dm lecture (2)
TRANSCRIPT
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dr. Dita Ria Selvyana, Sp.PD,
M.Sc
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What is diabetes (DM)?Glucose in your blood is fro ! ayor sources"
food and the liver
DM is a disease characteri#ed by elevated blood$lucose level, it is result of defective insulinsecretion or action (resistance) or both.
Resultin$ chronic hyper$lyceia is daa$e ordysfunction of various or$an (the eyes, %idneys,nerves, heart, and blood vessels).
&linical syptos" 'P cessive thirst(polydipsia) increased urination (polyuria),increased appetite (polypha$ia) and *ei$ht loss.
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+MPR-/-0ealthy pancreas have" 122 222
3an$erhans island and every3an$erhans" 122 4 cells (insulinproduction) 12.222.222
+nsulin and insulin receptors li%e %ey andthe door
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Historical milestones in DMDate Source bservation
1550 BC1-2ndcntry AD5thcentury
10thcentury
17th century18th century
19th century
19th century
20th century
20thcentury
Egypttian papyrusGalen !oman"# $retaeus Gree%"&usruta# '(aru%a )n*ian"
$+icenna $ra,ia"
-illis Englan*"Do,son# 'a.ley Englan*"
/ernar* renc("
anger(ans# Min%o.s%i#+onMering Germany"/anting o+ 14t("# /est#Macleo*# 'ollip 'ana*ian"Ho*ge%in# &anger Englan*"
Eessi+e ammount o urine&ugary urine# Eessi+et(irstDescri,e* sugary urine*istinguis(e* o,ese an*t(inpatients
&ugary urine# gangrene impotence ascomplicationsDia,etic urine containssugar&ugar in serum in*ia,etes# *ia,etes may
ollo. pancreatic *amageGlucose store* as glycogenon li+er# eocrine*egeneration o pancreasoccurs ater ligature o t(epancreatic *uctancreatic islets#
pancreatomy causes*ia,etes
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atient 15 Decem,er# 1922
atient 15 e,ruary# 1923
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P+DM+3G5W0 stiation" +ndonesia have people
*ith DM (!2'2)"
Rural " 6,! 7 fro adult (8!2 years old)
9rban" 1:,6 7 fro adult
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ist of Top Ten Global Number of People
ist of Top Ten Global Number of People
with Diabetes in 1995 and 2025 (in millions)
ith Diabetes in 1995 and 2025 (in millions)
!" 199#
!" 199#
+ndia&hinaRussian ;ederation1
>@
@:::
?
@6'A1!
>11
1!1@1!
?
>
1>>@ !2!@
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-op &ountries *ith Diabetes-op &ountries *ith Diabetes
um,ers o persons millions"um,ers o persons millions"
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&ource Dia,etes $tlas 2000
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@.
A.!
2,'62,1!7
162,2!',6@@ 7
!2,'!>,:7
1A,@
!>,@27
!1,:'>,:A:7
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-ype of DM1. -ype 1 (+DDM" insulin dependent DM)
!. -ype ! (/+DDM" non insulin dependentDM)
B obese B non obese
'. thers ($enetic cell function & insulin action,disease of exocrine pancreas, drugs, endocrinopathies,
infections, immune, others.
