TYPE COMPLICATION SUBCLASS PATHOGENESIS DESCRIPTION DIAGNOSIS TREATMENT

MICRO RETINOPATHY  Leading cause of blindness (20 – 74)  Routine comprehensive eye  PREVENTION – most effective
 Best predictors of development: examinations (DM patients) therapy
- Duration of DM  Routine NONDILATED eye  Slow progression: Intensive BP
- Degree of glycemic control examinations and glycemic control
 Other risk factors: HTN and nephropathy - First 6 – 12 mos of
 DM – 25x more likely to be legally blind improved glycemic control
 Severe vision loss:  transient worsening
- Progressive diabetic retinopathy - Long term: improved
- Macular edema glycemic control = less
retinopathy
 PROPHYLACTIC LASER
NON-  Pathophysiologic mechanism:  Late in first decade or early in second decade PHOTOCOAGULATION
PROLIFERATIVE 1. Loss of retinal pericytes  Found in many individuals w/ DM > 20 years - Very successful in
2. Increased retinal vascular permeability  Severe disease  greater chance of evolution to preserving vision
3. Alterations in retinal blood flow proliferative diabetic retinopathy w/in 5 years
-
4. Abnormal retinal microvasculature  Marked by:
 Advanced retinopathy = improved
1. Retinal vascular microaneurysms
glycemic control  less benefits
 All leading to RETINAL ISCHEMIA 2. Blot hemorrhages
3. Cotton-wool spots
 Characteristic of progression:
 Inflammatory process in the retinal - Changes in venous caliber
neurovascular unit - Intraretinal microvascular abnormalities
- More numerous microaneurysms and
hemorrhages

PROLIFERATIVE  Hallmark: NEOVASCULARIZATION in  Location of newly-formed vessels:  PANRETINAL LASER

response to hypoxemia - Near OPTIC NERVE PHOTOCOAGULATION
- Near MACULA
 Vessels rupture easily (leading to)
- Vitreous hemorrhage
- Fibrosis
- Retinal Detachment

MACULAR EDEMA  Clinically significant macular edema – both  Associated with 25% chance of moderate visual  FLUORESCEIN ANGIOGRAPHY  FOCAL LASER
Non-proliferative and Proliferative diabetic loss over the next 3 years  OPTICAL COHERENCE PHOTOCOAGULATION
nephropathy TOMOGRAPHY  ANTI-VASCULAR ENDOTHELIAL
GROWTH FACTOR THERAPY
(Anti-VEGF)
TYPE COMPLICATION SUBCLASS PATHOGENESIS DESCRIPTION DIAGNOSIS TREATMENT
GASTRO- Most prominent GI symptoms:  Primary goal = improved glycemic
INTESTINAL 1. GASTROPARESIS control
DYSFUNCTION 2. CONSTIPATION/DIARRHEA

GASTROPARESIS – delayed gastric emptying
 Development due to:
- Hyperglycemia itself
- Parasympathetic dysfunction secondary
to chronic hyperglycemia
 Symptoms:  NUCLEAR SCINTIGRAPHY after  Smaller more frequent meals –
 Anorexia ingestion of radiolabeled meal easier to digest (liquid), low in fat
 N&V - Doesn’t correlate well w/ and fiber – minimize symptoms
 Early satiety patient’s symptoms  METOCLOPRMIDE – not for long
 Abdominal bleeding  NONINVASIVE BREATH TESTS term use
 Retinopathy and neuropathy usually present - Not yet validated
 Esophageal dysfunction in long standing DM is
usually asymptomatic

CONSTIPATION/DIARRHEA – altered small and  Nocturnal diarrhea alternating w/ constipation –  Evaluation for CELIAC SPRUE  Symptomatic treatment – absence
large bowel motility feature of DM-related GI autonomic neuropathy of bacterial overgrowth
 DM 1 = evaluate for CELIAC SPRUE (due to
increased frequency)

GENITOURINARY  CYSTOPATHY  Begin with:  CYSTOMETRY  Scheduled voiding

DYSFUNCTION - Inability to sense full bladder  URODYNAMIC STUDIES  Self-catheterization
- Failure to void completely
 Bladder contractility worsens  postvoid residual
increase:
- Urinary hesitancy
- Decreased voiding frequency
- Incontinence
- Recurrent UTI

