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Ðề tài: Diabetes Mellitus (DM)

  1. #1

    Default Diabetes Mellitus (DM)

    Chủ Đề: Default Diabetes Mellitus (DM)

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    ►Ngày Gửi: 16-05-10 ►Đánh Giá: 5Sao

    1. Deffinition: Diabetes Mellitus (DM) also called Diabetes
    Metabolic disease characterized by high blood glucose concentration
    Abnormal in carbohydrate, protein, lipid metabolism owning to insufficient secretion of insulin or target tissue resistant

    2.Type 1 & Type 2 Diabetes
    Type 1 diabetes : Insulin-Dependent-Diabetes-Mellitus (IDDM)
    - 5-10% of DM
    - Onset: <30 years old ( children: Juvenile Diabetes)
    - Lack of/ no insulin secretion -> insulin deficiency -> hyperglycemia
    - Common cause: autoimmune (T cells attack and decimate the beta cells in the pancreas
    - The patients rely on insulin medication for survival
    Type 2 diabetes : Non-Insulin-Dependent-Diabetes-Mellitus (NIDDM)
    - ~90% of DM
    - Onset:>30 years old (50-60)
    - insulin insensitivity or resistant
    - Treatment variably: diet and weight control, regular physical activity, take medicine by mouth, insulin injection.

    3. Gestational Diabetes Mellitus (GDM):
    - GDM is DM occurs temporarily during pregnancy, resemble type 2 diabetes.
    - 2-5% all of pregnancy
    - cause: the placenta produce hormones (help the baby develop) that work by stopping the actions of insulin.
    GDM may improve or disappear within 6 weeks after delivery.
    - 20-50% of them will eventually develop type 2 later

  2. #2


    Metabolic decompensation in diabetes mellitus:
    - diabetic ketoacidosis (DKA)
    - hyperosmolar hyperglycemic syndrome (HHS)

    - myocardial infarction,
    - cerebrovascular accident,
    - sepsis
    - acute complications (aspiration, cardiac arrhythmias, and cerebral edema)

    - insulin to reverse hyperglycemia --> normal glycermie
    - fluid and electrolyte balance
    - precipitating illness

    1. Hyperosmolar Hyperglycemic Syndrome:
    one of fatal complications of type 2 DM, rare (1/1000)
    - Clinic: due to insulin levels:
    + effectively prevent lipolysis and ketogenesis --> no acidosis (most patient)
    + inadequate to facilitate peripheral glucose uptake and to prevent hepatic residual gluconeogenesis and glucose output. --> dehydration symptoms
    - increasing lethargy, unconsciousness and focal neurologic deficits (grand mal, focal seizures,hemisensory or motor deficits, ...)

    Hallmarks of the HHS: severe hyperosmolarity (>320 mOsm/L) and hyperglycemia (>600 mg/dL)

    Tests:____arterial blood gas: pH > 7,3 , serum bicarbonate >18 mEq/L
    lactic acidosis (+/-) , azotemia(+/-)
    ketonemia (-) , ketonuria (-)

    Effective Osmolarity (mOsm/L) = 2 * ([Na+] (mEq/L) + [Glucose] (mg%) / 18)

    2. Diabetic Ketoacidosis: 5% type 1 DM
    - hints: onset of type 1 diabetes, fatal complication of type 1 DM, severe insulin deficiency
    - result from the combined effects of deficient circulating insulin activity and the excessive secretion of counter-regulatory hormones
    - Clinic:
    + early stage: several days, with advancing polyuria, polydipsia, and other symptoms of progressive hyperglycemia.
    other common clinical features are weakness, lethargy, nausea, and anorexia.
    abdominal pain - classically periumbilical pain and can mimic an acute abdomen
    --> severe volume depletion
    + dry skin and mucous membranes, reduced jugular venous pressure, tachycardia, orthostatic hypotension, depressed mental function, and Kussmaul (deep, rapid) respirations --> dehydration and acidosis
    Tests:____arterial blood gas (serum HCO3- < 18 mEq/L, pH < 7,3) ~ DKA severity
    anion gap metabolic acidosis
    glucose (vary from 250 to more than 1000 mg/dL) , serum ketones (+)
    hyperosmolality: Hyponatremia, hyperkalemia, azotemia
    Ketonuria (+)
    ECG: electrolyte abnormalities / unsuspected myocardial ischemia

