DIABETES CONT ----

Transforming
Transforming education
education through
through ICT
ICT
 Other investigations
• Kidney fuction tests –u/e/cs
• Full heamogram
• Urinalysis/microcopy
• Fasting lipid profile
• HBA1C
 INVESTIGATIONS OR
PROCEDURES
DEPENDING ON COMPLICATIONS
• ECG
• CXR
• KUB ULTRASOUND
• BP Measurement
Management of
Diabetes
Lifestyle modification
Diet and Nutrition
 Food portions

20%

50%

20%

10%

vegetables fruits carbohydrates proteins

 INTRODUCTION

• The overall goal of diabetes management is to help

individuals with diabetes and their families gain:
– The necessary knowledge,
– Life skills,
– Support needed to achieve optimal health
• Diet and nutritional therapy is an integral
component of diabetes management and diabetes
self-management.

8
 INTRODUCTION

• Nutritional management of diabetes is

based on the principles of healthy
eating and still remains the
cornerstone of effective diabetes
therapy
• A qualified nutritionist/dietician is a
key member of the diabetes
management team.

9
 Aims of diet therapy

• The objective of nutritional therapy is to help people

with diabetes learn how to make appropriate
lifestyle choices.
• These choices can help people them to achieve
optimum metabolic control and prevent diabetes
complications through:
• Good blood glucose levels
• Optimum lipid profile
• Controlled blood pressure levels
• Optimum body weight
 Aims of diet therapy cont…
• To prevent and treat obesity, dyslipidaemia,
cardiovascular disease, hypertension and
nephropathy through modification of diet
and lifestyle
• To consider the person’s nutritional needs
while taking into account personal and
cultural preferences and lifestyle issues
• Respect the individual’s rights, decisions
and willingness to change
• Optimize quality of life
Goals of Nutrition Therapy for
Diabetes
• To attain and maintain optimal metabolic outcomes
• To improve health through healthy food choices and
physical activity
• To address individual nutritional needs
• To maintain near-normal blood-glucose levels by
balancing food intake with insulin or oral
medication and physical activity levels.
Goals of Nutrition Therapy for
Diabetes Cont…

• To prevent, delay or treat acute insulin-

related complications such as
hypoglycaemia, short-term illness and
exercise-related problems.
• To assist in the prevention and
treatment of acute and chronic
complications.
• To promote physical, social and psychological
well being.
 The Nutritional Care Process

• Proper Nutritional Care is integral to the successful

management of obesity, diabetes and hypertension.
• Compliance with the nutrition and meal planning
principles, however, remains one of the most challenging
aspects of care.
• An important first step in initiating Nutritional Care is
evaluating the nutrition status of the individual.
 Nutrition assessment

• Must be completed for every person with obesity,

diabetes or hypertension who presents for initial
care.
• It is an important tool for identifying existing or
potential problems and identify clients needing a
more comprehensive screening.
• It generates the information needed for a
comprehensive approach to nutrition intervention.
 Nutrition Assessment Cont….

• It is a pre-requisite for conducting dietary

counseling.
• It enables the diabetes educator to provide optimal
nutrition therapy that is individualized
• Some parameters will need to be assessed each
time the individual presents for care and they
include:
– weight,
– blood pressure,
– dietary intake and
– blood glucose.
 Nutrition Assessment Cont…..

