Reporters:JI Tabajonda, Jennifer M.JI Vio, Rachel Louise S.

Gross Anatomy

Microscopic Anatomy

Physiology

Glucagon single-chain polypeptide that contains

29 amino acid residues and has a molecular weight of 3483

increases blood glucose and relaxes smooth muscle of the gastrointestinal tract. 

potent stimulator of hepatic glycogenolysis, gluconeogenesis, and ketogenesis

Insulin

Preproinsulin (86 aa)

proteolytic processing

Proinsulin

site specific peptide cleavage

C-peptide Insulin

Effects of Insulin

Liver Adipose Muscle

Increased by insulin

FA synthesisGlycogen synthesisCHON synthesis

Glucose uptakeFA synthesis

FA synthesisGlycogen synthesisCHON synthesis

Decreased by insulin

KetogenesisGluconeogenesis

Lipolysis

Increased by glucagon

GlycogenolysisGluconeogenesisKetogenesis

Lipolysis

Diabetes Mellitus

Refers to a group of metabolic disorders that share the phenotype of hyperglycemia

With several distinct types Interaction of genetics and

environment Reduced Insulin secretion Decreased glucose utilization Increased glucose production

Classic Symptoms of Diabetes Polyuria Polydipsia Unexplained weight loss

Levels of Glycemia

Normal Pre- Diabetes

(IFG and IGT)

Diabetes Mellitus

FPG <100 mg/dl

(5.5 mmol/L)

100-125 mg/dL

(5.5-6.9 mmol/L)

> 126 mg/dL

(7.0 mmol/L)

2 hour PG < 140 mg/dL

(7.8 mmol/L)

140- 199 mg/dL

(7.8-11.0 mmol/L)

> 200 mg/dL

(11.1 mmol/L)

Criteria for the Dx of DM Fasting Plasma Glucose (FPG) ≥126 mg/dl (7.0 mmol/L) - Must be repeated on a separate day to

confirm diagnosis OR Postprandial Plasma Glucose (2h PG) ≥200 mg/dl (11.1 mmol/L) -Measured with Oral Glucose Tolerance

Test (OGTT) -Must be repeated on a separate days to

confirm diagnosis OR

Classic Symptoms + Casual Plasma Glucose (CPG) > 200 mg/dl (> 11.1 mmol/L).

-Considered diagnostic of diabetes but should be confirmed on a separate day with FPG or 2hPG.

- Casual plasma glucose ( plasma glucose taken without regard to the last meal)

Algorithm for Diagnosing Diabetes

Classic Symptoms of DM

RBS

140-200 mg/dl(<11.1 mmol/L

≥200 mg/dl(≥11.1 mmol/L)

20PGBS

<140 mg/dl140-199 mg/dl≥200 mg/dl

NORMAL IGT Repeat 20PGBS ≥200 mg/dl

DM

UERMMC-ISDFI

Asymptomatic PatientsCategorize Patients

Low Risk High Risk

Risk Factors:BMI > 23kg/m2(w to h ratio >1) orWaist cir >80 cm F,>90 cm for MFamily Hx of Type 2 diabetesAge >45 yoHPN (130/85 mmhg) Risk Factors:BMI > 23kg/m2(w to h ratio >1) orWaist cir >80 cm F,>90 cm for MFamily Hx of Type 2 diabetesAgeHPN (130/85 mmhg)

High risk- Screen as early as 20 years of age

FBS

<100 mg/dl 100-125 mg/dl (IFG) >/= 126mg/dl

NORMAL IFG Rpt FBS

<140 mg/dl 140-199 mg/dl >/= 200mg/dl

NORMAL IGT

Check 2hPGBS 2hPGBS<126 mg/dl

Check 2hPGBS

≥126 mg/dl

Diabetes

Classification

Type 1 Complete or near total insulin deficiency

Type 2 Insulin resistance impaired insulin secretion Increased glucose production Preceded by IFG and IGT

DM Type 3 and 4

DM type 3 Other specific types of Diabetes

DM type 4 Gestational Diabetes Mellitus

Pathophysiology

DM Type I Complete or near total insulin deficiency

circulating insulin is very low or absent plasma glucagon and the pancreatic beta cells fail to

respond to all insulin-secretory stimuli.

