Transcript Maximum Dose (mg/day)

Management of Type 2
Diabetes
123
General approach to therapy
Nonpharmacologic therapy
Pharmacologic therapy
Treatment of concomitant diseases
Treatment of acute complications
Treatment of chronic complications
Outcomeevaluation
69
Glycemic targets
● HbA1c < 7.0% (mean PG 150-160 mg/dl
Pre-prandial PG <130 mg/dl ●
Post-prandial PG <180 mg/dl ●
Individualization is key: ●
Tighter targets (6.0 - 6.5%) - younger,
healthier
Looser targets (7.5 - 8.0%+) -older,
comorbidities, hypoglycemia prone, etc.
●
●
Avoidance of hypoglycemia ●
125
Nonpharmacologic Therapy
Medical nutrition therapy ●
recommended for all DM patients ●
provides optimal metabolic and physiologicoutcomes (glucose, ●
lipids, BP, proteinuria, weight)
prevents/treats chronic DMcomplications ●
Regulates insulin administration with a balanced diet to ●
achieve/maintain a healthyweight
carbohydrate counting orexchanges
●
Promotes weight loss to overweight patients ●
caloricrestriction ●
Moderate weight loss has been shown to reduce CV risk as well as delay
or prevent the onset of DM in those with pre-diabetes (follow TLC)
General rule for weight loss diet is that it should supply 1000-1200
kcal/day for women and 1200-1600 kcal/day formen.
70
●
●
Nonpharmacologic Therapy
Exercise ●
improves insulin resistance, glycemiccontrol ●
reduces CV risk (HTN and elevated serumlipids) ●
helps with weight loss or maintenance ●
improves well-being ●
Patients withoutcontraindications ●
> 150 min/week moderate-intensity aerobic exercise(50- ●
70% of maximum heart rate)
resistance training for 30 min 3 times/week ●
Start exercise slowly in previously sedentary patients. ●
72
Nonpharmacologic Therapy
Psychological assessment and care ●
Determining the patient’s attitude regarding DM, expectations of ●
medical management and outcomes, mood and affect, general and
diabetes quality of life and financial, social and emotionalresources.
Immunization ●
Provide influenza vaccine annually to all diabetic patients ≥6 months
of age
Administer pneumococcal polysaccharide vaccine to alldiabetic
patients ≥2 years
One-time revaccination recommended for those >64 years previously immunized
at <65 years
if administered >5 years ago
Other indications for repeat vaccination: nephrotic syndrome, chronicrenal
disease, immunocompromised states
•
•
–
–
Administer hepatitis B vaccination to unvaccinated adultswith
diabetes who are aged 19 through 59years
Consider administering hepatitis B vaccination to unvaccinated adults
with diabetes who areaged ≥60 years
•
•
74
Therapeutic options:
● Oral agents & non-insulin injectables
● Metformin
● Sulfonylureas
● Thiazolidinediones
● DPP-4 inhibitors
● GLP-1 receptor agonists
● a-glucosidase inhibitors
● Amylin mimetics
128
9
12
Biguanide (Metformin)
Enhance hepatic & peripheral (muscle) tissue insulin ●
sensitivity
increases uptake of glucose intissues ●
No direct effect on β cells ●
Decrease hepatic glucoseproduction ●
Generic
Name
Dose (mg) Recommended Starting Maximum
Dosage (mg/day)
Dose
(mg/day)
Nonelderly Elderly
Metformin
500, 850,
1,000
500 mg Assess renal
twice a day function
2,550
Up to 24 hours No metabolism; renally secreted and
excreted
Metformin
extendedrelease
500, 750,
1,000
500–1,000 Assess renal
mg with
function
evening
meal
2,550
Up to 24 hours Take with evening meal or may split
dose; can consider trial if intolerant to
immediate-release
133
Duration of Metabolism or Therapeutic Notes
Action
Biguanide: Effects
Average HbA1c reduction: 1.5 to 2.0% ●
FBG reduction: 60 to 80 mg/dL ●
Reduce FBG levels when > 300 mg/dL ●
Decrease plasma triglycerides & LDL-C by ~8 to15% ●
Increases HDL-C: 2% ●
Weight loss: 2 to 3 kg ●
Use in all type 2 DMpatients ●
if tolerated & not contraindicated ●
only oral antidiabetic agent proven to reduce mortality risk ●