4. Gestasional
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1. -ype 1 DM@B!@7 of cases (pancreatic islet cell
deficiency)
Is a chronic-progressive autoimmune disease isletcell and insulin antibodies
he incidence is higher in children
!ssociated "ith autoimmune features and includes a
broad range of clinical presentation of all ageIdentification of autoantibodies in the general
population can predict type # $%
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!. -ype ! DM6@B>@7 of cases (defective insulin action
or secretion)
+nsulin resistance+nsulin secretory defect cell function)
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/ l Gl M t b li
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/oral Glucose Metabolis
G39&/
G/S+S
GLYCOGENOLYSIS
Insulin
HGP
Glucose
uptake +
G39&S
/RM3
G 35&G/
G 3 9& S
C Suppression
C Stiulation
-
+
LIVER PANCREAS
M9S&3
B
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PathophysioloyPathophysioloy o! "ype # $ia%eteso! "ype # $ia%etes
$ec&ease' lucose uptakeInc&ease' lucose p&o'uction
Hype&lyce(ia
I(pai&e' insulin actionI(pai&e' insulin sec&etion
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Patho$enesis of type ! diabetesPatho$enesis of type ! diabetes ""
-he-he (dys)B(dys)B0aronious EuartetF0aronious EuartetF
9+/-SS/-+3 9+/--9+/-SS/-+3 9+/--
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9+/-SS/-+3 9+/--9+/-SS/-+3 9+/--
0yper$lyceia
+ncreasedlipolysis
+paired +nsulinsecretion
+ncreased0GP
Decreased Glucoseupta%e
Decreased+ncretin eHect
uintus : ;+e
Deron
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SetaceousSetaceous
SetetSetet
0yper$lyceia
+ncreasedlipolysis
+paired +nsulin
secretion
+ncreased0GP
Decreased Glucoseupta%e
Decreased
+ncretin eHect
+ncrease$luca$onsecretion
+slet Bcell
Setaceous = smooth like fur
Deron
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&eptici*al &eptet&eptici*al &eptet
0yper$lyceia
+ncreasedlipolysis
+paired +nsulinsecretion
+ncreased0GP
Decreased Glucoseupta%e
Decreased
+ncretin eHect
+ncreaseGluca$onsecretion
+slet Bcell
/eurotransitterdysfunction
??
Septe C seven
Deron
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Pro$ression to -ype! Diabetes
0yperinsulineia
&opensated +nsulin Resistance/oral Glucose -olerance
B &ell ;ailureF Genes
-ype ! Diabetes
+paired Glucose -olerance
GenescEuired
besity Sedentary 3ifestyl $in$
+nsulin Resistance
ormal
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(ysiology o insulin secretion
Islet
transcription
factors
SS
UU
RR
))ATP/ADPATP/ADP
PyruvatePyruvate
Glucose-6-PhosphateGlucose-6-Phosphate
GlucoseGlucose
GlucokinaseGlucokinase NucleusNucleusSecretorySecretory
granulesgranules
CaCa!!
CaCa++++
Voltage-dependentVoltage-dependentCaCa2+2+ channelchannel
Depolari"ationDepolari"ation
ATP-sensitiveATP-sensitive
KK++channelchannel
#itochon$ria#itochon$ria
GlucoseGlucose
G%&TG%&T
InsulinInsulin
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&e! *e&sion #,
Insulin Resistance
A co&e 'e!ect in (ost type # 'ia%etes
patients
$e!inition
I(pai&e' &esponse to the physioloical
e!!ects o! insulin. inclu'in those on
lucose. lipi'. p&otein (eta%olis( an'*ascula& en'othelial !unction
Diab Care 1999;22:562Diab Care 2000; 23(Sul 1!:5"
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)&>) !E&)&?$'E+nsulin si$nallin$
besity and diet
ndocrine diseasesPre$nancyDru$Malnutrition in utero and early
childhood
Mutation
+nsulin receptorPost receptor defect
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)&>) !E&)&?$'E
D;&- ; +/S93+/&-+/
1. Muscle
!. dipose
'. 3iver
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'vereatingInactivity
(moing$iabetogenic drugs
*regnancy+ndocrine diseases$iabetogenic drugs
%alnutrition in utero
nno"n nno"n
- cell defectsInsulin resistance
Genetic !acto&sGenetic !acto&s
Glucose toxicity
yperglycaemia
/orsening -cell functions0 !myloid deposition%alnutrition in utero
I(pai&e' lucose
tole&ance
1I$$%
En*i&on(ental !acto&sEn*i&on(ental !acto&s
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NGT
/oro$lyceia
$GT
+paired $lucosetolerance
T2D%
-ype ! diabetes ellitus
-cell exhausted1ormo-, or hypo-
insulinemia
1ormal -cellhyper-
insulinemia#.2 years
3.3 years
Weyer et al. J Clin Invest. 1999; 104: 787-94
#-5per year
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5ears ;ro Dia$nosis
-! DMphase +
-! DM
phase ++
Sta$es of -ype ! DiabetesSta$es of -ype ! Diabetes
e,o+it
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Insulin secretion Insulin sensitivity
6 5 7 $% 36 5
86 -#66 5 IG 6 5
#6 5 Impaired glucose 86 5
metabolism
#66 5 1ormal glucose metabolism #66 5
he natural history of ype 7 $iabetes 39
3 At( t
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3@ At(ers typeGenetic defect of cell function
%'$9 #-4), mithochondrial $1! 3747 mutation
Genetic defect of insulin action
$iseases of exocrine pancreas
pancreatitis, trauma:surgery, neoplasia, cystic fibrosis
+ndocrinopathies
Infections ; rubella ,
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:. Gestasional DMPre$nancy induces state of insulinresistance *ith increases of the level of"
B Growth hormone
- progesterone
- placental lactogen
- cortisol
9ntreated $estasional DM has been sho*nperinatal ortality of :,: B ,:7 copared2,@ I 1,@7 in a siilar ethnicnoro$lyceic population.
