Diabetes mellitus: (DM): <ul><li>‘‘ Definition Diabetes mellitus results from a lake of,  </li></ul><ul><li>or   </li></ul...
<ul><li>Presentation:  </li></ul><ul><li>Patients may be a symptomatic. </li></ul><ul><li>Acute :  </li></ul><ul><li>Ketoa...
<ul><li>Subacute :  </li></ul><ul><li>History as above but longer and in addition lethargy , </li></ul><ul><li>infection (...
<ul><li>Complications  : </li></ul><ul><li>may be the presenting feature: </li></ul><ul><li>infections, </li></ul><ul><li>...
Classification
Type I ( insulin-dependent DM- IDDM) <ul><li>Usually  juvenile  onset but may occur at any age.  </li></ul><ul><li>charact...
Type II : (non insuline dependent DM,.  NIDDM, maturity onset DM)  <ul><li>Older age group, often obese, NB: NIDDMs may ev...
Causes of secondary diabetes <ul><li>Drugs (steroids and thiazides) </li></ul><ul><li>Pancreatic disease (pancreatitis, su...
<ul><li>* Fasting venous plasma glucose  >  7mmol/L  </li></ul><ul><li>a glucose of 6-7 mmol/L implies impaired fasting gl...
<ul><li>* Urine tests for glycosuria and random blood glucose tests are unreliable (but if 11.1 mmol/l and  symptoms are p...
<ul><li>Causes of insulin resistance : </li></ul><ul><li>* Obesity  *  Pregnancy </li></ul><ul><li>* Asian origin * Acute ...
Mechanism of insulin resistance:  <ul><li>Obesity probably  causes insulin  resistance by the associated  ↑ rate of releas...
Management: <ul><li>Advise weight loss and exercise mange  hyperglycaemia, with drugs or insulin. Vitamin E improves  insu...
<ul><li>Thiazolidinediones  (PPAR-gamma againsts)  ↑ insulin sensitivity eg rosiglitazone 4mg/24h.  </li></ul><ul><li>LFT ...
NICE  :  <ul><li>(recommends their use as an alternative  to insulin only if metformin with a sulfanyurea is not  working,...
Impaired glucose regulation that does not amount to diabetes <ul><li>This metabolic state lies between normal glucose home...
Impaired fasting glycaemia/glucase (IFG):  <ul><li>Fasting glucose levels above the normal range, but below the diagnostic...
Gestational diabetes:  <ul><li>This term now intrudes both gestational impaired glucose tolerance (GIGT) and gestations) d...
Diabetes management Principales: <ul><li>Patient motivation and education are the keys to success.  </li></ul><ul><li>Aim ...
<ul><li>Interestingly, tight blood pressure control is as effective in reducing microvascular disease,  </li></ul><ul><li>...
<ul><li>Basic investigations   Blood : </li></ul><ul><li>Glucose, U&Es, lipids, HbA1c , cholesterol. </li></ul><ul><li>Uri...
Fundoscopy and feet exam:  <ul><li>Assess feet and check for signs of neuropathy. </li></ul><ul><li>initial treatment If t...
Education/negotiation:  <ul><li>is crucial on drugs, diet, and the issues below: </li></ul><ul><li>•  Monitoring blood or ...
Healthy eating:  <ul><li>(saturated fats ↓ , sugar  ↓  starch-carbohydrates ↑ , moderate protein).  </li></ul><ul><li>Ensu...
Insulin Strength: <ul><li>l00u/mL Formulations of different durations:  </li></ul><ul><li>soluble insulin is short-acting ...
Oral hypoglycaemics:  <ul><li>Sulfonylureas : </li></ul><ul><li>These  ↑ insulin secretion. </li></ul><ul><li>tolbutamide ...
<ul><li>Metformin (a biguonide) Action:  </li></ul><ul><li>insulin sensitivity  ↑ ; hepatic glucorieogenesis  ↓  Se:  </li...
Acarbose (an  α -glucosidase inhibitor)  <ul><li>It decreases breakdown of starch to sugar.  </li></ul><ul><li>An adjust  ...
Thiazolidinediones:  <ul><li>Rosiglitazone e.g  4mg po.  </li></ul><ul><li>CL;: hepatic impairment, SE; headache, diarrhoe...
Other considerations:  <ul><li>ACE (many beneficial affects, not just BP ↓ ); aspirin and statins  to  ↓  overall risk. Ex...
Some commonly used insulin regiments  <ul><li>I- A single dose of  medium-acting insulin  with 3 doses  of short- acting  ...
<ul><li>3-  ‘Pen’ devices  are popular because of their ease of use (e.g. during   parties),  </li></ul><ul><li>Short-acti...
<ul><li>4-  If mealtimes are random, or pastprandial  glucose  ↑  very rapidly absorbed, genetically engineered human insu...
Assessment of the established  diabetic <ul><li>Continuing assessment of the diabetic patient has 3 main aims:  </li></ul>...
