DM pptx

PEAK ONSET 11-13 YEARS

MOST COMMON <20 YEARS

MOST COMMON METABOLIC DX IN KIDS

ODDS: 1 IN 400-600 KIDS

CAN OCCUR AS LATE AS 30-40 YEARS

1.25 MILL AMERICANS HAVE TYPE 1D

1. GENETIC SUSCEPTIBILITY:

   HLA HAPLOTYPES ON CHROMOSOME 6: DR4-DQ8 OR DR3-DQ2

2. T1DM OR T2DM IN FIRST DEGREE RELATIVE (T1D <10% GENETIC-BOOK)

3. VIRAL INFECTIONS

4. IMMUNIZATION

5. DIET

6. HIGHER SOCIOECONOMIC STATUS

7. OBESITY

8. VIT D DEFICIENCY

9. PERINATAL FACTORS SUCH AS MATERNAL AGE

10. LOW BIRTH WEIGHT

3 PS

POLYURIA

POLYDIPSIA

POLYPHAGIA

WEIGHT LOSS

HYPERGLYCEMIA

KETONURIA

DIABETIC KETOACIDOSIS

DEHYDRATION

DECREASED ENERGY LEVEL

CONFUSION

FRUITY ODOR BREATH-( IN KETOACIDOSISPatients with DKA may have a fruity odor (due to exhaled acetone; this is similar to the scent of nail polish remover) and deep respirations reflecting the compensatory hyperventilation (called Kussmaul respirations).UPTODATE

KIDS

FAILURE TO GROW AND GAIN WT

1. FUNDOSCOPY: NEOVASCULARIZATION

   RETINOPATHY

   MICROANEURYSMS

   SEE COTTON SPOTS,SOFT OR HARD EXUDATES-NERVE FIBER LAYER INTACT

2. VITAL SIGNS BMI

3. AUS HEART FOR RATE RHYTHM MURMUR CLICKS EXTRA HEART SOUNDS

4. PALPATE THYROID R/O THYROID DISORDERS

5. SKIN EXAM FOR DEHYDRATION

6. NEURO EXAM FOR NEUROPATHY

7. FEET - PULSES EDEMA NAIL THICKNESS GANGRENE

8. PSYCHOSOCIAL - DEPRESSION

FPG >126MG/DL

OR

2 HR BG >200 MG/DL IN OGTT 75 GM

OR

A1C >=6.5 %

OR

>=200 MG/DL IN SYMPTOMATIC PT

TO DISTINGUISH T1DM FROM T2DM

1. C-PEPTIDE INSULIN LEVEL < NORMAL T1 normal or above normal t2d ( NL: 0.5-2 NG/MM)

cpeptide is an inactive biproduct of insulin production in beta cells . Proinsulin splits into insulin and cpeptide, both released when >glucose to make glucose intracellular- c peptide measures endogenous insulin production only.

1. INSULIN LEVEL:LITTLE OR NO INSULIN IN T1DM-utd

   Insulin-to-glucose ratio – Some clinicians use a fasting plasma insulin-to-glucose ratio to assess the degree of insulin resistance.

2. PRESENCE OF AUTOANTIBODIES:

   A. ANTIGLUTAMIC ACID DECARBOXYLASE (GAD)

   anti GAD autoantibodies test

   B.INSULIN AUTOANTIBODIES

   C.ISLET CELL ANTIBODIES

NOTE:ENDOCRINE ABNORMALITIES IN GLUCOSE REGULATION: CUSHINGS, GROWTH HORMONE ACCESS, GLUCAGON SECRETING TUMORS

HGB AIC NOT RELIABLE WITH HEMOGLOBINOPATHIES (hemoglobin C disease, hemoglobin S-C disease, sickle cell anemia, and thalassemias.)

IDA

HEMOLYTIC ANEMIAS

SPHEROCYTOSIS

SEVERE HEPATIC OR RENAL DX

MULTIPLE DAILY INJECTIONS OR CONTINUOUS SUBCUTANEOUS INSULIN INFUSION:

INSULINS

RAPID ACTING : LISPRO humalog , ASPART novolog

SHORT ACTING: REGULAR -HUMULIIN R, NOVOLIN R humalog-lispro, novolog

INTERMEDIATE ACTING:NPH -HUMULIN N, NOVOLIN N

LONG ACTING: GLARGINES-LANTUS,TOUJEO .detemir-LEVEMIR,

degludecTRESIBA- 42 HOUR DURATION)

INSULIN PUMP: HUMALOG, NOVOLOG, APIDRA

dont use mixed in T1D as per ADA

ONSET OF ACTION :15 TO 30 MINUTES:

GIVE <15 MIN BEFORE OR AFTER MEAL

PEAK : 30 MIN-2.5 HOURS

DURATION: 3-6.5 HOURS

ONSET OF ACTION: 10-20 MIN

GIVE: 5-10 MIN PRE MEAL

PEAK: 1-3 HOURS

DURATION; 3-5 HOURS

ONSET OF ACTION: 10-15 MIN

GIVE:15 MIN BEFORE OR RIGHT AFTER MEAL

PEAK: 1-1.5 HOURS

DURATION: 3-5 HOURS

OOA: 15-30 MIN

GIVE: BEGINNING OF MEAL

PEAK: 53 MIN

DURATION: 2.5 - 3 HOURS

OOA: 30-60 MIN

GIVE:BLANK

PEAK: 2-3 HOURS

DURATION: 4-6 HOURS

OOA: 1-2 HOURS

GIIVE:BLANK

PEAK: 6-14 HOUR

DURATION:16-24

0.4 to 0.5 units/kg/day; conservative initial doses of 0.2 to 0.4 units/kg/day

OOA: 1 HOUR STARTS TO WORK

GIVE: ? NIGHT

PEAK: NONE

DURATION: >=24 HOURS

OOA: 1-2 HOURS

PEAK: 6-8 HOURS

DURATION : DOSE DEPENDENT: 12 HOURS FOR 0.2 U/KG

20 HOURS FOR 0.4 U/KG

OOA: UNKNOwn

PEAK : 12 HOURS

DURATION: 42 HOURS ( AFTER 8 DAILY DOSES)

RAPID

ASPART novolog

LISPRO humalog

human novolin r / humulin r

GLULISINE apdira

HUMAN( AFREEZA)

regular

INTERMEDIATE

NPH

LONG

GLARGINE

DETEMIR

DEGLUDEC

INITIAL TOTAL DAILY DOSE ( DD) 0.4-0.5 U/KG/DAY

USUAL TDD: 0.4-1.0 U/KG/DAY

DOSIING BROKEN DOWN TO 50% BASAL AND 50% PRANDIAL

BASAL: NPH INTER OR LONG ACTING( GARGINE,DEGLUDEC, DETEMIR)

1-2 DAILY INJECTIONS

PRANDIAL OR BOLUS: BEOFRE OR AT MEALTIMES-DEPENDS ON FORMULATION- LISPRO , ASPART, GLULISIN OR REGULAR

DIVIDE INTO MEALTIMES ( DIVIDE BY 3)

BASAL AND /OR PRANDIAL MUST BE TITRATED FOR GLUCOSE CONTROL AND AVOID HYPOGLYCEMIA

PRANDIAL FOR FPG ( PLASMA NOT BLOOD NOT FBG) >150 MG/DL

SUBTRACT 100 FROM THE BG AND DIVIDE BY 50

so: -100/50

EG

BG IS 200 MG/DL

200-100=100

100/50 =2

SO 2 EXTRA UNITS TO CORRECT ELEVATED BLOOD SUGAR ( THY WROTE OUT THE OLD SLIDING SCALE

1. DIABETES SELF MGT: MONITOR MULTIPLE X A DAY

2. NUTRITION : INDIVIDUAL AND CULTURALLY SENSITIVE

3. EXERCISE 150 MIN/ DAY MOD TO VIGOROUS AEROBIC DAILY OR AT LEAST 3 X WEEK.

4. DIABETES EDUCATION PERIODIC + CULTURAL SENS, DEVELOPMENTALLY APPROPRIATE

5. IDEAL BODY WEIGHT

6. SMOKING CESSATION OR AVOIDANCE

7. TAKE INSULIN AS PRESCRIBED

8. FOOT CARE

HYPOGLYCEMIA

HYPERGLYCEMIA-

DKA

RETINOPATHY

NEPHROPATHY : MICROALBUMINEMIA, MACROALBUMIINEMIA,

IMPAIRED GFR OR BOTH

ULCERATIONS

GANGRENE

CVD AND HLD

DEFINED AS LOW PLASMA GLUCOSE CONCENTRATION WITH OR WITHOUT SYMPTOMS

NO SPECIFIC GLUCOSE LEVEL TO DEFINE IT AS INDIVIDUAL

SYMPTOMS USU OCCUR < 65 MG/DL OR 3.6 MMOL/LIT

NEUROGENIC:

1. TREMORS

2. PALPITATIONS

3. ANXIETY

4. SWEATING

5. HUNGER

6. PARASTHESIAS

   NEUROGLYPENIC -WHAT A WORD!

   1. DIZZINESS

   2. WEAKNESS

   3. DROWSY

   4. DELIRIUM

   5. CONFUSION

   6. SEIZURES

   7. COMA

   
   

ASYMPTOMATIC: < 70MG/DL/3.9MMOL

RETEST 15-60 MINUTES

SYMPTOMATIC:

15-20 GMS OF REFINED CARBS:

1 TBSP SUGAR

4 OZ OJ

6-8 HARD CANDIES

3-4 GLUCOSE TABS

RETEST 15 MINS

F/U WITH COMPLEX CARB

SEVERE HYPOGLYCEMIA

REQUIRES ASST OF ANOTHER PERSON

GLUCAGON, CARB OR RESUSCITATION

“GLUCAGEN HYPOKIT” OR “GLUCAGON EMERGENCY” : IM IV SQ 1MG

REPEAT Q 15 MINS AS NEEDED

GLUCAGON INTRANASAL: 3MG ONE NARE, IF NO RESPONSE REPEAT IN 15 MINUTES,

CALL 911 IF NO RESPONSE TO GLUCAGON

PHYSICAL EXAM EVERY 3 MONTHS FOCUSED ON GROWTH AND DEVELOPMENT

FAMILY STRESS

PSYCHOLOGICAL IMPACT

CHECK FOR AUTOIMMUNE SOON AFTER DX AND EVERY 2-3 YEARS (THYROID, CELIAC) KATIE REMEMBER THIS IS CHROMOSOME 6 -RA, GUILLAN, EHLERS HASHIMOTOS ETC