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Diagnosis -HA
classi;cation" Jenous plasa $lucose($Kd3)
ormal asting 2( postBpran*ial
C 110C 140
Dia,etes mellitus asting 2( postBpran*ial
126 200
)mpaire*Glucose?olerance )G?"
asting 2( postBpran*ial
C 110140B199
)mpaire* astingGlucose )G"
asting 2( postBpran*ial
110 B 125C 140
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/)n t(e a,sence o symptom# t(e *iagnosis o DM must ,e con;rme*,y a secon**iagnosis test i@e@ asting# ran*om# or Aral Glucose ?olerance ?est
AG??" on a separate *ay
Sypto of
Sypto of
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D + = - S M 3 3 + - 9 S +G- +;G /RM3
Sypto ofDiabetes
Sypto ofDiabetes
&lassical Syp(L) &lassical Syp (B)
;=G
or
!hpp
81!
8!22
1!
!22
;=G
or
!h pp
112112 B 1!
112B1>>Repeat ;=G or !hpp
;=G
or
!h pp
81!
8!22
1!
!22
G--
!h pp
8!22 1:2 B 1>> 1:2
81!
8!22
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!is% actors o DM
;aily history
ver *ei$htKobeseKinactivity$e0ypertensionDyslipideia
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DM Relative *ith DM Ris% ofDM
?ype 1 Mot(erat(er&ister or ,rot(er
?.in sister or ,rot(er
2 910
50
?ype 2 Mot(erat(er/ot( parents
&ister or ,rot(er?.in sister or ,rot(er
1914
257599
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ssesent of the ne*ly
dia$nosed patient0ystory"
Duration of sypto" thirst, polyuria,*ei$ht loss
Possible secondary causes of diabetes
;aily history
Pressence of coplication of diabetes
Ris% factor for developin$ coplications"so%in$, hypertension, hyperlipideia
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FFF
aination"
=M+ (body ass inde *ei$ht (%$)Khei$ht!()&lues for secondary causes&ardiovascular syste (=P L pulse)Si$n of autonoic and peripheral neuropathy
yes for retinopathy+nvesti$ation"=lood test for" GDP, GD!