Pathophysiology of DM Type I

Autoimmune islet cell antibodies anti-insulin antibodies genetic susceptibility

HLA markers Infectious and/or environmental agents ?

 viruses (eg, mumps, rubella, Coxsackie B4), toxic chemicals, exposure to cow's milk in infancy, and cytotoxins

Dm Type 2

Predominantly insulin resistance with relative insulin deficiency to predominantly insulin deficiency with insulin resistance

Excessive hepatic glucose production Abnormal fat metabolism

*Insulin resistance, is the decreased ability of insulin to act effectively on target tissues (especially muscle, liver, and fat)

GDM

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

Does not exclude the possibility that undiagnosed glucose intolerance may have occurred prior to pregnancy

Usually 24-48 weeks

Pathophysiology

Placental hormones causing insulin resistance Estrogen, progesterone, cortisol, HPL

Decreased insulin secretion Borderline pancreatic function, cannot

produce insulin levels to meet metabolic needs

Pre-Diabetes

Impaired Fasting glucose FBS of 100-125 mg/dL

IGT 2HPGBS 140-199 mg/dL

Associated with the metabolic syndrome, which includes obesity (especially abdominal or visceral obesity), dyslipidemia of the high-triglyceride and/or low-HDL type, and hypertension.

Complications of Diabetes Mellitus

ACUTEDiabetic Ketoacidosis (DKA)Hyperglycemic Hyperosmolar State (HHS)

CHRONIC:Macrovascular (CAD,CVD,PVD)Microvascular (retinopathy, nephropathy,

neuropathy)Others (e.g. GI, GU, Dermatologic, Infectious)

Acute Complications of DMDKA and HHS are medical

emergencies

associated with potentially serious complications if not promptly diagnosed and treated.

associated with absolute or relative insulin deficiency, volume depletion, and acid-base abnormalities.

DKA vs HHSDKA HHS

Glucose (mg/dl) 250 - 600 600 - 1200

Sodium (mEq/L) 125 – 135 135 - 145

Potassium Normal to ↑ Normal

Magnesium Normal Normal

Chloride Normal Normal

Phosphate ↓ Normal

Creatinine Slightly ↑ Moderately ↑

Osmolality (mOsm/L) 300 – 320 330 - 380

Plasma Ketones ++++ +/-

Serum Bicarbonate <15 Normal to slightly ↓

Arterial pH 6.8 – 7.3 >7.3

Arterial pCO2 20 – 30 Normal

Anion gap [Na – (Cl+HCO3)]

↑ Normal to slightly ↑

DKA

Can occur in both type 1 and type 2 DM Signs & symptoms develop over 24hrs results from relative or absolute insulin

deficiency combined with counterregulatory hormone excess

DKA

Diagnostic Criteria:

Glucose >250mg/dl pH <7.3 High anion gap Positive ketones

Clinical Features of DKA

Precipitating events: Inadequate insulin administration Infection Infarction Drugs Pregnancy

Clinical Features of DKA

Symptoms: Nausea / vomiting Thirst / polyuria Abdominal pain Shortness of breath

Clinical Features of DKA

Physical Findings: Tachycardia Dehydration / Hypotension Tachypnea / Kussmaul respirations/

respiratory distress Abdominal tenderness (may

resemble acute pancreatitis or surgical abdomen)

Lethargy / obtundation / cerebral edema/ possibly coma

Diagnosis

Mild Moderate Severe HHS

Glucose (mg/dl)

>250 >250 >250 >600

Arterial pH 7.25-7.30 <7.24 <7.00 >7.30

HCO3 (mEq/L) 15-18 <15 <10 >15

Urine Ketones + + + Small

Serum Ketones

+ + + Small

Anion Gap >10 >12 >12 <12

Mental Status Alert Alert/drowsy

Stupor/coma

Stupor/coma

DKA

Anion Gap = Na – (Cl + HCO3) Normal: 8 - 12

Management of DKA

Hydration Insulin administration Glucose monitoring Electrolyte correction

HHS

Prototype case is an elderly type 2 DM patient with several week history of polyuria, weight loss, ↓oral intake that culminates in mental confusion, lethargy or coma.

