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Optometry Special Class
Diabetes Mellitus
Dr. Harry Tagbor
Diabetes Mellitus (Type I)
 FEATURES:
– A chronic disease caused by pancreatic
insufficiency (deficiency) of insulin production,
resulting in hyperglycemia and end-organ
complications such as accelerated
atherosclerosis, neuropathy, nephropathy, and
retinopathy.
– Patients require insulin
– Response to oral drugs uncommon
Diabetes Mellitus (Type I)
 FEATURES:
– Usually of rapid onset
– Nutritional status - normal or thin
– Disease lability
– Mean age of onset 8-12 years, peaking in
adolescence; onset about 1.5 years earlier in girls
than boys. Rapid decline in incidence after
adolescence.
– Prone to ketosis
Diabetes Mellitus (Type I)
 SIGNS AND SYMPTOMS:
– Polyuria and polydipsia
– Polyphagia is classic, but not common
– Anorexia is commonly observed
– Weight loss (usually from 10-30%, and often almost
devoid of body fat at time of diagnosis)
– Increased fatigue
– Decreased energy levels and lethargy
– Muscle cramps
– Irritability and emotional lability
Diabetes Mellitus (Type I)
 SIGNS AND SYMPTOMS:
– Vision changes, such as blurriness
– Altered school and work performance
– Headaches
– Anxiety attacks
– Chest pain and occasional difficult breathing
– Abdominal discomfort and pain
– Nausea
– Diarrhea or constipation
Diabetes Mellitus (Type I)
 CAUSES:
– An inherited defect which causes an alteration in
immunologic integrity, placing the beta cell at risk
of inflammatory damage. The mechanism of
damage is autoimmune.
– Environmental factors include:
 Viruses (such as mumps, Coxsackie, CMV, and hepatitis
viruses)
 Dietary factors - breast feeding may provide a degree of
protection against the disease while diets high in dairy
products are associated with increased risk
 Emotional and physical stress
Diabetes Mellitus (Type I)
 LABORATORY:
– Blood glucose
– Electrolytes
– Venous pH
– U/A for glucose and ketones
– FBC (WBC may be elevated)
– Hemoglobin Alc level
Diabetes Mellitus (Type II)
 DESCRIPTION:
1. Non-ketosis prone hyperglycemia and glucose
intolerance due to defects in insulin secretion and
peripheral insulin action. Accounts for 80% of
diabetic cases.
2. System (s) affected: Endocrine/Metabolic,
Nervous, Renal/Urologic, Cardiovascular
3. Predominant age: Typically occurs after age 40
4. Predominant sex: Female > Male in Caucasian
populations
Diabetes Mellitus (Type II)
 SIGNS AND SYMPTOMS:
– Related to hyperglycemia and complications
including nephropathy, neuropathy, and
retinopathy
– Polyuria; Polydipsia; Polyphagia
– Weight loss
– Weakness
– Fatigue
– Frequent infections
Diabetes Mellitus (Type II)
 CAUSES:
– Genetic factors and obesity are important
 RISK FACTORS:
– Family history
– Gestational diabetes
– Obesity
Diabetes Mellitus (Type II)
 POSSIBLE COMPLICATIONS:
 Appear to be due to effects of diabetes
mellitus on arterial walls in one form or
another
– Peripheral neuropathy
– Proliferative retinopathy
– Nephropathy and chronic renal failure
– Atherosclerotic cardiovascular and peripheral
vascular disease
Diabetes Mellitus (Type II)
 POSSIBLE COMPLICATIONS:
– Hyper-osmolar coma
– Gangrene of extremities
– Blindness
– Glaucoma
– Cataracts
– Skin ulceration
– Charcot joints
Diabetes Mellitus (Type II)
 EXPECTED COURSE AND PROGNOSIS:
– Maintenance of normal blood sugar levels
may delay or prevent complications of
diabetes
– In susceptible individuals, complications
begin to appear 10-15 years after onset, but
can be present at time of diagnosis since
disease may go undetected for years
Diabetes Mellitus (Type II)
 ASSOCIATED CONDITIONS:
– Hypertension is common (strict control
may retard renal complications)
– Hyperlipidaemia
– Impotence
The ocular manifestations
of DM
Eyelids Xanthelasmata
Conjunctiva Microaneurysms, venous dilatation
Extra-ocular muscles CN 3, 4 or 6 palsy with diplopia
Orbit Mucormycosis
