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Episode Notes

Source / episode info

  • Episode: 436
  • Title: Divine Intervention Episode 436: Eye Findings and The USML Es (floridly HY for Step 1-3)
  • Published: 2023-01-17
  • Source: Episode page

One-liner

Episode 436 is a comprehensive review of high-yield physical exam findings focusing on the eye, covering pupillary reflexes (cholinergic/anticholinergic toxicity), cranial nerve deficits (INO, Horner's syndrome), retinal pathologies (CRAO vs CRVO, diabetic retinopathy), and systemic associations like hypertension, connective tissue disorders, and drug toxicities.

High-yield summary

  • Pupil Assessment: Miosis suggests cholinergic toxicity (e.g., organophosphates) or opioid use; dilated pupils suggest anticholinergic toxicity (e.g., tricyclic antidepressants).
  • Ocular Motility Defects: Internuclear Ophthalmoplegia (INO) is an issue with the Medial Longitudinal Fasciculus (MLF), presenting as adduction deficits, and can be seen in Multiple Sclerosis (MS); Parinaud syndrome suggests a vertical gaze center lesion.
  • Retinal Emergencies: Central Retinal Artery Occlusion (CRAO) is typically non-occlusive/emboli related; Central Retinal Vein Occlusion (CRVO) involves blood stasis, hemorrhages, and cotton wool spots.
  • Papilledema: Indicates increased Intracranial Pressure (ICP). Causes range from mass lesions to pseudotumor cerebri (Idiopathic Intracranial Hypertension).
  • Systemic Associations: Findings like AV-nipping suggest severe hypertension; yellow deposits (drusen) are characteristic of Age-Related Macular Degeneration (AMD); and the "oil droplet sign" suggests Outboard syndrome.

Learning objectives

  • Differentiate between the causes and clinical presentations of pupillary sphincter defects (e.g., CN II vs CN III).
  • Recognize specific retinal findings associated with systemic diseases (HTN, Diabetes, Connective Tissue Disorders).
  • Apply knowledge of cranial nerve deficits to localize lesions (e.g., MLF lesion vs. CN III nucleus lesion).
  • Understand the pathophysiology and differential diagnosis for papilledema and optic neuropathy.
  • Correlate specific ocular findings (e.g., white reflex, oil droplet sign) with underlying genetic or metabolic disorders.

Board exam buzzwords

ConditionKey FindingAssociationBoard Exam Tip
Internuclear Ophthalmoplegia (INO)Adduction deficit (unilateral)Medial Longitudinal Fasciculus (MLF) lesionTest for accommodation: If adduction is impaired but accommodation is normal, suspect MLF.
Methanol PoisoningOptic nerve hyperemia/edemaIngestion of windshield washer fluidTreat with Fomepizole or Ethanol (inhibits aldehyde dehydrogenase).
Graves' DiseaseExophthalmos / Bulging pupilsTSH receptor stimulation on fibroblastsThe combination of hyperthyroidism signs + proptosis is highly suggestive.
PapilledemaSwelling of the optic discIncreased Intracranial Pressure (ICP)Requires measuring CSF opening pressure; differentiate between mass effect and pseudotumor cerebri.

Rapid review table

TopicKey PointContextExam Relevance
Pupillary Light ReflexAfferent vs Efferent defectsShining light in the eye (Afferents via CN II) vs. Constriction response (Efferents via CN III).If both pupils fail to constrict, suspect a CN II defect (afferent problem).
CRAO vs CRVOCRAO is non-occlusive; CRVO involves stasis/hemorrhage.CRAO: Embolus (e.g., cardiac source); CRVO: Venous outflow obstruction.Look for cotton wool spots and flame hemorrhages in CRVO.
Papilledema WorkupElevated ICP diagnosisRequires imaging (MRI) and CSF pressure measurement.Pseudotumor cerebri is a key differential when mass lesions are ruled out.
Optic Nerve GliomaAssociated with NF1/Lisch nodulesNeurofibromatosis Type 1The presence of hyperpigmented iris nodules (Lisch nodules) strongly suggests an underlying neurocutaneous syndrome like NF1.

Board-speak -> diagnosis

Board-speak / Vignette phraseDiagnosis / ConceptWhy it fits
A patient with a history of opioid use presents with bilateral miosis and respiratory depression.Opioid Toxicity/Cholinergic SyndromeOpioids cause profound respiratory depression, while the pupillary findings (miosis) are characteristic of central nervous system depression or cholinergic excess.
The patient has difficulty adducting the left eye when tracking an object laterally, but accommodation is intact.Internuclear Ophthalmoplegia (INO)INO specifically affects the MLF, causing adduction deficits without affecting the ability to focus (accommodation). This points away from a CN III or optic nerve issue.
A newborn examination reveals a white reflex instead of the expected red reflex.RetinoblastomaThe white reflex indicates leukocoria, which is highly suspicious for retinoblastoma and requires immediate investigation due to its association with increased risk of osteosarcomas.
On fundoscopic exam, there are flame-shaped hemorrhages and AV-nipping in the retina.Severe Hypertension / Hypertensive RetinopathyThese findings reflect chronic, severe increases in blood pressure leading to vessel damage (AV nicking) and leakage/hemorrhage.
A patient presents with a history of multiple MI events and has an eye that is displaced downward and inward.HomocystinuriaThe characteristic ocular finding associated with homocystinemia is the downward and inward displacement, often accompanied by marfanoid habitus (though Marfan's itself is autosomal dominant).
A patient presents with a bulging pupil acutely; if chronic, they are tachycardic and have E-fib.Hyperthyroidism / Graves' DiseaseThe combination of hyperthyroid signs (tachycardia, tremor) and proptosis/bulging pupils strongly suggests Graves' ophthalmopathy due to TSH receptor stimulation on fibroblasts.

Differential diagnosis / distinguishing features

Pupillary Constriction Defects

Key FeaturesDistinguishing FindingsNext Step
Afferent Defect (CN II issue)Both pupils fail to constrict when light is shone in either eye.Test other C Ns; investigate optic nerve pathology (e.g., papilledema, optic neuritis).
Efferent Defect (CN III issue)One pupil fails to constrict regardless of which eye the light shines into.Check for associated signs of CN III palsy (ptosis, muscle weakness); rule out compression/ischemia.

