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Ocular Disease 4 > Lecture 5 - HTN and Ocular Complications > Flashcards

Lecture 5 - HTN and Ocular Complications Flashcards

1
Q

what is normal BP for anyone younger than 60?

A

less than 140/90

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2
Q

what is normal BP for anyone with DM or CKD?

A

less than 140/90

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3
Q

what is normal BP for anyone older than 60 years old?

A

less than 150/90

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4
Q

what is a hypertensive crisis BP?

A

greater than 180/ 100

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5
Q

what are some symptoms related to end organ damage in HTN patients?

A

TIA, amourosis fugax, chronic kidney infections, polyuria, dyspnea, peripheral edema

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6
Q

what are some risk factors for HTN (modifiable)?

A

obesity (apple shape), salt intake, smoking/alcohol, physical inactivity, fatty diets/increased cholesterol, stress, metabolic syndrome

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7
Q

what happens to the heart with HTN?

A

the left ventricle becomes larger due to an increased resistance - fluid builds up in the lungs and peripheral body

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8
Q

what signs of HTN do you look for in the pre-testing part of the exam?

A

BP, EOMs (palsies), pupils (APD), BVA (macular involvement), SLEx (NVI and AC reaction) and DFE

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9
Q

what are some ocular diseases that occur secondary to HTN?

A

hypertensive retinopathy, vein occlusions, artery occlusions, CN3/CN4/CN6 palsies (CN6 higher than DM), OIS, macroaneurysm, sub-conjunctival hemorrhage, AION, and hypertensive choroidopathy

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10
Q

what is considered grade 1 hypertensive retinopathy?

A

mild increased ALR and mild arteriole narrowing

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11
Q

what is considered grade 2 hypertensive retinopathy?

A

more pronounced arteriole narrowing, AV ratio changes, focal constriction, AV crossing changes

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12
Q

what is considered grade 3 hypertensive retinopathy?

A

grade 2 + CWS, hemorrhages, exudates

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13
Q

what is considered grade 4 hypertensive retinopathy?

A

grade 3 + optic disc swelling

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14
Q

what is considered mild hypertensive retinopathy?

A

increased ALR, AV ratio changes, AV crossing changes, focal narrowing (diastolic >90 and >110)

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15
Q

what is considered moderate hypertensive retinopathy?

A

hemorrhages, CWS, hard exudates, aneurysms (diastolic BP >110)

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16
Q

what is considered severe hypertensive retinopathy?

A

moderate findings + ON swelling (diastolic BP > 110)

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17
Q

what is hypertensive encephalopathy?

A

the brain is swollen = severe HTN, headaches, nausea, +/- vomiting, papilledema and accelerated BP (perform crainial nerve assessment)

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18
Q

what is the pathogenesis of the vascular response in the chronic phase?

A

vasoconstrictive state - sclerotic state - exudative state

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19
Q

what happens in the vasoconstrictive state of the chronic phase?

A

initial response is vasoconstriction - generalized narrowing of arterioles, decrease in AV ratio (heart is working harder to excrete sodium/water)

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20
Q

what happens in the sclerotic state of the chronic phase?

A

persistently elevated BP causes hyperplasia and thickening of arteriole wall - increase in ALR and AV crossing changes (compression, deflection, humping, tapering)

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21
Q

what happens in the exudative state of the chronic phase?

A

when autoregulation fails and the high BP is transmitted to the capillaries - hemorrhages, CWS, hard yellow exudates, optic nerve swelling

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22
Q

what is the pathogenesis of the vascular response in the accelerated phase?

A

the upper limit of the retinal and cerebral vessel’s autoregulation is breeched = vasodilation, hyperperfusion, edema, retinopathy and/or encephalopathy

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23
Q

what did the ARIC (atherosclerosis risk in communities study) conclude?

A

generalized arteriolar narrowing and AV nicking have been associated with an increase in stroke and heart disease (2-3x greater risk when CWS, hemes or exudates)

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24
Q

what retinal signs indicate an emergent case of HTN?

A

bilateral disc edema and macular star (exudates)

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25
Q

what is hypertensive choroidopathy?

A

(rare) marked elevation in systemic BP - autonomic regulatory capacity exceeded - fibrin-platelet obstruction - obstruction of arteries and choriocapillaries - necrosis of RPE and fibrinous exudation

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26
Q

when is hypertensive choroidopathy seen?

A

associated with moderate-severe HTN retinopathy, younger patients (may be caused by adrenal gland tumor) >220/120 BP

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27
Q

what are the retinal signs of hypertensive choroidopathy?

A

Siegrist streaks (linear hyperpigmented areas over choroidal vessels) and Elschnig spots (changes in RPE from non-perfused areas in choriocapillaris = moth eaten appearance)

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28
Q

which ethnicity has a higher prevalence of HTN retinopathy?