• In defining the level of nutrition intervention for the

targeted diseases, a total review of patient data is
important. This will include:
– Age,
– Gender,
– Socio-economic circumstances
– Literacy and numeracy.
– Ability and willingness to change nutritional
habits and practices.
– Emotional state, especially if newly diagnosed.
– Clinical Information
 The Assessment Process

• This is a systematic process of collecting

objective information about the client,
his/her environment and the support
system.
• It provides some insight into some of the
challenges the client may face and the
resources that are available to cope with
them.
 The Assessment Process

Historical Data
• Provides an insight into any relevant past illnesses
or circumstances that may directly or indirectly
impact on the client’s nutrition needs and health
status.
• Important historical data to be reviewed include:
– Past medical history
– Social economic history
– Diet history
The Assessment Process
Data Collection
• Anthropometric • Biochemical
– Weight, – Blood Glucose,
– Height, – Lipid Profile,
– BMI, – RFTs,
– Waist – LFTs,
Circumference, – HBA1c
– Hip
Circumference,
 The Assessment Process
Data Collection
• Clinical • Behavioral
– Signs and symptoms of Information
– Alcohol Intake,
the disease(s) – Smoking,
– Symptoms of – Physical activity
Hyper/hypoglycemia • Dietary information
– Diagnosis and treatment – Diet History,
– Food security,
information – Food Preferences/Choices,
– Problems relating to – Taboos and beliefs
intake, e.g. chewing, – misconceptions,
– Allergies
swallowing
– Gastrointestinal
problems
– Blood Pressure,
 Other important assessment

• Determination of exercise/activity level

• Assessment of client's ability and readiness
to participate in care plan
• Assessment of client support network –
home/community
• Interpretation of data
• Use of the data to provide appropriate care
 Nutritional Care Plan

• The nutrition recommendations that are

integrated into the overall management plan
for the client are based on:
– Nutrition assessment
– Desired treatment outcomes
– Modification of lifestyles including eating
behaviors
 Nutritional Care Plan cont…

• The Nutritional Care Plan should outline:

– Objectives for meeting nutrition and educational needs
– Content of the counseling sessions
– Time frame for achieving the objectives
• Counseling sessions should then be planned to
provide instructions and recommendations for the
client.
• The counseling process may require several
sessions to address the care plan, the diet and to
evaluate the client’s understanding as well as
responses to the plan.
Management of Diabetes
Pharmacological therapy
 Presentation Outline

 ORAL GLUCOSE-LOWERING AGENTS (OGLAS)/

 Insulin therapy
 Combination therapy
 Non insulin injectables
 Treatment targets
 Drug therapy
Pharmacological management involves intake of oral or
injectable medications.
Groups of Oral Glucose Lowering Agents
(OGLA’s)

 Biguanides
 Sulfonylureas.
 α Glucosidase inhibitors.
 Insulin and insulin analogues
 Dipeptidyl peptidase inhibitors
 Non insulin injectables
Oral Glucose Lowering Agents
(OGLA’s)
Indications:
• Failure of lifestyle modifications
• When an individuals glycaemic targets are not met by
the combination of dietary modifications and physical
activity/exercise.
• Oral pharmacotherapy or insulin is indicated at the first
presentation of diabetes if:
– Fasting blood glucose level > 11.1 mmol/L or
– Random blood glucose level > 15 mmol/L.
 Types of OGLAs
 Sulponylurea:
 1st gen- Chlorpropamide (diabinase),
 Gen 2nd Glibenclamide, glimepiride (e,g Amaryl),
glipizide (eg Glucotrol and Glucotrol XL),
gliclazide (eg Diamicron-30mg,60mg)
 Biguanides: Metformin.(500mg,850mg)
 α glucosidase inhibitors: arcabose, miglitol.
 Types of OGLAs

 Thiazolidine diones: Pioglitazone, rosiglitazone.

 Meglitinides: Repaglinide.
 Dipeptidly peptidase IV inhibitors: sitaglpitin,
saxagliptin.
 Sulponylurea:

 These drugs exert their hypoglycaemic

effects by stimulating insulin secretion from
the pancreatic beta-cell. Their primary
mechanism of action is to close ATP-
sensitive K-channels in the beta-cell
plasma membrane, and so initiate a chain
of events which results in insulin release.
 SE –HYPOGLYCEAMIA
Biguanides: Metformin
 Trade name Glucomet
 metformin's inhibitory effect on liver glucose
production
 metformin increases insulin sensitivity, enhances
peripheral glucose uptake (by inducing the
phosphorylation of GLUT4 enhancer factor),
 decreases insulin-induced suppression of fatty acid
oxidation 
 and decreases the absorption of glucose from
the gastrointestinal tract
 Side effects

