diabetes mellitus pwr pt
TRANSCRIPT
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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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Pharmacological actions
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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Pharmacological actions
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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Preparation of insulin
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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Preparation of insulin
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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Newer insulin delivery devices
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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Newer insulin delivery devices
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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Newer insulin delivery devices
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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Newer insulin delivery devices
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
-
7/29/2019 Diabetes Mellitus Pwr Pt
90/96
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
-
7/29/2019 Diabetes Mellitus Pwr Pt
91/96
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
-
7/29/2019 Diabetes Mellitus Pwr Pt
92/96
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
-
7/29/2019 Diabetes Mellitus Pwr Pt
93/96
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
-
7/29/2019 Diabetes Mellitus Pwr Pt
94/96
Exenatide
Adverse effect : Nausea
Indication
Add on drug with metformin & or SU in type
2 DM
Injected SC 60 mins before breakfast & beforedinner
Pramlintide
-
7/29/2019 Diabetes Mellitus Pwr Pt
95/96
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
-
7/29/2019 Diabetes Mellitus Pwr Pt
96/96
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