MNT idk what last time Flashcards
Insulin functions and counter-regulatory hormone
Insulin is hormone produced by the beta-cells of the pancreas. It is necessary for use or storage of body fuels / glucagon
glucagon function and counter-regulatory hormone
a hormone produced by the a-cells of the pancreas that causes an increase in blood glucose levels by stimulating the release of glucose from liver glycogen stores / insulin
somostatin function and counter u know what
a polypeptide hormone secreted from the stomach,small intestine,and pancreas that tends to inhibit other gastrointestinal secretions and motility/ft decreases motility of the stomach and intestine and inhibits or regulates the release of severalGI hormones.
lab values to diagnose dm
AIC ≥ 6.5% FPG ≥ 126 2 hour PG ≥ 200 during OGTT In patients with classic symptoms of hyperglycemia or hyperglycemic crisis, a random PG ≥ 200
Diagnosis for gdm
plasma glucose level of 140/dl/mg
gtt
fasting 95 mg/dl
6.5
diagnosis for igt
the 2-hour blood glucose is between 140 and 199 mg/dl.
What weeks in the pregnancy we test for GDM?
24-28 weeks
Explain why decrease CHO in the morning is needed.
to CHO not as well tolerated at breakfast due to
increased cortisol and growth hormones
What are the recommendations of grams for CHO for the morning?
30 g
Characteristics for type 1 dm
Primary defect is pancreatic beta-cell destruction which leads to absolute insulin
deficiency.
Beta-cell destruction rates vary person to person but typically faster in infants
and children.
Pancreas produces much more insulin than is needed, so possible destruction of
beta-cells starts occuring months or years before symptoms occur. Hyperglycemia
doesn’t occur until > 90% of insulin secretory beta-cells are destroyed.
Immune-mediated diabetes mellitus: autoimmune destruction of
beta-cells in pancreas or idiopathic
auto-immune, environmental, genetic
characteristics of type 2 dm
Insulin resistance
• Target tissues: muscle, liver, adipose cells
Pancreatic beta-cell failure
• May increase secretion of insulin at first to compensate for resistance
• Eventually it will not be able to keep up
Age ≥ 45
Ethnicity: African American, Hispanic, Native American, Asian American, Pacific
Islander
Family History (parents and siblings)
HDL ≤ 35 and TG ≥ 250
HTN
Obesity with BMI ≥ 25
History of IFG or IGT
Vascular
insulin
U- 100 concentration = 100 units of insulin per ml of fluid
Onset – when it starts working
Peak – most action
Duration – how long
Injections via syringe or pen
RAPID ACTING
Examples: Insulin lispro (Humalog)
• Insulin aspart (Novolog)
• Insulin glulisine (Apidra)
• Onset: < 15 minutes
Peak: 60 – 90 minutes
Duration: 3 – 5 hours
Less hypoglycemic episodes than regular
REGULAR INSULIN
Short acting
Onset: 30 – 60 minutes
Peak: 2 – 3 hours
Duration: 5 – 8 hours
Take 30 – 60 minutes before meals
Example: Humalog R
INTERMEDIATE-ACTING
Neutral protamine Hagedorn (NPH) – only one that is
available
Cloudy appearance
Onset: ~ 2 hours
Peak: 6 – 10 hours
Duration: 10 – 16 hours
LONG-ACTING INSULIN
Slow dissolution at injection site – makes it relatively constant and has
peakless delivery over 24 hours
Acidic – so can’t mix with others
Given at bedtime – important that it is given at consistent time daily
Ex: Insulin glargine (Lantus)
Insulin determir (Levemir) – absorbed from tissues quickly and then is
bound to albumin in bloodstream. Prolonged action of 17 hours
lispro - All have an onset of action within
15 minutes, a peak in activity at 60 to 90 min, and a duration of action of 3 to 5 hours. They result in fewer hypoglycemic episodes compared with regular insulin.
regular - is a short-acting insulin with an onset of action 15 to 60 minutes after injection and a duration of action ranging from 5 to 8 hours. For best results the slow onset of regular insulin requires it to be taken 30 to 60 minutes be- fore meals.