Ocular Motility Palsies

Key FeaturesDistinguishing FindingsNext Step
Internuclear Ophthalmoplegia (INO)Adduction deficit only; accommodation is intact.Test for adduction deficits while keeping head fixed and testing accommodation.
Oculomotor Nerve Deficit (CN III)Ptosis, dilated pupil, weakness in all extraocular movements.Check pupillary reaction to light; assess for associated cranial nerve palsies.

Management pearls

  • Methanol Poisoning: Treat with Fomepizole or ethanol. The goal is to inhibit aldehyde dehydrogenase (ALDH) and prevent the formation of toxic aldehydes like formaldehyde and formic acid.
  • Retinoblastoma Screening: All children presenting with leukocoria (white reflex) must be evaluated for retinoblastoma, which requires screening due to its association with osteosarcoma risk.
  • Pseudotumor Cerebri Management: Treatment involves addressing the underlying cause of elevated ICP; medical management includes high-dose topical/oral corticosteroids and sometimes lumbar punctures or optic nerve sheath decompression.
  • Papilledema in Child Abuse: Always consider child abuse when finding papilledema, especially if accompanied by hemorrhages or signs of trauma.

Don't miss

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The difference between a true CN III palsy (which often involves pupil involvement) and an MLF lesion (which spares the pupil).
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Lisch nodules are hyperpigmented iris hamartomas strongly associated with Neurofibromatosis Type 1 (NF1).
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Homocystinuria: Is an autosomal recessive disorder leading to intellectual disability, marfanoid habitus, and ocular findings like downward/inward eye displacement.
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Outboard Syndrome: Caused by a defect in the COL4 A5 gene, resulting in Type IV collagen defects that manifest as lens luxation (lenticonus) and sometimes anterior lenticular synechiae.

Integration & clinical reasoning

  • Systemic Disease Integration: Ocular findings are often the first clue to systemic disease. For example, finding AV-nipping suggests chronic hypertension; finding yellow deposits suggests AMD.
  • Pharmacology/Ophthalmology Link: Be aware of drug toxicities affecting vision (e.g., Hydroxychloroquine retinopathy, Methanol poisoning). Always consider a full eye exam when starting new medications.
  • Neurology Integration: Ocular motor deficits require careful localization: Is the problem in the nucleus (CN III), the tract (MLF), or the muscle? This dictates the differential diagnosis.

OMM / COMLEX integration

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For COMLEX: know these viscerosomatics / Chapman points, but don't let OMM distract from emergent diagnosis and management.
  • Emergency Management Priority: In any acute ocular emergency (e.g., suspected CRAO or severe uveitis), standard ophthalmological/ophthalmic care takes absolute priority over OMT assessment.
  • ICP Monitoring: When evaluating for elevated ICP signs like papilledema, the primary focus is on ruling out acutely life-threatening causes (mass effect, hemorrhage) before considering non-invasive measures.

Concept connections / cross-references

  • For detailed information on systemic connective tissue disorders and vasculitis, see [ Episode 15 ].
  • For comprehensive review of metabolic disorders and genetic syndromes, see [ Episode 20 ].

High-yield association table

ConditionAssociationMechanismClinical Significance
Internuclear Ophthalmoplegia (INO)Adduction deficit; MLF lesionDamage to the Medial Longitudinal Fasciculus (MLF) in the brainstem.Suggests a central neurological process, often seen in MS or multiple sclerosis.
Graves' DiseaseExophthalmos / ProptosisAutoimmune stimulation of TSH receptors on fibroblasts.The combination of hyperthyroidism and proptosis is highly suggestive; requires careful monitoring for orbital complications.
Methanol PoisoningOptic nerve edema/hyperemiaFormation of toxic aldehydes (formaldehyde, formic acid) from metabolism.Requires immediate antidotal therapy (Fomepizole or ethanol).
HypertensionAV-nipping; Flame hemorrhagesChronic high blood pressure damages retinal arterioles and venules.Indicates severe, long-standing systemic hypertension requiring aggressive management.

Key terms glossary

TermDefinitionContextExample
LeukocoriaWhite or grayish reflex seen on fundoscopic exam instead of the red reflex.Ocular examination; highly suspicious for retinoblastoma.A newborn with leukocoria requires immediate screening for malignancy.
LenticonusCongenital narrowing/curvature of the cornea due to collagen defects.Genetics/Ophthalmology; associated with Outboard syndrome (COL4 A5 defect).The "oil droplet sign" or pinpoint expansion of the eye suggests this condition.
Pseudotumor CerebriIdiopathic Intracranial Hypertension (IIH); elevated ICP without a mass lesion.Neurology/Ophthalmology; causes papilledema and headache.Diagnosis requires ruling out secondary causes and measuring high CSF opening pressure.
Adduction MyastheniaDifficulty moving the eye inward (adducting) when head is fixed.Ocular motor assessment; suggests an MLF problem, not a CN III issue.Testing for adduction deficits while keeping the head still helps localize the lesion to the MLF.

Study optimization

TopicStudy ApproachPriorityResources
Oculomotor ExamPattern recognition; differential diagnosis based on specific findings (e.g., miosis, adduction deficit).HighReview board-specific vignettes and clinical pearls for CN deficits.
Retinal PathologyLinking systemic disease to retinal signs (HTN -> AV-nipping; DM -> PDR/CWS).Medium-HighFocus on the mechanism of damage, not just the finding itself.
Toxicology/PharmacologyKnowing drug side effects that affect vision or CNS function.HighMemorize antidotes (e.g., Fomepizole for methanol; Atropine for anticholinergic).

Question pattern recognition

  • Pattern: Adduction deficit with normal accommodation -> MLF lesion. This strongly suggests Internuclear Ophthalmoplegia, which is often seen in MS.
  • Pattern: White reflex on fundoscopic exam (Leukocoria) -> Retinoblastoma. Always assume malignancy until proven otherwise; requires screening for associated risks (e.g., osteosarcoma).
  • Pattern: Papilledema + headache/vomiting, but MRI is normal -> Pseudotumor Cerebri. This diagnosis requires measuring the CSF opening pressure to confirm elevated ICP and rule out secondary causes.

