專題報告主題:

Diabetes Mellitus (DM)糖尿病

日期:3/18(五) 1600-1730

報告人:莊承翰、詹雅衣、許瑞育實習生

指導藥師:鄭淑妃總藥師、許家禎藥師、王敏如藥師

Introduction

Diagnosis

Treatment

Case report

Discussion

2

Outline

國人洗腎原發原因以糖尿病居第一位(43.2%)。台灣腎臟醫學會

高血糖個案未來5年內發生心臟病、中風及腎臟疾病的危險性是一般人的1.5倍、2.9倍及2.4倍。國民健康局

3

前言

Age populations

Obesity

Physical inactivity

High sugar & Fat diet

Others

4

Epidemics

http://www.deo.ucsf.edu/types-of-diabetes/type-2.html

項目

盛行率

全體 男 女

高血糖 8.0% 8.7% 7.5%

表 96年20歲以上民眾高血糖盛行率高血糖定義：空腹8小時以上血糖值≧126mg/dL或服用降血糖藥物。

5

Pathogenitise

7

The Effect of Insulin

http://www.deo.ucsf.edu/type1/understanding-diabetes/how-the-body-processes-sugar/cotrolling-blood-sugar.html

8

Insulin Secretion

Panel 2. Insulin secretion-www.betacell.org

Metabolic disorders Fat metabolism

Carbohydrate metabolism

Protein metabolism

A relative or an absolute lack of insulin

Glucose intolerance Hyperglycemia

9

Causes of DM

Type 1 diabetes mellitus (T1DM)

Type 2 diabetes mellitus (T2DM)

Gestational diabetes mellitus (GDM)

Other specific type (uncommon)

10

Classification

11

T1DM & T2DM

The cells ignore the insulin or the body

does not produce enough insulin.

Normal insulin function, but not enough.

Hyperglycemia when 80% to 90% of

β-cells are destroyed.

12

Peripheral

insulin

resistance

Impaired

glucose

tolerance

Early diabetes

Late diabetes

Hyperinsulinemia

Defective glucorecognition

Deterioration of b-cell function

b-cell failure

Saltiel AR, Olefsky JM. Diabetes. 1996;45:1661-1669.

From Insulin resistance to T2DM

Environment

Characteristics Type 1 Type 2

Other names IDDM(Insulin-Dependent

Diabetes Mellitus)

NIDDM(Non-insulin-

Dependent Diabetes Mellitus)

Age at onset Can occur in any age, but

usually diagnosed in children

and young adults

Usually >40 y/o, but increasing

prevalence among obese

children

% of diabetic 5%-10% 90%

Pancreatic

function

Usually none Insulin present in low, normal

or high amounts

Pathogenesis Islet cell Ab (autoimmune

destruction of the beta cells

of the pancreas)

Defect in insulin secretion;

tissue resistance to insulin;

↑hepatic glucose output

(gluconeogenesis)

Family history Not strongly relative Strongly relative

Obesity Uncommon Common (60-90%) 13

Type 1 and type 2 Diabetes

Characteristics Type 1 Type 2

Clinical

presentation

Moderate to severe

symptom

Mild polyuria, fatigue;

often diagnosed on routine

physical examination

Symptom 3Ps (polyuria, polydipsia, polyphagia) , weight loss, fatigue

Same as T1DM , blurred vision, frequent infections, trauma slow healing, numbness in the hands/feet

Ketoacidosis Often present Rare, except in

circumstances of unusual

stress (eg. Infection)

Microvascular/

Macrovascular

complication

No

Rare

Common

Common

Affects about 7% of all pregnancies (In the U.S.)

Defined as glucose intolerance that is first recognized

during pregnancy

Some will develop to T2DM or glucose intolerance

later in life

Might cause fetus’s brain progress

Diet, exercise, and/or insulin administration

15

Gestational Diabetes Mellitus (GDM)

Maternal age > 35 y/o

Family history of diabetes

Obesity : >20% IBW or BMI >27 kg/m2

History of GDM or polyhydramnios

Prior infant weight > 9 lb. at birth (macrosomia) or with congenital anomalies

16

Risk Factors for GDM

Genetic defect of b-cell

Maturity-Onset Diabetes of the Young (MODY)

Impaired insulin secretion

Minimal or no insulin resistance

Usually develop < 25 y/o

Genetic defect in insulin action

Disease of exocrine pancreas

Endocrinopathies

Drug or chemical-induce

Infections17

Other specific type

18

Plasma Glucose Status Meaning

19

Diagnosis of DM

20

Diagnose of GDM

Can DM be treated?

