TID -

absolute in mein
-
alfuir of
Langemans by activated Lymphocytes B-cs population D
-
are altered 1. causes

80-90 % distruction ources panuras to fail.

>
-

Balls ↑
can be
destroyed as 2 :
enomutal and Genetic body idetes as forgin B cls
>
-

camy :
abrupt urination-polyurea
thirst polydipsia
:
marrie
-

hungermassive polypharia
-

DO
triggered by phyrisioquial stress of Unus .

accompanied by fatigue and withless.

>
-
Dignosis 76 glycosylated Mannogokin (normal
: . 5 is 5 . 1)
2 126 FBG (normal To-99)
100-125 FBG perdiabetic , Hyperglycemic > 200

post 180
glucose spills into the urive accombanid by of water
.
lass

Heperymenia ·

Hepatic production of Gluconeogenises

combined with accurated
-
Ketosis -

mobilisation of gathy acid from adipose true ,

hepatic fatty acid poxidation and syntims of 3

hydroxy but rate and acuto arifase
.

Diabetic betoacediactiesis A
type of Metabolic ccidosis ourus in 25% to 40% in
newly diagonal
-

paint O
--
TD
.

adminstring
trandbyreplacing
-

gids and electe sur

a

Hyper triacyle glyrounia :

Fatty acids are Convited to TAG ,

which is packed and
secreted in ULDL .
proviens
① STANDARD TREATMENT

Teatment 1-2
injection arryday of excombinant .
human insulin
>
- ⑨
:

·
blood Genoe 225-275
HBAIC -8-9% of total Haemoglobin
·

②INTENSIVE
· 3 or more times
of inmei infection
· blood 150
·
geore
HBAIL - 7%

Hypogenic type-1+ causes

by exces insulin occuring our 90% of the patents
,
.

of Glagon and epinephr peromotes

E

trigyens the revene

·

hepaticproduction of Geose .
·

Palente of tid also durleop dificing of Glucagon secretion

easte 4
usually .
years
·

·
combined eling of Gleagon and
epinephrin secretion creates
condition called hypoglycemic
symplous free
-

a .
unawarmers
·
excess excercius causes Mpogheemia.

Fight control >

-
Inchidrem light control of blood
guse before 8 because it .

affuts
Brain durlopment .

it can cause shokes and want altass

.
>
- wheras in elderly ,

in
-
major reason of light control is to prevent complications future
.
 TYPE-2 DIABETES

·
- Polyurea &Poludypsia Common)
sympos Polyphasia (uncommon)
,
·
Facos &
>
- Insulin assistance ,
and distructional pulls
.

Diagnons
· e

Hyperglycemia-D interim secretions , Bull falive

Insilinqvistance ① Hepatic Glucose production
Q Glucose upkate by mussels Eadspace tises
J
Glycoslugin of adipose tissue
↳ In in Ball could be non-diabetic
Obenty absence of defect
-

Obesity can counteractcover lull of insulin

-

Produces blood queose avels

↳ TID Balls gone Inspectional

-

are

cused in old indictive and sometimes in pregnant.

fat
-

, ,

they can't compensate insulin resistans

-

↳ causs- ① weight las

weight gain
> more isilien resistance
④ adipose Misus - &
.

Obesity changes in adipose trisue secration causing inbalance of

-

insulineouton &

↳ ILs
gulcose ① causing hyperglycemic
-
FFA so

↳ upting
adiponectiv ⑪ -
(
-
Ball falire-D insulin Secretion so , ⑪ rose uptake so
, hyperglycemia
>
- Metabolic changes
-

Iperglycemia - or ① betosis ①Geouse

-

Dislypodemia FFA - -
The (pared) and secreted to VLDC
.

VLDL causes Hypertriglycermenia

.

>
- Treatment -

Hypoglycemic agents :

Sulphonylureas , Theasolydenediones
- X
geosidase Mibitor