Clinical features of HHS

Precipitating events: serious, concurrent illness (e.g. MI,

CVA) Sepsis, pneumonia, and other

serious infections debilitating condition (prior stroke or

dementia) or social situation that compromises water intake

Clinical features of HHS

Physical findings: Profound dehydration Hypotension Tachycardia Altered mental status

Clinical features of HHS

Symptoms: Notable absence of nausea,

vomiting, and abdominal pain and the Kussmaul respirations

HHS

Diagnostic criteria:

Glucose >600mg/dl Total serum osmolality

>300mOsm/kg Absence of severe ketoacidosis

Management of HHS

Hydration Insulin administration Glucose monitoring Electrolyte correction

Chronic Complications of DM Macrovascular (CAD, CVD, PVD) Microvascular (retinopathy,

nephropathy,neuropathy)

Others (e.g. GI, GU, dermatologic, infectious)

Macrovascular Complications Largest cause of morbidity and

mortality Risk of CVD increased 2 to 4 fold Reduced survival post-MI. post-

CABG, and particularly PTCA Risk of stroke and PVD substantially

increased

Clinical Manifestations

Heart Angina pectoris Acute MI Silent MI Arrhythmias

Clinical Manifestations

Brain TIA (Transient ischemic attack) RIND (Reversible Ischemic

Neurological Deficits) Stroke in evolution Completed stroke

(infarction,embolism, hge) Lacunar infarcts

Clinical Manifestations

Limbs Peripheral vascular disease

(claudication; pain relieved by rest; pain does not go away with continued walk; primarily affects calves)

Poor wound healing, foot ulcers, gangrene

Neuropathy

Nephropathy

Retinopathy

MICROVASCULAR DAMAGE

DIABETES

AGE’s Diacyglyce

rol

Reactive oxygen species

PKC activation

•protein cross-linking•accelerate atherosclerosis•promote glomerular dysfxn•↓ NO synthesis•Induce endothelial dysfxn•Alter ECM composition & structure

Microvascular Complications

DM Retinopathy

DM is the leading cause of blindness in ages 20-74 in the US

Blindness is primarily the result of progressive diabetic retinopathy and clinically significant macular edema.

Incidence: Found in almost all individuals with DM for

> 20yrs and 25% incidence with 5 years, and 80% incidence with 15 years of type 1 DM

Pathophysiology of DM Retinopathy

loss of retinal pericytes

↑ retinal vascular permeability

altered retinal blood flow

abnormal retinal microvasculature

Retinal Ischemia

Neovascularization

•Vitreous hemorrhage•Fibrosis

Retinal Detachmen

t

Classifications of DM RetinopathyStage I – Non-proliferative Thickening of capillary endothelial

BM Reduction of pericytes Microaneurysms Multiple hemorrhages Macular edema Microvascular occlusion and

ischemia

Classifications of DM RetinopathyStage II – Proliferative Hallmark – Neovascularization in

response to retinal hypoxia newly formed vessels appear near

the optic nerve and/or macula and rupture easily

vitreous hemorrhage, fibrosis retinal detachment

Stages of DM Retinopathy

Normal -fine yellow line, red bld column

Gr I - broadened yellow line, rbc Gr II - broad yellow line, copper wire,

bld column not visible Gr III - Broad white line, silver

wire, bld column not visible Gr IV - Fibrous cord, blood column

not visible

DM Nephropathy

Occurs in 20-40% of patients with diabetes is the leading cause of End stage renal disease

Basement membranes of the glomerular capillaries are thickened

microalbuminuria and macroalbuminuria

in individuals with DM are associated with increased risk of cardiovascular disease

Stage Chronology Main Lesion

GFR Albumin excretion

Baseline

BP Reversible by Strict Insulin

1.Acute renal hypertrophy,hyperfx

(+) at dx of DM (reversible with good control

Inc kidney size, inc glomerular size

Inc by 20-50%

Maybe inc but reversible

Inc but reversible

Usually normal

yes

2. Normoalbuminuria (UAE <20ug/min

Almost all px normoalbuminuric in 1st 5 years

On renal biopsy, inc BM thickness

Inc by 20-40%

N by defn.(15-20 ug/min) maybe abN

Maybe abN after a few years

normal.

