Diabetes Notes
If you get a chance take a look at either or both of these websites.
http://www.diabetes.org/about-diabetes.jsp
http://diabetes.niddk.nih.gov/dm/pubs/statistics/
Diabetes= ‘to siphon’ Mellitus= ‘sweet’: characterized by sweet urine
“DM is not a single disorder but a group of chronic disorders of the pancreas resulting in inappropriate hyperglycemia caused by relative or total insufficiency of insulin, or cellular resistance to insulin.”
Type 1 DM: pancreatic islet cell damage and therefore total deficit of circulating insulin. [L/B] Type 1 diabetes is usually due to autoimmune destruction of the pancreatic beta cells, which produce insulin. [wiki]
Type 2 DM: results from insulin resistance with a defect in compensatory insulin secretion. [L/B] [abnormal resistance to insulin's effects coupled with inadequate levels of insulin secretion to compensate]. Type 2 diabetes is characterized by insulin resistance in target tissues, but some impairment of beta cell function is necessary for its development. [wiki]
Gestational [occurring during pregnancy]: Gestational diabetes is similar to type 2 diabetes, in that it involves insulin resistance; the hormones of pregnancy can cause insulin resistance in women genetically predisposed to developing this condition. [wiki]
Other Specific Types of DM: genetic defects in beta cell, diseases of the exocrine pancreas, drug induced in predisposed [drugs like thiazides, dilantin, thyroid hormone, glucocorticoids, etc], viral infections that attack beta cells…
Ultimately, all forms are due to the beta cells of the pancreas being unable to produce sufficient insulin to prevent hyperglycemia. [wiki]
The characteristic symptoms are excessive urine production (polyuria), excessive thirst and increased fluid intake (polydipsia), and blurred vision; these symptoms may be absent if the blood sugar is mildly elevated. [wiki]
Treatment
Type 1 diabetes, in which insulin is not secreted by the pancreas, is directly treatable only with injected or inhaled insulin, although dietary and other lifestyle adjustments are part of management.
Type 2 may be managed with a combination of dietary treatment, tablets and injections and, frequently, insulin supplementation.
Gestational diabetes typically resolves with delivery of the child. [wiki]
Normal levels of blood glucose: 80-120 mg/dL
Hormone interaction:
When low blood sugar [<70]: style=""> Also triggers breakdown of fat stores in adipose tissue.
When you have high blood sugar insulin [hormone created by beta cells in pancreas] is secreted to trigger cellular uptake of glucose from the bloodstream. It also prevents glycogenolysis. From the pancreas, insulin circulates first to the liver and then to systemic circulation. Glucose is then absorbed by the liver [site of storage of glucose as glycogen] and systemic cells until blood glucose has dropped again.
Backup system: the brain, nephrons, liver, and intestines do not require insulin to uptake glucose. However; your lungs, heart and muscles do, so you won’t make it long without insulin.
S&S:
Polyuria: caused by Serum hyperosmolarlity drawing fluid from intracellular to extracellular—[so you’re dehydrating the cells, forcing water into the blood.] The excess sugar in the blood acts as an osmotic diuretic: all the extra water in the blood is forced to urine.
Glucosuria: when blood levels of glucose are higher than 180, glucose is also forced into the urine. Which is probably a good trick of the body to get rid of excess urine.
Polydispia: thirst is caused by dehydration of the cells and corresponding release of water into the urine.
Polyphagia: because the cells are starving for glucose [despite the fact that they’re swimming in it], they initiate hunger response. Fatigue follows this lack of fuel in cells.
Blurred vision: macular edema is likely to have blurred vision, making it hard to do things like read and drive. In some cases, the vision will get better or worse during the day. [wiki] Results from swelling of the lenses of the eyes due to osmotic pressure. Extreme: Loss of vision from hemorrhagic damage due to diabetic retinopathy. [wiki]
Ketoacidosis: resulting from rapid, excessive breakdown of fats in the body. Bicarbonate is not produced to balance ketones from this catabolism, and the body becomes acidic. The body is also dehydrating. Scary because: CNS is depressed in the presence of ketones and acids, can cause coma and death. This is why we admit people to the hospital as soon as their blood glucose is over 250, ketones are present in the urine, or decreasing pH. Ketoacidosis and polyuria is followed by hypokalemia [obligate loss of potassium from kidney tubules as a cationic partner to the negatively charged ketone]
Risk factors in Type 2 diabetes:
Family Hx
Obesity [at least 20% over desired body weight] creates “peripheral insulin resistance” by ‘decreasing the number of insulin receptor sites in skeletal muscles and adipose tissue.’ Obesity also impairs beta cell secretion.
Physical inactivity
Race: Native Americans are 2.2 times as likely to have DM than whites, Hispanics 1.8 times, Blacks 1.7 times. 8.7% of white Americans have DM.
HTN, low HDL, or high triglycerides
Symptoms of hyperglycemia: wiki
· Polyphagia - frequent hunger, especially pronounced hunger. Polydipsia and polyuria occur when blood glucose levels rise high enough to result in excretion of excess glucose via the kidneys (glycosuria), producing osmotic diuresis.
