Theme 3: Diabetes Flashcards
C-peptide
this part is removed when converting proinsulin to insulin. this is a good measure of insulin synthesis for type 1
tests for type 1
c peptide and insulin autoantibody levels
in the absence of insulin in the liver… this is bad because
the unopposed action of glucogon promotes gluconeogenesis. This causes too much PROTEOLYSIS AND LIPOLYSIS
In the muscle, without insulin
the muscle does not receive any of the glucose that it needs for energy. because the muscle is so energy deprived, the ATP dependent transporters fail, and K+ leaks out of the cell and is lost in the urine. Thus, DIABETIC KETOACIDOSIS
Long term effects of no inuslin on brain, muscle and beta cells
The brain will down regulate glucose transporters because there is a massive amount of free glucose in the blood. The uscle will start to breakdown because of no energy, with a negative nitrogen balance and K loss. Also the beta cells will begin to die off because of glucose toxicity. Thus, poly urea, polydipsia, volume depletion, low HCO3, low pH, plasma K levels iwll be normal or even high, because it is not in the cell where it should be.
Unrestrained lipolysis and ketogenesis…
because of lack of insulin
Symptoms of untreated T1DM
Polyuria and polydipsia
Volume depletion (5+ liters), postural hypotension,
tachycardia
Loss of body fat and muscle, muscle weakness
Deep shallow breathing, breath smells of acetone
Labs (blood) glucose high, HCO3- low, pH low,
K+ normal or even high but body severely depleted
Osmotic diuresis with diabetes
because plasma glucose levels are really high and the renal threshold for glucose reabs at the kidney is 180.. thus becaue the urine becomes hyperosmotic, more water and salt is lost in the urine.
ketones
acetoacetic acid, beta hydroxybutyrate, acetone (thus sweet acetone breath)
Acidosis
acid produced from lipolysis (fat) and ketogenesis (liver) is initally buffered, by bicarb in the blood– this generate Co2, Kussmaul breathing– eventually this is overcome and blood pH becomes acidic
patient considerations for T1
life expectancy is now near normal, but not a normal life; with injected insulin, there is a risk of hypoglycemia always present, balanced with concequences of long term hyperglycemia
T2DM
common cause of early death (kidney failure, blindness, MI, stroke.)
usually asymptomatic
t2dm risk factors
asian american, latino, pacific islanders at a higher risk,
insulin resistance most commonly caused by obesity
low birth weight, fetal malnutrition
sleep disturbance
WESTERN LIFESTYLE HAS A BAD EFFECT
t2dm and central obesity
increased bmi increases insulin demand
insulin resistance and obesity
fact cells in obesity recruit INFLAMMATORY CELLS with release of cytokines. and these infl cytokines contribute to insulin resistance. c-reactive protein predicts risk for t2d and vascular disease
Insulin resistance due to inflammation from obesity, but not all people with insulin resistance on these cells get diabetes
80% are still non diabetic. they are able to make more insulin an do not get diabetes. Thus the genetic predisposition to t2 d is based on the beta cell response to insulin resistance. Those who develop diabetes have a LOWER BETA CELL MASS
T2dm when insulin demand is greater than insulin availability.. THUS WEIGHT LOSS
weight loss and lowered bmi helps with diabetes because it will lower the insulin demand to a level that is below insulin availability
Type 1 diabetes- ethnic risk factor.
caucians are at higher risk. it is an autoimmune diease. 1.5 million are affected in the US (30 mill t2dm)
t2dm
any type of insulin resistance, wether due to obesity, pregnancy, etc.
diabetes treatment
everyday, avoid high levels of blood glucose in order to prevent longer micro and macro vascular complications
other causes if increased insulin risk in addition to obesity
corticosteroid treatment, liver disease, muscle wasting diseases, pregnancy.
t2d patient considerations
do not make them feel guilty, this has a genetic component like male pattern balding.
changes in lifestyle is importnat for treatment, but this only comes with EDuCATION and help by explaining the context of their inheriting the genetic predisposition.
life expectancy is normal with appropriate care.
Clinical signs of diabetes
increased thirst, frequent urination, fatigue, weight loss Kussmaul breathing pattern Acetone breath Obese Acanthosis nigricans Serum glucose more than 100 High/Normal Potassium (when acute?) Diabetic Ketoacidosis, low pH With anion gap.. Glycosuria family history Increased risk of yeast infections
Associated with hypertension?
Look up stuff in Costanzo brs and physic!
diabetes treatment
everyday, avoid high levels of blood glucose in order to prevent longer micro and macro vascular complications
C-peptide
this part is removed when converting proinsulin to insulin. this is a good measure of insulin synthesis for type 1
other causes if increased insulin risk in addition to obesity
corticosteroid treatment, liver disease, muscle wasting diseases, pregnancy.
t2d patient considerations
do not make them feel guilty, this has a genetic component like male pattern balding.
changes in lifestyle is importnat for treatment, but this only comes with EDuCATION and help by explaining the context of their inheriting the genetic predisposition.
life expectancy is normal with appropriate care.
Clinical signs of diabetes
increased thirst, frequent urination, fatigue, weight loss Kussmaul breathing pattern Acetone breath Obese Acanthosis nigricans Serum glucose more than 100 High/Normal Potassium (when acute?) Diabetic Ketoacidosis, low pH With anion gap.. Glycosuria family history Increased risk of yeast infections
Associated with hypertension?
Look up stuff in Costanzo brs and physic!
C-peptide
this part is removed when converting proinsulin to insulin. this is a good measure of insulin synthesis for type 1
C-peptide
this part is removed when converting proinsulin to insulin. this is a good measure of insulin synthesis for type 1
