Diabetes Mellitus

Document Sample
Diabetes Mellitus Powered By Docstoc
Dr. Abdulmohsen Al Tuwijri

• Definition • Diabetes in History • Prevalence • Classification • Screening • Prevention • Management • Recommendations

1. Know definitions of: pre-diabetic state,
2. 3. 4. 5. 6.
impaired glucose tolerance, and DM. Know prevalence of DM. Understand etiologies and types of DM. Understand acute DM complications. Understand chronic DM complications. Understand current recommendations in the management of DM.

Part I

What is Diabetes?

Diabetes Mellitus is a group of metabolic disease characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both.
The chronic hyperglycemia of diabetes is associated with long-term damage, dysfunction, and failure of various organs, especially the eyes, Kidneys, nerves, heart, and blood vessels.

Diabetes in History !

The History of Diabetes Mellitus
Ancient Egyptians
The Middle Empire
2040 - 1785 B.C.

Women thirst:
• • • • • The Ebers Papyrus 1550 B.C. The first human description in history. Found more in women. Described to cause thirst. The papyrus found was turn so no more information about the treatment. • Glycated hair.
History of clinical Endocrinology.

The History of Diabetes Mellitus
Ancient Greeks
500 B.C.

Polyuria ? :
• He described a disease characterized by: • Polyuria.
• Lack of pain. • Weakness. • Fluid output is greater than fluid intake.

• Treat by: • Diet containing a minimum amount of food. • Regulated mode of life.
De Medicina ( English translation).


The History of Diabetes Mellitus
Islamic History
1000 A.C

• Polyuria and polydipsia.

• Physical wasting. • Energetic physical wasting. •Treatment: Diet Plants.

Li hsuan monograph on diabetes mellitus

The History of Diabetes Mellitus
Islamic history
1100 A.C. • It’s relation to foot gangrene. • Complication ( ie: impotence ). • Treatment: Diet, Plants, Veinsection.


‫ابن سيناء‬
Al canon fit Tibb.

The History of Diabetes Mellitus
Before 19th century
1500 A.C- 1800 A.C

Willis Sydenham Wirsung Sganarelle Morton Dobson Cawley Prout Von Fehling

Date Achievement
1621 1633 1642 1650 1689 1776 1788 1830 1848 Observed the sweetness of urine Regarded DM Blood disease Discovered the pancreatic duct Tasted the urine Mentioned a hereditary factor in DM Proved that sugar caused sweet urine & blood diabetes may follow injury to the pancreas Described Diabetic coma Described his test for sugar in the urine

The History of Diabetes Mellitus
Before 19th century
1500 A.C- 1800 A.C

Petters Langerhans Ebstein VonMering Minkowski Laguesse De Meyer Allen Folin

Date Achievement
1857 1869 1876 1890 1892 1893 1909 1913 1919 Isolated acetone from diabetic urine Described the islet cells of the pancreas Treated diabetes with sodium saliclate Produced DM by removal of pancreas in dogs Cured DM in dogs by reimplantation of pancreas Suggested that the islet cells produce hormone Named the hormone insulin Used prolonged fasting for treatment Presented blood sugar test

The History of Diabetes Mellitus
19th Century
1921 A.C

Insulin discovery
• Banting and Best separated the

insulin and used it for the first time in their dog. • Insulin was used in clinical setting for the first time in 1922 by Tompson.
Banting and Best 1921


Ancient Egyptians


Ancient Indians


Ancient Greeks


Ancient Greeks


Ancient Romans Chines Ancient Islamic period Before the 20th century

+500 +1000 +1500

Diabetes Mellitus appears with the civilization but disappear with it’s disappearance
The 20th century


History of diabetes management
1910 1920 1930 1940 1950 1960 1970 1980 1990 2000

Death Insulin discovery complication history

Natural history of Complication

Complication treatment

Complication Reduction

Prevention programs

What is the Prevalence of DM in KSA?

Insulin deficiency
Blood glucose


Insulin resistance

Polyuria and polydipsia. Weight loss with polyphagia. Blurred vision. Infection susceptibility. DKA or NKHS.

