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36-year old female lawyer diagnosed with diabetes mellitus, fasting blood…
36-year old female lawyer diagnosed with diabetes mellitus, fasting blood glucose of 12 mmol/L
Type I
Pathophysiology
Type IA:
Beta-cell destruction
attributable to autoimmune process (immune-mediated);
markers for T1DM
: autoantibodies to islet cell (ICA), insulin (IAA), glutamic acid decarboxylate (GADAb or GAD65), tyrosine phosphatases IA-2 and IA-2beta and zinc transporter ZnT8 (testing for ICA and GADAb available locally; detectable in up to 40% and 20% of T1DM patients respectively); immune markers detectable only after onset of autoimmune process
Long latent period: large no. of functioning beta cells must be lost before metabolic and symptomatic hyperglycemia occur
Type IB: idiopathic; no evidence of autoimmunity/known cause for beta cell destruction
Commonly occurs in childhood and adolescence but can occur at any age; patients are rarely obese but presence of obesity is not incompatible with diagnosis; may have other autoimmune disorders e.g. Graves' disease, Hashiomoto's thyroiditis and Addison's disease
Environmental factors (perinatal factors, viruses, diet, etc) have been implicated
Management
ALL patients require insulin treatment
Type II
Management
Initially (and often throughout lifetime) do not require insulin for survival; may require insulin at some stage of their disease
Target glycemic control: HbA1c </= 7%
Generally treat with oral agents when diet and exercise fail to control glycemia; multiple pharmacological agents may be needed to maintain target glucose control; 2 or more oral agents, or insulin therapy either alone or in combination with oral agents may be required (if 2 consecutive HbA1c failed to reach </=8% over 3-6 months interval)
1st choice: metformin; reasonable alternatives: sulfonylureas/DPP-IV inhibitors/alpha-glucosidase inhibitors
Factors to consider: 1) age [sulfonylureas esp. long-acting preparations, insulin secretagogues and insulin can cause hypoglycemia; in elderly patients, start with low-dose, shorting acting agents; 2) weight - metformin as 1st choice; 3) renal/hepatic impairment [metformin is contraindicated in severe renal/hepatic insufficiency where it's assoc. with lactic acidosis, thiazolidinediones can cause fluid retention in patients with renal dysfunction]; 4) cardiopulmonary comorbidities [thiazolidinediones are contraindicated in patients with ACS, IHD, all classes of heart failure]; 5) cost-benefit considerations; 6) risk of hypoglycemia
Pathophysiology
Hyperglycemia, insulin resistance and relative impairment in insulin secretion; hyperglycemia itself impair pancreatic beta cell function and exacerbate insulin resistance --> vicious cycle of hyperglycemia causing worsening metabolic state; prevalence rises markedly with increasing age °ree of obesity
Has strong familial and genetic pre-disposition; prevalence rates in adults aged >30 years in Singapore = 12.0%, >90% of patients with diabetes have T2DM
T2DM frequently undiagnosed for many years because hyperglycemia develops gradually and not severe enough to detect at earlier stages
Ketone-prone diabetes
: ketoacidosis is infrequent and usually occur in assoc. with stress of another illness e.g. infections; BUT increasingly clear that some T2DM patients are more susceptible to develop DKA without any precipitating cause; usually young, generally obese with strong family hx and low prevalence of autoimmune markers
Features
Symptoms
: polyuria (when glucose conc >180 mg/dL or 10 mmol/L), polydipsia, polyphagia, nocturia, blurred vision, weight loss;
Signs
: dry mouth, dry skin
Ix
Random plasma glucose
: >11.1 mmol/L;
fasting plasma glucose > 7mmol/L
; 2-hr post OGTT >11.1 mmol/L
HbA1c
: >6.1
Complications: check fasting lipid profiles, LFTs, urine albumin excretion (spot urine), serum Cr, serum TSH (for T1DM), routine eye exam, routine foot exam, neuropathy
Other types
Drug-induced
Drugs can impair glucose tolerance, act by decreasing insulin secretion, increasing hepatic glucose production or causing resistance to action of insulin
Glucocorticoids, oral contraceptives, antihypertensives (beta blockers, thiazide diuretics, nicotinic acid, statins, protease inhibitors, GnRH agonists, tacrolimus, sirolimus, cyclosporine and atypical anti-psychotic agents)
Other specific types
: relatively uncommon causes where underlying defect or disease process can be specifically identified e.g. genetic defects of beta cell function or insulin action, diseases of exocrine pancreas (pancreatitis, pancreatectomy) + induced by other endocrinopathies (Cushing's, acromegaly, glucagonoma, hyperthyroidism, etc, toxins and infections (congenital rubella, CMV)
Gestational
Onset or first recognition of any degree of glucose intolerance during pregnancy; does NOT include women with glucose intolerance that predates pregnancy; applies irrespective of insulin requirements and whether condition persists