Assess glycaemic control from:  <ul><li>I Glycated (glycosylated) haemoglobin (= HbA1c – levels relate to mean glucose lev...
<ul><li>The elderly may opt for less tight control.  </li></ul><ul><li>Complications increase in frequency with increasing...
Assessment of complications <ul><li>Check injection sites for infection, lipoatrophy, or lipohypertrophy. </li></ul>
•  Vasculor disease:  <ul><li>Commonest cause of death. Look for evidence of cere brovascular, cardiovascular, and periphe...
<ul><li>Also slow progression or renal disease.  </li></ul><ul><li>Treat lipid disorders: good glycaemic control helps.  <...
•  Kidneys <ul><li>( Check urine regularly. If dipstick is +ve for protein, collect 24h urine for creatinine clearance and...
•  Diabetic reonopatrty:  <ul><li>(Dilate pupils with 0.5% tropicamide.) Blindness is common but preventable.  </li></ul><...
Background:  <ul><li>Microaneurysms (dots), microhaemorrhages (blots) and hard exudates. Refer to specialist if near the m...
Pathogenesis:  <ul><li>Capillary endotheliai change —>. </li></ul><ul><li>vascular leakage—>. </li></ul><ul><li>microa neu...
•  Cataracts:  <ul><li>These occur earlier in DM (senile and juvenile ‘snowflake’ cataracts).  </li></ul><ul><li>The osmot...
Metabolic complications:  <ul><li>Diabetic feet. Neuropathy  </li></ul><ul><li>Amputation  is preventable:  </li></ul><ul>...
Signs:  <ul><li>Sensation ↓  (especially vibration) in ‘stocking’ distribution; absent ankle jerks; deformity (pea cavus, ...
Foot ulceration: <ul><li>Usually painless, punched-out ulcer in an area of thick callous ± superadded infection, pus, oede...
Management:  <ul><li>Regular  chiropody  to debride lesions (remove dead tissue).  </li></ul><ul><li>Relieve high-pressure...
Absolute indications for surgery <ul><li>•  Abscess or deep infection  </li></ul><ul><li>•  Spreading anaerobic infection ...
Types of neuropathy in diabetes <ul><li>Motor and sensory neuropathy </li></ul><ul><li>I-  Symmetric sensory polyneuropath...
Autonomic neuropathy:  <ul><li>Postural BP ↓  urine retention; impotence; diarrhoea s: night. The latter may respond to 3 ...
Diabetic patients with intercurrent illness: <ul><li>The stress of illness often increases basal insulin requirement If ca...
<ul><li>2-  Insulin-treated; moderate illness (eg pneumonia). Normal insulin and supplementary sliding scale of rapid-acti...
Hypoglycaemia : <ul><li>This is  the commonest endocrine emergency. Prompt diagnosis and </li></ul><ul><li>treatment is es...
Fasting hypoglycaemia :  <ul><li>(requires full investigation if documented). </li></ul><ul><li>Causes:  </li></ul><ul><li...
<ul><li>Liver failure plus some rare inherited enzyme defects. </li></ul><ul><li>Addison’s disease. </li></ul><ul><li>Isle...
Diagnosis and investigations: <ul><li>I-  Document hypoglycaemia by taking finger-prick (on filter-paper at </li></ul><ul>...
Interpretation of results <ul><li>1- Hypogtycaemia with high or normal insulin and no elevated ketones. Causes: insulinoma...
NB <ul><li>if insulinonia suspected, confirm with a suppressive test: eg infuse iv insulin and measure C-peptide.  </li></...
Post-prandial hypoglycaemia: <ul><li>This occurs particularly after gastric surgery, and in those with mild Type II Diabet...
Treatment : <ul><li>Treat with oral sugar, and a long-acting starch (eg toast); if coma, glucose 25 – 50g  iv or glucagon ...