Test yourself

Common mistakes to avoid

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Mistake 1: Confusing CRAO and CRVO. Remember, Central Retinal Artery Occlusion (CRAO) is usually due to an embolus/non-occlusive event; Central Retinal Vein Occlusion (CRVO) involves blood stasis, hemorrhages, and cotton wool spots.
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Mistake 2: Assuming all papilledema means mass lesion. Always consider Pseudotumor Cerebri (IIH) as a diagnosis when imaging is negative but ICP remains elevated.
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Mistake 3: Misinterpreting the pupillary reflex. Remember that an afferent defect (CN II) affects both pupils equally, while an efferent defect (CN III) affects one pupil unilaterally.

Common traps

⚠️
Trap 1: The "Adduction Deficit" Trap: If a patient has adduction deficit but normal accommodation, the answer is MLF. If they have adduction deficit AND impaired accommodation, suspect CN III or optic nerve pathology.
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Trap 2: The "Papilledema Cause" Trap: When presented with papilledema, do not assume it's always due to a mass lesion; consider IIH/Pseudotumor cerebri first if the MRI is negative.
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Trap 3: The "Cataract Cause" Trap: While age is the biggest risk factor for cataracts, remember that steroids and galactosemia are critical secondary causes that must be considered in a differential diagnosis.

Original transcript with highlights

Original transcript with highlights

Okay, welcome. My name is divine. This is episode 436 of the Divine Intervention Podcasts. In this podcast, I'm gonna be addressing high-yield physical exam findings on the USML Is and today I'm gonna be focusing on the eye. High-yield physical exam findings on the USML Is. I'm gonna be focusing on the eye. I'm just gonna put this out right there right now. This podcast is very high-yield. This stuff you will see it on your exam. This is one of those things you can pretty much guarantee. Step one, step two, step three, complex one, complex two, complex three. Literally, it doesn't matter. You're gonna see the stuff on your exam. In fact, if you're a resident preparing for your residency exams, you'll very likely see the stuff on your exam as well. For whatever reason, the USML Is, they focus very heavily on the eyes and the still of the eye can tell you exactly what may be going on in the patient on an exam. So today, I just want to point out certain clues that can guide you in certain directions on you on your exam. So first, let's look at the poop hills. So what if they give you a question about a person that has popularly meiosis? You see a question about a person that has popularly meiosis? What should you be thinking about? I really hope you're saying divine. I should be thinking about either opioids or some kind of colinegic toxic oil. Obviously with an opioid, the person is gonna have a profound respiratory depression. That's gonna be a very big thing.

But with a colinegic toxic drum, the person will have a lot of leakyness. They have a lot of diarrhea, a lot of rain, a lot of vomiting. They have a lot of abdominal pain and things like that. And you could also have a pretty cardio because remember your parasympathetic system is gonna slow down conduction through your AV node. And then if you see my dry assesses, again, think about either like a sympatomymeric toxicity or some kind of anti-colineurgic toxicity, right? Anti-colineurgics, right? So things like your tricyclic antidepressants, they can absolutely cause anti-colineurgic toxicity. And also don't forget like things like diaphidraminocrophaneuramine, those are anti-histamines that have a very powerful anti-colineurgic activity. Those people will be dry, they'll be very, very dry, they'll have a lot of constipation. If you see sympatomymetic cells that cause of the myiosis, then you know, you're probably thinking more along the lines of like cocaine intoxication or methamphetamine intoxication, things like that. Now what if you see a person that has bulging poop pills? So persons poop pills are bulging. When you see bulging poop pills on your exam, I want you to, if you see that in a race acutely, they have like a rock heart poop pill. I hope you're thinking about a curango-crocio glaucoma. But if you notice that, you know, these person has had bulging poop pills for a while. And the person is tachycardic, the person has e-fib, the person has led lag.

I want you to think about hyperthyroidism. I want you to think about greas' disease. Because remember, your fibroblast also expressed TSE receptors. So those tyrosystemalitin aminoplopulins, they will stimulate those TSE receptors. And on the fibroblast, you'll make them secret like a lot of glycosaminoglycans. And those things can absolutely cause the eye disease. And that also causes some of the the pre-tibial misidimine, you may find people that have hyperthyroidism. And then what if they give you a question about a person, you shine light in a poop pill. Hey, you notice that, wow, both of the poop pills do not constrict. Well, that's going to tell you that, hmm, this person seems like they have a relative offering popularity effect. It's pretty classic, right? Because remember, when you shine light in a person's eye, it goes in through crinonof two. And then that singular crinonof two projects to both crinonof threes, and you have bilateral popularity construction. If both poop pills do not constrict, that tells you that, oh, okay, well, the information must not be getting it. That's a crinol two defect. That's an offering popularity effect. But if there's an offering popularity effect, then there's going to be an efferent popularity effect. An efferent popularity effect, right? Remember, it'll be a person, regardless of the where you shine light in the person's eye, you'll notice that there's one poop pill that persistently does not constrict.

Because remember, in an offering popularity effect, when you shine light in the affected eye, both poop pills are not constrictable. When you shine light in the unaffected eye, both poop pills will constrict. But in an efferent, in an efferent popularity effect, it doesn't matter what eye you shine light in. The eye that is affected, they will always be one eye that is persistently not constricting. So if you notice an offering popularity effect, both eyes is an all-enough thing. Either both poop pills constrictor don't constrict. But in an efferent popularity effect, again, there are many different permutations of this, but I'm just discussing the classic classic effect. In an efferent defect, especially if it affects one eye, that one eye will persistently not constrict. Because there's no issue with information going in. There's lots of provincial information coming out. And then, what if they give you a question about a person, they tell you that, ooh, they're heads these fixed and they're trying to follow a movie object in the horizontal plane. And then they tell you that, ooh, this person has they have an adduction, not adduction adduction, AWD, auction, nice tagmas. Well, when you see that, I really hope you're thinking about a person that has interneclyophthalmoplesia. That's pretty classic with people that have multiple sclerosis. That's an INO problem, right? That's an MLF problem. And it's going to be the Ipsilateral MLF.

