Free OPS CRA Exam Flashcards

The inner barrier is the tight junctions between retinal capillary endothelial cells. The outer barrier is the tight junctions between retinal pigment epithelial cells, which keep normal choroidal leakage out of the retina. Breakdown of either barrier is what produces angiographic leakage.

The choriocapillaris has fenestrated capillary walls that let fluorescein pass freely into the extravascular choroid. In the posterior fundus it is arranged in a mosaic of lobules, which is why the early choroidal flush looks patchy rather than uniform.

Three anatomical features combine: taller and more heavily pigmented RPE cells centrally, xanthophyll pigment in the fovea, and the absence of retinal capillaries in the foveal avascular zone. None of these is pathology, so do not report it as blockage.

It fills with the choroidal flush rather than with the retinal arterioles, because a cilioretinal artery and the choroid are both supplied by the short posterior ciliary arteries. Recognizing this prevents mislabeling early filling of that vessel as an artifact.

Preretinal blood, as in proliferative diabetic retinopathy, blocks both the retinal and the choroidal circulations. Subretinal blood, as in exudative AMD, obscures only the choroidal circulation because the retinal vessels lie in front of it. What is hidden tells you the depth.

The classic angiographic sign of Stargardt disease. Widespread lipofuscin in the RPE absorbs the excitation light and masks background choroidal fluorescence, so the choroid stays dark. It is typically paired with a central bull's-eye fluorescence pattern in the macula.

Acute posterior multifocal placoid pigment epitheliopathy (APMPPE). The placoid lesions block choroidal fluorescence in the early frames and then stain in the late frames. Capturing both early transit and late images is essential or the pattern is missed.

Retinal hypoperfusion comes from arterial and venous occlusions and ischemic disease such as diabetes. Choroidal hypoperfusion comes from ophthalmic artery occlusion, giant cell arteritis, and hypertensive choroidopathy. In many occlusions the hypofluorescence is temporary and fills in on later frames.

Contraindications to dilation such as narrow angles, contact lenses, and iris-fixated or anterior chamber intraocular lenses; media opacities including corneal and lens scarring; and signs of inflammation or infection. It is performed before any drops are instilled.

Apply cold compresses to the site for five to ten minutes and reassess the patient until edema, pain, and redness resolve. Because fluorescein is buffered to a pH of 8 to 9.8, infiltration is painful and large volumes have caused skin sloughing, local necrosis, subcutaneous granuloma, and toxic neuritis.

No. The OPS BOC states that administering intravenous injections is not a certification requirement, so the Board has no authority to test or certify injection competency. Whether an unlicensed imager may inject is decided by state law, and credentials vary by state.

Fluorescein emits a narrow band that exposes only the green-channel photosites of an RGB sensor, so resolution is lost to interpolation. A monochrome sensor makes every pixel available to the fluorescence signal and is more light sensitive, which matters at the low light levels of angiography.

Charge from a saturated photosite overflows into neighboring photosites, producing bright streaks or haloes around the brightest areas of the image. It is an overexposure artifact, so reduce flash output or sensor gain rather than trying to correct it in software.

Gain amplifies the signal and the noise together. Noise is false pixel data generated by a poor signal-to-noise ratio and by that amplification. Brightening an underexposed file afterward increases noise the same way, so favor more light and lower gain when the exposure allows.

Diagnostic-quality digital color images saved with minimal or lossless compression: TIFF, PNG, JPEG, or PDF. Heavy lossy compression discards fine vessel and lesion detail permanently, so archive at low compression and reserve aggressive compression for non-diagnostic uses.

A reading center grades images from many sites, so field definitions, sequencing, and equipment settings must be identical everywhere. Certification confirms the imager and the camera meet protocol. Deviating from the protocol makes images ungradable and can exclude the patient's data.

A universal standard for transferring diagnostic images and their associated patient and study information between devices from different vendors. Conformance is what lets an ophthalmic imaging system connect to a hospital PACS and integrate with the electronic medical record.

