vascular issues Flashcards

1
Q

lipemia retinalis:

A

elevated serum triglyceride levels, make blood vessels look milky white, due to inc chylomicrons and triglyceride(level will be bw 1000mg/dl-2000)

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2
Q

CBC includes:

with differential?

A

RBCs and WBCs and platelets

w/diff get breakdown, including neutrophils, eosinophils, lymphocytes (%s and absolute counts)

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3
Q

hematocrit norm value?

A

37-47%

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4
Q

RBC absolute count norm value?

A

4.2-5.4 m/ul

amount of oxygen carrying protein

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5
Q

hemoglobin norm value?

A

12-16 gm/dl

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6
Q

what might low mean platelet volume correlate to? high platelet volume?

A

low=IBD

high=stroke, heart attack risk

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7
Q

platelet count norm value?

when to worry about retinal bleeding? (with what platelet counts?)

A

150-450 k/ul

-with 50 k/ul or less, worry about retinal bleeding

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8
Q

Thrombocytopenia=

A

low platelet count

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9
Q

3 possible ocular findings ass. with anemia?

A

1) conj pallor
2) retinal hemes (some say you only get with anemia and low platelet count)
3) ischemic optic neuropathy (usually rapid onset anemia, blood loss from trauma etc.)

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10
Q

Polycythemia

A

inc in RBCs, inc in blood volume and viscosity, decrease in flow

  • hematocrit can be 70-80%
  • hemoglobin 18.5
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11
Q

when blood becomes ___X more viscous than water, can get retinal changes

A

3-4X

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12
Q

what retinal changes can occur with polycythemia?

A
  • conj vascular engorgement
  • dark/thickening of blood vessels
  • ret hemes
  • ret vein occlusions
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13
Q

Primary vs secondary polycythemia

A

1=excess bone marrow production

2=hypoxic state (lung or heart disease, inc altitude)

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14
Q

normal serum viscosity?

A

1.4-1.8

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15
Q

what is waldenstrom’s macroglobulinemia?

A

small B cell lymphoma that secretes monoclonal Ig M which increases blood viscosity, causing tortuosity, sludging, venous dilation, segmentation
*normal IgM is 45-250mg/dl

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16
Q

waldenstrom’s macroglobulinemia can cause what ocularly?

A

hemes, edema, retinal artery and vein occlusions

  • central serous-like maculopathy
  • usually starts in periphery, later inc and can appear with CWS and exudates too
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17
Q

what is multiple myeloma? what do you see in eye?

A

too much IgG, similar eye findings as waldenstrom, also cysts near ora

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18
Q

most pars plana cysts are from what?

A

idiopathic

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19
Q

how do you tx polycythemia? what about waldenstrom?

A
P=blood let
WM=chemo, monoclonal abs etc
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20
Q

angiod streaks are caused by what and a risk factor for what?

A

breaks in Bruch’s membrane; risk factor for CNVM

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21
Q

what are some non-proliferative findings you might see with sickle cell in the eye?

A
  • salmon patches
  • black “sunbursts” of pigment epi hyperplasia
  • angiod streaks
  • schisis cavity
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22
Q

what is the main proliferative finding you might see with sickle cell in the eye?

A

“sea fans” which is peripheral neo

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23
Q

tx’s for sickle cell?

A

hydroxurea-Increases the concentration of fetal hemoglobin (holds more oxygen)
blood transfusions
bone marrow transplants

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24
Q

when to tx sickle cell in retina?

A

Bilateral proliferative disease
Elevated neovascular fronds
Rapidly growing fronds

Main treatment goal: try to get better overall control of the sickle cell disease with their doctor who is treating them medically

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25
Q

what are salmon patch hemes?

A

Salmon patch hemorrhages located in the mid periphery, it is an intraretinal 
hemorrhage believed to be caused by peripheral arteriole occlusions
-from sickle cell

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26
Q

why do you get black sunburst pigmentation with sickle cell?

A

Black sunburst pigmentation represents pigment epithelial hyperplasia 
following infarct of choriocapillaris or subretinal hemorrhages from sickling, 
hemosiderin (from reabsorbed hemorrhage)

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27
Q

More patients with SS sickle cell type get angioid streaks secondary to abnormal ____ in Bruch’s membrane.
•What do angioid streaks put the patient at higher risk for?

A

abnormal calcium

angiod streaks=higher risk for CNVM

28
Q

why is it impt to keep IOP low in sickle cell?

A

only a moderate increase in IOP can cause significant reduction in perfusion to ONH and retina putting patient at risk for ischemic optic atrophy and retinal artery occlusion

*Want to keep IOP below 25 mmHg for someone with sickle cell even if their nerves look fine

29
Q

Ocular involvement is more common in ___ leukemias.