UKPDS shows metformin is best suited for obese type 2 ●
DM patients; reduces mortality
134
Biguanide: Side effects & contraindications
Contraindications: ●
Most common adverse ●
effects:
GI: abdominal discomfort, ●
stomach upset, diarrhea
minimize with slow dosetitration
may improve with time ●
administer with food tolessen
adverse effects
switch to extended-release may
improve tolerability
Weight loss canoccur ●
anorexia ●
stomach fullness ●
●
●
●
Long term use – reductionin ●
vitamin B12 levels
High risk patients for lactic ●
acidosis (due to decrease
conversion of lactate to
glucose (decreased
gluconeogenesis) and increase
lactate production in the gut
and liver)
CHF, hypoxic states, shock, ●
septicemia, severe liverdisease,
alcohol use
Renal insufficiency ●
SCr ≥ 1.4 mg/dL inwomen ●
SCr ≥ 1.5 mg/dL in men ●
Intravenous dye procedures ●
risk of acute renal failure ●
withhold the day of procedure
may restart 2 to 3 dayspostprocedure
135
●
●
Sulfonylureas
Enhance insulin secretion ●
bind SUR receptors on pancreatic β cells ●
Elevated secretion of insulin from the pancreas travels ●
via the portal vein and subsequently suppresses hepatic
glucose production.
Classification: 1st & 2nd generation ●
differences in potency, adverse effects, serumprotein ●
binding
no therapeutic superiorityamong agents ●
Glipizide preferred over glyburide(Glibenclamide) ●
glyburide requires adjustment forrenal dysfunction; ●
higher risk of hypoglycemia
136
Sulfonylureas
Generic Name
Dose
(mg)
Recommended Starting Equivalent
Dosage (mg/day)
Therapeutic
Dose (mg)
None
Elderly
Elderly
Maximum
Dose
(mg/day)
Duration Metabolism or Therapeutic
of Action Notes
1st Generation
Acetohexamide
250,
500
250
125–250
500
1,500
Up to 16 Metabolized in liver;
hours metabolite potency equal to
parent compound; renally
eliminated
Chlorpropamide
100,
250
250
100
250
500
Up to 72 Metabolized in liver; also
hours excreted unchanged renally
Tolazamide
100,
250,
500
100–250
100
250
1,000
Up to 24 Metabolized in liver;
hours metabolite less active than
parent compound; renally
eliminated
Tolbutamide
250,
500
1,000–2,000
500–
1,000
1,000
3,000
Up to 12 Metabolized in liver to
hours inactive metabolites that are
renally excreted
137
Sulfonylureas
Generic Name
Dose
(mg)
Recommended Starting Equivalent Maximum
Dosage (mg/day)
Therapeutic
Dose
Dose (mg)
(mg/day)
None
Elderly
Elderly
Duration Metabolism or Therapeutic
of Action Notes
2nd Generation
Glipizide
5, 10
5
2.5–5
5
40
Up to 20
hours
Metabolized in liver to
inactive metabolites
Glipizide
2.5, 5,
10, 20
5
2.5–5
5
20
24 hours
Slow-release form; do not
cut tablet
Glyburide
1.25,
2.5, 5
5
1.25–2.5
5
20
Up to 24
hours
Metabolized in liver;
elimination ½ renal, ½ feces
Glyburide,
micronized
1.5, 3, 6
3
1.5–3
3
12
Up to 24
hours
Equal control, but better
absorption from micronized
preparation
Glimepiride
1, 2, 4
1–2
0.5–1
2
8
24 hours
Metabolized in liver to
inactive metabolites
138
Sulfonylureas
Most common side effect:hypoglycemia ●
higher with chlorpropamide & glyburide; longer t½ ●
high risk patients require lower doses ●
elderly ●
renal/hepaticdisease ●
patients that skipmeals ●
vigorous exercise ●
substantial weight loss ●
Weight gain alsocommon ●
Less common adverse effects:rash, hemolytic ●
anemia, GI upset, cholestasis
139
Sulfonylureas
Tolbutamide, chlorpropamide ●
hyponatremia may result from increasedantidiuretic ●
hormone
disulfram-type reactions can result when alcohol is ●
consumed
Titrate sulfonylureas doses every 1 to 2 weeks ●
Maximal effective dose ~60 to 75% stated max dose ●
At equipotent doses, all sulfonylureas equally effective ●
at lowering blood glucose
140
Sulfonylureas
All sulfonylureas are metabolized in theliver ●
CYP2C9 involved in sulfonylurea metabolism ●
Drug Interactions with Sulfonylureas
Interaction
Drugs
Displacement from protein
binding sitesa
warfarin, salicylates, phenylbutazone,
