. Foggy
- *Other: Macular degeneration, corneal scarring, cataracts, glucoma. increase incidence
- **Hyperglycemia;; causes blurred vision
- **hypoglycemia: causes double vision
Stages of Retinopathy
Legal blindness 20x more common in people with diabetes
New blood vessels grow b/c of occlusions. they go nowhere. don’t help with perfusion. Fatty tissue aneurysms in eye.
Nonproliferative diabetic retinopathy
blood vessels form; no blood perfusion; more form, crowds eye; **cotton woolly; Increases pressure in eye itself. Detached Retina. Blindness. Leaking blood vessels in fluid in eye Foggy
Proliferative retinopathy (Neovascular disease)
blood vessels form; no blood perfusion; more form, crowds eye; **cotton woolly; Increases pressure in eye itself. Detached Retina. Blindness. Leaking blood vessels. Foggy
Proliferative retinopathy (Neovascular disease)
- Laser Photocoagulation; zap cotton woollies and new blood vessels that are going no where; doesn’t cure just helps so it doesn’t get worse.
- Panretinal Photocoagulation; laser treatment. lg laser, Big guns, put you to sleep for procedure.
- Vitrectomy; vitreous humor and blood dip; blind. take out fluid and put clear solution in it. Under general anesthesia.
Treatment for Diabetic Retinopathy
save t
test
- preventing episodes of hyperglycemia.
- encouraging routine eye exams; every 6 months
- HTN; avoid valsalva maneuver
Client Teaching; Retinopathy
-Characterized by the presence of albumin in the urine, hypertension and edema; low albumin level, kidneys letting go
-Is the most common cause of Renal Failure in the US.; most bc diabetics; BUN & Cr lab values;
HTN; perfusion to kidneys diminished
Diabetic Nephropathy; kidneys
Control of hyperglycemia -control of hypertension prevention and early treatment of UTI's avoidance of nephrotoxic substances diet low in sodium and protein
client teaching Nephropathy
Is a progressive deterioration of nerves that results in loss of nerve function
Diabetic Neuropathy
Is a progressive deterioration of nerves that results in loss of nerve function
2 types:
*Diffuse Neuropathies; slow onset, involve motor and sensory nerves, involve the ANS.
BP doesn’t go up when standing quickly
ANP; not prop working
Diabetic Neuropathy
Slow onset, involve motor and sensory nerves, involve the ANS.
Diffuse Neuropathies
Usually caused by an acute ischemia event/physical trapping of a nerve. Leads to damage or death of nerve.
cant feel toes/feet
Focal Neuropathies
Distal symmetric polyneuropathy cause:
-sensory alteration such as parenthesias, or anesthesia, motor alteration including deformed feet such as hammertoes
-Autonomic neuropathy; including gastroparesis, bowel incontinence, neurogenic bladder, impotence, orthostatic hypotension, resting tachycardia, loss of warning signs of hypoglycemia.
cranial nerves; lose feelings. facial nerves. lack of blood
Poly-Neuropathies
sensory alteration such as parethesias or anesthesia, motor alteration including deformed feet such as hammertoes
Distal symmetric polyneuropathy
gastroparesis, bowel incontinence, neurogenic bladder, impotence, orthostatic hypotension, resting tachycardia, loss of warning signs of hypoglycemia
Autonomic neuropathy
such as pain radiating across back, side and front of chest or abdomen
Sensory and reflex loss (Focal Neuropathies)
diplopia or ptosis
Cranial nerve palsies
carpal tunnel syndrome, footdrop
Entrapment (Focal Neuropathies)
sensory impairment in sole of feet, weakness of intrinisic muscles of feet, burning pain & parethesias
Posterior tibial nerve damage (Focal Neuropathies)
Sensory and reflex loss
Cranial nerve palsies
Entrapment
Posterior tibial nerve damage
Focal Neuropathies causes
- The symptoms of diabetes plus a casual plasma glucose value more than 200 mg/dl. (A casual blood glucose value is obtained without regard to the last meal)
- A fasting plasma glucose level more than 126 mg/dl.
- The plasma glucose value in a 2 hr. sample of the oral glucose tolerance test is more than or equal to 200 mg/dl. The test should be performed using a loading dose of 75 grams of anhydrous glucose.