Iris Rubeosis iridis (neovascularisation)
Glaucoma Neovasucular glaucoma
Pupil Poor dilatation caused by RI
Lens Cataract
Vitreous body Vitreous haemorrhage
Retina Diabetic retinopathy
Optic nerve Ischaemic papillitis, optic atrophy
DIABETIC RETINOPATHY
 A sight-threatening chronic process based
primarily on damage to the retinal capillaries
(microangiopathy)
 Later the process involves larger vessels:
venules, arterioles and arteries
 A certain degree of retinopathy develops in
virtually every diabetic patient
DIABETIC RETINOPATHY
(pathogenic mechanisms)
 Capillary damage
– Capillary hypertension
– Systemic hypertension
– Insulin resistance
– Increased vascular permeability
– Endothelial dysfunction
– Hyperglycemic pseudohypoxia
– Non-enzymatic glycosylation
Capillary damage
Pericyte necrosis
(capillaries and veins)
Endothelial damage
Capillary non-perfusion
Retinal ischaemia
Vasoactive factors
Hyperperfusion
Abnormal autoregulation
Hypertension
New vessels
Growth factors
Hyperglycemia
PATHOGENIC MECHANISMS
Diabetes – Non-proliferative
disease
 Capillaries – leak and
become occluded
 Dot and Blot
hemorrhages
 Hard exudates
 Cotton wool spots
(ischemia)
Diabetes – Non-proliferative
disease
Diabetes – Proliferative
disease
 Neovascular
(Abnormal) vessels:
– Iris
– Optic Disc
– Retina
 Can cause:
– Severe Glaucoma
– Retinal detachments
– Vitreous Hemorrhages
Diabetes – Proliferative
disease
Diabetes – Macular Edema
 Affects 5-15% of
diabetic patients
 Leakage into the
macula from small
capillaries
 Results in severe
visual loss (e.g. no
useful reading
function)
DIABETIC RETINOPATHY
 **Revise grades of diabetic
retinopathy
Laboratory definition of
DM
 Normal values
– Fasting (plasma): 3.6 to 6.4mmol/l
– Random (plasma): 3.3 to 7.4 mmol/l
– GTT: 7.9 to 11.0 mmol/l or fasting < 7.8
mmol/l
Laboratory definition of
DM
 Indications for test
– The test is direct measurement of the
blood sugar and most commonly used in
the evaluation of diabetic patients
Laboratory definition of
DM
 Clinical priorities
– Serum glucose levels must be evaluated according
to the time of day they are obtained. Increased
levels follow a recent meal.
– Glucose determinations must be performed
frequently in new diabetic patients to determine
appropriate insulin therapy. Finger prick blood
glucose are often performed before meals and at
bed time.
– Many forms of stress can cause increased serum
glucose levels.
– Many drugs affect glucose levels.
Interpretation of results
 Interfering factors
– Acute stress (trauma, general anaesthesia,
infection, burns, myocardial infarction) increases
serum glucose levels.
– Caffeine may cause increased levels.
– IV fluids containing dextrose.
– Many pregnant women experience some degree of
glucose intolerance. If significant, it is called
gestational diabetes.
Interpretation of results
 Interfering factors
– Drugs (antidepressants, beta-adrenergic blocking
agents, corticosteroids, IV dextrose infusion,
diuretics, phenothiazines, estrogens) increase
glucose levels.
– Drugs (acetaminophen, alcohol, anabolic
steroids, insulin and other anti-diabetics)
decrease glucose levels
– Pancreatic disease and endocrine disorders
Interpretation of results
 A raised blood glucose is called hyperglycaemia.
 When definite it is diagnostic of Diabetes Mellitus.
 In an adult with symptoms, a random venous plasma
glucose of 11.1 mmol/l or more on two occasions or
a fasting value of 7.8 mmol/l or more on two
occasions is diagnostic.
 Random values below 7.8 mmol/l and fasting values
below 6.4 mmol/l excludes a diagnosis of diabetes
mellitus.
Interpretation of results
Plasma Fasting (mmol/l) Random (mmol/l)
Venous: >/= 7.8 (140mg%) >/= 11.1 (200mg%)
Capillary: >/= 7.8 (140mg%) >/= 12.1 (220mg%)
Whole blood
Venous: >/= 6.7 (120mg%) >/= 10.0 (180mg%)
Capillary: >/= 6.7 (120mg%) >/= 11.1 (200mg%)
Interpretation of results
 A low blood glucose level is called
hypoglycaemia.