Inc by about 1mmhg/yr

Hyperfiltration reduced

Classification of Renal Changes and Lesions in DM

3 incipient diabetic neuropathy UAE 20-200 ug/min(microalbuminuric)

Typically after 6-15yrs

Further BM thickening & mesangial expansion, arrestable with AHT

Still supranormal values, predicted to decline with development of proteinuria

Inc: 20%/yr

AbN aggravation of baseline UAE related to BP-inc

Incipient inc≈3mmhg/yr if untreated

Microalbuminuriastabilized,GFR also stable(if HbA1c is reduced). Structural damage slower

4.Proteinuria, clinical overt diabetic nephropathy

Afetr 15-25 yrs (in ≈35% of px)

Clear and pronounced abN

Decline ≈ 10ml/min/year with clear CHONuria

Progressive clinical CHONuria of glomerular origin

Pronounced inc in BP during exercise

High BP, inc by ≈5 mmhg/yr(if untreated)

Higher fall if GFR with poor control

5 End Stage renal failure

Final outcome after 25-30yrs or more

Glomerular closure and advanced glomerulopathy

<10 ml/min

Often some decline due to nephron closure

Not studied

High if untreated

No. previous glycemic important in prevention

Diabetic Neuropathy

occurs in ~50% of individuals with long-standing type 1 and type 2 DM

may manifest as polyneuropathy, mononeuropathy, and/or autonomic neuropathy

Slow progression

Stages of Diabetic NeuropathyStage Description S/Sx Abn

quantitative test

0 No neuropathy no no

1 Subclinical neuropathy

no yes

2 Clinically evident neuropathy

yes yes

3 Debilitating neuropathy

yes yes

Screening and Detection of Neuropathy Symptoms profile Neurologic examination Quantitative sensory testing (QST) Nerve conduction studies Quantitative autonomic function test

(QAFT)

Neurologic Examination

Cranial nerve deficits Sensory deficits Muscle changes Motor deficits Diminished or absent reflexes Autonomic disturbances

Treatment Goals

Halt progressive nerve fiber loss Early intervention Good glycemic control Decrease symptoms, especially pain Prevent ulcers and amputations

Other Complications

Gastrointestinal Delayed gastric emptying

(gastroparesis) Altered small or large bowel motility

(constipation or diarrhea)

Other Complications

Genitourinary Cystopathy Erectile dysfunction Female sexual dysfunction

Other Complications

Infections Pneumonia, UTI, and skin and soft

tissue infections are all more common in the diabetic population

Other Complications

Dermatologic Manifestations Protracted wound healing Skin ulcerations Diabetic dermopathy (e.g.

pigmented pretibial papules or “diabetic skin spots”; bullous diabeticorum; necrobiosis lipoidica; vitiligo; acanthosis nigricans; Lipoatrophy and lipohypertrophy )

Goals of treatment in type 2 DM Glucose control Decrease morbidity/mortality Preserve Beta cell function Maintenance of weight to as near

normal as possible BP control Eliminate symptoms Lipid control Decrease microvascular complications Decrease macrovascular complications

Pharmacologic Agents for Glycemic Control

Insulin Secretagogues (SU, Meglitinides)- ↑ insulin secretion

Insulin Sensitizers (Metformin, Thiazolidinediones)- ↑ peripheral glucose uptake- ↓ hepatic glucose production

Αlpha glucosidase inhibitors (Acarbose, Voglibose)- ↓ carbohydrate absorption

Factors to consider in use of OHAPatient

Age 60-70, AGI, glitazones, SU and meglitinidesMetformin may be used with caution, may lead to

lactic acidosisWeight

UW, insulin resistance, use insulin sensitizersOW, insulin deficiency use insulin secretagogues

Severity of hyperglycemiaRenal/ liver dse

Liver disease/ anti Koch meds, think of insulinDrugs

Efficacy and safetySite of actionTiming of BG lowering effect

Timing of BG lowering

Blood sugar lowering greater during fasting than post prandialMetforminSUInsulin

Blood sugar lowering greater during post prandial than fastingAGIInsulin sensitizersMeglitinidesinsulin