A

2x as frequent in african americans vs. caucasians

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29
Q

what is the follow up recommendation for mild HTN retinopathy?

A

less than 140/90 = RTC in 1-2 years

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30
Q

what is the follow up recommendation for moderate HTN retinopathy?

A

(>140-180/>90-110) = RTC in 3-6 months and MD in 2-4 weeks

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31
Q

what is the BP for a HTN crisis?

A

> 180/>110 + acute TOD

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32
Q

what is a hypertensive urgency?

A

(>180/>110) severe BP, may have headaches, no progressive TOD, and no disc edmea

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33
Q

what is a hypertensive emergency?

A

(>180/>110) life-threatening or progressive TOD, headaches, shortness of breath, dizziness, and disc edema (perform a neuro assessment for signs of a stroke)

34
Q

when do you send a patient to the ER?

A

bilateral disc edema and headaches

35
Q

when do you call 911 for a HTN patient?

A

severe (bilateral) disc edema with headaches, confusion (HTN encephalopathy), shortness or breath/chest pain, extremity swelling

36
Q

what are retinal signs of acute target end organ damage (TOD)?

A

exudates, hemorrhages, CWS

37
Q

what is the follow up for an urgent case with no TOD and mild HTN retinopathy?

A

BP control within 3-7 days and OD follow up in 3 months

38
Q

what is the follow up for an urgent case with evidence TOD and moderate HTN retinopathy?

A

BP control within 24-72 hours and OD follow up in 1 month

39
Q

what is the follow up for an urgent case with evidence TOD and severe HTN retinopathy?

A

BP control within minutes to hours and OD follow up in 1 month s/p from hospital

40
Q

what is atherosclerosis?

A

arterial wall thickening - occurs with increase in age and increase in cholesterol (LDL)

41
Q

what causes atherosclerosis?

A

accumulation of cholesterol and lipid in the tunic intima causing hyperproliferation of smooth muscles and narrowing of the lumen (slows blood flow and increases peripheral vascular resistance)

42
Q

what are considered hard plaques? soft plaques?

A

hard = calcium or cholesterol and soft = blood

43
Q

what are the systemic risk factors for a retinal venous occlusion?

A

hypertension (BRVO>CRVO), increased age (>50), increased LDL, DM, hyperviscosity (abnormal blood coagulation)

44
Q

what are the ocular risk factors for a retinal venous occlusion?

A

POAG (5x risk) and periphlebitis (inflammation of blood vessels)

45
Q

what is the pathogenesis of a retinal venous occlusion?

A

thickening of the arterial wall compresses the vein (share a common sheath) = resultant turbulence results in endothelial cell damage and thrombotic occlusion
stagnant blood = hypoxia = edema/swelling

46
Q

what causes a branch retinal vein occlusion (BRVO)?

A

thickening of the artery leads to compression of the underlying vein within the shared fascial sheath = commonly occurs superior temporal arcade at AV crossing in HTN/atherosclerosis

47
Q

what are the retinal features of a BRVO?

A

flame > blot hemorrhages, +/- CWS, non-ischemic, asymptomatic unless in macula

48
Q

what causes vision loss in BRVO?

A

CME, heme in macula, macular edema/exudates, S/P resolution of macular pigment disruption, S/P resolution associated with ERM formation, macular ischemia

49
Q

what are some associated features of BRVO?

A

CME, collateral vessels, sheathing of vessels, NVD/NVE (rare), vitreous hemorrhage (rare)

50
Q

what are the chronic BRVO sequelae?

A

collateral vessels or anastomoses, thicker lumen/vessel in curling pattern, does not leak

51
Q

what is the management for BRVO?

A

VA spontaneously resolves in about 3 months = follow every 4 weeks for 3 months (watch for collaterals, macular pigment disruption, and venous sheathing)
if not resolving order FA (PRP if neo develops)

52
Q

what did the BVOS (branch vein occlusion study) conclude?

A

to closely monitor for development of neo - do not PRP if there is only ischemia present (causes vision loss)

53
Q

what are some treatment options for BRVO?

A

avastin, kenalog injections, ozurdex implant

54
Q

what did the SCORE study conclude?

A

for BRVO with macular edema = trimcinolone (kenalog) injections gave a 3 or more line VA improvement

55
Q

what did the BRVO study conclude?

A

Avastin was given to eyes with BRVO + macular edema = fewer side effects vs steroid injection and 3 lines of VA improvement

56
Q

what is a central retinal vein occlusion (CRVO)?

A

obstruction of the vein at or posterior the lamina cribrosa = all 4 quadrants are affected (blood and thunder)
painless sudden VA loss (unilateral), dilated/tortuous veins, flame/blot hemes and +/- CWS

57
Q

what is non-ischemic CRVO?

