Diabetes Microvascular Complications (half of one lecture) Flashcards Preview

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Flashcards in Diabetes Microvascular Complications (half of one lecture) Deck (40):
1

Name some things diabetes is the most common cause of...

-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

2

What are the 3 most common microvascular complications of diabetes?

retinopathy, nephropathy, neuropathy
-->result of hyperglycemia

3

What is the mechanism for hyperglycemia-induced tissue damage?

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

4

What are the 2 major categories of diabetic retinopathy?

1. Non-proliferative (NPDR)
2. Proliferative (PDR)

5

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

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

6

Describe the pathophys of retinopathy

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

7

Describe the genetics of retinopathy

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

8

Macular edema

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

9

What is mild NPDR?

-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

10

What is moderate/severe NPDR?

-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

11

How do we diagnose macular edema?

Req specialized fundoscopic exam

12

What is the key characteristic of PDR?

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

13

What can proliferative retinopathy lead to?

1. Neovascularization

2. Preretinal and vitreous hemorrhage
-Acute vision loss, often resolves spontaneously

3. Fibrosis
-Retinal traction and detachment

4. Ischemia

14

How should retinopathy be prevented?

-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

15

How do we treat retinopathy ?

-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

16

Describe epidemiology of nephropathy

Most common cause of kidney failure in US
-Onset 5-20 yrs after diabetes
-Independent risk factor for both CV and overall mortality

17

What are the risk factors for nephropathy?

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

18

What are the pathologic changes in nephropathy?

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

How does nephropathy progress?

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

How do we prevent nephropathy?

-Glycemic control
-BP control
-Treatment of dyslipidemia
-Measurement of spot urine microalbumin to creatine ratio

21

What is the treatment of nephropathy?

-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

Epi of neuropathy

-Most common microvascular complication
-50-70% lifetime incidence of at least one form of neuropathy

23

Most common type of diabetic neuropathy?

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

24

List the risk factors for neuropathy

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

25

List the 4 types of diabetic neuropathy

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

26

What are the symptoms of peripheral neuropathy?

-Decreased sensation
-Paresthesia
-Hyperesthesia
-Worse at night
-Sensory symptoms worse than motor
-Axonal mostly (hands and toes)

27

Treatment of peripheral neuropthay

-Anticonvulsants
-TCAs
-SNRIs
-Topical agents
-Opioids
-Antioxidants

28

What are the 4 types of autonomic neuropathy

1. Cardiovascular
2. Gastrointestinal
3. Genitourinary
4. Peripheral/sudomotor

29

Describe cardiovascular autonomic neuropathy

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

30

Describe GI autonomic neuropathy

-Esophageal enteropathy
-Gastroparesis
-Diabetic enteropathy
-Gallbladder atony and elargement

31

Describe gastropareiss autonomic neuropathy

-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

Describe genitourinary autonomic neuropathy

-Urinary retention
-Erectile dysfxn

33

Describe peripheral autonomic neuropathy

-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

How do we prevent neuropathy?

-Glucose control
-BP control
-Dyslipidemia control
-Smoking cessation
-Dec alc intake

35

Diabetic foot ulcers

-MAjor cause of amputations, sepsis, death

36

What are the risk factors for diabetic foot ulcers

-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

Prevention of foot ulcers?

-Avid barefoot
-Proper fitting shoes
-Trimmed toenails, avoid sharp edges
-Daily foot inspection
-Daily foot washing
-Moisturizing cream

38

Treatment of NPDR without CSME

Risk factor mamagement

39

Treatment of PDR or CSME

Photocoagulation

40

Treatment of nephropathy

Renin-angiotensin inhibition
-note microalbuminuria