It's going to be a problem with the MLF on the same side as the affected eye. So if you're pressing, like you keep your head fixed, then you're told, ooh, look right. Like, object is being moved to the right. You're right, I supposed to AB docked. And then your left eye is supposed to AD docked. So if you have adduction, my statmas, then that tells you that, ooh, there must be something wrong with that I, that MLF, that feeds that I, that MLF that feeds that left eye is affected. So the person has a left MLF problem. And remember, my statmas, you can also find it as a component of wany keys. Remember, wany keys usually has a triad, right? It's like confusion of the amoplesia, which is usually my statmas and e-taxia. So just going to keep that in mind, you know, certain drugs of abuse can certainly be associated with my statmas. Just something you kind of want to, want to keep in mind. And again, some of you may be like, oh, divine. So you just said MLF, you know, you're going to have issues with adduction. Well, how do I differentiate an MLF problem from an actual bona fide cranial three issue? So the thing is when you have an MLF problem, you're going to notice that you have an AD docked my statmas. That's true. So you may be like divine. How do I tell that this is an MLF issue versus a meteorite decision? Well, the way you're going to tell those apart is literally by testing a commodity. So take an object and you bring it closer to both pupils.

If both pupils can adopt, if both media or retire can do their job, then that tells you that the person has more of an MLF issue and not a cradion of three issue. If you have a cradion of three issue, you're going to have problems with popularity. You're going to have issues with adduction of both pupils. Accommodation is not, is not going to work. So if you have adduction, my statmas, what accommodation is intact, the person has an MLF problem. But if you have adduction, my statmas, an accommodation is not intact. The person has an oculum or nerve problem. The person has an adverb or a cradion of three issue. And then what if they give you a chest x-ray about a person that has been a long-term smoker? And you notice that one side on the very top of the lungs, one side looks black, looks normal. Well, the other side looks very white at the top. And then they tell you that the person has like popularly ill-ses and they may have like hand weakness. If you see that, I really hope you're saying, ooh, divine. This sounds like a punk-host tumor. A punk-host tumor. Remember, sometimes we call these things a superior sulcus tumor. That can be a derivative term that you miss hearing the exams. That can be a derivative term you see on the exams. And then, so obviously, the person has a tumor that's, you know, compressing the sympathetic chain that goes to the eye, the cervical sympathetic chain. So they're going to have a horner syndrome.

Remember, in a horner syndrome, you're going to have two cysts, you're going to have a droopy eyelid, you're going to have meyosis, you're going to have an high droopy. And again, they can give you a question about a person that you know, suddenly, they develop this droopy eyelid and they have like this blue and blue peel. Right? Obviously, that person is having an uncle coronation. Remember, the uncle is the most medial portion of that temporal lobe. So that uncle, if he compresses cranial nerve three, that's going to be a problem. Because if you compress cranial nerve three, then you're not going to be able to have pulmonary meiosis. So you're going to have my dry asses. And again, you're also going to have a droopy eyelid. You're going to have a droopy eyelid because your nevato poppulpurus superioris is not functioning perfectly as it should. Again, I'm just trying to give you the different physical exam findings you may see in the eye and it may give you a certain direction concerning a disease. Because the imbi needs, again, to date test pure eye diseases, finally do. And I'm going to talk about some of them here. Well, many times the test eye diseases in the context of systemic pathologies. And again, if you like the way I'm integrating things, you may be interested in the courses that I have to offer. I do have a few courses that are going to be coming up within the month. I have a test taking class.

I'm sure you're taking please this Friday from 5 to 7 30 pm, mountain standard time. It's for step two and step three. And also for step one, for the clinically focused questions on step one, I have a 20 hour review course. I'm going to be taking place on the 23rd and 24th and the 26th and 27th of this month. It's going to be, you know, five hours each of those four days. And we're going to review a ton of stuff from internal medicine, surgery, peds, OB-GYN, neuro, psychiatry, multi-systems, processes, and disorders. And then if you struggle biostatistics, I'll encourage you to consider the class on the 30th of this month. It's for step one to step three. And then the social sciences and ethics class is also for step one to step three. As we know, social sciences and ethics is now 10 to 20 percent of all the USML exams, step one to step three. So if you want to get a very solid grounding in those things, then you want to consider attending one of these classes. Many people have taken these classes from them to be supremely helpful. Because again, I'm not going to give, beginning your lectures. I'm going to give you scenarios. And I'm not just going to be three scenarios that you're going to be giving you a puff of fist. I'm going to help you actually understand what's going on. And then if you're taking your step one or complex one exam, so you're taking step two or step three or complex two or three, they have a poor basic science foundation. I have a step one review class.

It's a 25 hour class. It's going to be taking place next month. We held the first iteration of this month. Many people found it to be extremely beneficial. I think you'll also find it to be beneficial. So let's go ahead and continue. So what if they give you a question about a person? And the person will tell you that for the past few months, the person has been having an upward gase policy. They tell you, you know, in the office, you tell the person to look upwards and they cannot. I would encourage you to think about Parynode syndrome. I want you to think about a Pinyloma. A Pinyloma, remember, it's a Pinyogland tumor. The Pinyogland is just above the superior polyculous. So if you have a Pinyloma, it can literally compress the superior polyculous. And the superior polyculous is your vertical gase center. It's not going to work properly. Although remember, if you also have a stroke of the superior cerebellar artery, that can also cause Parynode syndrome because the superior cerebellar artery is the blood supply to the superior polyculous. So that can be a vascular cause of Parynode syndrome. And also remember, if you see upward gase policy and you see a person, they have like shaking hands, they have like a lot of movement issues. I want you to think of progressive super nuclear policy, progressive super nuclear policy. That's something that's classically found in Parkinson's disease. And then what if they give you a question about a person?

