FINAL DIABETES & ITS ROLE IN PERIODONTICS...ppt

7/24/2019 FINAL DIABETES & ITS ROLE IN PERIODONTICS...ppt

http://slidepdf.com/reader/full/final-diabetes-its-role-in-periodonticsppt 1/140

Presented By:-

Dr. Vinay jain

1



CONTENTS

Introduction

History

Classifcation

Insulin

Blood Suar !eulation

Sins " Sy#$to#s

E%a#ination

Dianosis

2



Dia&etes #ellitus Ty$e I

Dia&etes 'ellitus Ty$e II

(estational Dia&etes

Co#$lication o) dia&etes

Predia&etes

In*uence o) Dia&etes on oral +ealt+

Periodontal #ani)estation o) dia&etes

Su##ary

3



INT!OD,CTION

Dia&etes is a c+ronic disease +ic+ occurs+en t+e $ancreas does not $roduce enou+insulin or +en t+e &ody cannot e/ecti0elyuse t+e insulin it $roduces. T+is leads to anincreased concentration o) lucose in t+e

&lood 1+y$erlyce#ia2.

It a/ects #ore t+an 345 #illion $eo$leorldide " is esti#ated t+at it ill a/ect

445 #illion &y t+e year 4545

Dia&etes is usually irre0ersi&le " alt+ou+$atients can +a0e a reasona&ly nor#al

li)estyle its late co#$lications results in 4



India is +o#e to t+irty-f0e #illion $eo$le it+dia&etes6nearly 37 $ercent o) t+e lo&aldia&etes &urden " $rojections s+o t+at t+isill increase to se0enty #illion &y 4547.

Dia&etes dis$ro$ortionately a/ects $eo$le o)or8in aes " accounts )or ,S94.4 &illion inannual +ealt+ care costs in India alone.

5



HISTO!

Term diabetes coined by Aretaeus of Cappadocia in 1st century

In 1675, Thomas Wiis added the !ord mellitus, from the "atin

meanin# $honey$, a reference to the s!eet taste of the urine%

&athe! 'obson in 1776, confirmed that the s!eet taste !as because

of an e(cess of a )ind of su#ar in the urine and bood of peope !ith

diabete%

*ushruta +6th century C- identified diabetes and cassified it as

Medhumeha% .e further identified it !ith obesity and sedentary

ifestye, ad/isin# e(ercises to hep $cure$ it%

"ater 0ohann eter ran) +1745121- first differentiated bet!een

diabetes meitus and diabetes insipidus

6



;ose$+ 0on 'erin and Os8ar 'in8os8i +o in 3<<= )oundt+at dos +ose $ancreas as re#o0ed de0elo$ed all t+e

sins and sy#$to#s o) dia&etes and died s+ortly a)terards

In 3=35 Sir Edard >l&ert S+ar$ey-Sc+a)er suested t+at$eo$le it+ dia&etes ere defcient in a sinle c+e#ical t+atas nor#ally $roduced &y t+e $ancreas6+e $ro$osed callin

t+is su&stance insulin

Bantin Best and colleaues 1es$ecially t+e c+e#ist Colli$2ent on to $uri)y t+e +or#one insulin )ro# &o0ine $ancreasesat t+e ,ni0ersity o) Toronto. T+is led to t+e a0aila&ility o) an

e/ecti0e treat#ent6insulin injections6and t+e frst $atientas treated in 3=44.

T+e distinction &eteen +at is no 8non as ty$e 3 dia&etesand ty$e 4 dia&etes as frst clearly #ade &y Sir Harold

Perci0al 1Harry2 Hi#sort+ and $u&lis+ed in ;anuary 3=@A 7



C>SSIIC>TION

T+e frst idely acce$ted classifcation o) dia&etes #ellitus as

$u&lis+ed &y HO in 3=<5 " in #odifed )or# in 3=<7 . T+e3=<5 and 3=<7 classifcations o) dia&etes #ellitus " alliedcateories o) lucose intolerance included clinical classes andto statistical ris8 classes.

T+e 3=<5 E%$ert Co##ittee $ro$osed to #ajor classes o)

dia&etes #ellitus " na#ed t+e# as:-

IDD' or Ty$e 3 "NIDD' or Ty$e 4.

. In t+e 3=<7 study rou$ re$orts t+e ter#s Ty$e 3 and Ty$e 4ere o#itted &ut t+e classes IDD' and NIDD' ere retainedand a class o) 'alnutritionrelated Dia&etes 'ellitus 1'!D'2as introduced.



Newer Classifcation

T+e classifcation enco#$asses &ot+ clinical stages "etiological types o) dia&etes #ellitus " ot+er cateories o)+y$erlyce#ia as suested &y FuGuya and 'atsuda.

Neer Classifcation contain staes +ic+ re*ects t+e 0ariousderee o) +y$erlyce#ia in indi0idual su&jects it+ any o) t+e

disease $rocesses +ic+ #ay lead to dia&etes #ellitus.

>ll su&jects it+ dia&etes #ellitus can &e cateoriGedaccordin to clinical stae and t+is is ac+ie0a&le in allcircu#stances.

T+e stae o) lycae#ia #ay c+ane o0er ti#e de$endin ont+e e%tent o) t+e underlyin disease $rocesses.

T+e etioloical classifcation re*ects t+e )act t+at t+e de)ect or$rocess +ic+ #ay lead to dia&etes #ay &e identifa&le at anystae in t+e de0elo$#ent o) dia&etes e0en at t+e stae o)



Neer Classifcation

Type 1

1&eta-cell destruction usually leadin to a&soluteinsulin defciency2

>utoi##une

Idio$at+ic

Type 2

1#ay rane )ro# $redo#inantly insulin resistanceit+ relati0e insulin defciency to a $redo#inantlysecretary de)ect it+ or it+out insulin resistance2

1



Other Specifc Types-

Genetic deects o beta-cell unctionC+ro#oso#e 45 HN 1'ODJ32

C+ro#oso#e K luco8inase 1'OD42

C+ro#oso#e 34 HN3 1'OD@2

C+ro#oso#e 3@ IP-3 1'OD2

'itoc+ondrial DN> #utation

1J'OD-'aturity Onset Dia&etes o) out+2

Genetic deects in insulin action Ty$e > insulin resistance

Diseases o the exocrine pancreasPancreatitis Trau#a L $ancreatecto#y Neo$lasia Cystic

f&rosis Hae#oc+ro#atosis

11



EndocrinopathiesCus+inMs syndro#e >cro#ealy (lucaono#a

Hy$ert+yroidis#.

Drug- or chemical-induced

Nicotinic acid (lucocorticoids T+yroid +or#one T+iaGidesDilantin.

InectionsConenital ru&ella Cyto#ealo0irus.

Uncommon orms o immune-mediated diabetes Sti/-#an syndro#e >ntiinsulin rece$tor anti&odies.

ther genetic syndromesDonMs syndro#e Fline)elterMs syndro#e Por$+yria TurnerMssyndro#e.

12



!ech o Insulin release

(lucose enters t+e &eta cells t+rou+ t+e lucosetrans$orter (,T4

(lucose oes into t+e lycolysis and t+e res$iratory cycle+ere #ulti$le +i+-enery >TP #olecules are $roduced &y

o%idation

De$endent on >TP le0els and +ence &lood lucose le0elst+e >TP-controlled $otassiu# c+annels 1F2 close and t+ecell #e#&rane de$olariGes

On de$olariGation 0oltae controlled calciu# c+annels1Ca42 o$en and calciu# *os into t+e cells

13



>n increased calciu# le0el causes acti0ation o) phospholipase C +ic+ clea0es t+e #e#&rane $+os$+oli$id

$+os$+atidyl inositol 7-&is$+os$+ate into inositol 37-tri$+os$+ate and diacyllycerol.

Inositol 37-tri$+os$+ate 1IP@2 &inds to rece$tor $roteins int+e #e#&rane o) endo$las#ic reticulu# 1E!2. T+is allos

t+e release o) Ca4 )ro# t+e E! 0ia IP@ ated c+annels and)urt+er raises t+e cell concentration o) calciu#.

Sinifcantly increased a#ounts o) calciu# in t+e cellscauses release o) $re0iously synt+esiGed insulin +ic+ +as&een stored in secretary 0esicles

14



15



Blood suar le0els are reulated &y neati0e )eed&ac8 in

order to 8ee$ t+e &ody in +o#eostasis.

T+e le0els o) lucose in t+e &lood are #onitored &y t+e cellsin t+e $ancreasMs Islets o) aner+ans.

I) t+e &lood lucose le0el )alls to danerous le0els 1as in0ery +ea0y e%ercise or lac8 o) )ood )or e%tended $eriods2t+e cells o) t+e $ancreas release lucaon a +or#one+ose e/ects on li0er cells act to increase &lood lucosele0els.

T+ey con0ert lycoen into lucose 1t+is $rocess is calledlycoenolysis2. T+e lucose is released into t+e&loodstrea# increasin &lood suar le0els.

"' *89A: :;98"ATI<

16



+en le0els o) &lood suar rise +et+er as a result o)lycoen con0ersion or )ro# diestion o) a #eal a di/erent+or#one is released )ro# &eta cells )ound in t+e Islets o)aner+ans in t+e $ancreas.