 Lactic acidosis almost never occurs with

metformin exposure during routine medical care.
Rates of metformin-associated lactic acidosis are
about nine per 100,000 persons/year, which is
similar to the background rate of lactic acidosis in
the general population
 Should not be given in renal failure /AKI
 (DPP IV INHIBITORS )
Dipeptidly peptidase IV inhibitors

 The mechanism of DPP-4 inhibitors is to increase

incretin levels (GLP-1 and GIP),BY
BLOCKING THE ENZYME Dipeptidly peptidase
IV which inhibit glucagon release, which in turn
increases insulin secretion, decreases gastric
emptying, and decreases blood glucose levels.
 Choice of OGLA

• The use of proven cost effective generic

drugs: discuss cost of available drugs with
your patient.
• Depend on the patient's characteristics,
lifestyle, degree of glycaemic control, access
to drugs, economic status and mutual
agreement between the doctor and the
person with diabetes,
• The sulphonylureas and Metformin are the
agents most widely available.
• Stocking these agents would meet the
diabetes-care needs of most diabetes
facilities.
 Choice of OGLA
 Monotherapy with any of the drugs should be the
initial choice.
 Use of the stepped-care approach is
recommended, as monotherapy is seldom
sufficient, because of the progressive nature of
the disease
 Combination therapy should be considered as
initial choice if HBAIC is greater than 8 %
 Precautions when using OGLA:

• If overweight (BMI > 25 kg/m2) Metformin should be the

first choice. If Metformin is contraindicated
thiazolidindiones (TZD) may be used.
• Long-acting sulphonylureas should be avoided in
elderly patients. In such patients, use short-acting
sulphonylureas such as glimepiride, gliclazide.
• Metformin should not be used in the elderly (over the
age of 75 years) and is also contraindicated in people
with elevated serum creatinine, (can lead to lactic
acidosis)
• liver disease and severe respiratory, cardiac and
peripheral vascular disease
 Precautions when using OGLA:

• Combination therapy using OGLAs with different

mechanisms of action is indicated if monotherapy with
one of the agents has failed. Never use two drugs from
the same class.
• The rapid acting secretagogues (meglitinides) and the
alpha glucosidase inhibitors allow for flexibility in the
glycaemic management but are relatively expensive,
• When oral combination therapy is insufficient, insulin
should be added to the treatment regimen or the OGLAs
replaced.
 Dipeptidyl peptidase IV inhibitors

 Dipeptidyl peptidase IV inhibitors (DPP4 Inhibitors): used

in type II diabetes patients in whom appropriate HBA1C
has not been attained.
 The mechanism of DPP-4 inhibitors is to increase incretin
levels (GLP-1 and GIP), which inhibit glucagon release,
which in turn increases insulin secretion, decreases gastric
emptying, and decreases blood glucose levels.

 NB-READ AND MAKE ADDITIONAL NOTES ON DPP4

Inhibitors
Insulin Therapy
 History of Insulin

 The discovery and isolation of insulin at the

University of Toronto in 1921–22 was one of the
greatest events in the history of medicine.
 The Discovery of Insulin highlights one of those
incredible moments in medical history where a
new treatment literally raises people from the
dead
Banting and Best -1921
 History of Insulin

 Living with Diabetes before the discovery of Insulin

 Children who suffered from juvenile diabetes(type
1Diabtes) survived anywhere from 1 month to 2 years.
 Symptoms included weight loss, coma, and eventually
death
 Doctors tried to treat diabetes with sugar, opiates,
starvation diets
Insulin Secretion