HTN SCREENING Q VISIT

HLD SCREEN ANNUAL

MICRO AND MACRO VASCULAR COMPS NEPHRO ANNUAL +

RETINOPATHY Q 2-3 YEARS

FOOT EXAM ANNUAL

ENDOCRINOLOGY

RD

DIABETES EDUCATOR

MENTAL HEALTH PROF-NEW DX AND PUMP INITIATION

OBSTETRICIAN DURING PREGNANCY

MANY SUBTYPES : MAIN ARE

T1D -LOW OR ABSENT INSULIIN, LOW C PEPTIDE <0.5 NG/ML,POSITIVE BETA CELL AUTOANTIBODIES, KETOSIS

T2D- PROGRESSIVE INSULIN SECRETORY DEFECT IN SETTING OF INSULIN RESISTANCE

T1D NO INSULIN

T2D INSULIN THAT DOESNT WORK PROPERLY

ODGERS-PAY ATTENION TO DETAILS

AACE ( ENDOCRINE)

AAFP

DIABETES AUSTR

DIABETES UK

CANADIAN TASK FORCE

RECOMMEND SCREENING FOR DM IN PERSONS WITH RISK FACTORS ONLY

BLURRY VISION 3 PS

FEELING TIRED

UNPLANNED WT LOSS

NAUSEA

CONSTANT THIRST

FEELING HUNGRY

FREQUENT URINATION

IRRITATION AND MOOD CHANGES

NUMBNESS HANDS AND FEET

ASYMTPOMATIC MAJORITY

HYPERGLYCEMIA FOUND ON ROUTINE LABS

3 PS -POLYURIA, POLYDIPSIA, POLYPHAGIA

FREQUENT INFECTIONS

SLOW HEALING WOUNDS

POLYURIA PRESENTS WHEN PG CONCENTRATION RISES SIGNIFICANTLY ABOVE 180 MG/DL WHICH IS THE RENAL THRESHOLD FOR GLUCOSE

MAY HAVE SYMPTOMS FOR WEEKS MONTHS YEARS BEFORE DETECTION.

GENES + ENVT

ENVT= VIRUSES MICROBIOME

NO PHYSICAL ACTIVITY, POOR DIET

LEADS TO T1D- INFLAMMATION AND AUTOIMMUNITY-B CELL DESTRUCTION- HYPERGLYCEMIA-COMPS

T2D-INFLAMMATION AND METABOLIC STRESS-B CELL DYSFUNCTION-

HYPERGLYCEMIA-T2D- COMPS

REMEBER THERE ARE OTHER TYPES OF DM

GENETIC PREDISPOSITION-PANCREAS- INCREASED HEPATIC GLUCOSE OUTPUT + DERANGED IINSULIN RELEASE -DECREASED GLUCOSE UPTAKE -HIGH PG-T2D

ENVT -OBESITY -INSULIN RESISTANCE- DECREASED GLUCOSE UPTAKE BY THE CELL-HIGH PG - T2D

ACCOUNTS FOR 90-95% OF ALL DM

T2D ENCOMPASSES PTS WHO HAVE INSULIN RESISTANCE AND RELATIVE ( RATHER THAN ABSOLUTE) INSULIN DEFICIENCY

MAIN CRITERIA BMI>25 + ONE OR MORE RISK FACTORS

HDL 35 MG/DL ( NORMAL 60 OR ABOVE)+/OR TRIGLYCERIDE > 250 MG/DL

( <150 NORMAL)

AIC 5.7% IGT-IMPAIRED GLUCOSE TOLERANCE OR IFG -IMPAIRED FASTING GLUCOSE ON PREVIOUS TESTING

HTN ->140/90 OR ON HTN MEDS

FIRST DEGREE RELATIVE W DM

HIGH RISK RACE: AA, LATINO, ASIAN AMER, PACI, NATIVE AMER

OTHER CLINICAL CONDITIONS ASSOC W INSULIN RESISTANCE:eg -OBESITY, ACANTHOSIS NIGRICANS

OVERWEIGHT BMI >25 OR >23 ASIANS OR OBESE

PHYSICAL INACTIVITY

HISTORY OF CVD

WOMEN WITH PCOS

WOMEN WHO HAD GEST DM OR BABY >9LBS AT BIRTH

REMEMBER THE HGB AIC-5.7

***ALL PTS 45 YEARS 3 YEAR SCREENING IF NORMAL

if normal RETEST Q 3 YEARS

PRE DIABETIC RETEST ANNUAL

ALL AT RISK PTS ANNUAL

DM PTS MORE FREQUENT- 3 MONTHLY SEE OTHER SLIDE

SERUM GLUCOSE RANDOM OR FASTING:

<100 MG/DL = NORMAL

100-125 MG/DL = PREDIABETES

126 OR > DIABETES

• MUST HAVE > /= 126MG/DL TWO SEPARATE OCCASIONS FOR DX OF DM

• CAN USE FINGERSTICK BLOOD GLUCOSE

<5.7% = NORMAL

5.7-6.4% = PREDIABETES

6.5 % DIABETES

ONLY ONE HGBAIC TO DIAGNOSE???DOUBTFUL

AS PER APEA YOU NEED TWO A1C TO DIAGNOSE

OGTT AFTER 75Gm GLUCOSE LOAD :

<140 MG/DL = NORMAL

140-199 MG/DL = PRE DIABETIC

> 200 MG/DL = DIABETES

ONLY ONE TEST TO DIAGNOSE DM

UA-PROTEIN, GLUCOSURIA ? KETONES (ME)

C PEPTIDE: IN PRESENCE OF A HIGH BLOOD SUGAR***

0.51-2.72NG/DL = NORMAL

<0.51 NG/DL = T1D TYPE ONE

>2.72 NG/DL = T2D-TYPE TWO

IF NOT DONE IN LAST YEAR DO:

LIPID PROFILE

LFT

SPOT URINARY ALBUMIN TO CREATININE RATIO

SERUM CREATININE, EGFR

TSH IF DYSLIPIDEMIA OR WOMEN >50

RISK OF DM AND CARDIAC DISEASE

PROGRESSION TO DM CAN BE DELAYED OR PREVENTED WITH DIET, EXERCISE , WEIGHT LOSS

PRE DIABETIC:

IMPAIRED FASTING GLUCOSE (IFG) 100-125 MG/DL ( X2X)

IMPAIRED GLUCOSE TOLERANCE (IGT) 140-199 MG/DL

HGB AIC 5.7-6.4

DIABETES RARELY LIVES ALONE

1. AGE/CHARACTERISTICS OF ONSET OF DM

2. EATING PATTERNS, NUTRITION ,WT, PHYSICAL ACTIVITY

3. NUTRITIONAL EDUCATION AND BEHAVIORAL SUPPORT NEEDS

4. PRESENCE OF COMORBIDITIES -ESP HTN HLD, PSYCHOSOCIAL AND DENTAL DX

5. DEPRESSION SXREEN PHQ2-9

6. DIABETES DISTRESS SCREEN DDS OR PAID

7. HX OF SMOKING, ALCOHOL SUBSTANCE USE

8. DSME, DSMS HISTORY AND NEEDS

OLMESARTAN EARLY TREATMENT WITH ARB REDUCES INCIDENCE OF MICROALBUMINURIA WITH T2DM

RANDOMIZED OLMESARTAN AND DIABETES MICROALBUMINURIA PREVENTION

however it was associated with increased cardiovascular mortality , FDA has not identified a cause for this

NIH 2013-WATCH-?OLD

HT, WT BMI

GROWTH + PUBERTAL DEVT -KIDS AND ADOLESCENTS

BP-INCLUDING ORTHOSTATIC IF NEEDED

EYES-FUNDOSCOPY

ORAL CAVITY- GUM DX , THRUSH OR LESIONS

NECK-PALPATE THYROID

CARDIAC: RATE RHYTHM MURMURS CLICK EH SOUNDS

SKIN - ACANTHOSIS NIGRICANS , INFECTIONS, NON HEALING WOUNDS, DRY SKIN FEET ESP

FEET- PULSES REFLEXES SENSATION, OVERALL SKIN CONDITION

DTRS-PATELLAR AND ACHILLES

PROPRIOCEPTION, MONOFILAMENT, VIBRATORY SENSATION check for stocking neuropathy

BP ORTHOSTATIC- ORTHOSTATIC BP DYSREGULATION IS COMMON IS AUTONOMIC NEUROPATHY , WHICH MAY BE PRESENT IN DM-EFFERENT VASOMOTOR FIBER DAMAGE

ANNUAL OPTHALOMOLGY FOR RETINOPATHY

TEETH GUMS - LINK BETWEEN GINGIVAL + PERIODONTAL DX AND CVD AND DM

DEVELOPS IN 20-40% PATIENTS W T2DM

SCREEN AT DIAGNOSIS

RANDOM/SPOT URINARY ALBUMIN TO CREATININE RATIO

REPEAT OVER 23 SPECIMENS OVER 3-6 MONTHS

IF ABNORMAL PT HAS ALBUMINURIA

NORMAL UACR IS 30MG/GM CR

AGE 75 80-130 MG/DL

HgbA1C <7.0 % FOR MOST NON PREGNANT ADULTS

PRE PRANDIAL CAPILLARY PG 80-130 MG/DL

PEAK POSTPRANDIAL CAPILLARY PG (1-2 HOURS AFTER MEALS) <180 MG/DL

HgbA1C 6.5% is STRINGENT GOAL FOR :

SHORT DURATION OF DM

T2DM TREATED WITH LIFESTYLE MODIFICATIONS

T2DM TREATED WITH METFORMIN ONLY

LONG LIFE EXPECTANCY

NO SIGNIFCANT CV DISEASE

watch for hypoglycemia w stringent goals*

HgbA1C of 8.0% eg

HISTORY OF SEVERE HYPOGLYCEMIA

LIMITED LIFE EXPECTANCY

ADVANCED MICROVASCULAR OR MACROVASCULAR COMPS

EXTENSIVE COMORBIDITIES

LONG STANDING DM WITH DIFFICULT TO ATTAIN GOAL DESPITE DSME , APPROPRIATE GLUCOSE MONITORING, EFFECTIVE DOSES OF MULTIPLE GLUCOSE LOWERING AGENTS INCLUDING INSULIN.