21

Type 1 DM Insulin

Diet

Physical activity

Amylin mimetic (ex. pramlintide)

Pancreas transplantation

Type 2 DM Diet

Physical activity

Antidiabetic agents

Insulin

Amylin mimetic22

Treatment

Physiology Reaction and Blood Sugar

Liver

Acts as the body’s glucose (or fuel) reservoir

Helps to keep circulating blood sugar levels

Both stores and manufactures glucose depending upon the body’s need

Blood sugar

Primarily dependent on the hormones insulin and glucagon

24

Liver & Blood Sugar

Glycogenolysis

Turns glycogen into glucose

Gluconeogenesis

Manufactures necessary sugar or glucose by harvesting amino acids, waste products and fat byproducts

25

Liver in Fasting State -1

http://www.deo.ucsf.edu/type2/understanding-diabetes/how-the-body-processes-sugar/the-liver-and-blood-sugar.html

25

Ketogenesis Begin is a low level of insulin

When sugar is in short supply, the liver also makes ketones, another fuel from fats

Burned as fuel by muscle and other body organs, while sugar is saved for the organs that need it

For the organs that always require sugar, including the brain, red blood cells and parts of the kidney

26

Liver in Fasting State -2

http://www.deo.ucsf.edu/type2/understanding-diabetes/how-the-body-processes-sugar/the-liver-and-blood-sugar.html

26

Accelerates transport of glucose from blood into cells Accelerates conversion of glucose into glycogen

(glycogenesis).

Accelerates transport of amino acids from blood into cells and increases rate of protein synthesis in the cells

Increases lipogenesis

Decreases glycogenolysis and gluconeogenesis

27

The role of insulin

Amylin

GLP-1 (glucagon-like peptide-1), GIP (glucose-dependent insulinotropic polypeptide)

Epinephrine, cortisol, and growth hormone

28

Other Hormones & Blood Sugar

Released along with insulin from beta cells

Reduce the production of sugar by the liver during a meal

Has much the same effect as GLP-1 Decreases glucagon levels

Slows the rate at which food empties from stomach

Make brain feel satisfying meal

29

Amylin

http://www.deo.ucsf.edu/type1/understanding-diabetes/how-the-body-processes-sugar/blood-sugar-and-other-hormones.html

29

Incretin hormones released from gut

Signal the beta cells to increase insulin secretion and decrease the alpha cells’ release of glucagon

GLP-1 also slows down the rate at which food empties from stomach, and makes the brain feel full and satisfied

For type 1 DM patients, having absent or malfunctioning beta cells, the releasing of GLP-1 during a meal cannot enhance insulin secretion

30

GLP-1 and GIP

http://www.deo.ucsf.edu/type1/understanding-diabetes/how-the-body-processes-sugar/blood-sugar-and-other-hormones.html

30

Along with glucagon

Called “stress” or “gluco-counter-regulatory” hormones, which make the blood sugar rise.

Enhance the production of glucose by the liver.

Counterbalance the effect of insulin .

31

Epinephrine, Cortisol, and Growth Hormone

http://www.deo.ucsf.edu/type1/understanding-diabetes/how-the-body-processes-sugar/blood-sugar-and-other-hormones.html

31

Treatment

DM Patient treatment goal

To ameliorate symptoms

Reduce the risk for microvascular and macrovascular disease complications

Improve life quality

Reduce mortality

33

34

ADA Goals for Adults with DM

Glycemic goals

A1c ＜6.5% (normal 4 %-6 %)

Preprandial plasma glucose 70-130 mg/dL (3.9-7.2 mmol/L)

Postprandial plasma glucose <180 mg/dL (<10 mmol/L)

Blood pressure <130/80 mmHg

Lipid

LDL <100 mg/dL (<2.6 mol/L)

TG <150 mg/dL (<1.7 mmol/L)

HDL-Men

-Women

>40 mg/dL (>1.1 mmol/L)

>50 mg/dL (>1.3 mmol/L)

Insulin Therapy

36

Proinsulin

Applied Therapeutics: The clinical use of drug, 2009, 9th Figure 50-3 Proinsulin.

Proinsulin=A chain+ B chain+ C chain(35 a.a)=86 a.a.Insulin=A chain(21 a.a.) + B chain(30 a.a.)