And they tell you that the person has been having visual difficulty. They tell you that they have an offering popularity effect in like an eye. So you notice that you're highlighting that popular and both popules are not constrict. And then they tell you that this person has all these hyperpigmented visions on their skin. Then I'll really hope you think about the optic nerve gliomas that are characteristic of neurofibromatosis type one. Remember, in F1, you don't just get crinon of two gliomas, but you can also get brown discolourations around the iris. Those are the things that are known as the Lesh nodules. Those are the things that are known as the Lesh nodules. And then what if they give you a question about a person? They have like very significant eye pain, very significant fevers. And then they tell you that you see ulcers that have a danger form appearance in the eye. When you see something like that, I really want you to think about herpes. I want you to think about herpes, keratitis. Don't forget the association with dangerous ulcers. What if they give you a question about a person? It is a newborn. And they tell you that this newborn, you know, when you're, when you, you go from the scopic exam, you observe a white reflex. Instead of a red reflex. Then I'll really hope you're saying, define this sounds an awful lot like a retinoblastoma. A retinoblastoma. Remember, retinoblastomas are from an RBG mutation.

When people have retinoblastomas, it increases the risk of osteosiracolmins in the future. And then what if they give you a question about a patient? They tell you that this patient has had multiple myocardial infarctions, multiple heart attacks. And they tell you that on on physical exam, on on for the scopic exam, they notice a downward and inward displacement of the pulpial. Well, if you see that, I really hope you think about homocystinuria. Homocystinuria. Remember, homocystinuria is an autosomor recessive disease. It's not autosomor dominant. It is autosomor recessive. It is autosomor recessive. And it's it's a deficiency of an enzyme known as cystothionein beta synthase or, you know, the empty HFR gene like meth, methylin tetrahedral folate reductis, that's another name. But if you have mutations in those enzymes, you're going to have issues with breaking down homocystin. And homocystin can, it can form a lot of bonds with stuff. So it can cause you to have like a lot of myocardial infarctions. It can cause you to have a lot of issues, a lot of atherosclerotic, vasculaic issues. So you want to kind of keep that at the back of your mind because remember, those people can also have a marphornoid happiness. So since there is a downward and inward displacement of the eye in homocystinuria, what do we find in marphans? Remember in marphans, those people are going to have an upward and outward displacement of the eye.

So remember, people that have marphans, do have marphans, is autosomor dominant in heritans. And people that have marphans, they have normal intelligence. People that have homocystinuria, they tend to have intellectual disability. Now, what if they give you a question about a patient? They tell you that this patient, you know, in their family, many people have eye problems, many people have hearing problems. They tell you that you see red blood cell casting the person's urine. And in detail, that on physical exam, you notice that this person has like what is called like an oil droplet sign. In fact, sometimes they call this anterior lenteconus. It's almost like they have like this pinpoint expansion of their of their of their eyes. If you see that, I really want you to think about outboard syndrome. There's this canola's lenteconus. Like, literally, their eyes because they have that collagen, that type of collagen defect. Remember, the gene defect is CUL45 because they have that type of collagen defect. Their their their cornea is not is not well shaped. So it looks like a corn. That's what's called lenteconus. lenteconus. If you see that, again, in the context of the other stuff, think about outboard syndrome. I want to see something about the USM in exams. They're going to answer your questions by just knowing one fact about the eye. You know, you need to know the context.

Notice, I'm supplying the eye findings, but I'm also supplying some of the other context that you may see on on your exam. Now, what if they give you a question about a patient that has a CD4 count of 50, you know, IV drug user or a person that has sex with like men having sex with men. And they you notice that this person has these white necrotic lesions in the eye. Well, I really hope you think about CMV or at night. So remember, CMV is one of the most common causes of retnightis in HIV patients. Remember, the way we treat CMV is with a gun cycle over here. We'd gong up on CMV with a gun cycle over here. Remember, again, CMV is one of those herpes viruses. And then what if they give you a question about a newborn that has lens or pacification, a newborn that has lens or pacification. So a newborn that has cataracts. If you see a newborn cataracts, then don't you think about some kind of galactose issue whenever you have excess galactose. So, see, for example, you have like galactokines deficiency or you have like essential galactose similar way you have a deficiency of galactose one force video radio transfer is galactose one force video radio transfer is we have a deficiency of those enzymes. You're going to build up a lot of galactose. I mean, be like divine. Who cares about the galactose? We'll let me tell you what you should care. That galactose is an all those sugar. There's such a thing as all those reductives in the body.

Now convert that galactose to galactitol radio, you'll convert that sugar to an osmotic something that's very osmotic. And I think in cause or pacification of the lens, it can absolutely cause cataracts. And you know, by the way, if you see an old person that is having trouble reading signs at night or they have trouble reading in the dark, they want to think about a person that has cataracts. Remember, age is the biggest risk factor. That's very high, you'll to know. Age is the biggest risk factor for cataracts. But there are many other things that incose cataracts like steroids, steroids can absolutely cause cataracts. Something you want to keep at the back of your mind. And then don't forget that if they give you a question about a person, the heart's heart failure will start it on a drug and they have yellow green vision. I want you to think about the juxtaposition. Remember, the juxtaposition can cause yellow green vision. Don't forget that you can also have like problems with vision if you're thinking of thambiotol. If thambiotol is one of those drugs that we use in the right pregnant for the management of TB. We use it in the right pregnant for the management of TB. And again, what did they give you a question about an old person? And they tell you that this old person giving lines don't look straight anymore. And the person has a lot of yellow deposits in the eye.

If you see that, I want you to think about age related, macular degeneration, those yellow deposits you're seeing in the eye is something that's known as drowsing, something that's known as drowsing. Those yellow deposits of drowsing are found in the eyes of people that have age related macular degeneration. And then what if they give you a question about a person that had a recent MI or they tell you that this person has an irregular heart beat. And then they tell you that they have the sudden loss of vision in one eye. And they tell you on physical example, notice fondle power like the fondle of the eye looks white. It shouldn't look white. If you see that, that means blood is not coming to the eye. That person has a central retinal artery occlusion. They will usually give you, they usually give you the relevant history like recent MI or pass medical history of e-fib. But if you're comparing a CRAO to a CRAO, central retinal vein occlusion, remembering people that have CRAO is not a blood-comminging problem, is a blood accident from the eye problem. So blood hydrostatic pressures of the blood vessels in the eye are going to build up. So you're going to have a lot of extravacition of blood. So those people, the thing that's going to happen is they're going to have fondle redness, they're going to have a lot of hemorrhages. Their eyes are going to have cotton wool spots, they're going to have this blood and fondle appearance of the eye.