HGBA1C TWICE ANNUALLY IF MEETING TREATMENT GOALS

HGBA1C Q 3 MONTHS IF NOT MEETING GOALS OR THERAPY CHANGED

CGM -CONTINUOUS GLUCOSE MONITORING HAS BEEN APPROVED BY THE FDA FOR USE INTHOSE OVER 18 YEARS OF AGE

*CGM REQUIRE CALIBRATION WITH SMBG ( FINGERSTICK) FOR MAKING ACUTE TREATMENT DECISIONS*

AGE

DISEASE DURATION/LIFE EXPECTANCY

HYPOGLYCEMIA RISK -INDIVIDUAL

COMORBIDITIES

SOCIAL SUPPORT

ATTITUDE /ADHERENCE ABILITY

AIC GOALS AS CLOSE TO NORMAL AS INDIVIDUAL CAN SAFELY GO

YOUNGER PTS /NEW DIAGNOSIS PTS HAVE STRICTER A1C GOALS

AIMS - REDUCE WT GAIN, REDUCE HYPOGLYCEMIA, GREATEST POTENTIAL TO MEET GOALS

INTRODUCING >>M-biguanide

METFORMIN

500 MG-2000 MG DAY-NO HIGHER

FOUNDATIONAL THERAPY BUT MUST HAVE LIFESTYLE CHANGES TOO-WT LOSS VIA HEALTHY DIET AND EXERCISE

DIET LOW CARB HI PROTEIN

START LOW AND GO SLOW- GI EFFECTS

BIGUAMIDE

AIC RED: 1-2 % HUGE!

EFFICACY : HIGH

HYPO RISK : NONE

WEIGHT : NEUTRAL OR LOSS

CHEAP

ALL T2D START ON METFORMIN

SGLT2 INH FDA APPROVED FOR ASCVD AND RENAL

AIC RED: <1.0

EFF: MODERATE

HYPO RISK: NONE

WT: LOSS

EXPENSIVE

USED FOR CV EVENT REDUCTION AND

HF RISK REDUCTION

RENAL DX RISK REDUCTION

*> GLUCOSE IN URINE > UTI , YEAST INFECTIONS

DPP4 INH

AIC: 0.5-0.8

EFFICACY: MODERATE

HYPO RISK: NONE

WEIGHT: GAIN

INSURANCE COVERAGE IMPROVING

TZD-thiazolidinediones

AIC RED: 0.5-1.0

EFFICACY: MODERATE

HYPO RISK: NONE

WEIGHT : *GAIN

GOOD FOR POST PRANDIAL HYPERGLYCEMIA

s/e :FDA

bladder carcinoma-increased risk

increased risk of bone fractures-controversial-risk factors-duration of drug therapy >2 years

Heart failure: increased risk, excacerbation, dose dependent edema

SULFONYUREA-OLD DRUG

AIC REDU: 1.0-2.0%

EFFICA: HIGH

HYPO RISK:* YES

WEIGHT: GAIN

SHY AWAY- COST EFFECTIVE SO SOME WILL BE ON IT

hypoglycemia risk and weight gain

GLINIDE

HGB AIC: 0.4-0.9%

EFFI: HIGH??

HYPO RISK: *YES

WEIGHT: GAIN

SHY AWAY, SOME PEOPLE MAY BE ON IT

GLP1RA

AIC RED: 0.6-1.5 %

EFF: HIGH

HYPO RISK: NONE

WEIGHT: LOSS LOSS LOSS!

NOW APPROVED FOR WT LOSS IF BMI >=30, OR BMI >=27-29+ 1 WT ASSOC COMORBIDITY EG HTN HLD CVD-PREFERRED

FDA: THYROID C CELL TUMORS IN RATS/SUICIDE INVEST

EARLY AGGRESSIVE RX LEADS TO BETTER OUTCOMES

MONOTHERAPY: METFORMIN,

STEPWISE APPROACH IF GOALS NOT MET

TREATMENT RESPONSE Q3 MONTHLY EVAL

HGBAIC>/=9% MAY DO COMBO THERAPY TO START,OR > 7 WITH MONOTHERAPY

WATCH FOR HYPO**

MEDCHOICE BASED ON PT, COMORBIDITY AND COST/COVERAGE

NO DPP-4I, GLP1ra AND/OR GIP TOGETHER

DM MUST BE CONTROLLED W + W/O FOOD SO FPG AND PPG( POST PRANDIAL PLASMA GLUCOSE)

TO ACHIEVE AIC GOALS

AT HI AIC FPG PREDOMINANT DRIVER OF HYPER

AS AIC DROPS BELOW 7.5% PPG PREDOMINATES

BASAL INSULIN TARGETS FPG

ONCE T2D AT BASAL RATE OF 50-60 UNITS DAILY THEY GET IMPROVEMENT IN FPG.

