The document discusses diabetes mellitus, detailing classifications (Type 1, Type 2, and MODY), diagnostic criteria (like HbA1c levels), and management strategies. It addresses complications such as diabetic ketoacidosis and non-ketotic hyperosmolar coma, along with treatment protocols. Key information includes insulin resistance mechanisms, glycemic index of foods, and the impact of family history on diabetes types.

1. DIABETES
- DR.AKIF A.B

2. HbA1C
VALUE CONDITION
<5.6% Normal Hb1AC
5.6-6.4% Impaired glucose tolerance
>/= 6.5% Diabetes mellitus
-It tells us about average blood sugar of previous 8-12wks
-Retrospective study
-Best investigation of choice for diagnosing Diabetes Mellitus.
-Good diabetes control = Hb1AC levels <7%

3. DIABETES
Fasting 2hrs Post
prandial
Normal 60-100mg/dl <140mg/dl
Impaired glucose
tolerance
100-126mg/dl 140-199mg/dl
Diabetes mellitus >126mg/dl >200mg/dl
Fasting is defined as no calorie intake for at least 8hr
2hrs post-prandial: an oral glucose tolerance test with 75gm of
glucose
1 mmol/lit of blood sugar = 18 mg% of blood sugar

4. 1) A young man has normal blood sugar & normal HbA1C but has glycosuria.
Most likely diagnosis is?
A Renal Glycosuria
B Pancreatic insufficiency
C Alimentary glycosuria
D High carbohydrate diet taken in the morning.

5. Ans. A Renal Glycosuria
Important points:
1. Glycosuria + Ketonuria : seen only in diabetes.
2. Only glycosuria (without diabetes) : is seen in a normal young adult,
pregnancy, hyperthyroid.
(Note: In hyperthyroid it is known as alimentary glycosuria)
3. Only ketonuria : seen in prolong starvation.
4. Renal glycosuria:is a benign condition, found in some young adults.
No treatment required. Blood sugar is normal. It is self limiting.

6. TYPE-1 DIABETES
- Ratio of type I & type II diabetes in India. = 5% : 95%
-Patient has normal Weight or under weight
- Presence of autoantibodies: islet cell antibodies (lCA) and anti-glutamic acid
decarboxylase (GAD) antibodies;
- Ketonuria on urine dipstick.
- Family history +/-
- Serum insulin levels are low
- HLA DR3, DR4
- Main treatment is insulin.

7. SCHMIDT SYNDROME OR
POLYGLANDULAR FAILURE SYNDROME)
-Autoimmune destruction of more than 80% of beta cells
-Type-1 Diabetes Mellitus

8. LATENT AUTOIMMUNE
DIABETES OF ADULTS (LADA)
- Also known as Type 1.5 DM
- Is a form of Type 1 DM, with slower progression to insulin dependence in later life.
-Initially there is not much need of insulin administration and patient can
be managed on hypoglycemic drugs but later in adulthood insulin
dependence occurs.
-Since initially it behaves as type 2 DM and later as Type 1DM , It is known
as Type1.5DM.

9. -Patient has over Weight
- No HLA association
- No autoantibodies
-Ketosis is uncommon.
-Non ketotic hyper osmolar coma is common.
-Family history strongly positive but not always positive.
- Insulin resistance is the main cause
- Serum insulin levels are very high ( hyper insulinemia )
- Treatment include weight loss, oral drugs & insulin
TYPE-2 DIABETES

10. 2.Q. A 29 years old person is known diabetic on oral hypoglycemic agents since
3 years. He has lost weight and never had DKA. His grand father is diabetic but
his father is nondiabetic. Which is the likely diagnosis: (AIIMS May 09)
A MODY
B DM type I
C DM type II
D Pancreatic diabetes

11. Ans. C. DM type II

12. 3.Q. A 29 years old person is known diabetic on oral hypoglycemic agents since
3 years. He has lost weight and never had DKA. His grand father and father
both are diabetic. Which is the likely diagnosis: (AIIMS Nov 09)
A )MODY
B )DM type I
C)DM type II
D ) Pancreatic diabetes

13. Ans. A MODY
In type II diabetes there is strong family history but in MODY there is definite
family history because it is autosomal dominant.
That’s why the answer of Q. 2 is C and
answer of Q 3 is A.
Because in Q. 2 Father is not diabetic but Grand Father is diabetic but
Q. 3 both Father and Grandfather are diabetic.

