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Diabetes Mellitus an overview. Aly A. Abdel-Rahim, MD.

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diabetes mellitus an overview

Diabetes Mellitusan overview

Aly A. Abdel-Rahim, MD

slide2

Diabetes is a disorder caused by the presence of too much glucose in the blood. A first depiction of this “sugar disease” was described in the “Ebers Papyrus”, a papyrus sold to the German Egyptologist Georg Moritz Ebers in 1872. It was said to have been found close to a mummy in the tomb of Thebes and appears to have been written between 3000 and 1500 BC.

history
History
  • Reference to diabetes was made 1550 BC.
  • In the 2nd Century AD, Aretaeus gave an excellent description of diabetes.
  • Thomas Willis in the 17th Century detected the sweet test of urine.
  • Mathew in the 18th Century showed that the sugar in urine comes from the blood.
history5
History
  • Minkowski and Von Mering discovered that disease of the pancreas is responsible for diabetes to develop in the 19th century.
  • In the 19th century treatment of diabetes was confined to food regulation which reduced urination but did not prevent wasting and complications.
history6
History
  • In the second half of the 19th Century, Paul Langerhans, a German student, identified clusters of cells within the pancreas responsible for the production on glucose lowering substance. “islets of Langerhans”.
  • Insulin: in Latin insula= island. So the name was coined before the hormone was discovered.
history7
History
  • Banting and Best “a student” worked in McLeod's labs in Toronto.
  • In 1921they made the exocrine cells atrophy by ligation of the pancreatic duct.
  • They made aqueous extracts of the remaining tissue keeping it cold and filtered it.
  • The extract was injected into a diabetic dog on 30 July 1921.
history8
History
  • They convinced themselves that they had discovered the active pancreatic hormone which normalizes the blood sugar.
history9
History
  • The first person to be treated with insulin was Leonard Thompson (1908-1935). The first injection was in 11 January 1922
history noble prize 1923
History: Noble Prize 1923

Banting

McLeod

Best

Collip

definition of diabetes
Definition of diabetes
  • A syndrome of chronic hyperglycaemia with other metabolic abnormalities together with micro and macro-vascular complications.
what is wrong with diabetes
What is wrong with diabetes
  • Insulin deficiency
  • Insulin resistance

Hyperglycaemia

classification of diabetes
Classification of diabetes
  • Type 1DM
  • Type 2DM
  • IFG: impaired fasting glycaemia
  • IGT: impaired glucose tolerance
  • GDM: Gestational diabetes mellitus
  • Secondary DM.
criteria of diagnosis
Criteria of diagnosis
  • FBS > 125.
  • PP > 200
  • OGTT.

normal:

  • FBS <100
  • PP <140
slide16
T1DM
  • Usually in young age
  • Characterized by absolute insulin deficiency.
  • Increased catabolism and liability to ketosis.
  • Stormy presentation.
  • must be treated with insulin.
slide17
T2DM
  • Usually in older age.
  • Relative insulin deficiency.
  • Increased insulin resistance.
  • Can be treated with OHA or insulin.
  • Slow onset, less likely to develop ketosis.
  • May present with complications.
slide18
MODY

Maturity onset diabetes of the youth

  • A special type of diabetes similar to type 2 diabetes but develop in young age groups.
  • Increased prevalence worldwide.
  • Associated with increased childhood obesity.
diabetes related to drugs
Diabetes related to drugs
  • Glucocorticoids
  • Diazoxide.
  • Thiazides.
  • Phyention
  • Pentamidine
slide20
GDM

Gestational diabetes mellitus

  • Diabetes discovered for the first time during pregnancy.
  • Every pregnant lady should be screened.
  • Usually disappears after labor.
  • Increased risk to develop T2DM later in life.
social profile related to diabetes in egypt
Social profile related to diabetes in Egypt
  • with an average income per person of $1,490 in 2001, fighting poverty remains a substantial challenge.
  • In it dropped to $1.390 in 2003 and then $1.310 in 2004. *
  • People living under poverty line (<1 $/day) 3.7%

*WHO statistics 2005

social profile related to diabetes in egypt28
Social profile related to diabetes in Egypt
  • Life expectancy is 69.1 years.
  • National poverty rate (% of population) 16.7 .
  • Child malnutrition, weight for age (% of under 5) 4.0 in 2003 increased to 8.6 2004.