Mild

Upper limit or

overweight

Lean/Underweig

ht

Any of the ff:•TZD•Met

•A-gluc inhibitors

Any of the ff:•A-gluc inhibitors

•TZD•Met

•Small doses of mild SU•Repaglinide•Nateglinide

ModerateFPG > 126-200 mg/dL

Overweight

Any of the ff:Metformin

Thiazolidinediones

underweight

SulfonylureasOr Repaglinide or

Nateglinide

Inc dose of 1st agent and/or combine any of the two with

SU or repaglinide or nateglinide or a-glucosidase

inhibitors

•Inc dose SU, glinide or combine•SU + Met or Repaglinide or

Nateglinide•SU + TZD or Repag or

Nateglinide•SU + a-gluc inhibitors

•SU+Met+TZD•Repag or Nate + TZD + Met

Severe >200

Upper limit or

overweight

Lean/Underweig

ht

•Met + SU or Repag or Nateglinide

•TZD + SU or Repag or Nateglinide

•A-gluc inhib + SU

A-gluc inhib + TZDSU + a-gluc inhib

Insulin therapy•Any of the above + insulin•Beyond this – more than 1 insulin injections as needed

Very severe >250-300, PPBS not restored to basal

Refer to Diabetes center or Diabetologist for insulin Therapy

Timing of BG lowering

Blood sugar lowering greater during fasting than post prandialMetforminSUInsulin

Blood sugar lowering greater during post prandial than fastingAGIInsulin sensitizersMeglitinidesinsulin

Dosing adjustment

Insulin secretagogues Titrate at 1-2 wks interval

Metformin Maximum lowering at 1-2 weeks Can be increased every 2-4 weeks

AGI Inc. dose every 2-4 weeks to minimize SE

TZD Max. lowering occurs at 16 weeks

OHA - SUDRUG Pharmacok

ineticsAction Char. Side

Effects

Glyburide    

Glipizide      

Glimepiride

DOA: 6-12 hrsM: HepaticE: excreted via urine & feces

DOA: 10-24hrsM: hepaticE: majority in urine, remainder in feces DOA: 12-24hrsM: HepaticE: urine

Bind to ATP-sensitive K+ ch to block K+ efflux resulting to depolarization thus ↑ Ca++ entry to cells thereby ↑ insulin release

OD dosing100x more potent than 1st gen

Cholestatic jaundiceHypoglycemiaWeight gainSIADHGI symptomsHematologic effects (thrombocytopenia, leukopenia, agranulocytosis)

OHA - Meglitinide

DRUG Pharmacokinetics

Action Char. Side Effects

Repaglinide

•DOA: 1-3hrs•M: hepatic p450 enzymes•E: majority in urine

•Closes an ATP-dependent K+ ch to block K+ efflux resulting to depolarizn thus ↑ Ca++ entry to cells thereby ↑ insulin release

Similar effect to bld glucose as SUUseful for px w/ allergy to sulfur

Arthralgia, diarrhea, headache, hypoglycemia, neausea, paresthesia

OHA - Biguanides

DRUG Pharmacokinetics

Action Char. Side Effects

Metformin • DOA: 10-12hrs•E: unchanged in urine

• ↑ insulin receptor binding in liver, adipose & muscle for increased glucose uptake• Inhibits hepatic gluconeo-genesis

•Useful in px w/ refractory obesity with ineffective insulin action

•Diarrhea, nausea, abdominal discomfort

OHA - TZDDRUG Pharmacok

ineticsAction Char. Side

Effects

Pioglitazone

Rosiglitazone

•DOA: 15-24hrs•M: hepatic by P450 enzymes•E: majority in feces, remainder in urine

•DOA:>24hrs•M: hepatic by P450 enzymes•E: urine & feces

•↑ glucose uptake in muscle and adipose•↓insulin resistance•↓heaptic gluconeo-genesis

•Less effective than SU & biguanides•Useful for monotx or w/ biguanide•Cause redistribution of ody fat with ↓in central obesity

•Edema, headache, hypoglycemia, upper resp tract infxn

OHA – α-glucosidase inhibitorDRUG Pharmacokin

eticsAction Char. Side Effects

Acarbose •DOA: 3-4hrs•M: intestinal flora•E: absorbed portion-urine; unabsorbed portion - feces

•Slows CHO digestion & absorption time to prevent exaggerated postprandial rise in blood glucose

•↓ post- prandial hyper-glycemia by 30-50%•No hypo-glycemia•↓insulin release due to ↓ blood glucose•↓non-enzymatic glycation of proteins•improves overall glucose control & insulin sensitivity

