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Endorine > Diabetes Microvascular Complications (half of one lecture) > Flashcards

Diabetes Microvascular Complications (half of one lecture) Flashcards

1
Q

Name some things diabetes is the most common cause of…

A
  • Blindness in ages 20-74
  • Kidney failure
  • Non-traumatic leg amputations
  • 2-4x higher death rates due to heart disease
  • 7th leading cause of death in USA
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2
Q

What are the 3 most common microvascular complications of diabetes?

A

retinopathy, nephropathy, neuropathy

–>result of hyperglycemia

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3
Q

What is the mechanism for hyperglycemia-induced tissue damage?

A

Not completely understood. Involves genetic factors, repeated acute changes in cellular metab and cumulative long-term changes in stable macromolecules due to hyperglycemia, leading to tissue damage. Also involves independent accelerating factors like hypertension, hyperlipidemia etc

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4
Q

What are the 2 major categories of diabetic retinopathy?

A
  1. Non-proliferative (NPDR)

2. Proliferative (PDR)

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5
Q

When is the ave onset of retinopathy in type 1 vs type 2?

A

Type 1: obset 2-5 yrs after diagnosis, nearly everyone affected by 20 yrs

Type 2: 20% at the time of diagnosis, obset 4-7 years prior to diagnosis. 50-80% incidence at 20 yrs

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6
Q

Describe the pathophys of retinopathy

A

Hyperglycemia–>dysreg retinal blood flow–>inc inflammation/oxidative stress, edema (inc vasc permeability), ischemia (microthrombosis), proliferation of new bvs

-hypertension, dyslipidemia and meds are also risk factors

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7
Q

Describe the genetics of retinopathy

A

Inc incidence in 1st deg relatives, associated with nephropathy in T1D pts

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8
Q

Macular edema

A
  • Thickening of the retina
  • Accounts for 75% of vision loss due to diabetes
  • Can occur at any stage of retinopathy and is clinically significant
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9
Q

What is mild NPDR?

A
  • Microaneurysms (small areas of dilated arteries), dot hemorrhages, and/or hard exudates (lipid leakage from within macrophages in the retina)
  • 5% annual progression to PDR
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10
Q

What is moderate/severe NPDR?

A
  • Findings of mild NPDR plus…
  • Soft exudates (cotton wool spots caused by nerve fiber layer infarcts), venous beading, intraretinal microvascular abnormalities (occluded vessels, dilated and tortuous capillaries)
  • Moderate: 15% annual progression PDR
  • Severe: 50-75% progression
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11
Q

How do we diagnose macular edema?

A

Req specialized fundoscopic exam

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12
Q

What is the key characteristic of PDR?

A

Neovascularization

-new bvs are fragile and can easily rupture. Rupture results in hemorrhage

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13
Q

What can proliferative retinopathy lead to?

A
  1. Neovascularization
  2. Preretinal and vitreous hemorrhage
    - Acute vision loss, often resolves spontaneously
  3. Fibrosis
    - Retinal traction and detachment
  4. Ischemia
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14
Q

How should retinopathy be prevented?

A
  • Glycemic control (highly effective in primary prevention–T1D–via metabolic memory as well, somewhat helpful at slowing progression of NPDR in T2D, more helpful with T1D)
  • Antihypertensive therapy
  • Maybe with lipid lowering, antiplatelet agents or carbonic anhydrase inhibitors
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15
Q

How do we treat retinopathy ?

A
  • NPDR with clinically significant macular edema (CSME): focal laser photocoagulation
  • High-risk and severe PDR: panretinal photocoagulation and medical therapy: Intravitreal glucocorticoids, VEGF inhibitors
  • Vitrectomy indications: nonclearing vitreous hemorrhage, traction retinal detachment involving fovea, severe PDR not responsive to PRP
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16
Q

Describe epidemiology of nephropathy

A

Most common cause of kidney failure in US

  • Onset 5-20 yrs after diabetes
  • Independent risk factor for both CV and overall mortality
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17
Q

What are the risk factors for nephropathy?

A
  • Poor glycemic control
  • Hypertension
  • Age
  • Genetic factors
  • Race (AAs, Pima Indian, Mexican-American)
  • Obesity
  • Tobacco use
  • Other microv disease like retinopathy
18
Q

What are the pathologic changes in nephropathy?

A

Glomerular disease
-mesangial expansion, basement membrane thickening, sclerosis

Albuminuria (protein in urine)

  • Microalbuminuria (high albuminuria)–»30-300mg/g creatinine
  • Proteinuria (macro/very high albuminuria)–»300mg/g creatinine
19
Q

How does nephropathy progress?

