Monica - Week 7 - Exam 2 Flashcards
what is diabetes mellitius?
- CHO metabolism disorder
- ↑ blood glucose d/t inability to produce or utilize insulin
what are 2 major risk factors for diabetes?
obesity and sedentary lifestyle
T/F diabetes is preventable and reversible in pre-diabetes stage
TRUE, BUT once you have actual diabetes → it can’t be cured; it can be managed
why is diabetes called a multi-factorial, multi-organ condition?
chronic ↑ in BG overtime can cause damage to other systems → CVD, renal damage, PVD, eyes (diabetic retinopathy), and nervous system disorders (peri. neuropathy)
diabetes is the leading cause of ____? (3)
blindness, renal failure, and non-traumatic lower extremity amputations
what are the immediate complication of hyperglycemia?
- ↓ immune function and wound healing (↓ WBC function efficiently → less able to fight infection)
- ↑ coagulability (thromboembolic events)
what are the long-term MICROvascular angiopathy and arteriosclerosis of hyperglycemia?
- retinopathy (small hemorrhage, cotton wool spots → blindness)
- neuropathy ( sensory motor nerves; ↓ blood flow → demylenation and degeneration)
- nephropathy = microalbuminuria/proteinuria (leading cause of KF in adults; damage to capill. (filter) → hyperpermeable → protein released in urine)
what is arteriosclerosis?
narrowing d/t the inflammation of arterial line
what are the long-term MACROvascualar angiopathy?
- coronary = angina, MI (leads to chest pain, ↓ O2 = MI)
- cerebral = TIA, CVA (↓ O2 to brain→TIA “mini stroke”; ↑ risk for CVA cerebrovascular accident)
- peripheral = peripheral vascular disease (PVD), limb loss
T/F diabetic’s TPA (natural clot buster) is effected, so they are not able to break down clots.
TRUE
what cells produce insulin?
beta cells
what stimulates an insulin release?
blood glucose rise
what happens to excess glucose?
converted to glycogen or converted to fatty acids
an inability to make insulin, failure to control BG, or insulin resistance is characteristics of ?
diabetes
what do alpha cells produce?
glucagon (counteracts insulin secretion and ↑ BG)
- glycogenolysis (break down of gly in liver)
- gluconeogenesis (make new glucose from fat/amino acids → ketones → DKA)
Type 1: where is is most common?
most common in children and adolescents < 20y/o
Type 1: possible causes?
genetic predisposition or autoimmune response (destruction of beta cells)
Type 1: characterized by?
a complete lack of endogenous insulin
Type 1: treatment?
need long term insulin therapy
Type 1: presenting condition?
- hyperglycemia (700-800)
- DKA
Type 2: can still make endogenous insulin but ______?
- not making enough = glucose can’t move into cell
- tissues poorly using insulin (cellular resistance)
- or both
Type 2: when there is a cellular resistance to insulin the liver attempts to _____–?
compensate by making more → hyperinsulinemia → beta cell exhaustion → blood sugars slowly rise
Type 2: contributing factors?
obesity and physical inactivity
Type 2: treatment?
may need oral and/or insulin treatment
***↑ exercise → can make cells more sensitive to insulin, weight loss, ↑ glucose use, good for ♥; ↑ HDL and ↓ LDL`
look at process map
understood
what are the uncontrollable risk factors of diabetes?
- age
- family hx of type 2 DM
- hx of GDM
- ethnicity (african-american, asian-american, hispanic, and native american) → ↑ rate of obesity
- genetic mutation → insulin resistance
what are the controllable risk factors of diabetes?
- obesity
- lack of physical inactivity
- metabolic syndrome (3 of each factor)
what are the characteristics of metabolic syndrome?
- ↓ HDL
- ↑ glucose levels, ↑ BP, ↑ triglycerides
- abdominal obesity
what are the complications of metabolic syndrome?
CAD, PVD, thrombotic events.
what are the 5 different tests to diagnose diabetes?
- fasting glucose (8hr fasting)
- random glucose (anytime, non-fasting)
- fingerstick blood glucose (FSBG - used in conjunction w insulin - not as reliable)
- oral glucose tolerance test (OGTT)
- glycosylated hemoglobin (hbg A1C/A1C)
what occurs in a OGTT?
- ingest a 75g glucose load drink and assess BG 2 hrs later (challenge test)
what occurs in a Hbg A1C?
looks at BG control over the preceding 3 months → glucose attaches to Hbg molecule and stays on for the life of the cell)
shows effectiveness of diabetic therapy
what is the normal, prediabetes, and diabetes levels for fasting blood glucose?
N: = 99
PD: 100 - 125
D: >/= 126
what is the normal, prediabetes, and diabetes levels for HgA1C?
N: = 5.6
PD: 5.7 - 6.4
D >/= 6.5
what is the normal, prediabetes, and diabetes levels for 2 hr post OGTT?
N: = 139
PD: 140 - 199
D: >/= 200
what is the normal, prediabetes, and diabetes levels for random blood glucose?
N: NA
PD: NA
D: >/= 200 + symptoms (polydipsia, polyuria, polyphagia)
what are the three way to lifestyle mainstays?
- following a meal plan
- increasing activity level + weight loss (if needed)
- self-monitoring of BG
what 3 characteristics of following a meal plan?