I- Type 1 diabetes: Etiologic classification II- Type 2 diabetes. of

diabetes mellitus

III- Other specific types.

IV- Gestational diabetes mellitus.

I- Type 1 diabetes:

Etiologic classification of

A. Immune mediated:
B lymphocyte
Cellular-mediated autoimmunity.

T lymphocyte


diabetes mellitus

Islet cell autoantibodies ( ICAs ). Autoantibodies to insulin ( IAAs ). Autoantibodies to glutamic acid decarboxylase ( GAD ). Autoantibodies to the tyrosine phosphatase IA-2 and IA-2B.

HLA-DR/DQ alleles can be either predisposing or protective.

Beta cell

I- Type 1 diabetes:

Etiologic classification of

Autoimmune destruction

Multiple genetic:
Graves’ disease Hashimoto’s thyroiditis Addison’s disease Vitiligo Pernicious anemia

Viral infection Obesity

diabetes mellitus

I- Type 1 diabetes:

Etiologic classification of
Beta cell destruction:
Rapid Slow


diabetes mellitus

infants and children adults

DKA Hyperglycemia Hyperglycemia to DKA children and adolescents adults Adults

I- Type 1 diabetes:

Etiologic classification of

B. Idiopathic:

diabetes mellitus

No autoimmunity DKA Minority of patients Strongly inherited No HLA association Insulin requirement may come and go

II- Type 2 diabetes.

Etiologic classification of

•Relative insulin deficiency ( initially). •No Autoimmune destruction of  -cell. •Obesity ( insulin resistance ). •No DKA (some times with stress ie infection). •Pass undiagnosed. •Macro- & micro-vascular complications. •Insulin is normal or high.

diabetes mellitus



Target tissue

II- Type 2 diabetes.

Etiologic classification of

•Relative insulin deficiency ( initially). •No Autoimmune destruction of  -cell. •Obesity ( insulin resistance ). •No DKA (some times with stress ie infection). •Pass undiagnosed. •Macro- & micro-vascular complications. •Insulin is normal or high.

diabetes mellitus



Target tissue

II- Type 2 diabetes.

Etiologic classification of

•Relative insulin deficiency ( initially). •No Autoimmune destruction of  -cell. •Obesity ( insulin resistance ). •No DKA (some times with stress ie infection). •Pass undiagnosed. •Macro- & micro-vascular complications. •Insulin is normal or high.

diabetes mellitus



Target tissue

II- Type 2 diabetes.

Etiologic classification of

•Relative insulin deficiency ( initially). •No Autoimmune destruction of  -cell. •Obesity ( insulin resistance ). •No DKA (some times with stress ie infection). •Pass undiagnosed. •Macro- & micro-vascular complications. •Insulin is normal or high.

diabetes mellitus



Target tissue

II- Type 2 diabetes.

Etiologic classification of

•Relative insulin deficiency ( initially). •No Autoimmune destruction of  -cell. •Obesity ( insulin resistance ). •No DKA (some times with stress ie infection). •Pass undiagnosed. •Macro- & micro-vascular complications. •Insulin is normal or high.

diabetes mellitus



Target tissue

II- Type 2 diabetes.

Etiologic classification of

Risk factors:

diabetes mellitus

Age Obesity Lack of physical activity Women H/O G.D.M Hypertension Dyslipidemia Ethnic and racial subgroups Strong genetic predisposition


III- Other specific types.

Etiologic classification of

Genetic defects of

-cell function:

Chromosome 12, HNF-1 (MODY3) Chromosome 7, glucokinase (MODY2) Chromosome 20, HNF-4 (MODY1) Mitochondrial DNA Others

Genetic defects in insulin action:
Type A insulin resistance Leprechaunism Rabson-Mendenhall syndrome Lipoatrophic diabetes Others

diabetes mellitus

Disease of the exocrine pancreas:
Pancreatitis Trauma/pancreatectomy Neoplasia Cystic fibrosis Hemochromatosis Fibrocalculous pancreatopathy Others

III- Other specific types.
Acromegaly Cushing’s syndrome Glucagonoma Pheochromocytoma Hyperthyroidism Somatostatinoma Aldosteronoma Others

Etiologic classification of

Drug or chemical-induced:

diabetes mellitus

Vacor Dilantin Thiazides Diazoxide Neoplasia Pentamidine  - interferon Nicotinic acid Cystic fibrosis Glucocorticoids Thyroid hormone Hemochromatosis  -adrenergic agonists Fibrocalculous pancreatopathy Others

III- Other specific types.