 FEMALE SEXUAL DYSFUNCTION  Reduced sexual desire  Vaginal lubricants

 Dyspareunia  Treatment of vaginal infections
 Reduced vaginal lubrication  Estrogen replacement
(systemic/local)

 ERECTILE DYSFUNCTION  May be one of the earliest signs of diabetic  PDE-5 inhibitors (Sldenafil)
neuropathy - Efficacy slightly lower in
 Increases in frequency w/ age and duration of diabetics
diabetes
 May occur in absence of other signs of diabetic
autonomic neuropathy

 RETROGRADE EJACULATION  May be one of the earliest signs of diabetic

neuropathy
 TYPE COMPLICATION SUBCLASS PATHOGENESIS DESCRIPTION DIAGNOSIS TREATMENT
MICRO NEUROPATHY  50% with long-standing DM  Improved glycemic control
 Risk factors: HTN and Hypertriglyceridemia - Improve nerve conduction
POLY-  DISTAL SYMMETRIC POLYNEUROPATHY  Most common form  PE Findings: velocity
NEUROPATHY  Frequent presentation: distal sensory loss & pain - Sensory loss - Symptoms may not necessarily
- 50% do not have symptoms - Loss of ankle DTR improve
 W/ hyperesthesia, paresthesia, or dysesthesia - Abnormal position sense  Treat RISK FACTORS
 Numbness, Tingling, Sharpness, Burning  Chronic Painful Diabetic

- Begins in the feet Neuropathy
- Spreads proximally - Duloxetine
 NEUROPATHIC PAIN  preceded by - Amitryptiline
improvement in glycemic control - Gabapentin
- Lower extremities - Valproate
- At rest; worsens at night - Pregabalin
- Acute (< 12 months) [usually treatment- - Opioids
related]/chronic forms  Acute Diabetic Neuropathy
- Progression: pain subsides but SENSORY - Resolve over time
DEFICIT in lower extremities persist - Medications may be
discontinued as progressive
neuronal damage from DM
 DIABETIC POLYRADICULOPATHY  May be accompanied by MOTOR WEAKNESS  occurs
 Characteristic: SEVERE DISABLING PAIN in  INTERCOSTAL/TRUNCAL RADICULOPATHY
the distribution of one or more nerve roots - Pain over thorax or abdomen
 DIABETIC AMYOTROPHY
- Involvement of lumbar plexus or femoral
nerve
- Severe pain in thigh or hip
- Pain in hip flexors or extensors**
 Usually self-limited
 Resolve over 6 – 12 months

MONO-  Dysfunction of isolated cranial or peripheral  Peripheral mononeuropathies or Mononeuropathy  Physical Exam:
NEUROPATHY nerves multiplex (simultaneous involvement of more than - Ptosis
 Pain and motor weakness in distribution of one nerve) may also occur - Ophthalmoplegia w/ normal
SINGLE NERVE (Mono)  Less common than polyneuropathy pupillary constriction to light
 Unknown pathogenesis  Can occur at: 
 Involvement of other cranial nerves: - Entrapment sites: Carpal Tunnel
 IV, VI, or VII (Bell’s palsy) - Noncompressive
 Most common involvement: THIRD cranial nerve
- Heralded by diplopia

AUTONOMIC  Can involve multiple systems: CVS, GI, GU,  CVS – resting tachycardia/orthostatic hypotension   Orthostatic Hypotension
NEUROPATHY motors, and metabolic systems  GI/GU – Gastroparesis and bladder emptying - Fludrocortisone
 Long standing DM  dysfunction of abnormalities - Midodrine
cholinergic, noradrenergic, and peptidergic (PP,  Sympathetic Nervous System: - Clonidine
- Octreotide
 substance P, etc.) system
 Can also reduce counterregulatory hormone
release (CATECHOLAMINES)
 Inability to sense hypoglycemia
 Complicate efforts to improve glycemic
control
- Upper extremities hyperhidrosis - Yohimbine
- Lower extremities: anhidrosis  Dry skin  Adequate salt intake, avoidance
w/ cracking – inc. risk foot ulcers of dehydration & diuretics, lower
 extremity support hose