Source: World Development Indicators database, August 2005

prevalence of diabetes in egypt
Prevalence of diabetes in Egypt
  • Herman : 9.3% above 20y of age.
  • Arab 4.3% above 20y of age.
  • Why the difference ???

region e.g.: desert and Nubians.

prevalence of diabetes in egypt30
Prevalence of diabetes in Egypt
  • Herman : 9.3% above 20y of age.
  • Arab 4.3% above 20y of age.
  • Why the difference ???

region e.g.: desert and Nubians.

diagnosis
Diagnosis
  • How to diagnose diabetes:
    • Signs and symptoms
    • Blood glucose test
    • OGTT
    • HbA1c
diagnosis32
Diagnosis
  • Most people are diagnosed with diabetes when they are suspected to have symptoms of polyurea, polydepsia, fatigue, loss of weight.
  • This is confirmed by fasting or PP blood glucose.
  • In case of doubt OGTT may be done.
  • Urine testing should not be used in diagnosis.
diagnosis33
Diagnosis
  • Peers and medical ‘advisors’ should be aware of the following:
  • T1DM & T2DM are two distinct diseases.
  • T1DM is stormy at presentation, delay in diagnosis can be disastrous.
  • Among the presentations of T1DM could be some non-specific symptoms like vomiting, abdominal pain….
diagnosis34
Diagnosis
  • T2DM may present with late symptoms, like numpness, disturbed vision, generalized oedema.
  • Patients with hypertension, dyslipidaemia, MI and family history of diabetes are very likely to develop T2DM.
pathophysiology of t1dm
Pathophysiology of T1DM

Absence of insulin secretion

Failure to use glucose as a fuel

Hyperglycaemia & using fat

Ketosis

pathophysiology of t1dm36
Pathophysiology of T1DM
  • Possible contributing factors:
    • Autoimmune disease.
    • HLA typing
    • Viruses
    • chemicals
pathophysiology of t1dm37
Pathophysiology of T1DM
  • Remission.
  • The honeymoon period
pathophysiology of t2dm
Pathophysiology of T2DM

Insulin resistance

hyperinsulinaemia

Relative hypoinsulinaemia

Hyperglycaemia, dyslipidaemia, atherosclerosis, HTN

pathophysiology of t2dm39
Pathophysiology of T2DM
  • Causes of insulin resistance:
    • Hereditary.
    • Decreased glucose transporters.
    • Decreased insulin receptors
    • Post receptor mechanisms
    • Chemical mediators e.g. TNFα
pathophysiology of t2dm40
Pathophysiology of T2DM
  • Loss of first phase of insulin secretion.
  • Delayed insulin release.
insulin45
Insulin
  • Action of insulin:
    • On glucose metabolism
    • On amino acid metabolism
    • On lipid metabolism
insulin46
Insulin
  • Short acting
insulin47
Insulin
  • Intermediate acting
insulin48
Insulin
  • Peak less insulin
  • Act for 24 hours no peak
insulin49
Insulin
  • Premixed insulin
insulin50
Insulin
  • Preparation of human insulin:
insulin51
Insulin
  • Preparation of human insulin:
insulin52
insulin
  • Plasmid preparation
insulin53
Insulin
  • Absorption
insulin54
Insulin
  • Variation of absorption:
    • Type
    • Dose
    • Site of preparation
    • Temperature.
    • circulation
insulin55
Insulin
  • Storage of insulin
insulin56
Insulin
  • injection
insulin57
insulin
  • injection:
insulin58
insulin
  • Devices
insulin59
Insulin
  • Side effect:
    • Hypoglycaemia
    • Atrophy
    • Hypertrophy
    • Sensitivity
    • Weight gain
slide60
Diet
  • Rules:
    • Balanced meal
    • Maintain body weight
    • Adequate nutrition
    • Regular meal time.
slide63
OHA
  • Sulphonylureas:
    • Mode of action
    • Side effect
    • Differences
    • Use
slide64
OHA
  • Metformin:
    • Action
    • When to use
    • Side effects
    • Warning.
slide65
OHA
  • Acarbose
    • Action
    • Effect
    • Side effect use
slide66
OHA
  • Non Sulphonylureas insulin secreatgauges:
    • Repaglinide
    • Natiglinide.
slide67
OHA
  • Insulin sensitizers:
    • Mode of action
    • Effect
    • Side effect
    • use
oral antihyperglycemic therapy for type 2 diabetes scientific review
Oral Antihyperglycemic Therapy for Type 2 Diabetes: Scientific Review
  • 63 published studies reviewed
  • Individually, oral agents lower A1c 1-2 %
  • In comparisons, roughly equal effects
  • In combination, roughly additive effects
  • Long-term benefits demonstrated only for
    • Metformin and Sulfonylureas