A

First, inc glomerular filtration. Then microalbuminuria develops with progression to proteinuria or, if control it, regression to normoalbuminuria. If didn’t control it, net result is a decrease in kidney fxn/GFR and progression to end=stage kidney failure

20
Q

How do we prevent nephropathy?

A
  • Glycemic control
  • BP control
  • Treatment of dyslipidemia
  • Measurement of spot urine microalbumin to creatine ratio
21
Q

What is the treatment of nephropathy?

A
  • ACE inhibitor/Angiotensin II receptor blocker (first line, dilate efferent arteriole to reduce glomerular pressure)
  • Other antihypertensive agents
  • Dietary restriction (no sodium, protein)
  • Weight loss
  • All in addition to glucose control
22
Q

Epi of neuropathy

A
  • Most common microvascular complication

- 50-70% lifetime incidence of at least one form of neuropathy

23
Q

Most common type of diabetic neuropathy?

A

-Diabetic polyneuropathy (peripheral neuropathy) is the most common type

24
Q

List the risk factors for neuropathy

A
  • Age
  • Duration of dis
  • Poor glucose control
  • BV damage
  • Mechanical injury to nerves
  • Genetic susceptibility
  • Hypertension
  • Dyslipidemia/hyperTGs
  • Tobacco use
  • Excessive alc use
25
Q

List the 4 types of diabetic neuropathy

A
  1. Distal symmetric sensorimotor polyneuropathy
  2. Autonomic neuropathy
  3. Polyradiculopathy (diabetic amyotrophy)
  4. Mononeuropathy (cranial, peripheral, mononeuritis multiplex)
26
Q

What are the symptoms of peripheral neuropathy?

A
  • Decreased sensation
  • Paresthesia
  • Hyperesthesia
  • Worse at night
  • Sensory symptoms worse than motor
  • Axonal mostly (hands and toes)
27
Q

Treatment of peripheral neuropthay

A
  • Anticonvulsants
  • TCAs
  • SNRIs
  • Topical agents
  • Opioids
  • Antioxidants
28
Q

What are the 4 types of autonomic neuropathy

A
  1. Cardiovascular
  2. Gastrointestinal
  3. Genitourinary
  4. Peripheral/sudomotor
29
Q

Describe cardiovascular autonomic neuropathy

A
  • Resting tachycardia (loss of parasymp tone)
  • Exercise intolerance (fixed HR, dec CO)
  • Postural hypotension (orthostatic and post prandial
  • Silent MI
30
Q

Describe GI autonomic neuropathy

A
  • Esophageal enteropathy
  • Gastroparesis
  • Diabetic enteropathy
  • Gallbladder atony and elargement
31
Q

Describe gastropareiss autonomic neuropathy

A
  • Delayed gastric emptying (issue with timing insulin injections)
  • Symptoms: early satiety, nausea, vomiting, worse glycemic control or none
  • Treatment: glycemic control, dietary mods, prokinetic agents
32
Q

Describe genitourinary autonomic neuropathy

A
  • Urinary retention

- Erectile dysfxn

33
Q

Describe peripheral autonomic neuropathy

A
  • aka Sudomotor neuropathy
  • Impaired perspiration
  • Peripheral edema
  • Callus formation (ulcers)
  • May contribute to neuroarthropathy (charcot joint, foot anatomy changes to create weird pressure pts)
34
Q

How do we prevent neuropathy?

A
  • Glucose control
  • BP control
  • Dyslipidemia control
  • Smoking cessation
  • Dec alc intake
35
Q

Diabetic foot ulcers

A

-MAjor cause of amputations, sepsis, death

36
Q

What are the risk factors for diabetic foot ulcers

A
  • Neuropathy (dec pain, dry skin and callus, abnormal weight bearing pressure pts)
  • Foot deformity (charcot)
  • Peripheral vasc dis
  • Poor glycemic control–>impaired wound healing
37
Q

Prevention of foot ulcers?

A
  • Avid barefoot
  • Proper fitting shoes
  • Trimmed toenails, avoid sharp edges
  • Daily foot inspection
  • Daily foot washing
  • Moisturizing cream
38
Q

Treatment of NPDR without CSME

A

Risk factor mamagement

39
Q

Treatment of PDR or CSME

A

Photocoagulation

40
Q

Treatment of nephropathy

A

Renin-angiotensin inhibition

-note microalbuminuria

Endorine (24 decks)

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