Etiologic classification of

Congenital rubella Cytomegalovirus Others

Uncommon forms of immune-mediated diabetes:
“ Stiff-man “ syndrome Anti-insulin receptor antibodies Others

diabetes mellitus

Other genetic syndromes sometimes associated with diabetes:
Down’s syndrome Klinefelter’s Turner’s syndrome Wolfram’s syndrome Friedreich’s ataxia Huntington’s chorea Laurence-Moon-Biedl syndrome Myotonic dystrophy Porphyria Prader-Willi syndrome Others

IV- Gestational diabetes mellitus.

Etiologic classification of

Any degree of glucose intolerance with onset or first recognition during pregnancy.


diabetes mellitus

- 1 ~ 14% of the total pregnancies. - 90% of pregnancies complicated by diabetes.

- Perinatal morbidity and mortality - Maternal complications - Risk factor for glucose intolerance

Impaired glucose tolerance Impaired fasting glucose Etiologic classification of Normal



diabetes mellitus


FPG = 100 - 125 mg/dl 5.6 - 6.9 mmol/l IGT: 2HPG = 140 - 199 mg/dl 7.8 -11.0 mmol/l)

Impaired glucose tolerance Impaired fasting glucose
Etiologic classification of


• They are known risk factors for future diabetes and

cardiovascular disease. • Intermediate stage for all types of diabetes. • Associated with insulin resistance syndrome or Metabolic Syndrome: Insulin resistance Hyperinsulinemia Obesity Dyslipidemia ( high triglyceride and/or low HDL ) Hypertension

diabetes mellitus

• Some patients cannot be clearly classified as T1D or T2D.
• Clinical presentation and disease progression vary considerably in
both types of diabetes.

• Occasionally, patients who otherwise have T2D may present with
ketoacidosis. Similarly, patients with T1D may have a late onset and slow progression of disease despite having features of autoimmune disease.

• Such difficulties in diagnosis may occur in children, adolescents,
and adults. The true diagnosis may become more obvious over time.

Criteria for the diagnosis of DM ?

Case Q
A Saudi lady, aged 56 years, with long-standing hypertension is found to have glycosuria at her regular check. FPG is 7.5 mmol/l. Does she have diabetes?

She probably has diabetes as the FPG is above the diagnostic criteria (>7.0 mmol/l). According to the diagnostic criteria, diabetes can be diagnosed on the basis of a single abnormal laboratory PG concentration in the presence of typical symptoms. If she is asymptomatic, then a further diagnostic PG is required. A repeat FPG >7.0 mmol/l would confirm this, otherwise a glucose tolerance test is required.

Criteria for the diagnosis of DM
1. FPG* >126 mg/dl (7.0 mmol/l) [Repeat]. OR 2. Symptoms of hyperglycemia and Casual plasma glucose * >200 mg/dl (11.1 mmol/l). OR 3. 2-h plasma glucose >200 mg/dl (11.1 mmol/l) during an OGTT *[Repeat]. ……………………………………………………………………………………….
* Fasting is defined as no caloric intake for at least 8 h. * Casual is defined as any time of day without regard to time since last meal. * The classic symptoms of hyperglycemia include polyuria, polydipsia, and unexplained weight loss. * OGTT: The test should be performed as described by the World Health Organization, using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water. * In the absence of unequivocal hyperglycemia, these criteria should be confirmed by repeat testing on a different day.

B. Diagnosis of diabetes
● The FPG test is the preferred test to diagnose diabetes in children and non pregnant adults. (E) ● Use of the A1C for the diagnosis of diabetes is not recommended at this time. (E) *** FPG X A1C : Standardization
Facilitation Cheep

Diagnosis of Diabetes :
Plasma Glucose Cutoff Points
FBS categories Normal IFG IGT

2- Hour BS on OGTT mg/dl < 140 _

mg/ dl < 100 > 100 and < 126

> 126

> 140 and < 200
> 200


Screening For Diabetes
• Should we screen for diabetes? • Who should we screen? • How should we screen?