SE Inzucchi. JAMA 2002; 287:360-372.

sulfonylureas e g chlorpropamide glyburide
Sulfonylurease.g. Chlorpropamide, Glyburide
  • Mechanism
    • Increase insulin secretion by pancreas
  • Advantages
    • Well established, Decrease microvascular risk, Convenient dosing
  • Disadvantages
    • Hypoglycemia, Weight gain
  • FDA Approval for combination therapy
    • Metformin, TZD, acarbose

Adapted from SE Inzucchi, JAMA 2002; 287:360-372.

non su secretagogues e g nateglinide repaglinide
Non-SU Secretagoguese.g. Nateglinide, Repaglinide
  • Mechanism
    • Increase insulin secretion by pancreas
  • Advantages
    • Targets post-prandial glycemia
  • Disadvantages
    • TID dosing, No long-term data
  • FDA Approval for combination therapy
    • Metformin

Adapted from SE Inzucchi, JAMA 2002; 287:360-372.

biguanides e g metformin
Biguanidese.g. Metformin
  • Mechanism
    • Decrease hepatic glucose production
  • Advantages
    • Well established, Weight loss, No hypoglycemia, Decrease micro & macrovascular risk, Convenient dosing, [Also prevents diabetes]
  • Disadvantages
    • GI distress, Lactic acidosis, Contraindications
  • FDA Approval for combination therapy
    • Insulin, SU and non-SU secretagogues, TZD

Adapted from SE Inzucchi, JAMA 2002; 287:360-372.

alpha glucosidase inhibitors e g acarbose miglitol
Alpha-Glucosidase Inhibitorse.g. Acarbose, Miglitol
  • Mechanism
    • Decrease gut carbohydrate absorption
  • Advantages
    • Targets post-prandial hyperglycemia, No systemic absorption, [Also prevents diabetes]
  • Disadvantages
    • GI distress, TID dosing, No long-term data
  • FDA Approval for combination therapy
    • Sulfonylureas

Adapted from SE Inzucchi, JAMA 2002; 287:360-372.

thiazolidindiones e g pioglitazone rosiglitazone
Thiazolidindionese.g. Pioglitazone, Rosiglitazone
  • Mechanism
    • Increase peripheral glucose disposal
  • Advantages
    • Physiologically “correct,” Convenient dosing, [Also prevents diabetes]
  • Disadvantages
    • Liver toxicity, Liver monitoring, Weight gain, Edema, No long-term data
  • FDA Approval for combination therapy
    • Insulin, sulfonylurea, metformin

Adapted from SE Inzucchi, JAMA 2002; 287:360-372.

