Talk on Diabetes and its Management

Diabetes MellitusDiabetes Mellitus

and itsand its

ManagementManagement

Talk by

Dr Anshu P Gokarn MBBS, MD(Pharmacology)

Dr Anshu P Gokarn 2

How My Talk Is Structured

PART - 1

1. Symptoms of Diabetes Mellitus

2. About our body & our pancreas

3. Glucose Metabolism : Role of Insulin

4. When Insulin Does Not Do Its Job - Diabetes Mellitus

5. Why is Diabetes Mellitus a Silent Killer

Dr Anshu P Gokarn 3


PART - 2

1. Diagonizing Diabetes Mellitus

2. Management of Diabetes Mellitus :

1. Diet & Excersise

2. Oral Medication

3. Insulin

3. Diabetes Management Algorithm

4. Hypo & Hyper Glycemia

5. Preventing & Controling Diabetes Mellitus - What you can do ?

Dr Anshu P Gokarn 4

Most of us have a close friend or relative who is suffering from “sugar” or “diabetes”.

Let us understand a little more about the disease that suddenly seems to be all around us….

Dr Anshu P Gokarn 5

Diabetes Mellitus

Affects over 300 million people globally.

India leads the world – 50 million Indians suffer from it.

Incidence increasing rapidly … specially in the developing world : India & China – due to lifestyle changes.

Affects the middle class and the rich – is a lifestyle disease – high caloric diet and lack of physical excersise.

Dr Anshu P Gokarn 6


PART - 1

1. Symptoms of Diabetes Mellitus

2. About our body & our pancreas

3. Glucose Metabolism : Role of Insulin

4. When Insulin Does Not Do Its Job - Diabetes Mellitus

5. Why is Diabetes Mellitus a Silent Killer

Dr Anshu P Gokarn 7

Symptoms of Diabetes Mellitus

PART 1

Dr Anshu P Gokarn 8

Diabetes Mellitus

Person has high blood sugar,

• either because the pancreas does not produce enough insulin,

• or because cells do not respond to the insulin that is produced.

High blood sugar produces classical symptoms :

• Frequent urination – polyuria

• Increased thirst – polydipsia

• Increased hunger – polyphagia

Dr Anshu P Gokarn 9

Symptoms of Diabetes MellitusSymptoms of Diabetes Mellitus

Dr Anshu P Gokarn 10

Hyperglycemia Can Cause Serious Long-Term Problems


About our body & our pancreas


PancreasPancreas

Is a solid organ lying in the abdomen.Is a solid organ lying in the abdomen.

The head of the pancreas fits in the CThe head of the pancreas fits in the C--shaped shaped curve of the duodenumcurve of the duodenum

Pancreas is a mixed gland withPancreas is a mixed gland with

•• Exocrine partExocrine part

•• Endocrine partEndocrine part

The endocrine part consists of groups of cells The endocrine part consists of groups of cells

called as called as Islets of Islets of LangerhansLangerhans


Islets of Islets of LangerhansLangerhans

Consist of different types of cells which Consist of different types of cells which

secrete different hormonessecrete different hormones

--cells cells : secrete glucagon: secrete glucagon

--cells : secrete insulincells : secrete insulin

--cells cells : secrete : secrete somatostatinsomatostatin

FF--cells : secrete pancreatic polypeptidecells : secrete pancreatic polypeptide


Secretions of Islets of Secretions of Islets of LangerhansLangerhans

GlucagonGlucagon

Increases blood glucose Increases blood glucose levelslevels

InsulinInsulin

Decreases blood glucose Decreases blood glucose levelslevels

SomatostatinSomatostatin

Inhibits secretion of glucagon and Inhibits secretion of glucagon and insulininsulin

Pancreatic polypeptidePancreatic polypeptide

Released in response to high protein dietReleased in response to high protein diet


Glucose Metabolism : Role of Insulin


Normal Body : Glucose/Insulin Self Correction Normal Body : Glucose/Insulin Self Correction


InsulinInsulin

InsulinInsulin is a hormone secreted by is a hormone secreted by the the --cells of the islets of cells of the islets of LangerhansLangerhans of the pancreasof the pancreas

The The --cells synthesize a cells synthesize a prehormoneprehormone called called PreproinsulinPreproinsulin

PreproinsulinPreproinsulin gets processed to gets processed to form form ProinsulinProinsulin

ProinsulinProinsulin splits to form Insulin and splits to form Insulin and CC--peptidepeptide


What is CWhat is C--peptide ?peptide ?

CC--peptide means Connecting peptide means Connecting peptide.peptide.

It is the portion of It is the portion of proinsulinproinsulin which which gets split off during formation of gets split off during formation of insulininsulin

Levels of CLevels of C--peptide are measured peptide are measured to assess to assess --cell functioncell function

CC--peptide levels are measured peptide levels are measured instead of insulin levels because instead of insulin levels because insulin gets metabolized in the liver insulin gets metabolized in the liver but Cbut C--peptide stays in circulation peptide stays in circulation for a long timefor a long time


What Are The Actions Of Insulin?What Are The Actions Of Insulin?

Insulin exerts it’s effects on carbohydrate, fat and Insulin exerts it’s effects on carbohydrate, fat and protein metabolismprotein metabolism

Effect on Carbohydrate metabolismEffect on Carbohydrate metabolism

•• Glucose transport :Glucose transport : uptake / entry of glucose into uptake / entry of glucose into cellscells

•• GlycogenesisGlycogenesis :: formation of glycogen from glucoseformation of glycogen from glucose

•• GlycolysisGlycolysis :: breakdown of glucose to produce breakdown of glucose to produce energyenergy

All these actions help in All these actions help in removing glucoseremoving glucose from blood from blood and henceand hence reduce blood glucose levelsreduce blood glucose levels..


Actions of Insulin….Actions of Insulin….

Effect on Fat / Lipid metabolismEffect on Fat / Lipid metabolism

•• Triglyceride synthesis in adipose tissueTriglyceride synthesis in adipose tissue

•• Fatty acid synthesis in liverFatty acid synthesis in liver

•• Enhances lipoprotein lipase activityEnhances lipoprotein lipase activity

Increases entry of fatty acids and Increases entry of fatty acids and triglycerides from lipoproteins into triglycerides from lipoproteins into adipose cellsadipose cells

AdipocytesAdipocytes


Actions of Insulin…Actions of Insulin…

These actions help in removal of fats from These actions help in removal of fats from

blood and help them to get deposited in blood and help them to get deposited in

adipocytesadipocytes..

