basics of complications of Diabetis

1. Complications of Diabetis
Dr Sravan Kumar M.D Medicine
Assistant Professor
MRIMS

2. • SGLT2 inhibitors are known to cause the
following except
1) Hyperkalemia
2) Decreased BMD
3) Hyponatremia
4) Euglycemic ketosis

3. • 56 year female diabetic patient skips her meal,
she develops sweating, palpitations initially later
becomes drowsy and has GTCS, her GRBS is 30
mg/dL, what is the first defence mechanism that
occurred in her against hypoglycemia
1) Increase in epinephrine
2) Decrease in insulin
3) Increase in glucagon
4) Increase in Acetylcholine

4. • Drug which acts through PPARα among the
following
1) Rosiglitazone
2) Fenofibrate
3) Riocigaut
4) Saxagliptin

5. • 20 year male presented to emergency with
cramps in both lower limbs followed by weakness
of both lower limbs ABG PH-7.2, HCO3-12, CL-
112, pco2-26 Na 136, K-2.5,
Urinary PH 6, what is the probable diagnosis
1) DKA
2) CONN SYNDROME
3) RTA
4) HYPOKALEMIC PERIODIC PARALYSIS

6. • HYPORENINEMIC, HYPOALDOSTERONISM RTA
(TYPE 4 RTA) is seen in
1) Addisons disease
2) Type 2 Diabetis Mellitus
3) Multiple Myeloma
4) Sjogrens Syndrome

7. r
Above fundus image is seen in
1) Hypertension
2) Diabetis
3) Hyperchylomicronemia
4) CRAO

8. Microvascular complication correlate with hyperglycemia

9. Pathophysiology of Diabetis complications

10. • Microvascular complications
– Related to hyperglycemia
– 10 years
• Macrovascular & Non Vascular Complications
– Insulin resistance
– May develop before hyperglycemia is established

11. Diabetic retinopathy

12. Macular edema detection
fluorescein angiography optical coherence tomography (OCT)
Angiography

13. treatment
• Fenofibrate – reduce progression of
retinopathy
Activate Lipoprotein lipase – Adipose tissue, heart, muscle
Decrease production of APO C3

14. Proliferative retinopathy
• Laser photocoagulation
• Anti VEGF ocular injection

18. Diabetic Nephropathy
Treatment : ACEIs or ARBs
GLP 1 agonists & SGLT2 inhibitors : DKD & CVDs
Type 4 RTA

22. • 70 x 70 ml = 4900 ml(5L)
• 20 % renal blood flow(1000ml)
• 20 % of renal plasma flow filtered (200 ml)
• Angiotensinogen – produced by liver
• Renin – Granular cells within wall of afferent
arteriole – converts Angiotensinogen to
angiotensin I
• ACE – present in lungs – converts angiotensin I to
ANGIOTENSIN II

24. 60 % Na
60 % Cl
90 % HC03
70 % Ca
85 % phosphorous
100 % Glucose
Aminoacids
NH3 is produced

25. 10 % HCO3 H + NH3
NH4

26. RTA
• PH < 7.35
• Hypokalemia (Sr K < 3.5)
• Anion Gap = Normal (Na+K – ↑ Cl+ ↓ HC03)
• Hyperchloremic metabolic acidosis
• Urine PH > 5.5
• Urine Anion Gap = (Na + K – Cl)
– Normally – Negative (NH4 in urine)
– Positive – (No NH4 in urine)

27. ANION GAP

28. Na 136 AG 12
HC03 24
Cl 100
136
Na 136 AG 26
HC03 10
Cl 100
136
Na 136 AG 12
HC03 10
Cl 114
136

31. Type 4 RTA hyporeninemic hypoaldosteronism
• PH < 7.35
• Hyperkalemia (Sr K > 5.5)
• Anion Gap = Normal (Na+K – ↑ Cl+ ↓ HC03)
• Hyperchloremic metabolic acidosis
• Urine PH > 5.5
• Urine Anion Gap = (Na + K – Cl)
– Normally – Negative (NH4 in urine)
– Positive – (No NH4 in urine)

33. Diabetic Neuropathy
• 50 % of Diabetics
• most common type is distal symmetric
polyneuropathy (DSPN)
• Cranial nerve most commonly involved –
occulomotor nerve
– Pupillary sparing(pupillay fibres are peripherally
located)
• Pregabalin, Duloxetine

34. • Dyslipidemia
– High Triglycerides
– Low HDL
• Most common site of foot ulcer
– Great toe or metatarsophalangeal areas
– Off loading –complete avoidance of weight
bearing on ulcer

35. Hypoglycemia
• Blood glucose < 70 mg/dL
• Whipple’s triad:
– 1) symptoms consistent with hypoglycemia
– 2) a low plasma glucose concentration measured
with a precise method
– 3) relief of symptoms after the plasma glucose
level is raised

36. • 4 gm of glucose circulates in the blood
• 60 % consumed by brain
• 100 gm glycogen in liver, 400 gm glycogen in
muscle
• Hepatic glycogen stores are sufficient to
maintain plasma glucose levels for ̴8 h

37. 1
2
3
Defences against Hypoglycemia

38. • Symptoms of hypoglycemia - BG < 55 mg/dL
• Drugs causing hypoglycemia
– Insulin, sulfonylureas, or glinides
• Drugs not causing hypoglycemia
– Metformin, thiazolidinediones, α-glucosidase
inhibitors, glucagon-like peptide 1 (GLP-1)
receptor agonists, and dipeptidyl peptidase IV
(DPP-IV) inhibitors

39. • hypoglycemia unawareness
loss of the warning adrenergic and cholinergic
symptoms that previously allowed the patient
to recognize developing hypoglycemia and
therefore to abort the episode by ingesting
carbohydrates.

40. Hypoglycemia
• Ethanol blocks gluconeogenesis but not
glycogenolysis.
• Drugs causing Hypoglycemia
– ACEIs, ARBs, B blockers, Quinolones, Indomethacin,
Quinine
• Non Beta Cell tumour causing Hypoglycemia
– Hepatoma, Adreno cortical carcinoma, carcinoid
• Beta cell tumour
– Insulinoma (part of MEN 1)
• Nesidioblastosis -diffuse islet involvement with β-
cell hypertrophy and sometimes hyperplasia.

41. Treatment
• 15–20 g of oral glucose
• IV administration of glucose - 25 g
• IM glucagon (1.0 mg in adults)

42. Fasting

43. • Glycolysis – Cytoplasm
• Krebs cycle – Mitochondria
• Glycogenesis - Cytoplasm
• Glycogenolysis – Cytoplasm
• Gluconeogenesis – oxaloacetate production in
Mitochondia, which moves to cytoplasm
• Beta oxidation of fatty acids – Mitochondria
• Ketone bodies production – Mitochondria