Week 3 Flashcards
Q: Which region of the brain is responsible for controlling pupillary reflexes?
A: The pretectal area (aka the olivary pretectal nucleus, OPN)
Its important to understand the pupil reflexes both afferent and efferent pathways. Understand the direct and consensual responses. And understand that an APD occurs only if the lesion is anterior to the LGN.
Lecture: 54, Visual Pathways Objective 1: List five destinations of the optic tracts and their general functions.
Q: A 57 yo patient comes to your office after being hit by a baseball which he failed to see coming from his left side. Examination reveals that he sees nothing in his left visual field in both eyes except in the center of his visual field which appears to be spared. Where do you determine the brain lesion to be that causes the visual field defect, and what is the name for the phenomenon the results in maintained visual acuity in the central portion of the visual field?
A: The lesion is either in calcarine occipital cortex or in the optic radiations just anterior to the calcarine region. Sparing of the central visual field in such cases is termed “macular sparing.” Macular sparing after occipital vascular lesions is due to dual blood supply from posterior and middle cerebral arteries. Macular sparing after incomplete lesions can be due to the much larger portion of the brain dedicated to the fovea. Macular sparing is not seen with lesions earlier in the visual pathways.
Lecture: 54, Visual Pathways Objective 4: Identify brain lesion sites based on the location of a scotoma in the visual field, or on the nature of the visual field deficits.
Q: A lesion affecting the optic chiasm (position 2) produces what pattern of visual field deficit?
Lecture: 54, Visual Pathways
Objective 4: Identify brain lesion sites based on the location of a scotoma in the visual field, or on the nature of the visual field deficits.
Q: What light-sensitive cell in the retina is responsible for regulating circadian rhythms?
A: Melanopsin-containing retinal ganglion cells (RGCs)
Lecture: 55, Oculomotor pathways
Objective 2: Diagram or list the steps in the pathways for pupil constriction and dilation.
Q: A patient visits your clinic complaining of diplopia. You perform an eye exam and discover that the patients eyes converge well to focus on a single object, but when looking left, the right eye doesn’t move left. Where is this lesion, what is the term for the condition and what disease is it most often associated with?
A: Failure of the medial rectus in one eye during conjugate nasal eye movements, but a retained ability to utilize the medial rectus for convergent eye movements in the same eye is a clear indicator of a lesion affecting the medial longitudinal fasciculus (MLF). The condition is termed internuclear ophthalmoplegia (or ophthalmoparesis) and is most often seen in patients with multiple sclerosis
Lecture: 55, Oculomotor pathways
Objective: Explain internuclear ophthalmoplegia to a lay person or patient.
Q: The ideal, orderly arrangement of what material allows the cornea to be transparent?
A: Collagen I
Lecture: 56, Review of Anatomy and Physiology of the Eye
Objective 1: Explain the properties of the cornea and lens that make them transparent, and what could change this.
Q: Paralysis of the ciliary muscle would primarily cause difficulty focusing on objects near or far?
A: Near. When the ciliary muscle is relaxed, the lens is flatter and more capable of resolving objects at a distance. In order to focus on near objects, the ciliary muscle must contract around the lens (it acts as a sphincter making contact with 360 degrees of the lens’ equator via the zonule fibers)—this causes the lens to become rounder and focus near objects better.
Lecture: 56, Review of Eye Anatomy
Q: Obstruction of what outflow structure causes angle closure glaucoma?
A: Trabecular meshwork
Lecture: 56, Review of Eye Anatomy
Objective 3: Explain the role of outflow facility and aqueous flow rate in controlling intraocular pressure and ways in which high intraocular pressure could be corrected.
Q: Upregulation of what factor in response to hypoxia results in choroidal neovascularization?
A: Vascular Endothelial Growth Factor (VEGF)
Lecture: 56, Review of Anatomy and Physiology of the Eye
Objective 4: Describe differences between the retinal and choroidal circulations in terms of anatomy, flow rate, control mechanisms, and role in supporting retinal energy metabolism
Q: A mad scientist invents a drug that specifically targets and destroys rod cells. Would a victim of the mad scientist treated with this drug be able to read after the obliteration of all their rods.
A: Yes, the acuity of the fovea is overwhelmingly due to the high concentration of cones. However, vision in the dark would be very poor.
Lecture: 57, Retinal Anatomy and Physiology
Objective 3: Understand the distribution across the retinal surface of rods and cones and the significance for vision.
Q: What factor binds to ion channels in photoreceptor cells, allowing them to stay open in the dark and depolarize the cell so that it provides an inhibitory signal to ON bipolar cells?
A: cGMP
Lecture: 57, Retinal Anatomy and Physiology
Objective 2: Understand the basic cascade that mediates phototransduction in rods and cones.
Q: A patient presents to your clinic due to markedly decreased vision in the left eye. You decide to perform fluorescein angiography and notice the dye takes 45 seconds to reach the arteries of the left eye from the injection site on the arm. What is the most likely cause of this patient’s loss of vision in the left eye?
A: Fluorescein dye usually takes 8-12 seconds to reach the eye via the ophthalmic arteries (arm to eye). A delay in this transit time is usually due to occlusive vascular disease
Lecture: 58, Ophthalmology: Basic Eye Exam & Ancillary Testing
Objective 5: Describe the uses of basic ophthalmic testing (Fluorescein angiography, optical coherence tomography and visual field testing).
Q: A child who was hit in the left eye presents to your clinic with a swollen eye after being hit with a baseball. They exhibit mild proptosis and have a limited upgaze. What features of the orbital are most likely to have been fractured in this case?
A: The medial orbital wall mostly composed of the ethmoid bone and the orbital floor composed of the maxillary and zygomatic bones divided by the zygomatic suture, are possible areas of fracture. Given the limitation in upgaze, floor fracture should be most considered. Somtimes the eye can look sunken in (enophthalmos) as well.
Lecture: 59, Clinical anatomy of the orbit
Objective 6: Explain relationships of orbital anatomy to clinical problems (inflammation, masses, and trauma).
Q: A patient presents to your clinic complaining of eye irritation. Upon slit lamp examination with fluorescein you notice a branching pattern on her cornea. What part of her medical interview will most likely be most informative as to the etiology of this condition?
A: Branching lesions on the eye are indicative of herpes keratitis. The lesion itself is called a herpetic dendrite. Asking history about occurrence of cold sores around the lipds and sexual history may be helpful (although HSV can be spread by sharing silverware, glasses, kiss, etc).
Lecture: 60, Anterior Segment Disease
Objective 3: Identify different reasons an eye can be “red”. Be able to form a basic differential diagnosis for the red eye. Understand which types of red eye are due to local processes such as infection vs systemic disease.
Q: What is the central process that drives wet age related macular degeneration and how is it treated?
A: The physiologic change that result in vision loss in wet AMD is neovascularization (which is why it is also called neovascular AMD). Neovascular tissue breaks through the retinal pigment epithelium (RPE) causing exudation and destruction). Because it is driven by neovascularization, anti-VEGF treatments are the front line to block vascular endothelial growth factor
Lecture: 61, Posterior segment disease
Objective 5: Identify age related macular degeneration as a major cause of vision loss in the elderly and be able to differentiate between features of exudative vs non-exudative disease.