Effect on Protein metabolismEffect on Protein metabolism

•• Increased transport of amino acids into cellsIncreased transport of amino acids into cells

•• Enhances protein synthesisEnhances protein synthesis


How How does glucose does glucose enters cells?enters cells?

Insulin acts on Insulin Receptors present on Insulin acts on Insulin Receptors present on cell membranecell membrane

Glucose Transporters [Glucose Transporters [GLUTsGLUTs] come to the ] come to the cell surfacecell surface

Glucose enters the cells through GLUTsGlucose enters the cells through GLUTs


GLUTGLUT INSULIN RECEPTORINSULIN RECEPTOR


What are Insulin Receptors What are Insulin Receptors

These are the receptors present on cell These are the receptors present on cell membrane which bind the circulating insulinmembrane which bind the circulating insulin

Actions of insulin are mediated by insulin Actions of insulin are mediated by insulin receptorsreceptors

The number and sensitivity of insulin receptors The number and sensitivity of insulin receptors varies with insulin levels, exercise, food and varies with insulin levels, exercise, food and other factorsother factors

If number and/or sensitivity of If number and/or sensitivity of insulin insulin receptors is reduced, receptors is reduced, the individual develops the individual develops Insulin Insulin ResistanceResistance


When Insulin Does Not Do Its Job


What is Insulin Resistance?What is Insulin Resistance?

Insulin Resistance is the inability of insulin to act Insulin Resistance is the inability of insulin to act effectively on peripheral target tissues effectively on peripheral target tissues [especially muscles and liver][especially muscles and liver]

Resistance to action of insulin impairs glucose Resistance to action of insulin impairs glucose utilization by peripheral cells and increases utilization by peripheral cells and increases hepatic glucose outputhepatic glucose output

This further signals the pancreas to release more This further signals the pancreas to release more insulininsulin

Hence, excessive levels of insulin build up in the Hence, excessive levels of insulin build up in the plasma [plasma [HyperinsulinaemiaHyperinsulinaemia]]


Insulin Resistance…..Insulin Resistance…..

Insulin Resistance is a Insulin Resistance is a prominent feature of prominent feature of type 2 diabetes. type 2 diabetes.

Obesity contributes to Obesity contributes to insulin resistance.insulin resistance.

Insulin resistance is a Insulin resistance is a part of part of Syndrome XSyndrome X..


Syndrome X ?Syndrome X ?

Syndrome X is a condition which includes:Syndrome X is a condition which includes:

Insulin ResistanceInsulin Resistance

HypertensionHypertension

DyslipidaemiaDyslipidaemia

Central ObesityCentral Obesity

Endothelial dysfunctionEndothelial dysfunction

Accelerated cardiovascular diseaseAccelerated cardiovascular disease


What happens due to What happens due to lack lack of Insulin ?of Insulin ?

Lack of insulin affects:

Carbohydrate metabolism

Fat metabolism

Protein metabolism

Leading to various biochemical abnormalities….


What happens due to What happens due to lack lack of Insulin ?of Insulin ?

These biochemical abnormalities include….These biochemical abnormalities include….

ReducedReduced entryentry ofof glucoseglucose intointo variousvarious peripheralperipheral tissuestissues..

GlycogenolysisGlycogenolysis [breakdown[breakdown ofof glycogenglycogen toto glucose]glucose]

IncreasedIncreased liberationliberation ofof glucoseglucose intointo circulationcirculation fromfrom liverliver

GluconeogenesisGluconeogenesis [synthesis[synthesis ofof glucoseglucose fromfrom fattyfatty acidsacids andand aminoamino acids]acids]

Leading to Leading to HyperglycaemiaHyperglycaemia [excessive glucose in blood][excessive glucose in blood]

LipolysisLipolysis..

ReducedReduced entryentry ofof fattyfatty acidsacids andand triglyceridestriglycerides intointo adipocytesadipocytes

Leading to Leading to DyslipidaemiaDyslipidaemia [[disturbed lipid profile] disturbed lipid profile]

DecreasedDecreased inin entryentry ofof aminoamino acidsacids intointo musclemuscle..

Leading to Leading to Muscle WastingMuscle Wasting


More About Diabetes Mellitus


Diabetes MellitusDiabetes Mellitus

Is a clinical syndrome Is a clinical syndrome

characterized by characterized by

HyperglycaemiaHyperglycaemia

due to due to

Absolute or RelativeAbsolute or Relative

lack of Insulin.lack of Insulin.


Recap : Signs & Symptoms of DiabetesRecap : Signs & Symptoms of Diabetes

PolyuriaPolyuria [increased[increased urination]urination]

PolydipsiaPolydipsia [increased[increased thirstthirst ]]

PolyphagiaPolyphagia [increased[increased hunger]hunger]

HyperglycaemiaHyperglycaemia [increased[increased bloodblood glucoseglucose levels]levels]

GlycosuriaGlycosuria [excretion[excretion ofof glucoseglucose inin urine]urine]

andand inin uncontrolleduncontrolled casescases -- ketosis,ketosis, acidosisacidosis andand comacoma


Types of Diabetes MellitusTypes of Diabetes Mellitus


Types of Diabetes?Types of Diabetes?

According to the American Diabetes Association [2000]; diabetes According to the American Diabetes Association [2000]; diabetes

is classified as follows:is classified as follows:

I.I. Type 1 diabetesType 1 diabetes

II.II. Type 2 diabetesType 2 diabetes

III.III. Other specific types of diabetesOther specific types of diabetes

a.a. Genetic defects of Genetic defects of --cell functioncell function

b.b. Genetic defects in insulin actionGenetic defects in insulin action

c.c. Diseases of exocrine pancreasDiseases of exocrine pancreas

d.d. EndocrinopathiesEndocrinopathies

e.e. DrugDrug-- or chemicalor chemical--inducedinduced

f.f. InfectionsInfections

g.g. Uncommon forms of immuneUncommon forms of immune--mediated diabetes etc.mediated diabetes etc.

IV.IV. Gestational diabetes [GDM]Gestational diabetes [GDM]


What is Type 1 Diabetes?What is Type 1 Diabetes?

Type 1 DM is characterized by destruction of Type 1 DM is characterized by destruction of --cellscells, , usually leading to absolute insulin deficiencyusually leading to absolute insulin deficiency

It is further classified as:It is further classified as:

Type 1A : results from autoimmune Type 1A : results from autoimmune --cell destructioncell destruction

Type 1B : immunologic markers are not found, hence cause of Type 1B : immunologic markers are not found, hence cause of --cell destruction is not knowncell destruction is not known

Type 1 was previously known as IDDM or Juvenile Onset of Type 1 was previously known as IDDM or Juvenile Onset of Diabetes.Diabetes.