15. MATURITY ONSET
DIABETES OF YOUNG (MODY)
-Age of presentation = 25yrs
-6types (Type1-6)
-MC MODY in India = Type-3
-No antibodies
-No obesity
-DKA uncommon
-No insulin resistance
-Gene defect = HNF1
-Autosomal Inheritance
-Family history of sucessive
generations

16. Remember Gene names……chromosome names not required.

18. 4.Q. Acute fulminant diabetes is related to:
A) DKA
B )Viral infection
C ) MI
D ) Pregnancy

19. B )Viral infection

20. 5.Q. Patient of which of the following type of diabetes is most likely to have normal
blood sugar?
A Potential
B Latent
C MODY
D LADA

21. A) Potential

22. POTENTIAL DIABETES
Person himself at present is non-diabetic but has a strong family history
of type 2 diabetes.
LATENT DIABETES
A person becomes diabetic under stressful conditions like pregnancy.
Person again becomes non-diabetic when stress is removed.

23. BRITTLE DIABETES
It is seen in children with type 1 diabetes. Some times patient’s sugar becomes very
high leading to DKA,
sometimes patient goes into hypoglycemia
ACUTE FULMINANT
DIABETES MELLITUS
It is acute onset diabetes, can occur in any age, occurs after viral infection. Serum
insulin level are reduced but there are no antibodies against insulin or beta cell.
(PNQ)
The viral infections associated with diabetes are :
Mumps, Measles, Coxsackie virus, Cytomegalovirus, Rubella, EB virus

24. TROPICAL DIABETES
-Diabetes mellitus associated with chronic malnutrition and, sometimes, chronic
pancreatitis.
-Also called malnutrition-related diabetes.
-Chronic pancreatitis patient are usually in Africa where they consume Casava.

25. Recent advances in Pathology of
Type II diabetes
-Genes for type II diabetics that cause the insulin resistance and the beta cell
failure- a gene on chromosome 2 encoding a cysteine protease, calpain –10, has
been reported in some patient.
- Several adipokines, secreted by fat cells, can affect insulin Action.
-Example of adipokines
1. Leptin
2. Adiponectin
3. TNF
4. Resistin
i. Adipokines which reduce insulin resistance - a. Leptin b. Adiponectin.
ii. Adipokines which increase insulin resistance – a. TNF-alpha b. Resistin

26. INITIAL MANAGEMENT
OF DIABETES
Treatment of diabetes mellitus (H-18th Pg-2990)
1. Patient Education : For any obese type II diabetic patient initial therapy is
diet therapy and exercise.
(a) (Reduce weight to maintain normal BMI)
BMI = body weight (kg) / height in meters2
BMI > 25 overweight
30 obese
(b) In Obesity down regulation of insulin receptors occurs.
(c) Avoid food of high glycemic index (i.e. any food like sugar, glucose powder etc.
which are absorbed immediately in GIT and raised blood sugar very fast).

27. 100% Glucose
80-89% Corn Flakes, carrots, potatoes (mashed), maltose, honey, idli.
70-79% Bread (whole meal), millets, rice (white), broad beans, potato (new),
uppama
60-69% Bread (white), paratha (Wheat), rice (brown, unhusked), shredded
wheat, beetroot, banana, raisins, sprouted green gram, sucrose.
50-59% Buck wheat, noodles (white), peas (frozen), pongal sweet corn,
potato chips.
40-49% Noodles (whole mal), porridge oats (dahlia), beans, potato (sweet),
oranges (juice), peas (dried), bengal gram, black gram.
30-39% Black-eyed peas, apple, skimmed milk, curd/yogurt, tomato soup, ice
cream
20-29% Kidney beans, lentils (all daals), fructose, rajmaah
10-19% Soyabeans, groundnuts
GLYCEMIC INDEX

