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Diabetes Mellitus
 

Diabetes Mellitus

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    Diabetes Mellitus Diabetes Mellitus Presentation Transcript

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