T+is +or#one insulin causes t+e li0er to con0ert #orelucose into lycoen 1t+is $rocess is called lycoenesis2and to )orce a&out 4L@ o) &ody cells 1$ri#arily #uscle and)at tissue cells2 to ta8e u$ lucose )ro# t+e &lood t+usdecreasin &lood suar.

17



1



Sins " Sy#$to#s

Syste#ic ei+t loss 1insulin defciency2

O&esity - #ay &e a&do#inal 1insulin resistance2

+ite s$ots on s+oes- lycosuria 1e%cretion o) lucose into t+eurine2

Dry #out+ or tonue

S8in in)ections- &oil candidiasis

Dee$ si+in res$iration

S#ell o) acetone in $atientQs &reat+in 1dia&etic 8etoacidosis2

1



Slo +ealin o) ounds

Blurred 0ision

Polydi$sia

Polyuria

Poly$+aia

et+ary

Nausea 0o#itin a&do#inal $ain

2



E%a#ination

Hands:-

i#ited joint #o&ility 1c+erioart+ro$at+y2 in +ic+ su&jects+os ina&ility to e%tend t+e #etacar$o$+alaneal orinter$+alaneal joints o) 3 fner &ilaterally

21



es:-

-'uscle astin sensory a&nor#ality +air loss etc.

eet:-

-De)or#ity o) t+e )eet #ay &e $resent es$ecially in c+arcotneuro$at+y

-unal in)ections e/ectin t+e s8in &eteen toes " nails asell as a&scess )or#ation

->t+erosclerosis o) arteries " t+ic8enin o) &ase#ent

#e#&rane o) ca$illaries resultin in tissue $er)usion ")or#ation o) anrene

22



Dianosis

Dianosis o) dia&etes is done t+rou+ a series o) tests

T+ese test could &e:

,rine Test

BenedictQs Test

Fetone Test

Blood Test

Blood suar

astin Plas#a (lucose Test

(lucose Tolerance Test

(lycosylated H&

23



,rine testin

Glucose

Testin s+ould &e $er)or#ed 3-4 +ours a)ter #eal

T+e test can &e

-BenedictQs test

-Di$stic8 test

24



"enedict#s $est

*ampe of urine = enedict>s rea#ent

.eat

n cooin#

25



Dipstic% test

T+ese are stri$ o) $a$er t+at c+ane t+eir color in $resence

o) suar $rotein 8etone at urinary $H " ot+er su&stancesin urine.

T+e c+ane o) color de$ends on c+e#icals used in $re$arindi$stic8s

26



Blood Test

Blood Suar

Blood suar concentration or lucose le0el re)ers to t+e

a#ount o) lucose $resent in t+e &lood o) a +u#an or ani#al.

Nor#ally in #a##als t+e &lood lucose le0el is #aintained

at a re)erence rane &eteen a&out @.A and 7.< #' 1##olLl2.

It is ti+tly reulated as a $art o) #eta&olic +o#eostasis.

27



astin Plas#a (lucose Test

> &lood sa#$le is dran a)ter an <-+our )astin $eriod to

c+ec8 )or &lood lucose le0els in t+e &ody.

T+e &est ti#e to carry out t+is test is in t+e #ornin. T+e

results are read as )ollos:

!ane Dianosis

=5 # or &elo Nor#al

=5-34A # Pre-dia&etic or i#$aired )astin lucoserane

34A # and a&o0e Dia&etic

2



4-+our $ost$randial &lood suar #easures &lood lucosee%actly 4 +ours a)ter #eal. Nor#al 0alue K537 #Ld

Cateories

3. 4+P( R35 #Ld nor#al lucose tolerance

4. 4+P( 35 #Ld and less t+an 455 #Ld i#$aired

lucose tolerance@. 4+P( 455 #Ld $ro0isional dianosis o) dia&etes

!ando# &lood suar 1!BS2 #easures &lood lucose reardlesso) )ood consu#$tion. Se0eral rando# #easure#ents #ay &e

ta8en t+rou+out t+e day. !ando# testin is use)ul &ecauselucose le0els in +ealt+y $eo$le do not 0ary idely t+rou+outt+e day.

Nor#al 0alue 3<5 #Ld

2



Glucose Tolerance Test

T+e lucose tolerance test is also carried out a)ter an <-+our )astin$eriod.

Patient Pre$aration

T+e $atient is instructed not to restrict car&o+ydrate inta8e in t+e

days or ee8s &e)ore t+e test.Procedure

T+e $atient s+ould +a0e &een )astin )or t+e $re0ious <-3 +ours

1ater is alloed2.

,sually t+e O(TT is sc+eduled to &ein in t+e #ornin as lucose

tolerance e%+i&its a diurnal r+yt+# it+ a sinifcant decrease in

t+e a)ternoon. > Gero ti#e 1&aseline2 &lood sa#$le is dran.

3



T+e $atient is t+en i0en a lucose solution to drin8. Standard

dose o) 3.K7 ra#s o) lucose $er 8ilora# o) &ody ei+t to a

#a%i#u# dose o) K7 . It s+ould &e drun8 it+in 7 #inutes.

Blood is dran at inter0als )or #easure#ent o) lucose 1&lood

suar2 and so#eti#es insulin le0els.

Nor#al &lood 0alues )or a K7-ra# oral lucose tolerance testused to c+ec8 )or ty$e 4 dia&etes:

Normal range ,nder 335 #Ldl )astin ,nder 35 at 4+rsImpaired &asting Glycemia range O0er 335 to under 34A #Ldl

)astin ,nder 35 at 4 +rs

Impaired Glucose $olerance range ,nder 34A #Ldl )astin,nder

or eUual to 35 at 4 +rs.

Diabetes range O0er or eUual to 34A #Ldl )astin O0er oreUual to 455 at 4+rs. 31



(lycated H&

(lycosylated +e#olo&in test 1H&>3c2 is a &lood test. It

#easures t+e a#ount o) lycosylated +e#olo&in in t+e &lood.

T+is +e#olo&in is lin8ed to lucose. T+e test #easure t+ea#ount o) lucose or suar is in t+e &lood (lyco+e#olo&in.

,nderlyin Princi$le

+en lucose is a&sor&ed into t+e &loodstrea# so#e o) it is$ic8ed u$ &y t+e +e#olo&in in red &lood cells.

T+is lycated 1lucose-carryin2 +e#olo&in +olds onto t+elucose until t+e red &lood cells die in a&out 345 days.

32



? A buidup of #ycated hemo#obin !ithin the red ce therefore refects the a/era#e

e/e of #ucose to !hich the ce has been e(posed durin# its ife cyce%? &easurin# #ycated hemo#obin assesses the effecti/eness of therapy by

monitorin# on#term serum #ucose re#uation%

?There are a number of techni@ues used to measure .bA1c% "aboratories use

.i#hperformance i@uid chromato#raphy +."C-

Immunoassay

oronate Affinity Chromato#raphy

33



Value

!ane Dianosis

.7 A.5 Nor#al

R K (ood Dia&etes Control

K -< 'oderate Dia&etes Control

W< >ction suested to i#$ro0e dia&etic

control

34



Guo YH Zhu BL (200! In a study to in0estiate t+e e/ect

o) $eriodontal initial t+era$y on t+e le0el o) lycated H&

1H&>Ic2 and $eriodontal status in non-insulin de$endent

dia&etes #ellitus1NIDD'2$atients it+ $eriodontitis. !esults

s+oed t+at t+e $ercentae o) &leedin on $ro&in and

$ro&in de$t+ ere sinifcantly reduced in all $atients a)ter

$eriodontal t+era$y +ic+ included oral +yiene

instructionultrasonic scalin and su&ini0al scalin..T+e

lycosylated +e#olo&in le0el as sinifcantly decreased in

$atients it+ ad0anced $eriodontitis+ile $atients it+

#oderate $eriodontitis s+oed no c+anes )olloin

t+era$y.

35



DI>BETES 'EIT,S TPE I

Ty$e 3 dia&etes is an autoi##une disease t+at results in destruction

o) insulin-$roducin &eta cells o) t+e $ancreas.

ac8 o) insulin causes an increase o) )astin &lood lucose 1around K5-

345 #Ld in nondia&etic $eo$le2 t+at &eins to a$$ear in t+e urine

a&o0e t+e renal t+res+old 1a&out 3=5-455 #Ldl in #ost $eo$le2.

T+e #ost defnite la&oratory test to distinuis+ ty$e 3 )ro# ty$e 4

dia&etes is t+e C-peptide assay +ic+ is a #easure o) endoenous

insulin $roduction since e%ternal insulin +as not 1to date2 included C-

$e$tide.

36



Epidemiology

In estern countries al#ost all t+e $atients Ha0e Ty$e I D'.

Ty$e I D' is $ro#inent disease o) c+ild+ood reac+in a $ea8

incidence around t+e ti#e o) $u&erty &ut can $resent at any

ae.

T+e +i+est rates o) Ty$e I D' in t+e orld is seen in inland

" ot+er Nort+ Euro$ean countries.

E%ce$tionally Island o) Sardinia +ic+ )or un8non reasons

+as second +i+est rate in t+e orld.