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Upcoming SlideShare
Loading in …5
×

Diabetes Mellitus

2,192 views

Published on

Published in: Health & Medicine
0 Comments
1 Like
Statistics
Notes
  • Be the first to comment

No Downloads
Views
Total views
2,192
On SlideShare
0
From Embeds
0
Number of Embeds
4
Actions
Shares
0
Downloads
70
Comments
0
Likes
1
Embeds 0
No embeds

No notes for slide

Diabetes Mellitus

  1. 1. Diabetes mellitus: (DM): <ul><li>‘‘ Definition Diabetes mellitus results from a lake of, </li></ul><ul><li>or </li></ul><ul><li>diminished effectiveness of endogen insulin and is characterized by hyperglycaemia. </li></ul>
  2. 2. <ul><li>Presentation: </li></ul><ul><li>Patients may be a symptomatic. </li></ul><ul><li>Acute : </li></ul><ul><li>Ketoacidosis unwell hyper ventilation, </li></ul><ul><li>ketones on breath, weight loss, </li></ul><ul><li>polyuria and polydipsia., fatigue </li></ul>
  3. 3. <ul><li>Subacute : </li></ul><ul><li>History as above but longer and in addition lethargy , </li></ul><ul><li>infection (pruritus vulvae, boils). </li></ul>
  4. 4. <ul><li>Complications : </li></ul><ul><li>may be the presenting feature: </li></ul><ul><li>infections, </li></ul><ul><li>neuropathy, </li></ul><ul><li>retinopathy </li></ul><ul><li>arterial disease e.g. myocardial infarction or claudication). </li></ul>
  5. 5. Classification
  6. 6. Type I ( insulin-dependent DM- IDDM) <ul><li>Usually juvenile onset but may occur at any age. </li></ul><ul><li>characterized by insulin deficiency. </li></ul><ul><li>Patients always need insulin, and are prone to ketoacidosis and weight loss. </li></ul><ul><li>Associated with other autoimmune diseases (HLA DR3 & DR4; +ve islet cell antibodies around time of diagnosis). Concordance is >30% in identical twins. </li></ul><ul><li>4 genes are important one determines islet sensitivity to damage (eg from viruses or cross-reactivity from cows’ milk antibodies). </li></ul>
  7. 7. Type II : (non insuline dependent DM,. NIDDM, maturity onset DM) <ul><li>Older age group, often obese, NB: NIDDMs may eventually need insulin: </li></ul><ul><li>this does not mean that IDDM has developed. </li></ul><ul><li>Insulin is likely to be needed in those with ketoanuria, </li></ul><ul><li>glucose >25mmol/L, sudden onset weight dehydration If Ketoacidosis then lDDM exists. </li></ul><ul><li>— 100% concordance in identical twins. </li></ul><ul><li>Due to impaired insulin secretion and/or insulin resistance. </li></ul>
  8. 8. Causes of secondary diabetes <ul><li>Drugs (steroids and thiazides) </li></ul><ul><li>Pancreatic disease (pancreatitis, surgery in which >90% pancreas is removed, haemochromatosis cystic fibrosis, pancreatic cancer). </li></ul><ul><li>Endocrine (Cushing’s disease, acromegaly, phaeochromocytoma, throtoxicosis) </li></ul><ul><li>Others (acanthosis nigricant. congenital lipodystrophy with insulin </li></ul><ul><li>receptor antibodies. and glycogen storage diseases). </li></ul>
  9. 9. <ul><li>* Fasting venous plasma glucose > 7mmol/L </li></ul><ul><li>a glucose of 6-7 mmol/L implies impaired fasting glucose. </li></ul><ul><li>* If the patient has no diabetic symptoms. diagnosis should not be based on a single glucose value. </li></ul><ul><li>* If there is any doubt the 2-hour value in an OGTT should be used (look for a level >l1.1mmol/L Method for performing a 2-hour oral glucose tolerance test: </li></ul><ul><li>• Fast overnight and give 75g of glucose in 300 ml water to drink </li></ul><ul><li>• Venous plasma gIucose before and 2h after drink. </li></ul>Diagnosis: (WH0 criteria adopted by UK in June 2000)
  10. 10. <ul><li>* Urine tests for glycosuria and random blood glucose tests are unreliable (but if 11.1 mmol/l and symptoms are present, this is diagnostic of DM). </li></ul><ul><li>* Severs hyperglycaem’a in acute infection, trauma, or circulatory or other stress may be transitory delay formal o (but not management). </li></ul><ul><li>Plasma HbA1c values: If >7%. DM is likely (specificity 99.6% sensitivity 99%) and risk of microvascular complication occurs. </li></ul><ul><li>Screening for glycosuria : This is easy but 1% of the population have low renal threshold for glucose; the sensitivity is only 32% (specificity: 99%). </li></ul>
  11. 11. <ul><li>Causes of insulin resistance : </li></ul><ul><li>* Obesity * Pregnancy </li></ul><ul><li>* Asian origin * Acute and chronic renal failure </li></ul><ul><li>*Acromegaly * Isolaiazzid </li></ul><ul><li>* Rifampicin * Sympathetic tone ↑ </li></ul><ul><li>* Werner’s syndrome * Polycystic ovaries </li></ul><ul><li>* Ataxia * Teiangiectasia </li></ul><ul><li>* Cystic fibrosis </li></ul>
  12. 12. Mechanism of insulin resistance: <ul><li>Obesity probably causes insulin resistance by the associated ↑ rate of release of non-esterified fatty acids causing post-receptor defects in insulin’s action. Other mechanisms . </li></ul><ul><li>Mutation of the gene encoding receptor . </li></ul><ul><li>Circulating autoantibodies to the extracellular domain of the insulin receptor </li></ul>