Criteria for Screening
• Important public health problem • Early asymptomatic stage exists • Suitable screening test • An accepted treatment is available • There is evidence that early intervention
improves outcome.

Testing healthy individuals
• T1D :
– More than one antibodies (ICA, IAA, GAD, IA-2). – No effective method can prevent or delay it. – Screening is not cost-effective.

• T2D :
– 50% of T2D are undiagnosed. – Chronic complications precede diabetes. – Risk factors.

A. Criteria for testing in asymptomatic adults
1. Testing should be considered in all adults who are overweight and have one or more additional risk factor of:
● ● ● ● ● ● ● ● ● ● physical inactivity first-degree relative with diabetes members of a high-risk ethnic population women who delivered a baby weighing 4 Kg or were diagnosed with GDM hypertension (140/90 mmHg or on therapy for hypertension) HDL cholesterol level 35 mg/dl (0.90 mmol/l) and/or a triglyceride level 250 mg/dl (2.82 mmol/l) women with polycystic ovarian syndrome (PCOS) IGT or IFG on previous testing other clinical conditions associated with insulin resistance (e.g., severe obesity and acanthosis nigricans) history of CVD

2. In the absence of the above criteria, testing should begin at age 45y 3. If results are normal, testing should be repeated at least at 3-year intervals, with consideration of more frequent testing depending on initial results and risk status.

B. Criteria for testing in asymptomatic children
● Overweight * Plus any two of the following risk factors:
● Family history of T2D in first or second-degree relative ● Race/ethnicity ● Signs of insulin resistance or conditions associated with insulin resistance (e.g., acanthosis nigricans, hypertension, dyslipidemia, or PCOS) ● Maternal history of diabetes or GDM

Time: Age of initiation: age 10 years or at onset of puberty, if puberty occurs at a younger age. Frequency: every 2 years Test: FPG (preferred)

*Overweight: BMI 85th percentile for age and sex, weight for height 85th percentile, or
weight 120% of ideal for height

C. Screening for GDM

• Carry out GDM risk assessment at the first prenatal


visit. Women at very high risk for GDM should be screened for diabetes ASAP after the confirmation of pregnancy.

• All women of higher than low risk of GDM, should

undergo GDM testing at 24–28 weeks of gestation.

Screening for GDM …
Criteria for very high risk (any of):

Criteria for low risk (all of) :
● Age < 25 years ● Weight normal before pregnancy ● Member of an ethnic group with a low prevalence of diabetes ● No known diabetes in first-degree relatives ● No history of abnormal glucose tolerance ● No history of poor obstetrical outcome

● Severe obesity
● Prior history of GDM or delivery of large-for-gestational-age infant ● Presence of glycosuria ● Diagnosis of PCOS ● Strong family history of type 2 diabetes

Screening for GDM …
1. 1. One-step approach (preferred in clinics with high prevalence of GDM):
Perform a diagnostic 100-g OGTT in all women to be tested at 24–28 weeks. A diagnosis of GDM requires at least two of the following plasma glucose values: FPG : 95 mg/dl (5.3 mmol/l) 1 h: 180 mg/dl (10.0 mmol/l) 2 h: 155 mg/dl (8.6 mmol/l) 3 h: 140 mg/dl (7.8 mmol/l)

2. Two-step approach: Perform initial screening by measuring plasma or
serum glucose 1 h after a 50-g OGTT, (> 140 mg/dl) . Then Perform a diagnostic 100-g OGTT on a separate day in women who exceed the threshold on 50-g screening.
*The 100-g OGTT should be performed in the morning after an overnight fast of at least 8 h.

Can diabetes be prevented/delayed?

• These interventions include an intensive lifestyle modification program that
has been shown to be very effective (58% reduction after 3 years), and use of the pharmacologic agents metformin, acarbose, orlistat, and rosiglitazone, each of which has been shown to decrease incident diabetes to various degrees ( ~ 30%). 5–10% of body weight, as well as on increasing physical activity to at least 150 min/week of moderate activity such as walking.