37



Etiology

Genetics(enetic )actors account )or a&out 3L@rd o) susce$ti&ility o)

Ty$e I D'

O0er 45 di/erent reions o) +u#an eno#e s+o so#e

lin8ae it+ Ty$e I D'

'ost interest +as )ocused on t+e +u#an leu8ocyte antien1H>2 reion it+in #ajor +istoco#$ati&ility co#$le% on t+es+ort ar# o) c+ro#oso#e A

T+e H> +aloty$es D!@ " D! are associated it+ increasedsusce$ti&ility.

3



"n#iron$ental %actors

It +as &een $ro$osed t+at lac8 o) e%$osure to $at+oenic

#icrooranis#s in early c+ild+ood li#its #aturation o) i##une syste#

" increase susce$ti&ility to autoi##une disease

&iruses

T+e e0idence t+at 0iral in)ection #i+t cause so#e )or# o) Ty$e I D' is

deri0ed )ro# t+e studies +ere 0irus $articles 8non to cause

cyto$at+ic or autoi##une da#ae to X cells +a0e &een isolated )ro#

$ancreas.

Se0eral 0iruses +a0e &een i#$licated includin #u#$s co%saci8e 0irus

B retro0irus ru&ella cyto#ealo0irus " e$stein &arr 0irus.

3



Diet

-So#e researc+ers &elie0e t+at t+e autoi##une res$onse is in*uenced&yanti&odies aainst coMs #il8 $roteins.

-Bo0ine Seru# >l&u#in 1BS>2 a #ajor constituent o) coQs #il8 +as &eeni#$licated in trierin Ty$e I Dia&etes

-C+ildren +o +a0e &een i0en coQs #il8 early in in)ancy are #oreli8ely to

de0elo$ Ty$e I D'

-BS> #ay cross t+e neonatal ut " raise t+e anti&odies +ic+ &ecauseo)

close +o#oloy &eteen BS> t+e X c+ain o) class II antien " +eats+oc8 $rotein e%$ressed &y X cells could cross react it+ " cause da#ae to

Beta cell co#$onents

4



'tress

Stress #ay $roress t+e de0elo$#ent o) Ty$e I D' &y sti#ulatin

t+e secretion o) counter reulatory +or#ones " $ossi&ly #odulatin

i##une acti0ity.

>utoi##unity

Ty$e I dia&etes is a slo T cell #ediated autoi##une disease.

a#ily studies +a0e $roduced e0idence t+at destruction o) t+e

insulin secretin cells in t+e $ancreatic islets ta8es $lace o0er #any

years

Hy$erlyce#ia acco#$anied &y t+e classical sy#$to#s o) dia&etes

occur only +en K5-=5 o) &eta cells +a0e &een destroyed

41



'he$icals

So#e c+e#icals and drus $re)erentially destroy $ancreatic

cells. Vacor a rodenticide introduced in t+e ,nited States in

3=KA selecti0ely destroys $ancreatic &eta cells resultin in

ty$e 3 dia&etes a)ter accidental or intentional inestion.

Vacor as it+dran )ro# t+e ,.S. #ar8et in 3=K= &ut is still

used in so#e countries.

Yanosar is t+e trade na#e )or stre$toGotocin an anti&iotic

and antineo$lastic aent used in c+e#ot+era$y )or

$ancreatic cancerZ it also 8ills &eta cells resultin in loss o)

insulin $roduction.

42



ancreatic pro)le$s

Ot+er $ancreatic $ro&le#s includin trau#a $ancreatitis or

tu#ors 1eit+er #alinant or &enin2 can also lead to loss o)

insulin $roduction.

43



Clinical eatures

>lt+ou+ co##only associated it+ c+ild+ood onset ty$e 3can occur at any ae.

Initially e%oenous insulin reUuire#ents are #ini#al+oe0er X-cell reser0e is e0entually e%+austed and insulinreUuire#ents escalate and #anae#ent &eco#es arduous.

Ty$e 3 is do#inated &y sins o):->ltered #eta&olis#PolyuriaPolydi$sia and

Poly$+aia.

44



$reatment o $ype I diabetes mellitus

- Ty$e 3 is treated it+ insulin re$lace#ent t+era$y6usually &yinsulin injection or insulin $u#$

Insulin In(ection

Syrines )or insulin users are desined )or standard ,-355

insulin. T+e dilution o) insulin is suc+ t+at 3 #l o) insulin*uid +as 355 standard [units[ o) insulin. Since insulin 0ialsare ty$ically 35 #l eac+ 0ial +as 3555 units.

45



Insulin syrines are #ade s$ecifcally )or sel) injections and

+a0e )riendly )eatures:

S+orter needles 1insulin injections are su&cutaneous rat+er

t+an intra#uscular2

iner aue needles )or less $ain and

'ar8ins in insulin units to si#$li)y drain a #easured doseo) insulin.

46



Insulin )ump

T+e de0ice includes:

T+e $u#$ itsel) 1includin controls $rocessin #odule and&atteries2

> dis$osa&le reser0oir )or insulin 1inside t+e $u#$2

> dis$osa&le in)usion set includin a cannula )or su&cutaneousinsertion 1under t+e s8in2 and a tu&in syste# to inter)ace t+e

insulin reser0oir to t+e cannula.

Dosing

> &olus dose t+at is $u#$ed to co0er )ood eaten or to correct a

+i+ &lood lucose le0el. > &asal dose t+at is $u#$ed continuously at an adjusta&le &asal

rate to deli0er insulin needed &eteen #eals and at ni+t.

47



Insuin pump, sho!in# an infusion set oaded into sprin#oaded insertion de/ice% A

reser/oir is attached to the infusion set +sho!n here remo/ed from the pump-% 4

Pancreas Trans$lantation



Pancreas Trans$lantation

Pancreas trans$lants are enerally $er)or#ed toet+er it+ or so#e

ti#e a)ter a 8idney trans$lant.

Islet Cell Trans$lantation

Islet cell trans$lantation is e%$ected to &e less in0asi0e t+an a

$ancreas trans$lant +ic+ is currently t+e #ost co##only used

a$$roac+ in +u#ans.

In one 0ariant o) t+is $rocedure islet cells are injected into t+e

$atientMs li0er +ere t+ey ta8e u$ residence and &ein to $roduce

insulin.

T+e li0er is e%$ected to &e t+e #ost reasona&le c+oice &ecause:-

-It is #ore accessi&le t+an t+e $ancreas and

-Islet cells see# to $roduce insulin ell in t+at en0iron#ent.

4



Gene therapy approach

(ene t+era$y can &e used to $anu*acture insulin +irectly: anoral #edication consistin o) 0iral 0ectors containin t+e insulin

seUuence is diested and deli0ers its enes to t+e u$$erintestines.

T+ose intestinal cells ill t+en &e+a0e li8e any 0iral in)ected celland ill re$roduce t+e insulin $rotein. T+e 0irus can &e controlled toin)ect only t+e cells +ic+ res$ond to t+e $resence o) lucose suc+t+at insulin is $roduced only in t+e $resence o) +i+ lucose le0els.

Due to t+e li#ited nu#&ers o) 0ectors deli0ered 0ery )e intestinalcells ould actually &e i#$acted and ould die o/ naturally in a)e days.

T+ere)ore &y 0aryin t+e a#ount o) oral #edication used t+ea#ount o) insulin created &y ene t+era$y can &e increased ordecreased as needed.

>s t+e insulin $roducin intestinal cells die o/ t+ey are &oosted &yadditional oral #edications.

5



> disorder t+at is c+aracteriGed &y +i+ &lood lucose in t+e

conte%t o) insulin resistance and relati0e insulin defciency.

O)ten initially #anaed &y increasin e%ercise and dietary

#odifcation #edications are ty$ically needed as t+e disease

$roresses.

Traditionally considered a disease o) adults ty$e 4 dia&etes is

increasinly dianosed in c+ildren in $arallel to risin o&esity

rates due to alterations in dietary $atterns as ell as in li)e

styles durin c+ild+ood.

Ty$e 4 #ay o unnoticed )or years &e)ore dianosis since

sy#$to#s are ty$ically #ilder 1e.. no 8etoacidosis co#a

etc2 and can &e s$oradic.

TB; II 'IA;T;* &;""IT8*

51



Pat+oenesis-

Insulin !esistance-

Increased +e$atic $roduction o) lucose " resistance to t+eaction o)

insulin in &ot+ o&ese " non o&ese $atient in ty$e II D'

Insulin resistance #ay &e due to:

i2 >n a&nor#al insulin #olecule

ii2 >n e%cessi0e a#ount o) circulatin antaonists or taret

tissuede)ects

iii2 Se0ere Hy$erlyce#ia

52

Pancreatic X cell )ailure



In Ty$e II D' t+ere is only #oderate reduction in t+e total

#ass o) $ancreatic islet tissue +ic+ is consistent it+

#easura&le )all in $las#a insulin concentration +en relatedto &lood lucose le0el.

T+e #ost consistent $at+oloical c+ane is de$osition o)

a#yloid +ic+ is acco#$anied &y atro$+y o) t+e nor#al tissue

$articularly islets e$it+elial cells.

De$osition o) a#yloid is $ro&a&ly not a cause o) dia&etes &ut

rat+er re*ects a $at+oloical $rocess +ic+ is increased in

Ty$e II D'.