  13. 13. Management: <ul><li>Advise weight loss and exercise mange hyperglycaemia, with drugs or insulin. Vitamin E improves insulin sensitivity and delays oxidation of LDL (The postulated common factor in development of atheroma, hypertension, hypercholesterolaemia, and diabetes: this LL down-regulates nitric oxide production). </li></ul><ul><li>We don’t know if vitamin E saves lives. </li></ul>
  14. 14. <ul><li>Thiazolidinediones (PPAR-gamma againsts) ↑ insulin sensitivity eg rosiglitazone 4mg/24h. </li></ul><ul><li>LFT ↑ check LFTs </li></ul><ul><li>They have complex metabolic effects, including ↓ leptin expression , and ↑ p85alpha K gene expression ( a gene that allows insulin to work ) They also augment insulin’s down regulation of angiotensinogen gene expression; this may explain why thiazilsiniones decrease blood pressure. </li></ul>
  15. 15. NICE : <ul><li>(recommends their use as an alternative to insulin only if metformin with a sulfanyurea is not working, or tolerated. </li></ul><ul><li>They are better combined with metfarmin than with sulfanyureas. </li></ul>
  16. 16. Impaired glucose regulation that does not amount to diabetes <ul><li>This metabolic state lies between normal glucose homeostasis and diabetes. </li></ul><ul><li>Impaired glucose tolerance (IGT): </li></ul><ul><li>Fasting plasma glucose <7mmol/l and OGTT 2-hour glucose > 7.8mmol/L but <11.l mmol/L </li></ul>
  17. 17. Impaired fasting glycaemia/glucase (IFG): <ul><li>Fasting glucose levels above the normal range, but below the diagnostic level for DM, a fasting plasma glucose > 6.l mmol/L but <7mmol/L. </li></ul><ul><li>Diabetes UK (formerly BDA) recommends all those with IFG should have an OGTT to exclude diabetes. </li></ul><ul><li>1FG and IGT are not interchangeable and represent different abnormalities of glucose regulation fasting and post-prandial). </li></ul><ul><li>Both have the risk of progress to diabetes and rnacrovsscular disease. </li></ul><ul><li>Although prospective data are sparse, there may be lower risk o progression in IFG than in IGT. </li></ul><ul><li>Both should be managed with lifestyle advice (ag exercise and diet). </li></ul>
  18. 18. Gestational diabetes: <ul><li>This term now intrudes both gestational impaired glucose tolerance (GIGT) and gestations) diabetes mellitus (GDM). </li></ul><ul><li>Use the same diagnostic values as IGT and diabetes above. </li></ul><ul><li>As glucose tolerance changes during pregnancy, </li></ul><ul><li>the gestation at ‘which use diagnosis was made needs to be stated . </li></ul><ul><li>> 6 weeks postpartum, So a further 75g GGTT whether she still has diabetes or IGT/IFG. </li></ul><ul><li>Regardless of the 6-week post-pregnancy result these women are at risk of later diabetes. </li></ul>
  19. 19. Diabetes management Principales: <ul><li>Patient motivation and education are the keys to success. </li></ul><ul><li>Aim to avoid complications, which include hypoglycaemia as well as the long-term con— sequences of hyperglycaemia. </li></ul><ul><li>Strict plasma glucose control does reduce renal, CNS and retinal damage. However, a balance is required for each patient between lower blood glucose readings and the risk of hypo ‘glycaemia. </li></ul>
  20. 20. <ul><li>Interestingly, tight blood pressure control is as effective in reducing microvascular disease, </li></ul><ul><li>but also reduces macrovascular disease, and mortality. </li></ul><ul><li>This emphasizes the importance of a global assessment of a individuals risk—glucose, blood pressure, cholesterol, and smoking history. </li></ul><ul><li>Don’t treat DM in isolation. </li></ul>
  21. 21. <ul><li>Basic investigations Blood : </li></ul><ul><li>Glucose, U&Es, lipids, HbA1c , cholesterol. </li></ul><ul><li>Urine: </li></ul><ul><li>Urine analysis, urinary protein excretion. </li></ul>
  22. 22. Fundoscopy and feet exam: <ul><li>Assess feet and check for signs of neuropathy. </li></ul><ul><li>initial treatment If there is ketonuria, </li></ul><ul><li>dehydration, or the patient is ill, hospital admission is required. </li></ul><ul><li>Children are liable to become ketotic rapidly, so prompt psediatric referral is a must. </li></ul><ul><li>If pregnant. </li></ul><ul><li>share care with an interested obstetrician. </li></ul><ul><li>Stress the need for special pre-conception counselling. </li></ul>
  23. 23. Education/negotiation: <ul><li>is crucial on drugs, diet, and the issues below: </li></ul><ul><li>• Monitoring blood or urine glucose and adopting treatment accordingly. </li></ul><ul><li>Explain that when ill more, not less, insulin is needed. Recognition and </li></ul><ul><li>treatment of hypoglycaemia (eg sweets/sugars) is essential. </li></ul><ul><li>• Introduce to a specialist nurse/dietician, chiropodist. and diabetic association. </li></ul><ul><li>• Regular follow-up and regular exercise ( ↓ insulin resistance & ↓ risk of MI). </li></ul><ul><li>• Patients must inform their driving licence authority . </li></ul>