Remember if you see cotton wool spots in the eye, don't just think of CRAO, you can also think about diabetic retinal pathy, especially people that have diabetes for a very prolonged period of time. Remember diabetic retinal pathy can come in two flavors. It can come in the proliferative flavor or in the non-proliferative flavor. Though you're going to see cotton wool spots in many, in almost both of them. But if you see a lot of blood vessels, if you see the term neo-vascularization, proliferation of blood vessels within the eye, then you want to think about a person that has proliferative retinopathy, proliferative retinopathy. I remember that proliferative retinopathy with trade with laser, photo-coagulation, laser photo-coagulation. Now what if they give you a question about a patient? They tell you that this patient is a diabetic and then you have the sodium on said vision loss in one eye and it's a painless vision loss. And they tell you on one of those copy exams, you see these floating bodies in the eye, you see floating bodies in the eye. If you see something like that, you want to think about retinopathy. Because think about it when you're diabetic and you have proliferative retinopathy. All those blood vessels that are proliferating, they're going to be playing like a tug of war with your retina. If you proliferate enough, you'll have enough power and force to literally yank down your retina. If that happens, you're going to get a retina retina detachment.

Now what if they give you a question about a patient? They tell you that this patient is, you know, it's like a one or two-year-old having a lot of motor problems, having a lot of neurological issues. And you see a chariot spot in the eye. If you see a chariot spot in the eye, then I want you to think about T-Sax disease. Some of you may be like, divine, but you remember chariot spots can also be found in Neem and PIC. So how do you differentiate both? Remember in T-Sax disease, they'll have a chariot spot in the eye, but they will not have a pato-splino-megaly. But people that have Neem and PIC and addition to having said chariot spot, they will also have a pato-splino-megaly. Remember T-Sax disease is a deficiency of hexosamony Bs A, so you have a build-up of GM2 gangbliocyte. But when people that have Neem and PIC disease, it's a deficiency of Sphingo-Milinis. Sphingo-Milinis. Sphingo-Milinis is a lipid derived agent. So those people again, remember in Neem and PIC, they will also have issues with pato-splino-megaly because they're going to have issues as well within their particular endothelial systems. That's basically the lever and the splint. So they're going to have pato-splino-megaly. I've talked some more about pathophysic and my life. It's a story of diseases, podcasts. So you can go ahead and listen and listen to that. That something is pretty high up to know there. And then what if they give you a question about a person that has tunnel vision?

And you see that it's a child. If it's a child, they want to be thinking about a craniofarin-juma. Remember those things that are derived from Rathke's pouch. They can compress the optic chiasm and you have bite temporal hemianopsia. But if you see it in an adult, they want to think about a pituitary adenoma. Probably like a prolectinoma. Remember prolectinomas can cause low libido, they can cause gynecomastia, they can cause gallatbrilla. So keep those things in mind. Criofarin-juma is usually more in kids. Pituitary adenomas like a prolectinoma, which is the most common. Usually find out, find that in. And I do. Remember prolectinomas, I'm going to respond very well to dopamine agonists like a bregulin or bromo-cryptin. And then what if they give you a question about a person? They tell you that this child has hemorrhage in the eyes. But they tell you that this child has been coming for the last few weeks and the immunization history is not known. They want to think about peritosis. Remember peritosis, I think of it as the cough plus disease. You're going to have a really, really bad cough. But crazy stuff is going to happen. You can vomit as a result of set cough. You can pass out, have syncopal episodes from set cough. You can have a hemorrhage in the eyes because they're just coughing so hard. So you're literally raising the pressure so suddenly in the eye. They can literally blow the blood vessels in your eye. Remember we're going to treat that with aerithromycin.

We're going to use a microlitre. And you don't just treat the patient. You're going to treat the close, the close contacts of that person. And then what if you see a person that has a bulging or take this person that has papilladema? Well if you see a person that has papilladema, it's a little child. Unless it's a child of a teenage mom or you know, they tell you that the child has these weird fractures that has come to the emergency room many times. Think about child abuse. Think about child abuse. Remember in child abuse, you can see papilladema, you can see right no hemorrhages. But if you see this same situation, you know papilladema in a person that has this really studying on set severe headache, you probably want to think about some kind of stroke like a sub-arachnoid hemorrhage. That person is having a buildup of intra-cranial pressures. But if they give you a question about a person that is on acne therapy of some sort or a person is an obese woman or a person is on all trans-retinoic acid for EML or the person is on some kind of therapy for just acne or like on a tetracycline for example. And you see they have papilladema, it's an obese woman, she has like chronic headaches and all these things. They don't want to think about pseudo-tomo cerebride. When you think about pseudo-tomo cerebride, remember another name for that disorder is idiopathic intra-cranial hypertension. Those people are going to have very high CSF opening pressures.

It's really over 200 on the immune exams. And then what if they tell you again about cotton wool spots, again I've talked about, you can have this endabetic retinopathy, you can also actually have this in systemic hypertension. You see flame-shaped hemorrhages in the eye. Think about systemic hypertension. In a very old podcast I've talked about this concept of AV-nicking, heterovienosnicking. Basically the thing that happens there is that the vessels in your eye, they're going to look like copper wires like silver wires. I'll encourage you like these different pathologies I mentioned and you'll have mentioned a lot. I'll encourage you to just look up examples of this. So if you see them on your exam, you can recognize them. But that AV-nicking, usually indicates that a person has very severe hypertension, like from renal otterists to no season, no person or fibromuscular dysplasia in a younger female. A person has like conned syndrome, really half primary, high-proud, no-stronism. Those things can all cause significant severe hypertension. What if they give you a question about a person, they tell you that this person had just had an MI recently, went to the cath lab, was revascularized, the stent was placed. And then they tell you that this person, you can see these refractal-godim buddies in their eyes. If you see that, I want you to think about cholesterol and volization syndrome.