28. Q.Which adipokine reduces in insulin resistance
A Leptin
B TNF alpha
C Resistin
D All of the above

29. A. Leptin

30. Complications Of DM
1) Somogyi phenomenon
2) Dawn phenomenon
3) Diabetic Ketoacidosis
4) Non-ketotic hyperosmolar coma
5) Diabetic retinopathy
6) Diabetic neuropathy
7) Diabetic nephropathy

31. 1)SOMOGYI PHENOMENON
-Early morning (3-4am) hypoglycemia due to excess administration of
Insulin at night but again at morning around 6-7am there will be hyperglycemia.
Explanation of 6am hyperglycemia is given below
When the blood glucose level falls below normal, the body responds by releasing the
endocrine hormone glucagon as well as the stress hormones epinephrine, cortisol
and growth hormone.
- Glucagon facilitates release of glucose from the liver that raises
the blood glucose immediately, and
- the stress hormones cause insulin resistance for several hours,
sustaining the elevated blood sugar.

32. 1)SOMOGYI PHENOMENON

33. 1)SOMOGYI PHENOMENON
Normal glucose at night
High Insulin given at 9pm
Leads to hyperglycemia
In morning
Glucagon and other stress
hormones are released
Due to hypoglycemic stress
Leads to hypoglycemia
At around 2-3pm

34. DAWN PHENOMENON
-Early morning Hyperglycemia at around 2-3am
- Due to low dose administration of Insulin

35. DIABETIC KETOACIDOSIS
Diabetic
ketoacidosis
Lactic
acidosis
Non ketotic
hyperosmolar
coma
pH Low <7.3 Low <7.3 Normal
HCO3- LOW LOW Normal
Urine ketones +++ -ve -ve
Blood sugar >300mg% >300mg% >800mg%

36. DIABETIC KETOACIDOSIS
CLINICAL FEATURES –
Symptoms –
Nausea,
vomiting,
Abdominal pain
Altered mental function.
Shortness of breath
Signs –
1. Tachycardia
2. Dry mucous membrane
3. Dehydration
4. Hypotension
5. Kussmaul respiration Q
6. Tachypnea
7. Abdominal tenderness
8. Fever. May be there
9. Fruity odour of the breath

37. INVESTIGATIONS Of DKA
1. Hyperglycemia – Blood sugar 400 – 600 mg%
2. TLC – Leucocytosis. It is a feature of DKA. It does not indicate infection.
Presence of fever indicate infection
3. K+ - increase (shifting of K+ from intracellular to extracellular compartment
due to decrease Insulin)
4.S. Osmolality 300 – 320mosm/Kg
5.Urine ketones – Positive
6. Metabolic acidosis - Low HCO-
3
7. increase anion gap.

38. Q. Which of the following is the best parameter to know about the control of DKA?
A Random blood sugar
B pH of the blood
C Urine ketone
D Serum potassium

39. B) pH of the blood

40. Treatment Of DKA
a. Fluids → 0.9% saline.
b. Insulin → Regular Insulin is given I/V in DKA. It is not given
subcutaneous.
c. Treat precipitating events → Non compliance, infection by antibiotics.
d. K+ replacement → Initially when patient comes initially he is hyperkalemic,
later on when patient is treated with insulin, serum potassium level goes down
and may required potassium replacement.
e. Injection HCO3 I/V if Ph <7
Note : Insulin causes movement of K+ from ECF to ICF leading to hypokalemia
For Pg entrance this is enough ….if u want to know more about
management read in harrison/ davidson latest edition

41. Q. A diabetic patient with blood glucose of 600 mg/dL and Na 122 mEq/L was
treated with insulin. After giving insulin the blood glucose decreased to 100 mg/dL.
What changes in blood Na level is expected? (LQ)
A Increase in Na+ level
B Decrease in Na+ level
C No change would be expected
D Na+ would return to previous level spontaneously on correction of blood glucose.

