The term "diabetes

meIIitus" was derived

from 2 terms :
The Greek word
Diabetes to Siphon
or pass through
and the Latin word
mellitus sweet as
honey
11
2
What |s d|abetes?
8ody does not moke or proper/y use insu/in
no lnsulln producLlon
lnsufflclenL lnsulln producLlon
reslsLance Lo lnsulln's effecLs
-o insu/in to move q/ucose from b/ood into ce//s
hlgh blood glucose means
fuel loss cells sLarve
shorL and longLerm compllcaLlons
I DIA8L1LS MLLLI1US I DIA8L1LS MLLLI1US
2
II DIA8L1LS II DIA8L1LS 1LS 1LS
TIcrc arc iIrcc major forms of dialcics.
Tgpe 1 D1obe1es (IDDM} (Juvcnilc onsci}
Tgpe 11 D1obe1es (NIDDM} (Maiuriiy onsci}
es1o11ono1 D1obe1es
Seoondorg ]orms:
!ancrcaiic Dialcics
Hormonal Dialcics
Iairogcnic Dialcics
3
DIA8L1LS MLLLI1US IAC1CkS DIA8L1LS MLLLI1US IAC1CkS
Hcrcdiiy
Auio-immuniiy
Infcciions
Olcsiiy
Dici
Insulin aniagonism
4
Sk|n prob|ems
Sk|n Infect|ons |ead|ng to bo||s
carbunc|es or abscesses
Cra| Gen|ta| cand|d|as|s
3
DIA8L1LS DIA8L1LS 1L I 1L I
8YMPTOM8:
ivcrea.ea tbir.t
ivcrea.ea vrivatiov
reigbt to.. ae.ite ivcrea.ea
aetite
vav.ea
&8E:
vvcertaiv, ti/et, botb gevetic ava
evrirovvevtat factor.
rovitivg
abaovivat aiv
fatigve
ab.evce of vev.trvatiov
ON8ET:
occvr at av, age, bvt it v.vatt, .tart. iv
eote ,ovvger tbav 0. ,vtov. are
v.vatt, .erere ava occvr raiat,.
lL resulLs from prlmary beLa cell desLrucLlon
leadlng Lo absoluLe lnsulln deflclency
6
Type 2 diabetes is a progressive
metaboIic disorder characterised by:
InsuIin
resistance
Type 2
diabetes
.-ceII
dysfunction
7
Type 2
diabetes
8YMPTOM8:
ivcrea.ea tbir.t
ivcrea.ea vrivatiov
ivcrea.ea aetite
atigve
btvrrea ri.iov
&8E:
a robtev iv tbe ra, ,ovr boa, va/e. or v.e.
iv.vtiv.
freqvevt ava,or .tor
beativg ivfectiov.
;ivctvaivg btaaaer, ragivat,
./iv)
erectite a,.fvvctiov iv vev
ON8ET:
v.vatt, occvr. graavatt,.
Type 2 diabetes meIIitus
8
Gestat|ona| D|abetes ( GDM ) Gestat|ona| D|abetes ( GDM )
Some women develop gestational diabetes late in pregnancy.
Although this form of diabetes usually goes away after the baby is
born, a woman who has had gestational diabetes is more likely to
develop type 2 diabetes later in life. Gestational diabetes is caused by
the hormones of pregnancy or a shortage of insulin, which usually
begins about 20 to 24 weeks into the pregnancy.