*WHEN PPG PREDOMINATES CONSIDER ACTOS

PT MUST MONITOR PRE AND POST PRANDIAL( 1-2 HOURS POST MEAL)

EXERCISE:

150 MINS MODERATE AEROBIC SPREAD OVER AT LEAST 3 DAYS A WEEK , NOT MORE THAN 2 DAYS SEDENTARY

RESISTANCE 2 OR > X A WEEK

AVOID ALCOHOL

AVOID SMOKING

WT LOSS 5-10%

MEDICAL NUTRITION THERAPY

3 VISITS W RD AT DIAGNOSIS AND ONGOING SEMI ANNUAL-ANNUAL-

3 VISITS SHOWN TO BE HIGHLY EFFECTIVE

LIFESTYLE ONLY-Q3 MONTHS UNITL AIC GOAL MATCHED AND SUSTAINED

MED RX - Q 3 MONTHS UNTIL GOAL MET THEN Q3 - 6 MONTHS ONCE AT GOAL

MED RX- Q 3 MONTHS ONGOING IF GOAL NOT REACHED OR CHANGE IN MED RX

LABS: ANNUAL

TOTAL URINARY PROTEIN ONCE MICROALBUMINURIA PRESENT

LIPID PROFILE ANNUAL/BIANNUAL IF ELEVATED

TSH ANNUAL ESP WOMEN

1. CAD-LIPID , BP, SMOKING

2. EKG > 50 IF STARTING EXERCISE PROGRAM*

3. FATTY LIVER DX-ASSOC >BMI, WAIST CIRC, >TRIG, <HDL

4. HEARING TEST-ALL FREQU> DM

5. OSA

6. DENTAL SCREEN/PERIODONTAL

7. COGNITIVE IMPAIRMENT -LINK DM+ CVD+ ALZHEIMERS-NEURAL CELLS < GLUCOSE UPTAKE FORM TANGLES

8. DEPRESSION

9. FRACTURES- > HIP FRACTURES DESPITE > BONE MINERAL DENSITY

10. RENAL IMPAIRMENT

11. ANNUAL EYE EXAM

12. CANCER SCREEN -LIVER, PANCREAS( HOW TO SCREEN???) ENDOMETRIUM, COLON/RECTUM BREAST BLADDER

HIGHER CA RISK - THOUGHT DUE TO HYPERINSULINEMIA OR HYPERGLYCEMIA

T1D OR T2D 3 MEDS+/OR INSULIN NOT AT GOAL :

ENDOCRINOLOGIST

FAMILY PLANNING-DM AFFECTS FERTILITY, COMPLICATES PREGNANCY

RD -MEDICAL NUTRITION THERAPY

OPTHALM ANNUAL

DENTAL ANNUAL

DMSE DIABETIC SELF MANAGEMENT EDUCATION

DSMS- DIABETIC SELF MGT SUPPORT

PODIATRY

MENTAL HEALTH PROFESSIONAL

DSME- ALL DM PATIENTS SHOULD PARTICIPATE: FACILITATE KNOWLEDGE,SKILLS, ABILITY NECESSARY FOR SELF CAR

DSMS- TO ASSIST WITH IMPLEMENTING AND SUSTAINING SKILLS AND BEHAVIORS FOR ONGOING SELF MGT.

1. AIC RECORDS REVIEW - WITH PREVIOUS TREATMENT REGIMENS

2. RESULTS OF PT GLUCOSE MONITORING ( SMBG)AND USE OF DATA

3. HYPOGLYCEMIA EPISODES AND AWARENESS, FREQUENCY AND CAUSES-IF ON SULFONY AMARYL- STOP IF HYPO EPISODES

4. HX OF HTN, > LIPIDS, TOBACCO USE

5. MICROVASCULAR COMPS-EYES, KIDNEY, FEET/HANDS ,ULCERS, SEXUAL DYS, GASTROPARESIS

6. MACROVASCULAR: HEART, CEREBROVASCULAR DX, PAD

FIRST LINE PHARMACOTHERAPY BASED N : GLYCEMIC MGT NEEDS. CARDIORENAL RISKS, COMORBIDITIES COST ACCESS

*CONSIDER COMBO PHARMACY AT INITIATION IF HGB AIC >= 1.5% ABOVE TARGET GOAL

CONSIDER EARLY INSULIN INITIATION IF HGB AIC >10% , BG >300 , SIGNS OF CATABOLISM

ASCVD: GLP1-RA OR SGLT -2 i

IF HGBAIC >TARGET CONSIDER INCORPORATING BOTH

CONSIDER LO DOSE ACTOS (NO HF)

HEART FAILURE: SGLT2i- FARXIGA/DAPAGLIFOZIN, JARDIANCE/EMPAGLIFOZIN

NO TZD, NO SAXAGLIPTIN-dpp4 .IF AIC ABOVE TARGET

CKD -ENSURE ON MAXIMALLY TOLERATED ACEi/ARB: -SGLT2i- IF AIC ABOVE TARGET USE GLP 1RA ALSO

SGLT2i CAN BE INITIATED AS LOW AS EGFR 20ML/MIN.

