FINAL: DIABETES Flashcards
Where is insulin produced?
in the BETA islet cells of the pancreas:
○ Alpha Islet cells produce glucagon
○ Insulin released form the B cells is not the true form used by the cells
▪ There’s a process of activation
○ The insulin then attaches to many cells
▪ Mainly muscle, fat, and tissue cells
▪ There are certain cells that don’t use
insulin
○ Without insulin attaching to the cell, glucose CANNOT enter the cell
** diabetes is a disease where the body doesn’t produce or use insulin properly **
What is DM and what does it affect?
a GROUP of metabolic disorders
- Impaired metabolic functioning affecting fat, carbs, and protein metabolism
- Characterized by HYPERglycemia (in all types)
Who is DM more prevalent in?
all age groups but affects more of the minority population and older adults (65+):
- American Indian/Alaskan Natives
- Black
- Hispanic
- Asian
- White
** it is the 7th leading COD in the USA **
What can DM cause in a patient?
○ Number 1 cause of blindness
○ Number 1 cause of END-stage Renal Disease (ESRD)
▪ Number 2 = HTN
○ Number 1 cause of lower extremity of amputations
○ Major r/f for MI and CVA
○ Large medical expenses and diminished QOL (1/3 of medicare budget)
What are some historical perspectives of DM?
- Egyptians found urine to be sweet
- Greeks described polydipsia (excess thirst) and polyuria of sweet urine
- Research in the US (1921) Banting & Best discovered the hormone insulin in dogs
Which diabetes develops as a child?
Type I: they MUST inject insulin or they will die
** ABSOLUTE INSULIN DEFICIENCY **
▪ Caused by either:
□ Type 1A- Immune mediated response
(autoimmune destruction of B cells)
□ Type 1B - Idiopathic (unknown etiology)
Describe some elements of type II diabetes:
○ Most common
○ Can be managed w/ diet
○ Others take oral meds that stimulate the pancreas and the insulin process
○ Progressive disease
▪ After about 10 yrs, they are likely to
need to have insulin supplements
▪ Due to exhaustion of cells
○ Combination of decreased insulin production and cellular resistance to insulin
** Unmanaged Type II can lead to Beta cell exhaustion and lack of insulin production and require insulin injections **
What are some contributing factors to hyperglycemia?
- Pancreas:
○ Impaired insulin secretion/production - GI:
○ Absorption of glucose from diet - Liver:
○ Inappropriate glucose production
▪ Breaks down glycogen stores even if
there is BG from GIT absorption - Muscle:
○ Decreased insulin-stimulated glucose
uptake
▪ Glucose sparing for the brain and other
vital organs
Describe the effects of the pancreatic hormone insulin:
○ Secreted by B cells in pancreas
○ Lowers the blood glucose by attaching to cells’ insulin receptors, allowing glucose to enter the cell
▪ If there is excess glucose, it is stored as
glycogen
○ Prevents the breakdown of fat and glycogen stores in the liver and lipid tissues
▪ Works to build fat to reduce the blood
sugar levels
▪ Also inhibits gluconeogenesis
○ Increases protein synthesis, fatty acid transport into ADIPOSE tissues
▪ Increases transport of AA into protein
cells
○ Inhibits the lipase in adipose- preventing breakdown of fats
○ Target Cells:
▪ Some cells don’t require insulin for
glucose uptake (liver, brain, RBC)
▪ All other cells require insulin to uptake
glucose into the cells.
What controls glucose levels?
□ Insulin secretion
□ Uptake of glucose by peripheral tissues
□ Glucose production in the liver
- Can either store glucose as glycogen or
through gluconeogenesis -> breakdown
glycogen stores to increase blood glucose
levels
- Liver can inappropriately increase blood
glucose levels in diabetics
What is the pathogenic process of diabetic hormones?
▪ Autoimmune destruction of B cells (type I)
▪ Insulin resistance (type II)
□ Obesity is a risk factor for type II
▪ Diminished tissue responsiveness to insulin
□ Leads to hyperglycemia, then eventually
overt diabetes
What is the effect of glucagon in the body and when is it used?
○ It increases blood glucose levels
▪ Coverts stored glycogen in liver to
glucose
▪ Released of glucagon stimulated by low
blood sugar levels
○ Used for children with HYPOglycemia to induce the liver to break down glycogen stores to increase blood glucose levels
What is the effect of amylin in the body and when is it used?
○ Islet amyloid polypeptide
○ Co-secreted from the B cells of the pancreas (along with insulin)
○ Released in response to nutritional stimuli
▪ Slows the movement of food through
the stomach to lower the postprandial
blood glucose (2 hours after meals)
□ Blood sugar should be normal at this
time (below 140)
□ Persons with diabetes, manage the
level between 140-180
▪ This is the clinical significance (lowers
postprandial glucose)
○ May cause degeneration of the beta cells and contribute to development of T2DM
What is the effect of somatostatin in the body and when is it used?