Beta cell no. is reduced to 45-@5 +ereas al$+a cell #ass is

un c+anes resultin in increased lucaon secretion.

53



Etioloy

(enetics

(enetic )actors are #ore i#$ortant in t+e etioloy o) Ty$e IID' t+an Ty$e I

(eno#e ide searc+es +a0e identifed susce$ti&ilities eneson c+ro#oso#e 3U 34U " 45U &ut t+e underlyin enes+a0e not yet &een identifed

In addition t+ere is also a #utation to t+e Islet >#yloidPoly$e$tide ene t+at results in an earlier onset #orese0ere )or# o) dia&etes.

54



En0iron#ental actors

i)estyle

E$ide#ioloical studies o) Ty$e II D' $ro0ides e0idence t+at

o0ereatin es$ecially +en co#&ined it+ o&esity " under

acti0ity

Ot+er #ore direct studies +a0e s+on t+at #iddle aed $eo$le

it+ dia&etes eat sinifcantly #ore " less acti0e t+an non

dia&etic si&lins.

O&esity $ro&a&ly acts as a dia&etoenic )actor 1t+rou+

Increasin t+e resistance to t+e action o) insulin2 in t+ose

enetically $redis$osed to de0elo$ ty$e II dia&etes.

55



>e

>e is an i#$ortant ris8 )actor o) Ty$e II D'

Ty$e II D' is $rinci$ally a disease o) t+e #iddle aed "elderly a/ectin 35 o) t+e $o$ulation o0er ae

56



Prenancy

Durin nor#al $renancy insulin sensiti0ity is reduced

t+rou+ t+e action o) $lacental +or#ones " t+is a/ects

lucose tolerance.

T+e insulin secretin cells o) $ancreatic islets #ay &e una&le

to #eet t+is increased de#and in o#en enetically

$redis$osed to de0elo$ dia&etes.

!e$eated $renancy #ay increase t+e li8eli+ood o)

de0elo$in irre0ersi&le dia&etes $articularly in o&ese o#en.

57



CLEarly sy#$to#s #ay &e not+in #ore t+an c+ronic )atiues

eneraliGed ea8ness and #alaise 1)eelin o) unease2E%cessi0e urine $roductionE%cessi0e t+irst and increased *uid inta8eBlurred 0ision 1ty$ically )ro# lens s+a$e alterations due to

os#otic e/ects e.. +i+ &lood lucose le0els2,ne%$lained ei+t losset+ary Itc+in o) e%ternal enitalia'eta&olic derane#ents are usually #ildQ o)ten t+e

dianosis is #ade on routine &lood tests.Des$ite a #ilder clinical course t+an ty$e 3 o)ten at t+e ti#e

o) dianosis t+ere is e0idence o) end oran da#ae1in)arcts \renal )unction neuro$at+y etc.2

5



'anae#ent

T+era$eutic oals

T+ere are to #ain oals o) treat#ent:

-!eduction o) #ortality and conco#itant #or&idity 1)ro#

assorted dia&etic co#$lications2-Preser0ation o) Uuality o) li)e

5



)re*ention

-Onset o) ty$e 4 dia&etes can o)ten &e delayed t+rou+$ro$er nutrition and reular e%ercise.

-In 4557 an e0idence re$ort &y t+e >ency )or Healt+care!esearc+ and ]uality concluded t+at [t+ere is e0idence t+atco#&ined diet and e%ercise as ell as dru t+era$y1#et)or#in acar&ose2 #ay &e e/ecti0e at $re0entin$roression to D'.

6



Treat#ent-

4 &asic ty$es o) diet are used in t+e treat#ent o) dia&etes:

o enery ei+t reducin diets "

ei+t #aintenance diet

'anae#ent o) o&ese $eo$le 1&ot+ dia&etic " non dia&etic2

it+ a diet lo in refned car&o+ydrate " +i+ in unrefned

car&o+ydrate " restricted in total enery content results in

increased insulin sensiti0ity

T+is $ro#otes in decline in &lood lucose in o&ese dia&etic

$atients

61



o enery ei+t reducin diet

Dietary $rescri$tions +ic+ cause a daily defcit o) 755 Fcal

$ro0ide a realistic diet " o) around 5.7 F induces a ee8ly

ei+t loss.

Caloric restriction is essential )or t+e o&ese dia&etic $atient

treated it+ insulin " #ost oral aents to try to #ini#iGe

t+e ei+t ain +ic+ t+ese can $ro#ote.

62



ei+t #aintenance diet

T+ese are necessary )or indi0iduals it+ nor#al &ody #ass

inde% " ideally s+ould &e +i+ in car&o+ydrate " lo in )at

it+ $articular attention &ein $aid to t+e ty$e o) )at

inested.

+ile total enery inta8e re#ain constant

63



Car&o+ydrate

T+e diet #ost o)ten reco##ended )or $eo$le +o su/er )ro#

dia&etes #ellitus is +i+ in dietary f&er es$ecially solu&le f&er &ut

lo in )at 1es$ecially saturated )at2.

T+e consu#$tion o) 37 #s o) solu&le f&er 1$resent in &eans $ulses

oats $eas )ruit " 0eeta&les2 can $roduce 35 reduction in )astin

&lood lucose lycated H& D c+olesterol.

at

>s dia&etes is a ris8 )actor )or #acro 0ascular disease t+e inta8e o)

)at s+ould &e restricted to @5-@7 o) enery.

64



Drus

-Various aents are i#$ortant in reducin +y$erlyce#ia in$atients it+ ty$e 4 dia&etes #ellitus

-Treat#ents include

132 >ents +ic+ increase t+e a#ount o) insulin secreted &yt+e $ancreas

142 >ents +ic+ increase t+e sensiti0ity o) taret orans toinsulin and

1@2 >ents +ic+ decrease t+e rate at +ic+ lucose is

a&sor&ed )ro# t+e astrointestinal tract.

65



arious dru#s are #i/en !hich can be cassified as

66

(estational dia&etes



(estational dia&etesIntroduction

(estational dia&etes 1or estational dia&etes

#ellitus (D'2 is a condition in +ic+ o#en

it+out $re0iously dianosed dia&etes

e%+i&it +i+ &lood lucose le0els durin

$renancy.

(estational dia&etes and i#$aired lucose

tolerance 1I(T2 in $renancy a/ects &eteen

o) all $renancies and &ot+ +a0e &een

associated it+ $renancy co#$lications.

67



(estational dia&etes is )or#ally defned as [any deree o) lucose

intolerance it+ onset or frst reconition durin $renancy

It is &elie0ed t+at +or#ones $roduced durin $renancy increase

a o#anMs resistance to insulin resultin in i#$aired lucose

tolerance.

o#en it+ estational dia&etes are at increased ris8 o)de0elo$in ty$e 4 dia&etes #ellitus a)ter $renancy +ile t+eir

o/s$rin are $rone to de0elo$in c+ild+ood o&esity it+ ty$e 4

dia&etes later in li)e .

It occurs in &eteen 7 and 35 o) all $renancies 1&eteen 3-

3 in 0arious studies1>#erican Dia&etes >ssociation 4552

6



Classifcation

-T+ere are 4 su&ty$es o) estational dia&etes 1dia&etes +ic+&ean durin $renancy2:

$ype +,

>&nor#al oral lucose tolerance test 1O(TT2 &ut nor#al &lood

lucose le0els durin )astin and 4 +ours a)ter #ealsZ diet

#odifcation is su^cient to control lucose le0els

$ype +.

>&nor#al O(TT co#$ounded &y a&nor#al lucose le0els

durin )astin andLor a)ter #ealsZ additional t+era$y it+

insulin or ot+er #edications is reUuired.

6



Pat+o$+ysioloy

T+e +all#ar8 o) (D' is increased insulin resistance.

Prenancy +or#ones and ot+er )actors are t+ou+t to inter)ere

it+ t+e action o) insulin as it &inds to t+e insulin rece$tor.

Cortisol and $roesterone are #ainly res$onsi&le &ut +u#an$lacental lactoen $rolactin and estradiol contri&ute too.

>s a result lucose re#ains in t+e &loodstrea# +ere lucose

le0els rise. 'ore insulin is needed to o0erco#e t+is resistanceZ

a&out 3.7-4.7 ti#es #ore insulin is $roduced in a nor#al

$renancy. 1Carr DB et al 3==<2

7



Insulin resistance is a nor#al $+eno#enon e#erin in t+e second

tri#ester o) $renancy +ic+ $roresses t+erea)ter to le0els seen in non-

$renant $atients it+ ty$e 4 dia&etes.

o#en it+ (D' +a0e an insulin resistance t+ey cannot co#$ensate it+

increased $roduction in t+e X-cells o) t+e $ancreas.

Because lucose tra0els across t+e $lacenta 1t+rou+ di/usion

)acilitated &y (,T@ carriers2 t+e )etus is e%$osed to +i+er lucose le0els.

T+is leads to increased )etal le0els o) insulin 1insulin itsel) cannot cross t+e

$lacenta2. T+e rot+-sti#ulatin e/ects o) insulin can lead to e%cessi0e

rot+ and a lare &ody 1#acroso#ia2.

