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OPTM 737 > Test 1: Diabetes > Flashcards

Test 1: Diabetes Flashcards

1
Q

etiology of diabetes

A

incidence is higher in Hispanics and African americans

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2
Q

type 1 diabetes

A

5-10%
characterized by destruction or loss of function of the insulin producing pancreatic beta cells resulting in absolute dependence on exogenous insulin to prevent hyperglycemia and ketoacidosis
inherited/genetic component
formerly called insulin dependent or juvenile diabetes

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3
Q

two forms of type 1

A

immune mediated disease

idiopathic-more common in African and Asian populations

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4
Q

most patients with type 1 DM demonstrates classic signs of

A

polyuria
polydipsia
polyphagia
unexplained weight loss
patients commonly present with diabetic ketoacidosis
patients with T1 DM should have dilated eye exam within 3-5 years of dx

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5
Q

type 2 DM

A

90-95%
caused by relative insulin deficiency, either the body doesn’t produce enough insulin or the body can’t use the insulin it makes effectively (insulin resistance)
formerly termed non-insulin dependent or adult onset diabetes
people diagnosed with T2 DM should have dilated retinal examination
pts typically undiagnosed for 5-8 years

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6
Q

pre-diabetes

A

when blood glucose levels don’t meet the criteria for diabetes but are higher than normal levels
persons with pre-diabetes have: impaired glucose tolerance (IGT), impaired fasting glucose (IFG) levels, an A1C test level between 5.7% and 6.4%
currently pre-diabetes, IGT and IFG aren’t billable reasons or dilated retinal exam

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7
Q

gestational diabetes

A

5-10% of pregnancies
gestational diabetes any degree of glucose intolerance with onset or first diagnosis during pregnancy
GDM is caused by the hormones secreted during pregnancy or by a shortage of insulin
more common in black, hispanic, and american indian women, as well as women who are obese or have a family history of type 2
onset of GDM is usually during 2nd or 3rd trimester, glucose tolerance typically returns to normal within 6 weeks postpartum
due to short duration of GDM, DR doesn’t usually occur hx of GDM increased the risk of developing type 2 in the next 10-20 years by 35-60%

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8
Q

other types of diabetes

A

1-5%
diabetes can also occur secondary to genetic defects n beta cell function or insulin action, pancreatic diseases or other endocrinopathies, medications (steroids), toxic chemicals, infections, or uncommon forms of immune mediated diabetes

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9
Q

DM diagnosis based on

A 
plasma glucose criteria or A1C criteria 
FPG >/= 126
2-h PG >/= 200
random plasma glucose >/= 200
A1C >/= 6.5%
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10
Q

therapeutic principles of T2 DM meds

A

individualized treatment ask the patient what their target A1C is
14 step algorithm - use meds that minimize the risk of hypoglycemia, minimize weight gain, considers the starting A1C levels and lifestyle factors (including cost)

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11
Q

clinical diabetic exam

A

careful VA and refraction if needed
carful pupils and EOMs
slit lamp exam with gonio when appropriate
dilated fundus exam
check blood pressure
if BVA reduced - consider OCT to evaluate for the presence and extent of DME, consider IVFA to detect areas of non-perfusion including foveal ischemia and/or subclinical neo

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12
Q

ocular complications of DM

A

transient refractive shifts - data is mixed but both hyperopic shifts seem to be more common in hyperglycemia
cornea - decreased sensitivity and increased risk of abrasions, caused by reduced adhesion of corneal epithelium to stroma
lens - cataracts occur more often and younger, caused by osmotic stress from intracellular accumulation of sorbitol in the lens secondary to elevated intraocular glucose

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13
Q

other complications of DM

A

EOM palsy: neuropathy of CN 3, 4, 6, likely caused by localized demyelination of the nerve due to ischemia, can be first manifestation of DM, usual recovery 1-3 months
optic neuropathy: increased risk of subclinical neuropathy, anterior ischemic optic neuropathy and diabetic papillopathy
diabetic papillopathy: disc edema without pallor, bilateral 50% doesn’t always have APD, can occur with macular edema, VA usually recovers to 20/50
glaucoma: uncertain association with POAG, increased risk of NVG with PDR

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14
Q

diabetic retinopathy

A

the most common microvascular complication of diabetes
the leading cause of new cases of blindness and low vision among americans 20-74
diabetic retinopathy accounts for ~12% of all new cases of blindness each year
the strongest predictor for the development of DR is duration of disease

