Introduction

• Type 1 diabetes (formerly Insulin Dependent Diabetes Mellitus or Juvenile

◦ immune mediated destruction of beta cells and loss of insulin produc
▪ 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. G
◦ severe insulin deficiency; these patients require exogenous insulin 
◦
• Type 2 diabetes
◦ insulin insensitivity (resistance) in peripheral organs requiring increa
keep up 
▪ insulin levels are usually normal to high but may diminish after
◦ gradual onset
◦ 90%+ of diabetes cases
◦ typically in older individuals, though increasingly found in children wi
◦ 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 p
◦ damage mediated by
▪ non-enzymatic glycosylation which makes vessels more perme
▪ increased synthesis of type IV collagen in basement membrane
▪ osmotic damage secondary to glucose conversion to sorbitol by
Presentation
• Symptoms 
◦ Type I
▪ polyuria
▪ polydipsia
▪ polyphagia
▪ fatigue
▪ weight loss
▪ Diabetic ketoacidosis (DKA) - is commonly the initial presentati
▪ the symptoms of type I diabetes mellitus often develop rap
▪ 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 dev
many of the long-term macrovascular and microvascular dis
▪ Type 2 diabetics may have had underlying disease for many ye
retinopathy, nephropathy or other complications, as discuss
• Signs/Physical Exam Findings 
◦ Physical examination in diabetic patients should focus on identifying
◦ Type II:
▪ Foot examination - pulses (may be diminshed), signs of ulcerat
▪ Vascular disease examination - Coronary artery disease and pe
pulses
▪ hypertension is commonly coexistent
▪ orthostatic hypotension may result from autonomic neurop
▪ Neurologic examination - diminished sensation to touch or temp
▪ Fundoscopic (eye) examination - hemorrhages, exudates, neov
▪ 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 t
to-date; however, they should monitored in the future
▪ DKA presents with: Kussmaul respirations, dehydration, hypote
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 m
◦ Hemoglobin A1c of > 6.5% 
• Monitoring/evaluation of glycemic control
◦ hemoglobin A1c
▪ represents mean glucose level from previous 8-12 weeks (appr
▪ useful to gauge the 'big-picture' overall efficacy of glucose cont
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 mo
diet or activity
▪ Treatment goals: < 130 mg/dL fasting and < 180 mg/dL peak po
Treatment
• See Diabetes pharmacology (link)
◦ Recall that diet and exercise should always be a part of any manage
◦ Strict glycemic control is the best treatment for diabetes (type I or typ
develop
• Complication treatment:
◦ macrovascular disease (CAD, PVD, stroke) - RISK FACTOR REDUC
aspirin, regular exercise, improved diet
▪ Target blood pressure (130/80) and LDL (<100) is lower in diab
◦ peripheral neuropathy
▪ duloxetine (serotonin/norepinephrine reuptake inhibitor), amitr
◦ diabetic kidney disease
▪ ACE-inhibitor or ARB - good BP control slows progression of
◦ gastroparesis 
▪ initially with exercise, dietary modification
▪ metoclopramide, erythromycin 
◦ retinopathy
▪ ophthalmologist referral for regular eye-exams and photocoagu
◦ foot ulcers
▪ regular foot exams and care by a podiatrist
▪ debridement and antibiotics for ulcers without signs of osteomy
▪ 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 diabet
◦ 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 -
▪ 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 pati
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/infe
◦ central neuropathy
▪ 3rd nerve palsy sparing the pupil - pain, double vision, ptosis; c
▪ 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 obs
▪ 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