Tri 7 Endocrinology #7725 Test 5 Summer 2000 Dr. Sanders
1
DIABETES
(American diabetes association clinical practice recommendations 1998). This is
relatively prominent. There is plenty of fund raising to “cure” the disease. 30-40% of people
have DM and don’t know it. Our textbook is relatively current, but some tests are obsolete.
Over the years there were a number of diagnostic schemes to detect DM. You either have it or
you don’t. DM is common that chiropractors see – they will either have it or they will develop
it.
Diabetes mellitus is a group of metabolic diseases characterized by hyperglycemia
resulting from defects in insulin secretion, insulin action, or both. Note, hyperglycemia is not
DM. Hyperglycemia: 1) there is a defect in insulin production 2) there is a problem in insulin
action 3) both.
CLASSIFICATION OF DIABETES MELLITUS AND OTHER CATEGORIES OF GLUCOSE
REGULATION – the expert committee on the diagnosis and classification of diabetes
mellitus.
CLASSIFICATION OF DM:
Type 1 – idiopathic.
Type 2 – idiopathic.
Other specific types (caused by an identifiable process).
Gestational DM – idiopathic.
The terms insulin-dependent DM and non-insulin-dependent DM and their acronyms, IDDM
AND NIDDM, are eliminated.
The terms type 1 and type 2 are retained, with Arabic numerals being used rather than roman
numerals.
TYPE 1: encompasses the vast majority of cases that are primarily due to pancreatic islet -cell
destruction and that are prone to ketoacidosis.
While most type 1 diabetes is characterized, in the majority of cases, by the presence of islet cell,
GAD, IA-2, IA-3, (insulin autoantibodies) that identify the autoimmune process that leads to
-cell destruction. In some subjects, no evidence of autoimmunity is present. These cases
are classified as type 1 idiopathic, though we know the mechanisms, the cause is unknown.
Had the label of insulin dependent, juvenile onset, and others.
TYPE 2: includes the most prevalent (85-90%) form of diabetes, which results from insulin
resistance with or without an insulin secretory defect.
OTHER – these cause secondary forms of DM:
Genetic defects of -cell function
Diseases of the pancreas
Drug/chemical induced
Uncommon immune forms
Genetic defects in insulin activity
Endocrinopathies
Infections
Other genetic syndromes
Tri 7 Endocrinology #7725 Test 5 Summer 2000 Dr. Sanders
2
GESTATIONAL DM – defined as any degree of glucose intolerance with onset or first
recognition during pregnancy. This is not a case of a diabetic that becomes pregnant, it is a
person that becomes pregnant and develops DM that may or may not resolve. GDM
complicates ~4% of all pregnancies in the U.S., resulting in ~135,000 cases annually. The
prevalence may range from 1-14% of pregnancies, depending on the population studied.
Maternal complications related to GDM also include an increased rate of cesarean delivery
and chronic hypertension. Although many patients diagnosed with GDM sill not develop
diabetes later in life, others will be diagnosed many years postpartum as having type 1
diabetes, type 2 diabetes, IFG (intolerance of fasting glucose), or IGT (impaired glucose
tolerance).
IMPAIRED GLUCOSE TOLERANCE – the stage termed impaired glucose tolerance (IGT) has
been retained.
MALNUTRITION-RELATED DM – this class of DM is eliminated. While it appears that
malnutrition may influence the expression of other types of diabetes, the evidence that
diabetes can be directly caused by protein deficiency is not convincing. It is more likely a
result of genetics that expressed itself through frank starvation.
DIAGNOSTIC CRITERIA FOR DM (National Diabetes Data group 3/98).
Three ways to diagnose diabetes are possible:
1. Symptoms (polyuria, polydipsia, polyphagia, etc) with casual plasma glucose >200.
Casual is defined as any time of day without regard to time since last meal.
2. FBG >126 mg/dL; fasting is defined as no caloric intake for at least 8 hours. There are
challenges to this diagnostic criteria. Though our text says 140, in the past six months it
changed to 126. There are three types of glucose: normal (was 80-120), diagnostic
(140), and the “in-betweeners”… what was discovered, was that people in the 126 to 139
range tended to develop complications.
3. An OGTT (oral glucose tolerance test) with the 2 hour post-load value >200mg/dL.
This is a rare test anymore and you can not perform it on an ill patient. This is not
reproducible, if over age 65 it doesn’t work.
Symptoms and casual glucose >200mg/dL or FBG>126mg/dL or 2hr (OGTT)>200mg/dL. Each
must be confirmed by repeat testing.
FBG<110mg/dL = normal fasting glucose.
FBG>110 and <126mg/dL = IFG
FBG>126mg/dL = provisional diagnosis of diabetes.
2 hour post-load of glucose (2h PG)<140 = normal glucose tolerance
2 hour PG >140 AND <200 mg/Dl = IGT
2 hour PG>200 mg/dL = provisional diagnosis of diabetes (the diagnosis must be
confirmed).
HbAlc measurement is not currently recommended for diagnosis of diabetes.