• Patients with IGT (A) or IFG (E) should be given counseling on weight loss of

● In addition to lifestyle counseling, metformin may be considered in those who are at very high risk (combined IFG and IGT plus other risk factors) and who are obese and under 60 years of age. (E) ● Monitoring for the development of diabetes in those with pre-diabetes should be performed every year. (E)

Part II


A sedentary man aged 50 years has had T2D for 5 months, BMI has fallen from 32 to 30 kg/m2 on diet and exercise alone. Results are now steady, with FPG 8.1 mmol/l, HbAlc 7.4% and creatinine 72 umol/l.

Glycaemic control is suboptimal and, 5 months later, this is probably the best he will achieve with diet alone. You could continue with diet alone if he was still losing weight; If not, Metformin is the next step.

Drug groups & names


Dose & time of administration

Common side



A- Sulfonylurea: Glibenclamide (Daonil) Glipizide (glucotrol) Glimepiride (amaryle) Gliclazide (Diamicron) Glinides: Repaglinide(parandine) Nateglinide(starlix)

2.5-20mg/d 15-30m Before meal
1-8mg/d with meal

Hypoglycemia, wt gain

Use with caution in pt with renal & hepatic impairment

0.5-4mg max.16mg b.m 120mg b.m


caution in patient susceptible to hypoglycemia (elderly & liver disease)

B- Biguanide Metformin (glucophage)

starting dose 500mg b.d, after meal. Max. dose 2550mg divided 3 doses.

Anorexia, diarrhea, abd. discomfort.

Use with caution in pt with renal, hepatic & heart diseases. ↓LDL

C- Acrobose(precose)& Miglitol. D- Glitazones ●Troglitazone ●Rosiglitazone(Avandia) ●Pioglitazone(actos)

Take with meal 25mg TDS max.100mgTDS Take with meal 4-8mg/d o.d or b.d 15-30mg not exceed 45mg/d

Flatulence, abd. bloating & cramping

Contraindicated in IBD

edema, ↑ALT Wt gain ↑LDL & triglyceride

Caution in pt with CHF, Discontinue if ALT↑ above 3x.

type Start Peak of action Duration of action

lispro short acting (Regular)

15 min 30 min

1h 1-3 h

2-3 h 5-6 h

Intermediate NPH,Lente
Long action (Ultralente) (Lantus)

2-3 h

4-6 h

12-14 h

slow of sustained insulin release

18-24 h


A. Initial evaluation

Medical history

● Age and characteristics of onset of diabetes (e.g., DKA, asymptomatic laboratory finding) ● Eating patterns, nutritional status, and weight history; growth and development in children and adolescents ● Diabetes education history ● Review of previous treatment regimens and response to therapy (A1C records)

● Current treatment of diabetes, including medications, meal plan, physical activity patterns, and results of glucose monitoring and patient’s use of data

Medical history …
• Acute complications:
● ● ● ● DKA frequency, severity, and cause Hypoglycemic episodes Hypoglycemia awareness Any severe hypoglycemia: frequency and cause

●Chronic complications:
● Microvascular: retinopathy, nephropathy, neuropathy (sensory, including history of foot lesions; autonomic, including sexual dysfunction and gastroparesis) ● Macrovascular: CHD, cerebrovascular disease, PAD

● Other: psychosocial problems, dental disease

Physical examination
● Height, weight, BMI ● Blood pressure determination, including orthostatic measurements when indicated ● Fundoscopic examination* ● Thyroid palpation ● Skin examination (for acanthosis nigricans and insulin injection sites) ● Comprehensive foot examination:
● ● ● ● Inspection Palpation of dorsalis pedis and posterior tibial pulses Presence/absence of patellar and Achilles reflexes Determination of proprioception, vibration, and monofilament sensation

Laboratory evaluation
● A1C ● Fasting lipid profile, including total, LDL, and HDL cholesterol and triglycerides ● Liver function tests ● Test for urine albumin excretion with spot urine albumin-to-creatinine ratio ● Serum creatinine and calculated GFR ● Thyroid-stimulating hormone in T1D, dyslipidemia or women over age 50

