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Flashcards in Intro to diabetes Deck (17):

Other than type 1, type 2, and gestational, what are some causes of diabetes?

genetic beta cell defects, genetic defects in insulin action, diseases of the exocrine pancreas, drug induced, infections, stiff person syndrome


What is LADA?

LADA: latent autoimmune diabetes of adulthood: 10% of pts with "type 2 DM" are leaner, have higher A1Cs, and have antibodies like a type I diabetic. tends to be somewhat slower in onset than childhood type 1 DM.


What is flatbush diabetes?

entity that is esp. seen in African Americans
now called ketosis prone diabetes- they don't fit typical DM 1 profile but they are prone to ketosis


What is MODY?

maturity onset diabetes of youth. non-insulin dependent disease. no autoantibodies. often autosomal dominant transmission.
caused by monogentic mutations that affect insulin secretion. pts are often lean, but it looks like DM type II. they get diabetes before age 25.


What should I know about neonatal diabetes?

it exists, and about half of it is transient, while the other half is permanent


What should I know about beta cell growth in childhood?

Beta cell mass growth varies wildly in childhood
as we age, there is tremendous variation around the mean number of beta cells. people with much lower beta cell mass are more prone to diabetes than those with a higher reserve


How is insulin secreted?

glucose enters teh cells through glut-2 receptors. it is broken down to ATP. At a certain ATP:ADP level, ATP binds inward rectifying K channels called Kir6.2. Kir6.2 is closed. This depolarizes the cell and opens Ca2+ channels. Calcium influx causes the release of insulin from secretory granules into the body


What are some monogenic forms of DM?

glucokinase is an enzyme that is important for glucose detection. defects cause insulin resistance because a higher glucose threshold is required for glucokinase activity. this diabetes is stable, mild, and not really associated with the same degree of complications.
HNF-alpha gene mutations are more serious


non-genetic factors that cause DM

aging, high caloric intake, overweight, central adiposity, sedentary lifestyle, low birth weight


compare type 1 and type 2 diabetes with respect to onset symptoms, insulin requirement, b cell descrution, obesity, insulin resistance, familial, and HLA associations, autoantibodies, seasonal onset

type 1: abrupt, always symptomatic, always requires insulin, involves b cell destruction, obesity is unusual, no insulin resistance, not usually familial, and there are HLA associations. autoantibodies present, there is a seasonal onset
type 2: gradiual, often asymptomatic, sometimes insulin is required, about 10% have b cell destruction, usually obese, insulin resistant, usually familial, not associated with HLA types. 10% have autoantibodies, no seasonal onset


Dx of DM

HbA1C >6.5 or symtpoms plus casual glucose > 200 mg/dl or fasting plasma glucose > 126 or 2 hr plasma glucose > 200 during a 75 g glucose challenge


What is impaired fasting gluose

levels of 100-126 mg/dl fasting


what is impaired glucose tolerance?

2 hr glucose >140 but <200 during glucose challenge


What factors promote glucugon and insulin secretion

glucugone: GH, cortisol, epinephrine
insulin: VIP, GIP (and some others like enteroglucagon, cholecystokinin-pancreozymin)


What does insulin do?

anabolic metabolic state to replenish energy stores:
glucose is made into glycogen in liver and muscle
FFA made into triglycerides in adipose tissue and liver
AAs made into proteins


What metabolic abnormalities contribute to insulin resistance?

central obesity, aging, reduced physical activity, hyperinsulinemia, smoking elevated FFAs, drugs, elevated cytokines


What are some consequences of uncompensated insulin resistance?

muscle: decr. glucose utilization
liver: incr. glucose production and triglyceriad and VLDL secretion
adipose: incr. FFA release
causes glucose intolerance, hypertiglyceridemia, and elevated FFAs