  24. 24. Healthy eating: <ul><li>(saturated fats ↓ , sugar ↓ starch-carbohydrates ↑ , moderate protein). </li></ul><ul><li>Ensure that some starchy carbohydrate (bread, potato pasta) is taken at each meal. </li></ul><ul><li>If renal impairment or micro albuminuria , restrict protein, and consider ACE. </li></ul>
  25. 25. Insulin Strength: <ul><li>l00u/mL Formulations of different durations: </li></ul><ul><li>soluble insulin is short-acting (peak 2-4h, fasting - 8h). </li></ul><ul><li>Longer-acting suspensions have onest of action of 1- 2 h, peck 4 - 12h and duration 16 – 35 h. </li></ul>
  26. 26. Oral hypoglycaemics: <ul><li>Sulfonylureas : </li></ul><ul><li>These ↑ insulin secretion. </li></ul><ul><li>tolbutamide is short-acting; useful in elderly as hypogiycaemia unlikely (0.5—1 g in 2 - 3 doses) Clilazide is medium-acting (40 - 160mg po as a single daily dose, or up to 320mg in divided doses). </li></ul><ul><li>Less frequently used is glibenclomiae - medium-acting l2.5-l5mg/24h P0 at breakfast). </li></ul>
  27. 27. <ul><li>Metformin (a biguonide) Action: </li></ul><ul><li>insulin sensitivity ↑ ; hepatic glucorieogenesis ↓ Se: </li></ul><ul><li>anorexia; D& V; B12 absorption ↓; not hypoglycaemia. </li></ul><ul><li>It has been shown to decrease mortality in obese subjects. </li></ul><ul><li>Avoid in hepatic and renal impairment. </li></ul><ul><li>Dose: 500—1000mg/8h P0 after food. May be used as first-line therapy: </li></ul><ul><li>unlike sulfonylureas, weight gain is not a problem. </li></ul>
  28. 28. Acarbose (an α -glucosidase inhibitor) <ul><li>It decreases breakdown of starch to sugar. </li></ul><ul><li>An adjust to oral hypoglycaemics (50mg chewed at start of each meal, start with a once-daily dose; max 200mg/8h). </li></ul><ul><li>SE: wind (can be terrible; less if slow dose build-up), abdominal distension/pain, diarrhoea. </li></ul>
  29. 29. Thiazolidinediones: <ul><li>Rosiglitazone e.g 4mg po. </li></ul><ul><li>CL;: hepatic impairment, SE; headache, diarrhoea, dyspepsis, fatigue, anaemia, fluid retention (caution in CCF). </li></ul><ul><li>Do LETs every 2 months for the 1 year. </li></ul><ul><li>Stop if AIT up >3-fold. This new drug ↓ insulin resistance </li></ul>
  30. 30. Other considerations: <ul><li>ACE (many beneficial affects, not just BP ↓ ); aspirin and statins to ↓ overall risk. Exercise also helps. </li></ul>
  31. 31. Some commonly used insulin regiments <ul><li>I- A single dose of medium-acting insulin with 3 doses of short- acting insulin (15 – 30 mins before each meal). </li></ul><ul><li>This tends to be favoured by younger subjects (it offers greater flexibility in lifestyle), </li></ul><ul><li>2-A mixture of short- and longer insulin (eg saluble and Lente) at 7 AM and 6 PM (ie ½ h before meal). </li></ul><ul><li>Give 2/3 of total insulin in the morning and ,2/3 as Lente (or medium-acting). </li></ul><ul><li>To Improve control before breakfast, adjust evening Lente; before lunch - morning soluble; before supper - morning Lente; before bed evening soluble. </li></ul>
  32. 32. <ul><li>3- ‘Pen’ devices are popular because of their ease of use (e.g. during parties), </li></ul><ul><li>Short-acting insulin is given 15 - 30 mins before each meal, </li></ul><ul><li>with basal insulin requirement being provided by a conventional evening dose of long-acting insulin; </li></ul><ul><li>mixed soluble (short) and isophane preparations (medium) are also available (e.g. PenMix 10/90, 20/80, 30/70, 40/60, 50/50). </li></ul><ul><li>Other biphasic human insulin’s; Insuman Comb SO® for the Optipen®, 20 – 30 mins before a meal. </li></ul><ul><li>The 50 refers to % of soluble insulin (the rest is isophane); 15%, 25%, and 50% are the options. Onset is at >30min, duration 12 -19hrs </li></ul><ul><li>Pre-filled and reusable pens are prescribable in the UK, e.g. Autopen®, BD Pen®, Novopen; their accompanying needles are also prescribable (eg Microfine+® and Novofi </li></ul>
  33. 33. <ul><li>4- If mealtimes are random, or pastprandial glucose ↑ very rapidly absorbed, genetically engineered human insulin lispro (Humalog) can be injected just be eating. It helps iron-out glucose variability and can ‘tendency to pre-lunch hypoglycaemia ↑. It can be mixed with Ultralente (needed at night if lispro injections separated by > 5 h). </li></ul><ul><li>Encourage regular home blood glucose monitoring in all patients (esp. those with hypoglycaemic unawareness consider ‘allowing ‘ laxer glycaemic control here). Discuss the pros and cons with your patient, </li></ul><ul><li>Begin with at least 6u of soluble insulin before meals, monitoring blood glucose; transfer to one of the above when control is achieved </li></ul>