 Insulin is secreted by the β

cells of the islets of
Langerhans of the
pancreas.
 -HIGH blood glucose
increases insulin
secretion. Glucose is
stored in fat cells
 -when blood glucose
falls, insulin secretion
goes down

46
 Use of Insulin
• Insulin is the mainstay
treatment for people
with type 1 diabetes and
many patients with type
2 diabetes mellitus.
• Patients with type 1
diabetes lack functional
B- cells(cells that produce
Insulin )and require
insulin for survival.
Indications for use of insulin in
type 2 diabetes
 Initial presentation with severe hyperglycaemia
and are symptomatic
 Presentation in hyperglycemic emergency
 Peri-operative period especially major or
emergency surgery
 Other medical conditions requiring tight
glycaemic control e. g acute MIs, strokes,
infection, trauma
Indications for use of insulin in
type 2 diabetes
 Organ failure (e.g. renal, liver, heart)
 Pregnancy and breastfeeding
 Latent autoimmune diabetes of adults (LADA)
 Contraindications to OGLAs
 Failure to meet glycaemic targets with OGLAs
( secondary failure of OGLA s)
 Types of Insulin and their properties

Insulin Onset of Peak action Duration of Injections per day

preparation action (h.) action(.h)
Rapid-acting 10-20 1-2 3-5 Immediately before
analogues -
NovoRapid min meals or with meals
Humalog
Soluble 30-60 2-4 6-8 30 min before meals
Actrapid min
Humulin R
Intermediate 1-2h. 5-7 13-18 Once or twice
(NPH) - lente
insulin
Biphasic 30.min 2-8 14-16 hrs twice
mixture 30/70
Mixtard 30
Humulin 70/30

Long acting 1-2 hours peakless 24 h Once

analogue -
Lantus
 Insulin regimen and dose

Supplemental/ basal Therapy:

 NPH insulin administered at 22.00 hrs given as a
Total Daily Dose calculated by: Kg x 0.2 IU of
insulin (70 kg patient x 0.2 IU = 14 IU insulin).
 The OGLAs are continued (half maximum dose of
sulphonylureas and Metformin dose of 2 g/day)
 Monitor blood glucose levels when possible.
 Insulin regimen and dose

Substitution Therapy
 OGLAs are discontinued (unless the patient is obese
where METFORMIN will be continued),
 PRE-MIXED insulin is introduced twice daily at a
dosage of 0.2 IU/kg body weight.
 This is split into 2/3 in the morning and 1/3 in the
evening, at 30 minutes before the morning and the
evening meals.
 If the requirement of insulin exceeds 30 units/day,
referral should be considered to a level 4 or higher
facility.
Insulin -Administration sites

Front Back

Insulin is injected in areas`with adequate subcutaneous fat

53
 Insulin - Administration

Causes of differences in absorption of Insulin

• Injection sites
⁻ Abdomen faster than arm
⁻ Arm faster than thigh
• Absorption increased by
₋ Exercise,
₋ High temperature,
₋ localised massage.
• Absorption decreased by
– Low temperature.
– Intra-individual variations- 20- 25% in the same person
Storage of Insulin - Insulin
not in use:
 Keep insulin in the fridge at 4-8 °C
 Human insulin is stable for 30 months from the
manufacturing date at these temperatures,
compared to 24 months for analogues.
 Store the insulin in a separate container, at the
bottom of the fridge and away from the freezer
compartment.
 Do not store insulin in the fridge door, as this will
cause exposure to fluctuating temperatures.
Storage of Insulin - Insulin not in
use:
• Insulin must not be frozen. Changes in the crystalline
structure cause the action profile of the insulin to be
unpredictable.
• When damaged by heat, insulin becomes cloudy,
suspension changes becoming granular appearance and
brownish colour.
• If a refrigerator is not available, insulin can be stored in the
coolest part of the room or covered with a wet flannel
cloth, or in a clay pot submerged in water and protected
with plastic
Storage of Insulin – Insulin in
use:
 Insulin currently in use by the person with diabetes
may not need to be stored in the fridge.
 Insulin however must be kept away from the sun.
 Human insulin is stable at 25 °C for 6 weeks and at
37 °C for 4 weeks.
 Analogues will maintain stability for 4 weeks at
temperatures of 30 °C and lower.
Patients Advice