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When you have diabetes,
youre"
-*enty ties ore li%ely to developQ+D/5 disease
;our ties ore li%ely to have a S-RQ
;our ties ore li%ely becoe =3+/D
-*o to four ties ore li%ely to have a
0R- attac%
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Researchers continue to a%e $reatpro$ress *hat tri$$ers coplicationDM N ho* to ana$e or prevent the
=lood su$ar close to noral reduceris%s of coplication
&ontrolled blood su$ar not to late to
start (s soon as be$in ana$in$ bloodsu$ar level slo* the pro$ression ofcoplication N reduce chances ofdevelopin$ coplication
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&MP3+&-+/S of DM
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&9-
1.Diabetic %etoacidosis (DQ)
!.0yper$lyceic hyperosolar state (00S)
'.0ypo$lyceia
&0R/+&
1.Microan$iopathy (retinopathy,
nephropathy, neuropathy,&ardioyopathy, Diabetic foot, etc)
!.Macroan$iopathy (0eart attac%K+M,Stro%e, PD)
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&hronic coplicationsDevelopent of other diseases 3on$Bter DM coplications are those
that develop $radually and that aybecoe disablin$ or liveBthreatenin$.-hey include nerve, %idney, eye, heartand blood vessel disease
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M+&RJS&93R
R-+/P-05
/P0RP-05
&RD+M5P-05
/9RP-05
9-/M+& &RD+&
GS-R+&
9RG/+-3
&0R/+& &MP3+&-+/S
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&0R/+& &MP3+&-+/
M&RJS&93R
&0D !)& 2 4
DE$?H
60
&R=RJS&93R
&?!AE 4
PR+P0R3 JD40 50 //B-R9M-+&MP9--+
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!etinopat(yRetina is bac% part of eye, is nourished byany tiny vessel. -he blood vessels areoften aon$ the Orst to be daa$ed by
blood su$arveryone *ith type 1 DM N K12 type ! DM
developed retinopathy after !2 years
Most people only ild vision probles. ;or
others *ith severe includin$ blindnessDM is leadin$ cause blindness in adults
(each year 1!222 I !:222 cases)
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+f bleedin$ is heavy or occurs in the
certain it can obscure your vision/e* blood vessel (neo vascularisation)
also can for scar tissue can push N pullon your retina and distour vision
Special treatent by an optalolo$ist*th 3aser or Jitrectoy
+portant to cath the disease early sothat it can be treated
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0o* is it -reated?
(retinopathy)Re$uler eye eainations to identityproble early
3aser procedure to seal *ea% blood vessel
+n ost cases only one eye is treated at atie ay several treatents pain
=leedin in the iddle eye need sur$icalprocedure to reove the blood an replace
*ith clear uidDetached (ablatio) retina by scar tissue
reEuires sur$ery to position the retina inplace
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/ephropathy+nside %idney are illion tiny bloodvessel Olter *aste fro the blooddisposed to urine
DM can daa$e this delicate Olterin$syste, before developed any sypto
More 'K12 type 1 DM nephropathy
1K12 type ! DM nephropathy
-ype DM youn$er, lon$er have DM hi$herris% of %idney daa$e
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Si$n N syptomS*ellin$ of an%les, feet and handsShortness of breath0i$h blood pressure
&onfusion or diculty concentratin$Poor appetite
/ausea and voitin$
Dry, itchy s%in;ati$ue
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0o* is treated?
(nephropathy)-reatent depends on ho* advance thedisease is. Qeepin$ =G level noral canprevent your condition fro $ettin$*orse, possibly iprove.
& inhibitors ay help hypertensionN heart proble
R= can iprove %idney function anddecrease icroalbuinuria
3o* protein diet sees to reduce*or%load of %idney (consult doctors Ndietician)
Severe daa$e *ith (SRD) transplant,0eodialyse or &PD (continous
abulatory peritoneal dialyse) 59
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/europathy0ave an intricate net*or% of nerves runsthrou$hout the body, connectin$ brain touscles, s%in and other or$ans.