Organize archival systems to meet state and federal retention rules, coordinate network transfers into the patient database, and observe network security including firewalls, access control, and protection of wireless transmissions. Patient identifiers travel with the images, so HIPAA applies to the archive itself.

A mask shapes the light into a doughnut that is reflected off a mirror with a central aperture and projected through the outer part of the dilated pupil. The image reflected off the retina exits through the central, un-illuminated portion of that ring and passes back through the aperture.

Thirty degrees is the normal angle of view and produces an image about 2.5 times life size. Variable-angle cameras cover roughly 45 to 60 degrees with proportionately less magnification and need a more widely dilated pupil. Narrow-angle work is 20 degrees or less.

With no subject in the field, turn the eyepiece to maximum plus, relax your eyes on a distant object with both eyes open, then rotate toward zero and stop the instant the reticle is sharp. Repeat until three consecutive settings agree, and recheck before each patient.

A bright hazy crescent along one edge of the frame, produced when the illuminating ring is partly clipped by the iris because the camera is off-center in the dilated pupil or at the wrong working distance. Correct it by recentering the camera and resetting the working distance, not by changing exposure.

A focal opacity such as a lens or corneal scar can often be bypassed by shifting the camera within the dilated pupil to find a clear optical path, giving a sharp view around it. The CRA portfolio requires a matched pair of the same eye documenting both the hazy and the clear approach.

The camera is shifted laterally a few millimeters between the two exposures. The illuminating beam then strikes opposite slopes of the cornea, and the resulting cornea-induced parallax produces a hyperstereoscopic effect when the pair is fused in a stereo viewer.

A simultaneous stereo camera records both stereo views in a single exposure, placing two images side by side on one frame. Sequential stereo takes two separate exposures with a lateral camera shift, so patient or eye movement between frames can degrade or destroy the stereo effect.

The fundus camera focuses at or near infinity, so the focus control compensates for the patient's refractive error. Plus and minus diopter compensation lenses extend the range for high hyperopia, aphakia, and high myopia, and an astigmatic correction device addresses significant corneal astigmatism.

Replacing viewing bulbs, flash tubes, and fuses, and cleaning the optics including the objective and relay lenses. Dust or a fingerprint on the objective produces central haze and flare that no amount of exposure or alignment adjustment will remove.

A confocal aperture sits in front of the detector at a focal plane conjugate to the retina and blocks light that is not image-forming. Combined with a narrow-band laser scanning the retina point by point in a raster, this yields high-contrast, finely detailed images at video frame rates.

Those procedures compromise corneal clarity and leave residual topical fluorescein on the cornea. Corneal haze scatters light, and residual fluorescein glows under blue or blue-green illumination, cutting contrast in monochromatic images and competing with retinal fluorescence during angiography. Image first, or on a separate visit.

Green light around 540 to 570 nm is absorbed by blood but partly reflected by retinal pigment, giving the best overall fundus contrast and clear rendition of vessels, hemorrhages, drusen, and exudates. Vogt described the technique in 1925 and coined the term red-free.

It reveals the nearly transparent anterior retinal layers by scattering off them against a dark background. The nerve fiber layer, internal limiting membrane, retinal folds, cysts, and epiretinal membranes stand out. Blue-green around 490 nm is usually used because very short blue scatters excessively in the media.

The confocal SLO technique uses 488 nm excitation with a barrier filter at 500 or 520 nm, the same wavelengths used for fluorescein angiography. Even a trace of intravenous fluorescein swamps the low-level lipofuscin signal. Fundus-camera filter sets shifted toward red can be used before or after angiography.

The exciter transmits blue-green light at 465 to 490 nm, fluorescein's peak excitation range. The barrier transmits a narrow yellow-green band at 520 to 530 nm, fluorescein's peak emission. Narrow band-pass interference filters are used so the two transmission curves barely overlap.

Crossover between the spectral transmission curves of the exciter and barrier filters lets reflected light from bright fundus structures reach the sensor without any dye present. Mismatched or aged filters are the usual cause. A control photograph taken before injection reveals it.

