Diabetes Type II Flashcards
1
Q
4 clinical classes of diabetes
A
- type I
- type II
- secondary diabetes: when diabetes occurs as a result of other disorders or treatments
- gestational diabetes
2
Q
prediabetes
A
- impaired fasting glucose (IFG) or impaired glucose tolerance (IGT) can be diagnosed with hyperglycemia insufficient for criteria for diabetes
- IFG = FPG 100-125mg/dl
- IGT = 2hr plasma glucose 140-199ng/dl
- HbA1c between 5.7-6.4%
- IFG and IGT are both risk factors for future type 2 diabetes and CV dz
3
Q
criteria for dx of diabetes
A
-sxs of diabetes and plasma glucose 200mg/dl or greater (classic sxs include polyuria, polydipsia and unexplained weight loss)
OR
-FPG of 126 mg/dl or greater (no food at least 8 hrs before)
OR
- 2hr plasma gluc 200mg/dl during OGTT (performed using glucose load containing equivilant of 75g anhydrous glucose dissolved in H2O
- HbA1c >6.5 (diagnostic w/ sxs, otherwise confirm 2 weeks later)
- each must be confirmed on subsequent day unless unequivocal sxs of hyperglycemia are present
4
Q
type 2 DM pathogenesis
A
- failure of beta cells to compensate for insulin resistance
- obesity is most common cause of insulin resistance
- there is a genetic predisposition to beta cell failure
- progressive disease –> B cell fn leads to impaired glucose tolerance and can lead to type 2 DM; B cell dysfunction STARTS LONG BEFORE GLUCOSE RISES and worsens after diabetes develops
- hyperglycemia may cause additional defects in insulin secretion and insulin action (glucotoxicity)
5
Q
frequency of Type 2 DM
A
- 90% of patients with diabetes have this type
- increasing obesity in pop, older pop, and increase in pop of high-risk minority groups –> all causing prevalence to rise
6
Q
Age of type 2 diabetics
A
-once thought to mainly affect individuals > 40, it is now increasingly in younger people, particularly in highly susceptible racial and ethnic groups
7
Q
Presentation of type 2 DM
A
- MOST PTS WITH DIABETES ARE ASYMPTOMATIC FOR YEARS!!
- frequently not diagnosed until complications develop
- 1/3 of pts with type 2 DM are undiagnosed
- polyuria, polyphagia, weight loss all occur long after hyperglycemia has been present
- other sxs: blurred vision, lower extremity paresthesias, yeast infections, balanitis
- hyperosmolar hyperglycemic state (HHS) can be initial presentation of type 2 DM
8
Q
Goals of management for type 2 DM
A
- elimination of symptoms (many pts are asymptomatic)
- microvascular risk reduction by controlling BG and BP (eye and kidney dz)
- macrovascular risk reduction (heart dz and PAD) by lipid and BP control, smoking cessation and aspirin therapy
- metabolic risk reduction through control of BG
9
Q
factors that contribute to insulin resistance
A
- genetics
- obesity and inactivity
- aging
- medications
- rare disorders
10
Q
problems that occur due to insulin resistance
A
- type 2 DM
- HTN
- dyslipidemia
- athersclerosis
- PCOS
11
Q
diabetes self management education either individualized or group classes
A
- instruct pts on SMBG
- instruct on diet and lifestyle recommendations
- address psychosocial issues with regards to diabetes and how this may affect pts ability to self manage diabetes
- provide support and answer questions
12
Q
lifestyle modifications for improved metabolic control
A
- EXCERCISE: the best insulin sensitizer. Exercise for 30 mins and get residual 4-6 hrs of improved insulin sensitivity
- REDUCE CARB CONSUMPTION: avoid white carbs and sugars, encourage carbs from veggies rather than grains
- WEIGHT LOSS: even modest weight loss improves insulin sensitivity
- smoking cessation
- aspirin therapy 75-162mg/d: prevents CV problems
13
Q
medical management of T2DM
A
- Biguanides = 1st LINE!!!
- Thiazolidinediones
- Sulfonylureas
- Meglitinides
- Incretin mimetics (injectable)
- Dipeptidyl peptidase-4 (DPP4) inhibitors
- Welchol
- Alpha glucosidase inhibitors
- SGLT2 inhibitors
14
Q
Biguanides
A
- 1st LINE TX!!
- reduces hepatic glucose production, may improve glucose utilization at periphery
- insulin HAS TO BE PRESENT for these to work!
- ADEs: diarrhea, lactic acidosis w/ liver or renal impairment
- drugs: metformin (glucophage, glucophage XR, Glumetza, Fortamet)
15
Q
Thiazolidinediones
A
- aka TZD
- THESE ARE THE BEST INSULIN SENSITIZERS!
- reduce insulin resistance at periphery and maybe liver too
- insulin MUST BE PRESENT for TZDs to work
- increase TGs slightly and increase LDL
- ADEs: edema (caution pts with CHF), weight gain (worse w/ insulin), elevate LFTs
- drugs: avandia, actos
16
Q
actos warning
A
- increased bladder cancer risk
- longer use and higher dose = greater risk
17
Q
sulfonylureas
A
- directly stimulate first phase insulin secretion in pancreatic beta cells
- ADEs: hypoglycemia, weight gain
- drugs: glyburide, glipizide, glimepiride, tolbutamide
- these are very old drugs –> tell pancreas to make insulin
18
Q
meglitinides
A
- non-sulfonylurea insulin secretogegues with rapid onset and short acting, so less post meal hypoglycemia
- ADEs: hypoglycemia, weight gain
- drugs: repaglinide, nateglinide
- take these before a meal
19
Q
incretin mimetics
A
- similar activity to naturally occurring glucagon like peptide 1 (GLP1) –> GLP1 released from cells in gut in response to food, binds receptors on beta cells to stimulate insulin release
- DOES NOT CAUSE INSULIN SECRETION UNLESS BG RISES!