=rain senses pain, control the uscles,and perfor autoatic tas% such asbreathin$ and di$estion
/europathy aHect K12 type ! DM
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Si$n N sypto
Many %ind of nerve daa$eMany %ind of nerve daa$e
Wea%ened uscles N an unsteady *al%
utonoic nerves can increase heart
rate N perspiration level+n en can interfere to ability erection
+n sensory nerves daa$e unable
detect sensation such as pain, *arth,coolness an* teture
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Si$n N sypto&oonly daa$e often in the le$s
-in$lin$ feelin$, nubness, pain orcobination these sensation
=urnin$ pain coes and $oes
Discofort as a cra*lin$ sensation
=e$in in tips of toe or On$er or bothand $radualy spread up*ard
Daa$e nerve in toe, if untreated canlose of all sensation hi$h ris% forinTury *ithout reali#in$
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Si$n N sypto
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Si$n N sypto;oot care very iportant
+f lost feelin$ in the feet and not to
chec% the each day, ay not reali#ehave a cut or open *ound until seriousinfection
-he ain cause of aputations in DM
2.222 aputation each year in DM
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0o* is it treated?(neuropathy)Good =G control *ill reduce your
syptos
-o relieve pain" pain reliever orantidepressantor antisei#ureedication
&apsaicin crea (hot pepper etract)
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0eart and blood vessel
DM draatically increased your ris% ofdevelopin$ one of any cardiovascularprobles, includin$"
&hest pain (an$ina)0eart attac%Stro%e/arro*in$ of the arteries (le$s and brain poor
blood circulation) peripheral vascular disease
0i$h blood pressureDM can daa$e ayor arteries (supply heart N
brain) easier for fatty deposits (plaEues)increase pressure in arteries N reduce bloodcirculation
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Si$n N syptoSyptos heart disease vary. arly sta$eproduce no sypto. 3ater ay include"
Shortnss of breath
Pain of the chest, Ta* or ar;ati$ue or *ea%ness
S*ellin$ (edea)
Rapid or irre$uler heart beat (palpitation)
People *ith DM are particular ris% for silent(asyptoatic) heart attac%s *ithouttypical sytops (painless)
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0o* it is treated?Many fors of heart disease are treated*ith edicationto prevent syptofro *orsenin$
+f accuulation of plaEues in the arteriesay procedure an$ioplasty to openarteries soeties bypass arteriessur$ery
-o prevent includin$ healthy diet, oreeercise, stoppin$ so%in$, losin$*ei$ht (if over *ei$ht)
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Ris% of infection0i$h =G ipaired function the iune
cells to O$ht oH $er Nbacteria infection
3ocation" outh, $us, lun$s, s%in, feet,bladder and $enital
0i$h =G daa$e nerve other*isealert infection
daa$e nerves to control bladdersensation fail alert bladder is fulloverstreched lose uscle tone abilityyo epty copletely bacteria ay$ro* infection
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Si$n and syptoMany vary dependin$ location ofinfection
3o* $rade fever
Gu " red and bleedin$
=ladder" freEuent urination, ur$ency andburnin$ sensation
Ja$ina" itchin$ NKor dischar$e in va$ina;oot" redness N pus are *arnin$ an
infection
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0o* it is treated?ntibiotic to %ill bacteria foot inTury" procedure to clean the
inTured area and reove infected tissue
Reduce ris% of $u disease by brushin$and ossin$ the teeth re$ularly
Reduce ris% of bladder infection by $oin$
the bathroo re$ularly and a%in$ sureto epty the bladder
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+MP-/& i DM
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+MP-/& in DMRefers" inability an erection of the penis