37

Properties of InsulinInsulin Brand Name Onset (hr) Peak (hr) Duration Appearance

Rapid acting

Lispro

Aspart

Glulisine

Inhaled

human insulin

Humalog

Novorapid

Apidra

5–25 min

15–30

min

30–90 min

1–2

<5hr

6hr

Clear

Powder

Short Acting

Regular Humulin R 0.5–1 2–3 5–8hr Clear

Intermediate Acting

NPH Humulin N 2–4 4–12 12–18hr Cloudy

Long Acting

Glargine

Detemir

Lantus

Levemir

1.5

3–8

No pronounced

peak

Relatively flat

20–24 hr

5.7–

23.2hr

Clear

Clear

38

Onset and Duration of Insulin

R.A. Harvey et al. Lippincott’s illustrated Reviews: Pharmacology 3rd ed., 2006 p 285

39

Combination Insulins

Type/Duration of Action Brand Name Manufacturer

NPH/regular mixture (70%/30%) Humulin 70/30

Novolin 70/30

Lilly

Novo Nordisk

NPH/regular mixture (50%/50%) Humulin 50/50 Lilly

Insulin aspart protamine/insulin aspart

mixture (70%/30%)NovoMix 30 Novo Nordisk

Insulin lispro protamine/insulin

lispro(75%/25%)Humalog Mix25 Lilly

Insulin lispro protamine /insulin

lispro mixture(50%/50%)

Humalog Mix

50/50Lilly

40

Insulin Injection

40

Hypoglycemia (tachycardia, sweating, blurred vision, hunger, tremulousness, confusion, vertigo and coma) <60 mg/dL－may or may not be symptomatic

<40 mg/dL－symptomatic <20 mg/dL－associated with seizure and coma Treatment of hypoglycemia

Oral administration of glucose or sugar 50% glucose solution (i.v.) Glucagon (i.m. or s.c)

Lipodystrophy Allergic reactions

41

Adverse Effect

Insulin pump

Continuous S.C. infusion by pump

Can program an extra dose of insulin at meals

Inhaled insulin

Taken before meals as an rapid-acting insulin, in conjunction with an injected basal insulin

Reduce number of daily injections required

The lower bioavailability

42

Other Preparations of Insulin

Restore near-normal glucose patterns throughout the day while minimizing the risk of hypoglycemia

Current regimens generally use intermediate- or long-acting insulin to provide basal coverage

Rapid- or short-acting insulin to meet the mealtime requirements

43

Aims of Insulin Therapy

44

Empiric Insulin Doses

Type 1 diabetes

Initial dose 0.3-0.5 Unit/kg

honey moon phase 0.2-0.5 Unit/kg

With ketosis, during illness,

during growth

1-1.5 Unit/kg

Type 2 diabetes

With insulin resistance 0.7-1.5 Unit/kg

Normal Early peak

Immediate release of stored insulin

Late phase Release of newly formed

insulin to normalize glycemia

Type 1 DM Almost no release

Type 2 DM Release slowly

45

Insulin Release

R.A. Harvey et al. Lippincott’s illustrated Reviews: Pharmacology 3rd ed., 2006 p 282.

45

Insulin Levels throughout the Day

http://www.deo.ucsf.edu/type1/understanding-diabetes/how-the-body-processes-sugar/controlling-blood-sugar.html

46

Low steady secretion of insulin

Overnight, fasting and between meals

Spikes of insulin

At mealtimes

Typical split-mixed regimen

Variation of A Regimen that

incorporates ultralenteor glargine insulin

Variation of C Continuous

subcutaneous insulin infusion

Multiple Daily Injection

47

Goals of Physiological (Basal-Bolus) Insulin Therapy

Monitoring

parameter

(mg/dL)

Adults School Age

(6–12 years)

Adolescent

s and young

adults(13-

29 years)

Pregnancy

Fasting 70-130 90-180 90-130 60-90

2 hr

postprandial

180 ≦120

2-4 AM ＞70 100-180 90-150 60

A1C 6.5% 8% 7.5% 5-6%

Urine

ketones

Absent to

rare

Absent to

rare

Absent to

rare

rare

48

49

Glysolated Hemoglobin ( A1c)

A1c Estimated Average

Glucose (mg/dL)

5% 97

6% 126

7% 154

8% 183

9% 212

10% 240

11% 269

12% 298

49

Oral Anti-diabetic Drugs Therapy(OHA)

Type 2 DM treatment of Oral Drugs classification

Insulin secretagogues Sulfonylureas

Non-sulfonylureas

(Meglitinides)

Insulin sensitizers Biguanides

Thiazolidinediones

(Glitazones)

Delaying carbohydrate absorption α – glycosidase antagonists

Gut hormones DPP- IV Inhibitiors

GIP , GLP-1 , Amylin analogs

51

Sulfonylureas

Pharmacology Enhance insulin secretion

Bind to sulfonylurea receptor(SUR) on pancreatic beta cells

Pharmacokinetics All sulfonylureas are metabolized by liver

CYP2C9 is involved with the hepatic metabolism of the majority of sulfonylureas

52

Sulfonylureas

Side effects Hypoglycemia alert(most common)

Hyponatremia (serum sodium<129mEq/L)

Weight gain

DDI(related to CYP2C9)

53

DrugDuration of biologic

effect, hUsual daily dose, mg Dosing per day

First-generation sulfonylureas

Acetohexamide 12 to 18 500 to 750 Once or divided

Chlorpropamide (Diabinese) 24 to 72 250 to 500 Once

Tolbutamide (Orinase) 14 to 16 1000 to 2000 Once or divided

Second-generation sulfonylureas

Glipizide 14 to 16 2.5 to 10 Once or divided

(Glucotrol)

(Glucotrol XL) 5 to 10 Once

Gliclazide 24 40 to 240 Once

(Diamicron R)

(Diamicron MR)

Glyburide (Glibenclamide) 20 to 24+ 2.5 to 10 Once

(Diabeta)

(Micronase)

(Glynase)

Glimepiride (Amaryl) 24+ 2 to 4 Once

Sulfonylureas

54

Meglitinides

Pharmacology Similar to sulfonylureas, it also enhance insulin secretion

Primarily used to target postpradial glycemia (because it is a short-acting insulin secretagogues)

Pharmacokinetics Rapidly absorbed(0.5 ~ 1 hr)and t1/2=1~1.5 hrs Nateglinide and Repaglinide can be metabolized by liver

or other pathways like renal or biliary

Side effects Hypoglycemia(lower) Similar risk for weight gain

55

Meglitinides

56

Biguanides

Pharmacology

Enhancement of insulin sensitivity

Metformin only

Pharmacokinetics

B.A.=50~60%

NOT METABOLIZED BY LIVER

Renal inffciency is contraindicated for metformin use

In men : serum creatinine ≥1.5mg/dL

In women : serum creatinine ≥ 1.4mg/dL

57

While comparison with sulfonylurea or insulin Reduce all-cause mortality

Reduce the risk of stroke

Reduce CV death

Side effects GI side effects(Diarrhea ,nausea/vomiting or flatulence )

Lactic acidosis(<1%)

Biguanides

58

Biguanides

Q: Only metformin ? What about Buformin(Bigunal) or Phenformin?

59

Thiazolidinedione(TZD or -glitazones)

Pharmacology

Bind to the peroxisome proliferator activator receptor-γ(PPAR-γ)

Enhance insulin sensitivity

Pharmacokinetics

Mainly metabolized by liver

Side effect

Weight gain

Water remain - induce CV risk60

Progress slowly

Liver toxicity of Troglitazone

Patient

Should not start if ALT> 2.5times ULN

DC if ALT> 3 times ULN

Thiazolidinedione(TZD or -glitazones)

61

Not suggest for understatement Ischemic heart diease

CHF(Contraindication for Class III & IV)

＃目前此類藥物不可做為第一線用藥， 而使用Avandia前須簽同意書。

Thiazolidinedione(TZD or -glitazones)

62

α-Glucosidase inhibitor

Pharmacology Competitive inhibit starch and di-saccharides metabolism,

cause glucose intake decrease

Acarbose & Miglitol

Pharmacokinetics Work on intestine

Commonly use for after-meal plasma glucose control (take with meals)

Side effects GI discomfort (bloating, diarrhea…)

63

α-Glucosidase inhibitor

64

DPP-IV inhibitor

Pharmacology 能阻止內生性的GLP-1遭分解

GLP-1具有降低血糖、刺激胰島素分泌、抑制升糖素分泌的作用

Pharmacokinetics Sitagliptin 做成水溶性磷酸鹽，Oral B.A.可達87%，

Protein binding達38%，t1/2約12hrs

另外還有Saxagliptin (新藥，是Januvia 2-3倍強度) 為DPP-IV 抑制劑，也可以使GLP-1濃度上升

65

DPP-IV inhibitor

66

Pharmacology Exendin-4可與GLP-1 receptor結合，產生擬似血糖素樣胜肽作用

(GLP-1 mimetic effect)