- Polydipsia - frequent thirst, especially excessive thirst:
- Polyuria - frequent urination, especially excessive urination
- Blurred vision
- Fatigue
- Weight loss
- Poor wound healing (cuts, scrapes, etc.)
- Dry mouth
- Dry or itchy skin
- Impotence (male)
- Recurrent infections such as vaginal yeast infections, groin rash, or external ear infections (swimmer's ear)
Symptoms of acute hyperglycemia may include:
- Ketoacidosis
- A decreased level of consciousness or confusion
- Dehydration due to glycosuria and osmotic diuresis
- Acute hunger and/or thirst
- Impairment of cognitive function, along with increased sadness and anxiety[8][9]
Hypoglycemia: wiki
If the amount of glucose supplied by the blood falls, the brain is one of the first organs affected. In most people, subtle reduction of mental efficiency can be observed when the glucose falls below 65 mg/dl (3.6 mM). Impairment of action and judgement usually becomes obvious below 40 mg/dl (2.2 mM). Seizures may occur as the glucose falls further. As blood glucose levels fall below 10 mg/dl (0.55 mM), most neurons become electrically silent and nonfunctional, resulting in coma. These brain effects are collectively referred to as neuroglycopenia.
Hypoglycemia
HHS: Hyperosmotic Hyperglycemic State/Nonketotic hyperosmolar coma: [in this case ketones are not part of the equation because there is enough insulin to keep faty acid catabolism down. Hyperosmotic state concentrates the blood with glucose and sodium, sucking water out of cells and the brain cells. Think severe dehydration.] (nonketotic hyperglycaemia) is a type of diabetic coma associated with a high mortality seen in diabetes mellitus type 2. The preferred term used by the American Diabetes Association is hyperosmolar nonketotic state (HNS). Other commonly used names are hyperosmolar hyperglycemic nonketotic coma (HHNKC) or hyperosmotic non-ketoic acidosis (HONK).
Nonketotic coma is usually precipitated by an acute illness, myocardial infarction or stroke. A relative insulin deficiency leads to a serum glucose that is usually higher than 33mmol/l (600 mg/dl), and a resulting serum osmolarity that is greater than 350 mOsm. This leads to polyuria (an osmotic diuresis), which, in turn, leads to volume depletion and hemoconcentration that causes a further increase in blood glucose level. Ketosis is absent because the presence of some insulin inhibits lipolysis, unlike diabetic ketoacidosis.
The increasing hemoconcentration and volume depletion may result in:
- Hyperviscosity and increased risk of thrombosis
- Disturbed mentation
- Neurologic signs including focal signs such as sensory or motor impairments or focal seizures or motor abnormalities, including flacidity, depressed reflexes, tremors or fasciculations.
- Ultimately, if untreated, will lead to death.
The treatment involves slow hydration, replacement of electrolytes and intravenous insulin. Anticoagulants (such as low molecular weight heparins) are often commenced as there is a significant rate of thrombosis in patients with NKHC. Mortality is 30% to 50%.
Chronic complications
Vascular disease
Chronic elevation of blood glucose level leads to damage of blood vessels (angiopathy). The endothelial cells lining the blood vessels take in more glucose than normal, since they don't depend on insulin. They then form more surface glycoproteins than normal, and cause the basement membrane to grow thicker and weaker. In diabetes, the resulting problems are grouped under "microvascular disease" (due to damage to small blood vessels) and "macrovascular disease" (due to damage to the arteries).
Image of fundus showing scatter laser surgery for diabetic retinopathy
The damage to small blood vessels leads to a microangiopathy, which can cause one or more of the following:
- Diabetic retinopathy, growth of friable and poor-quality new blood vessels in the retina as well as macular edema (swelling of the macula), which can lead to severe vision loss or blindness. Retinal damage (from microangiopathy) makes it the most common cause of blindness among non-elderly adults in the
- Diabetic neuropathy, abnormal and decreased sensation, usually in a 'glove and stocking' distribution starting with the feet but potentially in other nerves, later often fingers and hands. When combined with damaged blood vessels this can lead to diabetic foot (see below). Other forms of diabetic neuropathy may present as mononeuritis or autonomic neuropathy. Diabetic amyotrophy is muscle weakness due to neuropathy.
- Diabetic nephropathy, damage to the kidney which can lead to chronic renal failure, eventually requiring dialysis. Diabetes mellitus is the most common cause of adult kidney failure worldwide in the developed world.
Macrovascular disease leads to cardiovascular disease, to which accelerated atherosclerosis is a contributor:
- Coronary artery disease, leading to angina or myocardial infarction ("heart attack")
- Stroke (mainly the ischemic type)
- Peripheral vascular disease, which contributes to intermittent claudication (exertion-related leg and foot pain) as well as diabetic foot.
- Diabetic myonecrosis ('muscle wasting')
Diabetic foot, often due to a combination of neuropathy and arterial disease, may cause skin ulcer and infection and, in serious cases, necrosis and gangrene. It is the most common cause of adult amputation, usually of toes and or feet, in the developed world.
Carotid artery stenosis does not occur more often in diabetes, and there appears to be a lower prevalence of abdominal aortic aneurysm. However, diabetes does cause higher morbidity, mortality and operative risks with these conditions.[37]
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