oror inability an erection lon$ enou$hfor seual intercourse
Physical" ecess blood su$ar can daa$ethe nerves N blood vessel no lon$er
counication nerves to sall bloodnerves to sall bloodvesselvesselN lar$e blood vessel narro*ed orlar$e blood vessel narro*ed or
bloc%edbloc%ed not enou$h blood to erection(coon in DM)
Psychological:aniety, stress ordepression ipaired =rain and 0orones=rain and 0orones
respondrespond
Medication:dru$s for hypertension,
aniety N depression 70
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MD+&-+/ of
+MP-/&)@ SildenaOl (Jia$ra, ndro#, de$ra,Sila$ra)isnt eHective for everyone 1 hour before activity eHective : hours
++. lprostadil (synthetic of prosta$landin B1)
not a pill self intraurethral (a $rain rice) or self inTection therapy (@B!2 inutes before
and 1 hour erection)
+++. Jacuu device
+J. Penile iplanta. seiri$id, benabled rod (peranenterection)
b. inantable (*ith pup in scrotu producean erection only *hen you *ant)
J. &ounselin$ (if psycholo$ycal factors) 71
P ti li ti
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Preventin$ coplication-i$ht =G control noral or nearB
noralDiabetes &ontrol and &oplication -rialDiabetes &ontrol and &oplication -rial
(D&&-)"(D&&-)"-i$ht =G control reduce @27ris% of any coplication
9nited Qin$do Prospective Diabetes9nited Qin$do Prospective DiabetesStudy (9QPDS)"Study (9QPDS)"
Qeep =G noral" 1K: fe*ercoplications (eyes, %idneys and nerves)
and reduce ris% of heart diseaseQuaoto studyQuaoto study" the intensive insulintherapy have delay in the start andpro$ression of eye, %idney and nervecoplication
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M$$GEME? o DM1. D9&-+/2@ EIE!')&E
3@ >?!)?)A D)E?4@ H$!M$'AAGJ
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E*ucationJery iportant, included"Pathophysiolo$y of DM
-ar$ets of DM ana$eent
Mana$eent of nutrition and diet
Phaacolo$i% interventionercise and physical activity
Self onitorin$ blood $lucose (SM=G)
Prevent and ana$e of acute and chronic
coplicationPsychosocial aspect
Mana$eent of Stress
0ealth care syste
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'riteria o DM
managementGood Moderate Poorasting ,loo* glucose mgK*" 80 B 109 110 125 120
2Hour post pran*ial mgK*" 110 144 145 179 180
H,$1c " C 6#5 6#5 8 8
?otal '(olesterol mgK*" C 200 200 239 240
D '(olesterol mgK*" C 100 100 129 130
HD '(olesterol mgK*" 45
?riglyseri*e mgK*" C 150 150 199 200
/M) %gKm2" 18#5 B 22#9 23 25 25
/loo* ressure mmHg" C 130K80 130B140K80B90
140K90
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M$$GEME? o DM1@ ED>'$?)A!.UR&+S3@ >?!)?)A D)E?4@ H$!M$'AAGJ
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EcersiceMinial '2 inutes (fat burnin$), 1@2inutesK*ee%s
&R+P"
&ontinous
Rhythic
+nterval (Sai)
Pro$resivendurance aiu P93SCA27 (!!2B
a$e in year)
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>?!)?)A an* D)E?+portant of ;ood1.JariousKcontents
!.Schedule
'.-otal *ei$ht or calories
Standard diet" '27 for all fats ( 127 for saturated
fats)
@2B27 for carbohydrate (cople hi$h Obre)
1@B!27 for proteinSu$ar liited !@ $Kday
Sodiu $Kday, if hypertensive ' $Kday
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>?!)?)A an* D)E?
+deal body *ei$ht"Men (12 c) 0ei$ht in c I 122 C VQ$s ( 812 c) >27 (0ei$ht in c I 122)C VQ$sWoen (1@2 c) 0ei$ht in c I 122 C VQ$s (81@2 c) >27 (0ei$ht in c I 122)C V
Q$s
/oro*ei$ht" >2B1127 (+deal =W) or =M+ 1A,@ I !@ '2 caloriesKQ$=WKday9nder*ei$ht" >27 (+deal =W) or =M+ 1A,@
:2 caloriesKQ$ =WKdayver*ei$ht" 112 B 1!27 (+deal =W) or =M+ !@B'2 !2 caloriesKQ$ =WKdaybese" 81!2 7 (ideal =W) or =M+ 8'2
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M$$GEME? o DM1@ ED>'$?)A2@ EIE!')&E
3@ >?!)?)A D)E?