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15
Q

grading systems of DR

A
  1. ETDRS - one of the major outcomes was a standardized grading system of the different levels of DR, some argue the ETDRS scale is overly complicated and not practical for clinical practice
  2. international grading is a simplified system that is commonly used
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16
Q

NPDR characterized by the presence of

A 
hemorrhages and/or micro aneurysms 
hard exudates 
soft exudates CWS
IRMA
venous beading
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17
Q

characteristics of PDR

A

new vessels on or within 1 DD of disc (NVD)
new vessels elsewhere on the retina but not on or within one DD of the optic disc NVE
fibrous proliferation on or within 1 DD of the optic disc FPD or elsewhere on the retina FPE
pre retinal hemorrhage
vitreous hemorrhage

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18
Q

CSME

A

retinal thickening = 500 um from the center of the macula
HE = um of the center of the macula with thickening of the adjacent retina
an area of retinal thickening >/= DA of which any portion is within = DA from the center of the macula

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19
Q

diabetes and pregnancy

A

the main risk factor of DR worsening during pregnancy is the baseline severity of DR
women with pre existing diabetes who are planning or become pregnant should have a dilated retinal exam to a planned pregnancy or during the first trimester, with f/u during each trimester of pregnancy
pts with GDM don’t develop retinopathy therefore retinal evaluation for DR in these patients is not indicated

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20
Q

recommend exams in DR pregnancy

A 
gestational - none
no to minimal NPDR - 1st & 3rd tris 
mild to mod NPDR - every try 
high risk NPDR - monthly 
PDR - monthly - treat
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21
Q

treatment of DR and DME

A

laser photocoagulation: focal laser, grid laser, pan retinal photocoagulation used for severe NPDR and PDR
intravitreal injections - used for neo and DME, steroid triamcinolone, anti-vegfs
intravitreal implants
vitrectomy - used for non clearing VH, traction RD, combo retinal detachment, macular pucker
peripheral retinal cryotherapy: can be used for high risk complications in eyes with hazy media that prevents PRP, rarely used because of accelerated traction detachment

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22
Q

laser photocoagulation focal treatment

A

ETDRS established as standard treatment for CSME

a focal laser pattern is used to photocoagulative discrete leaking micro aneurysms identified with a prior FA

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23
Q

laser photocoagulation grid treatment

A

used to treat diffuse (aka florid) CSME without identifiable discrete foci of leakage

24
Q

pan retinal photocoagulation

A

the current standard treatment for high risk PDR, the goal of treatment is to cause regression of neo, sometimes used preventatively in severe NPDR
destruction of peripheral retina reduces the oxygen demand of the retina, decreases the production of VEGF and prevents or slows neovascular growth
~1200-2400 laser burns are scattered over the retina voiding the central macula
patients with PRP can still progress ETDRS showed that 60% will need additional treatment for DME and 17% will need vitrectomy

25
Q

complications and side effects of PRP

A

pt edu
PRP is uncomfortable and several sessions might be needed
complications and side effects: VF constriction, night blindness, color vision changes, decreased accommodation, scotoma, anisocoria, glaucoma and tractional RD
PRP can worsen retinal thickening in pts with center involved macular edema
in eyes without center involved macular edema, the risk for significant worsening of the edema PRP is low

26
Q

anti-VEGF injections

A

ranibizumab lucentis - approved for DME/DR
afibercept eyelea - approved for DME/DR
bevacizumab avastin - off label for DME

27
Q

intravitreal steroids

A

dexamethasone implant ozurdex - approved for DME
fluocinolone implant Iluvien - approved for DME
triamcinolone 40 mg/mL injection - off label for DME

28
Q

injections and implants complications

A

complications and considerations of anti-VEGF: cost, frequency of dosing, increasing incidence of endophthalmitis, other complications include inflammation, RD, vitreous hemorrhage, and traumatic cataract
complications of intravitreal steroids: glaucoma, cataracts

29
Q

treatment of mild to moderate NPDR

A

none

30
Q

treatment of severe NPDR

A

PRP considered

31
Q

treatment of PDR/high risk PDR

A

PRP

32
Q

treatment of DME (fovea not included)

A

focal/grid and possibly anti-VEGF

33
Q

treatment of DME (fovea involved)