retail price per month of selected antidiabetic regimens
Retail Price ($ per month) of Selected Antidiabetic Regimens
  • Chlorpropamide 500 mg qD 18
  • Glyburide (generic) 10 mg bid 48
  • Glimepiride 8 mg qD 56
  • Acarbose 100 mg tid 68
  • Metformin (generic) 850 mg tid 78
  • Nateglinide 120 mg tid 90
  • Rosiglitazone 8 mg qD 130
  • Repaglinide 4 mg tid 160

www.drugstore.com, August 2003

hypoglycaemia79
Hypoglycaemia
  • Most common complication of diabetes
    • 100% of Type 1 patients affected
    • ~ 10%/year severe (requiring assistance)
    • much less common in Type 2
  • Multiple causes:
    • exercise/activity drug overdose
    • reduced food intake alcohol use
    • delayed meal
symptoms of hypoglycemia
Symptoms of Hypoglycemia

AdrenergicNeuroglycopenic

tachycardia dizziness

palpitations confusion

sweating sleepiness

tremor coma

hunger seizure

slide81

Hypoglycemia

Symptoms and Signs

  • Sweating, tremors, pounding heart beats.
  • Pallor, cold sweat, irritability
  • May develop coma.

108

prevention of hypoglycemia
Prevention of Hypoglycemia
  • Consistent meal times, appropriate to drug regimen
  • Consistent carbohydrate intake, or matched to drug dose
  • Adjustments for extra exercise
    • extra food, e.g. 15 gm carb/30 min
    • reduce drug, e.g. prior dose by 20-30%
  • Accurate drug dosing
  • Blood glucose monitoring
treatment of hypoglycemia
Treatment of Hypoglycemia
  • Oral carbohydrate:
    • 10-15 gms, repeat after 15 minutes if needed
    • glucose tabs preferred; food acts slower, adds unneeded calories (fat, protein)
  • IV Glucose
    • 20-50 cc of D50
  • Glucagon
    • 1 mg IM
hyperosmolar hyperglycemic nonketotic syndrome85
Hyperosmolar Hyperglycemic Nonketotic Syndrome

Clinical presentation

Severe hyperglycemia (BG > 600)

No or minimal ketosis

Hyperosmolarity

Profound dehydration

Altered mental status

causes of hhns
Causes of HHNS
  • Drugs: glucocorticoids, diuretics
  • Acute stressors: infection, burns, CVA, MI, gastroenteritis
  • Other chronic disease: renal, heart, old stroke
  • Procedures: surgery
prevention of hhns
Prevention of HHNS
  • Awareness of the syndrome
  • Maintenance of adequate hydration
  • Control of blood glucose during acute stress with insulin
diabetic ketoacidosis
Diabetic Ketoacidosis
  • An acute, life threatening metabolic acidosis complicating IDDM and some cases of NIDDM with intercurrent illness (infection or surgery)
  • Usually coupled with an increase in glucagon concentration with two metabolic consequences:
    • 1) Maximal gluconeogenesis with impaired

peripheral utilization of glucose

    • 2) Activation of the ketogenic process and

development of metabolic acidosis.

diabetic ketoacidosis90
Diabetic Ketoacidosis
  • Usually seen in Type 1 DM, but CAN OCCUR in Type 2
  • Often with acute stress, such as infection, MI, etc.
  • Recurrent DKA almost always related to omission of insulin, psychosocial problems
  • Preventive measures same as for HHNS
clinical presentation
Clinical Presentation
  • Anorexia, N/V, along with polydepsia and polyuria for about 24 hrs. followed by stupor (or coma).
  • Abdominal pain and tenderness could be present (remember DDx of acute abdomen).
  • Kussmaul breathing with fruity odor “acetone”
  • Sings of dehydration ( HR, postural BP, etc.)
  • Normal or low temperature:

NB.: if fever is present it suggests infection

while leukocytosis alone is not because

DKA per se can cause fever.

slide92

Has to be treated in Hospital

Always refer to Endocrinologist

  • Insulin: is a prerequisite for recovery
  • IVF: the usual fluid deficit is 3-5L
  • Potassium: replacement is always necessary
  • Bicarbonate:
acute complications of diabetes
Acute Complications of Diabetes

SUMMARY:

  • Acute complications can be prevented or greatly reduced
  • Prevention depends on effective patient education
slide95

Causes of Death Among People With Diabetes

Cause

% of Deaths

40

15

13

13

10

4

5

Ischemic heart disease

Other heart disease

Diabetes (acute complications)