71



Sy#$to#s

Ty$ically o#en it+ estational dia&etes e%+i&it nosy#$to#s 1anot+er reason )or uni0ersal screenin2 &utso#e o#en #ay de#onstrate:-

-Increased t+irst-Increased urination

-atiue

-Nausea and 0o#itin

-Bladder in)ection

-east in)ections and

-Blurred 0ision.

72



-Tests )or estational dia&etes #ellitus includes

a2 Non-c+allene &lood lucose tests

-astin lucose test

-4-+our $ost$randial 1a)ter a #eal2 lucose test

-!ando# lucose test

-+en a $las#a lucose le0el is )ound to &e +i+er t+an34A #Ldl 1K.5 ##olLl2 a)ter )astin

or

-O0er 455 #Ldl 133.3 ##olLl2 on any occasion and i) t+is isconfr#ed on a su&seUuent day t+e dianosis o) (D' is#ade and no )urt+er testin is reUuired.

-T+ese tests are ty$ically $er)or#ed at t+e frst antenatal 0isit.

'ia#nosis

73



&2 Screenin lucose c+allene test

Oral lucose tolerance test 1O(TT2

PrereUuisites

-Nor#al diet )or @ days &e)ore rest

-No diuretic 35 days $rior to test

-35 +ours o) )astin $rior to test-Test is done in t+e #ornin at rest

-Patient is (i0en K7 # 1355 # &y ot+er aut+ors2 lucosein 475 #l ater orally

74



Criteria )or lucose tolerance test

T+e #a%i#u# &lood lucose 0alues durin $renancy:-astin =5 #L dl

-3 +our 3A7 #Ldl

-4 +ours 37 #Ldl

-@ +ours 347 #Ldl.

I) any 4 or #ore o) t+ese 0alues are ele0ated t+e $atient is

considered to +a0e an i#$aired lucose tolerance test.

75



c! Glycosylate+ he$o,lo)in (H) 1(

It is nor#ally accounts )or 7-A o) t+e total +e#olo&in #ass.

> 0alue o0er 35 indicates $oor dia&etes control in t+e

$re0ious -< ee8s.

I) t+is is detected early in $renancy t+ere is a +i+ ris8 o)conenital ano#alies .

I) detected in late $renancy it indicates increased incidence

o) #acroso#ia and neonatal #or&idity and #ortality.

76



'anae#ent

-T+e oal o) treat#ent is to reduce t+e ris8s o) (D' )or#ot+er and c+ild.

Counselin

-Counselin &e)ore $renancy 1)or e%a#$le a&out$re0enti0e )olic acid su$$le#ents2 and #ultidisci$linary#anae#ent are i#$ortant )or ood $renancy outco#es.

-'ost o#en can #anae t+eir (D' it+ dietary c+anesand e%ercise. Sel) #onitorin o) &lood lucose le0els canuide t+era$y.

77



Diet

->ny diet needs to $ro0ide su^cient calories )or $renancyty$ically 4555 - 4755 8cal it+ t+e e%clusion o) si#$lecar&o+ydrates.

-T+e #ain oal o) dietary #odifcations is to a0oid $ea8s in

&lood suar le0els.

-T+is can &e done &y s$readin car&o+ydrate inta8e o0er#eals and snac8s t+rou+out t+e day and usin slo-release car&o+ydrate sources.

-Since insulin resistance is +i+est in #ornins &rea8)astcar&o+ydrates need to &e restricted #ore.

7



'edical Nutrition T+era$y

'edical nutrition t+era$y s+ould include t+e $ro0ision o) adeUuate

calories and nutrients to #eet t+e needs o) $renancy and s+ould &econsistent it+ t+e #aternal &lood lucose oals t+at +a0e &eenesta&lis+ed.

Noncaloric seeteners #ay &e used in #oderation.

Diet t+era$y is critical to success)ul reulation o) #aternal dia&etes.

> $rora# consistin o) t+ree #eals and se0eral snac8s is used )or#ost $atients. Dietary co#$osition s+ould &e :

-75 to A5 $ercent car&o+ydrate

-45 $ercent $rotein

-47 to @5 $ercent )at it+ less t+an 35 $ercent saturated )ats u$ to 35$ercent $olyunsaturated )atty acids and t+e re#ainder deri0ed )ro#

#onosaturated sources.

7



Sel) #onitorin

Sel) #onitorin can &e acco#$lis+ed usin a +and+eldca$illary lucose dosae syste#.

I) #onitorin re0eals )ailin control o) lucose le0els it+t+ese #easures or i) t+ere is e0idence o) co#$lications li8ee%cessi0e )etal rot+ treat#ent it+ insulin #i+t &eco#enecessary.

T+e #ost co##on t+era$eutic rei#e in0ol0es $re#eal

)ast-actin insulin to &lunt s+ar$ lucose rises a)ter #eals.

Care needs to &e ta8en to a0oid lo &lood suar le0els dueto e%cessi0e insulin injections.



Insulin t+era$y

Insulin t+era$y is reco##ended +en #edical nutritiont+era$y )ails to #aintain sel)-#onitored lucose at t+e)olloin le0els:

%astin, +ole &lood lucose R=7 #Ldastin $las#a lucose R357 #Ld

or

1-hour postpran+ial +ole &lood lucose R35 #Ld3-+our

$ost$randial $las#a lucose R377

#Ld or

2-hour postpran+ial +ole &lood lucose R345 #Ld

4-+our $ost$randial $las#a lucose R3@7 #Ld

1



Tice daily 1 &e)ore &rea8)ast and &e)ore dinner2 injectionso) a co#&ination o) s+ort and inter#ediate actin insulins

are usually su^cient to control #ost $atients ot+erise asu&cutaneous insulin $u#$ is used.

T+e total frst dose o) insulin is calculated accordin to t+e$atientQs ei+t as )ollo:

In t+e frst tri#ester .......... ei+t % 5.KIn t+e frst tri#ester .......... ei+t % 5.K

In t+e second tri#ester........ ei+t % 5.<In t+e second tri#ester........ ei+t % 5.<

In t+e t+ird tri#ester........... ei+t % 5.=In t+e t+ird tri#ester........... ei+t % 5.=

2



Oral Hy$olyce#ic >ents-

'et)or#in +as s+on $ro#isin results.

Treat#ent o) $olycystic o0arian syndro#e it+ #et)or#indurin $renancy +as &een noted to decrease (D' le0els.

> recent rando#iGed controlled trial o) #et)or#in 0ersusinsulin s+oed t+at o#en $re)erred #et)or#in ta&lets toinsulin injections and t+at #et)or#in is sa)e and eUuallye/ecti0e as insulin.

3

Co#$lications o) D'



Co#$lications o) D'

-Dia&etes 'ellitus leads to a 0ariety o) co#$lications.

-T+ese co#$lications are li)e t+reatenin " can &esu##ariGed into >cute " C+ronic.

>cute co#$lications

Dia&etic 8etoacidosis

Non 8etotic +y$eros#olar co#a

Hy$olyce#iaDia&etic co#a

4



C+ronic Co#$lications

In dia&etes t+e resultin $ro&le#s are rou$ed under [micro*ascular

disease[ 1due to da#ae to s#all &lood 0essels2 and [macro*ascular

disease[ 1due to da#ae to t+e arteries2.

!icro *ascular disease include

Dia&etic !etino$at+y

Dia&etic Neuro$at+yDia&etic Ne$+ro$at+y

Dia&etic cardio#yo$at+y

5



!acro*asular Disease

Coronary artery disease

Stro8e

Peri$+eral 0ascular disease

Dia&etic #yonecrosis

Dia&etic oot

6

>cute Co#$lications



>cute Co#$lications


.ia)etic /etoaci+osis 1DF>2 is a $otentially li)e-t+reatenin

co#$lication in $atients it+ dia&etes #ellitus.

It +a$$ens $redo#inantly in t+ose it+ ty$e 3 dia&etes &ut it can

occur in t+ose it+ ty$e 4 dia&etes under certain circu#stances.

DF> results )ro# an a&solute s+ortae o) insulinZ in res$onse t+e

&ody sitc+es to &urnin )atty acids and $roducin acidic 8etone

&odies t+at cause #ost o) t+e sy#$to#s and co#$lications.

Predo#inant sy#$to#s are nausea and 0o#itin $ronounced t+irst

e%cessi0e urine $roduction and a&do#inal $ain t+at #ay &e se0ere.

7



In se0ere DF> &reat+in &eco#es la&ored and o) a dee$

as$in c+aracter. T+e a&do#en #ay &e tender to t+e $oint t+at an acute

a&do#en #ay &e sus$ected suc+ as acute $ancreatitis

a$$endicitis or astrointestinal $er)oration.

Co/ee round 0o#itin occurs in a #inority o) $atientsZ t+is

tends to oriinate )ro# erosions o) t+e eso$+aus

De+ydration Tac+ycardia " lo &lood 0olu#e #ay &e

o&ser0ed

PATHOGENESIS



smotic'iuresis

:ena .ypoperfusion

Impaired ;(cretion of

Detones E .ydro#en ions

uid E ;ectroyte'epetion

omitin#

Acidosis.yper#ycaemia

9ycosuria

9ucose Detones

Ketoacidosis

is a state of

uncontrolled catabolism

associated with

insulin deficiency.