:.P0RM&3G5
82
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H$!M$'AAGJ1.+/&RSD +/S93+/S&R-+/
2@ )'!E$&ED )&>) &E&)?)L)?J3@ $H$ G>'A&)$&E )H)/)?A!&
4@ )&>)
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+/&RSD +/S93+/
S&R-+/Sulfonilureas";irst line treatent in non obese patients
*ith type ! DM
Stiulatin$ a receptor on the surface cellsclosing >@channel and opening
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+/&RSD +/S93+/
S&R-+/
85
Sulfonylurea 3en$thofaction
=e$insofaction
Dailydose($)
Route ofecretion
Gli,enclami*e
16 24( 2 4( 1#25 15 ! : 50# / :50
Glicla
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H$!M$'AAGJ1@ )'!E$&ED )&>) &E'!E?)A!. +/&RSD +/S93+/
S/S+-+J+-53@ $H$ G>'A&)$&E )H)/)?A!&
4@ )&>)
86
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+/&RSD +/S93+/
S/S+-+J+-5=i$uanides;irst line treatent for obese patient *ith type !DM
9sed cobination *ith insulin treatent-he 9QPDS sho*ed si$niOcantly better etforin
copared *ith the other therapies in reducedcoplication and ortality in the over*ei$ht DM
lthou$h 1B! Q$ *ei$ht loss is seen, but notsi$nifucant in over a 12 years period, and nota%e hypo$lyceia
Decreasin$ hepatin $luconeo$enesis, increasin$uscle $lucose upta%e and insulin sensitivity
3on$ period 2,A I !,27 0b1c reduction
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+/&RSD +/ S93+/
S/S+-+J+-5Side eHects"-he aTor side eHects of etforin is$arointestinal *ith nausea, voitin$ anddiarrhoea proinent (ta%en *ith eals orstarted at lo* dose inii#ed side
eHects/ot $iven to hi$h ris% patients *ith"
Severe cardiac failureRenal failure0epatic cirrhosisRespiratory failurelcoholis
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)'!E$&E )&>)
&E&)?)L)?J-hia#olidinedionePPR D agonist reducing b!#c #5)!ct on adipose tissue, liver and muscle as insulin
sensitiEers, potentiating the action of insulinImproved glycaemic control and beneficial effects on
lipid profile, lood *ressure and microalbuminuria
e careful "ith hepatic failure fatalities troglitaEone)
BosiglitaEone 4-2mg:day) & *ioglitaEone #-36mg:day)
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H$!M$'AAGJ1@ )'!E$&ED )&>) &E'!E?)A2@ )'!E$&ED )&>) &E&)?)L)?J
'. 3P0 G39&S+3S+/0+=+-RS
4@ )&>)
90
3P0 G9&S+DS
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3P0 G9&S+DS+/0+=+-RScarbose
ct by inhibitin$ disaccharidases in the sallbo*el
Delay en#yatic di$estion of coplecarbohydrate delay absortion $radual uin of $lucose concetration in portal vessels
Reducin$ postprandial hyper$lyceia (0b1c"2,@7)
Side eHects"
Si$niOcant carbohydrate alabsorption
atulence, abdoinal bloatin$ and diarrhoeaReduced the startin$ dose of @2 $Kday and
aintenance @2B122 $ each eal
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H$!M$'AAGJ1@ )'!E$&ED )&>) &E'!E?)A2@ )'!E$&ED )&>) &E&)?)L)?J
3@ $H$ G>'A&)$&E )H)/)?A!&
:.+/S93+/
92
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93
Ward WQ, et al. Diabetes Care
1>A:6":>1I@2!.
/oral -ype ! diabetes1!2
122
A2
2
:2
!2
2I'2 2 '2 2 >2 1!2
-ie (inutes)
I'2 2 '2 2 >2 1!2
-ie (inutes)
Plasainsulin(X
9Kl) 1!2
122
A2
2
:2
!22
!2$ $lucose!2$
$lucose
Plas
ainsulin(X9Kl)
Pattern of insulin secretion is altered early in type! diabetes
+ndication of +nsulin therapy"
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py
-ype 1 DM
-ype ! DM 9ncontrolled *ith diet,eercise and 0 (included aller$yand contraBindication).