Cancer

Cerebrovascular disease

Pneumonia/influenza

All other causes

Geiss LS et al. In: Diabetes in America. 2nd ed.1995:233-257.

complications of diabetes long term
Complications of Diabetes: Long term
  • Macrovascular
    • Ischaemic heart disease – heart attacks; stroke
    • Peripheral vascular disease – gangrene, amputations
  • Microvascular
    • EYE – retinopathy - blindness
    • NERVE - neuropathy (peripheral and autonomic)
    • KIDNEY – nephropathy; dialysis
  • Infections
magnitude of problem
Magnitude of Problem
  • Diabetic retinopathy: most common cause of blindness before age 65
  • Nephropathy: most common cause of ESRD
  • Neuropathy: most common cause of non-traumatic amputations
  • 2-3 fold increase in cardiovascular disease
microvascular complications
Microvascular Complications
  • Diabetic retinopathy
      • background retinopathy
      • macular edema
      • proliferative retinopathy
  • Diabetic nephropathy
  • Diabetic neuropathy
      • distal symmetrical polyneuropathy
      • mononeuropathy (peripheral, cranial nerves)
      • autonomic neuropathy
slide99

Increased risk of complications with lack of glucose control...

Only 27% of DM US patients on OADs have HbA1c<7%**

15

Retinopathy

13

Nephropathy

Neuropathy

11

Microalbuminuria

Relative Risk

9

7

5

3

1

6

7

8

9

10

11

12

HbA1C(%)

*Endocrinol Metab Clin 1996;25:243 - 254 (Diabetes Control Complications Trial) ** NHANES III

slide100

chronic complications* population based - Egyptians

  • prevalence known D new D
  • %
    • retinopathy 41.5 15.7
    • nephrop. 6.7 6.8
    • neuropathy 21.9 13.6
    • foot ulcers 0.8 0.8
  • associations
    • ret; nephr; neuro :  glucose

*microvasc + neuropathic; n: 1451

retinopathy and blindness in diabetes patients
Retinopathy and Blindness in Diabetes Patients
  • It is estimated that retinopathy affects 80%-97% of patients with diabetes of ³15 years’ duration
  • Diabetes is the leading cause of new cases of blindness in adults*
  • Diabetic retinopathy accounts for the majority of these cases
  • Minimum cost of blindness for working-age adult is estimated at $12,769 per year

*Blindness is defined as visual acuity £20/200

Klein R, Klein BEK. In: Diabetes in America. 2nd ed.1995:293-338.

diabetic retinopathy
Diabetic Retinopathy
  • Background retinopathy
    • present in 90% of patients after 10 years
    • asymptomatic
    • red dots (microaneurysms)
    • dot, blot, and flame shaped hemorrhages
    • hard waxy exudates of lipid and protein
    • best detected by dilated eye exam or photos
diabetic retinopathy104
Diabetic Retinopathy
  • Macular edema
    • sight threatening edema of the macula
    • usually reduces visual acuity early
    • can only be diagnosed by ophthalmologic exam
    • focal photocoagulation reduces risk of blindness by 50%
diabetic retinopathy106
Diabetic Retinopathy
  • Proliferative retinopathy
    • growth of small, fragile blood vessels that may bleed (vitreous hemorrhage)
    • associated with growth of fibrous tissue that may cause retinal detachment
    • may occur on the optic disk or elsewhere
    • high risk of blindness (50% in 3 years)
    • hypertension, isometric exercise, high contact sports may increase risk of bleeding
kidney disease in diabetes patients
Kidney Disease in Diabetes Patients
  • 27,851 new cases of ESRD in diabetes patients in 1995
    • 40% of all new cases in the US
  • Nearly 99,000 diabetes patients required dialysis or kidney transplantation that year
  • Annual cost of ESRD:
    • $45,000 in diabetic patients ages 45-64

National Diabetes Fact Sheet. November 1, 1997:1-8.

U.S. Renal Data System, USRDS 1997 Annual Data Report.