•Abdominal pain, diarrhea, flatulence, jaundice

Guideline for use of Insulin Secretagouges

Action Generic Trade Name Preparation Daily dose

Short Tolbutamide Rastinon 500mg/tab ½ - 6tabs

Intermediate Glibenclamide

Gliclazide

Glipizide

Glimepiride

Euglucon

Daonil

Orabetie

Diamicron MR

Diamicron

Dianorm

Clizid

Minidiab

Solosa

2.5/5.0mg/tab

5.0mg

30mg/tab

80mg/tab

5 mg/tab

1,2,3 mg/tab

½-3 tabs

1-4 tab/day pre breakfast

½ - 4 tab

½ - 6 tabs

1-4 mg

Long acting Chlorpropamide Diabenese 250mg/tab ½ - 2 tabs

Generic Trade Name Preparation taken pre meals

Daily dose

Repaglinide Novonorm .5, 1 and 2mg tab .5mg tab TID to 2 mg tab TID

CLASS D PHENYLALANINE DERIVATIVE

Nateglinide Starlix 120 and 240 mg tab 120mg tab TID, to 240 mg tab TID

Generic Trade Name Preparation taken aftermeals

Daily dose

Meglitinides

Biguanide

Metformin Glucophage 500 & 850mg tab 500mg ½- 4 tabsFornidd 500mg tab

Humamet 500 and 850mg tab 850mg ½- 2 tabs

Guideline for Alpha Glucosidase InhibitorGeneric Name

Trade Name Preparation Daily Dose

Acarbose Glucobay

Gluconase

50-100mg tab 1 tab after 1 tbsp of food

Voglibose Basen 0.2 and 0.3 mcg tablet 1 tab after 1 tbsp of food

Generic Name Trade Name Preparation Daily Dose

Rosiglitazone Avandia 4 and 8mg/tab 4 mg/tab BID

8mg/tab OD

Pioglitazone Actos 15-30mg tablet 15mg tab OD to BID

30mg/tab OD

Guideline for use of Rosiglitazone

Newer Drugs

DPP4 inhibitorsMOA :small molecules that enhance the

effects of GLP-1 and GIP, increasing glucose-mediated insulin secretion and suppressing glucagon secretion 

Inhibits degradation of GLP-1 and glucose-dependent insulinotropic peptide (GIP), the main insulinotropic peptides of intestinal origin (incretins ) by Dipeptidyl peptidase IV

Sitagliptin 100 mg (Januvia) once daily with or without food

Sitagliptin 100mg + metformin (Janumet)Vidagliptin

New drugs

Incretins Exenetide

derived from a compound found in the saliva of the Gila monster

 functional analog of Glucagon-Like Peptide-1 (GLP-1), a naturally occuring peptide which enhances insulin secretion in response to elevated plasma glucose levels.

specifically indicated as adjunctive therapy to improve glycemic control in patients with Type 2 diabetes mellitus who are taking metformin, a sulfonylurea, or a combination of both, but have not achieved adequate glycemic control.

initiated at 5 mcg per dose 60 mins AC BID SubQ

When to start Insulin?

May be started Marked FPG >280mg/dL HBA1c of >9% Rapid uncontrolled weight loss GDM not controlled by dietary

modificaation Must be started

Acute stress, injury, surgery, steroid tx Renal/hepatic/allergies to OHA Patient’s choice

SHORT and RAPID ACTING

Contents Onset Peak Duration

RAPID

Insulin lispro

15-30 min 1-2 hrs 3-5 hours

Short Acting

Regular

0.5-0.7 hr 1.5-4 hr 5-8 hours

Intermediate Acting

Contents Onset Peak Duration

Insultard 1-4 hrs 8-10 hrs 12-20 hrs

Lente 2-4 hrs 8-12 hr 12-20 hr

Long Acting

Contents Onset Peak Duration

Ultralente, Ultratard

3-5 hrs 10-16 hrs 18-24hrs

Pre mixed

Contents Onset Peak Duration

70 NPH/30 regular

30-60 mins dual 12-20

Different Insulin RegimenInsulin alone( currently accepted)Single dose – Less optimal control of post prandial bld

glucose but convenient for the px (once a day injxn)e.g humulin 15-30 units N SQ at 6am

Split dose – better control than single dosee.g. humulin 15 units N SQ at 6am (2/3 as am dose) humulin 5 units N SQ at 6pm (1/3 as pm dose)