○ Released by the Delta pancreatic cells
○ Inhibits the release of insulin & glucagon
○ Decreases GI activity after ingestion of food
▪ Thus increasing the amount of time it
takes for the food to absorbed into the
bloodstream
○ Clinical significance: synthetic forms of hormone not used in diabetes but used in acromegaly and other growth hormone disorders.
What 4 hormones control the regulation/absorption of glucose, AA, & fatty acids?
- insulin
- glucagon
- amylin
- somatostatin
What is incretin (GILA MONSTER) and its effects on the body?
Intestinal hormones in response to ingestion of food
▪ Increases the insulin response to get
glucose in the cells
▪ Responses to incretin in T2DM is
decreased (not as effective)
What are the two main types of incretins and what are they degraded by?
- GIP
- GLP-1
** GIP and GLP-1 are rapidly degraded by the DPP-4 Enzyme **
What is exenatide and when is it used?
a synthetic GLP-1 that is resistant to the DPP-4 enzyme, and thus lasts longer in the bloodstream
□ Since the synthetic GLP-1 is in the
bloodstream longer, it potentiates the
insulin release
▪ Given by injection to potentiate insulin release
▪ A synthetic DPP-4 agent (Januvia) has been developed to decrease hyperglycemia
□ DPP-4 AGENT used to deactivate DPP-4
ENZYME
□ Is that why the DPP-4 agent is used to
decrease hyperglycemia???
What are some other specific types of diabetes?
○ Most of the times these are genetic in nature
○ Endocrine disorders (Cushing’s): Prolonged cortisol release, causes increased/prolonged gluconeogenesis
○ Diseases of the Pancreas (pseudocysts)
○ Gestational DM: develops during pregnancy (may or may not end after pregnancy)
How is DM diagnosed?
- Fasting Blood Glucose (FBG)- (Traditional Method)
○ 126 mg/dl or higher
▪ Diagnostic of DM
▪ Normal = 70-100
○ This is the blood glucose after 8 hrs of
fasting - Hgb A1C
○ 6.5% or higher to Dx
▪ Normal is about 4-6%
▪ Diabetic want to keep it below 7%
○ Shows how long the RBC has been in
circulation and being glycosylated
(coated) with glucose
▪ Hgb is saturated with glucose over
time
▪ If you have high blood glucose levels
for a long time, the A1C level will be
higher
> Like in poorly managed diabetes,
there is circulating glucose in the
blood and it glycosylates the RBC - 2 hours Plasma Glucose
○ 200 mg or higher to Dx
▪ This is postprandial (2 hours after
meals)
○ This test is done by giving an oral dose
of glucose
▪ Oral Glucose Tolerance Test (OGTT) of
75 grams of glucose - With signs of HYPERglycemia, do a random glucose screening
○ Anything over 200 mg = DM
How is gestational diabetes diagnosed and treated?
Dx:
○ FBG = 92+
○ 1 hr = 180 mg/dl or higher
○ 2 hr = 153
Tx:
○ Preferably treated with INSULIN supplements
○ Or can use glyburide or Metformin
** ANY FORM/DEGREE OF HYPERGLYCEMIA is teratogenic and can cause abnormalities **
What causes islet cell destruction in type 1 DM?
** IT IS A MULTIFACTORIAL DISEASE **
○ Genetic predisposition
- Genetics
□ Diabetes can aggregate in families
□ Concordance rate for twins is 50%
□ Exact mode of inheritance is unknown
○ Autoimmunity (The reason someone has Type I DM, the CD4 & CD8 (T-cells) are attacking the pancreas and causing a total inability to produce insulin)
▪ 90% pts have circulating islet cell
antibodies within a year of Dx
▪ Approximately 10% have other
autoimmune disorders include:
□ Grave’s Disease, & Addison’s Disease
○ Environmental insult/effects
▪ Viruses are suspected as initiators the
insult and causes Type I diabetes
▪ There has probably been a long latency
period of the virus in the body with
subsequent beta cell loss
▪ Chemical toxins and ingestion of cows
milk as an infant
What are the s/sx of type I DM?
○ Polydipsia, polyuria, polyphagia, & weight loss
▪ Increase the eating but losing weight
▪ Glucose is a very large molecule
□ As it move through renal tubule, it filters
out as urine and it draws water through
osmosis.
□ Some weight loss is due to the loss of
water weight
> And also due to the glucose being
excreted as urine and not going into the
cells for use/storage
□ GLUCOSE IS AN OSMOTIC DIURETIC
(polyuria)
> Causing the thirst, hunger, and weight
loss
○ Most common in younger population (under 30)
○ Leaving untreated can progress to Diabetic Ketoacidosis (DKA) = coma/death
How is Type I DM treated?
through exogenous INSULIN (primary), Medical Nutrition Therapy (MNT), and physical activity
When should pts w/type I DM check their insulin?
○ Fasting Blood Glucose as needed to monitor Diagnoses
○ Need blood glucose monitors when injecting insulin
▪ Type I check a minimum of 4 times per
day before meals
○ A1C- check this 3-4 times annually for T1 & T2
○ Medicare/Medicaid will cover most of these costs