However, these terms are now considered obsolete because However, these terms are now considered obsolete because type 2 patients eventually require insulin and 5type 2 patients eventually require insulin and 5--10% of type 1 10% of type 1 DM develops after 30yrs of ageDM develops after 30yrs of age


What is Type 2 Diabetes?What is Type 2 Diabetes?

Type 2 DM is characterized by Type 2 DM is characterized by

Variable degrees of insulin resistanceVariable degrees of insulin resistance

Impaired insulin secretionImpaired insulin secretion

Increased glucose productionIncreased glucose production

Type 2 DM has a strong genetic componentType 2 DM has a strong genetic component

Obesity, particularly central obesity, is very common in type 2 Obesity, particularly central obesity, is very common in type 2 DMDM

Type 2 was previously called NIDDM or Maturity onset Type 2 was previously called NIDDM or Maturity onset diabetesdiabetes

Now obsolete as :Now obsolete as :

Type Type 2 patients 2 patients eventually require insulin eventually require insulin

Type 2 seen even at Type 2 seen even at young age, particularly in young age, particularly in obese obese adolescentsadolescents


A form of glucose intolerance that is diagnosed in some women during pregnancy.

Gestational diabetes occurs more frequently among African Americans, Hispanic/Latino Americans, and American Indians. It is also more common among obese women and women with a family history of diabetes.

During pregnancy, gestational diabetes requires treatment to normalize maternal blood glucose levels to avoid complications in the infant.

After pregnancy, 5% to 10% of women with gestational diabetes are found to have type 2 diabetes.

Women who have had gestational diabetes have a 20% to 50% chance of developing diabetes in the next 5-10 years.

Gestational diabetes Gestational diabetes


Latent Autoimmune Diabetes in Adults (LADA) is a form of autoimmune (type 1 diabetes) which is diagnosed in individuals who are older than the usual age of onset of type 1 diabetes.

Alternate terms that have been used for "LADA" include Late-onset Autoimmune Diabetes of Adulthood, "Slow Onset Type 1" diabetes, and sometimes also "Type 1.5

Often, patients with LADA are mistakenly thought to have type 2 diabetes, based on their age at the time of diagnosis.

LADA LADA -- Latent Autoimmune Diabetes in Adults Latent Autoimmune Diabetes in Adults

http://www.diabetesmonitor.com/dictionary/a-e.htm

http://www.diabetesmonitor.com/dictionary/p-t.htm











About 80% of adults apparently with recently diagnosed Type 2 diabetes but with GAD auto-antibodies (i.e. LADA) progress to insulin requirement within 6 years.

The potential value of identifying this group at high risk of progression to insulin dependence includes:

the avoidance of using metformin treatment

the early introduction of insulin therapy

LADA LADA -- Latent Autoimmune Diabetes in Adults Latent Autoimmune Diabetes in Adults


MODY – Maturity Onset Diabetes of the Young - is a monogenic form of diabetes with an autosomal dominant mode of inheritance:

◦ Mutations in any one of several transcription factors or in the enzyme glucokinase lead to insufficient insulin release from pancreatic ß-cells, causing MODY.

◦ Different subtypes of MODY are identified based on the mutated gene.

Originally, diagnosis of MODY was based on presence of non-ketotic hyperglycemia in adolescents or young adults in conjunction with a family history of diabetes.

However, genetic testing has shown that MODY can occur at any age and that a family history of diabetes is not always obvious.

MODY MODY -- Maturity Onset Diabetes of the Maturity Onset Diabetes of the YoungYoung




Within MODY, the different subtypes can essentially be divided

into 2 distinct groups: glucokinase MODY and transcription

factor MODY, distinguished by characteristic phenotypic

features and pattern on oral glucose tolerance testing.

Glucokinase MODY requires no treatment, while transcription

factor MODY (i.e. Hepatocyte nuclear factor -1alpha) requires

low-dose sulfonylurea therapy and PNDM (caused by Kir6.2

mutation) requires high-dose sulfonylurea therapy.



Diabetes Mellitus - Risk Factors


Risk Factors for Type 2 DMRisk Factors for Type 2 DM

Family history of diabetesFamily history of diabetes

Obesity, esp. centralObesity, esp. central

Age Age >> 45 years45 years

Race / ethnicityRace / ethnicity

Previously identified IFG [impaired fasting glucose] Previously identified IFG [impaired fasting glucose] or IGT [impaired glucose tolerance]or IGT [impaired glucose tolerance]

History of GDM or delivery of baby over 9 lbsHistory of GDM or delivery of baby over 9 lbs

Hypertension [BP Hypertension [BP >> 140/90 mm Hg]140/90 mm Hg]

HDLHDL--c c << 35mg/35mg/dLdL and/or TG level and/or TG level >> 250mg/250mg/dLdL


Why is Diabetes Mellitus a Silent Killer


Complications due to Diabetes?Complications due to Diabetes?

Complications in diabetes occur due to Complications in diabetes occur due to

•• Excessive glucose in bloodExcessive glucose in blood

•• Disturbed lipid profileDisturbed lipid profile

•• Insulin resistanceInsulin resistance

•• Increased rate of atherosclerosis, etc.Increased rate of atherosclerosis, etc.

Complications Complications of diabetes can be of diabetes can be ::

a. Acute a. Acute

b. b. LongLong--termterm


Acute Complications of DiabetesAcute Complications of Diabetes

a. Acute Complicationsa. Acute Complications

1. 1. Diabetic Diabetic ketoacidosisketoacidosis ::

•• Disturbed metabolism of glucose Disturbed metabolism of glucose and fats and fats leads to formation of excessive acetyl leads to formation of excessive acetyl CoACoA

•• Excess acetyl Excess acetyl CoACoA gets converted to gets converted to ketoneketone bodiesbodies

•• KetoneKetone bodies reduce pH of body fluidsbodies reduce pH of body fluids

•• This leads to the condition called as diabetic This leads to the condition called as diabetic ketoacidosisketoacidosis

•• Signs include: dehydration, hypertension, tachycardia, Signs include: dehydration, hypertension, tachycardia, hypothermia.hypothermia.