When initiating insulin therapy and

thereafter, advice on:
 Hypoglycaemia.
 Sick days.
 Physical activity.
 Self Blood Glucose Monitoring.
 Diet.
 Treatment targets
INDEX GOAL

HBA1c <6.5%)
Fasting blood glucose 4-7.2 mmol/L
Post prandial glucose <10mmol/L Preferably
8.3mm/l
Lipids
• LDL <2.6mmol/L (100MG%)
•HDL >1.1mmol/L (>40mg%)
•TRIGLYCERIDES <1.7mmol/L (150mg%)
Evidence in Primary Prevention
Name of Study Design Outcome

West of Scotland 6595 men 31 % risk reduction in

Coronary Prevention Mean TC 272; LDL>155 coronary deaths and
Study (WOSCOPS) diet + placebo nonfatal MI
Diet + pravastatin Benefit >treating mild
HTN but 3 x less than
that in 4S study

Air Force/Texas Coronary 5614 Men; 991 women 37 % risk reduction in

Atherosclerosis 45-73 y.o. coronary events
Prevention Study mean TC 221; LDL 150
(130-190)
Diet + placebo
Diet + lovastatin
 Evidence in Secondary Prevention
Name of Study Design
Scandinavian Simvastatin Survival 4444 patients (angina or h/o MI)
Study (4S) TC 212-309; 5 year f/u
Placebo v. simvastatin 20-40 qd
Goal TC <200
CARE 4159 h/o MI 2 yrs prior
Borderline Average TC 209; LDL
139; HDL 39
Pravastatin 40 qhs x 5 yrs
LIPID 9014 men and women with
recent MI or unstable angina
TC 155-270
Pravastatin or placebo
Heart Protection Study 20,536; simvastatin 40 qd; 33%
LDL<116;25% 116-135; 42%
LDL>135 h/o CVD, DM, or
treated HTN; 5.5 yrs
Outcome
Total mortality (8 v.12%)
Major events (19 v. 28%)
CHD deaths 42% lower
Revascularization 37%
CVA (2.7 vs 4.3)
1% LDL decrease=1.7% RR
Coronary death/MI 10.2 v. 13.2
Revascularization 14.1 v. 18.8
Stroke frequency 2.6 v. 3.8
% LDL reduction unrelated to
events
CHD deaths 6.4 v. 8.3
Total mortality 11 v. 14
Stroke 20% decrease
Bypass 8.9 v. 11.3
All cause mortality RRR 13%
CHD death RRR 17%
Major events RRR 24%
Similar in 3 tertiles of LDL and in
those with LDL<100
Mechanism of Benefit of Statins in
Secondary Prevention
 Regression of atherosclerosis
 Plaque stabilization
 Reduced inflammation
 Decreased thrombogenicity
 Reversal of endothelial dysfunction
 Others
 Reduced monocyte adhesion to endothelium
 Reduced oxidative modification of LDL
 Increased mobilization and differentiation of
endothelial progenitor cells leading to new
vessel formation
Adverse Effects of Statins
 In general, less than with other agents. Fairly tolerable and safe
 Myopathy
Ranges from myalgias (2-11%), myositis(0.5%) to rhabdomyolysis (<0.1%) (possibly ARF)
Few weeks-4 months onset
Symptoms and CK should normalize over days to one month after d/c
Pravastatin and Fluvastatin less risk
Increased risk in
 ARF/CRF
 Obstructive liver disease
 Hypothyroidism
 Concomittant use of drugs interfering with CYP3A4??
 Gemfibrozil combined therapy
 Hepatic
 0.5 to 3% persistent elevations in amino-transferases in first 3 months and dose-dependent
 Several randomized trials have found no difference compared with placebo
 FDA recommends LFTs before and 12 weeks after starting and with any dose elevation and
periodically
 CNS
 Case reports of memory loss associated with statins (mainly lipophilic)
 If memory loss and recent initiation of statin, then d/c and use a hydrophilic statin such as
pravastatin or rosuvastatin
 No significant difference with placebo in trials
 Fibric Acid Derivatives
Decrease Triglycerides (35-50%)
 Reduced hepatic secretion of VLDL through activation of PPAR-alpha
receptors in liver
 Stimulate lipoprotein lipase and thus clearance of TG-rich lipoproteins
 Raise HDL (15-25%)
 Direct stimulation of HDL apolipoprotein synthesis A-I,II
 Increased transfer of apo A-I with diminished cholesterol transfer from
HDL to VLDL
 Increases LDL buoyancy
 May also improve endothelial function and favorable effect on macrophage
responses (possible reduction in CHD risk independent of effect on
lipoproteins)
 Agents
 Gemfibrozil- 600 mg po BID (11% raise in HDL). Modest LDL reduction but
little effect in combined hyperlipidemia. Can increase LDL in pure
hypertriglyderidemia
 Fenofibrate 200 mg capsules or iii caps 67 mg qd (renal dosing and can
decrease Cyclosporin levels). Better for LDL lowering
 Side effects
 Gallstone formation
 Dyspepsia, diarrhea, nausea, vomiting, abdominal pain, eczema, rash,
vertigo and myalgias
 Adverse drug interaction
 Gemfibrozil- inhibits glucuronidation of lipophilic statins and increases
levels thus increasde risk of myopathy. Also decreases warfarin by 30%
 Bile Acid Sequestrants
 Lower LDL (10-15%)
 BINDING BILE ACIDS IN INTESTINE CAUSING A DECLINE IN HEPATIC CHOLESTEROL POOL;
THUS SYNTHESIS OF apo B/E (LDL) RECEPTORS
 Max doses cause 30% reduction
 Raise HDL
 Intestinal formation of nascent HDL