sulfonamides
Alters sulfonylurea hepatic
chloramphenicol, monoamine oxidase
metabolism (cytochrome P450) inhibitors, cimetidine, rifampinb
Altered renal excretion
aMany drug
allopurinol, probenecid
interactions metabolism-based
bInducer
141
Sulfonylureas
Average HbA1c reduction: 1.5 to2% ●
FBG reduction: 60 to 70 mg/dL ●
Most patients do not reach glycemic goal with ●
monotherapy
1˚ failure: < 30 mg/dL drop in FBG ●
low C-peptide ●
high (> 250 mg/dL) FBG ●
2˚failure: good initial response, but insufficientto ●
reach or maintain glycemicgoal
5 to 7% per year failure rate ●
142
TZDs: Thiazolidinediones
● May be used in type 2 DM therapy
● Enhance insulin sensitivity at muscle, liver, fat tissues
● Decrease hepatic glucose production
● Requires presence of insulin
Generic
Name
Dose (mg)
Recommended Starting
Dosage (mg/day)
Nonelderly
Pioglitazone 15, 30, 45
15
Rosiglitazone
2, 4, 8
2–4
146
Elderly
15
2
Maximum Duration Metabolism or Therapeutic
Dose
of Action Notes
(mg/day)
45
24 hours Metabolized by CYP2C8 and
CYP3A4; two metabolites have
longer half-lives than parent
compound
8 mg/day or 24 hours Metabolized by CYP2C8 and
4 mg twice a
CYP2C9 to inactive metabolites
day
that are renally excreted
TZD Adverse Effects
May increase ALT ●
CI if ALT > 2.5 times upper limit of normal (ULN) ●
discontinue if ALT > 3 times ULN ●
troglitazone (1st approved TZD) removed from market in ●
2000 due to deaths from liver failure
Fluid retention ●
edema, dilutional anemia, pulmonary edema, HF ●
CI in NYHA Class III & IV ●
black box warning for chronic heartfailure ●
147
TZD Adverse Effects
● Weight Gain
● 1.5 to 4 kg
● fluid retention & fat accumulation
● Increased fracture risk
● upper & lower limbs of postmenopausalwomen
● Ovulation
● anovulatory patients can resumeovulation
● pregnancy & contraception precautions required
● pregnancy category C
148
TZDs
● Average HbA1c reduction ~1.5%
● FBG reduction: 60 to 70 mg/dL at maxdoses
● Maximal glycemic-lowering effects after3 to 4 months
● Triglycerides:
● pioglitazone: 10 to 20% decrease
● rosiglitazone: neutral effect
● LDL:
● pioglitazone: no significant increase
● rosiglitazone: 5 to 15% increase
● HDL: both increase 3 to 9 mg/dL
149
α-Glucosidase Inhibitors
● Competitively inhibit enzymes in the small intestine
● delay sucrose & complex carbohydrate breakdown
● Reduce postprandial hyperglycemia
● Used in both type 1 & type 2 DM
Generic
Name
Dose (mg)
Recommended Starting Dosage
(mg/day)
Nonelderly
Maximum Dose
(mg/day)
Duration of Metabolism or
Action
Therapeutic
Notes
Elderly
Acarbose
25, 50, 100 25 mg one to three 25 mg one to
25–100 mg three
times a day
three times a day
times a day
1–3 hours Eliminated in
bile
Miglitol
25, 50, 100 25 mg one to three 25 mg one to
25–100 mg three
times a day
three times a day
times a day
1–3 hours Eliminated
renally
150
α-Glucosidase Inhibitors
● Adverse effect:
● GI side effects mostcommon
●
flatulence, bloating, abdominal discomfort,diarrhea
● may elevate serumaminotransferase
● Contraindications:
● IBD
● colonic ulceration
● intestinal obstruction
● cirrhosis
151
α-Glucosidase Inhibitors
Efficacy ●
reduce postprandial glucose 40 to 50 mg/dL ●
FBG relatively unchanged (~10% reduction) ●
average HbA1c reduction: 0.3 to 1% ●
beneficial in patients close to target HbA1c with near- ●
normal FBG but high postprandial levels
152
α-Glucosidase Inhibitor
May be monotherapy or used with metformin, ●
sulfonylureas, insulin
Initiate with very lowdose ●
25 mg with one meal aday ●
Increase gradually to maximumdose ●
50 mg TID patients ≤ 60 kg ●
100 mg TID patients > 60 kg ●
Take with 1st bite of a meal ●
must be present to inhibit enzyme activity ●
153
Incretin-Based Therapies
The most recent advances in therapy for type 2 diabetes have revolved ●
around the discovery and exploration of the effects of incretins.