A

focal/grid and anti-VEGF

34
Q

treatment of vitreous hemorrhage

A

vitrectomy

35
Q

treatment of tractional RD

A

vitrectomy, membrane peel, PRP

36
Q

current treatment of DME

A

anti-VEGF therapy first line for center involving DME
focal or grid laser treatment should be considered in patients with CSME, pts with extensive foveal ischemia are poor laser candidates
if nonresponsive to treatment consider corticosteroid therapy
with diffuse or extensive ME, ME in presence of foveal ischemia, or those with poor response to prior focal or grid laser may benefit from intravitreal antiVEGF or corticosteroid therapy either alone or in combo with laser

37
Q

PRP is indicated for any one of the following high risk characteristics

A

NVD greater than 1/4 to 1/3 of disc area in size
any degree of NVD when associated with pre retinal hemorrhage or VH
NVE greater than 1/2 of the disc area in size when associated with a pre retinal hemorrhage or VH
any NVI or neo of the angle
anti-VEGF therapy can be added as an adjunct to PRP with or without pars plana vitrectomy

38
Q

vitrectomy may indicated for any one of the following conditions

A

dense, non clearing VH causing decreased vision
traction RD involving and progressing within macula
macular epiretinal membrane ERMs
dense pre macular hemorrhage
chronic ME not responsive to other treatment
severe retinal neo and fibrous proliferation that is unresponsive to laser photocoagulation

39
Q

ABCs of diabetes

A 
A= A1C, target for most people is 7% or less but individualized by patient, fasting blood glucose target 70-130, post prandial blood glucose target (1-2 hours after eating) less than 180
B = blood pressure, for most people with DM target is below 140/80
C = cholesterol, LDL bad cholesterol under 100, triglycerides under 150, HDL good cholesterol for men above 40 for women above 50
S = smoking cessation
40
Q

multiple glucose tests exist including

A

capillary glucose - test aka finger stick test
fasting glucose test - nothing to eat 8-12 hours prior to test
post prandial glucose test - after a meal
serum glucose test - done at the lab, typically 11-15% higher then capillary glucose test

41
Q

diagnostic fasting plasma glucose levels

A

normal 70-99
pre diabetes 100-126
diabetes above 126

42
Q

glycated hemoglobin

A

HbA1C

measures the three month average plasma glucose concentration

43
Q

impaired fasting glucose

A

IFG

signifies the zone between the upper limit of normal fasting glucose (FPG) and the lower limit of diabetic FPG

44
Q

impaired glucose tolerance

A

a transition phase between normal glucose tolerance and diabetes with blood glucose levels that are between normal and diabetic, the diagnosis of IGT can only be made with oral glucose tolerance testing which measures the body’s ability to metabolize glucose

45
Q

oral glucose tolerance test

A

OGTT
was the gold standard for diagnosing T2DM
is still used commonly during pregnancy for diagnosing gestational diabetes

46
Q

micro aneurysms

A

the earliest clinical sign of DR, these occur secondary to capillary wall out pouching due to pericyte loss

47
Q

dot and blot hemorrhages

A

occur as micro aneurysms rupture in the deeper layers of the retina, such as the inner nuclear and outer plexiform layers

48
Q

flame shaped hemorrhages

A

hemorrhages that occur in the more superficial nerve fiber layer

49
Q

retinal edema and hard exudates

A

caused by the breakdown of the blood retina barrier, allowing leakage of serum proteins, lipids, and protein from the vessels

50
Q

cotton wool spots

A

NFL infarctions from occlusion of precapillary arterioles

51
Q

venous beading

A

frequently occur adjacent to areas of nonperfusion, they reflect increasing retinal ischemia and their occurrence is the most significant predictor of progression to PDR

52
Q

intraretinal microvascular abnormalities

A

IRMA

remodeled capillary beds without proliferative change, can usually be found on the borders of the non-refused retina

53
Q

neovascularization

A

hallmark of PDR

54
Q

pre retinal hemorrhages

A

appear as pockets of blood within the potential space between the retina and the posterior hyaloid face, as blood pools within this space, the hemorrhages may appear boat shaped

55
Q

hemorrhage into the vitreous

A

may appear as a diffuse haze or as clumps of blood clots within the gel

56
Q

fibrovascular tissue proliferation

A

usually seen associated with the neovascular complex, may appear avascular when the vessels have already regressed

57
Q

traction retinal detachments

A

usually appear tented up, immobile and concave

OPTM 737 (6 decks)

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