    Need: look for infection

    - Complications:
    + Lactic acidosis
    + Arterial thrombosis (stroke, myocardial infarction, ...)
    + Cerebral edema
    + Rebound ketoacidosis


    1. Washington Manual of Medical Therapeutics, 32nd ed, chapter 17
    2. Cecil medicine 23rd ed, chapter 247 + 248
    thay đổi nội dung bởi: hoanganh_89, 17-05-10 lúc 10:29 AM

  3. #3

    Default Alcoholsim, Chronic Pancreatitis can Lead to Diabetes

    Regulation of Blood Glucose:
    1. The liver: stores and releases glucose properly.
    2. The pancrea: insulin and glucagon
    3. Adrenal glands: epinephrine, in case of severe hypoglycemia.
    4. GH and Cortisol: in case of prolonged hypoglycemia.

    So, the blood glucose concentration in a patient with severe liver disease or diseases that damage the pancrea can not be maintain in a normal range.

    It is possible for alcohol to cause diabetes (though most cases of diabetes are not caused by alcohol). Alcohol abuse is the cause of 80% of cases of chronic pancreatitis* and around 1 in 3 people with chronic pancreatitis develop diabetes.

    *The events that initiate an inflammatory process in the pancreas are still not well understood.

  4. #4

    Post Insulin Resistance Syndromes

    Insulin Resistance Syndromes

    1. General:
    - insulin resistance indicates the presence of an impaired biologic response to either exogenously administered or endogenously secreted insulin
    - present years before the onset of diabetes

    - in the development of glucose intolerance and diabetes

  5. #5


    2. Causes:

    3. Clinic:
    - hyperglycemie
    - hyperinsulinemia (+)
    - 3 types:
    a. Type A, which affects young women and is characterized by severe
    hyperinsulinemia, obesity, and features of hyperandrogenism;
    b. Type B, which affects middle-aged women and is characterized by
    severe hyperinsulinemia, features of hyperandrogenism, and autoimmune disorders
    c. Polycystic ovary syndrome (PCOS)

    4. Results:
    - abnormalities of the signaling pathways that link receptor activation with multiple cellular effects
    - prevent the efficient uptake and utilization of glucose by most cells of the body, -brain cell
    - hyperglycemie
    - cell utilization: glucose ↓↓ , fats and proteins ↑↑

    --> abnormal muscle and fat metabolism
    Increased hepatic glucose and lipid production
    Impaired insulin secretion

    --> The metabolic syndrome, or syndrome X:

    + insulin resistance,
    + hypertension,
    + dyslipidemia (low HDL and elevated triglycerides),
    + central or visceral obesity,
    + type 2 diabetes or IGT/IFG,
    + accelerated cardiovascular disease.
    Details: Harrison's Principles of Internal Medicine 17th ed, Chapter 236

    1. Harrison's Principles of Internal Medicine 17th ed
    2. Cecil medicine 23rd edition
    3. Williams Textbook of Endocrinology_11th ed
    thay đổi nội dung bởi: hoanganh_89, 19-05-10 lúc 10:18 AM

  6. #6

    Post Insulin injection

    1. Insulin preparations.
    After SC injection, there is individual variability in the duration and peak activity of insulin preparations and day-to-day variability in the same subject (Table 21-1).

    - Rapid-acting insulins include regular insulin, lispro, insulin aspart, and glulisine.
    Regular insulin can be administered IV, intramuscularly, or SC.
    IV: maximum effect in 10-30 minutes and is quickly dissipated.

    - Intermediate-acting insulins include NPH (isophane) and lente (zinc).
    released slowly from SC sites
    peak : 6–12 hours, followed by gradual decline.

