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Snapshot
  • A 56-year-old woman comes to your clinic for her annual physical exam. She reports increased urinary frequency and thirst but is otherwise feeling generally well. She is obese, does not exercise, and regularly eats fried foods. A random blood glucose level is 223 ml/dL, and her hemoglobin A1c is 9.2.
Introduction
  • Type 1 diabetes (formerly Insulin Dependent Diabetes Mellitus or Juvenile Diabetes)
    • immune mediated destruction of beta cells and loss of insulin production by pancreas
      • Hypoparathyroid may also have antibodies against insulin
    • 5-10% of diabetes cases
    • classically occurs in thin people younger than 30
      • most commonly presents before age 20
      • NOT related to obesity
    • sudden onset (after about 90% beta cells destroyed)
    • uncommon to have a family history
    • associated with HLA DR3 and DR4
      • also seen concurrently with other autoimmune diseases (e.g. Graves', Hashimoto's, ect.)
    • severe insulin deficiency; these patients require exogenous insulin 
  • Type 2 diabetes
    • insulin insensitivity (resistance) in peripheral organs requiring increased insulin production to where the pancreas cannot produce enough insulin to keep up 
      • insulin levels are usually normal to high but may diminish after the disease is present for many years
    • gradual onset
    • 90%+ of diabetes cases
    • typically in older individuals, though increasingly found in children with obesity
    • common to have a family history
    • associated with obesity (greatest risk factor)
    • amyloid deposition in β-cells
  • Complications are due to long-term poor glycemic control
    • if a diabetic maintains glucose in the normal range, there is nothing pathological about the disease
    • damage mediated by
      • non-enzymatic glycosylation which makes vessels more permeable
      • increased synthesis of type IV collagen in basement membrane
      • osmotic damage secondary to glucose conversion to sorbitol by aldose reductase
Presentation
  • Symptoms 
    • Type I
      • polyuria
      • polydipsia
      • polyphagia
      • fatigue
      • weight loss
      • Diabetic ketoacidosis (DKA) - is commonly the initial presentation
        • the symptoms of type I diabetes mellitus often develop rapidly (days to weeks) and often manifest after a preceding illness
      • hypoglycemia
        • sympathetic and parasympathetic nervous activation
    • Type II
      • polyuria
      • polydipsia
      • polyphagia
      • fatigue
      • weight loss (however, these patients are typically overweight)
      • blurry vision
      • candidal infections (especially vaginitis)
      • neuropathy - numbness, tingling of hands and/or feet
      • hyperosmolar nonketotic coma (link)
      • hypoglycemia
    • Consider the time-course and natural history of disease
      • Type I diabetics often present in acute manner shortly after developing the disease - they have not had the disease long enough to develop many of the long-term macrovascular and microvascular disease complications
      • Type 2 diabetics may have had underlying disease for many years (5-10+ years) and may often present initially with profound neuropathy, retinopathy, nephropathy or other complications, as discussed below
  • Signs/Physical Exam Findings 
    • Physical examination in diabetic patients should focus on identifying potential complications of the disease:
    • Type II:
      • Foot examination - pulses (may be diminshed), signs of ulcerations/infections 
      • Vascular disease examination - Coronary artery disease and peripheral vascular disease - cold, hairless lower extremities with diminished pulses
        • hypertension is commonly coexistent
        • orthostatic hypotension may result from autonomic neuropathy in advanced disease
      • Neurologic examination - diminished sensation to touch or temperature; loss of proprioception; loss of ankle deep tendon reflexes
      • Fundoscopic (eye) examination - hemorrhages, exudates, neovascularization 
      • Infection - fungal infections - vaginitis or thrush common
      • Skin - acanthosis nigricans (neck or axilla) 
    • Type I:
      • In new cases of disease, the above complications are unlikely to be detectable on physical exam due to the short time-course of the disease to-date; however, they should monitored in the future
      • DKA presents with: Kussmaul respirations, dehydration, hypotension, altered mental status
Evaluation
  • Diagnosis of DM is made by one of the following:
    • random blood glucose level of > 200mg/dL AND diabetic symptoms
    • 2 separate fasting glucose levels of > 126 mg/dL