 If less than 2.2 mmol/l it is
accompanied by symptoms such as
fainting, fits, sweating, hunger, pallor,
confusion or violence
Interpretation of results
 Causes of hypoglycaemia
– Severe malnutrition
– Kwashiorkor
– Severe liver disease
– Alcoholic excess
– Insulin secreting tumours
– Addison’s disease
– Drugs
– Neonatal hypoglycaemia
– Malaria

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diabetes (2).ppt

  • 1. Optometry Special Class Diabetes Mellitus Dr. Harry Tagbor
  • 2. Diabetes Mellitus (Type I)  FEATURES: – A chronic disease caused by pancreatic insufficiency (deficiency) of insulin production, resulting in hyperglycemia and end-organ complications such as accelerated atherosclerosis, neuropathy, nephropathy, and retinopathy. – Patients require insulin – Response to oral drugs uncommon
  • 3. Diabetes Mellitus (Type I)  FEATURES: – Usually of rapid onset – Nutritional status - normal or thin – Disease lability – Mean age of onset 8-12 years, peaking in adolescence; onset about 1.5 years earlier in girls than boys. Rapid decline in incidence after adolescence. – Prone to ketosis
  • 4. Diabetes Mellitus (Type I)  SIGNS AND SYMPTOMS: – Polyuria and polydipsia – Polyphagia is classic, but not common – Anorexia is commonly observed – Weight loss (usually from 10-30%, and often almost devoid of body fat at time of diagnosis) – Increased fatigue – Decreased energy levels and lethargy – Muscle cramps – Irritability and emotional lability
  • 5. Diabetes Mellitus (Type I)  SIGNS AND SYMPTOMS: – Vision changes, such as blurriness – Altered school and work performance – Headaches – Anxiety attacks – Chest pain and occasional difficult breathing – Abdominal discomfort and pain – Nausea – Diarrhea or constipation
  • 6. Diabetes Mellitus (Type I)  CAUSES: – An inherited defect which causes an alteration in immunologic integrity, placing the beta cell at risk of inflammatory damage. The mechanism of damage is autoimmune. – Environmental factors include:  Viruses (such as mumps, Coxsackie, CMV, and hepatitis viruses)  Dietary factors - breast feeding may provide a degree of protection against the disease while diets high in dairy products are associated with increased risk  Emotional and physical stress
  • 7. Diabetes Mellitus (Type I)  LABORATORY: – Blood glucose – Electrolytes – Venous pH – U/A for glucose and ketones – FBC (WBC may be elevated) – Hemoglobin Alc level
  • 8. Diabetes Mellitus (Type II)  DESCRIPTION: 1. Non-ketosis prone hyperglycemia and glucose intolerance due to defects in insulin secretion and peripheral insulin action. Accounts for 80% of diabetic cases. 2. System (s) affected: Endocrine/Metabolic, Nervous, Renal/Urologic, Cardiovascular 3. Predominant age: Typically occurs after age 40 4. Predominant sex: Female > Male in Caucasian populations
  • 9. Diabetes Mellitus (Type II)  SIGNS AND SYMPTOMS: – Related to hyperglycemia and complications including nephropathy, neuropathy, and retinopathy – Polyuria; Polydipsia; Polyphagia – Weight loss – Weakness – Fatigue – Frequent infections
  • 10. Diabetes Mellitus (Type II)  CAUSES: – Genetic factors and obesity are important  RISK FACTORS: – Family history – Gestational diabetes – Obesity
  • 11. Diabetes Mellitus (Type II)  POSSIBLE COMPLICATIONS:  Appear to be due to effects of diabetes mellitus on arterial walls in one form or another – Peripheral neuropathy – Proliferative retinopathy – Nephropathy and chronic renal failure – Atherosclerotic cardiovascular and peripheral vascular disease
  • 12. Diabetes Mellitus (Type II)  POSSIBLE COMPLICATIONS: – Hyper-osmolar coma – Gangrene of extremities – Blindness – Glaucoma – Cataracts – Skin ulceration – Charcot joints
  • 13. Diabetes Mellitus (Type II)  EXPECTED COURSE AND PROGNOSIS: – Maintenance of normal blood sugar levels may delay or prevent complications of diabetes – In susceptible individuals, complications begin to appear 10-15 years after onset, but can be present at time of diagnosis since disease may go undetected for years
  • 14. Diabetes Mellitus (Type II)  ASSOCIATED CONDITIONS: – Hypertension is common (strict control may retard renal complications) – Hyperlipidaemia – Impotence