● ● ● ● ● ● Annual dilated eye exam Family planning for women of reproductive age Registered dietitian for MNT Diabetes self-management education Dental examination Mental health professional, if needed


Summary of glycemic recommendations for adults with diabetes:
• Preprandial capillary plasma glucose
70–130 mg/dl (3.9–7.2 mmol/l)

• Postprandial capillary plasma glucose
< 180 mg/dl (10.0 mmol/l)

• A1C

< 7.0%

Key concepts in setting glycemic goals:
● Goals should be individualized based on: ● duration of diabetes ● pregnancy status ● age ● comorbid conditions ● hypoglycemia unawareness ● individual patient considerations

• More stringent glycemic goals (i.e., a normal A1C, 6%) may
further reduce complications at the cost of increased risk of hypoglycemia


• A1C • CBGM

1. Self-monitoring of blood glucose (SMBG) ● SMBG should be carried out three or more times daily for patients using multiple insulin injections or insulin pump therapy. (A)

● When prescribing SMBG, ensure that patients receive initial instruction in, and routine follow-up evaluation of, SMBG technique and their ability to use data to adjust therapy. (E)

2. A1C
● Perform the A1C test at least two times a year in patients who are meeting treatment goals (and who have stable glycemic control). (E) ● Perform the A1C test quarterly in patients whose therapy has changed or who are not meeting glycemic goals. (E)

Correlation between A1C level and mean plasma glucose levels*
AIC (%) 6 7 8 9 10 11 12 MPG (mmol/l) 7.5 9.5 11.5 13.5 15.5 17.5 19.5 (mg/dl) 135 170 205 240 275 310 345

[+ [+ [+ [+ [+ [+ [+

1.5] 2.5] 3.5] 4.5] 5.5] 6.5] 7.5]

………………………………………………………………………………………… MPG = Mean Plasma Glucose * based on data from the DCCT (Diabetes Care 25:275–278, 2002).

3. Continuous Glucose Monitoring (CGM)

• In recent years, methods to sample interstitial fluid glucose

(which correlates highly with blood glucose) in a continuous and minimally invasive way have been developed.

• Although continuous glucose sensors would seem to show great
promise in diabetes management, as yet no rigorous controlled trials have demonstrated improvements in longterm glycemia.

D. Nutritional recommendations for patients with diabetes

• Protein to provide 10-20% of kcal/d
• Saturated fat to provide < 10% of kcal/d (< 7% for those with •
elevated LDL). Polyunsaturated fat to provide < 10% of kcal/d.

• Remaining calories to be divided between carbohydrate &

monounsaturated fat, based on medical needs & personal tolerance. hypertension. Caloric sweeteners ,including sucrose, is acceptable.

• Sodium < 3 gm/d, to be reduced to < 2 gm if patient suffers from
• • Low glycemic index foods (i.e. apple, peach, pear, banana, yoghurt,
low fat milk, brown rice, peanuts ).

E. Diabetes Self Management Educations (DSME)

● People with diabetes should receive DSME according to national standards when their diabetes is diagnosed and as needed thereafter. (B) ● DSME should address psychosocial issues, since emotional well-being is strongly associated with positive diabetes outcomes. (C)

F. Physical activity
● People with diabetes should be advised to perform at least 150 min/week of moderate-intensity aerobic physical activity (50–70% of maximum heart rate). (A)

G. Psychosocial assessment and care
● Assessment of psychological and social situation should be included as an ongoing part of the medical management of diabetes. (E) ● Psychosocial screening and follow-up should include, but is not limited to, attitudes about the illness, expectations for medical management and outcomes, affect/mood, general and diabetesrelated quality of life, resources (financial, social, and emotional), and psychiatric history. (E) ● Screen for psychosocial problems such as depression, anxiety, eating disorders, and cognitive impairment when adherence to the medical regimen is poor. (E)

H. Hypoglycemia
● Glucose (15–20 g) is the preferred treatment for the conscious individual with hypoglycemia, although any form of carbohydrate that contains glucose may be used. ● Glucagon should be prescribed for all individuals at significant risk of severe hypoglycemia, and caregivers or family members of these individuals should be instructed in its administration. • Glucagon administration is not limited to health care professionals. (E)

I. Immunization
● Annually provide an influenza vaccine to all diabetic patients > 6 months of age. (C)
● Provide at least one lifetime pneumococcal vaccine for adults with diabetes.
Revaccination for pneumococcal vaccine :
– Individuals > 65 years of age previously immunized when they were < 65 years of age if the vaccine was administered 5 years ago. – Nephrotic syndrome – chronic renal disease – Other immunocompromised states, such as after transplantation.