42. Ans. A Increase in Na + level
In diabetes pseudohyponatremia occurs i.e. the measured serum sodium
is reduced as a consequence of the hyperglycemia.
i. There is a reduction of (1.6 meq) of serum sodium for each 100 mg/Dl
rise in the serum glucose.
ii. A normal serum sodium in the setting of DKA indicates a more
profound water deficit.
So when we treat a case of DKA, as the blood glucose level falls then
measured serum sodium rises.
(Ref. Harrison, 18th edition, 2978)
Extra Edge::
Causes of pseudohyponatremia:
1. Severe hyperglycemia (DKA, NKHOC)
2. Hyperlipidemia
3. Hyperproteinemia (Multiple myeloma)

43. Complications of DKA
i. Cerebral edema (most dangerous complication, seen mostly in children)
ii. Venous thrombosis
iii. ARDS
iv. MI
v. Acute gastric dilatation
Acidosis leads to damage of blood brain barrier and thus leads to
cerebral edema

44. Q. Mr. Ram Lal, 80 years, a known case of diabetes, was brought to
emergency ward in unconscious state. His blood sugar was 900 mg%,
dry tongue. BP; 80/50. Urine ketones negative. Which of the following fluid
you will give to treat his marked dehydration.
A Injection RL
B Injection N/2 saline
C Give plain water by Ryle’s tube
D Injection N saline

45. Ans. D Injection N saline
This is a case of NKHOC.
Ideal replacement fluid in this condition N/2 saline but in this case the patient
BP is 80/50 i.e. he is in hypovolemic shock so to begin with in this case N saline
should be given.
Once the systolic BP is above 90mmHg then N/2 saline should be started.
Supposed in this question patient’s BP was 110/70 i.e. normal BP than best answer
would have been N/2 saline.)

46. Q. A 70 years old patient was brought to emergency ward in a comatose state.
His ABG was done and findings are as follows Na = 132 meq/lit,
K = 6.5 meq / lit, HCO3 = 10 meq/ lit, blood glucose 20 mmol/lit
BUN = 4 mmol/lit
What is your diagnosis. (AIIMS Nov 09)
A Non ketotic hyperosmolar diabetic coma
B D.K.A
C Hypoglycemic coma
D Lactic acidosis

47. Ans. D Lactic acidosis
In this case the RBS is 20mmol/lit i.e. 20 X 18 = 360 mg%.
So this is not a case of hypoglycemia.
Here in this question HCO3 is 10meq/lit so it is not a case of NKHOC.
So because this case has metabolic acidosis either it is a case of DKA or lactic acidosis.
But as patient age is 70 years it is more likely to be lactic acidosis.
Supposed in this question patient age was 17 year than the answer was DKA !!!)
Normal HCO3 levels = 22-26meq/l

48. LACTIC ACIDOSIS
-Lactic acidosisis characterized by low pH in body tissues and blood.
-Lactic acidosis is characterized by lactate levels >5 mmol/L and serum pH <7.35.
-It is very common in type 2 diabetic patient who are on metformin therapy.
-Associated with Vitamin b1 deficiency
-Signs:
a. Deep and rapid breathing
b. Vomiting
c. Abdominal pain.
Treatment:
1. Lactic acidosis is typically associated with tissue hypoperfusion.
Appropriate measures include treatment of shock, restoration of circulating fluid
volume, improved cardiac function, identification of sepsis source
2. Sodium bicarbonate is given I/V
3. Thiamine

49. NON KETOTIC
HYPEROSMOLAR COMA (NKHOC)
Symptoms –Classically patient is
i. Elderly
ii. H/O polyuria of several weeks with weight loss and decrease oral intake.
iii. Mentally confused
Signs –
a. Tachycardia
b. Hypotension
c. Dehydration
d. Altered sensorium, coma
Extra Edge:
Nausea, Vomiting, Abdominal Pain, Kussmaul respiration & Ketosis are
not the features of NKHOC.

50. Investigation of NKHOC
a. Blood sugar 900 – 1100 mg/dl
b. Serum osmolality > 350mosm/kg
c. Pseudo hyponatremia
e. pH normal i.e. no acidosis
f. Ketonuria is absent. i.e. no ketosis

51. Treatment of NKHOC
1. Fluid → Total fluid deficit (9 – 10L) should be reversed over 1 –2 day
Initially give normal saline to stabilize the patients hemodynamically
Then Give 0.45% saline
2. Regular Insulin to be given intravenous
3. Subcutaneus heparin because these patients are prone to venous
thrombosis.