Tri 7 Endocrinology #7725 Test 5 Summer 2000 Dr. Sanders
3
THE DISEASE
Several pathogenic processes are involved in the development of diabetes. DM is a multisystemic disease primarily affecting the nervous and vascular systems. This is where
chiropractic comes in to help. These range from autoimmune destruction of the -cells of the
pancreas with consequent insulin deficiency to abnormalities that result in resistance to
insulin action. The basis of the abnormalities in carbohydrate, fat, and protein metabolism in
diabetes is deficient action of insulin on target tissues. Deficient insulin action results from
inadequate insulin secretion and/or diminished tissue responses to insulin at one or more
points in the complex pathways of hormone action. Impairment of insulin secretion and
defects in insulin action frequently coexist in the same patient, and it is often unclear which
abnormality, if either alone, is the primary cause of the hyperglycemia.
Symptoms of marked hyperglycemia include: polyuria, polydipsia, weight loss, polyphagia,
blurred vision.
As physicians, our responsibility is to find, recognize, and diagnose the process.
COMPLICATIONS
Acute metabolic – the patient will die without treatment. This is what the diabetic works to
prevent on a daily basis.
Hypoglycemia – the most frequent; 10-25% of patients, more common in type 1.
Ketoacidosis – most often in recognized diabetics; hyperglycemia, acidosis, osmotic diuresis,
abdominal pain, anorexia, nausea. This is a killer.
Nonketotic hyperosmolar syndrome - >320mOsm/L, >600mg/dL, dehydration; caused by
lack of fluid intake. This is also a killer.
Chronic - common denominator is nerves and vessels.
Retinopathy – diabetes is the leading cause of blindness in persons aged 3 years. Blindness
occurs 20 times more frequently in diabetic patients than in others. Is most often seen
after the disease has been manifest for at least 15 years. Approximately 10-15% of type 1
diabetic patients become legally blind whereas in type 2 diabetic patients the risk is
approximately half that value. The primary cause of visual loss is retinopathy.
Regardless of the type of diabetes, the severity of retinopathy increases with increasing
duration of the disease. The earliest retinopathic changes are classified as nonproliferative retinopathy. These lesions generally do not affect visual acuity.
Proliferative retinopathy is characterized by the growth of fine … new blood vessels and
fibrous tissue from the inner retinal surface … optic nerve head. Prevalence rates of both
non-proliferative and proliferative retinopathy are higher in type 1 than in type 2 diabetes.
Nephropathy – end stage renal disease (ESRD) from diabetic nephropathy is a major cause of
death, particularly in type 1 diabetes, in which it affects 30-35% of patients. Diabetes is
the leading cause and accounts for one third of the ESRD cases in the united states. In
patients destined to develop ESRD, gross proteinuria (greater than 0.3 gram of albumin
per day) begins approximately 15 years after the diagnosis of diabetes.
Neuropathy – symptomatic, potentially disabling neuropathy affects nearly 50% of diabetic
patients. It may be symmetrical or focal and often involves the autonomic nervous
system as well. The prevalence of symmetrical neuropathy is similar in type 1 and 2
diabetes, whereas focal neuropathy is most common in older type 2 diabetes.
Tri 7 Endocrinology #7725 Test 5 Summer 2000 Dr. Sanders
4
Distal sensorimotor neuropathy – this syndrome, characterized by axonal loss, is the most
common presentation of diabetic neuropathy. The process involves all somatic nerves
but has a distinct … predilection for distal sites, i.e. the distal sensorimotor nerves of the
feet and hands. Patients complain of numbness and tingling in the extremities, especially
the feet.
Diabetic foot – the syndrome is characterized by plantar ulcers that heal slowly and follow
apparently insignificant trauma. In severe cases, gangrene may be a complication and
amputation the outcome. Diabetes accounts for about one half of non-traumatic limb
amputations.
Atherocsclerosis – involving the arteries of the heart, lower extremities, and brain is the
major cause of death from diabetes. The atherosclerotic process is indistinguishable from
that affecting the non-diabetic population but begins earlier and is more severe. The
predilection of atherosclerosis is uniformly observed over the entire spectrum of diabetes
– from difficult-to-control insulin dependent patients to patients with mild hyperglycemia
requiring insulin. The risk of MI is 2 to 3 fold greater in diabetes.
Hypertension.
TREATMENT GOALS
Short term
A. Restore metabolic control to as close to normal as possible.
B. Improve sense of well-being.
Long term - Minimize risk of diabetic complications: accelerated atherosclerosis,
microangiopathy (retinopathy, nephropathy), neuropathy.
LIFESTYLE MODIFICATIONS FOR THE PATIENT WITH DIABETES
Diet
1. Weight reduction (when appropriate). This increases the receptor density as the cell
size reduces.
2. Carbohydrates: 45-60% (depending on severity of diabetes and triglyceride).
3. Restriction of saturated fat (to < 10% of calories).
4. Increased monounsaturated fat (depending on the need to limit carbohydrate.
5. Decreased cholesterol intake to <300 mg per day.
6. Sodium restriction in patients prone to HTN.
Exercise
1. Type: aerobic strongly preferred. Avoid heavy lifting, straining, and Valsalva
maneuvers that raise BP.
2. Intensity: increase pulse rate to at least 120-140, depending on the age and
cardiovascular state of the patient.
3. Frequency: 3-4 days per week.
4. Duration: 20-30 minutes preceded and followed by stretching and flexibility exercises
for 5-10 minutes.