our goals for today l.
Skip this Video
Loading SlideShow in 5 Seconds..
Our goals for today PowerPoint Presentation
Download Presentation
Our goals for today

Loading in 2 Seconds...

play fullscreen
1 / 48

Our goals for today - PowerPoint PPT Presentation

  • Uploaded on

Our goals for today. Define diabetes and subtypes Distinguish between the etiology of the prevalent forms of diabetes Discuss basic features of gestational diabetes Understand the pharmacological management of diabetes. Strange but true……….

I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
Download Presentation

PowerPoint Slideshow about 'Our goals for today' - RexAlvis

An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.

- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
our goals for today
Our goals for today
  • Define diabetes and subtypes
  • Distinguish between the etiology of the prevalent forms of diabetes
  • Discuss basic features of gestational diabetes
  • Understand the pharmacological management of diabetes
strange but true
Strange but true………
  • Greeks noticed that urine of diabetics attracted flies (linked this to increased sugar)
  • Chinese tested for diabetes by noticing whether ants were attracted to urine
  • Europeans tasted urine for sweetness
soft drinks
Soft Drinks……
  • A 50 ml pop drink contains 10 teaspoons sugar
  • 360 ml can of pop contains 160 calories
  • (and same caffeine as in a cup of coffee)
  • Between 1985 and 1997:
  • Schools purchased 30% less milk and
  • 1,100% more soft drinks
Increased sugar in urine leads to loss of water—THIRST
  • Loss of sugar in urine=loss of calories—WEIGHT LOSS
  • Hunger
  • Dry mouth
  • Increased urination
  • Blurred vision
  • Frequent infections
  • Slow healing of cuts, bruises
type 1 diabetes
Type 1 Diabetes
  • Previously called “juvenile onset diabetes” or “insulin dependent diabetes”
  • Canadian connection (Charles Best, medical student partner in discovery of insulin)
insulin 1
Insulin (1)

Things to remember:

  • Glucose UNITS: multiply or divide by 18 (mg/dL is larger than mmol/L)
  • Normal pancreas secretes half of insulin as bolus after a meal. To replace this: need a short acting insulin

Secretes other half gradually during day and night (basal secretion). To replace this: need long acting insulin

insulin 2
Insulin (2)

Insulin to cover meals: short or rapidly acting insulin.

NOVOLOG (insulin aspartate)

HUMALOG (lispro)

For later meal: intermediate acting insulin

NPH (neutral protamine of Hagedorn)

For basal insulin: long acting insulin



extent and duration of various types of insulin
Extent and duration of various types of insulin

Figure 41-2 from Katzung, 8th edition, 2001

HYPOGLYCEMIA is the most prominent adverse effect of insulin.

type 2 diabetes
Type 2 Diabetes
  • Previously called “adult onset diabetes” or “maturity onset diabetes” or “non-insulin dependent diabetes”
first thing to do
First thing to do………….

Lifestyle modifications:

  • Exercise (actually the mere attempt to exercise regularly—no weight loss—can be beneficial)
  • Diet(work with nutritionist)
pharmacological management 1
Pharmacological management(1)

Oral medications initiated when 2-3 months of lifestyle

modifications cannot maintain optimal plasma glucose


First generation: tolbutamide

Second generation: glyburide, glipizide


Metformin used as monotherapy

pharmacological management 2
Pharmacological management(2)
  • ALPHA-GLUCOSIDASE INHIBITORS: (Acarbose) inbibits pancreatic alpha-glycosidase hydrolase enzymes in intestine.
  • THIAZOLIDINEDIONES (Rosiglatone, Pioglitazone)—adjunct to exercise and diet or as monotherapy (PPAR activators—nuclear peroxisome proliferator-activated receptors)
papr activators
PAPR activators
  • Activation of genes that mediate a variety of characteristic actions of insulin
  • PAPR receptors: regulate storage and catabolism of dietary fats.
  • PAPRγ highly expressed in adipose tissue: leads to induction of adipocyte genes—e.g. lipoprotein lipase and fatty acid transporter 1…………improves insulin action in muscle and liver.
dpp 4 inhibitors januvia canada approved for one a day use in 2007
DPP-4 inhibitors (Januvia®)Canada: Approved for one a day use in 2007
  • DPP found in all major organs—esp kidney, liver (also capillary surfaces, circulation (soluble form)
  • No weight gain or hypoglycemia
complications of diabetes
Complications of diabetes..
  • MACROVASCULAR: coronary artery disease, peripheral vascular disease, cerebrovascular disease
  • MICROVASCULAR: leading cause of blindness, kidney failure and amputations

Definition : “any degree of glucose intolerance with onset or first recognized during pregnancy”. IncludesPatients that may previously have undiagnosed diabetes, or may develop diabetes coincidentally with diabetes.Occurs in 5-10% of all pregnancies

risk factors
Risk Factors
  • Previous diagnosis of GDM or impaired glucose tolerance
  • Glycosurea, history of glucose intolerance
  • Family history (first relative with type 2 DM)
  • Maternal age (>35yr)
  • Ethnicity
  • Overweight/obese: BMI> 30kg/m2 (increases risk 2-8X)
  • Previous high birth weight child (>4000g)
  • Largely unknown. Main feature is insulin resistance.
  • Pregnancy hormones may modify binding of insulin to IR…plasma glucose levels rise and insulin release is increased (feedback).
  • Insulin resistance: secures glucose supply to fetus?
  • Normal pregnancy: nearly doubled insulin release
  • Prolactin? Estradiol?
  • Fat (Obesity)
  • Immune system?
  • Gene Mutations
  • Placental cytokines(TNF-α, resistin, leptin) increase IR
  • Placental hormones ( cortisol, progesterone, human placental growth hormone) increase IR.
  • Human chorionic somatomammotropin increases throughout pregnancy and increases maternal insulin release
  • Most women with GDM don’t remain diabetic after birth of child
  • Risk to baby: Growth abnormalities and chemical imbalances (admit to ICU?). Maternal hyperglycemia during week 6-7 of pregnancy: embryo toxicity (CNS, MSK, CV, spontaneous abortion). Hypoglycemia at birth. Jaundice. Increased RBC. Poorly developed lungs (respiratory distress). Later develop diabetes (~50% chance)
  • Risk for mother: Hypertension, UTI and type 2 diabetes (50% chance). Cesarean sections. Increased risk for developing GDM in later pregnancies.
treatment 1
Treatment (1)

Non-pharmacological: Cornerstone treatment

  • Medical nutritional therapy (MNT) –caloric and nutritional support for pregnancy but maintain target blood glucose without excess weight loss/gain (frequent, smaller meals, foods with low glycemic index etc)
  • 30 min daily exercise ( insulin sensitivity, weight loss)
  • If exercise and diet (2 weeks) does not help, use drug treatment
treatment 2
Treatment (2)


  • Insulin: during excessive fetal growth or when maternal glucose levels are not maintained. Use human insulin (least immunogenic)—INJECT—need oral medication. Increase dosage in 3rd trimester
  • Glyburide: minimal placental transfer. Not approved for GDM
  • Metformin: crosses placenta. Many women still need insulin. Not approved for GDM
take away messages

Take Away Messages……….

Diabetes is a progressive disease: high rates of morbidity and mortality.

Most diabetics die of cardiovascular complications.

Treatment of diabetes is a partnership: patient, physician, home support, nutritionist….others.

Insulin types and use (type 1 and type 2 diabetes).

Oral hypoglycemics (type 2 diabetes).

Gestational diabetes—risks for baby and also for mother.