- they also suppress glucagon secretion, reduce appetite, and delay food absorption (slow movement through stomach)
- ADEs: n/v/d, dizziness, HA, weight loss, hypoglycemia (worse with sulfonylurea)
- drugs: exanatide, bydureon, liraglutide, albigultide, dulaglutide, trulicity
- THIS IS HER FAVORITE DRUG CLASS - TRULICITY AND OZEMPIC ARE HER FAVORITES because they are once weekly
20
Q
Dipeptidyl peptidase-4 (DPP4) inhibitors
A
- DPP4 inactivates incretin hormones
- by inhibiting DPP4, active incretin is prolonged –> increases insulin release and decreases glucagon levels
- inhibit breakdown of GLP1
- ADEs: comparable to placebo
- drugs: Januvia, onglyza, tradjenta, nesina
- use these BEFORE GLP1 agonist –> once you give them GLP1s, you never come back to these
21
Q
Colesevalam hydrochloride (Welchol)
A
- MOA: non-absorbed, lipid-lowering polymer that binds bile acids in intestine - impedes their reabsorption. Exact mechanism unkown
- dosing: 3.8g/day
- ADEs: constipation, nasopharyngitis, dyspepsia, hypoglycemia, nasuea, HTN
22
Q
Alpha-glucosidase inhibitors
A
- saccharides that are competitive inhibitors of AG enzymes (brush borders of small intestines, needed to digest carbs)
- oligosaccharides cant be broken down and cant be absorbed –> lowers glucose values but allows complex carbs to pass to colon –> ADEs!!
- ADEs: flatulence, cramping, diarrhea
- drugs: precose, glyset
- dosing: take at start of a meal, increase as tolerated depending on ADEs
23
Q
cycloset
A
- ergot derivative
- dopamine receptor agonist
- dosing 1.8-4.8mg qd within 2 hrs of waking
- ADEs: n/v/d, dizziness, fatigue, HA, constipation
- Used a lot for prolactinomas
24
Q
SGLT2 inhibitors
A
- sodium glucose co-transporter 2 inhibitors
- inhibit glucose reabsorption from the renal tubules
- also improves weight and reduces BP b/c it has diuretic activity
- ADEs: yeast infecitons, UTIs (greatest risk in females and uncircumcised males), increased thirst, increased urination
- need to have adequate glomerular filtration for this to work
- drugs: Jardiance (showed improved CV health)
25
Insulin and Symlin
- used to treat type 2 DM, typically at much higher doses and in combo with other meds
- insulin is always safe if dosed appropriately and may be best first-line option for pts with significant renal or hepatic impairment
26
Tx of sxs of diabetes
- LIFESTYLE, DIET AND EXERCISE, METFORMIN are the cornerstones of therapy
- if TG are high, HDL is low
- ACE and AARBs are the two preferred methods to treat BP (also help kidney to prevent proteinuria) --> DONT USE IN WOMEN OF CHILD BEARING AGE
- Statin therapy if hx of MI or LDL >100, reduce risk of CV events --> DONT USE IN WOMEN OF CHILD BEARING AGE
27
Glycemic goals
- AACE HbA1c goal of <6.5%
- ADA HbAtc goal is <7%
- 2 hr post prandial measurement <140mg/dl
- BP <130/80
- the older the pt, the less aggressively we manage them
28
Accord trial
-showed us that people aggressively managed with type II had an overall higher risk of mortality
29
hyperosmolar hyperglycemic state
- occurs in elderly patients with type II DM
- similar to DKA except insulin deficiency is less profound. Less ketosis so abdominal sxs less likely and pts dont seek medical care
- impaired thirst mechanism exacerbates tendency toward HHS, these pts are more dehydrated than those with DKA and have higher BUN and creatinine
- Emergent situation
- Can appear like a stoke
30
sxs of HHS
- due to hyperglycemia --> polyuria, polydipsia, blurred vision and weight loss if prolonged
- weakness, lethargy, malaise and HA
- less nausea, vomiting and abdominal pain. Probably due to lack of ketotic or acidotic state
- focal neurological signs (hemisensory deficits, hemiparesis, aphasia) mimic CVA
31
tx of HHS
- hospitalization is required
- rehydration to restore plasma volume and correct electrolyte deficits
- provide adequate insulin to restore and maintain normal glucose metabolism
- watch for complications of tx
32
chronic complications of hyperglycemia
-CV complications: coronary a. dz, myocardial infearction, peripheral vascular dz, cerebral vascular dz
33
target numbers for diabetics: BP, LDL, HDL, TGs
- BP <130/80
- LDL <100
- HDL >45 men, >55 women
- TGs <150
- quit smoking and take daily aspririn
- smoking narrows vessels which makes BP worse
34
microvascular complications of chronic hyperglycemia
- neuropathy
- foot ulcers
- nephropathy
- retinopathy
35
diabetic neuropathy
- distal symmetric polyneuropathy (stocking glove distribution)
- entrapment neuropathy
- autonomic neuropathy (neurogenic bladder, sexual dysfunction, gastroparesis, orthostatic hypotension)
36
diabetic foot ulcers
-develop primarily as a consequence of vascular dz, neuropathy and foot deformities
37
diabetic nephropathy
-diabetes is the MCC for nephropathy
38
retinopathy
-leading cause of blindness in the US
39
follow up visits type 2 DM
- pts not at goal should be seen q3mos w/ HbA1c each visit
- pts at goal seen q4-6mos
- regular foot exams w/ 10g monofilament at appointments anually
- 24 hr urine done anually