STRONGEST BENEFIT WHEN UACR >=200 MG/G

AIC ABOVE TARGET-CONSIDER + GLP1RA

GLUCOSE LOWERING EFFICACY:

VERY HIGH: DULAGLUTIDE/TRULICITY (HIGH DOSE), SEMAGLUTIDE OZEMPIC, TIRZEPATIDE/MOUNJARO

HIGH: METFORMIN, EXTENATIDE, LIXISENATIDE

INTERMEDIATE: DPP -4i JANUVIA

WEIGHT LOSS EFFICACY:

VERY HIGH: SEMAGLUTIDE OZEMPIC, TIRZEPATIDE/MOUNJARO

HIGH: DULAGLUTIDE/TRULICITY.LIRAGLUTIDE/VICTOZA’

INTERMEDIATE: GLP1-RA.EXTENATIDE, LIXISENATIDE,SGLTi

INTRMEDIATE: JANUVA DPP4i, METFORMIN

COST AND ACCESS:

ORAL AGENTS IN GENERIC FORM /LOWER COST: SULFONYUREAS-AMARYL, GLIPIZIDE,GLIMEPIRIDE. TZD PIOGITAZONE

CONSIDER LOWER COST INSULINS: REGULAR , NPH

IF AIC >TARGET ADD AGENTS

DO NOT COMBINE DPP4i, GLP1RA AND /OR TIRZAPETIDE/MOUNJARO**

COMP LIFESTYLE CHANGES AND NON INSULIN AGENTS SHOULD BE CONSIDERED PRIOR TO INSULIN THERAPY

*CONSIDER EARLY INSULIN INITIATION W EXTREME HYPERGLYCEMIA eg BG>=300MG/DL AIC >10 % OR SIGNS OF CATABOLISM PRESENT-

REASSESS AND MODIFY RX EVERY 3-6 MONTHS TO AVOID THERAPEUTIC INERTIA

INJECTABLE THERAPY TO LOWER AIC?

GLP1RA OR GLP1RA/GIP AND TITRATE TO MAINTENANCE DOSE

IF NOT APPR/WORKING …. ADD INSULIN- BASAL FIRST

LONG ACTING OR NPH- TOUJEO/LANTUS-GLARGINE , DEGLUDEC/TRESIBA, DETEMIR/LEVEMIR

10 units once daily or 0.1 to 0.2 units/kg once daily

TITRATE TO FPG TARGET

USE EBP ALGORITHM:

> 2 UNITS EVERY 3 DAYS UNTIL FPG TARGET OBTAINED

*HYPOGLYCEMIA IS NEVER ACCEPTABLE

IF IT OCCURS REDUCE DOSE 20-30%

ASSESS BASAL INSULIN DOSE ADEQUACY AND EVALUATE FOR OVERBASALISATION

AIC ABOVE TARGET

ON BEDTIME NPH? CONVERT TO BID NPH

TOTAL DOSE =80% OF CURRENT

2/3 IN AM

1/3 AT BEDTIME

NOT ON NPH?

ADD PRANDIAL INSULIN:

GIVE ONE DOSE AT MEAL WHICH IS LARGEST OR HAS LARGEST PPG( POSTPRANDIAL GLUCOSE) EXCURSION

PRANDIAL CAN BE DOSED INDIVIDUALLY OR MIXED WITH NPH AS APPROPRIATE

START: 4 UNITS /DAY OR 10% OF BASAL INSULIN DOSE

IF AIC <8% CONSIDER LOWERING BASAL DOSE BY 4 UNITS/DAY OR 10% OF BASAL DOSE

TITRATE: >DOSE 1-2 UNITS OR 10-15% BASAL TWICE WEEKLY

IF HYPOGLYCEMIA < DOSE BY 10-20%

AIC STILL ABOVE TARGET

1. STEPWISE ADD’L PRANDIAL 1 THEN 2 THEN 3 INJECTIONS TO REACH FULL BASAL -BOLUS REGIMEN

I.E. PRANDIAL INSULIN W MEALS AND BASAL INSULIN

2.SELF MIXED/SPLIT INSULIN REGIMENS W NPH

START: TOTAL NPH =80% CURRENT NPH

2/3 BEFORE BREAKFAST

1/3 BEFORE DINNER

ADD 4 UNITS OF SHORT/RAPID INSULIN TO EACH INJECTION OR 10% OF REDUCED NPH DOSE-TITRATE ACCORDING TO PT NEED

3. BID PREMIX INSULIN- NOVOLOG 70/30.DC ORAL MEDS EXCEPT METFORMIN,GLP1RA AND SGLT2i

INSULIN NAIVE: 0.2 to 0.3 units/kg/day or 10 to 12 units/day

2/3 DOSE AT BREAKFAST

1/3 DOSE AT DINNER

abdominal obesity, hyperglycemia, dyslipidemia, and hypertension

Increased waist circumference, with ethnic-specific waist circumference cut-points (table 2) 31.5 INC W, 35.4 IN MEN

●Triglycerides ≥150 mg/dL (1.7 mmol/L) or treatment for elevated triglycerides

●HDL cholesterol <40 mg/dL (1.03 mmol/L) in men or <50 mg/dL (1.29 mmol/L) in females, or treatment for low HDL

●Systolic blood pressure ≥130, diastolic blood pressure ≥85, or treatment for hypertension