Split mix: Better control than single or split dose e.g humulin N 14, Humulin R 6 units at

6am humulin N 7,Humulin R 3 units at 6 pmBIDS (Bedtime Insulin and Daytime Sulfonylureas)Combined insulin & oral hypoglycemic agents

e.g. Diamicron 80mg/tab, TID PO 30 min before meals Humulin N 20 units SQ at night

Different Insulin Regimen

Insulin + Oral Hypoglycemic Agents

Add insulin treatment on top of oral hypoglycemic agents. Choose any of the 3 regimens in (usually single dose or split dose

e.g. Humulin N 20 units SQ at 6am single dose

+ Diamicron 80mg 1 tab TID 30 min premeals

Medical Nutrition Therapy Calculate Desirable Body weight Determine the TEA Distribute to energy allowance CHO,

CHON, fats

Estimation of DBW A. HAMWI Method

Build Adult Women Adult Men

Medium 100 lbs for the 1st 5 ft of ht

5 lbs per inch for each inch above 5 ft

106 lbs for the 1st 5 ft of ht

6 lbs per inch for each inch above 5 ft

Small Subtract 10% Subtract 10%

Large Add 10% Add 10%

Determination of the TEA

To determine the TEA of adult, multiply DBW with the corresponding values accdg to the ff activities

ACTIVITY Kcal/kg DBW/day

Bed rest but mobile (hospital px) 27.5

Sedentary (most sitting e.g. typist, bank tellers, cashier, administrators

30

Light (office workers, most professionals e.g. lawyers, doctors, nurses, accts, teachers)

35

Mod (students, painters, most vendors, housewife w/o maid, most men and women in light industry))

40

Very active(unskilled laborers, athletes, dancers, fishermen, steel workers, soldiers on active service)

45

For example, a laborer whose DBW is 75kg, will require an energy allowance of kcal per day. TEA = 75 kg x 45 kcal/kg = 3375 kcal Distribution of TEA into CHO, CHON and Fat Percentage of CHO, CHON and Fat Distribution

CHO: 55 – 70 % TEACHON: 10 - 20 % TEA

Fat: 20 – 30 % TEAEx: 3375 calories ( 60% CHO, 15% CHON, 25% Fat) CHO: 3375 x 0.60 = 2025 cal CHON: 3375 x 0.15 = 506.25 cal Fat: 3375 x 0.25 = 843.75 cal 

Calculate the number of grams of CHO, CHON and Fats by dividing the calories for each nutrient by the corresponding physiologic fuel values

4 kcal/g CHO4 kcal/g CHON9 kcal/g Fat

Ex: CHO: 2025 / 4 = 506.25

gCHON: 506.25 / 4 = 126.56

g Fat: 843.75 / 9 = 93.75

g Diet Rx: 3375 kcal ; CHO: 506.3 g; CHON: 126.6 g; Fat: 94 g

Medical Nutritional Therapy (MNT)

term used by the ADA to describe the optimal coordination of caloric intake with other aspects of diabetes therapy (insulin, exercise, weight loss

three types of MNT

10 prevention measures - directed at preventing or delaying the onset of type 2 DM in high-risk individuals (obese or with pre-diabetes)

2o prevention measures of MNT - preventing or delaying diabetes-related complications in diabetic individuals by improving glycemic control

3o prevention measures of MNT - managing diabetes-related complications (cardiovascular disease, nephropathy) in diabetic individuals

Exercise

cardiovascular risk reduction, reduced blood pressure, maintenance of muscle mass, reduction in body fat, and weight loss

lowering plasma glucose increasing insulin sensitivity ADA recommends 150 min/week

(distributed over at least 3 days) physical activity

Guidelines for Ongoing Medical Care for Patients with Diabetes

Self-monitoring of blood glucose (individualized frequency) A1C testing (2–4 times/year) Patient education in diabetes management (annual) Medical nutrition therapy and education (annual) Eye examination (annual) Foot examination (1–2 times/year by physician; daily by

patient) Screening for diabetic nephropathy (annual; see Fig. 338-11) Blood pressure measurement (quarterly) Lipid profile and serum creatinine (estimate GFR) (annual) Influenza/pneumococcal immunizations Consider antiplatelet therapy

Thank You!