 Available agents
 Cholestyramine 8 grams/day. 24-30 grams/day can lower LDL up to 24%
 Colestipol 10 grams/day
 Colesevelam 1.5-4.5 grams/d

 Adverse effects
 Usually limit use
 Mainly GI (nausea, bloating, cramping)- least problematic with colesevelam
 Increased liver enzymes
 Also drug interactions (impair absorption)
 Digoxin, warfarin, and fat soluble vitamins (give one hour before or 4 hours after bile acid
sequestrant)
 Contraindications: pts with elevated TG
 Mechanism of Action
Nicotinic Acid
 Inhibits hepatic VLDL production and its metabolite LDL
 Raises HDL by reducing lipid transfer of cholesterol from HDL to VLDL and by delaying HDL
clearance
 Increase in LDL size
 Reduction in plasma fibrinogen levels

 Formulations and dosing

 Immediate release (crystalline): 100 TID and titrated to tolerance
 Sustained release
 Niacor
 Niaspan: 500 mg qhs x one month and then titrated to 1000 mg usually given daily after
evenng meal

 1-1.5 grams/day for HDL raising

 3 grams/day for VLDL and LDL lowering and possibly lowering lipoprotein a levels
 OTC IR preps are cheaper and effective
 OTC preps labeles “NO FLUSH” usually not efficacious