  34. 34. Assessment of the established diabetic <ul><li>Continuing assessment of the diabetic patient has 3 main aims: </li></ul><ul><li>I- To educate. </li></ul><ul><li>2- To find out what problems the patient is e (glycaemic control and morale). </li></ul><ul><li>3- To find, or pre-empt, complications. </li></ul>
  35. 35. Assess glycaemic control from: <ul><li>I Glycated (glycosylated) haemoglobin (= HbA1c – levels relate to mean glucose level over previous 8 weeks (i.e RBC half-life). </li></ul><ul><li>The target HbAIc must be set individually. </li></ul><ul><li>Tight control is desirable in pregnancy or those with microvascular complications. </li></ul>
  36. 36. <ul><li>The elderly may opt for less tight control. </li></ul><ul><li>Complications increase in frequency with increasing HbA1c Note that fructosomine (glycated plasma protein) levels relate to control over previous 1-3 weeks. </li></ul><ul><li>May be useful in pregnancy to assess shorter-term control, also if there is a condition interfering with HbA1c measurement (eg some haemoglobinopathies). </li></ul><ul><li>1. History of hypoglycaemic attacks (and whether symptomatic). </li></ul><ul><li>2. 3 Home fingerstick glucose records may be useful </li></ul>
  37. 37. Assessment of complications <ul><li>Check injection sites for infection, lipoatrophy, or lipohypertrophy. </li></ul>
  38. 38. • Vasculor disease: <ul><li>Commonest cause of death. Look for evidence of cere brovascular, cardiovascular, and peripheral vascular disease. MI is 3-5 </li></ul><ul><li>times more common in DM and is more likely to be ‘silent’ (i.e without classic symptoms). </li></ul><ul><li>Stroke is twice as common. Women are at particular relative risk—DM removes The cardiovascular advantage conferred by female gender. </li></ul><ul><li>Reduce other risk factors NB: ACE. </li></ul>
  39. 39. <ul><li>Also slow progression or renal disease. </li></ul><ul><li>Treat lipid disorders: good glycaemic control helps. </li></ul><ul><li>HMG CoA reductase inhibitors (eg simvastatin) are first-line. </li></ul><ul><li>Fibrates may be useful for ↑ triglycerides and ↓ HDL. </li></ul><ul><li>An aspirin a day may ↓ risk of MI in diabetics as in non-diabetics (no significant risk to the eye). </li></ul>
  40. 40. • Kidneys <ul><li>( Check urine regularly. If dipstick is +ve for protein, collect 24h urine for creatinine clearance and for quantifying albuminuria. </li></ul><ul><li>Measuring rnicroalbuminuria ( helps detect early renal disease. </li></ul><ul><li>Control BP with ACE- inhibitor if tolerated (cautions and CL), </li></ul>
  41. 41. • Diabetic reonopatrty: <ul><li>(Dilate pupils with 0.5% tropicamide.) Blindness is common but preventable. </li></ul><ul><li>Arrange regular fundoscopy for all patients, including retinal photography, if ossib1e Refer if maculopathy or pre-proliferative changes. </li></ul><ul><li>Pre-symptomatic screening enables laser photocoagulation to be used. </li></ul>
  42. 42. Background: <ul><li>Microaneurysms (dots), microhaemorrhages (blots) and hard exudates. Refer to specialist if near the macula. </li></ul><ul><li>pre-proliferotive retinopathy: Cotton-wool spots (small retinal infarcts) and extensive microhaomorrhages. </li></ul><ul><li>Proliferative retinapathy: </li></ul><ul><li>New vessels form. Needs urgent referral. </li></ul><ul><li>Maculopathy: </li></ul><ul><li>More common in NIDDM. Suspect f visual acuity. </li></ul>
  43. 43. Pathogenesis: <ul><li>Capillary endotheliai change —>. </li></ul><ul><li>vascular leakage—>. </li></ul><ul><li>microa neurysms. </li></ul><ul><li>Capillary occlusion—> hypoxia + ‘schaemia —> new vessel formation. </li></ul><ul><li>High retinal blood flow caused by hyperglycaemia (and BP ↑ and pregnancy) triggers these events, and causes capillary oericyte damage. </li></ul><ul><li>Microvascular occlusion causes cotton wool spots; there may blot haemorrhoges at interfaces with perfused retina. </li></ul><ul><li>New vessels form on disc or schaemic areas, profferace, bleed. fibrosis. and can detach the retina. </li></ul>
  44. 44. • Cataracts: <ul><li>These occur earlier in DM (senile and juvenile ‘snowflake’ cataracts). </li></ul><ul><li>The osmotic changes in the lens induced in acute hyperglycaemias reverse after normoglycaemia (so wait before buying glasses). </li></ul><ul><li>• Rubeosis Irides: </li></ul><ul><li>New vessels on the iris: occurs late and may lead to glaucoma. </li></ul>
  45. 45. Metabolic complications: <ul><li>Diabetic feet. Neuropathy </li></ul><ul><li>Amputation is preventable: </li></ul><ul><li>good care saves legs feet regularly . </li></ul><ul><li>Distinguish between ischaemia (eg critical toes) and peripheral neuropathy (injury/infection over pressure points, eg the metatarsal heads). </li></ul>Symptoms: Numbness, tingling, and burning, often worse at night .