NPH - NPH is the only available intetmediate-aaing insulin (Lente insulin has been discontinued). Its appearance
is cloudy,and its onset of action is about 2 hours after injection, with a peak effect from 6 to 10 hours.
basal - analog that becauseof its slow dissolution at the injection site results in a rela- tively constant and peaklessdelivery over 24 hours
insulin - combination rapid acting or short acting pumped continuous with bolus
Insulin secretagogues Sulfonylureas
drugs administered orally to lower blood glucose levels/ katp channel of pancreatic beta cells
Sulfonylureas: promote insulin secretion by beta cells of the
pancreas
Disadvantages: weight gain and hypoglycemia
Examples:
• Glipizide (Glucotrol)
• Glyburide (Glynase Prestabs)
• Glimepiride (Amaryl)
Meglitinide
lower blood levels /pancreatic beta cells
secretagogues
Biguanide
enhance insulin action / liver
metaformin
Thiazolidinediones
drugs administered orally that are used to control or lower blood glucose level/ liver
TZDs or glitazones
Decrease insulin resistance in peripheral tissues and thus enhance
ability of muscles and fat to take up gluocse
Improve lipids and don’t cause hypoglycemia on their own
Adverse effects: weight gain and edema
Examples:
• Actos
Alpha-glucosidase inhibitors
intestines/ blockes glucose digestion/absorbtion
Delay CHO absorption in small intestine by inhibiting enzymes that
digest CHO
Lower post-prandial glycemia
GI side effects include: flatulence, diarrhea, cramping, abdominal pain
Examples:
• Acarbose (Precose)
• Miglitol (Glyset)
Januvia
The mechanism of DPP-4 inhibitors is to increase incretin levels (GLP-1 and GIP),[2][3][4] which inhibit glucagon release, which in turn increases insulin secretion, decreases gastric emptying, and decreases blood glucose levels.
Byetta, Human Amylin
increases insulin secretion
benefits of exercise and grams needed for longer and 30 mins
Physical activity should be an integral part of the treat- ment plan for persons with diabetes. Exercise helps all per- sons with diabetes improve insulin sensitivity, reduce car- diovascular risk factors, control weight, and improve well-being
15 grams
how are ketones formed
Ketones are formed when there is not enough sugar or glucose to supply the body’s fuel needs. This occurs overnight, and during dieting or fasting. During these periods, insulin levels are low, but glucagon and epinephrine levels are relatively normal. This combination of low insulin, and relatively normal glucagon and epinephrine levels causes fat to be released from the fat cells. The fats travel through the blood circulation to reach the liver where they are processed into ketone units. The ketone units then circulate back into the blood stream and are picked up by the muscle and other tissues to fuel your body’s metabolism. In a person without diabetes, ketone production is the body’s normal adaptation to starvation. Blood sugar levels never get too high, because the production is regulated by just the right balance of insulin, glucagon and other hormones.
Sogmogyi and Dawn Phenomenon
dawn -Body needs less insulin from (1 – 3 AM) than at dawn (4 – 8 AM)
T1DM – make sure long-acting insulin doesn’t peak at this time.
Increased need for insulin will cause BG to be higher at dawn
Overnight excessive hepatic glucose production (common in T2DM)
Metformin often used
sogmogi - Rebound hyperglycemia”
Hypoglycemia triggers secretion of counter-regulatory hormones
Glucagon, epinephrine, growth hormone, cortisol
Hepatic glucose production stimulated
Decrease evening insulin dose or take long-acting insulin
guidelines for sickness
DKA risk during acute illness: flu, colds, vomiting, diarrhea
MNT: 150 – 200 gm CHO/day to prevent DKA
45 – 50 gm CHO every 3 – 4 hours along with medication adjustments
Monitor BG at least 4 times daily
Obtain liquids
Call health care provider if sick more than 1 day
hypoglycemia
BG normally: 60 – 100
Affects small number of people
Symptoms when BG < 65
Brain and nervous system are starved of glucose causing:
Sweating, shaking, weakness, hunger, headaches, irritability