If untreated, it leads to If untreated, it leads to ketoacidoticketoacidotic comacoma


Acute Acute ComplicationsComplications

2. 2. HyperglycaemicHyperglycaemic coma:coma:

Excessive glucose in blood Excessive glucose in blood disturbs disturbs brain functionsbrain functions

Is accompanied by dehydration and Is accompanied by dehydration and uraemiauraemia

Management includes insulin and fluid & Management includes insulin and fluid & electrolyte replacementelectrolyte replacement

3. 3. LacticacidosisLacticacidosis::

Excessive lactic acid production reduces pH of Excessive lactic acid production reduces pH of body fluidsbody fluids

Occurs due to anaerobic Occurs due to anaerobic glycolysisglycolysis


LongLong--standing Complications of Diabetes ? standing Complications of Diabetes ?

TheseThese developdevelop overover aa periodperiod ofof monthsmonths toto yearsyears duedue toto slowslow progressiveprogressive changeschanges occurringoccurring inin thethe bloodblood vessels,vessels, nervesnerves andand variousvarious organsorgans ofof thethe bodybody..

LongLong--standingstanding complicationscomplications includeinclude::

a)a) MicrovascularMicrovascular ComplicationsComplications

b)b) MacrovascularMacrovascular ComplicationsComplications

c)c) DiabeticDiabetic NeuropathiesNeuropathies

d)d) DiabeticDiabetic footfoot

e)e) CataractCataract

f)f) OtherOther complicationscomplications


MicrovascularMicrovascular Complications of DiabetesComplications of Diabetes

These are the complications involving the small These are the complications involving the small blood vesselsblood vessels

Excessive glucose in blood gets converted to Excessive glucose in blood gets converted to sorbitolsorbitol, which is toxic and damages blood vessel , which is toxic and damages blood vessel wallswalls

Excess glucose also binds to proteins in blood Excess glucose also binds to proteins in blood vessel walls by vessel walls by glycationglycation reactionreaction

These complications includeThese complications include

•• Diabetic Retinopathy Diabetic Retinopathy

•• Diabetic NephropathyDiabetic Nephropathy


MicrovascularMicrovascular Complications….Complications….

Diabetic RetinopathyDiabetic Retinopathy

Damage to the retinal Damage to the retinal blood vessels due to blood vessels due to

longlong--standing diabetesstanding diabetes

Diabetic NephropathyDiabetic Nephropathy

Damage to renal blood Damage to renal blood vessels due to vessels due to

longlong--standing diabetesstanding diabetes

Later Later onon,,

nephronsnephrons get get

damaged damaged tootoo


These are the complications involving larger blood vessels due These are the complications involving larger blood vessels due to longto long--standing diabetesstanding diabetes

Occur due to Occur due to

•• accelerated atherosclerosisaccelerated atherosclerosis

•• DyslipidaemiaDyslipidaemia

These These include increased incidence of include increased incidence of stroke, stroke, CHD [coronary CHD [coronary heart diseaseheart disease, peripheral arterial diseases, peripheral arterial diseases etc.etc.

MacrovascularMacrovascular Complications….Complications….


CHD [Coronary Heart Disease]CHD [Coronary Heart Disease]

Also called as IHD [Also called as IHD [ischaemicischaemic heart disease]heart disease]

IschaemiaIschaemia = lack of blood supply to a tissue= lack of blood supply to a tissue

damage to coronary blood vessels damage to coronary blood vessels increases increases risk of heart attacksrisk of heart attacks

CHD includes:CHD includes:

AnginaAngina –– pain in chest due to lack of blood pain in chest due to lack of blood supply to heart musclessupply to heart muscles

MI [myocardial infarction]MI [myocardial infarction] –– death of cardiac death of cardiac tissue due to lack of blood supplytissue due to lack of blood supply




StrokeStroke Damage Damage to cerebral to cerebral

arteries leads to lack of arteries leads to lack of blood supply to brain blood supply to brain tissuetissue

Resulting neurological Resulting neurological dysfunction [paralysis dysfunction [paralysis etc.] is called strokeetc.] is called stroke

Peripheral Arterial Peripheral Arterial DiseaseDisease

Damage Damage to arteries of legs to arteries of legs leads to pain while walkingleads to pain while walking

Increasing damage can lead Increasing damage can lead to to ischaemicischaemic necrosis of necrosis of tissues and may even tissues and may even require amputation of legrequire amputation of leg


Diabetic NeuropathyDiabetic Neuropathy

Damage Damage to nerves occurs due to to nerves occurs due to

excessive glucose and other factorsexcessive glucose and other factors

Includes:Includes:

Peripheral neuropathy Peripheral neuropathy –– damage occurs to nerves of arms damage occurs to nerves of arms and legs leading to and legs leading to loss of ability to sense touch, pain, loss of ability to sense touch, pain, temperaturetemperature etc.etc.

Autonomic neuropathy Autonomic neuropathy –– damage to nerves of autonomic damage to nerves of autonomic nervous system leading to nervous system leading to GI disturbances, urinary GI disturbances, urinary incontinence, impotenceincontinence, impotence etc.etc.

Long standing complications…. Long standing complications….


Long standing complications….Long standing complications….

HypertensionHypertension

SustainedSustained elevationelevation ofof bloodblood pressurepressure aboveabove normalnormal limitslimits isis calledcalled asas hypertensionhypertension..

HypertensionHypertension maymay developdevelop inin diabeticsdiabetics duedue toto ::

•• IncreasedIncreased raterate ofof atherosclerosisatherosclerosis

•• InsulinInsulin resistanceresistance

•• EndothelialEndothelial dysfunctiondysfunction

•• DiabeticDiabetic nephropathy,nephropathy, etcetc..


Long standing complications….Long standing complications….

Diabetic FootDiabetic Foot

Ulcers develop in feet Ulcers develop in feet

These are foul smelling and These are foul smelling and become infected with become infected with bacteriabacteria

CataractCataract

Lens of the eye becomes Lens of the eye becomes opaqueopaque

Due to Due to glycationglycation of lens of lens proteinsproteins


Other Complications …..Other Complications …..

Increased incidence of infections like Increased incidence of infections like

•• UTI UTI

•• SSkin kin infectionsinfections

•• Fungal Fungal infections infections

Bone metabolism disordersBone metabolism disorders

Fetal abnormalities in diabetic mothers, etc.Fetal abnormalities in diabetic mothers, etc.