 Side effects
 Flushing (less common with controlled release) minimized with ASA 30 minutes before and
limited in 7-10 days
 Nausea, paresthesias, pruritis (20% each)
 Elevation of hepatocellular enzymes and possible hepatotoxicity, jaundice and fulminant
hepatitis (generally less common with Niaspan and crystalline niacin)
 Insulin resistance and worsening hyperglycemia (less with crystalline Niaspan)
 Hyperuricemia (AVOID IF H/O GOUT)
 Hypotension in combination with other vasodialtors (can increase unstable angina)
 Diet Supplements
 Fish Oil (source of omega-3 polyunsaturated fatty acids)
 Salmon, flaxseed, canola oil, soybean oil and nuts
 At high doses > 6 grams/day reduces TG by inhibition of VLDL-TG synthesis and
apolipoprotein B
 Possibly decreases small LDL (by inhibiting CETP)
 Several studies have shown lower risk of coronary events
 2 servings of fish/week recommended??
 Pharmacologic use restricted to refractory hypertriglyceridemia
 Number of undesirable side effects (mainly GI)
 Soy
 Source of phytoestrogens inhibiting LDL oxidation
 25-50 grams/day reduce LDL by 4-8%
 Effectiveness in postmenopausal women is questionable
 Garlic
 Mixed results of clinical trials
 In combination with fish oil and large doses (900-7.2 grams/d), decreases in LDL
observed
 Cholesterol-lowering Margarines
 Benecol and Take Control containing plant sterols and stanols
 Inhibit cholesterol absorption but also promote hepatic cholesterol synthesis
 10-20% reduction in LDL and TC however no outcome studies
 AHA recommends use only in hypercholesterolemia pts or those with a cardiac event
requiring LDL treatment
 Other agents include soluble fiber, nuts (esp. walnuts), green tea
 Overall a combination diet with multiple cholesterol-lowering agents causes much more
significant LDL reductions
 Measurement of Lipoproteins

 Lipoprotein analysis 12-14 hours fasting

 TC and HDL-C can be measured fasting or non-fasting
 LDL-Cholesterol = Total cholesterol –VLDL (1/5 TG)-HDL
 Validity depends on TG <400 mg/dL
 Measured directly if patients have profound hypertrig
 Errors in TC, HDL, and TG can affect values
 Non-HDL cholesterol= TC – HDL-C
 All cholesterol in atherogenic lipoproteins incl LDL, Lipoprotein a, IDL,
VLDL
 Acute phase response (i.e. MI, surgical trauma or infection)
 Can reduce levels of TC, HDL, LDL, apo A+B through impairment of
hepatic lipoprotein production and metabolism
 Raise Lpa and TG
 Lipoprotein analysis should be done as outpatient one month after event
 Screening Recommendations

 Adult Treatment Panel III (NCEP) National Cholesterol

Education Program: . A program designed to reduce illness
and death from coronary heart disease (CHD) in the US
 Fasting lipid profile at least once q 5 years for all persons 20
y.o. or older
 If non-fasting obtained and TC >200 or HDL <40, f/u panel
recommended
 If no known CHD and serum LDL <160 (0-1 risk factors) or
LDL <130 (2 or more risk factors) then re-screen in 5 years
 Borderline high cholesterol and <2 risk factors, re-screen in
1-2 years
 Risk Assessment
 CHD equivalents:
 Symptomatic carotid artery disease
 Peripheral arterial disease
 AAA
 DM
 Multiple risk factors that confer a 10-year risk of CHD > 20%
 Identify major risk factors other than LDL:
 Smoking
 HTN BP >140/90 or on anti-hypertensive medication
 Low HDL <40 mg/dL
 Family history premature CHD (CHD in men 1st degree relative <55; women
<65 y.o.)
 Age (men > or =45; women >or =55)
 Other potential risk factors
 Chronic renal insufficiency (Cr > 1.5 mg/dL OR GFR <60 cc/min) per Up-To-
Date
 Obesity, physical inactivity, impaired fasting glucose, markers for
inflammation
 HDL > 60 mg/dL is a negative risk factor
 If patient without CHD or equivalent has 2 or more major risk factors, then
calculate the Framingham risk (age,TC,HDL,smoking,SBP)
THANK YOU