Those things you're seeing in their eyes, as they did the cardiac cath, as they put the stent in the coronary vessels, they pretty much dislodged cholesterol crystals all over the body. Those cholesterol crystals can go to the eye. When they get to the eye, they're known as Hulenhorst plucks. Hulenhorst plucks, H-O-W-L-E-N-H-O-R-S-T, Hulenhorst plucks. Just keep that in mind when a person has a cholesterol and volization syndrome. And then what if a person has this sodium onset vision loss, like it sounds like a curting that's coming down, you want to think about amorosis fugax. Usually that's a person that has like a curated problem, they have like a TIE pretty much, a scossing hypoper fusion of the eye and they're getting in trouble. And then what if they give you a question about a person that you know has these neurologic deficits that come and go and it's a female in her 30s and they tell you that this person has this painful sodium onset of vision loss and the person you know is just not doing well. You want to think about optically arthritis. Remember optically arthritis is a characteristic finding in multiple sclerosis. And by the way, it's an ophthalmologic emergency. Those things are going to need an mRNA of the brain and MRI of the brain with IV contrast. They're going to need IV steroids. If you don't treat them, they're going to be complied. I want to keep that in mind.

And remember if you see a person that is beginning to have vision problems on one eye, I you notice that, hmm, these people have this unilateral headache. You want to think about a person that may have a claustrahedic, one thing about claustrahedic, that's a usual presentation. Usually people that have claustrahedics, they'll have tearing from that pupil and things like that. But also don't forget temporal arthritis, especially in a woman that's over age 50, temporal arthritis, sometimes we call it giant cell arthritis. Something you want to keep at the back of your mind, for example. And then remember, what if they give you a question about a person, they tell you that this is a lady in her 40s and her 50s. She tells you that she has been having trouble seeing that night. And then they tell you that during the physical exam, you keep testing an apopial, testing an apopial, testing an apopial. And over time it becomes droopy. That person has myostiniae gravis. That lady literally has myostiniae gravis. Because you notice her symptoms are fatigable. It literally gets worse with use. I talked about myostiniae gravis. I believe in the literally episode 455. Remember, those people have anti-nicotinicacidoculin receptor antibodies. And then if you see a person that has dry eyes, don't forget about show grains. Remember in show grains, those people have these different antibodies that can attack like the lacrimal glands, the silvery glands so they can have dry eyes and dry mouth.

And then don't forget, if you see anterior U Vitis, in a person that has chronic joint pain as a kid, think about oligoticula, JRA. Those people need amylslytlamp exams. And then don't forget that sarcoidosis also is associated with U Vitis. And please, please, please, please, don't forget the drugs that can affect the eye. Hydroxychloroquine can cause a retinopathy. In fact, if you're on hydroxychloroquine, you deserve an amyl eye exam. And then don't forget that methanol can also damage your optic nerve. Methanol can damage your optic nerve. That's where we give for mepizol. For mepizol is an inhibitor of alcohol dehydrogenics. When you inhibit that, then you will not make formaldehyde and for mecacid. That for mecacid is not good for the eye. I'll tell you that. So again, if you see like optic nerve hyperemia in a person that has again consumed something, think about methanol poisoning. So I'm going to go ahead and stop here. So thank you for joining me here today. Remember that methanol poisoning, I guess I'll just say that it's associated with wind, shield, washer fluid, wind shield, washer fluid with methanol poisoning. Okay, so I'm just going to go ahead and stop here today. Again, I also want to want you to rainfall all the USM Lion, all the complex exams, pre-clean comments, cool exams, 30-ish-off exams. I have review courses for step one, for step two, for step three, for biostatistics, for social sciences and ethics, for testing and strategies.

If you're interested in any of these things, you should shoot me an email. Also, I would like to interview personal statements, rec letters, and things like that. And also discussing rank list. That's actually something I do with a lot of with a lot of people. And then finally, I have these podcasts on the major apps, Apple podcasts, Google podcasts, Spotify. So just check those out. I also have a You Tube channel called Divine Intervention, USM Li podcasts and videos. That's why I post the videos that I make. And then finally, I also have a new website called Divine Intervention, Life Lessons.com. There's actually an Apple podcast associated with that is the Divine Intervention Life Lessons podcast is an Apple podcast. And basically, I make like two podcasts every week. And from a biblical perspective, I try to offer a life lesson. You know, just a common problem that people face. I try to address it in those podcasts. And again, many people have listened to it and found it to be really, really helpful. So I really hope you find this podcast to be helpful. I'm seriously begging you, this podcast, you should listen to it before your exam. I can almost promise you, you will get a few questions right on any USM Li exam you take from this single podcast. This is probably one of the highest yield podcasts I have ever made in my entire life. So please pay attention to this stuff, know this stuff. The reason I'm saying this stuff is because it's very high yield.

So seeing the next episode, have a wonderful rest of your day. Bye for now.

Practice questions — USMLE style

Question 1 — Neurology/Toxicology

A 45-year-old male presents to the emergency department after being found intoxicated. On physical examination, he is noted to have dry mucous membranes, urinary retention, and severe constipation. Ocular examination reveals bilateral mydriasis (dilated pupils) and decreased lacrimation. The physician suspects an anticholinergic overdose. Which of the following substances would most likely cause this constellation of findings?

  • A) Diphenhydramine
  • B) Naloxone
  • C) Acetylthiocholine
  • D) Pilocarpine

Answer: A. Anticholinergics block acetylcholine receptors, leading to classic signs like dry eyes (decreased lacrimation), urinary retention, and constipation. Diphenhydramine is a common first-generation antihistamine with potent anticholinergic activity. Naloxone is an opioid antagonist that reverses respiratory depression but does not cause these specific peripheral effects. Acetylthiocholine is a substrate for acetylcholinesterase, and pilocarpine is a direct agonist of muscarinic receptors (a cholinergic agent), which would cause the opposite findings (miosis, diarrhea).