Dx of Diabetes
Type I is an autoimmune disease with the presence of autoantibodies to proteins. The presence of islet cell antibodies (ICA) is an indicator. blood; very expensive
*Measurement of C-peptide levels indicates beta secretory function of the pancreas. C-peptide levels correlate well with insulin levels.
So which kind of Diabetes?
Type I is an autoimmune disease with the presence of autoantibodies to proteins. The presence of islet cell antibodies (ICA) is an indicator. blood; very expensive
- Measurement of C-peptide levels indicates beta secretory function of the pancreas. C-peptide levels correlate well with insulin levels.
- decrease in C-peptide; Type I DM
- Pancrease pre-insulin with C-peptide gets to liver. C-peptide takes off insulin. hangs in liver. Increase C-peptide adequate insulin.
So which kind of Diabetes?
Fasting Plasma Glucose more than or equal to 100 and less than 126 mg/dl.
- Sometimes known as Pre-diabetes.
- Can lead to Metabolic syndrome.
Insulin Physiology Impaired Fasting Glucose
- They are age 45 or older.
- If they are obese
- have an immediate family relative with Diabetes
- member of a high risk ethnic group.
- delivered a baby more than 9 lbs.
- Hx of gestational diabetes
- have HTN, HDL cholesterol less than 35 mg/dl or
- Triglyceride level of 250 mg/dl or more
- Dx with Impaired fasting glucose
Individuals should be screened for Diabetes if
- Fasting blood glucose.
- Glycoslated hemoglobin assays (HbA1c levels); tells you amount of glucose that attaches to RBC; 120 days RBC, takes on more glucose than should. Normal is 6%. 6.5-7 or above is a problem. 7-10% severe problem
- Urine glucose and ketone levels
- urine test for presence of protein (albumin)
- Serum Cr. levels
- Serum Electrolytes
Monitoring Diabetes
*Type-1; Insulin
*Type 2; usually with oral diabetes medications but, at times may require insulin; After 10-15 years go on insulin; bc of build up insulin
*Gestational; Usually insulin if diet does not seem to control condition.
practice diff. then in book (insulin only in book); women can still stay on orals if pregnant
Managing Diabetes: Pharmacologic Treatment of DM
Mimic the normal pattern of insulin secretions as closely as possible.
- Insulin: Synthetic (using recombinant DNA)
- Insulin Analogs
Goal of Insulin Therapy
Onset of Action
Peak Effect
Duration of action
***Need to know when blood will be affected by insulin
Characteristics of Insulin
*Type-1; Insulin
*Type 2; usually with oral diabetes medications but, at times may require insulin; After 10-15 years go on insulin; bc of build up insulin; Drugs, exercise, and diet
*Gestational; Usually insulin if diet does not seem to control condition.
practice diff. then in book (insulin only in book); women can still stay on orals if pregnant
Managing Diabetes: Pharmacologic Treatment of DM
- Rapid-acting; covers the meal immediately following injection
- Short-acting
- Intermediate-acting; covers subseq meals
- Intermediate; and short-acting mixtures
- Long-acting-Lantus (glargine); constant level of insulin & controls
Types of Insulin
- Lipodystrophy; same place, harden like cellulite
- Lipoatrophy; dimpeling; use different place
- Insulin Resistance; build up over time
Complications of Insulin Therapy
- Lipodystrophy; same place, harden like cellulite
- Lipoatrophy; dimpling; use different place
- Insulin Resistance; build up over time
Complications of Insulin Therapy
- Extremes of temperature
- Exposure to light
- Lantus insulin
Storage of Insulin; AVOID
- Subcutaneous route
- IV route; regular insulin only
- Insulin Pump; (AKA; continuous sub. infusion)
- Fasting acting insulin only
Insulin can be administered
-Reducing insulin resistance.
-Augmenting insulin secretion or replacing insulin
Gut; carb metabolism; liver; elevate glucose production.
muscle decrease uptake of insulin/resistance
Type 2 DM; real time insulin pump/monitor
Pharmacological Goals
- Sulfanylureas; increase production insulin from pancreas
- Meglitinides Analogues; increase production insulin from pancreas and others
- Biguanides; Metformin *Popular type 2 Diabetes; Important drug. can cause kidney issues; must hydrate!!