  46. 46. Signs: <ul><li>Sensation ↓ (especially vibration) in ‘stocking’ distribution; absent ankle jerks; deformity (pea cavus, claw toes, loss of transverse arch, rocker-bottom sole). </li></ul><ul><li>Neuropathy is patchy, so examine all areas. If the foot pulses cannot be felt, consider Doppler pressure measurement. </li></ul><ul><li>Any evidence of neuropathy or vascular disease puts the patient at high risk of foot ulceration. Educate (daily foot inspection, comfortable shoes—ie very soft leather, increased depth, cushioning insoles, weight- distributing cradles, extra cushioning - no barefoot walking, no corn- plasters). </li></ul><ul><li>Regular chiropody. Treat fungal infections . </li></ul>
  47. 47. Foot ulceration: <ul><li>Usually painless, punched-out ulcer in an area of thick callous ± superadded infection, pus, oederna, erythema, crepitus, odour. </li></ul><ul><li>Assess degree of: </li></ul><ul><li>1- Neuropathy (clinical). </li></ul><ul><li>2- lschiaemia (clinical and Doppler’s; consider angiography - even elderly patients may benefit from </li></ul><ul><li>angioplasty). </li></ul><ul><li>3- Bony deformity, eg Charcot joint (clinical, x-ray). </li></ul><ul><li>4- Infection (do swabs, blood culture, x-ray: probe ulcer to assess depth). </li></ul>
  48. 48. Management: <ul><li>Regular chiropody to debride lesions (remove dead tissue). </li></ul><ul><li>Relieve high-pressure areas with bed rest ± therapeutic shoes (Pressure Relief Walkers and similar shoes may be as good as total contact casts); </li></ul><ul><li>metatarsal head surgery may be needed. </li></ul><ul><li>ischemia, shoes must be wide- fitting with deep toe boxes to protect vulnerable forefoot margins and toes. </li></ul><ul><li>If there is cellulitis, admission is mandatory for iv antibiotics: </li></ul><ul><li>start with benzyipenicillin 600 mg/6h iv and flucloxacillin 500 mg/6h iv ± metrondazole 500mg/8h iv, refined when microbiology results are known. </li></ul><ul><li>Get surgical help early: normoglycaemia helps. </li></ul>
  49. 49. Absolute indications for surgery <ul><li>• Abscess or deep infection </li></ul><ul><li>• Spreading anaerobic infection </li></ul><ul><li>• Severe ischaemia –gangrene/rest pan </li></ul><ul><li>• Suppurative arthritis </li></ul><ul><li>The degree of peripheral vascular disease, patient’s general health, and patient request will determine whether local excision and drainage, vascular reconstruction, and/or amputation (and how much) is appropriate. </li></ul>
  50. 50. Types of neuropathy in diabetes <ul><li>Motor and sensory neuropathy </li></ul><ul><li>I- Symmetric sensory polyneuropathy – distal numbness, tingling, and visceral pain, e.g. worse at night Consider aspirin, paracetamol, or a tricyclic drug (± a low-dose phenorthiazine or caroamazepine,) Capsaicin cream can relieve pain: it acts as a counter-irritant. </li></ul><ul><li>2- Mononeuritis multiplex - especially III and VI cranial nerves. </li></ul><ul><li>3- Amyotrophy - painful wasting of quadriceps; reversible. </li></ul>
  51. 51. Autonomic neuropathy: <ul><li>Postural BP ↓ urine retention; impotence; diarrhoea s: night. The latter may respond to 3 doses of tetracycline 250mg P0 or long-term codeine phosphate (the lowest dose which controls symptoms. </li></ul><ul><li>e.g. l5 mg/8h po). </li></ul><ul><li>Vomiting associated with gastraparesis may respond to anticmetica. </li></ul><ul><li>Postural hypotension may respond to fludrocortisone 0.lmg - 0.3mg/24h P0 (SE aedema), Consider hydrochloride 30 - 6Omg/8h P0 for neuropathic oedema. </li></ul>
  52. 52. Diabetic patients with intercurrent illness: <ul><li>The stress of illness often increases basal insulin requirement If calorie Intake ↓ (if voniting) then increase long-acting insulin (by -‘-20%); reducing short-acting in proportion to meal size. </li></ul><ul><li>Check blood sugar often. </li></ul><ul><li>I- Insulin-treated; mild illness (eg gastroenteritis). Maintain calorie </li></ul><ul><li>Intake with oral fluids (lemonade etc.). Continue normal insulin. </li></ul><ul><li>Test blood glucose and urine ketones regularly (eg twice daily). </li></ul><ul><li>Increase insulin if blood glucose consistently >l0mmol/L </li></ul>