Incretins are insulinotropic hormones secreted from specialized ●
neuroendocrine cells in the small intestinal mucosa in responseto
carbohydrate ingestion and absorption.
The two hormones accounting for most incretin effects are: ●
glucose-dependent insulinotropic polypeptide (GIP) ●
glucagonlike peptide-1 (GLP-1) ●
GIP and GLP-1 stimulate pancreatic β-cells in a glucose-dependent ●
manner, contributing to the early phase insulin response.
GLP-1 also inhibits pancreatic α-cells, thus reducing glucagon secretion ●
and hepatic glucoseproduction.
Incretin action is efficient, but short lived. As they enter the blood ●
vessels, incretins undergo rapid metabolism via proteolytic cleavage by
dipeptidyl peptidase-4 (DPP-4) to inactive metabolites. Thus, only
small amounts are needed to exert their effects on glucose metabolism.
154
GLP-1 Mimetics/Analogs: Exenatide
Synthetic analog of amino acid peptide exendin-4 ●
isolated from Gila monster saliva ●
Mechanism similar to humanGLP-1 ●
enhances insulin secretion ●
suppresses postprandial glucagon when bloodglucose ●
elevated; reduces hepatic glucoseproduction
Slows gastric emptying, reduces food intake,promotes ●
weight loss
Unlike GLP-1, exenatide does not increasegastric ●
secretions
156
Exenatide
Indication: adjunctive therapy for type 2DM ●
Not recommended in end-stage renal disease or ●
dialysis patients
prolongs t½ ●
increases incidence of GI sideeffects ●
Adverse effects: ●
nausea, vomiting, diarrhea ●
may improve overtime ●
dose-related, slowly titratedose
157
●
Exenatide
Postmarketing cases of acutepancreatitis ●
May delay absorption of other medications: slow ●
gastric emptying
not recommended for patients withgastroparesis ●
Dose ●
start with 5 mcg BID ●
may titrate to 10 mcg BID whentolerated ●
inject subcutaneously within 60 min of morning & ●
evening meals
158
Exenatide
Average HbA1c reduction ~0.9% ●
Significantly decreases postprandialglucose ●
excursions
Modest effects onFBG ●
Average weight loss in studies: 1 to 2 kg over 30 weeks ●
long-term, open-labeled trials show continued weight ●
loss for at least 2.5 years with 10 mcg BID dose
Improvements in triglycerides & HDL seenwith ●
exenatide 10 mcg BID
159
DPP-IV Inhibitors
● Inhibit DPP-IV which degrades GLP-1
● prolongs GLP-1 t½
● GLP-1 deficient in type 2 DM
● Partially reduces elevated postprandial glucagon
● Stimulates glucose-dependent insulin secretion
Generic Name
Dose (mg)
Recommended Starting
Dosage (mg/day)
Nonelderly
Sitagliptin
25, 50, 100 100 mg daily
Saxagliptin (N) 2.5, 5
5 mg daily
Elderly
Maximum Duration Metabolism or Therapeutic
Dose
of Action Notes
(mg/day)
25 to 100 mg 100 mg daily 24 hours 50 mg daily if: creatinine
daily based on
clearance > 30 to < 50
renal function
mL/minute
25 mg if: creatinine
clearance < 30 mL/min
2.5–5 mg daily 5 mg daily
based on renal
function
24 hours 2.5 mg daily if creatinine
clearance <50 mL/min or if
on strong inhibitors of
CYP3A4/5
162
DPP-IV Inhibitors
May be used as monotherapy or in combination ●
therapy
Average HbA1c reduction 0.7 to1.0% ●
Mild hypoglycemia mayoccur ●
Postmarking reports of serious hypersensitivity ●
reactions
anaphylaxis ●
angioedema ●
exfoliative skin conditions (Stevens-Johnsonsyndrome) ●
163
Amylin Receptor Agonists
(Amylinomimetics)
Amylin, or islet amyloid polypeptide, is a hormone ●
found in the β-cells where it is co-manufactured,
stored, and released with insulin in response to food
intake.