    • 2 hour postprandial glucose level (glucose tolerance test) of > 200 mg/dL
    • Hemoglobin A1c of > 6.5% 
  • Monitoring/evaluation of glycemic control
    • hemoglobin A1c
      • represents mean glucose level from previous 8-12 weeks (approx lifespan of an RBC)
      • useful to gauge the 'big-picture' overall efficacy of glucose control in patients (either Type 1 or Type 2) to assess the need for changes in medication/insulin levels
      • Treatment goal of A1c < 7.0%
    • "finger-stick" blood glucose monitoring
      • useful for insulin-dependent (either type 1 or 2) diabetics to monitor their glucose control and adjust insulin doses according to variations in diet or activity
      • Treatment goals: < 130 mg/dL fasting and < 180 mg/dL peak postprandial 
Treatment
  • See Diabetes pharamacology (link)
    • Recall that diet and exercise should always be a part of any management plan for type II diabetics
    • Strict glycemic control is the best treatment for diabetes (type I or type II), as it minimizes the incidence and severity of complications that may develop
  • Complication treatment:
    • macrovascular disease (CAD, PVD, stroke) - RISK FACTOR REDUCTION - lipid control (statins), blood pressure control, smoking cessation, daily aspirin, regular exercise, improved diet
      • Target blood pressure (130/80) and LDL (<100) is lower in diabetics than in the nondiabetic population
    • peripheral neuropathy
      • duloxetine (serotonin/norepinephrine reputake inhibitor), amitriptyline, pregabalin, NSAIDs
    • diabetic kidney disease
      • ACE-inhibitor or ARB - good BP control slows progression of proteinuria and decrease in GFR  
    • gastroparesis 
      • metoclopramide, erythromycin 
      • exercise, dietary modification
    • retinopathy
      • ophthalmologist referal for regular eye-exams and photocoagulation or other procedure as needed 
    • foot ulcers
      • regular foot exams and care by a podiatrist; amputation as final resort in an infected limb
    • neurogenic bladder 
      • intermittent self-catheterization
      • bethanchol
Prognosis, Prevention, and Complications
  • Macrovascular complications - accelerated atheroscelrosis
    • Coronary artery disease (CAD) - leading to MI or CHF
      • 4 times more likely in DM patients
      • Coronary artery disease is the leading cause of death in diabetic patients
    • Peripheral vascular disease (PVD)
    • Stroke
  • Microvascular complication
    • nephropathy
      • arteriosclerosis leading to hypertension
      • thickening of the glomerular basement membrane 
      • nodular glomerular sclerosis - hyaline deposited in glomerulus -- this is pathognomonic for a diagnosis of diabetes
        • Kimmelstiel-Wilson nodules
      • diffuse glomerular sclerosis
      • basement membrane thickening
      • progressive proteinuria as a result of an increased GFR 
        • screen for microalbuminuria 
        • if protein comes up as positive on a urine dipstick, the patient has already progressed from microalbuminuria (30-300 mg/24 h) to outright proteinuria
      • chronic renal failure (ESRD)
    • ocular
      • retinopathy
        • proliferative changes involve neovascularization of retina
        • nonproliferative changes involve microaneurysms
      • cataracts
      • glaucoma
      • blindness
    • peripheral neuropathy  
      • numbness and paresthesias
      • burning sensation
      • ↓ deep tendon reflexes
      • ↓ vibration and temperature sense
      • can mask the symptoms of PVD or of developing ulceration/infection of foot
    • central neuropathy
      • 3rd nerve palsy sparing the pupil - pain, double vision, ptosis; cannot ADduct the eye
      • also CN IV and VI
    • autonomic dysfunction
      • impotence
      • neurogenic bladder - urinary retention and incontinence
      • gastroparesis  
        • nausea & vomiting, early satiety
        • should be evaluated with upper endoscopy to rule out obstructing mass 
        • confirm diagnsis with gastric emptying study
      • GI discomfort - constipation and/or diarrhea
      • postural hypotension
    • skin dysfunction
      • necrobiosis lipoidica diabeticorum
        • yellow plaques on legs
    • diabetic foot 
      • combination of vascular and nerve disease
        • largest risk factor = presence of neuropathy 
      • higher likelihood of infection, pressure ulcers
      • can lead to amputation
    • infectious disease - increased susceptibility to infection
      • impaired/delayed wound healing
      • UTIs
        • due to increased glucose in urine
      • Rhinocerebral mucormycosis
      • Pseudomonas malignant external otitis
 
 

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