• Balance CHO intake with pancreas function or insulin
injections
• Reduce demand on pancreas
• Reduce post-prandial BG spikes and A1c
what 2 characteristics of ↑ activity and ↓ weight?
- Reduce blood glucose directly
* Reduce insulin resistance
what 2 characteristics of self monitoring BG?
- Identify individual patterns and help target therapy
* Routine monitoring of glucose levels and A1c
Protein: glucose effects
- Very little converted to glucose
- Stimulates some insulin secretion
- Slows digestion
- Intake: 15-20% calories/day
fat: glucose effects
- Slows digestion, slow ↑ of BG
- Blunts post meal spike; ↑ risk of CVA
- Promotes satiety
- Less saturated fat (<7%)0
- Poly- and monounsaturated
- Low cholesterol, low Na+
- Intake: 25-30% calories/day
alcohol: glucose effects
- Inhibits gluconeogenesis - good in some way; can cause hypoglycemia in conjunction w/ insulin or oral drug
- Best to drink with meals
- Sugar-free mixes
- Dry, light wines
CHO: glucose effects
• Greatest effect on post-prandial spikes • Whole grains, fruits, veggies healthier • Daily allowance 130 gm/day • Intake: 50% of calories/day
3 different methods of CHO counting?
- consistent CHOs
- “exchange” list system
- myPlate
what are the 3 characteristics of consistent CHOs?
- CHO load divided equally into 3-4 meals
- 1 serving of CHO = 15 grams
- 45-60 grams/meal and 15-30 grams/snack
what are 2 characteristics of exchange list system?
• 1 serving of food choice = 15 grams of CHO
• food choice can be exchanged for another within list
ex: 1 ear of corn for 1/3 cooked pasta
what is myPlate system?
• ½ plate with veggies and fruit, ¼ starch, ¼ protein, dairy
what are food items with 15 grams of CHO?
1 slice bread, ½ c. cooked oatmeal, ½ banana,
1 small baked potato, ⅓ c. cooked beans or rice,
½ c. croutons, 1 small apple, 1 c. milk, ½ c. fruit juice
what is the indication for metformin?
- management of type 2 DM and pre diabetes
- introduced when lifestyle mod are inefficient in control
- first line drug of choice
what type of med is metformin?
biguanide
what are the actions of metformin?
o makes tissues less resistant to endogenous insulin
o ↓ amount of glucose produced by the liver
o ↓ intestinal glucose absorption
what are AEs of metformin?
nausea, diarrhea, abdominal bloating, metallic taste
what are NIs with metformin?
o take with meals
o assess BG and Kidney function → contraindicated w/renal insufficiency o DC before procedures requiring radiographic contrast
media
- hold for 1 - 2 days prior to procedure and 48 hrs. post-procedure
- HCP to assess renal function and restart
what are the 3 common sulfonylureas?
glipizide, glyburide, glimepiride
how do the sulfonylureas work?
o stimulate the release of insulin from the pancreas (pt needs functional beta cells)
o ↑ sensitivity to insulin at receptor sites
o may ↓ hepatic glucose production
what are the AEs of sulfonylureas?
hypoglycemia (shaky, sweating, confusion, aggitation) and increased appetite (weight gain)
what are the NIs for sulfonylureas?
o administer 30 mins. before meals
o cross-sensitivity with sulfonamide allergy (sulfa)
o may be combined with metformin
o hold post-op until able to intake regular meal
what are incretins?
hormones found in GI tract
what do incretins do?
stimulate pancreatic insulin secretion
what does incretin dysfunction result in?
post-prandial hyperglycemia
what does dipeptidyl peptidase (DDP-4) do?
destroys incretin hormones
what 3 actions do DDP-4 inhibitors do?
- inhibit enzyme from destroying incretin
hormones - stimulates pancreas to secrete insulin
- reduces fasting and post-prandial glucose
what are the DDP-4 drug names?
Drugs: sitagliptin and saxagliptin
what is the name of the DDP-4 combo drug and what is the combo?
Combo: Janumet (sitagliptin and metformin)
what is the drug-drug interaction for DDP-4?
may ↑ risk of hypoglycemia with
sulfonylureas or insulin
what are the NIs for DDP-4?
o assess for hypoglycemic sxs
○ no regard to food
what is the purpose of insulin?
- mimic the pancreatic secretory patterns of insulin
* achieved through basal and post-prandial insulin
what are the different types of insulin?
rapid-, short-, intermediate-, and long-acting
forms
what is the goal of insulin combination therapy?
combined w/therapy to stimulate fasting and postprandial pancreatic insulin
when should rapid acting insulin be given?
15 min before a meal; 3 - 4 times a day
when should short acting insulin be given?
30 min w/in time frame
when should intermediate acting insulin be given?
1 - 2 a day
when should long acting insulin be given?
once a day; can be given in conjunction with spikes; steady release
refer to sliding scale insulin picture
understood
what are the effects of corticosteroids and stress hyperglycemia (physical/emotional/recovery stress)?
- ↑ blood glucose levels
* insulin therapy may be needed • patient teaching
what should be considered with IV therapy?
- may ↑ blood glucose depending on solution
- assess type of IVFs and oral intake
- assess need for IVFs if taking PO
what should we do as far as patient education?
- assess knowledge
- teach monitoring and management therapy
- meal plans
T/F: people are normally prediabetic for 10 years prior to their diabetes diagnosis
T