Its actions seem to be centrally mediated and include ●
slowing gastric emptying, suppressing glucagon
secretion, and modulating the regulation of
appetite.
Amylin is absent in patients with type 1 diabetes. In ●
patients with type 2 diabetes, its concentrations are
altered to mirror those of insulin at different points in
the progression of thedisease.
164
Amylinomimetics: Pramlintide
● Adjunctive therapy for patients using insulin
● Synthetic analog of amylin
● neurohormone co-secreted from β-cells with insulin
● Suppresses postprandial glucagonsecretion
● Reduces food intake
● Slows gastric emptying
165
Pramlintide
Subcutaneous injection in abdomen or thigh ●
variable absorption with arminjection ●
Adverse effects: ●
GI most common ●
nausea, vomiting, anorexia ●
may decrease overtime ●
dose-related, slowly titrate doseupwards ●
May delay absorption of other medications; slow ●
gastric emptying
166
Pramlintide
Reduce preprandial insulin dose 30 to 50%at ●
pramlintide initiation
Basal insulin dose may be reduced if FBG close to goal ●
Dosing ●
type 2: 60 to 120 mcg prior tomeals ●
type 1: 15 to 60 mcg prior tomeals ●
2.5 units on 100 units/ml insulin syringe = 15 mcg of ●
pramlinitide
167
Pramlintide
Average HbA1c reduction 0.4 to0.6% ●
Decreases prandial glucoseexcursions ●
Little effect of FBG concentrations ●
Main advantage in type 1 DM is that it stabilizes wide ●
postprandial glycemic swings
Average weight loss in controlled trials: 1 to 2 kg ●
168
Management strategies for Type 2 DM
● Implementation strategies:
● Initial therapy
● Advancing to dual combination therapy
● Advancing to triple combination therapy
● Transitions to & titrations of insulin
186
Treatment of
acute complications
hypoglycemia
hyperosmolar hyperglycemic state
205
1- Hypoglycemia
● low blood sugar,
● defined clinically as a blood glucose level of less than 50 mg/dL.
● Individuals with DM can experience symptoms of hypoglycemia at varyingblood
glucose levels.
● Patients who have regular blood glucose levels as high as 300 to 400 mg/dL may
experience symptoms of hypoglycemia once blood glucose levels are lowered to the
middle to upper 100 mg/dLrange.
● Most people whose blood glucose levels are controlled adequately may experience
symptoms when levels fallbelow 70 mg/dL.
● Symptoms include: shakiness, sweating, fatigue, hunger, headaches, and
confusion.
● Common causes include:
delayed or inadequate amounts of food intake, especially carbohydrates,
● excessive doses of medications (e.g., sulfonylureas and insulin),
● exercising when insulin doses are reaching peak effect,
● inadequately adjusted drug therapy in renally or hepatically impaired patients.
●
206
Hypoglycemia – management
The key to successful management of hypoglycemia is ●
recognition and prevention.
Patients experiencing symptoms of hypoglycemiashould: ●
check their blood glucoselevel, ●
consume 15 g of carbohydrate, and wait 10 to 15 minutes for ●
symptom resolution (15 – 15 – 15)
Examples of acceptable treatments may include a small box of raisins,
approximately 120 mL of orange juice, approximately 240 mL of skim
milk, or three to six glucose tablets.
In patients receiving an α-glucosidase inhibitor in combination with a
sulfonylurea or insulin, hypoglycemia should be treated with glucose
tablets or skim milk owing to the mechanism of action of the αglucosidase inhibitors.