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GDM SM1CMS
Clycosurla
LlevaLed blood glucose levels
usually appears beLween 2428 weeks
gesLaLlon
uegree of hyperglycemla ls noL as severe as ln
oLher Lypes of dlabeLes
10
SLCCNDAk DIA8L1LS SLCCNDAk DIA8L1LS
1hls condlLlon ls observed when dlabeLes occurs secondary
Lo some dlseases
ancreaLlc dlabeLes
ancreaLlLls
PaemochromaLosls
Mallgnancy of ancreas
Abnormal concenLraLlons of anLagonlsLlc hormones
PyperLhyroldlsm
PypercorLlclsm llke Cushlng's syndrome
PyperplLulLarlsm llke acromegaly
lncreased glucagon acLlvlLy
laLrogenlc
ln geneLlcally suscepLlble cases may be preclplLaLed by Lherapy llke
corLlcosLerolds Lhlazlde dlureLlcs
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ther ProbIems to be Considered:
- Psychogenic polydipsia
- Nephrogenic diabetes insipidus
- High-output renal failure
- Transient hyperglycemia with illness and other stress
- Steroid therapy
DIFFERENTIALS
- Diabetes nsipidus
- Hyperthyroidism
- Pheochromocytoma
- Renal Glucosuria
- Toxicity, Salicylate
12 12
M|croang|opathy
Metabo||ctox|c damage
(neuropathy)
Macro
ang|opathy
0l00Ilt 0t00l) t0NIltIl0I: 0\0l\l0
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Diabetic Foot CompIications
15% of all diabetes develop serious foot condition
Common problems
Callus formation
Ulceration
Gangrene
Charcot's joints
Ulceration and Gangrene are serious problems and
they may lead to amputation (removal of limbs)
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III- Pathophysiology:
ancreas and Insu||n
13 13
The Pancreas
Function:
The pancreas produces two enzymes --insulin
and glucagon-- that control the level of sugar in the
blood. n addition the pancreas produces a mixture of
enzymes, called pancreatic juice, which is released into
the small intestine to help digest starch, proteins, and
fats.
Location:
stretches across the back of the abdomen,
behind the stomach.
16
Locat|on of the ancreas
17 17
The actions of insuIin
g|uconeogenes|s
18
Actions of GIucagon
- ncreased glycogenolysis
- ncreased gluconeogenesis
- ncreased lipolysis
- ncreased ketogenesis
- Decreased glycolysis
- Decreased cholesterol synthesis
19
oth insuIin and gIucagon are released by the pancreas, a
long, tapered gland that lies behind the stomach. Most of the
pancreas produces digestive enzymes, which travel via ducts into the
small intestine. But embedded in this tissue are nests of hormone-
producing cells the islets of Langerhans which secrete insulin and
glucagon into a network of surrounding blood vessels.
High bIood sugar IeveIs stimulate the release of insulin
(produced by the beta cells in the islets), which increases the uptake
of glucose by cells. nside the cells, the glucose may be used as
energy, converted to glycogen for storage (mainly in the liver and
muscles), or used in the production of fats.
GIucagon is produced by the alpha cells in the islets, and is
released by the pancreas when blood glucose is low. t stimulates the
breakdown of stored glycogen to glucose, which is then released into
the bloodstream.
20 20
PATHOPHYSIOLOGICAL BASIS OF SYMPTOMS AND SIGNS OF
UNCONTROLLED DM
21
IsIets of
Langerhans
.-cell destruction nsulin Deficiency
Adipo-
cytes
MuscIe
Liver
Decreased Glucose Utilization
Glucagon
Excess
Increased
Protein
CataboIism
Increased Ketogenesis
GIuconeogenesis
Increased LipoIysis
HypergIycemia
Ketoacidosis
PoIyuria
VoIume DepIetion
Ketonuria
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Lab Studies:
- Urine glucose
+ A positive urine glucose test suggests but is not diagnostic
for DDM. Diagnosis must be confirmed by test results showing
elevated blood glucose levels.
+ Test urine of ambulatory patients for ketones at the time of
diagnosis.
+ Urine ketones
+ Ketones in the urine confirm lipolysis and gluconeogenesis,
which are normal during periods of starvation.
+ With hyperglycemia and heavy glycosuria, ketonuria is a
marker of insulin deficiency and potential DKA.
23 23
24
G|ycem|c Contro|
Norma| 8|ood G|ucose
|eve|s
8eLween 70 100 mg/dl
before meals
180mg/dl
Lwo hours afLer meals
yperg|ycem|c state
400 mg/dl
ypog|ycem|c state
70 mg/dl
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Criteria for the Diagnosis of Diabetes
Symptoms of diabetes plus random plasma glucose
concentration K 200 mg/dl (11.1 mmol/l).
The classic symptoms of diabetes include:
polyuria, polydepsia, and unexplained weight loss.
R
PG K 126 mg/dl (7.0 mmol/l).
asting is defined as no caloric intake for at least 8 h.