  53. 53. <ul><li>2- Insulin-treated; moderate illness (eg pneumonia). Normal insulin and supplementary sliding scale of rapid-acting. insulin four times daily (before meats and bedtime snack); </li></ul><ul><li>3- Insulin-treated; severe illness (eg Ml, severe trauma). IV soluble insulin by pump and iv dextrose . </li></ul><ul><li>4- Diet arid tablet treated moderate/severe illness If on metformin, stop. If on sulfonytureas and illness likely to be self-limiting. keep on tablets, supplement with SC insulin, and sliding scale or iv infusion . Tail off insulin as patient recovers. </li></ul>
  54. 54. Hypoglycaemia : <ul><li>This is the commonest endocrine emergency. Prompt diagnosis and </li></ul><ul><li>treatment is essential. </li></ul><ul><li>Definition: Plasma glucose <2.5mmol/L Threshold for symptoms varies. Symptoms Autonomic—Sweating; hunger, tremor, </li></ul><ul><li>Neuroglycopenic - Drowsine personality change; fits; rarely focal symptoms, eg transient hemiplegia, loss of consciousness, Two types: </li></ul>
  55. 55. Fasting hypoglycaemia : <ul><li>(requires full investigation if documented). </li></ul><ul><li>Causes: </li></ul><ul><li>By far the commonest cause is insulin or sulfonylurea treatment in a known diabetic in the non-diabetic subject with fasting hypoglycaemia the following mnemonic is useful: EXPLAIN. </li></ul><ul><li>Exogenous drugs, eg insulin or oral hypoglycaemics . Does he have access to these? Is there a diabetic in the family? Alcohol, eg alcoholic on a binge with no food. Also: aminoglutethimide; 4- quinolones; pen tomidine: quinine sulfate, </li></ul><ul><li>Pituitary insufficiency. </li></ul>
  56. 56. <ul><li>Liver failure plus some rare inherited enzyme defects. </li></ul><ul><li>Addison’s disease. </li></ul><ul><li>Islet cell tumours (insulinorna) and immune hypoglycaemia (eg anti- insulin receptor antibodies in Hodgkin’s disease). </li></ul><ul><li>Non-pancreatic neoplasms (especially retropentoneal fibrosarcomas </li></ul><ul><li>and haemangiopericytomas). </li></ul>
  57. 57. Diagnosis and investigations: <ul><li>I- Document hypoglycaemia by taking finger-prick (on filter-paper at </li></ul><ul><li>home for later analysis) during attack, or lab glucose if in hospital. </li></ul><ul><li>2- Exclude liver failure and malaria. </li></ul><ul><li>3- Admit for 72h fast. Do glucose, insulin & C-peptide if symptomatic. </li></ul>
  58. 58. Interpretation of results <ul><li>1- Hypogtycaemia with high or normal insulin and no elevated ketones. Causes: insulinoma; sulfonylurea administration; insulin administration (no detectable C-peptide); insulin autoantibodies. </li></ul><ul><li>2- Insulin low or undetectable, no excess ketones. Causes: Non-pancreatic neoplasm; anti-insulin receptor antibodies. </li></ul><ul><li>3- Insulin low or undetectable, ketones high. Causes: Alcohol: pituitary or adrenal failure. </li></ul>
  59. 59. NB <ul><li>if insulinonia suspected, confirm with a suppressive test: eg infuse iv insulin and measure C-peptide. </li></ul><ul><li>Normally exogenous insulin suppresses C-peptide, but this suppression does not occur in patients with insulinomas. </li></ul><ul><li>Localize the insulinoma using CT. If none is visible, sophisticated techniques (eg utra-operative pancreatic ultra sound) may be needed. </li></ul>
  60. 60. Post-prandial hypoglycaemia: <ul><li>This occurs particularly after gastric surgery, and in those with mild Type II Diabetes. </li></ul><ul><li>Investigation: Prolonged OGTT. </li></ul>
  61. 61. Treatment : <ul><li>Treat with oral sugar, and a long-acting starch (eg toast); if coma, glucose 25 – 50g iv or glucagon 0.5-lmg SC (± a repeat after 20 mins; follow with carbohydrate). </li></ul><ul><li>If episodes frequent, advise many- small meals high in starch, If post-prandial glucose ↓ . </li></ul><ul><li>slowly absorbed carbohydrate (high fibre, complex carbohydrates). </li></ul><ul><li>Insulinomas: </li></ul><ul><li>surgical removal if possible: diazoxide and a thiazide diuretic. </li></ul>

×