diabetes mellitus pwr pt

7/29/2019 Diabetes Mellitus Pwr Pt

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Diabetes Mellitus

It is a metabolic diorder characterized

by hyperglycaemia, glycosuria, hyper

lipaemia, negative nitrogen balanceand sometimes ketonaemia.

Hallmark of DM:

Polyuria, Polydipsia, Polyphagia


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Types Of DM

Type I DM

Previously called Insulin Dependent Diabetes

Mellitus (IDDM) or Juvenile onset diabetes.

Type II DM

Previously called Non InsulinDependant Diabetes Mellitus (NIDDM)


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Type 1 DM

Previously called Insulin Dependent Diabetes Mellitus(IDDM) or Juvenile onset diabetes.

Absolute lack of insulin & regular injections ofinsulin are needed to save life.

Type I A Autoimmune

Type I B Idiopathic viral


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TypeII DM

Previously called Non Insulin DependantDiabetes Mellitus (NIDDM)

Characterized by variable degrees of insulin

resistance, impaired insulin secretion, and

increased glucose production.

90-95% of diabetics are of type II


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Complications

Microvascular Complications1) Diabetic Retinopathy2) Diabetic Nephropathy - Due to accumulation ofsorbitol3) Diabetic Neuropathy - Due to demyelination ofaxons

Macrovascular Complication1) Coronary artery disease2)Peripheral vascular disease3)Cerebrovascular disease


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Diagnosis

FBSL = 126 mg/dl DM

RBSL >= 200 mg /dl DM

PPBSL =200 mg/dl DM


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Diagnosis

Glycosylated haemoglobin HbA1c provides

an integrated measure of control over the life

span of red cells approximately 120 days.

HbA1c < 7%

The rate of glycosylation in RBC is directly

proportional to glucose concentration.


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History of Insulin

In 1921 Banting, Canadian Surgeon & Best,

fourth year medical student discovered insulin.

In 1923 noble prize was awarded to Banting &

Best


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Pharmacological actions

Insulin affects all three main sources of

metabolic energy - carbohydrates, fats and

proteins. Actions involve three principal

tissues liver, muscle, adipose tissue.

Causes reduction in blood sugar and facilitates

the uptake, utilization and storage of glucose,

amino acids and fats after a meal


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Carbohydrate metabolism:1. Decreases gluconeogenesis2. Decreases glycogenolysis3. Increases glycolysis (liver, muscles)

4. Increases glycogenesis (liver, muscles)5. Increases glucose uptake (fat, muscles)

Fat metabolism:

6. Increases lipogenesis7. Decreases breakdown of triglycerides8. Increases TG synthesis


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Protein metabolism9. Decreases protein breakdown

10. Decreases amino acid uptake

11. Increases protein synthesis


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Preparation of insulin

1) Conventional

Produced from Beef or Pork pancreas.

Beef insulin differs by 3 amino acid

Pork insulin differs by 1 amino acid

Thus pork insulin being more homologous to human insulin is lessimmunogenic than beef insulin.

They contain~1% (10,000 ppm) of other proteins which are potentiallyantigenic


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Preparations of insulin

2) Purified insulin

a) Single peak insulin

Purified by gel filtration; reduces content of proinsulin but will

not significantly reduce the content of insulin derivatives orpancreatic peptidase.

b) Monocomponent (highly purified) insulin Purified by

both gel filtration and further by ion-exchange chromatography;further decreases proinsulin & also reduces contamination byinsulin derivatives or pancreatic peptides.


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3) HUMAN INSULIN

Not obtained from human pancreas, but is obtained by :

Recombinant DNA technology in E coli- proinsulin recombinant bacterial (prb)

Yeast- precursor yeast recombinant (pyr)

Enzymatic modification of porcine insulin (emp)


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4) Insulin analogues

Produced using recombinant DNA technology but

differ from human insulin in amino acid sequence.

Binds to insulin receptors & act on them like

insulin.

They do not aggregate in solutions

Insulin Lispro, Insulin Aspart, Insulin Glulysine, Insulin Glargine,Insulin Detemir


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Rapid acting

Insulin LisproProduced by reversing prolin lysine at the carboxy terminus B28

& B29 positions.

Insulin AspartThe proline at B28 of human insulin is replaced by asparticacid.

Insulin Glulysine

Glutamic acid replaces lysine at B29 & lysine replacesasparagines at B3


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Rapid acting

Advantages

Rapid absorption from subcutaneous tissue &

shorter duration of action compared to regular

insulinUseful in controlling hyperglycaemia that

occurs immediately after meals.

Hypoglycaemia is less.Glucose control as assessed by HbA1c is

significantly improved


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Rapid acting

Rapid acting are injected 15 mins before

meal.

Rapid acting & SA insulin is the only form

of hormone that is used in SCI pumps.

Used in combination with LA insulin to provideimmediate insulin following a meal & to maintain a

baseline level of insulin between 2 meals.


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Short acting insulins

Regular (soluble) insulin

It is a soluble crystalline zinc insulin. In solution, these ashexamers but as the drug is diluted by interstitial fluid

the hexamers breakdown into dimers & finally asmonomers which have a faster absorption. Regularinsulin is injected 30-45 mins before meals SC to contropost prandial hyperglycaemia in combination with anintermediate or LA preparations.


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Short acting insulin

Indications for IV infusions

Ketoacidosis

Perioperative period

During labour & delivery

Intensive care situations


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Intermediate acting insulin

Neutral Protamine Hagedorn (NPH) or isophane insulin

Has a Neutral pH , contain Protamine & was

developed by Hagedorn. It is a suspension of insulin incomplex with zinc & protamine.

Lente insulin


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NPH

After SC injection , proteolytic tissue enzymes

degrade the protamine slowly to permit

sustained absorption of insulin.

NPH does not retard action of regular insulin

when the 2 are mixed vigorously or when they

are available commercially.


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Lente Insulin

Mixture of 30% semilente

(relatively rapid onset of action) +

70% ultralente

(delayed onset & prolonged duration of action).

Relatively rapid absorption with

sustained & prolonged action make lente

insulin useful & most commonly used

insulin.


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Long acting

Ultralente Protamine zinc insulin

Glargine Detemir

They have a slower onset & a prolonged peak ofaction. Provide a low basal concentration ofinsulin throughout the day.


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Long acting

Ultralente insulin

Cloudy zinc suspension at neutral Ph in acetate buffer

Large insulin zinc crystals , dissolves slowly at the site

of action .

It is usually combined with semilente preparation &

is administered sc


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Long acting

Protamine zinc insulin

Rarely used because of its very unpredictable &

prolonged course of action.


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Insulin glargine

Slow & long acting peak less.

Asparagine is replaced by glycine at A21, an twoarginine residues are added to the C-terminus of the Bchain.Lower incidence of nocturnal hypoglycemia.

Has an acidic pH and hence should not be mixed withother insulins which have a neutral pH.

Injection can be painful, given once daily or bd.


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Insulin detemir

New basal insulin analogue.

Terminal threonine is dropped from B30

position and a saturated fatty acid isattached to the

terminal B29 lysine.

More slowly absorbed than other long acting insulins, effect lasts longer (> 24 hours).


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Pharmacokinetics

Insulin is a high molecular weight polypeptide,is rapidly inactivated if administered orally.

Insulin is usually administersd SC

Administered IV in emergency. Monomers are absorbed faster compared to

dimers or hexamers.

Liver & kidney are the principal sites ofhormone uptake & degradation. Plasma t1/2 is


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Pharmacokinetics

Insulin released from the pancreas & circulatingin plasma is in the monomeric form which ishighly diffusible & biologically active.

Therapeutically used insulin preparation containinsulin in tetrameric or hexameric form whichare minimally diffusible; hence monomericinsulin must first be released from the injected

insulin , thus delaying its onset of action


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Pharmacokinetics

Addition of zinc & / protamine slows down

its absorption & prolongs its DOA .

Absorption of SC insulin is fastest from theabdominal wall is less rapid from the arm &

least rapid from the thigh.


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Adverse Effects

1)Hypoglycaemia2)Counter regulatory sympatheti stimulation

Sweating, Anxiety, Palpitation, Tremor

3)Deprivation of brain of glucose- Dizziness,headache, behavioural changes, visualdisturbances, hunger fatigue, weakness, &sometimes fall in BP

Treatment : glucose oral or iv


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Somogyi effect

An unrecognized hypoglycemic episodeduring night is followed by rebound

hyperglycemia with glycosuria next morning.

Post hypoglycaemic hyperglycaemia.

Dawn phenomenon

Morning hyperglycaemia due to

inadequate insulin dose.


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Adverse Effects

1)Allergy: Urticaria, angioedema may be observed with beef or porkinsulin but rarely with human insulin.

2)Edema

3)Insulin Lipodystrophy

Lipohypertrophy: Spongy lump due to lipogenic property of insulininjected, repeatedly into a given area . It is advisable to rotatethe injection site.

Lipoatrophy: Loss of fat tissue due to allergic reaction seen with

conventional insulin preparation. Inject human insulin at theborders of the lipoatrophic area. Resolution may tak as muchas 4-6 months.


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Drug interactions

1) Beta adrenergic blockers: Prolong hypoglycemia by inhibitingcompensatory mechanisms ( B1 selective agents are less liable).

Warning signs of hypoglycemia like palpitation, tremor andanxiety are masked.

2) Thiazides, furosemide, corticosteroids, oral contraceptives,salbutamol, nifedipine tend to raise blood sugar and reduceeffectiveness of insulin.

3) Acute ingestion of alcohol can precipitate hypoglycemia bydepleting hepatic glycogen.

4) Salicylates, lithium and theophylline may also accentuatehypoglycemia by enhancing insulin secretion and peripheralglucose utilization


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Indications

1) Type I DM insulin is must.

NPH insulin is often combined with a SA regular insulin& is administered SC before meals.

Dose 0.4-0.8 U/kg/day2)Type II DM

Primary or secondary failure of OHA.Temporarily to

tide over infections,Trauma, Surgery, Perioperativeperiod,Pregnancy & duringlabour


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Indications

Any complications of DM

Ketoacidosis,

Non ketotic hyperosmolar coma & Gangrene of the extremities.

Dose 0.2-1.6 U /kg/day


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Insulin resistance

When insulin requirement is

increased

Conventionally > 200 U/day, but Physiologically > 100 U/ day,

insulin resistance is said to have developed.


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Insulin resistance

Acute :It develops rapidly and is usually a

short term problem.

Causes : Infection, trauma, Surgery & stress.Corticosteroids and other hyperglycaemic

hormones may be produced in excess as a

reaction to the stress & oppose insulin action.


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Insulin resistance

Ketoacidosis

Ketone bodies and FFA inhibit glucose uptakeby brain and muscle.

Treatment is to overcome the precipitating causeand to give highdoses of regular insulin.Theinsulin requirement comes back to normal once

the condition has been controlled.


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Insulin resistance

Chronic

This is generally seen in patients treated for years with

conventional preparations of beef or pork insulins.

Antibodies to homologous contaminating

proteins are produced which also bind insulin.

It is more common in type 2 M.


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Insulin resistance

Switch over to the more purified newer preparations.

Respond well to pork or human insulin.

After instituting highly pure preparations,insulin requirement gradually declines

over weeks and months.

Majority of patients stabilize at 60 U/ day.


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Diabetic ketoacidosis (Diabetic coma)

Ketoacidosis:Generally occurs in Type I DM.

It is infrequent in type 2 DM.

Causes are : Infection, Trauma, Stroke,Pancreatitis, Stressful conditions and Inadequatedoses of insulin.

Cardinal Features are : Vomiting,Hyperventilation, Dehydration, Hypotension,Impaired consciousness.


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Treatment Of DKA

1)Insulin :Regular insulin is used to rapidlycorrect the metabolic abnormalities. A bolusdose of 0.1-0.2U/kg IV is followed by0.1U/kg/hr infusion. Usually, within 4-6 hoursblood glucose reaches 300 mg/ dl. Then the rateof infusion is reduced to 2-3/hr.

2) Intravenous fluids:It is vital to correct

dehydration. Normal saline is infused IV initially at therate of 1 L/hr, reducing progressively to 0.5L/4 hours.After the blood sugar has reached 300mg/dl 5%glucose in NS is administered.


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Treatment Of DKA

3) KCL:Though K may be lost in urine duringketoacidosis, serum K is usually normal due toexchange with intracellular stores.When insulin

therapy is instituted ketosis subsides and K is drivenintracellularly dangerous hypokalemia can occur.After4 hours it is appropriate to add 10-20 m Eq/hr KClto the IV fluid.

4) Sodium bicarbonate:It is not routinely needed.Acidosis subsides as ketosis is controlled. If acidosis isnot corrected 50 mEq of sod. bicarbonate is added


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Treatment Of DKA

5) Antibioticsand other supportive measure and

treatment of precipitating cause must be

instituted simultaneously.

Newer insulin delivery devices:

Made to improve ease and accuracy of insulinadministration & to achieve tight glycaemiacontrol.


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Newer insulin delivery devices

1. Insulin syringes :Prefilled disposible syringescontain specific types or mixtures of regular &modified insulins.


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2. Pen devices

Fountain pen like use insulin cartridges for s.c.injection through a needle. Preset amounts (in 2

U increments)are propelled by pushing aplunger; convenient in carrying and injecting.


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3. Inhaled insulin

The fine powder is delivered through a nebulizer.Absorption is rapid. It is used to control

mealtime glycaemia. Pulmonary fibrosis andother complications are apprehended on long-term use.


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4) Insulin pump

Portable infusion devices connected to a subcutaneouslyplaced cannula : provide 'continuous subcutaneous

insulin infusion (CSII). Only regular insulin is used.5)Implantable pumps:

Consist of an electromechanical mechanism whichregulates insulin delivery from a percutaneouslyrefillable reservoir. Mechanical pumps, fluorocarbonpropellant and osmotic pumps are being developed


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External artificial pancreas

Other routes

Intra peritoneal

Oral

Rectal


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Classification

Oral hypoglycaemic agents

1) Insulin secretagogues: Sulphonylureas,Meglitinides

Sulphonylureas

First Generation: Tolbutamide, Chlorpropamide

Second Generation: Glibenclamide, Glipizide,Gliclazide, Glimepiride


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Meglitinide (Phenyl Alanine

analogues): Repaglinide, Nateglinide

2) Biguanides: Metformin

3)Thiazolidinediones (Glitazones):Rosiglitazon, Pioglitazone


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4) Alpha Glucosidase Inhibitors:

Acarbose, Voglibose, Miglitol

5) Aldose Reductase Inhibitors:

Tolrestat, Epalrestat, Zopolrestat

6) Miscellaneous: Guargum


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7) Newer Drugs

Incretin mimetics : Exenatide

Amylin agonists : Pramlintide

Dipeptidyl peptidase4 inhibitors

Sitagliptin

Vildagliptin


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Sulphonylureas

MOA: Main action is on beta cells. Stimulatesinsulin secretion & thus reduces blood glucoselevels. SU binds to SU receptors & block ATP

sensitive K channels, reduces permeability of K ,this depolarizes the beta cell & leads to calciumchannel opening. The resulting increased

calcium influx induces degranulation & releaseof insulin.


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Sulphonylureas

Thus these drugs are effective only in patients

having properly functioning pancreatic beta cells.

Increases the number of insulin receptors in liver.

Glimepiride, gliclazide & glipizide increases the

sensitivity of peripheral tissues to insulin.


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Pharmacokinetics

SU are well absorbed after oral administration.

Absorption of glipizide & glimipiride is delayed whengiven with food.

All SU are highly PPB 90-99 %.PPB is least forchlorpropamide & greatest for glyburide.

Chlorpropamide has a long t1/2 of 24-48 hours .

Second generation agents have short t1/2 3-5 hours buttheir hypoglycemic effects are evident for 12-24 hours& often be administered once daily.


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Pharmacokinetics

All SU are metabolized in liver and

excreted in urine.

Thus SU should be administered

with caution to patients with either

renal or hepatic insufficiency.


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Adverse Effects

Less with second generation agents

Hypoglycemia more common with elderly patients withimpaired hepatic & renal function on LA SU.

Non specific side effects nausea, vomiting, flatulence,diarrhoea or constipation & Weight gain.

Hypersensitivity reaction: Rashes, photosensitivity &rarely agranulocytosis

Chlorpropamide: Cholestatic jaundice, Dilutionalhyponatremia, Disulfiram like effect with alcohol


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Disulfiram like effect

Ethyl alcohol

Acetaldehyde

aldehyde dehydrogenase

Acetate

CO2 + H2O


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Drug Interactions

Drugs that enhance sulfonylurea action

(a) Displace from protein binding:Phenylbutazone,sulfinpyrazone, salicylates, sulfonamides,

(b) Inhibit metabolism/excretion:Cimetidine,sulfonamides, warfarin, chloramphenicol.

(c) Synergise with or prolong pharmacodynamic action:

Salicylates, propranolol , sympatholytic, antihypertensives, lithium, theophylline, alcohol (byinhibiting gluconeogenesis).


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Interactions

Drugs that decrease sulfonylurea action

(a) Induce metabolism

Phenobarbitone, phenytoin, rifampicin.

(b) Opposite action/ suppress insulin release

Corticosteroids, diazoxide, thiazides,

furosemide, oral contraceptives.


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Indication

Type II DM who cannot achieve appropriate

control with changes in diet alone.

Less effective in severely obese type II DM

possibly because of:

1) Insulin resistance that often accompanies obesity.

2) SU causes weight gain due to fluid retention &edema.


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Contraindications

Pregnancy & gestational DM

SU crosses placental barrier & may cause

foetal hypoglycemia or hypoglycemia at

birth.

Lactation

SU is secreted in milk


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Dose

Glibenclamide : 2.515 mg od / bd

Glipizide : 2.5 - 20 mg od / bd

Gliclazide : 40 - 240 mg od /bd

Glimepiride : 18 mg od

Taken 30 mins before meals


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Meglitinide

Repaglinide, NateglinideNon sulfonylurea drug, has similar MOA as SU on the

beta cell SU receptor. Binds to SUR blocks ATPsensitive K channel depolarization insulin release.

Repaglinide induces rapid onset short lasting insulinrelease.It is administered before each major meal to control post

prandial hyperglycemia , in type II DM, inadequatelycontrolled with diet & exercise as an alternative to SUor to supplement metformin or LA insulin.

Dose should be omitted if a meal is missed


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Pharmacokinetics

Rapidly & completely absorbed from GIT. t 1/21 hour & DOA 2-4 hours

Repaglinide cleared by liver ideal choice in

patients with renal impairment.Nateglinide cleared by renal mechanism.

DOSE

Repaglinide 0.5-16 mg immediately before meals.

Nateglinide 60-120 mg immediately before meals.


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Adverse effects

Hypoglycemia lower risk because ofshort lasting action.

Weight gain

Allergic reactions

Headache , dyspepsia & arthralgia


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Biguanides

Metformin

Phenformin

Banned in India in 2003 due to lactic acidosis


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MOA Of Biguanides

Anti hyperglycemic & not hypoglycemic agents.

Do not cause insulin release from pancreas butpresence of some insulin is essential for their

action . Suppress hepatic neo glucogenesis &glucose output from liver.

Enhance insulin mediated glucose disposal in

muscle & fat.Retard intestinal absorption of glucose.


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Unlike SU Biguanides

1. Do not lower blood glucose levels in normal persons.

2. Do not stimulate insulin release, so do not depend on

functional pancreatic beta cells for its action.

3. Can be given to obese patients as it do not cause weight

gain . Do not stimulate appetite causes anorexia &

weight loss


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Pharmacokinetics

t1/2 is 2-3 hours & DOA 6-10 hours

Not bound to PP

Not metabolised & is excreted unchanged by the

kidneys.

In renal insufficiency the active compound can

accumulate & increase the risk of lactic acidosis


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Adverse effects

Anorexia, nausea, vomiting, metallic tastediarrhoea, epigastric fullness & constipation .

Long term use may decrease absorption ofvitamin B12.

Lactic acidosis though a rare problem yet

patients of renal or hepatic disease &

alcohol ingestion are predisposed to it.


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Indications

Obese Type II DM as monotherapy

or concomitantly with other oral anti

diabetics (SU, thiazolidinediones)

Polycystic ovarian disease

Enhances fertility


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Dose

500 mg tablet with breakfast

500 mg tablet with evening meal

Twice or thrice daily.

Maximum dose : 2500 mg daily


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Thiazolidinediones (glitazones)

Rosiglitazone

Pioglitazone

Troglitazone

Introduced in 1998 was withdrawn from themarket in 2000 because of hepatotoxicity


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MOA Of Thiazolidinediones

Selective agonists for the nuclear PeroxisomeProliferator Activated Receptor gamma (PPARgamma) which enhances the transcription of

several insulin responsive genes.PPAR gamma is mainly found in adipocytes,myocytes & hepatocytes Stimulates GLUT 4expression & translocation so entry of glucose

into muscle & fat improves.Hepatic gluconeogenesis is suppressed.

T d d


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Thiazolidinediones

Decreases HbA1c levels.

Pioglitazone lowers while rosiglitazone

elevates TG levels.

Act synergistically with SU, metformin &

insulin.

Ph ki i


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Pharmacokinetics

Onset delayed may take several

weeks for maximal effect.

Eliminated as metabolites in urine & faeces.

Drug enzyme inducers.

Ad ff


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Adverse effects

1)Weight gain due to fluid retention & edema.2)Headache , myalgia & mild anaemia.

3)Hepatoxicity is rare yet regular LFT are advisable

CHF may be ppt or worsened.4)Anovulatory women may resume ovulation

(polycystic ovary syndrome), Anovulatory due to

insulin resistance.


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Drug interactions

1)Failure of OCP may occur during Pioglitazone therapy.

2)Ketoconazole inhibits metabolism of

pioglitazone.

CONTRAINDICATIONS:

1)Liver disease2)CHF

I di i


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Indications

Type II DM exhibiting substantial amount of insulinresistance i.e. who require high doses of insulin ( > 100

u/day)

However insulin sensitizing action of glitazones takesseveral weeks to develop

If a glitazone is to be added to the diabetic regimen, thedosage of SU or insulin s/b decreased to compensatefor any enhanced insulin sensitivity.

D


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Doses

Pioglitazone : 15-45mg daily orally.

Rosiglitazone : 2-8 mg daily orally.

Al h l id i hibi


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Alpha glucosidase inhibitors

Acarbose

Miglitol

Voglibose

MOA


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MOA

Alpha glucosidases facilitate digestion of complexstarches, oligosaccharides & disaccharides intomonosaccharides so that these are absorbed from theSIAcarbose is a complex oligosaccharide which

reversibly inhibits alpha glucosidases , the final enzymefor the digestion of CHO in the brush border of SI.

It slows down & decreases digestion & absorption ofpolysaccharides & sucrose .

Postprandial glycaemia is reduced without increasinginsulin levels. Regular use tends to lower HbA1c ,body

weight & serum TG

Ph ki i


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Pharmacokinetics

Acarbose is minimally absorbed but

miglitol is, however absorbed.

Some part of acarbose is excreted as such

through faeces while a part is metabolized by

intestinal bacterial flora.

Ad ff


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Adverse effects

1)Flatulence2)Diarrhoea.3)Abdominal pain: Due to fermentation of unabsorbed

CHO in lower GIT.

DOSES

Acarbose : 25100 mg tds with first bite ofeach main meal

Miglitol : 25100 mg tds with first bite ofeach main meal


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Alpha glucosidase inhibitors do not stimulate insulinrelease & therefore d/n result in hypoglycaemia.

Hypoglycaemia may occur if used along with SU.

Treat with glucose & not sucrose, because its

breakdown by these drugs is already blocked.

Ald R d t I hibit


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Aldose Reductase Inhibitors

Tolrestat Epalrestat

Zopolrestat

Inhibits aldose reductase enzyme which converts

glucose to sorbitol.

Sorbitol is responsible for complications

of DM like neuropathy & nephropathy.

G G


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Guar Gum

Dietary fibre obtained from Indian cluster beans.Forms viscous gel on contact with water.

Administered before meals, decreases CHO absorption.

Adverse Effects: Flatulence, bloating, diarrhoea & nausea.

Used as an adjunct to oral hypoglycaemics.

Dose : 5 mg tds

I ti


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Incretins

Type of gastrointestinal hormone that cause an increase in the

amount of Insulin released from the beta cells of the islets of

Langerhans after eating, even before blood glucose levels become

elevated.

2 types: GLP-1 (Glucagon - like peptide-1)

GIP (Glucose-dependent Insulinotropic Peptide)

E n tid


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Exenatide

Synthetic long acting analogue of GLP-1 (incretin

mimetic) derived from the salivary gland of

Gila monster lizard

1. GLP -1 is an incretin which stimulatespostprandial insulin secretion .

2. Suppresses glucagon secretion.

3. Delays gastric emptying.4. Suppresses appetite.

E n tid


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Exenatide

Adverse effect : Nausea

Indication

Add on drug with metformin & or SU in type

2 DM

Injected SC 60 mins before breakfast & beforedinner

Pramlintide


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Pramlintide

Synthetic analogue of amylin.Amylin is a polypeptide produced by pancreatic beta cells

which :

a) reduces glucagon secretion from alpha cells.

b) delays gastric emptying.

c) decreases appetite. Adverse effects : hypoglycemia &nausea

Indications : Type 1 & Type 2 DM as an adjuvantto insulin / SU/ metformin for control of meal timeglycemia. Injected SC just before each meal

Dipeptidyl peptidase 4 inhibitors


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Dipeptidyl peptidase4 inhibitors

Sitagliptin, Vildagliptin

Inhibits DPP-4 an enzyme they degrades incretin hormone likeGLP-1 . Thus potentiates the action of incretin resulting in

limitation of postprandial hyperglycemia.

Adverse effects: URTI

Indications: Type 2 DM as an add on drug to SU /metformin / thiazolidinediones. Administered orally

diabetes mellitus pwr pt

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