●
●
If the blood glucose level has dropped below 50 mg/dL, as much as ●
30 g of carbohydrate may be necessary to raise blood glucose
levels adequately.
207
● For patients with hypoglycemia experiencing a loss of
consciousness,
a glucagon emergency kit should be administered by ●
intramuscular or subcutaneousroute,
Glucagon dose: ●
for a child younger than 5 years of age is 0.25 to 0.5 mg;
for children 5 to 10 years of age, 0.5 to 1 mg;
for patients older than 10 years, 1 mg)
●
●
●
If glucagon is unavailable  IV glucose ●
emergency medical personnel should be contacted. ●
The patient should be rolled onto his or her side to ●
patients receiving theprevent aspiration since many
glucagon injection will vomit.
208
2- Hyperosmolar Hyperglycemic state (HHS)
Diabeticemergency – arise from inadequate insulin ●
Typically older type 2 DM patients ●
Fluid deficits & blood glucose concentrations generally greater than ●
DKA
Blood glucose can be of greater than 600 mg/dL ●
serum osmolality > 320 mOsm/kg  osmotic diuresis and fluid deficits ●
Lacks the lipolysis, ketonemia and acidosis associated with DKA ●
Precipitating Factors ●
infection/illness ●
prolonged hyperglycemia ●
prolonged dehydration ●
renal insufficiency ●
213
HHS - treatment
Lower blood glucose levels gradually ●
Treatment ●
Fluid replacement ●
hypotonic fluids (0.45% saline) should be usedif serum
sodium > 150 meq/L
low-dose insulin infusions (1 to 2 units/hour) ●
Avoid rapid correction of glucose levels ●
no greater than 75 to 100mg/dL ●
may result in cerebraledema ●
214
●
Recommended Monitoring
blood pressure
each visit
body weight/BMI
each visit
hemoglobin A1c
not atgoal: every 10-12 weeks
at goal: every 6 months
fasting lipid profile
not at goal: each visit
at goal: annually
foot exam
each visit: physical exam; monofilament annually
urine albumin
assessment
annually
dilated
annually; more frequently with identified abnormalities
ophthalmologic exam
pneumococcal
vaccine
At least 1 lifetime vaccination, vaccinate patients > age
64 if last vaccination was > 5 years ago
influenza vaccine
annually unless contraindicated
smoking cessation
each visit
220
PREVENTION AND
MANAGEMENT OF
DIABETES COMPLICATIONS
Cardiovascular Disease (CVD) in
Individuals with Diabetes
CVD is the major cause of morbidity, mortality for
those with diabetes
Common conditions coexisting with type 2 diabetes
(e.g., hypertension, dyslipidemia) are clear risk
factors for CVD
Diabetes itself confers independent risk
Benefits observed when individual cardiovascular risk
factors are controlled to prevent/slow CVD in people
with diabetes
•
•
•
•
ADA. VI. Prevention, Management of Complications. Diabetes Care 2013;36(suppl 1):S28-29.
Recommendations:
Hypertension/Blood Pressure Control
Screening and diagnosis
Blood pressure should be measured at every routine •
visit
Patients found to have elevated blood pressure should •
have blood pressure confirmed on a separate day (B)
Goals
People with diabetes and hypertension should be •
treated to a systolic blood pressure goal of <140
mmHg (B)
Lower systolic targets, such as <130 mmHg, may be •
appropriate for certain individuals, such as younger
patients, if it can be achieved without undue
treatment burden (C)
Patients with diabetes should be treated to a diastolic •
blood pressure <80 mmHg (B)
ADA. VI. Prevention, Management of Complications. Diabetes Care 2013;36(suppl 1):S28-S29.