52. Q. Complication in Diabetics mellitus type-II occurs around: (LQ)
A 5 years of onset
B 10 years of onset
C 15 years of onset
D 20 years of onset

53. Ans. B 10 years of onset In type II diabetes the chronic complication usually
start after 10 years of onset of diabetes.

54. Chronic Complications of diabetes are:
1. Vascular:
a. Micro vascular
b. Macro vascular
1. Microvascular
i. Eye: a. Retinopathy b. Macular edema
ii. Neuropathy
iii. Nephropathy
2. Macrovascular
i. CAD
ii. PAD
iii. CVA
3. Non vascular
i. Gastrointestinal
ii. Genitourinary
iii. Dermatologic
iv. Infectious
v. Cataracts
vi. Glaucoma
vii. Periodontal disease

55. 1. Vascular disease
i. Cardiovascular disease is increased in individuals with type 1 or type 2
DM.
ii. The Framingham Heart Study revealed a marked increase in PAD, CHF,
CAD, MI, and sudden death (risk increases from one- to fivefold) in DM.
iii. MI is 3-5 times commoner in and is more likely to be 'silent' (without
classic symptoms). Diabetes is a major risk factor for CAD.
iv. CAD is the commonest cause of death in diabetic.
v. Earliest dyslipidemia to occur is diabetes is raised Tg.
- In both the DCCT (type 1 diabetes) and the UKPDS (type 2 diabetes),
cardiovascular events were not reduced immediately by intensive treatment
during the trial but were reduced at follow-up 10–17 years later (this effect
has been termed legacy effect or metabolic memory).

56. Q. The most characteristic finding in diabetic nephropathy is: (LQ)
A Diffuse glomerulosclerosis
B Nodular glomerulosclerosis
C Armani-Ebstein reaction
D Fibrin caps

57. 1. ↑GFR is the 1st manifestation of diabetic nephropathy.
2. Then is the stage of Microalbuminuria.
It is the most reliable marker of diabetic nephropathy.
-diabetes is the commonest cause of CRF
-Protein restriction is helpful in diabetic nephropathy – (H, 18th Pg- 2985)
(8) Dietary advice- Protein intake = 0.8 gm/kg/day in micro Albuminuria,
< 0.8 gm/ kg /day = in macro albuminuria
B) Nodular glomerulosclerosis

58. Pathology of Diabetic nephropathy
(1) Capillary BM thickening
(2) Diffuse glomerulosclerosis (Most common). In this there is increase in
mesangial matrix.
(3) Nodular glomerulosclerosis. (It is the most characteristic feature).
(4) It is accompanied by accumulation of hyalin material.
(5) If it is within capillary loop (Fibrin cap) or it is attached to Bowman
capsule (Capsular drop)
(6) Armani Ebstein Reaction : Collection of glycogen clumps within the
renal tubules found in diabetic nephropathy

64. Q. In diabetic patient fundus examination should be checked how
frequently? (AIIMS May 09)
A 6 Months
B 1 year
C 2 years
D 5 years

65. Ans. B 1 year.
Diabetic retinopathy will be discussed in ophtho.

66. Q. The most common presentation of diabetic neuropathy is: (LQ)
A Amyotrophy
B Mononeuropathy
C Symmetrical sensory neuropathy
D Autonomic neuropathy

67. Ans. C Symmetrical sensory neuropathy

68. Q. Frequency of the tuning fork use for vibration sense is?
A 128
B 256
C 512
D 1024

69. A 128

70. Q.Drug used for DM gastropathy (AIIMS)
A Erythromycin
B Sulpha drug
C Tetracycline
D Ranitidine

71. A Erythromycin
Since erythromycin stimulates motilin receptors. And thus improves
Gastric paralysis.

72. Skin involvement in DM
a. Pigmented pretibial papules
b. Necrobiosis lipoidica
c. Acanthosis nigricans
d. Granuloma annulare
e. Lipoatrophy and lipohypertrophy
f. Scleredema
g. Dupuytren’s contracture.
Extra edge: Protease inhibitor can cause lipodystrophy.

73. Pigmented pretibial papules
MC skin manifestation of diabetes

74. Acanthosis nigricans

75. Acanthosis nigricans

76. DIABETIC RETINOPATHY
DRUGS AND INSULIN
WILL BE DISCUSSED LATER