R
2-h PG K 200 mg/dl (11.1 mmol/l) during OGTT
The test should be performed as described by W HO using
a glucose load containing equivalent of 75-g anhydrous
glucose dissolved in water.

ther Tests:
Oral glucose tolerance test
+ Obtain a fasting blood sugar level, then
administer a PO glucose load (2 g/kg for children aged <3 y,
1.75 g/kg for children aged 3-10 y [max 50 g],
or 75 g for children aged >10 y). Check the blood glucose
concentration again after 2 hours. A fasting whole-blood
glucose level higher than 120 mg/dl (6.7 mmol/L) or a 2-hour
value higher than 200 mg/dl (11 mmol/L) indicates diabetes.
Mild elevations, however, may not indicate diabetes when the
patient has no symptoms and no diabetes-related antibodies.
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- GIycated hemogIobin
There is hemoglobin in all red blood cells. Hemoglobin
is the part of the red blood cell that carries oxygen to the
tissues and organs in the body. Hemoglobin combines with
blood glucose to make glycosylated hemoglobin or hemoglobin
A1c. Red blood cells store glycosylated hemoglobin slowly
over their 120-day life span. When you have high levels of
glucose in your blood, your red blood cells store large amounts
of glycosylated hemoglobin. When you have normal or near
normal levels, your red blood cells store normal or
near normal amounts of glycosylated hemoglobin. So, when
you measure your glycosylated hemoglobin, you can find out
your level of blood glucose, averaged over the last few
months.
27 27
VaIues vary from Iab to Iab but beIow is a common vaIue system
for HemogIobin A1C
HemogIobin A1C NormaI: Less than 6.5
ExceIIent: 6.5-7.5
Good: 7.5-8.5
Fair: 8.5-9.5
Poor: Greater than 9.5
HbA1C(%) Average Iood GIucose (mg/dI)
4 60
5 90
6 120
7 150
8 180
9 210
10 240
11 270
12 300
13 330
28 28
29 29
Frequency of monitoring HbA1c Frequency of monitoring HbA1c
month month
unsLable uM unsLable uM
change of LreaLmenL change of LreaLmenL
month month
sLable uM sLable uM
Triad of Treatment Triad of Treatment
Diet Diet
Medication Medication
raI raI hypogIycemics hypogIycemics
InsuIins InsuIins
Exercise Exercise
30 30
Five components of diabetes
management
nuLrlLlonal managemenL
Lxerclse
MonlLorlng
harmacologlc Lherapy
LducaLlon
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V- TREATMENT:
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TYPE 1
32
Introduction
At Kantha Bopha hospital we have been
practicing two ways of insulin injections by
using:
Short-acting insulin (Atrapid/Novorapid)
ntermediate-acting insulin (InsuIatard)
Long-acting insulin (Levemir)
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Patients and Methods:
We use 2 methods of the insulin treatment protocol
managed by professor Shuenle in Zurich (Switzerland )
1- Two injections daiIy: (old system)
short-acting insulin (Actrapid) + ntermediate-acting
insulin (InsuIatard)
Fin the same syringe before breakfast and the dinner
2- Four injections daiIy: (new system)
The short-acting insulin (Novorapid): before breakfast,
lunch, dinner, and
The long-acting insulin (Levemir) at bedtime.
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33
%7eatment of %5e I Diabetes %7eatment of %5e I Diabetes
Old Insulins System
33
36
%7eatment of %5e I Diabetes %7eatment of %5e I Diabetes
ew Insulins System
36
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Diabetes Diabetes Oral Medications Oral Medications
Sulfonylureas
Biguanides
Sulfonylureas and biguanide combination
drugs
Thiazolidinediones
Alpha-glycosidase inhibitors
Meglitinides
Classes
38 38
HypergIycemia
GLUCOSE
ABSORP%ION
aIpha-gIucosidase inhibitors
INTESTINE
PANCREAS
INSULIN Sec7etion
Sulphonylurea (SU)
Non-SU : Meglitinides
& Nateglinide
GLUCOSE
PRODUC%ION
Biguanides Biguanides
Thiazolidinediones Thiazolidinediones
LIVER
MUSCLE
PERIPHERAL
GLUCOSE UP%AKE
Thiazolidinediones Thiazolidinediones
Biguanides Biguanides
ADIPSE
TISSUE
echanisms of action
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