A

acute

30
Q

what kind of disease is leukemia?

A

The leukemias are a group of neoplastic disorders characterized by abnormal proliferation of white blood cells.

31
Q

Ocular complications of leukemia may be due to a direct involvement by leukemic infiltrates or secondary to ________

A

anemia or thrombocytopenia

32
Q

what are some of the eye findings in leukemia?

A

-Roth spots (leukemic infiltration), CWS, hemes
-Heme with leukemic infiltrates in the center
-Optic neuropathy infiltration of the optic nerve.
-Sheathing of the retinal vessel
-Platelet fibrin deposits (similar to hollenhorst plaque)
-Venous tortuosity from hyperviscosity.
-Serous retinal detachments (CSR)
KEY FINDINGS
o Roth spots
o Sub-retinal hemes and intraretinal hemes
o exudates

33
Q

what is ITP (Idiopathic thrombocytopenic purpura)?

A

autoimmune conditionwhere body produces autoantibodies that attack and destroy platelets
-Similar to hemolytic anemia

34
Q

thrombocytopenia is associated with what ocular findings?

A
decreased platelet disorder associated with: 
	increased bleeding
	retinal hemorrhages
	vitreous hemorrhages
	hyphemas
	conjunctival petechial hemorrhages

35
Q

what is thrombocytosis? what can it lead to?

A

High platelet counts

Can lead to the formation of blood clots, TIA, or heart attacks.

36
Q

Platelet conditions are often associated with what systemic conditions?

A

leukemia, lymphoma and autoimmune disease

37
Q

most common finding with HIV?

A

CWS

38
Q

What causes CWS HIV retinopathy?

A
  • Immune complex deposition

- Direct infection of the retinal vessels with HIV

39
Q

CWS usually do not manifest until CD4 is below ____

Normal CD4 is ___ cells per cubic millimeter of blood


A

Usually do not manifest until CD4 is below 200-400.

Normal is 500-1500 cells per cubic millimeter of blood

40
Q

Coumadin is used to treat a number of conditions including:

A

-pulmonary embolism
-deep vein thrombosis (DVT)
•in legs- reason why you need to walk around an airplane; birth control, knee surgery are causes
-recurrent myocardial infarction
-thromboembolic events such as stroke

41
Q

If a patient on Coumadin comes in with a bleed, when should you send them for an INR?

A

send them for an INR that day- need their levels adjusted

42
Q

Most common retinopathy with interferon is:

A
  • Cotton Wool Spots – Deposition of immune complexes in the retinal vasculature and leukocyte infiltration.
  • Also hemorrhages
43
Q

should you D/C interferon when you see retinopathy?

A

Should do a 
pre-exam when interferon is started then follow every one to three months, some doctors choose to follow every 6 months.
*Usually drug is not discontinued if retinopathy develops unless the optic nerve is involved, just watch closely

44
Q

what is interferon used to tx?

A

Drug is used most commonly for MS, some cancers and Hepatitis C treatment
*more likely to get retinopathy with hep C tx than MS

45
Q

when should you d/c interferon?

A
  • retinal vein occlusion
  • transient vision loss
  • CWS encroaching the macula or CME (macular involvement)
  • Remember CWS cannot be in macula b/c there is no NFL
46
Q

HTN defined as BP over:

what is pre hypertensive?

A

Defined as blood pressure equal to or in excess of 140/90 in a relaxed state= older definition
Systolic pressure of 120-139 should be considered pre-hypertensive

**If diastolic is greater than 90 or systolic is greater than 140 should be sent to PCP and blood pressure should be re-measured

47
Q

in what htn situation would you refer immediately to ER?

to PCP ASAP?

A

Cases for immediate referral to ER:

  • Diastolic is greater than 130
  • Systolic is greater than 200
  • Disc edema

Cases for ASAP referral to PCP:

  • Diastolic greater than 110
  • Any hypertensive retinopathy
48
Q

what is hyalinization?

A
  • Irregular thickening of BM of vessel with deposits of extracellular 
substances

  • Collagenization of the intima and media
  • Loss of structural detail and narrowing the of lumen
  • occurs with arteriole sclerosis
49
Q

In accelerated hypertension as in toxemia the patients can experience headache, diplopia, 
photopsia and scotomas.
WHat is toxemia?

A

Toxemia- too much protein during pregnancy/ gestational hypertension

50
Q

what kind of changes to RPE and choroid can occur in HTN?

what are siegrist streaks?

A

Hyperpigmentation can develop over choroidal arteries in patients with chronic hypertension.

