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CS TIPS_EYES_2010
| Question | Answer |
|---|---|
| Ptosis | A drooping of the upper eyelid indicative of a congenital or acquired weakness of the levator muscle or a paresis of a branch of CN III. |
| Xanthelasma | Depositions of lipids in the upper and lower eyelids indicative of abnormal lipid metabolism. |
| Blepharitis | Inflammation of the eyelid with associated crusting and itching. Caused by infection, autoimmune conditions, et al. (Expect bepharitis to be more generalized than a stye or chalazion, which are lumps or swellings of the eyelid). |
| Hordeolum (stye) | Infection of the sebaceous glands at the base of the eyelashes usually by Staphylococci. Painful. |
| Chalazion | A blockage of the meibomian (tarsal) glands on the edge of the eyelid. NOT Painful. |
| Conjuctiva (CLEAR) | Clear membrane (as opposed to the white sclera) covering the eye surface. Helps keep the eye moist and serves as a barrier to microbial invasion. |
| Conjuctiva (Conjunctivitis) | Inflammation of the conjunctivae caused by infection, or allergic reactions. Usually associated with an erythematous, cobblestoned appearance, especially on the posterior surface of the eyelid. |
| Arcus Senilis of the Cornea | a ring around the edge of the cornea caused by lipid deposition. A normal finding in patients >60 years old. In younger patients, this may represent a lipid metabolism disorder. |
| Corneal Light Reflex | Shine penlight directly at patient’s eyes. Look for the reflection off the cornea. It should shine equally on the nasal portion of each cornea. Asymmetry of the reflection may indicate strabismus and/or amblyopia. |
| Scleral Icterus | Jaundice or yellowing of the sclera secondary to hyperbilirubinemia |
| Exopthalmos | “Bulging Eyes” or an increased volume of orbital content. |
| Exopthalmos (bilateral) | commonly associated with Hyperthyroidism. Graves’s disease is a common cause of autoimmune induced hyperthyroidism especially prevalent in women. |
| Exopthalmos (unilateral) | consider a retro-orbital tumor or mass. |
| Strabismus | Patient cannot focus both eyes on an object simulatenously. May have deviation of one eye out of position relative to the other. |
| Paralytic strabismus | is caused by either weakness of an extra-ocular muscle or damage to the nerve supplying it |
| Non-paralytic strabismus | has no primary muscle weakness and is usually associated with intraocular pathology.If deviation is present it is called tropias. |
| Exotropia | turns outward |
| Esotropia | turns inward |
| Abnormal Pupils: Anisocoria | unequal pupils. Check pt’s history! Normal in 20% of healthy individuals. But may be associated with destruction of the sympathetic or parasympathetic pathways during trauma. |
| Abnormal Pupils: Miosis | “Pinpoint pupils!” Abnormally constricted pupils. Often associated with opoid abuse (e.g. morphine or heroin) |
| Abnormal Pupils: Mydriasis | Abnormally dilated pupils. Multiple causes including Midriatic drops, Midbrain lesions Hypoxia, Oculomotor (CNIII) damage, Acute angle glaucoma, Drug abuse, Psychedelics (e.g. LSD), Amphetamines (stimulate SNS), Antihistamines Tri cyclic antidepres |
| Pupils fail to constrict | Think PSNS problems |
| Horner’s Syndrome | Hemi-sided loss of the cervical sympathetic innervation to the face and eye. Results in ipsilateral ptosis (eyelid drooping), miosis (pinpoint pupil), vasodilation (warm, red skin), anhydrosis (lack of sweating). May be congenital or trauma or cancer. |
| CN III Palsy | Damage to CNIII results in ptosis (because orbicularis oculi is unopposed), mydriasis (remember the PSNS piggybacks on CNIII), abduction and depression of the pupil (eye shifts “down and out”). |
| Lens • Cataracts- | clouding or increased opacity of the lens leading to blurring or loss of vision. o Risk Factors: increased age, corticosteroid use, UV light exposure, smoking, diabetes mellitus. |
| Retinoblastoma | a malignant tumor of the retina often found in children < 2 years old. Usually presents with loss of the reflex in the affected eye and replacement with a white reflex instead. |
| Glaucoma | disease consisting of damage to the optic nerve usually caused by increased intra-ocular pressure from blocked exit of the aqueous humor from the anterior chamber of the eye. |
| o Open angle (chronic glaucoma) | Trabecular meshwork becomes blocked over time. Often asymptomatic except for gradual loss of vision over a period of years. |
| o Closed angle (acute glaucoma)- | opening between the cornea and iris narrows resulting in a rapid buildup of pressure. History: Intense ocular pain, blurred vision, visual halos, red eyes, dilated pupils, or rapid loss of vision. Systemic symptoms such as nausea and vomiting may present. |
| Fundoscopic Examination: Normal Strucutures | Fundus: posterior retina. Optic Disc- where vessels and nerve enters eye, should be yellow to creamy pink with well defined margins. Macula lutea- yellowish area without blood vessels where visual acuity is heightened. Contains the fovea. |
| Fovea | area of highest visual acuity on the retina. |
| • Physiologic Findings: Fundoscopic Examination | • Myelinated nerve fibers- soft, ill defined margins around the optic disc. No pigment changes visible. • Darker skinned patients will have more melanin pigment in their retina resulting in a darker overall appearance. See. Pic pg. 294 |
| • Papilledema | - caused by increased intra-cranial pressure o Optic disc loses definition, pushed out central vessels, and dilated veins. Venous pulsations not visible. Visual alterations are late findings. |
| Glaucomatous cupping of the optic disc | caused by increased intra-ocular pressure and the death of ganglion cells secondary to glaucoma. o Findings: cupping around the edges of the optic disc, blood vessels may disappear around the edge of the disc. |
| Drusen Bodies | usually caused by aging, associated with senile macular degeneration o Small discrete yellow spots on the retina that enlarge over time. |
| • Diabetic Retinopathy | o Background changes- dot hemorrhages, hard exudates (bright yellow lipid depositions [left pic]), soft exudates “cotton wool spots” (gray infracted tissue [middle pic]) |
| • Diabetic Retinopathy: o Proliferative changes | local hypoxia leads to neovascularization (new vessel growth), but the new vessels are weak and leak easily leading to hemorrhage and vision loss. [right pic] |
| • Hypertensive Retinopathy o Features: | Increased light reflex from the arterioles, arteriole narrowing, AV nicking, shiny retina, cotton wool spots (areas of infarcts seen at diastolic > 110 mmHg), flame hemorrhages, papilledma (late find assoc with malignant hypertension e.g. systolic > 200) |
| Hypertensive Retinopathy o Features: | hard exudates (cholesterol depositions) o Normal arterial-venous size ratio is 3:5, it will be decreased in hypertensive retinopathy as arterioles become constricted or fibrotic. |
| Pupils fail to dilate- | Think SNS problems. |
| Open Angle (Chronic Glaucoma) History | History: Tiny blind spots appear at the edges of the visual field, blurred vision, appearance of colored halos around lights, adjustment problems upon entering a dark room, repeated difficulties that new eyeglass prescriptions do not help |
| AV Nicking | Hypertensive Retinopathy |
| Cotton Wool Spots | Diabetic Retinopathy |
| Drusen Bodies | Macular Degeneration (Aging) |
| Retinal Hemorrhages in infant | Shaken Baby Syndrome. |
Created by:
ankurshah
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