Question 2 — Ophthalmology/Neuroscience

A patient undergoes an ophthalmological examination. When light is shone into the right eye, both pupils fail to constrict. However, when light is shone into the left eye, both pupils constrict normally. The physician suspects a specific pupillary defect. Which of the following best describes this finding?

  • A) Efferent Pupillary Defect (EPD), suggesting an issue with the efferent pathway.
  • B) Afferent Pupillary Defect (APD), suggesting damage to the optic nerve II.
  • C) Relative afferent pupillary defect, indicating a problem with the cranial nerve III.
  • D) Argyll Robertson pupil, suggesting syphilis infection.

Answer: B. An Afferent Pupillary Defect (APD) occurs when there is impaired signal transmission from the retina back to the brainstem via the optic nerve II. Since both pupils fail to constrict when light is shone into the right eye, the issue lies with the afferent pathway of that eye. The finding is described as an APD and points toward a lesion affecting CN II (e.g., optic neuritis or retrobulbar process).

Question 3 — Genetics/Metabolic Disorders

A 12-year-old boy presents for routine physical examination. His family history is notable for multiple instances of joint issues and cardiovascular problems. On the physical exam, the patient exhibits downward and inward displacement of both eyeballs (exophthalmos). Laboratory testing reveals elevated homocysteine levels. Which metabolic defect is most likely responsible for this presentation?

  • A) Ehlers-Danlos Syndrome
  • B) Marfan Syndrome
  • C) Homocystinuria
  • D) Osteogenesis Imperfecta

Answer: C. Homocystinuria, caused by a deficiency in cystathionine beta synthase (or related enzymes), leads to the accumulation of homocysteine. This metabolic derangement is associated with vascular issues and characteristic ocular findings, including downward and inward displacement of the eyes. Marfan syndrome (B) is an autosomal dominant connective tissue disorder that typically causes upward and outward displacement of the eyes (proptosis).

Question 4 — Infectious Disease/Ophthalmology

A previously healthy immunocompromised patient presents to the clinic with bilateral conjunctivitis and multiple white, necrotic-appearing lesions in both corneas. The patient has a history of advanced HIV infection. Given the clinical picture and underlying immune status, what is the most likely diagnosis?

  • A) Bacterial keratitis requiring topical antibiotics
  • B) Herpes Simplex Keratitis requiring acyclovir
  • C) CMV retinitis requiring ganciclovir
  • D) Gonococcal conjunctivitis requiring ceftriaxone

Answer: C. Cytomegalovirus (CMV) retinitis is a common and serious opportunistic infection in immunocompromised patients, particularly those with advanced HIV. The clinical presentation of white, necrotic lesions in the cornea/retina in this setting strongly suggests CMV involvement. Treatment requires specific antiviral agents like ganciclovir. Bacterial keratitis (A) would typically present differently, while Herpes Simplex Keratitis (B) is also possible but CMV retinitis is a classic high-yield association with advanced HIV and necrotic lesions.

Quick fire review

What finding suggests opioid or cholinergic toxin exposure?

Profound pupillary miosis (pinpoint pupils).

What finding suggests anticholinergic toxicity?

Pupillary mydriasis, dry skin/mucous membranes, and constipation.

If a patient has adduction myastagnia but intact accommodation, what is the most likely diagnosis?

Medial Longitudinal Fasciculus (MLF) lesion (e.g., Multiple Sclerosis).

What finding suggests an efferent pupillary defect?

One pupil persistently fails to constrict regardless of which eye light shines into.

What constellation of findings—ptosis, miosis, and anhidrosis—is characteristic of sympathetic chain damage?

Horner syndrome.

If a newborn has a white reflex instead of the normal red reflex on ophthalmoscopy, what should be suspected?

Retinoblastoma (due to RB1 gene mutation).

What is the classic finding in diabetic retinopathy that suggests impending retinal detachment?

Proliferative changes leading to vitreous hemorrhage and traction.

What metabolic disorder causes cataracts due to excess galactose accumulation?

Galactose-1-phosphate uridyltransferase deficiency (Galactosemia).

Which type of glaucoma is suspected if bulging pupils are seen acutely, but the patient has signs of chronic systemic disease like hyperthyroidism and tachycardia?

Chronic angle-closure glaucoma.

What condition presents with a downward and inward displacement of the eyeball, often associated with myocardial infarctions?

Homocystinuria (due to cystathionine beta synthase deficiency).

Which specific finding in the eye is highly suggestive of advanced systemic hypertension or vasculitis?

AV-nipping (arteriovenous nipping) or flame-shaped hemorrhages.

What condition causes a vertical gaze palsy, and what structure might be compressed?

Parinaud syndrome; compression of the superior colliculus/superior collicular pathway.

If a patient has papilledema and is on hydroxychloroquine, what must be done annually?

Fundoscopic exam (retinopathy screening).

What specific finding differentiates Marfan Syndrome from Homocystinuria regarding eye displacement?

Marfan syndrome causes upward and outward displacement; Homocystinuria causes downward and inward displacement.

Quick recall / Anki-style questions

What metabolic disorder causes cataracts due to excess galactose accumulation?

Galactose-1-phosphate uridyltransferase deficiency (Galactosemia).

Which type of glaucoma is suspected if bulging pupils are seen acutely, but the patient has signs of chronic systemic disease like hyperthyroidism and tachycardia?

Chronic angle-closure glaucoma.

What condition presents with a downward and inward displacement of the eyeball, often associated with myocardial infarctions?

Homocystinuria (due to cystathionine beta synthase deficiency).

Which specific finding in the eye is highly suggestive of advanced systemic hypertension or vasculitis?

AV-nipping (arteriovenous nipping) or flame-shaped hemorrhages.

What condition causes a vertical gaze palsy, and what structure might be compressed?

Parinaud syndrome; compression of the superior colliculus/superior collicular pathway.

If a patient has papilledema and is on hydroxychloroquine, what must be done annually?

Fundoscopic exam (retinopathy screening).

What specific finding differentiates Marfan Syndrome from Homocystinuria regarding eye displacement?

Marfan syndrome causes upward and outward displacement; Homocystinuria causes downward and inward displacement.