DIABETES MELLITUS
• Group
no..29
• Stuti, Fenil, Ravi, Neha, Dharti.
• Group mentor:-DR. Alok Parekh
History of patient
Patient is 61yr old, residing at pandesara, come to
 Chief complain of..
l Breathlessness since 7 days
l Cough since 3 weeks
 No complain of fever & Hemoptysis

H/O Diabetes Mellitus since 10 years
 H/O Coronary Angioplasty in 2008

First time diagnosed with accidental Hairfall & weig
 No H/O Polyuria, Polydipsia, Polyphagia
l Due to Controllled Diabetes Mellitus
 No H/O Palpitation
 No any Edema (Diabetic Nephropathy)


Operated for cataract in both eyes

No fatigue, weakness ( Cells are starving)
stigation
Haemoglobin
Total RBC
Total WBC
= 9.9 gm %
= 3.88 millions/ cu.mm
= 16,200 / cu.mm
Random Blood Sugar= 469 mg/dl
Serum Creatinine
= 1.4 mg% (0.4 – 1.2 )
Advanced
Glycated
Endproducts
groups of Proteins
AGEs)
+
s of Reducing sugar
metic reaction)
GE with Hyperglycemia)
RAGEs is present on
Inflammatory cells
Endothelium
Vascular smooth muscle.
So More Chances of
Microvascular disease
Macrovascular disease
Renal cell disease
Atherosclerosis due to endothelial damage
enesis of AGE
ollagen (In large vessels)
se in elasticity
helial injury
AGE is resistant to proteolytic digestion
of AGEs difficult
y increase AGE
osis Due to AGE
elial Componant of Vessels
nt Blood Flow
ted Plasma proteins
DL in large vessels
on of LDL- cholesterol
of the vessels
ogenesis
y due to AGE
of Renal glomeruli
to Basement membrane
&
e of Basement membrane
Protein during filteration
inuria
y + Diabetic Nephropathy
ed haemoglobin
emoglobin (Protein)
oglobin = 120 days
main for 120 days
c control of last 120 days
ion of all Other protein
ty of Other Complication
G
pH
Report
pO2 =
pCO2
HCO3SpO2 =
= 7.4
(7.35 – 7.45)
110 mm Hg ( 90 – 100 )
= 22 mm Hg (32 – 40 )
= 15.4 mmol/l ( 22 – 28 )
99%
( 90 – 100 )
Fully Compansated Metabolic Acidosis
ed Here
metabolic Acidosis
HCO3 conc. is low = Metabolic Acidosis.
But with that CO2 = Low = Washed out
So pH level = Maintained at Normal
So , it is fully copensated metabolic acidosis.
Chest X – Ray
Left side Hazziness in Lower & Middle zone
 Right side Mild Hazziness lower zone
 Obliterated Costro-Phrenic angle

Conclusion :
 Left side huge pleural effusion
 Right side mild pleural effusion
 Left middle & lower zone pneumonitis
Decrease
Immunity
s in
diabetes
2) AGE afect Microvessels

Decrease Blood Supply to Distal tissue
 Decrease chemotaxis at injured site
 Delay healing of injured site
3) AGE affect Nerves
 Neuropathy
 Sensory loss in the limbs
 Repeated Injury
4) Cell has more glucose
 Nutrition for Bacteria = Bacteria “Like It”

of “Diabetec Foot”
What to be needed in this patient?
Serum Ketone Body Level
 Serum Insulin Level
 Serum C-peptide level
 Serum Protein level
 Urinary Micro-protein level ( 30 – 300 mg/day)
 Pleural Fluid Examination
 Sputum Culture

1)Aspirin
 Antiplatelet Action
 Cyclo-oxygenase inhibitor
 Suicide inhibition
1)Oral Hypoglycemic drugs
1)Glipizide (Sulfonylurea group)
 Block K+ of Beta cell of pancrease
 Increase Calcium Influx of in the Cell
 Increase Insulin Release from The Beta Cell
2)Metformin (Biguanide group)
 Inhibit Gluconeogenesis in Liver
 Decrease activation of Following Enzyme

Phophoenolpyruvate Carboxykinase (PEPCK)

Glucose 6 Phosphatase
Mechanism of Sulfonylurea (Glipizide)
Treatment
3. Nikoran & Sorbotrate
1) Nitrate Like Action
2) Dilate the Coronary Artery
4. Pantoprazole
1) Proton Pump Inhibitor
2) Decrease H+ Secreation in GIT.
3) Prevent Peptic Ulcer & Drug induce Gastritis
5. Thyroxine = For Correction of Hypothyroidism
6. Antibiotic
Question to be learn from this case.
1) Why cataract is common in patient of uncontrolled DM?
2) What is Advance Glycate End Products?
3) What is nephropathy & why it is common with patient of
uncontrolled DM?
4) What chances of infection and repeated injury to foot is
common with uncontrolled DM?
5) Why hypercholesteremia occurs in patient of uncontrolled
DM?
6) What is significant of micro-proteinuria?
7) Why metabolic acid can more commonly with type – 1 DM?
8) What is difference between uncomponsated ,partially
componsated & fully componsated metabolic acidosis?
9) What advantage of during C-Peptide level & Glycated
haemoglobin, after diagnosis of diabetes mellitus?