Summary of recommendations for glycemic, blood pressure, and lipid control for adults with diabetes

• A1C < 7.0%*
• Blood pressure < 130/80 mmHg • LDL < 100 mg/dl (2.6 mmol/l)†
*Referenced to a nondiabetic range of 4.0–6.0% using a DCCT-based assay. †In individuals with overt CVD, a lower LDL cholesterol goal of 70 mg/dl (1.8 mmol/l), using a high dose of a statin, is an option.


1. Blood pressure control
● Blood pressure should be measured at every routine diabetes visit.

● Patients with diabetes should be treated to a systolic blood pressure < 130/ 80 mmHg. (C)

• Details on this topic will be discussed on related lecture


CVD … 2. Dyslipidemia ● In most adult patients, measure fasting lipid profile at least annually. ● Statin therapy should be added to lifestyle therapy, regardless of baseline lipid levels, for diabetic patients:
● With overt CVD (A) ● Without CVD who are over the age of 40 and have one or more other CVD risk factors. (A)

• Details on this topic will be discussed on related
lecture …

A. CVD …

3. Antiplatelet agents


Use aspirin therapy (75–162 mg/day) as a
– Primary prevention strategy in those with T1D or T2D at increased cardiovascular risk, including those who are 40 years of age or who have additional risk factors (family history of CVD, hypertension, smoking, dyslipidemia, or albuminuria). (A) – Secondary prevention strategy in those with diabetes with a history of CVD. (A)

A. CVD …

3. Antiplatelet agents …
● Aspirin therapy is not recommended in people under 30 years of age, due to lack of evidence of benefit, and is contraindicated in patients under the age of 21 years because of the associated risk of Reye’s syndrome. (E)
● Other antiplatelet agents may be a reasonable alternative for high-risk patients with aspirin allergy, with bleeding tendency, who are receiving anticoagulant therapy, with recent gastrointestinal bleeding, and with clinically active hepatic disease who are not candidates for aspirin therapy. (E) ● Combination therapy using other antiplatelet agents (such as clopidrogel) in addition to aspirin should be used in patients with severe and progressive CVD. (C)

A. CVD … 4. Smoking cessation

Recommendations ● Advise all patients not to smoke. (A) ● Include smoking cessation counseling and other forms of treatment as a routine component of diabetes care. (B)

A. CVD …

5. CHD screening and treatment
• In asymptomatic patients, evaluate risk factors to stratify
patients by 10-year risk, and treat risk factors accordingly.(B)

• In patients 40 years of age with another cardiovascular risk

factor, ACEI, aspirin, and statin therapy (if not contraindicated) should be used to reduce the risk of cardiovascular events. (B)

● In patients with known CVD, ACEI, aspirin, and statin therapy (if not contraindicated) should be used to reduce the risk of cardiovascular events. (A) ● In patients with a prior myocardial infarction, add B-blockers (if not contraindicated) to reduce mortality. (A)

B. Nephropathy screening and treatment
● To reduce the risk or slow the progression of nephropathy, optimize glucose control and blood pressure control. (A) ● Perform an annual test to assess urine albumin excretion in T1D (D5) and T2D (D0). (E) ● Measure serum creatinine at least annually in all adults with diabetes regardless of the degree of urine albumin excretion. • Serum creatinine should be used to estimate GFR and stage the level of chronic kidney disease (CKD), if present. (E)

B. Nephropathy …

In the of the nonpregnant patient with micro- or macroalbuminuria, either ACE inhibitors or ARBs should be used. (A)