合成的Exendin-4稱為Exenatide (Byetta)

Pharmacokinetics 體內被DPP-IV 水解，S.C.後t1/2約2-4hrs

Side effects

Nausea and vomiting, diarrhea,headache, dizziness

GLP-1 agonists

#通常用在飯後皮下注射給藥，控制Type 2 DM67

Pharmacology 是Amylin 的合成類似物，減少升糖素(glucagon)的釋出反應，可皮下注射調節飯後血糖的濃度

可活化中樞系統之Amylin受體，因此能使糖化血色素減少及降低飯後葡萄糖的濃度

Pharmacokinetics 體內約20 min達 Peak concentration， t1/2約0.5hrs ，主要由腎排除

Side effects Nausea and vomiting, hypoglycemia

Amylin agonists

#通常用在飯前皮下注射給藥，治療Type 1與2 DM 68

Total Data

69

糖尿病二型 guildline

70 70 XD

Case Report

Mr. Li 61y/o 169.3 cm 58.2 kg BMI:20.305

DOA：2011-02-08 DOD：2011-02-24

Section：META

Chief complaint： Syncope last afternoon, denied fever, alcohol, head injury ;

conscious clear at ER

History of present illness ： Type 2 Diabetes Mellitus 40+, under OADs and Levemir control,

but poor compliance

72

Case report-1

Past medical history：

status post debridement and full thickness skin graft

Perforated peptic ulcer s/p subtotal gastrectomy + gastrojejunostomy 30+ yrs ago

Hypertension

Vitreous Hemorrhage OD

73

Case report-2

Personal history

Alcohol : nil

Smoking : nil

Drugs allergy : nil

Family history:

DM

HTN

74

Case report-3

Vital signs：T/P/R:35/103/20,BP:131/ 77 mmHg Lab data ：

EKG showed sinus rhythm Ccr=(140-age)*Wt(kg)/Serum creatinine creatinine *72

=43.73858….中度慢性腎病75

Emergency Department Course

Hgb12-15

NA 135-147

K 3.4-4.7

free Ca2+ 0.9-1.5

BUN7-20

9.9 g/dL

134 mmol/L

4.1 mmol/L 1.03 mmol/L

24 mg/dl

Cr0.5-1.5

GLU65-115

CK/MB/TnI24-168/-/0-0.05(AMI>1.5)

CRP0-0.05

1.46mg/dl

492 mg/dl

75/-/0.04 0.13mg/dl

Drug Profile

77

2007-2011年用藥紀錄

2007.4.21

• Amaryl tab 2 mg BID

• Glucophage tab 500 mg BIDCC

2007.11.10

•Amaryl tab 2 mg BID•Glucophage tab 500 mg BIDCC•Insulatard HM 100 iu/Ml HS

2008.1.28

•Amaryl tab 2 mg BID

•Glucophage tab 500 mg BIDCC

•Lantus inj 100 iu/Ml QD

2008.5.19

• Glucophage tab 850 mg BIDCC

• Lantus inj 100 iu/Ml QD

2009.1..13

• Humulin-R 100 iu/mL

• Glucophage tab 850 mg

• Lantus pen 100 iu/mL

78

2007-2011年用藥紀錄(續)

2009.12.16

• Glucophage tab 850 mg BIDCC

• Lantus pen 100 iu/Ml QD

2010.5.14

• Mixtard 30 inj 100 iu/mL

2011.1.21

• Starlix FC tab 120 mg

• Levemir flexpen 100 io/mL

• glucophage tab 500 mg

2011.2.24

• Humulin-N 100 iu/mL

• Novorapid penfil 100 u/3L

點我>0<

商品名/學名/含量/劑型日期+頻次/

途徑2/8 2/9 2/10 2/11 2/12 2/13 2/14 2/15 2/16 2/20 2/22 2/24

2011/3/9(出院)