"ac) of Insuin in ody





Dia&etic 8etoacidosis #ay &e dianosed +en t+e

co#&ination o) +y$erlyce#ia 1+i+ &lood suars2 8etones on

urine analysis and acidosis are de#onstrated.

> 455A >#erican Dia&etes >ssociation state#ent 1)or adults2

cateoriGes DF> into one o) t+ree staes o) se0erity:

!ild Blood $H #ildly decreased to &eteen K.47 and K.@51nor#al [email protected] seru# &icar&onate decreased to 373< ##olLl 1nor#al a&o0e 452Z t+e $atient is alert

!oderate $H K.55K.47 &icar&onate 3537 #ild drosiness#ay &e $resent

'e*ere $H &elo K.55 &icar&onate &elo 35 stu$or or co#a#ay occur

1

Non 8etotic Hy$eros#olar Co#a



y$

Non8etotic +y$eros#olar co#a 1non8etotic +y$erlyce#ia2 is

a ty$e o) dia&etic co#a associated it+ a +i+ #ortalityseen in dia&etes #ellitus ty$e 4.

T+e condition is c+aracteriGed &y se0ere +y$erlyce#ia

it+out sinifcant +y$er8etone#ia or acidosis

Pat+o$+ysioloy

Non8etotic co#a is usually $reci$itated &y an in)ection

#yocardial in)arction stro8e or anot+er acute illness.

> relati0e insulin defciency leads to a seru# lucose t+at is

usually +i+er t+an @@ ##olLl 1A55 #Ldl2 and a resultin

seru# os#olarity t+at is reater t+an @75 #Os#.

2



T+is leads to $olyuria 1an os#otic diuresis2 +ic+ in turn

leads to 0olu#e de$letion and +e#oconcentration t+at

causes a )urt+er increase in &lood lucose le0el.

Clinical eature

Hy$er0iscosity and increased ris8 o) t+ro#&osis.

Vo#itin

Disordered #ental )unctionin.

Neuroloic sins includin )ocal sins suc+ as sensory or

#otor i#$air#ents or )ocal seiGures or #otor a&nor#alitiesincludin *acidity de$ressed re*e%es tre#ors .

,lti#ately i) untreated ill lead to deat+.

3



Hy$olyce#ia

Hy$olyce#ia 1&lood lucose R @.7 ##olLl 2 occurs o)ten in

dia&etic $atients treated it+ insulin &ut relati0ely in)reUuently

in t+ose ta8in sul$+onylurea drus.

Se0ere +y$olyce#ia can result in serious #or&idity " +as a

reconiGed #ortality o) 4- insulin treated $atients.-Co##on sy#$to#s include:-

+utonomic

Seatin tre#&lin $oundin +eart +uner an%iety

Neuroglycopenic

Con)usion drosiness s$eec+ di^culty Ina&ility to concentrate

Non specifc

Headac+e nausea tiredness

4



Hy$olyce#ia induced secretion o) lucaon &eco#es i#$aired in

#ost $eo$le it+in de0elo$#ent o) Ty$e I D'.

>)ter se0eral years #any $atients also de0elo$ a de)ecti0e adrenaline

to +y$olyce#ia.

Causes

-'issed delayed or inadeUuate #eal

-,ne%$ected e%ercise->lco+ol-Errors in oral +y$olyce#ic or insulin dose-'ala&sor$tion-(astro$aresis-Du#$in

5



Dia&etic co#a

Dia&etic co#a is a #edical e#erency in +ic+ a $erson it+

dia&etes #ellitus is co#atose 1unconscious2 &ecause o) one o)

t+e acute co#$lications o) dia&etes:

Se0ere dia&etic +y$olyce#ia


Hy$eros#olar non8etotic co#a in +ic+ e%tre#e +y$erlyce#ia

and de+ydration alone are su^cient to cause unconsciousness.

6

Se0ere +y$olyce#ia



,nconsciousness due to +y$olyce#ia can occur it+in 45 #inutes to an

+our.

Titc+in or con0ulsions #ay occur.

Paleness a ra$id +eart &eat " seatin : all sins o) t+e adrenaline res$onse

to +y$olyce#ia.

,nconsciousness due to +y$olyce#ia is treated &y raisin t+e &lood lucoseit+ intra0enous lucose or injected lucaon.

>d0anced dia&etic 8etoacidosis

Dia&etic 8etoacidosis 1DF>2 i) it $roresses and orsens it+out treat#ent

can e0entually cause unconsciousness )ro# a co#&ination o) se0ere

+y$erlyce#ia de+ydration and s+oc8 and e%+austion.

7

N 8 t ti + l



Non8etotic +y$eros#olar co#a

De0elo$s #ore insidiously t+an Dia&etic Feto >cidosis.

E%tre#e +y$erlyce#ia is acco#$anied &y de+ydration dueto inadeUuate *uid inta8e.

Co#a )ro# NFHC occurs #ost o)ten in $atients +o de0elo$ty$e 4 D' or steroid dia&etes and +a0e an i#$aired a&ilityto reconiGe t+irst and drin8

T+e treat#ent consists o) insulin and radual re+ydration

it+ intra0enous *uids





Dia&etic !etino$at+y

'ost co##on cause o) &lindness in adults &eteen @5 " A7 years o) ae

Dia&etes induced +y$erlyce#ia increases retinal &lood *o "

#eta&olis#.

T+e uncontrolled &lood *o increases $roduction o) 0asoacti0e

su&stances " endot+elial cell $roli)eration resultin in ca$illary closure

-CL

-'icroaneurys#s

-!etinal +e#orr+aes

-E%udates

-Cotton ool s$ots

-Neo0asculariGation

-i&rosis

Di & ti N t+



Dia&etic Neuro$at+y

-T+is is t+e early " co##on co#$lication a/ectina$$ro%i#ately @5 o) dia&etic $atients

/istopathology

>%onal deeneration o) &ot+ #yelinated " un#yelinatedner0e f&ers.

T+ic8enin o) Sc+ann cell &asal la#ina.

Patc+y se#ental de#yelination.

T+ic8enin o) &ase#ent #e#&rane " #icrot+ro#&i inintraneural ca$illaries.

1



'ymptoms

Nu#&ness " tinlin o) e%tre#itiesDiarr+ea

,rinary incontinence 1loss o) &ladder control2

DiGGiness #uscular ea8ness di^cult salloin s$eec+i#$air#ent

Burnin or electric $ain

$reatment

T+e only to drus a$$ro0ed &y t+e D> )or dia&etic $eri$+eralneuro$at+y are t+e antide$ressant dulo%etine and t+eanticon0ulsant $rea&alin

11

Dia&etic Ne$+ro$at+y



Dia&etic Ne$+ro$at+y

Dia&etic ne$+ro$at+y also 8non as i$$elstiel-ilson

syn+ro$e and intercapillary ,lo$erulonephritis is a

$roressi0e 8idney disease caused &y anio$at+y o) ca$illaries

in t+e 8idney lo#eruli.

It is c+aracteriGed &y ne$+rotic syndro#e and di/use

lo#erulosclerosis.

T+e earliest detecta&le c+ane in t+e course o) dia&etic

ne$+ro$at+y is a t+ic8enin in t+e lo#erulus.

>t t+is stae t+e 8idney #ay start alloin #ore seru#

al&u#in 1$las#a $rotein2 t+an nor#al in t+e urine

1al&u#inuria2

12

Clinical eatures



Clinical eatures-

Ede#a: sellin usually around t+e eyes in t+e #orninsZlater eneral &ody sellin #ay result.

oa#y a$$earance or e%cessi0e )rot+in o) t+e urine1caused &y t+e $roteinura2

,nintentional ei+t ain 1)ro# *uid accu#ulation2

anore%ia 1$oor a$$etite2

nausea and 0o#itin

#alaise 1eneral ill )eelin2

)atiue

+eadac+e

)reUuent +iccu$s

eneraliGed itc+in

13

Dia&etic Cardio#yo$at+y



Dia&etic cardio#yo$at+y 1DC'2 is a clinical condition dianosed +en

0entricular dys)unction de0elo$s in $atients it+ dia&etes in t+e

a&sence o) coronary at+erosclerosis and +y$ertension.

One $articularity o) Dia&etic Cardio 'yo$at+y is t+e lon latent $+ase

durin +ic+ t+e disease $roresses &ut is co#$letely asy#$to#atic.

In #ost cases DC' is detected it+ conco#itant +y$ertension or

coronary artery disease.

One o) t+e earliest sins is #ild le)t 0entricular diastolic dys)unction

it+ little e/ect on 0entricular fllin.

>lso t+e dia&etic $atient #ay s+o su&tle sins o) DC' related to

decreased le)t 0entricular co#$liance or le)t 0entricular +y$ertro$+y or

a co#&ination o) &ot+.

14



Dia&etic 'yonecrosis

!are co#$lication o) dia&etes caused &y in)racted #uscle

tissue usually in t+e t+i+.

T+e #ean ae at $resentation is @K years it+ a re$orted

rane o) 3= to A years.

T+e #ean ae o) onset since dianosis o) dia&etes is 37 years.

T+e )e#ale: #ale ratio is 3.@:3.

Its #ajor sy#$to# is t+e acute onset #uscle $ain usually in

t+e t+i+ in t+e a&sence o) trau#a. Sins include #uscle

tenderness and sellin.