    - Long-acting insulins: Glargine and detemir
    once or twice a day.
    administered once daily as a SC injection at bedtime

    - Mixed insulin therapy. Rapid-acting insulins (regular, lispro, and aspart) can be mixed with intermediate-acting (NPH and lente) or long-acting (ultralente) insulins
    The rapid-acting insulin should be drawn first, cross contamination should be avoided, and the mixed insulin should be injected immediately.

    * Besides, inhaled insulin administered within 10 minutes before meals.
    Patients have to be trained in the appropriate procedure for inhalation of insulin.
    - rapid onset of action, faster than regular insulin with a duration of action between that of insulin lispro and regular insulin.
    - Hypoglycemia, cough, and bitter taste were reported.
    - not currently recommended in smokers / pulmonary disorders including asthma patients

    2. Position: SC insulin delivery.
    - The anterior abdominal wall, thighs, buttocks, and arms are the preferred sites for SC insulin injection.
    - Absorption is fastest from the abdomen, followed by the arm, buttocks, and thigh
    - Injection sites should be rotated across separate regions, to minimize erratic absorption. Exercise or massage over the injection site may accelerate insulin absorption.

    3. Initial insulin dosage (optimal glycemic control)
    - approximately 0.5-1.0 units/ kg/d for the average nonobese patient. --> adjusted
    - two-thirds of the total daily dose is injected in the morning and one-third in the evening.
    - two-thirds of each injection comprises intermediate-acting insulin and one-third is rapid-acting insulin (rule of third).
    - The units of individual insulin components of each injection are then adjusted using values from preprandial and bedtime blood glucose monitoring.

    4. Monitoring.
    - Blood glucose: >= 4 times/day (preprandially and at bedtime) in hospitalized patients with type 1 DM.
    - HbA1c (if no recent result is available)
    - Urine : ketones? whenever hyperglycemia (>300 mg/dL) persists.


    Washington Manual of Medical Therapeutics, 32nd Edition 2007

  7. #7


    These are the questions given by some people in class tonight:

    1/ Why do we classify type 1 and type 2?
    2/ How often does the child of diabetic mother get inborn diabetes mellitus (DM)? when?
    3/ When do we titrate the insulin in blood?
    4/ What is insulinoma?
    5/ When could we infuse dextrose for a DM, blood glucose is 240 mg%, K+ = 4. So how much is real K+?
    7/ Where is the problem of retina in DM?
    8/ A patient has just had an operation of hemorrhagic pancreatitis (necrotic). In how long could that person have diabetes? how many percent?

    Welcome you answer the above sentences!!!
    thay đổi nội dung bởi: boorin88, 26-05-10 lúc 03:40 PM

  8. #8


    Trích Nguyên văn bởi boorin88 View Post
    3/ When do we titrate the insulin in blood?
    + be used, along with glucose and C-peptide levels, to help diagnose insulinomas
    + help diagnose the cause of documented acute or chronic hypoglycemia.
    + check for insulin resistance, + C-peptide + glucose tolerance test (GTT).
    + determine when a type 2 diabetic might need to start taking insulin to supplement oral medications.

    Details: http://www.labtestsonline.org/unders...ulin/test.html

    Trích Nguyên văn bởi boorin88 View Post
    4/ What is insulinoma?
    Insulinoma is a tumour of the pancreas that is derived from beta cells and secretes insulin.

    Signs and Symptoms: neuroglycopenic symptoms:
    - recurrent headache
    - lethargy
    - diplopia
    - blurred vision particularly with exercise or fasting
    --> Severe hypoglycemia may result in seizures, coma, and permanent neurological damage.

    - insulin ≥ 3 μU/mL (18 pM)
    - C-peptide ≥ 200 pM
    - proinsulin ≥ 5 pM
    - β-hydroxybutyrate ≤ 2.7 mM
    - blood glucose ≥ 25 mg/dL (1.4 mM).
    thay đổi nội dung bởi: hoanganh_89, 06-06-10 lúc 06:07 PM

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