Autofluorescence is genuine fluorescence from natural fluorophores with no dye given, seen in optic nerve drusen, astrocytic hamartomas, RPE lipofuscin, and the aging crystalline lens. Pseudofluorescence is not fluorescence at all, only reflected light leaking through mismatched filters.

About ten seconds in a normal patient. The major choroidal vessels are impermeable but the choriocapillaris leaks freely, and the RPE acts as an irregular filter, so the flush shows little detail. Start shooting before the dye is visible so the earliest frames are not lost.

About 12 seconds: retinal arterioles fill one to two seconds after the choroid. A prolonged arm-to-retina time points either to a problem with the injection itself or to a circulatory issue in the patient, such as cardiac or peripheral vascular disease.

After the retinal capillary bed fills, thin columns of fluorescein appear along the walls of the larger veins while the center of the lumen stays dark. The columns widen until the whole lumen is filled. It is a normal finding, not a filling defect.

About 30 seconds after injection, in the peak venous phase, once the veins have filled completely over the preceding ten seconds. This is the phase in which the perifoveal capillary network is best visualized, so it is the frame to protect when assessing the foveal avascular zone.

The mid or recirculation phase runs roughly 2 to 4 minutes after injection, with arteries and veins about equally bright and fluorescence slowly fading as the kidneys clear the dye. Late-phase images are captured about 7 to 15 minutes after injection; the CRA portfolio guide accepts any frame taken 5 minutes or later as late phase.

Transmission or window defect, leakage, pooling, and staining. Autofluorescence and pseudofluorescence are listed separately because they are apparent hyperfluorescence occurring without any dye in the eye.

A window defect stays the same size throughout the study and its brightness rises and falls with the choroidal fluorescence, because it is only loss of RPE pigment revealing normal choriocapillaris fluorescence. Leakage is extravasated dye, so it enlarges and intensifies as the angiogram progresses.

Blocked fluorescence, where material such as blood, lipid exudate, lipofuscin, xanthophyll, or melanin sits in front of the fluorescence, and filling defects, where retinal or choroidal perfusion is abnormal. Blockage is anatomic; a filling defect is vascular.

Staining is late hyperfluorescence from dye accumulating within tissue, seen in drusen, chorioretinal scars, sclera, and normally the optic nerve head. Pooling is dye collecting in a distinct anatomic space, such as the serous detachment of central serous chorioretinopathy.

Indocyanine green fluoresces in the near infrared, excited around 805 nm and emitting around 835 nm, so its light penetrates the RPE, blood, and serous fluid that obscure fluorescein. It is also about 98 percent protein bound, so it stays within the fenestrated choriocapillaris instead of diffusing away.

The normal adult dose is 500 mg, packaged as 5 mL of a 10 percent solution or 2 mL of a 25 percent solution, given as a bolus into a peripheral vein. The pediatric dose is adjusted to 35 mg per 10 pounds of body weight.

Only the unbound portion. About 80 percent of the dye binds to plasma proteins, and those bound electrons are unavailable for excitation. With a molecular weight of 376, free fluorescein diffuses out of every capillary bed in the body except those of the retina and central nervous system.

Transient nausea, sometimes with vomiting, typically starting 30 to 60 seconds after injection and lasting one to two minutes. It needs no treatment. Historical series reported adverse reactions in 5 to 10 percent of patients; a more recent large study found just over 1 percent.

OCT uses low-coherence interferometry to build cross-sectional images of the retinal layers, directly showing intraretinal and subretinal fluid and its depth. Because it documents edema non-invasively, it has essentially replaced oral fluorescein angiography for confirming cystoid macular edema.

Roughly 200 degrees of retina in a single image, against 30 to 60 degrees for a standard fundus camera, reaching far peripheral pathology in diabetic retinopathy and vein occlusion. Eyelid and lash artifacts are the main quality limit; CRA Portfolio B (100 degrees or wider) allows no more than 5 percent lid and lash artifact in most images.