Metabolism: Diabetes Mellitus, Obesity Flashcards
(100 cards)
1
Q
Is the process of biochemical reactions occurring in the body’s cells that are necessary to produce energy, repair cells and maintain life
A
Metabolism
2
Q
Through the release of hormones, such as insulin, the endocrine system controls the cellular activity that regulates growth and body metabolism.
A
How metabolism works
3
Q
- 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.
A
Statistics on Diabetes Mellitus
4
Q
kills more quickly
A
hypoglycemia
5
Q
kills slowly overtime
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hyperglycemia
6
Q
People live longer.
Obesity has increased in the general population
The use of insulin and other anti-diabetic agents.
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Reasons why more people have Diabetes than ever before..
7
Q
- 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.
A
People with Diabetes
8
Q
- 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.
A
Blood glucose homeostasis is maintained through the action of insulin and glucagon.
9
Q
- increased plasma glucose levels
- increased plasma levels of amino acids.
- increased plasma levels of fatty acids.
- incretin hormones-GLP-1 and amylin
A
How does the pancreas know to secrete insulin?
10
Q
70-100 mg/dl
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Normal blood glucose level is between.
11
Q
- 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.
A
Counterregulatory System
12
Q
Complex disorder of carbohydrate, fat and protein metabolism that is primarily a result of a deficiency or complete lack of insulin secretion.
A
Diabetes Mellitus
13
Q
- 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.
A
Classifications of Diabetes Mellitus
14
Q
- 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.
A
Type I Diabetes Mellitus
15
Q
- 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.
A
Type 2 Diabetes Mellitus
16
Q
- 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
A
Possible causes of Diabetes Mellitus; Type 2
17
Q
*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.
A
Cardinal Signs DM1
18
Q
180 mg/dl glucose in blood starts to pee it out.
A
glucose in urine; DKA (total lack of insulin)
19
Q
thick blood
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hemoconcentration
hyperosmolarity
20
Q
- 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.
A
Treatment for DKA Type I DM
21
Q
Called Maturity onset diabetes of the young (MODY)
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Children Type 2 Diabetes Mellitus
22
Q
Regular insulin only kind given in an IV!!
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Need to know DM
23
Q
- Administration of Insulin
- Symptoms of hyper/hypoglycemia
- serum glucose monitoring
- Diet
- Long term complications**
- Prudent Living
- Sick day rule
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Pt teaching for type I diabetes
24
Q
- Polyuria
- polydipsia
- polyphagia
- blurred vision
- weightloss
- fatigue
- poor wound healing
If CHF patient: 0.045% NS for dehydration.
A
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
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0.1 unit per kg/hr of insulin;
To determine IV drip of insulin
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-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
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*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)
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*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)
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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)
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-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
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- 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
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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
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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
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Forget to eat
took too much insulin
need to eat; energize cells
Ran marathon; not enough carbs
Change 1 type or manufacturer to another
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Hypoglycemia; blood glucose less than 60 mg/dl
| Kills Fast
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- 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
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Can give:
6 life savors
1 tsp honey
Applejuice; no OJ b/c of K+; cardiac patients
4-6 oz soda
```
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Keep checking q 15 mins for raising of glucose levels to normal
15/15 rule
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* disorientation (seems drunk)
* seizures
* somnolence (difficulty arousing from sleep)
* loss of consciousness
* **death
Neuroglycopenic symptoms; Life Threatening
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TIRED
tremors and tachycardia
irritability
restlessness
excessive hunger
diaphoresis and depression
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Treatment
parenteral glucagon and/or IV 50% dextrose (usually instantly) Book will say 20mins
Neuroglycopenic symptoms
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beta blockers: which block receptors; can become hypoglycemic in diabetes
Avoid beta blockers in Diabetics
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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)
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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)
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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
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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
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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)
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- Coronary Artery Disease; increases chance of stroke
- Cerebral Vascular Disease
- Peripheral Vascular Disease (higher incidence in Type 2 Diabetics)
Macrocirculation; Atherosclerotic changes lead to
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- Coronary Artery Disease; increases chance of stroke
- Cerebral Vascular Disease
- Peripheral Vascular Disease (higher incidence in Type 2 Diabetics)
Macrocirculation; Atherosclerotic changes lead to
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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
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is the nerve layer that lines the inside of the eye and converts light into nerve signals that the brain can interpret.
The Retina
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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
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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
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* **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
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New blood vessels grow b/c of occlusions. they go nowhere. don't help with perfusion. Fatty tissue aneurysms in eye.
Nonproliferative diabetic retinopathy
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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)
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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)
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- 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
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save t
test
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- preventing episodes of hyperglycemia.
- encouraging routine eye exams; every 6 months
- HTN; avoid valsalva maneuver
Client Teaching; Retinopathy
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-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
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Control of hyperglycemia
-control of hypertension
prevention and early treatment of UTI's
avoidance of nephrotoxic substances
diet low in sodium and protein
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client teaching Nephropathy
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Is a progressive deterioration of nerves that results in loss of nerve function
Diabetic Neuropathy
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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
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Slow onset, involve motor and sensory nerves, involve the ANS.
Diffuse Neuropathies
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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
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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
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sensory alteration such as parethesias or anesthesia, motor alteration including deformed feet such as hammertoes
Distal symmetric polyneuropathy
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gastroparesis, bowel incontinence, neurogenic bladder, impotence, orthostatic hypotension, resting tachycardia, loss of warning signs of hypoglycemia
Autonomic neuropathy
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such as pain radiating across back, side and front of chest or abdomen
Sensory and reflex loss (Focal Neuropathies)
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diplopia or ptosis
Cranial nerve palsies
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carpal tunnel syndrome, footdrop
Entrapment (Focal Neuropathies)
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sensory impairment in sole of feet, weakness of intrinisic muscles of feet, burning pain & parethesias
Posterior tibial nerve damage (Focal Neuropathies)
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Sensory and reflex loss
Cranial nerve palsies
Entrapment
Posterior tibial nerve damage
Focal Neuropathies causes
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- 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
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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?
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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?
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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
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- 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
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- 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
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*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
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Mimic the normal pattern of insulin secretions as closely as possible.
- Insulin: Synthetic (using recombinant DNA)
- Insulin Analogs
Goal of Insulin Therapy
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Onset of Action
Peak Effect
Duration of action
***Need to know when blood will be affected by insulin
Characteristics of Insulin
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*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
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- 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
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- Lipodystrophy; same place, harden like cellulite
- Lipoatrophy; dimpeling; use different place
- Insulin Resistance; build up over time
Complications of Insulin Therapy
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- Lipodystrophy; same place, harden like cellulite
- Lipoatrophy; dimpling; use different place
- Insulin Resistance; build up over time
Complications of Insulin Therapy
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- Extremes of temperature
- Exposure to light
- Lantus insulin
Storage of Insulin; AVOID
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- Subcutaneous route
- IV route; regular insulin only
- Insulin Pump; (AKA; continuous sub. infusion)
- Fasting acting insulin only
Insulin can be administered
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-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
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* 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
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- 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)
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- 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)
90
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!
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- Inhibits the work of the intestinal enzyme Alpha-Glucoside to slow carbohydrate digestion and delay glucose absorption.
- Acarbose (Precose), Miglitol (Glyset)
Alpha-Glucoside Inhibitors
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- 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
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* *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
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- 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
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- 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
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- Carbohydrate counting
- Exchange list; weight watchers, etc
- Alcohol consumption
- prevent weight gain
Diet control strategies
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- 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
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- 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
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- 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
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- Whole pancreas transplantation
| - Islet cell transplantation; severely sick long term from Diabetes
Advances; DM