  • RPE above the sclerotic choroidal arteries become hyperplastic and the choricocapillaris become narrowed.
  • Changes in the periphery = called Siegrist Streaks
  • Siegrist streaks develop when HTN is affecting the choroid
51
Q

The quadrant most commonly affected in BRVO?

A

The quadrant most commonly affected is the superotemporal (63%) because it has the most A/V crossing

  • What would a patient complain of with a superior temporal vein occlusion? Inferior distortion
  • *Nasal quadrant BRVOs are rare.
52
Q

T/F: BRVO usually occurs in the fifth and sixth decade of life and is the second most prevalent retinal vascular disease to diabetes

A

true

53
Q

only cause of BRVO?

A

HTN

54
Q

the 2 main complications of BRVO?

A

chronic macular edema and secondary retinal neovascularization

55
Q

what is Bonnet’s sign?

A

Bonnet’s sign- flame shaped heme at A/V crossing

  • Very high risk for the vein to bleed when seen at the site of A/V nicking
  • Tell patients to get BP under control if you see this
56
Q

what are some other fundus findings you might see with BRVO?

A

Dilated and tortuous veins
Dot and blot hemorrhages:
-intraretinal hemorrhages from site of obstruction out to periphery 
in the section of retina normally drained by the affected vein
-Microaneurysms with subsequent intraretinal edema

57
Q

T/F: BRVO is typically bilateral?

A

false

58
Q

how should you tx non-ischemic BRVO?

A

If BRVO is not too large and the macula is not involved- just watch
-check monthly to insure bleeding is not increasing, Watch once a month for 6 months

If significant amount of retina is affected and there is macular edema with decreased VA (worse than 20/40)

  • send to a retinal specialist for consideration of using an anti-VEGF or grid laser treatment (mostly anti-VEGF nowadays)
  • Corticosteroids have also been found to be effective
59
Q

how should you tx ischemic BRVO?

A

Assess for macular edema and treat with either anti-VEGF or intravitreal corticosteroids.

  • Laser of the peripheral retina can be considered if extensive ischemia is present to prevent neo.
  • With ischemic, you cannot get macula back to normal
  • Usually they wait until they see neo in order to laser
60
Q

what was the outcome of the BRVO study?

  • ABout what % end up with 20/40 or better vision even if left untreated?
  • If had what VA at the time of the event had excellent prognosis?
A

o Management of BRVO- first 6-12 months
o Basically shows what happens if we do nothing to treat:
 Many patients with BRVO improve significantly during the first 6-12 months with or without treatment.
 Slightly greater than 50% end up with 20/40 or better vision even if left untreated.
 If 20/40 at the time of the event excellent prognosis.
 About 1/3 of patients with BRVO affecting the macula region may improve 1-2 lines of VA without treatment.

61
Q

Many individuals with macular edema often describe visual acuity as worse in the morning and better in the afternoon. WHy?

A

In the morning when these patients wake up, the fluid is right over the macular region. As the day goes on, the fluid falls due to gravity and VA is improved slightly

62
Q

what was the outcome of the BRVO Study Past Management (1980)?

A

*Argon laser photocoagulation successfully reduced vision loss from perfused macular edema
-if 20/40 or worse (due to macular edema) patients were treated with laser 
photocoagulation applied in grid pattern throughout leakage area.
-After 3 years follow up about 2/3 of the treated group gained two or more lines compared with 1/3 in the untreated group
ALSO: wait to see neo before you treat with laser because only 50% of people with ischemic BRVO (with large areas of non-perfusion) went on to even develop neo

63
Q

what was compared in the SCORE study?

A

Purpose: Safety and efficacy of standard care of grid laser vs. intraviteral traimacinolone acetonide corticosteroid injection (Kenalog)
-Testing steroid injections on macular edema associated with BRVO treatment

64
Q

what was the outcome of the SCORE study?

A

Conclusion: For BRVO, laser was still considered the gold standard
•Kenolog (the steroid), although slightly more effective, the side effects of cataract formation and glaucoma did not outweigh the benefits.
•Patients developed cataracts within 3-6 months of injections
•In pseudophakic patients the benefits did outweigh the risk since the patients were
already pseudophakic.

65
Q

what was the point of the BRAVO study?

outcome?

A

purpose: Efficacy of Ranibizumab (lucentis) vs sham injections for the treatment of macular edema secondary to a BRVO
- Lucentis did improve macular edema moreso than sham, but even after decreasing swelling vision probably won’t return

66
Q

when should you send BRVO pt to ret specialist?

A

o Send to retina specialist if macula edema causing vision of 20/40 or worse or if a lot of hemorrhaging or very large amount of retina effected.

67
Q

How often can you do steroid injection?

A

o Also remember that a steroid injection can be given once every 3 months