TYPE COMPLICATION SUBCLASS PATHOGENESIS DESCRIPTION DIAGNOSIS TREATMENT

MICRO NEPHROPATHY  Involve effects of:  20 – 40% of diabetics  Interventions to slow progression
1. Soluble Factors  Risk factors: RACE and FAMILY HISTORY of albuminuria:
- GF, ATII, Endothelin, advanced  Commonly have diabetic retinopathy - Improved glycemic control
glycation end products/AGEs  Leading cause of CKD, ESRD, and CKD requiring - Strict BP control
2. Hemodynamic alterations in renal renal replacement therapy - Administration of ACE-I or
vasculature  Prognosis on diabetic dialysis patients = POOR ARB
- Glomerular hyperfiltration  Albuminuria – increased risk of CVD - Dyslipidemia should also be
- Hyperperfusion treated
 Smoking – accelerates decline of renal function
- Increased glomerular capillary pressure  Later phase of declining renal
3. Structural changes in glomerulus function: insulin requirements fall
- Increased extracellular matrix  GLOMERULAR HYPERPERFUSION and RENAL  Kidney: site of degradation
- BM thickening HYPERTROPHY  Re-evaluate use of glucose
- Mesangial expansion - First years after onset of DM lowering agents as GFR decrease
- Fibrosis - Associated with increase in GFR - METFORMIN and
 First FIVE YEARS: SULFONYLUREAS are
- Glomerular BM thickening contraindicated in advanced
 Some effects are mediated through Angiotensin
- Glomerular hypertrophy renal insufficiency
II receptors
- Mesangial volume expansion  BP < 140/90 mmHg
 Macroalbuminuria:
- GFR returns to NORMAL  ARBs – alternative due to ACE-I
- Steady decline in GFR
 5 -10 YEARS (TYPE I DM) associated cough or angioedema
- ~50% reach ESRD in 7 – 10 years
- Excrete small amounts of albumin in urine - After 2 to 3 mos 
Persistent Albuminuria
 Only 50% of those with microalbuminuria progress increased to maximum
MICRO 30 – 29 mg/24h
to macroalbuminuria over the next 10 years tolerated dose
MACRO > 300 mg/24h
 Microalbuminuria – short duration in DM 1  Alternative to ACE-I and ARBs:
- Diuretics
- CCBs (nondihydropyridines)
DM 2  Albuminuria may be secondary to factors  May be present at diagnosis  Long  ALBUMINURIA – should be
- Beta blockers
unrelated to DM: asymptomatic period – micro and macro detected at early stage
 NEPHROLOGY CONSULTATION
- HTN  More commonly accompanied by HTN  Annual SERUM CREATININE
- GFR < 60 mL/min per 1.743 m2
- CHF  Microalbuminuria may be less predictive of - Estimate GFR
- Prostate disease diabetic nephropathy & likelihood of progression to - DM: decline in GFR in the
- Infection type II DM (inc. CV mortality) absence of albuminuria  Complications of
 Annual Microalbuminuria ATHERSCLEROSIS  leading
measurement cause of death in diabetics with
- Albumin-to-creatinine nephropathy and hyperlipidemia
ration in spot urine  Renal transplant from living donor
 Screening for Albuminuria: – requires chronic immune-
- 5 yrs after onset of DM 1 suppression
- Time of diagnosis DM 2  Pancreas-kidney transplants
 Normoglycemia
 Freedom from dialysis
Type IV Renal  DM 1 or DM 2  Patients with DM = predisposed to radiocontrast-
Tubular Acidosis  Hyperkalemia and academia induced nephrotoxicity
- Risk Factors:
- Exacerbated by Medications 1. Volume Depletion
- ACE-I, ARBs, Spironolactone 2. Preexisting nephropathy
 Individuals undergoing radiocontrast procedures:
- Well hydrated before & after dye exposure
- Serum creatinine monitored 24 – 48h after
- Metformin should be held if indicated