●FPG ≥100 mg/dL (5.6 mmol/L) or previously diagnosed type 2 diabetes; an oral glucose tolerance test is recommended for patients with an elevated FPG, but it is not required

International Diabetes Federation (IDF)

DIETS

2023 META ANALYSIS

MEDITERANEAB

LO FAT

SOME EVIDENCE FOR 8 HOUR FASTING PERIODS

EXERCISE

AEROBIC AND MUSCLE STRENGTHENING

LIPID LOWERING:

Evidence does not support metabolic syndrome as a coronary risk equivalent that would prompt statin initiation [121]. Nevertheless, metabolic syndrome is a "risk enhancing factor" that may warrant statin therapy even in individuals whose ASCVD risk would not otherwise meet the threshold for treatment

DM PREVENTION

SAME AS FOR PREDIABETES

START METFORMIN

BP SAME AS STANDARD

SUGGEST COMBO OLEMSARTAN /AMLODIPINE

THIAZIDES CAN CAUSE HYPERGLYCEMIA AND AFFECT LIPID PROFILE -

IF NOT :UTD:Alternatively, clinicians can initiate thiazide diuretics in combination with ACE inhibitors or ARB agents as these medications may counteract the hyperglycemia-inducing effects of thiazides

TWO MOST SERIOUS COMPLICATIONS OF DM

DKA -KETOACIDOSIS AND HYPERGLYCEMIA

HHNK NO KETOACIDOSIS BUT MORE SEVERE HYPERGLYCEMIA

DRUGS

LITHIUM

SGLT2I-USED MORE OFTEN

COCAINE

2ND GENREATION ATYPICAL ANTIPSYCHOTICS

ACUTE ILLNESS

INFECTION

STROKE/TIA

MI

PANCREATITIS-ACUTE

NEW ONSET DM (20%)

DRUGS

BETA BLOCKERS

CCB

STEROIDS

TPN

THIAZIDE DIURETICS

ENDO

THYROTOXICOSIS

CUSHINGS

ACUTE ILLNESS:

INFECTION -UTI SEPSIS PNA

STROKE/TIA

PNCREATITIS

BURNS-SEVERE

PD-peritoneal dialysis

PE

DEHYDRATION ELDERLY

dka evolves rapidly over 24 HOUR PERIOD

FIRST HYPERGLYCEMIA

3 PS

NEUROGLYCOPENIC SX

LETHARGY

FOCALSIGNS

OBTUNDATION

HYPERVENTILATION-

ABDOMINAL PAIN

NAUSEA AND VOMITING 46% ? FROM METABOLIC ACIDOSIS AND ELECTROLYTE ABNORMALITIES

S/S DEHYDRATION-DRY ORAL MUCOSA

TACHYCARDIA

PEAR DROP KETONE BREATH AND KUSSMAULS-COMPENSATORY HYPERVENTILATION

DEVELOPS OVER LONGER PERIOD W 3 PS AND WT LOSS ->FEW DAYS

SAME -NEUROGLYCOPENIC SX LETHARGY FOCALAND OBTUNDATION

NEURO SIGNS MORE COMMON

ABD PAIN AND >VENTILATION NOT COMMON

SEIZURES

SAME DEHYDRATION SX

NO KUSSMAULS

MANAGE CAB( CIRC,AIRWAY BREATHING

MENTAL STATUS

PRECIPITANTS

VOLUME STATUS

SERUM GLUCOSE

SERUM ELECTROLYTES AND CALCULATE ANION GAP,

BUN CREATININE

CBCW DIFF

UA AND URINE KETONES BY DIPSTICK

PLASMA OSMOLALITY

SERUM BETA-HYDROXYBURATE -IF KETONES PRESENT

ABG IF LOW SERUM BICARB

EKG

OTHER INFECTION RELATED LABS

DKA >250 HHNK OR HHS>600

SERUM BICARB MEQ/L DKA <10 (SEVERE) HHNK>18-SERUM BICARB REALLY REDUCED IN DKA, NORMAL OR MILD REDCTION IN HHS

URINE KETONES DKA + HHS SMALL

SERUM OSMOLALITY DKA VARIABLE HHS >320

ANION GAP DKA >10->12 , HHK VARIABLE

ALTERATION IN MENTALSTATUSBOTH CAN LEAD TO STUPOR AND DROWSY

ANION GAP = SERUM NA -(SERUM CHLORIDE +BICARBONATE)

THAT IS WHY DKA HAS KUSSMAULS -ELEVATED ANION GAP METABOLIC ACIDOSIS ->RESPS TO REDUCE CO2 AND MITIGATE FALL IN ARTERIAL PH

TRIAD OF FDKA IS

HYPERGLYCEMIA

KETONEMIA-NITROPRUSSIDE TEST

ANION GAP METABOLIC ACIDOSIS

SERUM GLUCOSE USU <800 MG/DL

HHS

LITTLE OR NO KETOACID ACCUMULATION

SERUM GLUCSE MUCH HIGHER

NEURO SIGNS FIRST

PH>7.30

SERUM BICARB >20NEQ/L

SERUM GLUCOSE >600

NO KETONES IN URINE AND BLOOD-MAY GET MILD KETOSIS