Co-Diovan(Valsartan +

Hydrochlorothiazide) FC tab 80/12.5 mg

QD/PO

Norvasc(Amlodipine) tab 5 mg

QD /PO

Starlix(Nateglinide) FC tab 120 mg

QD-BL*#1QD-BD*#1

QD-BBF*#0.5/P

OGlucophage tab 500

mgBIDCC /PO

Humulin-R inj 100iu/ml 1iu (UD

QD-BBFQD-BL

QD-BD /SC

Humulin-N inj 100iu/ml 1iu (UD

HS /SC ST ST

Novorapid penfill 100 u/ml 3ml

TIDAC /SC ST ST ST

Levemir flexpen 100 iu/ml 3ml

QD-INSL /SC

HS

Ferrum hausmann chewa.tab 100 mg

QD /PO

Chloramphenicol oph sol0.25% 10ml

QID /OU

STST

ST ST

STSTST

HS

Discussion-1

81

近兩年空腹血糖v.s.糖化血色素值

82

2/8-2/24住院期間血糖值

橫軸:日期 縱軸:血糖值

0

100

200

300

400

500

600

日期

2011

/2/9 2

1:36

2011

/2/11

06:3

7

2011

/2/12

15:1

8

2011

/2/13

22:0

2

2011

/2/15

06:1

5

2011

/2/16

06:4

8

2011

/2/17

10:2

0

2011

/2/18

15:2

5

2011

/2/19

22:2

6

2011

/2/20

22:5

5

2011

/2/21

21:5

3

2011

/2/22

21:5

8

2011

/2/24

06:5

4

血糖值

線性 (血糖值)

What causes bad PG controll ?

1.Irregular meals(dessertsor something else)

2.Medication Compliance (which influences glucose)

3.Hypersensitivity for medication(Caused hypoglycemia)

4.Individual tolerance(feeling of SMBG)

5.Worsing of DM

Discussion-2

FIGURE 24-32 Long-term complications of diabetes85

Complication

Patient’s Complication

Macrovascular Skin necrosis over the lower leg ulcer over the big toe

Microvascular Had been a sudden blurred vision (HYPERTENSIVE

RETINOPATHY , CRVO, NIDDM RETINOPATHY)

86

From HA1C Control to Retinopathy

87

Complication Treatment

Macrovascular Skin necrosis over the lower leg

STSG Neomycin Ointment 0.5% Augmentin tab 375 mg Betadine sol 10% 100 ml

ulcer over the big toe FTSG

Microvascular Had been a sudden blurred vision

Trental tab 100 mg Transamin cap 250 mg Fluorometholone Oasis oph sol

88

From DM to Nephropathy

89

I GOT PROTEINURIA !!

90 90

DM comes, Dyslipidemia follows

91

Screening Test

Glucose monitor : Once half year (HbA1c)

Cardiac vascular health:

Check blood pressure daily

Check plasma lipid

Eye : Check once in two years

Kidney : Check micro proteinuria annually

Peripheral perfusion : Foot exam at least once a year

92

Prevention complication

Diet

Exercise

Not smoking

Taking a low-dose aspirin every day if indicated (for adults only)

Proper and exact medications

Monitoring goals

Avoid getting trauma

93

Discussion-3

Control diet amount Avoid high caloric foods such as organs, crab egg, fish egg

Egg yolk control under three per week

Quit sugar

Cut oil Use vegetable oil while cooking.

Choose steam, water boil mostly to cook your food

Decrease salt intake

DM patient diet formula-casual time

95

Calorie 30-35 cal/Kg/day, equals to 2 slice of toast, or a bottle of coke

45% to 65% of daily caloric intake carbohydrates

Protein Insignificant Proteinuria, daily protein 0.8-1.0 g/Kg/day

Significant Proteinuria, daily protein 0.8/Kg/day

Study show protein can improve DM p’t PG control

Glycemic control Does not recommend restricting diets to <130 grams of

carbohydrate a day

96

DM patient diet formula - while ill

Aerobic exercise Improves insulin resistance and glycemic control

Reduces cardiovascular risk factors

Weight maintenance

Improves well-being

Physical activity goals At least 150 minutes/week of moderate intensity exercise

Exercise

97

Light exercise Patient had surgery on his leg, suggest exercise which need not

too much walking, such as swimming

Wear elastic socks

Warm feet bath

Increase protein in take Patient has miner kidney problem

Patient doesn’t take enough protein at home

Patient show terrible PG control

Keep candies at hand98

Suggesting health care for patient

Applied Therapeutics: The clinical use of drug

Pharmacotherapy: a pathophysiologic approach

http://www.deo.ucsf.edu/index.html

Up to date

國民健康局

行政院衛生署全民健康保險醫療品質資訊公開網(DM)

行政院衛生署

全民糖尿病觀測站

99

Reference

100

Thanks for your attention