A

80% of cases - less severe presentation and better prognosis, VA 20/60-20/100, less likely to develop NVI, less likely to have APD, 15% may convert to ischemic CRVO within first 4 months

58
Q

what is ischemic CRVO?

A

VA worse than 20/200, +APD, venous tortuosity, extensive hemes, extensive CWS, disc edema, extensive capillary drop out on FA and poor prognosis

59
Q

when can neo glaucoma occur with CRVO?

A

may occur within first 3 months of disease onset (90 day glaucoma)

60
Q

what are some associated features of CRVO?

A

macular edema (cystoid), varying degrees of disc edema, optic disc colateral vessels, NVI, exudative RD, vitreous heme

61
Q

what is a hemicentral retinal vein occlusion (HRVO)?

A

in about 20% of eyes the central retinal vein enters the optic nerve as 2 separate branches (superior and inferior) and only half of the retina is involved (outcome is more like CRVO)

62
Q

what did the ischemic or non-ischemic central vein occlusion study conclude?

A

ischemic CRVO = at least 10DD of retinal capillary non-perfusion at posterior pole
non-ischemia CRVO = less than 10DD of retinal capillary non-perfusion
FA is most useful test to evaluate conditions

63
Q

what is the work up for CRVO?

A

complete history (>age 50, DM, HTN, birth control pills), BO, gonio, OCT of macula, FA if not recent onset, and blood work (younger patient - hyperviscosity concern)

64
Q

what is the treatment for CRVO?

A

no proven treatment - can use anti-VEGF for edema and monitor for neo (prophylactic PRP does not help), lower IOP if needed, treat underlying conditions

65
Q

when do you follow up with a patient with CRVO and 20/40 or better VA?

A

exam every 1-2 months for 6 months after diagnosis, annual exams as condition stabilizes

66
Q

when do you follow up with a patient with CRVO and 20/50-20/200 VA?

A

exam monthly - bimonthly for first 6 months after diagnosis, exams every 6 months - year after

67
Q

when do you follow up with a patient with CRVO and 20/200 VA?

A

exam every month for 6 months, then every 2 months until 8 months, then every 4 months until 2 years after presentation

68
Q

when do you follow up with a patient with ischemic CRVO?

A

follow every 4 weeks for first 6-9 months then every 3 months

69
Q

when do you follow up with a patient with non-ischemic CRVO?

A

every 4 weeks for first 3 months then every 3-6 months (conversion to ischemic typically occurs during first 6-12 months)

70
Q

what do you watch for during the resolution phase of CRVO?

A

NVI/NVE, collateral vessels, macular pigment disruption, macular ERM, macula sub-retinal fibrosis (scaring)

71
Q

what is the management for macular edema in CRVO?

A

avastin injections, triamcinolone (kenalog), ozurdex, PRP once NVI/NVG develops

72
Q

what is a central retinal artery occlusion (CRAO)?

A

sudden painless, severe vision loss (CF or worse), +APD, whitening of posterior pole over hours, cherry red spot macula, box-carrying of blood flow in retinal vessels

73
Q

what are some associated features of CRAO?

A

amaurosis fugax, visible emboli, carotid artery disease, giant cell arteritis, NVI, arterial collaterals on optic disc

74
Q

who typically gets CRAO?

A

M>W, mean age 60, HTN, DM, ipsilateral carotid artery disease, cardiac valvular disease, endocarditis

75
Q

how does the occlusion occur in CRAO?

A

hard or soft emboli - can affect the ophthalmic artery, cilioretinal arteries and retinal arteries, hollenhorst plaque (increases mortality 3x)

76
Q

what are the late stages of CRAO?

A

after 4-6 weeks the retina returns to normal (less white), optic disc pallor and may form disc collaterals

77
Q

what is a branched retinal artery occlusion (BRAO)?

A

retinal whitening in an area of vessel blockage, +VF defect, VA may or may not be affected

78
Q

who typically gets a BRAO?

A

M>F, more common in OD, HTN, DM, carotid artery disease, giant cell arteritis, cardiac disease, cardiac valve disease, Susac disease (young females with MS like symptoms and hearing loss, bilateral recurrent BRAO)

79
Q

what are 3 main retinal emboli in BRAO?

A

cholesterol (hollenhorst) at bifurcation, platelet (fibrin - long white, intra-arterial plugs) and calcific (closer to the disc, solid white)

80
Q

what are the key features of BRAO?

A

retinal whitening in territory of obstructed vessel, visible emboli and VF defect that corresponds with territory of obstructed vessel

81
Q

what is the treatment and management for CRAO/BRAO?

A

no proven treatment, patient education and monitoring, letter to PCP, carotid doppler and order blood work

Ocular Disease 4 (6 decks)

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