Recommendations:
Hypertension/Blood Pressure Control
Treatment
Patients with a blood pressure (BP) >120/80 mmHg should be advised on lifestyle changes to
•
reduce BP (B)
Patients with confirmed BP ≥140/80 mmHg should, in addition to lifestyle therapy, have prompt
•
initiation and timely subsequent titration of pharmacological therapy to achieve BP goals (B)
Lifestyle therapy for elevated BP (B)
•
Weight loss if overweight
DASH-style dietary pattern including reducing sodium, increasing potassium intake
Moderation of alcohol intake
Increased physical activity
–
–
–
–
Pharmacological therapy for patients with diabetes and hypertension (C)
A regimen that includes either an ACE inhibitor or angiotensin II receptor blocker; if one class is not tolerated,
substitute the other
•
–
Multiple drug therapy (two or more agents at maximal doses) generally required to achieve BP
targets (B)
Administer one or more antihypertensive medications at bedtime (A)
If ACE inhibitors, ARBs, or diuretics are used, kidney function, serum potassium levels should be
monitored (E)
In pregnant patients with diabetes and chronic hypertension, blood pressure target goals of 110–
129/65–79 mmHg are suggested in interest of long-term maternal health and minimizing impaired
fetal growth; ACE inhibitors, ARBs, contraindicated during pregnancy (E)
•
•
•
•
ADA. VI. Prevention, Management of Complications. Diabetes Care 2013;36(suppl 1):S29.
Recommendations:
Dyslipidemia/Lipid Management
Screening
In most adult patients, measure fasting lipid profile at least annually (B) •
In adults with low-risk lipid values •
(LDL cholesterol <100 mg/dL, HDL cholesterol >50 mg/dL, and triglycerides <150
mg/dL), lipid assessments may be repeated every 2 years (E)
Treatment recommendations and goals (1)
To improve lipid profile in patients with diabetes, recommend lifestyle modification
•
(A), focusing on
Reduction of saturated fat, trans fat, cholesterol intake
Increased n-3 fatty acids, viscous fiber,
plant stanols/sterols
Weight loss (if indicated)
Increased physical activity
–
–
–
–
Statin therapy should be added to lifestyle therapy, regardless of baseline lipid levels
with overt CVD (A)
without CVD >40 years of age who have one or more other CVD risk factors (A)
–
–
For patients at lower risk (e.g., without overt CVD, <40 years of age) (C)
Consider statin therapy in addition to lifestyle therapy if LDL cholesterol remains >100 mg/dL
In those with multiple CVD risk factors
•
•
–
–
ADA. VI. Prevention, Management of Complications. Diabetes Care 2013;36(suppl 1):S31.
Recommendations:
Dyslipidemia/Lipid Management
Treatment recommendations and goals (cont’d)
In individuals without overt CVD •
Primary goal is an LDL cholesterol
<100 mg/dL (2.6 mmol/L) (B)
–
In individuals with overt CVD
Lower LDL cholesterol goal of <70 mg/dL
(1.8 mmol/L), using a high dose of a statin,
is an option (B)
–
If targets not reached on maximal tolerated statin therapy
Alternative therapeutic goal: reduce LDL cholesterol ~30–40% from baseline (B)
•
–
Triglyceride levels <150 mg/dL (1.7 mmol/L), HDL cholesterol >40 mg/dL (1.0 mmol/L)
in men and >50 mg/dL (1.3 mmol/L) in women, are desirable (C)
However, LDL cholesterol–targeted statin therapy remains the preferred strategy (A)
•
•
–
benefit Combination therapy has been shown not to provide additional cardiovascular
above statin therapy alone and is not generally recommended (A)
Statin therapy is contraindicated in pregnancy (B)
•
•
ADA. VI. Prevention, Management of Complications. Diabetes Care 2013;36(suppl 1):S31.
Recommendations:
Smoking Cessation
Advise all patients not to smoke or use •
tobacco products (A)
Include smoking cessation counseling and •
other forms of treatment as a routine
component of diabetes care (B)
ADA. VI. Prevention, Management of Complications. Diabetes Care 2013;36(suppl 1):S34.
Recommendations:
Coronary Heart Disease Screening
Screening
In asymptomatic patients, routine screening for CAD is not •
recommended, as it does not improve outcomes as long as
CVD risk factors are treated (A)
Treatment
To reduce risk of cardiovascular events in patients with
•
known CVD, consider
ACE inhibitor (C) –
Aspirin* (A) –
Statin therapy* (A) –
In patients with a prior MI •
β-blockers should be continued for at least 2 years after the event –
(B)
Avoid thiazolidinedione treatment in patients with
symptomatic heart failure (C)
Metformin use in patients with stable CHF
Indicated if renal function is normal (C) –
Should be avoided in unstable or hospitalized patients with CHF –
(C)
•
•
ADA. VI. Prevention, Management of Complications. Diabetes Care 2013;36(suppl 1):S34.