  • 15. The ocular manifestations of DM Eyelids Xanthelasmata Conjunctiva Microaneurysms, venous dilatation Extra-ocular muscles CN 3, 4 or 6 palsy with diplopia Orbit Mucormycosis Iris Rubeosis iridis (neovascularisation) Glaucoma Neovasucular glaucoma Pupil Poor dilatation caused by RI Lens Cataract Vitreous body Vitreous haemorrhage Retina Diabetic retinopathy Optic nerve Ischaemic papillitis, optic atrophy
  • 16. DIABETIC RETINOPATHY  A sight-threatening chronic process based primarily on damage to the retinal capillaries (microangiopathy)  Later the process involves larger vessels: venules, arterioles and arteries  A certain degree of retinopathy develops in virtually every diabetic patient
  • 17. DIABETIC RETINOPATHY (pathogenic mechanisms)  Capillary damage – Capillary hypertension – Systemic hypertension – Insulin resistance – Increased vascular permeability – Endothelial dysfunction – Hyperglycemic pseudohypoxia – Non-enzymatic glycosylation
  • 18. Capillary damage Pericyte necrosis (capillaries and veins) Endothelial damage Capillary non-perfusion Retinal ischaemia Vasoactive factors Hyperperfusion Abnormal autoregulation Hypertension New vessels Growth factors Hyperglycemia PATHOGENIC MECHANISMS
  • 19. Diabetes – Non-proliferative disease  Capillaries – leak and become occluded  Dot and Blot hemorrhages  Hard exudates  Cotton wool spots (ischemia)
  • 21. Diabetes – Proliferative disease  Neovascular (Abnormal) vessels: – Iris – Optic Disc – Retina  Can cause: – Severe Glaucoma – Retinal detachments – Vitreous Hemorrhages
  • 23. Diabetes – Macular Edema  Affects 5-15% of diabetic patients  Leakage into the macula from small capillaries  Results in severe visual loss (e.g. no useful reading function)
  • 24. DIABETIC RETINOPATHY  **Revise grades of diabetic retinopathy
  • 25. Laboratory definition of DM  Normal values – Fasting (plasma): 3.6 to 6.4mmol/l – Random (plasma): 3.3 to 7.4 mmol/l – GTT: 7.9 to 11.0 mmol/l or fasting < 7.8 mmol/l
  • 26. Laboratory definition of DM  Indications for test – The test is direct measurement of the blood sugar and most commonly used in the evaluation of diabetic patients
  • 27. Laboratory definition of DM  Clinical priorities – Serum glucose levels must be evaluated according to the time of day they are obtained. Increased levels follow a recent meal. – Glucose determinations must be performed frequently in new diabetic patients to determine appropriate insulin therapy. Finger prick blood glucose are often performed before meals and at bed time. – Many forms of stress can cause increased serum glucose levels. – Many drugs affect glucose levels.
  • 28. Interpretation of results  Interfering factors – Acute stress (trauma, general anaesthesia, infection, burns, myocardial infarction) increases serum glucose levels. – Caffeine may cause increased levels. – IV fluids containing dextrose. – Many pregnant women experience some degree of glucose intolerance. If significant, it is called gestational diabetes.
  • 29. Interpretation of results  Interfering factors – Drugs (antidepressants, beta-adrenergic blocking agents, corticosteroids, IV dextrose infusion, diuretics, phenothiazines, estrogens) increase glucose levels. – Drugs (acetaminophen, alcohol, anabolic steroids, insulin and other anti-diabetics) decrease glucose levels – Pancreatic disease and endocrine disorders
  • 30. Interpretation of results  A raised blood glucose is called hyperglycaemia.  When definite it is diagnostic of Diabetes Mellitus.  In an adult with symptoms, a random venous plasma glucose of 11.1 mmol/l or more on two occasions or a fasting value of 7.8 mmol/l or more on two occasions is diagnostic.  Random values below 7.8 mmol/l and fasting values below 6.4 mmol/l excludes a diagnosis of diabetes mellitus.
  • 31. Interpretation of results Plasma Fasting (mmol/l) Random (mmol/l) Venous: >/= 7.8 (140mg%) >/= 11.1 (200mg%) Capillary: >/= 7.8 (140mg%) >/= 12.1 (220mg%) Whole blood Venous: >/= 6.7 (120mg%) >/= 10.0 (180mg%) Capillary: >/= 6.7 (120mg%) >/= 11.1 (200mg%)
  • 32. Interpretation of results  A low blood glucose level is called hypoglycaemia.  If less than 2.2 mmol/l it is accompanied by symptoms such as fainting, fits, sweating, hunger, pallor, confusion or violence
  • 33. Interpretation of results  Causes of hypoglycaemia – Severe malnutrition – Kwashiorkor – Severe liver disease – Alcoholic excess – Insulin secreting tumours – Addison’s disease – Drugs – Neonatal hypoglycaemia – Malaria