- Alpha-Glucoside inhibitors;
- Thiazolidenediones (AKA; Insulin Sensitizing Agents)
Oral Antidiabetic Agents
- Are related to the sulfonamides but lack antibacterial action.
- Stimulate the pancreas to produce insulin
- Increase the sensitivity of peripheral tissue to insulin
- 2nd generation; Glipizide (Glucotrol, Glucotrol XL); Glycuride (Micronase); Glimepride (Amaryl)
Sulfonylureas (Oral Antidiabetic Agent)
- Has many of the same actions as sulfonylureas-increase insulin release to treat postprandial hyperglycemia but they act rapidly and have a short duration of action.
- Their effects are glucose dependent, decreasing when the patient’s blood glucose level decreases.
- REPAGLINIDE; (Prandin) & Nateglinide (Starlix)
Meglitinides analogues (Oral Antidiabetic Agent)
The three mechanisms whereby the Biguanides work are:
- reduce liver production of glucose thereby reducing fasting blood glucose release
- reduces intestinal absorption of glucose
- increases cells sensitivity to insulin
- only one in the USA; Metformin (Glucophage)
Biguanides; Antihyperglycemic agents
Metformin!
- Inhibits the work of the intestinal enzyme Alpha-Glucoside to slow carbohydrate digestion and delay glucose absorption.
- Acarbose (Precose), Miglitol (Glyset)
Alpha-Glucoside Inhibitors
- Directly stimulates peripheral glucose uptake and storage.
- Inhibits glucose and triglyceride production in the liver
- Rosiglitazone (Avandia)-concern for heart-related deaths, bone fractures and macular edema. Pioglitazone (Actos) not a concern at this time.
Insulin Sensitizing Agents
Glitazone or Thiazolidinedione
- *Combination agent: Glucovance; combines glyburide (a sulfonylureas) with Metformin (a biguanide)
- *Amylin analogues-Pramlintide (Symlin): delays gastric emptying, reduces after-meal blood glucose levels and triggers satiety in the brain.
- *Incretin analgues; agents lower plasma glucose levels. Exenatide (Byetta)
- *DPP-IV inhibitors; slow the inactivation of incretin hormones; Sitagluiptin (Januvia)
Newer Drugs
- Maintain bld. glucose levels as near normal by balancing; activity, food intake & insulin or oral glucose lowering meds.
- Achieve optimal blood lipid levels.
- Provide adequate calories for maintaining reasonable wt.
- Preventing complications.
Goal of Nutritional Therapy in Diabetes
- Protein; 10 to 20% of the total kcalories.
- Fats; 30% or less of total kcalories and less than 7% from saturated fat.
- Carbohydrates; 45-60% of the total kcalories. [Important to know control of carbs for diabetes]
- Fiber; 25 grams/day; keeps you full
ADA. Nutritional recommendations/day
- Carbohydrate counting
- Exchange list; weight watchers, etc
- Alcohol consumption
- prevent weight gain
Diet control strategies
- Insulin or oral antidiabetic agents should be taken
- Attempt to eat frequent small amounts of CHO
- Fluid intake is important for avoiding dehydration
- Blood glucose and urine ketones should be checked q 4 hrs.
- *take insulin bc glucose levels go up! EAT!!
Sick Day rules for Diabetics
- Avoid exercise if frequent episodes of hyper/hypoglycemia.
- Type I diabetic should perform exercise when bl. glucose levels are 80 to 250 mg/dl. and No ketones are present in the urine.
- Exercising at peak insulin action time may lead to hypoglycemia
- food intake may need to be increased.
- Fluid intake is essential
Exercise Guidelines DM
- Begin training slowly, extending activity over a prolonged period
- May have to take a carbohydrate drink (5 to 10%) before, during or after 1 hour of exertion
- Monitor glucose level
- Carry a simple sugar, such as hard candy in case of hypoglycemia symptoms.
Exercise promotion DM
- Whole pancreas transplantation
- Islet cell transplantation; severely sick long term from Diabetes
Advances; DM