PART - 2

1. Diagonizing Diabetes Mellitus

2. Management of Diabetes Mellitus :

1. Diet & Excersise

2. Oral Medication

3. Insulin

3. Diabetes Management Algorithm

4. Hypo & Hyper Glycemia

5. Preventing & Controling Diabetes Mellitus - What you can do ?


Diagonizing Diabetes Mellitus

PART 2


Tests For Diagnosing Diabetes Tests For Diagnosing Diabetes

Tests involving measurement of glucose levels Tests involving measurement of glucose levels

include:include:

Fasting blood glucose [ FBG ]Fasting blood glucose [ FBG ]

Post Post PrandialPrandial Blood Glucose [ PPBG ]Blood Glucose [ PPBG ]

GlycosylatedGlycosylated HaemoglobinHaemoglobin { { HbHb AA1C 1C } levels} levels

Glucose Tolerance Test { in selected cases }Glucose Tolerance Test { in selected cases }

Other tests include:Other tests include:

Urine analysis Urine analysis –– for glucose, proteins, for glucose, proteins, ketoneketone bodiesbodies

Other tests for screening of complicationsOther tests for screening of complications


Fasting & PostFasting & Post--PrandialPrandial Blood GlucoseBlood Glucose

FBGFBG [[fastingfasting bloodblood glucoseglucose]] :: levellevel ofof glucoseglucose inin bloodblood onon emptyempty stomachstomach (for(for atat leastleast 88 hourshours))

PPBGPPBG [[postpost--prandialprandial bloodblood glucoseglucose]] :: bloodblood glucoseglucose levelslevels atat 22 hourshours afterafter mealsmeals


GlycosylatedGlycosylated HaemoglobinHaemoglobin HbAHbA1C1C

GlycosylationGlycosylation = enzymatic reaction in which glucose binds with a = enzymatic reaction in which glucose binds with a proteinprotein

HaemoglobinHaemoglobin present in the RBCs consists of a pigment ‘present in the RBCs consists of a pigment ‘haemhaem’ ’ and a protein ‘and a protein ‘globinglobin’’

Glucose normally binds with the Glucose normally binds with the globinglobin of the of the HbHb leading to leading to formation of a complex called formation of a complex called glycosylatedglycosylated HbHb

HbAHbAicic is the specific portion [1c] of adult is the specific portion [1c] of adult haemoglobinhaemoglobin [[HbAHbA] ] bound with glucosebound with glucose

Normal levels of HbANormal levels of HbA1c1c are are <6%<6%

In diabetes, due to high levels of glucose in blood, the levels of In diabetes, due to high levels of glucose in blood, the levels of HbAHbA1c1c are raisedare raised

HbAHbA1c 1c is a more sensitive test than plasma glucose measurementis a more sensitive test than plasma glucose measurement


HbAHbA1c1c formationformation

HbAHbA1c1c is the complex formed when glucose is the complex formed when glucose

combines with [the combines with [the globinglobin of] of] haemoglobinhaemoglobin

GLUCOSEGLUCOSE

RBCRBC

GLYCOSYLATED HbGLYCOSYLATED Hb


Diabetes Diabetes Diagnostic CriteriaDiagnostic Criteria

Diabetes Diagnostic Criteria

Condition 2 Hour Glucose

mg/dl Fasting Glucose

mg/dl Hba1c

%

Normal <140 <110 <6.0

Impaired Fasting

Glycaemia <140 ≥110 And <126 6.0–6.4

Impaired Glucose

Tolerance ≥140 < 126 6.0–6.4

Diabetes Mellitus

≥200 ≥126 ≥6.5

Pre

-Dia

be

tes


HbaHba1c 1c and Blood Glucoseand Blood Glucose


Pre-diabetes : people at increased risk of developing

diabetes. People with :

• Impaired fasting glucose (IFG) - fasting blood sugar level is elevated (100 to 125 milligrams per decilitre or mg/dL)

• Impaired glucose tolerance (IGT) - blood sugar level is elevated (140 to 199 mg/dL after a 2-hour oral glucose tolerance test)

Pre-diabetes: Impaired glucose tolerance and impaired fasting glucose


People with pre-diabetes are already at increased risk for other adverse health outcomes such as heart disease and stroke.

Progression to diabetes among those with pre-diabetes is not inevitable.

Studies suggest that weight loss and increased physical activity among people with prediabetes prevent or delay diabetes and may return blood glucose levels to normal.

Pre-diabetes


Management of Diabetes Mellitus


The major components of the treatment of diabetes are:

Management of DMManagement of DM

•• Diet and ExerciseDiet and Exercise AA

•• Oral hypoglycaemic Oral hypoglycaemic therapytherapy BB

•• Insulin TherapyInsulin Therapy CC


Management of DiabetesManagement of Diabetes

The specific aims of treatment for type 2 diabetes are:The specific aims of treatment for type 2 diabetes are:

GlycaemicGlycaemic controlcontrol

•• Diet/lifestyle changesDiet/lifestyle changes •• ExerciseExercise •• MedicationMedication

Treatment of associated conditions Treatment of associated conditions

•• HyperlipidaemiaHyperlipidaemia •• HypertensionHypertension •• ObesityObesity •• CHDCHD

Screening and management of complications Screening and management of complications

•• Cardiovascular diseaseCardiovascular disease •• NephropathyNephropathy •• RetinopathyRetinopathy •• NeuropathyNeuropathy


•• Diet and ExerciseDiet and Exercise AA



The following principles are recommended as dietary guidelines for people with diabetes:

Dietary fat should provide 25-35% of total intake of calories but

saturated fat intake should not exceed 10% of total energy. Cholesterol consumption should be restricted and limited to 300 mg or less daily.

Protein intake can range between 10-15% total energy (0.8-1 g/kg of desirable body weight). Requirements increase for children and during pregnancy. Protein should be derived from both animal and vegetable sources.

Carbohydrates provide 50-60% of total caloric content of the diet. Carbohydrates should be complex and high in fibre.

Excessive salt intake is to be avoided. It should be particularly restricted in people with hypertension and those with nephropathy.

Dietary GuidelinesDietary Guidelines


•• Regulating Regulating intake of carbohydrates and fatintake of carbohydrates and fat

•• Reducing weight if obeseReducing weight if obese

•• ExerciseExercise

•• Dietary adjuncts to reduce absorption of Dietary adjuncts to reduce absorption of carbohydrates e.g. guar gum etc.carbohydrates e.g. guar gum etc.

A. Diet & Lifestyle ManagementA. Diet & Lifestyle Management


Goals Goals of eating right of eating right ::

Weight control & reducing body fat

Blood glucose control

Prevent and manage short-term & long-term complications of diabetes

Providing nutritional requirements


Slimming tipsSlimming tips

Be realistic about your target weight

Aim to lose weight gradually

Eat regular meals

Make small changes you can stick to


Physical activity promotes weight reduction and improves insulin sensitivity, thus lowering blood glucose levels.

Together with dietary treatment, a programme of regular physical activity and exercise should be considered for each person. Such a programme must be tailored to the individual’s health status and fitness.

People should, however, be educated about the potential risk of hypoglycaemia and how to avoid it.

Exercise Exercise


1. SALT: You get enough salt from vegetables in inorganic form, so reduce the intake of extra salt.

2. SUGAR: Sucrose, a table sugar, provides nothing but calories and carbohydrates. Substitute sucrose with natural sugar, like honey, jaggery (gur), etc.

3. FAT: Excessive fat intake is definitely not a good habit. Try and exclude fried items from the diet But, remember, a small quantity of oil is needed to absorb fat-soluble vitamins, especially vitamin E.

4. WHOLE MILK AND PRODUCTS: Try to switch to low fat milk and its products like yogurt (curd).

5. WHITE FLOUR (MAIDA) AND ITS PRODUCTS: Replace these with whole grains, whole wheat (ATTA) or soya breads and unpolished rice.

6. FOODS WITH A HIGH CARBOHYDRATE (SUGAR) CONTENT: Avoid white rice, potatoes, carrots, breads and banana – they increase the blood-sugar levels.

Foods to Avoid/Reduce intake of :Foods to Avoid/Reduce intake of :


Recommended Recommended food food for diabeticsfor diabetics

Bitter gourd (karela) This vegetable contains a high dosage of 'plant insulin'.

It lowers the blood sugar levels effectively.

Have the juice of three to four karelas early morning on an empty stomach.

As a vegetable, too, it can be taken on a regular basis.

Powder the seeds of karela (measuring 1 teaspoon), mix with water and drink it.

Fenugreek (methi) It is the most common food used to control diabetes.

Gulp a teaspoonful of these seeds with a glass of water daily.

Soak the seeds overnight. Have the water in which the seeds were soaked.

You can make a chutney with methi seeds. You can also eat them sprouted, dried and powdered, or mix them in wheat flour to make chapattis.


Recommended foods for diabeticsRecommended foods for diabetics

Indian blackberry (jamun)

This fruit is very effective in preventing and controlling diabetes.

Powder the stone of the fruit and eat it -- it contains glucoside, which prevents the conversion of starch into sugars.

Garlic

This is used to lower blood-sugar levels. Garlic is rich in potassium and replaces the potassium which gets lost in urine. It also contains zinc and sulphur, which are components of insulin. Take about three to four flakes of freshly crushed garlic daily.

Onion

Because of its diuretic and digestive properties, onion works against diabetes. Raw onion is more useful.



Flaxseed

This is the richest source of Omega 3 fatty acids. It helps control diabetes because it maintains the sensitivity of the cell membrane, facilitates insulin, and thereby the uptake of glucose by the cells.

Fibre

Soluble fibre, found in apples, kidney beans (rajma), oatmeal, soyabean, etc, help control diabetes.

These aid slow digestion and absorption of nutrients, resulting in a slow and steady release of glucose.

They soak up excess bile acids found in the intestinal tract, the same acids that are converted to blood cholesterol.

They also help empty the stomach and bring about a feeling of satisfaction that can help Type 2 diabetics to achieve weight loss goals.



Cinnamon solution

Water extracts of cinnamon have been found to promote glucose metabolism and reduce cholesterol. You can boil cinnamon sticks in water and drink this water.

Antioxidants

Diabetes is often associated with conditions like heart disease, diabetic retinopathy, immune deficiency and

kidney disease. Many are caused by free radical damage. Therefore, make sure you include foods containing antioxidants, like amla, fresh seasonal fruits, pomegranates and green/black tea in your diet.


•• Oral hypoglycaemic Oral hypoglycaemic therapytherapy BB



B. B. Oral AntiOral Anti--Diabetic AgentsDiabetic Agents

These drugs depend on endogenous supply of insulinThese drugs depend on endogenous supply of insulin

Include various classes like:Include various classes like:

•• SulphonylureasSulphonylureas (Insulin (Insulin SecretagoguesSecretagogues))

•• BiguanidesBiguanides

•• --glucosidaseglucosidase inhibitorsinhibitors

•• MeglitinidesMeglitinides

•• ThiazolidinedionesThiazolidinediones

Used as adjunct to dietary and lifestyle modificationsUsed as adjunct to dietary and lifestyle modifications

Used as Used as monotherapymonotherapy or in combinationor in combination


If glycaemic control is not achieved (HbA1c > 6.5% and/or; FPG > 7.0 mmol/L or; RPG >11.0mmol/L) with lifestyle modification within 1 –3 months, ORAL ANTI-DIABETIC AGENT should be initiated.

In the presence of marked hyperglycaemia in newly diagnosed symptomatic type 2 diabetes (HbA1c > 8%, FPG > 11.1 mmol/L, or RPG > 14 mmol/L), oral anti-diabetic agents can be considered at the outset together with lifestyle modification.

B. Oral B. Oral AntiAnti--Diabetic Diabetic MonotherapyMonotherapy


First line therapy:

Obese type 2 patients, consider use of metformin, acarbose or TZD.

Non-obese type 2 patients, consider the use of metformin or insulin secretagogues

Metformin is the drug of choice in overweight/obese patients. TZDs and acarbose are acceptable alternatives in those who are intolerant to metformin.

If monotherapy fails, a combination of TZDs, acarbose and metformin is recommended. If targets are still not achieved, insulin secretagogues may be added.

B. Oral B. Oral AntiAnti--Diabetic Diabetic MonotherapyMonotherapy


Combination oral agents is indicated in:

Newly diagnosed symptomatic patients with HbA1c >10

Patients who are not reaching targets after 3 months on monotherapy

B.2 Combination Oral B.2 Combination Oral AgentsAgents


If targets have not been reached after optimal dose of combination therapy for 3 months, consider adding intermediate-acting/long-acting insulin (BIDS).

Combination of insulin+ oral anti-diabetic agents (BIDS) has been

shown to improve glycaemic control in those not achieving target despite maximal combination oral anti-diabetic agents.

Combining insulin and the following oral anti-diabetic agents has

been shown to be effective in people with type 2 diabetes: ◦ Biguanide (metformin) ◦ Insulin secretagogues (sulphonylureas) ◦ Insulin sensitizers (TZDs)(the combination of a TZD plus insulin is not an

approved indication) ◦ α-glucosidase inhibitor (acarbose)

Insulin dose can be increased until target FPG is achieved.

B.3 Combination Oral B.3 Combination Oral & & InsulinInsulin


How do How do SulphonylSulphonyl UreasUreas act?act?

SUs stimulate the SUs stimulate the --cells of the pancreas and cells of the pancreas and

increase the secretion of insulinincrease the secretion of insulin

In longIn long--term, they also improve insulinterm, they also improve insulin--sensitivitysensitivity

Useful for management of type 2 DM especially in Useful for management of type 2 DM especially in

nonnon--obese patientsobese patients

Main adverse effects include: Main adverse effects include:

risk of hypoglycaemia, weight gainrisk of hypoglycaemia, weight gain


Examples of Examples of SulphonylSulphonyl UreasUreas

FIRST GENERATIONFIRST GENERATION

ChlorpropamideChlorpropamide

TolbutamideTolbutamide

TolazamideTolazamide, etc., etc.

SECOND GENERATIONSECOND GENERATION

GlibenclamideGlibenclamide

GliclazideGliclazide

GlipizideGlipizide GlipizideGlipizide extended releaseextended release

GlimepirideGlimepiride, etc., etc.

Second generation Second generation sulphonylureassulphonylureas are more potent than first are more potent than first generationgeneration

GlibenclamideGlibenclamide should be avoided in elderly and should be avoided in elderly and renallyrenally impairedimpaired

GliclazideGliclazide has beneficial has beneficial antiplateletantiplatelet effectseffects


How do How do BiguanidesBiguanides act ?act ?

BiguanidesBiguanides have peripheral actions only. i.e.,have peripheral actions only. i.e.,

Reduce hepatic glucose outputReduce hepatic glucose output

Enhance action of insulin on peripheral cellsEnhance action of insulin on peripheral cells

Increases glucose utilization by peripheral cellsIncreases glucose utilization by peripheral cells

No effect on pancreas or insulin secretionNo effect on pancreas or insulin secretion

ee.g.g. . MetforminMetformin

Main adverse effects: Main adverse effects:

GI disturbances, GI disturbances, lactoacidosislactoacidosis


What are What are --GlucosidaseGlucosidase Inhibitors?Inhibitors?

Agents which inhibit enzyme Agents which inhibit enzyme --glucosidaseglucosidase in the in the

intestines and prevent absorption of carbohydratesintestines and prevent absorption of carbohydrates

Help in reducing the post Help in reducing the post prandialprandial rise in glucoserise in glucose

ee.g.g. . AcarboseAcarbose, , VogliboseVoglibose

Used as adjunct to diet controlUsed as adjunct to diet control


How do How do MeglitinidesMeglitinides act?act?

MeglitinidesMeglitinides stimulate insulin secretion from stimulate insulin secretion from

pancreas by causing closure of ATPpancreas by causing closure of ATP--sensitive Ksensitive K++

channels in channels in --cellscells

Effectiveness depends on number of Effectiveness depends on number of --cells cells

presentpresent

ee.g.g. . RepaglinideRepaglinide, , NateginideNateginide

Have a fast onset of actionHave a fast onset of action

Should be used with caution in patients with liver Should be used with caution in patients with liver

dysfunctiondysfunction


How Do How Do ThiazolidinedionesThiazolidinediones Act?Act?

TZDs stimulate PPARs and improve insulin TZDs stimulate PPARs and improve insulin

sensitivitysensitivity

Improve Improve glycaemicglycaemic control and also have control and also have

beneficial effect on lipid profilebeneficial effect on lipid profile

They depend on presence of endogenous insulin They depend on presence of endogenous insulin

for their actionfor their action

ee.g.g. . RosiglitazoneRosiglitazone, , PioglitazonePioglitazone

TroglitazoneTroglitazone was withdrawn because of was withdrawn because of

hepatotoxicityhepatotoxicity


What Are PPARs ?What Are PPARs ?

PPARs = PPARs = PeroxisomePeroxisome ProliferatorProliferator Activated ReceptorsActivated Receptors

PPARs are a subPPARs are a sub--family of nuclear receptorsfamily of nuclear receptors

Activation of PPARs stimulates the transcription of genes Activation of PPARs stimulates the transcription of genes

which are responsible for regulating glucose and fat which are responsible for regulating glucose and fat

metabolismmetabolism

RosiglitazoneRosiglitazone activates PPARactivates PPAR--

PioglitazonePioglitazone activates PPARactivates PPAR-- and PPARand PPAR--


Oral Hypoglycaemic MedicationsOral Hypoglycaemic Medications


In elderly non-obese patients, short acting insulin secretagogues can be started but long acting Sulphonylureas are to be avoided. Renal function should be monitored.

Oral anti-diabetic agents are not recommended for diabetes in pregnancy

Oral anti-diabetic agents are usually not the first line therapy in diabetes diagnosed during stress, such as infections. Insulin therapy is recommended for both the above

Targets for control are applicable for all age groups. However, in patients with co-morbidities, targets are individualized

When indicated, start with a minimal dose of oral anti-diabetic agent, while reemphasizing diet and physical activity. An appropriate duration of time (2-16 weeks depending on agents used) between increments should be given to allow achievement of steady state blood glucose control

General Guidelines for Use of Oral General Guidelines for Use of Oral AntiAnti--Diabetic Agent Diabetic Agent in Diabetesin Diabetes


•• Insulin therapyInsulin therapy CC



When is Insulin used?When is Insulin used?

Exogenous Insulin is Exogenous Insulin is

Essential for treatment of type 1 DMEssential for treatment of type 1 DM

May eventually be required in type 2 DM May eventually be required in type 2 DM where oral where oral antidiabeticantidiabetic agents are not agents are not enough to control glucose levelsenough to control glucose levels

Is used during surgery in diabetics when oral Is used during surgery in diabetics when oral drugs are withheld for sometimedrugs are withheld for sometime


Insulin SourcesInsulin Sources

SourcesSources

Bovine Bovine & Porcine & Porcine –– not used todaynot used today

HumanHuman

Recombinant/syntheticRecombinant/synthetic

Depending on duration of action :Depending on duration of action :

Short actingShort acting

Intermediate actingIntermediate acting

Long Long actingacting

CombinationCombination


Recombinant InsulinRecombinant Insulin


Where is insulin injected?Where is insulin injected?


Short-term use:

Acute illness, surgery, stress and emergencies

Pregnancy

Breast-feeding

Insulin may be used as initial therapy in type 2 diabetes

in marked hyperglycaemia

Severe metabolic decompensation (diabetic ketoacidosis, hyperosmolar nonketotic coma,

lactic acidosis, severe hypertriglyceridaemia)

Long-term use:

If targets have not been reached after optimal dose of combination therapy or BIDS,

consider change to multi-dose insulin therapy. When initiating this,insulin secretagogues

should be stopped and insulin sensitisers e.g. Metformin or TZDs, can be continued.

Insulin Insulin TherapyTherapy


The majority of patients will require more than one daily injection if good glycaemic control is to be achieved. However, a once-daily injection of an intermediate acting preparation may be effectively used in some patients.

Twice-daily mixtures of short- and intermediate-acting insulin is a commonly used regimen.

In some cases, a mixture of short- and intermediate-acting insulin may be given in the morning. Further doses of short-acting insulin are given before lunch and the evening meal and an evening dose of intermediate-acting insulin is given at bedtime.

Other regimens based on the same principles may be used.

A regimen of multiple injections of short-acting insulin before the main meals, with an appropriate dose of an intermediate-acting insulin given at bedtime, may be used, particularly when strict glycaemic control is mandatory.

Insulin Insulin regimensregimens


Overview of Insulin and ActionOverview of Insulin and Action



Diabetes Management Algorithm


Diabetes Management

Algorithm


Combination Therapy in DiabetesCombination Therapy in Diabetes

Diabetes is a progressive disorderDiabetes is a progressive disorder

Type 2 diabetics eventually require combinations Type 2 diabetics eventually require combinations of of antidiabeticantidiabetic drugs for effective drugs for effective glycaemicglycaemic controlcontrol

The additional agents are added in a stepwise The additional agents are added in a stepwise manner depending upon the quality of control of manner depending upon the quality of control of diabetic conditiondiabetic condition

The drugs used in Combinations have additive The drugs used in Combinations have additive action and offer a better action and offer a better glycaemicglycaemic controlcontrol


Commonly Used Regimens Commonly Used Regimens in in DiabetesDiabetes

SulphonylureaSulphonylurea or or MeglitinideMeglitinide + + MetforminMetformin or or ThiazolidinedioneThiazolidinedione

SulphonylureaSulphonylurea + + --glucosidaseglucosidase inhibitorinhibitor

Insulin + Insulin + MetforminMetformin or or ThiazolidinedioneThiazolidinedione

MetforminMetformin + + ThiazolidinedioneThiazolidinedione


Hypo & Hyper Glycemia


Hyperglycemia Hypoglycemia

• When controlling diabetes, blood sugar can become too high or too low. These conditions should be taken seriously. Fortunately, one can easily re-establish control of blood sugar.

• When there is too much sugar in the blood, this condition is called hyperglycemia. Hyper is Latin and means "more." Glycemia is also Latin and means "sugar in the blood."

• Hyperglycemia is caused by eating too much food, eating sugary foods, or by not taking one’s medication. It can also occur when one is sick. If not treated, hyperglycemia can lead to a coma.


• Hypoglycemia occurs when too little sugar is present in the blood. Hypo is Latin and means "less."

• Hypoglycemia usually occurs with patients who take insulin or other medications.

• Taking too much insulin can cause it. That is why it is also known as insulin shock.

• Hypoglycemia can also be caused when the food intake is reduced or a meal is skipped. . Signs of low blood sugar, or hypoglycemia .



• If not treated, low blood sugar can lead to fainting or seizures. Diabetics experience different signs when their blood sugar is low and they learn to recognize these signs.

• Some patients do not experience any signs when their blood sugar is low. These patients must depend on blood sugar testing to find out if they have hypoglycemia..



Symptoms of Hypoglycemia


If you sugar is 70 or lower you should treat it with….

½ a glass of juice

¼ glass of soft drink

2 or more glucose tablets if necessary

Treatment of Treatment of low blood low blood sugarsugar


Symptoms of HyperglycemiaSymptoms of Hyperglycemia


If your sugar is above 240 you should do the followings:

Drink lots of sugar-free fluids like water or diet drinks

Eat the right food and the right amounts

Check your blood sugars more often

Check keytones if over 240

Call doctor or nurse if you have a positive keytones

Treatment of high Treatment of high blood blood sugarsugar


Summing Up

Preventing & Controling Diabetes Mellitus

What you can do ?


Be physical active….

Eat a healthy diet

Abcs(know and control) Hb1ac, blood pressure, cholesterol, and smoking

Take your medication

B.E.A.T. DIABETESB.E.A.T. DIABETES


Getting regular medical careGetting regular medical care

Schedule for routine medical care

Once (repeat at age 65) Pneumococcal vaccine

1 time/year Flu shot

1 time/year Urine microalbumin/

creatinine ratio

2 times/year Dental exam

At least 1 time/year Foot exam

1 time/year Dilated eye exam

At least every other year Cholesterol

At least 2 times/year Blood pressure

2-4 times/year HbA1c


A – A1c, or hemoglobin A1c test. ADA goal is 7% or less.

AACE goal is 6.5% or less.

B – Blood pressure < 130/80 mmHg for non-pregnant adults.

C – Cholesterol HDL (good) cholesterol – >40 mg/dl (men);

>50 mg/dl (women)

LDL (bad) cholesterol – <100 mg/dl

Triglycerides – <150 mg/dl

ABC of Diabetes CareABC of Diabetes Care


Recap Recap -- Diabetes Diabetes can be controlled by can be controlled by

Healthy diet may include changing what one eats, quantities, and how often. Exercise helps diabetic patients in many ways - lowers glucose levels, helps weight loss, maintains a healthy heart and healthy circulation. In addition, exercising helps relieve stress and strengthens muscles. Blood/urine sugar testing is important in order to find out if the sugar level is where it should be. If the blood/urine sugar is too low or too high, a change in diabetes medication, diet, or exercise may be needed. Blood sugar should be checked often. In cases of very high blood sugar levels that do not respond to diet and exercise plans, medications may be needed. If insulin is needed, it can only be injected. Insulin is needed for all patients with Type 1 diabetes and for some patients with Type 2 diabetes.


Patients should be educated to practice self-care. This allows the patient to assume responsibility and control of his / her own diabetes management. Self-care should include:

• Blood glucose monitoring

• Body weight monitoring

• Foot-care

• Personal hygiene

• Healthy lifestyle/diet or physical activity

• Identify targets for control

• Stopping smoking

SelfSelf--CareCare


Avoid diabetic productsAvoid diabetic products

Cost

Laxative effects

Focus on ‘sugar free’

Still raise blood glucose levels

Still contain same calories

Good News for Type 1 Diabetes


Thank You

Queries ?

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