15

Dia&etic oot



Dia&etic oot-

oot is )reUuent site o) co#$lications )or dia&etes seen al#ost

in 35-37 o) dia&etic $atients.

Occurs as a result o) trau#a in t+e $resence o) neuro$at+y "

$eri$+eral 0ascular disease it+ in)ection occurrin as a

secondary $+eno#enon )olloin ulceration in $rotecti0e

e$ider#is

16

In*uence o) Dia&etes on oral Healt+



Oral co#$lications o) dia&etes #ay include:-

>lterations in sali0ary *o

Increased incidence o) in)ection

Burnin #out+

>ltered ound +ealin

Increased $re0alence and se0erity o) $eriodontal disease.

_erosto#ia and $arotid land enlare#ent

>lterations in oral *ora it+ reater $redo#inance o) Candida

>l&icans +e#olytic stre$tococci " sta$+ylococci

Increased caries rate #ay &e associated it+ decreased sali0ation or

it+ increased lucose concentrations in sali0a " (C

17

Periodontal 'ani)estation



o) Dia&etesStron e0idence to su$$ort t+is state#ent co#es )ro# t+e

National Healt+ and Nutrition sur0ey III 1NH>NES III2 +ic+e%a#ined <45= $artici$ants &eteen 3=<< and 3==

1

Dia&etes " $eriodontitis: a to ay street



1



i 3 t t /i



roin3a$$atory cyto/ines4

Patients it+ in*a##atory $eriodontal diseases o)ten +a0e

ele0ated seru# le0els o) $roin*a##atory cyto8ines.

In $atients it+ dia&etes +y$erin*a##atory i##une cells can

e%acer&ate t+e ele0ated $roduction o) $roin*a##atory

cyto8ines.

T+is +as t+e $otential to increase insulin resistance and #a8e it

#ore di^cult

)or t+e $atient to control +is or +er dia&etes

111

Periodontiu#



9in#i/a ;nar#ement

9in#i/a oyp

'eep eriodonta oc)et 9in#i/a Infammation

Increased Tooth &obiity

eriodonta Abscess

Tooth oss E Increased a/% one destruction

Dia&etes'ellitus

112

oss o) attac+#ent



oss o) attac+#ent

Dia&etes #ay in*uence not only t+e $re0alence and se0erity o)

$eriodontitis &ut also t+e $roression o) disease.

Periodontal attac+#ent loss +as &een )ound to occur #ore)reUuently in #oderate to $oorly controlled dia&etic $atients o)&ot+ Ty$e I " II dia&etes #ellitus t+an in t+ose under control1est)elt et. al.3==42

Taylor and colleaues 13==<2 de#onstrated t+at ty$e 4dia&etes sinifcantly increased t+e rate o) al0eolar &one loss$roression o0er a 4-year $eriod +en co#$ared to

nondia&etic su&jects. T+e ris8 )or $roressi0e &one loss as .4ti#es reater in dia&etic su&jects it+ t+e reatest increase inris8 occurrin in $atients under t+e ae o) @ years.

113



Dia&etes #ay e%ert an e/ect on t+e $eriodontiu# t+rou+

Cyto8ine dysreulation.

T+is is su$$orted &y studies in +ic+ $oor lyce#ic controlas sinifcantly correlated it+ reater $roduction o)cyto8ines and +i+er cyto8ine le0els in ini0al *uid1Ene&retson et al0 4552.

TN dysreulation

urt+er#ore dia&etic #ice e%+i&it $roloned in*a##ation inres$onse to )0 gingi*alis +ic+ is due in $art to TN

dysreulation 1Naui& et al0 4552. Increased in*a##ationcould a/ect t+e net loss o) &one &y increasin &one lossin+i&itin re$air o) resor&ed &one or &ot+.

114



>$o$tosis o) &one linin cells

T+e fndin t+at dia&etes sinifcantly increased a$o$tosis o)&one-linin cells raises t+e $ossi&ility t+at en+anceda$o$tosis #ay inter)ere it+ t+e re$air o) resor&ed &one.Increased a$o$tosis o) PD cells could also a/ect t+e re$air$rocess since it is t+ou+t to &e a ric+ source o) cellsca$a&le o) di/erentiatin into osteo&lasts 1Isa8a et al0

45532

T+e +i+er rates o) a$o$tosis could &e due to t+e sa#e#ediators t+at +a0e &een i#$licated in $roloned

in*a##ation na#ely cyto8ines suc+ as TN or ad0anced

lycation end-$roducts.

115

Periodontal a&scess



Periodontal a&scess

-T+e #ost classic descri$tion o) undianosed or $oorly controldia&etes is $atient $resentin it+ #ulti$le $eriodontala&scess.

Harrison et. al. 13=<@2 re$orted a case o) dee$ nec8 in)ection

o) su&#ental su&linual " su&#andi&ular s$aces secondaryto $eriodontal a&scesses in0ol0in #andi&ular incisors in a$oorly control dia&etic $atient.

,eta et. al. 13==@2 in a $o$ulation study de#onstrated t+at

Dia&etes as a $redis$osin )actor )or de0elo$#ent o)$eriodontal a&scess )or#ation due to su$$ression o)neutro$+il )unction.

116

Bacterial Pat+oens



Bacterial Pat+oens

- lucose in ini0al *uid " &lood o) dia&etic $atientsinduces Uualitati0e c+ane in &acteria t+at can contri&ute tose0erity o) $eriodontal disease.

-Patients it+ Ty$e I D' " $eriodontitis +a0e &een re$ortedto +a0e a su&ini0al *ora co#$osed #ainly o):

Capnocytophaga sp1.22

Patient it+ ty$e II D' " $eriodontitis

)re*etella Intermedia

Campylobactor 3ectus)ophyromonas Gingi*alis

+ggregatibactor +ctinomycetemcomitans 1 Ya#&on et al.3=<<2

117

Se$$ala " >ina#o 13==A2 s+oed t+at in an insulin



$$ 1 2

de$endent dia&etic $o$ulation it+ a lare $ro$ortion o)$oorly control dia&etics sinifcant increase in t+e

$ercentaes o) s$iroc+etes " #otile rods " decreased le0elo) cocci in t+e $eriodontal lesions ere seen co#$ared it+ell controlled dia&etes le0els.

11



.e*ecti#e a+hesion



)ossible explanation )or t+e a&nor#al leu8ocyte )unction india&etes #ellitus #i+t &e a don-reulation o) ad+esion#olecules t+at reulate leu8ocyte recruit#ent durin t+e courseo) in*a##atory $rocesses.

Sanno#iya P et. al13==K2. ortes YB et. al.13==32 in a study

s+oed t+at:-

I#$aired local e%udati0e cellular reaction in allo%an-induceddia&etic rats is a conseUuence o) de)ecti0e leu8ocyte-endot+elialinteractions.

Intra0ital #icrosco$ic e%a#ination o) t+e internal s$er#atic)ascia #icrocirculatory netor8 s+oed t+at a reduced nu#&ero) leu8ocytes rollin alon t+e 0enular endot+eliu# is o&ser0ed)ro# t+e early staes o) dia&etes.

12

Polyol Pat+ay



121



De)ecti0e 'iration



-In0estiators de#onstrated i#$aired c+e#otactic $e$tide)or#yl-

'et-eu-P+e-induced #iration o) neutro$+ils t+rou+

endot+elial cell #onolayers suestin t+at sustainedsti#ulation o) neutro$+ils

it+ >(Es #i+t reduce t+eir a&ility to res$ond to $+ysioloicalc+e#otactic sti#uli. 1Collison FS et al 45542

123

(luta#ine



(luta#ine $lays an i#$ortant role in $rotein 1as an a#ino acid

source2 li$id 1&y N>D1P2H $roduction2 and nucleotide synt+esis1&y $urine " $yri#idine $roduction2 " in N>DPH o%idase acti0ity.

(luta#ine raises t+e in *itro bacterial %illing acti*ity 4 t+e rateo) reacti0e o%yen s$ecies $roduction &y neutro$+ils.

Pit+on-Curi et al. s+oed t+at luta#ine +as a $rotecti0e e/ecton neutro$+il a$o$tosis. (luta#ine o%idation and luta#inaseacti0ity are sinifcantly decreased in neutro$+ils )ro# dia&eticrats.

T+ere)ore decreased luta#ine utiliGation #ay contri&ute to t+ei#$aired in*a##atory res$onse in dia&etic $atients &yincreasin t+e occurrence o) a$o$tosis in neutro$+ils.

124

E/ect on Cyto8ines 'onocytes " #acro$+aes



Hi+er le0els o) I-3X " P(E4 is seen in $eriodontitis in

dia&etic $atients as co#$ared to non dia&etics.

!elease o) cyto8ines 1I-3X P(E4 TN-2 &y #onocytes +as

&een s+on to &e sinifcantly reater in dia&etics t+an innon dia&etic controls.

125

>ltered collaen 'eta&olis#



Increased collaenase acti0ity " decreased collaen

synt+esis osteo$orosis " reduction in t+e +ei+t o) al0eolar&one occur in dia&etic ani#als

C+ronic +y$erlyce#ia ad0ersely a/ects t+e synt+esis#aturation " #aintenance o) collaen " e%tracellular #atri%

in t+e +y$erlyce#ic state.

Nu#erous $roteins " #atri% #olecules undero a nonenGy#atic lycosylation resultin in accu#ulation o)>d0anced (lycation End $roducts 1>(Es2.

>(Es $lay a central role in dia&etes co#$lications

126

Increased &indin o) >(Es to #onocytes " #acro$+aes



result in destructi0e cell $+enoty$e it+ increased sensiti0ityto sti#uli resultin in e%cessi0e release o) cyto8ines

>ccu#ulation o) >(Es in $atients it+ dia&etes alsoincreases t+e intensity o) t+e i##uno in*a##atory res$onseto $eriodontal $at+oens &ecause in*a##atory cells suc+as #onocytes and #acro$+aes +a0e rece$tors )or >(Es.

>ltered #acro$+ae $+enoty$e due to cell sur)ace &indinit+ >(E $re0ents de0elo$#ent o) #acro$+aes associatedit+ re$air.

Interactions &eteen >(Es and t+eir rece$tors onin*a##atory cells result in t+e increased $roduction o)$roin)la##atory cyto8ines suc+ as I-3X and TN-.

127

T+is interaction #ay &e t+e cause o) t+e #ar8ed ele0ation in(C le0els o) I-3X " TN- seen in su&jects it+ dia&etes



(C le0els o) I 3X " TN seen in su&jects it+ dia&etesco#$ared it+ t+ose it+out dia&etes

Cross lin8in o) collaen &y >(Es )or#ation #a8es it lesssolu&le " less li8ely to &e nor#ally re$aired or re$laced.

Cellular #iration across cross lin8ed collaen is i#$eded "

tissue interity is i#$aired.

Collaen in $atients it+ $oorly controlled dia&etes is aed "#ore susce$ti&le to &rea8donQ

12

E/ect on connecti0e tissue



!educed $roduction " utiliGation o) insulin in +y$erlyce#ic

en0iron#ent can reduce rot+ $roli)eration " #atri% synt+esis &yini0al " PD f&ro&lasts " osteo&lasts.

!eacti0e o%yen s$ecies $roduced &y )or#ation o) >(Es are da#ainto cellular )unction o) ini0al tissues 1due to o%idati0e stress2

Vascular c+anes suc+ as t+ic8enin o) ca$illary &ase#ent #e#&ranein +y$erlyce#ic en0iron#ent can i#$air o%yen di/usion #eta&olicaste eli#ination P'N #iration " di/usion o) anti&odies.

Bindin o) >(Es to 0ascular endot+elial cells can trier res$onses

t+at induces coaulation leadin to 0asoconstriction " #icrot+ro#&us )or#ation resultin in i#$aired $er)usion o) tissue.

(lucose >(E " nicotine in+i&it t+e synt+esis o) steroid #ar8ers o)ound +ealin.

12

E/ect on +ealin " TLt res$onse



ound +ealin is i#$aired due to cu#ulati0e e/ects on

cellular )unctions. T+ese )unctions include:

32 Decreased synt+esis o) collaen &y f&ro&last

42 Increased deradation &y collaenase

@2 (lycosylation o) e%istin collaen at ound #arins2 De)ecti0e re#odelin " ra$id deradation o) nely

synt+esiGed $oorly cross lin8ed collaen

13

)eriostat



)eriostat

Do%ycycline Hyclate- in+i&its collaenase acti0ity andreduces t+e collaenase acti0ity in ini0al cre0icular *uido) $atients it+ adult $eriodontitis

Indicated )or use as an adjunct to scalin and root $lanin to

$ro#ote attac+#ent le0el ain and to reduce $oc8et de$t+s

Periostat is a0aila&le as a ta&let145#2 to &e ta8en orallyto ti#es a day 1a&out an +our &e)ore or to +ours a)ter#eals2. S+ould &e ta8en it+ $lenty o) *uids.

Ty$ical treat#ents rane )ro# @#ont+s to 34#ont+s

131

Periostat is t+e frst and only t+era$eutic aent desined to



#odulate t+e +ost res$onse and +el$s to slo t+e$roression o) $eriodontal disease.

Periostat s+ould &e used +en traditional SCL!P treat#entsalone are ine/ecti0e &ut &e)ore surery is indicated.

Su&ini0ally deli0ered do%ycycline +yclate $roducesadditional )a0ora&le clinical results to $eriodontal t+era$y inty$e 3 D' $atients.

132



PE!IODONT> C>!E ON

DI>BETICS P>TIENTS

133

Protocol )or Treat#ent:Clinician s+ould #a8e sure t+at $rescri&ed insulin +as



Clinician s+ould #a8e sure t+at $rescri&ed insulin +as&een ta8en )olloed &y a #eal

'ornin a$$oint#ents are a$$ro$riate &ecause o)o$ti#al insulin le0els

'onitor 0itals includin &lood lucose $rior totreat#ent

Procedures $er)or#ed #ay alter t+e $atientQs a&ility to#aintain caloric inta8e t+ere)ore $ost-o$ insulin doses

s+ould &e altered accordinly Tissues s+ould &e +andled as atrau#atically and#ini#ally as $ossi&le 1less t+an 4 +rs2

E$ine$+rine s+ould not &e used in concentrationreater t+an 3:355555 due to e$ine$+rine e/ects oninsulin

Diet reco##endations s+ould &e #ade to #aintain$ro$er lucose &alance

reUuent recall and )astidious +o#e oral care s+ould&e stressed

134



T+e #ost co##on dental o^ce co#$lication seen india&etic $atients ta8in insulin is sy#$to#atic lo &loodlucose or hypoglycemia.

Hy$olyce#ia does not usually occur until &lood lucosele0els )all &elo A5 #Ldl. Hoe0er in $atients it+ $oorlyce#ic control +o +a0e $roloned hyperglycemia 1high&lood lucose le0els2 a ra$id dro$ in lucose can $reci$itatesins and sy#$to#s o) +y$olyce#ia at le0els ell a&o0e A5

#Ldl.

135

I) + l i d i d t l t t t t+ + ld &



I) +y$olyce#ia occurs durin dental treat#ent t+era$y s+ould &ei##ediately ter#inated. I) a luco#eter is a0aila&le t+e &lood lucose

le0el s+ould &e c+ec8ed. Treat#ent uidelines include t+e )olloin.1 'ealey B 3==<2

3. Pro0ide a$$ro%i#ately 37 o) oral car&o+ydrate to t+e $atient:

to A oG o) juice or soda

@ or ts$ o) ta&le suar

Hard candy it+ 37 o) suar4. I) t+e $atient is una&le to ta8e )ood or drin8 &y #out+ or i) t+e $atient

is sedated:

(i0e 47 to @5 #l o) 75 de%trose intra0enous 1IV2 +ic+ $ro0ides 34.7to 37.5 o) de%trose or

(i0e 3 # o) lucaon IV 1lucaon results in ra$id release o) storedlucose )ro# t+e li0er2 or

@. I) $atient is una&le to ta8e )ood &y #out+ and intra0enous line is not in$lace i0e:

(i0e 3 # o) lucaon intra#uscularly or su&cutaneously 1i) no IV access2.

136

In $eriodontal t+era$y #ay render t+e $atient una&le t5 eat)or so#e ti#e adjust#ent in insulin or oral aent dosaes



j #ay &e reUuired.

It is a&solutely critical t+at $atients eat t+eir nor#al #eal&e)ore dental treat#ent. Ta8in insulin it+out eatin is t+e$ri#ary cause o) +y$olyce#ia.

>s a eneral uideline well controlled diabetic patientsha*ing routine periodontal treatment may ta%e their normalinsulin doses as long as they also eat their normal meal0

137



!is8 )actors )or

+y$olyce#ia in $atients

S8i$$in or delayin #eals

Injection o) too #uc+ insulin

E%ercise

Increasin e%ercise le0el it+out adjustin insulin orsul)onylurea dose

>lco+ol consu#$tion

Ina&ility to reconiGe sy#$to#s o) +y$olyce#ia

>n%ietyLstress

Patient #ay con)use sins o) +y$olyce#ia it+ an%iety Denial o) arnin sinsLsy#$to#s

Past +istory o) +y$olyce#ia

Hy$olyce#ia unaareness

(ood lon-ter# lyce#ic control 13

S,''>!



Dia&etes is an e$ide#ic disease it+ a ide s$read#ani)estations " li)e t+reatenin co#$lication on ot+er &odyorans. In 4555 accordin to t+e orld Healt+ OraniGationat least 3K3 #illion $eo$le orldide su/er )ro# dia&etesor 4.< o) t+e $o$ulation. Its incidence is increasin ra$idly

and it is esti#ated t+at &y t+e year 45@5 t+is nu#&er illal#ost dou&le. T+e #anae#ent o) dia&etes s+ould includenot only t+e treat#ent o) disease " underlyin co#$lication&ut also t+e eli#ination o) ris8 )actors " c+ane in dietary+a&it " li)estyle.

13



TH>NF O,

Date post:	20-Feb-2018
Category:	Documents
Upload:	vinay-jain
View:	218 times
Download:	0 times

FINAL DIABETES & ITS ROLE IN PERIODONTICS...ppt

Documents