Gestasional DM
Severe hepatic and %idney failure.cute +nfection(cellulitis, $an$ren),
severe tuberculosis, critical illness(stro%eKM+)
DQ N 00S (0/Q)Mayor sur$ical and fracture of bones9nder*ei$ht, DM related
alnutrition
&orticosteroid teraphy 94
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-ype of 0uan +nsulin
#$e#$e %e&i'i'&%e&i'i'& eakseaks Duratio'Duratio'
Sho&t actionSho&t action
)ctrai*)ctrai*
+umuli' ,+umuli' ,
15-30 m't15-30 m't 2-"hr2-"hr 6-.hr6-.hr
P&e(i/e'P&e(i/e'
+umuli' 30/0+umuli' 30/0
itar* 30/0itar* 30/0
15-30m't15-30m't 1-.hr1-.hr 1"-15 hr1"-15 hr
Inte&(e'iate actian 0Inte&(e'iate actian 0++
+umuli' +umuli'
4'sulatar*4'sulatar*2-"hr2-"hr
1-.hr1-.hr
1"-15 hr1"-15 hr
95
E*olution o! insulin &ei(ens %einsE*olution o! insulin &ei(ens %eins
;ith un'e&stan'in Physioloical Insulin Sec&etion P&o!ile;ith un'e&stan'in Physioloical Insulin Sec&etion P&o!ile
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96
122122
#3#3
3232
4343
522522 ,#22,#22 ,622,622 #222#222 #122#122 122122
7&eak!ast7&eak!ast LunchLunch $inne&$inne&
Plas(aInsul
in
Plas(aInsulin890(l:
90(l:
y
"i(e"i(e
522522
7olus &ei(ens7olus &ei(ens
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97
122122 ,622,622 #222#222 #122#122 122122
7&eak!ast7&eak!ast LunchLunch $inne&$inne&
Plas(aInsul
in
Plas(aInsulin
522522,#22,#22522522
"i(e"i(e
Act&api' Act&api'Act&api'
,
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98
122122 ,622,622 #222#222 #122#122 122122
7&eak!ast7&eak!ast LunchLunch $inne&$inne&
Plas(aInsul
in
Plas(aInsulin
522522,#22,#22522522
"i(e"i(e
Insulata&'
Act&api' Act&api'Act&api'
Insulata&'
,
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99
122 ,622 #222 #122 122
7&eak!ast Lunch $inne&
Plas(aInsulin
522,#22522
"i(e
>i/ta&'?@2 &e + 42 inte&(e'iate:
P&e(i/ &ei(ens
>i/ta&'?@2 &e + 42 inte&(e'iate:
,i/ta&'
P&e(i/ %eco(es choice
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100
+ere $ou see a bolus of i'suli' *eliere* i' the Subcuta'eous
sace77
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101aco%sen L et al. Eur J Clin Pharm#222D36@
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p(ysiology
102
Slow to appear ~ Unwanted high sugar levels
Slow to disappear ~ Unwanted low sugar levels (Hypo)
122122
#3#3
3232
4343
522522 ,#22,#22 ,622,622 #222#222 #122#122 122122
7&eak!ast7&eak!ast LunchLunch $inne&$inne&
Plas(aInsulin
P
las(aInsulin8
90(l:
90(l:
"i(e"i(e
522522
P&e(i/ Analoue ?No*o>i/:Matches normal
Hu(an insulin ?Hu(an >i/ta&':
No&(al physioloical
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?ype o $nalogue insulin
#$e#$e be&i'i'&be&i'i'& eakseaks *uratio'*uratio'Rapi' actionRapi' action
9$sro (+umalo&!9$sro (+umalo&!
)sart (oo ,ai*!)sart (oo ,ai*!
:luisi'e ()i*ra!:luisi'e ()i*ra!
5-15 m't5-15 m't 2 hr2 hr "-6hr"-6hr
P&e(i/e'P&e(i/e'
+umalo& 25/5+umalo& 25/5
oomi 30/0oomi 30/0
5-15m't5-15m't 2-"hr2-"hr 12-1" hr12-1" hr
Lon actionLon action
9a'tus9a'tus
9eemir9eemir
oo eakseaks 2" hr2" hr
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105
&istem o+oetN
Sites of +/S93+/ inTectionSites of +/S93+/ inTection
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B B
B B
B B
B
Sites of +/S93+/ inTectionSites of +/S93+/ inTection
(ove every ! *ee%s)(ove every ! *ee%s)