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Medicine I: Module 4 > Diabetes Type II > Flashcards

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
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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
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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
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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)
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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
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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

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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
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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
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9
Q

factors that contribute to insulin resistance

A
  • genetics
  • obesity and inactivity
  • aging
  • medications
  • rare disorders
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10
Q

problems that occur due to insulin resistance

A
  • type 2 DM
  • HTN
  • dyslipidemia
  • athersclerosis
  • PCOS
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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
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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
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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
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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)
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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
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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
Q

Insulin and Symlin

A
  • 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
Q

Tx of sxs of diabetes

A
  • 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
Q

Glycemic goals

A
  • 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
Q

Accord trial

A

-showed us that people aggressively managed with type II had an overall higher risk of mortality

29
Q

hyperosmolar hyperglycemic state

A
  • 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
Q

sxs of HHS

A
  • 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
Q

tx of HHS

A
  • 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
Q

chronic complications of hyperglycemia

A

-CV complications: coronary a. dz, myocardial infearction, peripheral vascular dz, cerebral vascular dz

33
Q

target numbers for diabetics: BP, LDL, HDL, TGs

A
  • 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
Q

microvascular complications of chronic hyperglycemia

A
  • neuropathy
  • foot ulcers
  • nephropathy
  • retinopathy
35
Q

diabetic neuropathy

A
  • distal symmetric polyneuropathy (stocking glove distribution)
  • entrapment neuropathy
  • autonomic neuropathy (neurogenic bladder, sexual dysfunction, gastroparesis, orthostatic hypotension)
36
Q

diabetic foot ulcers

A

-develop primarily as a consequence of vascular dz, neuropathy and foot deformities

37
Q

diabetic nephropathy

A

-diabetes is the MCC for nephropathy

38
Q

retinopathy

A

-leading cause of blindness in the US

39
Q

follow up visits type 2 DM

A
  • 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

Medicine I: Module 4 (7 decks)

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