● In patients with T1D, with hypertension and any degree of albuminuria, ACE inhibitors have been shown to delay the progression of nephropathy. (A) ● In patients with T2D, hypertension, and microalbuminuria, both ACE inhibitors and ARBs have been shown to delay the progression to macroalbuminuria. (A) ● In patients with T2D, hypertension, macroalbuminuria, and renal insufficiency (serum creatinine 1.5 mg/dl), ARBs have been shown to delay the progression of nephropathy. (A)

B. Nephropathy …
● If one class is not tolerated, the other should be substituted. (E) ● When ACE inhibitors, ARBs, or diuretics are used, monitor serum creatinine and potassium levels for the development of acute kidney disease and hyperkalemia. (E) ● Consider referral to a physician experienced in the care of kidney disease when there is uncertainty about the etiology of kidney disease (active urine sediment, absence of retinopathy, rapid decline in GFR), difficult management issues, or advanced kidney disease. (B)

B. Nephropathy …

Definitions of abnormalities in albumin excretion

Category Normal

Spot collection (g/mg creatinine) <30 30–299

Macro (clinical)-albuminuria

Stages of CKD

B. Nephropathy …

Description (Kidney damage*)

1 = GFR > 90 with normal or increased GFR 2 = GFR 60–89 with mildly decreased GFR 3 = GFR 30–59 with Moderately decreased GFR 4 = GFR 15–29 with Severely decreased GFR 5 = GFR <15 or dialysis Kidney failure ……………………………………………………………………………………
*Kidney damage defined as abnormalities on pathologic, urine, blood, or imaging tests. GFR (ml/min per 1.73 m2 body surface area)

C. Retinopathy screening and treatment

International Clinical Diabetic Retinopathy Disease Severity Scale

C. Retinopathy screening and treatment …
● To reduce the risk or slow the progression of retinopathy, optimize glycemic and blood pressure control. (A) • Refer sever nonproliferative and proliferative retinopathy.

D. Neuropathy screening and treatment
● All patients should be screened for distal symmetric polyneuropathy (DPN) at diagnosis and at least annually thereafter, using simple clinical tests. (B) ● Educate all patients about self-care of the feet. For those with DPN, facilitate enhanced foot care education and refer for special footware. (B) ● Screening for signs and symptoms of autonomic neuropathy should be instituted at diagnosis of T2D and 5 years after the diagnosis of T1D. Special testing is rarely needed and may not affect management or outcomes. (E)

D. Neuropathy

(Table of drugs to treat symptomatic DNP )

Tricyclic drugs Amitriptyline 10–75 mg at bedtime Nortriptyline 25–75 mg at bedtime Imipramine 25–75 mg at bedtime
Anticonvulsants Gabapentin 300–1,200 mg TID. Carbamazepine 200–400 mg TID. Pregabalin† 100 mg TID.
*Dose response may vary; initial doses need to be low and titrated up; †has FDA indication for treatment of painful diabetic neuropathy.

E. Foot care
● For all patients with diabetes, perform an annual comprehensive foot examination to identify risk factors predictive of ulcers and amputations. The foot examination can be accomplished in a primary care setting and should include the use of a monofilament, tuning fork, palpation, and a visual examination. (B) ● Provide general foot self-care education to all patients with diabetes. (B)

E. Foot care …

● Initial screening for peripheral arterial disease (PAD) should include a history for claudication and an assessment of the pedal pulses. Consider obtaining an ankle-brachial index (ABI), as many patients with PAD are asymptomatic. (C)
● Refer patients with significant claudication or a positive ABI for further vascular assessment, and consider exercise, medications, and surgical options. (C)

Summary of recommendations for adults with diabetes
• •

Target Value
< 7% 70 -130 mg/dL < 180 mg/dL < 130/80 mmHg < 100 mg/dL > 40 mg/dL for men > 50 mg/dL for women < 150 mg/dL

pre-prandial plasma glucose

post-prandial plasma glucose

• • •

Blood pressure LDL- cholesterol HDL- cholesterol Triglycerides

Home Message
• DM is a chronic, multifactorial disease, lead to
many complications, need many interventions and teamwork care.

We have to work together to reduce the


burden of diabetes

Shared By: