DM Sementara

8/13/2019 DM Sementara

1/9

General Objectives of Diabetes Management:

To relieve symptoms

To correct associated health problems and to reduce morbidity, mortality andeconomic costs of diabetes

To prevent as much as possible acute and long-term complications and toprovide timely intervention

To improve the quality of life and productivity of the individual ith diabetes

A. Diet

Diet is a basic part of management in every case! Treatment cannot be effective

unless adequate attention is given to ensuring appropriate nutritionDietary treatment should aim at:

a! ensuring eight control

b! providing nutritional requirements

c! allo ing good glycaemic control ith blood glucose levels as close tonormal as possible

d! correcting any associated blood lipid abnormalities

The following principles are recommended as dietary guidelines for peoplewith diabetes:

Dietary fat should provide 25-35% of total intake of calories but saturatedfat intake should not e"ceed 10% of total energy! #holesterol consumptionshould be restricted and limited to $%% mg or less daily!

&rotein inta'e can range bet een 10-15% total energy (%!)-* g+'g ofdesirable body eight ! equirements increase for children and duringpregnancy! &rotein should be derived from both animal and vegetablesources!

#arbohydrates provide 50-60% of total caloric content of the diet.#arbohydrates should be comple" and high in fibre!

."cessive salt inta'e is to be avoided! /t should be particularly restricted inpeople ith hypertension and those ith nephropathy!

!ercise


2/9

&hysical activity promotes eight reduction and improves insulin sensitivity,thus lo ering blood glucose levels!

Together ith dietary treatment, a programme of regular physical activityand e"ercise should be considered for each person! 0uch a programme must

be tailored to the individual1s health status and fitness!&eople should, ho ever, be educated about the potential ris' ofhypoglycaemia and ho to avoid it!

Mechanism of 2ction

0ulfonylureas interact ith receptors on pancreatic b-cells to bloc' 2T&-sensitive potassium channels

This, in turn, leads to opening of calcium channels

3hich leads to the production of insulin

0econd Generation 0ulfonylureas

"lipi#ide

$!idi#ed to inacti e metabolites

&alf-life - ' to ( hours

)otency - &igh

*'.5 to (0 mg+d,

."tended-release preparation- glipi4ide G/T0

5 Glipi4ide gastrointestinal therapeutic system

5 Does not induce eight gain

#linical 6ses of 0ulfonylureas

7ypoglycemic agents for treatment of Type 8 diabetes mellitus

2ct by increasing endogenous insulin secretion 9 not indicated for Type * Most effective hen cell function has not been severely compromised

/ncreased insulin secretion favors lipogenesis

Most appropriate in non- or mildly obese

6p to *;% < of ideal body eight


3/9

#hoice of 0ulfonylurea

onsider:

Duration of action, potency, metabolism, side effects

/n presence of renal dysfunction:

- Dual routes of elimination

Glyburide or glimepiride

- Metaboli4ed to inactive metabolites

Glipi4ide

0econd generation 06s bind nonionically to plasma albumin and have fe er druginteractions than earlier 06s, hich bind albumin ionically and compete ith other

drugs for binding sites

=iguanides : improves insulin1s ability to move glucose into cells (esp! muscle

- mechanism improves insulin sensitivity by increasing peripheral glucose upta'e

and utili4ation!

- >hou et al (8%%* sho ed that metformin stimulates the hepatic en4yme 2M&-

activated protein 'inase- Metformin as first described in the scientific literature in *?@A (6nger et al !

- /t as first mar'eted in Brance in *?A? but did not receive BD2 approval for Type

8 diabetes until *??C!

etformin is a widely used monotherapy/ and also used in combinationwith the sulfonylureas in treatment of type ' diabetes

=iguanides

Birst Generation- &henformin

&henethylbiguanide

2dverse .ffects


4/9

actic acidosis

is' of cardio-

vascular disorder

#urrently in use in the 6!0!

arely produces lactic acidosis e"cept under predisposing conditions

echanism of action: antihyperglycemic

orrect ele ated hepatic glucose output

nhibit gluconeogenesis

nhibit glucose- -phosphatase acti ity glycogen sparing insulin resistance

ediated by acti ation of 52A )-acti ated protein 3inase*A )4, in hepatocytes and muscle

Do not increase insulin secretion

ot hypoglycemic/ e en at high doses

Do not produce hypoglycemia

6econdary beneficial effects on lipids

7educed triglycerides

7educed total cholesterol

7educed 8D8

ncreased &D8

nsulin le els unchanged or reduced

9eight loss/ some reduction of blood pressure

Appropriate for obese Type ' diabetics


5/9

!creted unchanged in the urine

&alf-life - appro!imately ' hours

Does not bind to plasma proteins

6hould not be used with renal or hepatic dysfunction

Also appro ed for pre ention of Type ' diabetes in high ris3indi iduals

se also for polycystic o ary syndrome: insulin resistance witho arian hyperandrogenism

Thia4olidinediones (T>D1s : ma'e cells more sensitive to insulin (esp! fatty cells

binds to and activates the gamma isoform of the pero"isome proliferator-activated

receptor (&&2 E !

&&2 E is a member of the steroid hormone nuclear receptor superfamily, and isfound in adipose tissue, cardiac and s'eletal muscle, liver and placenta

upon activation of this nuclear receptor by a ligand such as a T>D, &&2 EFligandcomple" binds to a specific region of D 2 and thereby regulates the transcription ofmany genes involved in glucose and fatty acid metabolism!

Thia4olidinediones: osiglita4one

;ioa ailability of oral dose is


6/9


7/9

.ffective regardless of age, genetic factors, body eight, duration or severityof disease

2carbose

Metaboli4ed ithin the digestive tract by en4ymes and intestinal bacteria

o systemic bioavailability

I 8 < is absorbed as intact molecule

2dverse effects: Gastrointestinal disturbances

Blatulence

ausea

Diarrhea

6se gradual dose titration

#ontraindicated for inflammatory and obstructive bo el disease,colonic ulcers

Meglitinides : 0timulate more insulin production J dependant upon level of glucosepresent

epaglinide and ateglinide

Mechanism of action:

t decrease 2T&-sensitive K L conductance

t 2dditional high affinity binding site identified in mouse -cells forrepaglinide

2ction is glucose dependent

7igh potency .licited insulin release is rapid and brief

t Ta'en ith meals for postprandial hyperglycemia

t educed ris' of long-lasting hypoglycaemia


8/9

Dipeptidyl-&eptidase C /nhibitors

2gent in #lass: 0itagliptin, 0a"agliptin

Mechanism of action:

slo s the inactivation of incretin hormones (glucagon-li'e peptide *and glucose-dependent insulinotropic polypeptide

/ncreases glucose-stimulated insulin secretion

#auses glucose-stimulated glucagon suppression

primarily lo ers postprandial glucose levels but has also been sho nto reduce fasting plasma glucose

D&&-/ inhibitors e"hibit both short term and long term actions of G &-*

2ugment glucose induced insulin secretion

/nhibit glucagon secretion

0lo gastric emptying

/ncrease insulin biosynthesis

&romote beta cell differentiation

Oral 2gent Monotherapy

/f glycaemic control is not achieved (7b2*c N ;!@< and+orJ B&G N A!% mmol+orJ &G N**!%mmol+ ith lifestyle modification ithin * F$ months, O 22 T/-D/2=.T/# 2G. T should be initiated!

/n the presence of mar'ed hyperglycaemia in ne ly diagnosed symptomatictype 8 diabetes (7b2*c N )D!


9/9

on-obese type 8 patients, consider the use of metformin or insulinsecretagogues

Metformin is the drug of choice in over eight+obese patients! T>Ds andacarbose are acceptable alternatives in those ho are intolerant to

metformin!/f monotherapy fails, a combination of T>Ds, acarbose and metformin isrecommended! /f targets are still not achieved, insulin secretagogues may beadded

#ombination Oral 2gents

#ombination oral agents is indicated in:

e ly diagnosed symptomatic patients ith 7b2*c N*%

&atients ho are not reaching targets after $ months on monotherapy

DM Sementara

Documents

Transcript of DM Sementara