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Flashcards in Case Vignettes Deck (47)
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1
Q

A 48-year-old man presents to clinic for his physical. He reveals to you that he hasn’t been sleeping well for the past few months, and has felt like he is drained of energy, to the point that he doesn’t have much interest in his work or hobbies, and finds it difficult to concentrate at work. He says he feels sluggish, and has been moving slower than usual as well. Overall, he says, he has been feeling “down.” He reports no history of difficulty sleeping before this point. What are the criteria to come up with a diagnosis for this patient, and what might you want to rule out?

A

Major Depressive Disorder: 5 of the following (including at least one of the first two):
1. depressed mood
2. diminished interest or pleasure (anhedonia)
3. weight loss or weight gain (or change in
appetite)
4. insomnia or hypersomnia
5. psychomotor agitation or retardation
6. fatigue or loss of energy
7. feeling worthless or excessively guilty
8. decreased concentration or indecisiveness
9. suicidal ideation
The symptoms cause clinically significant distress or
impairment in social, occupational, or other important
areas of functioning.

Can be remembered as SIGECAPS: 
•change in Sleep
•loss of Interest
•Guilt
•lack of Energy
•poor Concentration
•change in Appetite
•Psychomotor retardation or agitation
•Suicidal ideation

Things to rule out:
The episode is not attributable to the physiological
effects of a substance or another medical condition (hypothyroid, for example, or sleep disorders - you’d have to rule those out)
The occurrence of the major depressive episode is not
better explained by schizoaffective disorder,
schizophrenia, schizophreniform disorder, delusional
disorder, or other specified and unspecified schizophrenia
spectrum and other psychotic disorders
There has never been a manic episode or a hypomanic
episode (ruling out bipolar disorder)

2
Q

You are taking a history from a 57-year-old woman. She tells you, “I’m a prophet. I hear the divine word through my television. It’s my job to save everyone I know from the apocalypse.” What kind of findings are these, and how will you document them? What kind of diagnosis might she have?

A

Delusions - specifically religious delusions
Ideas of reference - feels like TV, radio, or other media is speaking directly to them.

These findings could be present in schizophrenia, schizoaffective disorder, mania associated with bipolar disorder type I, or anything with psychotic symptoms.

3
Q

You are evaluating a patient for opioid use disorder. The patient has some reservations about starting methadone or buprenorphine, and says, “I don’t want to end up dying of an overdose, but I don’t have the time to commit to these kinds of intensive treatment.” What are some approaches you can take with this patient to ensure that the patient gets appropriate therapy?

A

1) Motivational interviewing. You’ve already elicited change talk (“I don’t want to end up dying of an overdose”) but the patient has resistance to change and ambivalence about change. You could try reflections (“You’re worried that taking these medications will take a lot of time, but you don’t want to die of an overdose”) in order to elicit more change talk. You should also try the Explore-Provide-Explore model of structuring interventions (explore what the patient thinks, provide more info with permission, explore their reaction).

2) On the side of opioid interventions, you may want to discuss the pros and cons of methadone treatment and buprenorphine treatment.
- Methadone requires treatment at a treatment center, and supervision of the person taking the medications, but is effective if patients are compliant. It doesn’t have a risk of inducing withdrawal when you take it.
- Buprenorphine can be provided by a physician who has been trained to do so, so it doesn’t require a treatment center. It can also be given in combo with naloxone (as Suboxone) to prevent overdose if the patient tries to overdose. It does have a risk of inducing withdrawal since it has such high affinity for the receptor.

4
Q

Jane is a 21-year-old patient who you are treating for depression. She is curious about what causes depression, and asks you if it’s true that depression is caused by a neurotransmitter imbalance. How do you answer her, and how do you explain some of the possible theories for the etiology of depression?

A

It’s true that manipulation of serotonin signaling is important in the mechanism of action of many antidepressants. However, the etiology of depression probably is due to changes in neuro plasticity. The current reigning theory for the etiology of depression is that depression is a failure of neuroplasticity. Increased glucocorticoids from stress lead to decreased neurogenesis, and increased glutamate leads to excitotoxicity. Glucocorticoids also block BDNF (brain-derived natriuretic peptide), which is needed for neural remodeling and neuroplasticity. However, this theory is not perfect and more research is needed.

5
Q

Mike is a 44-year-old man who comes to your clinic for a physical. When you ask him how things are going at work, he tells you that he has been having some difficulties. He says, “I don’t think my manager and I get along very well. I’m not sure what I did, but he really seems to dislike me. I’m sure it’s because I turned in a report late to him three months ago, and since then I’ve just felt like he’s very hostile to me. It’s not like he’s said anything, but he’s always scowling any time I see him around the office, and I just feel like I must not be performing up to standard to make him feel that way.” What kind of cognitive distortion(s) do you identify in this statement?

A

Personalization - “it must be something I did”

Over generalization - “I’m always messing up”

6
Q

Using the language of cognitive distortions, how would you describe this common sentiment experienced by medical students? “Why am I not studying all the time? I should be studying more. I should probably be putting in several more hours each day. If I don’t study enough, then I’ll fail the test, and then I’ll have to retake it, and might have to retake the block!” At what point does this cross the line into a pathological state?

A

Shoulds and musts - “I should be doing X”
Catastrophizing - “If I don’t do X, then Y will happen, and then Z…”

This becomes pathological when it causes significant distress or impairment to the person having these thoughts.

7
Q

John Smith is a 25-year-old man who tells you at his physical that when he gets very stressed at his job, he tends to come home and yell at his wife. What kind of psychological defense is he manifesting, and how mature would you consider it to be?

A

Acting out - he’s taking an action rather than reflecting on the problem or thinking about his feelings. This is one of the least mature psychological defenses.

8
Q

Mary Smith is a 47-year-old woman with type 2 diabetes and obesity. At her physical, she tells you, “When I was first diagnosed with diabetes, and had to learn to eat fewer carbs, I tried not to think too hard about it and I basically pretended I didn’t have diabetes. Kept on baking cookies, cakes, muffins, and eating them whenever I felt like it. Now, though, I’ve learned to control it, and when I feel like baking, well, I maybe save one muffin for myself and bring the rest of the batch down to the local food pantry. I get to bake, and I’m helping someone out too.” What two psychological defenses did she describe?

A

Denial - early after her diagnosis, she refused to acknowledge that she had T2DM
Altruism - she channels her feelings about her diabetes into serving others

9
Q

Your patient is a woman who has experienced a sexual assault. She tells you, “When I see mentions of sexual assault on social media, I’ve taught myself not to feel anything. It’s like I make myself numb on purpose. That way I don’t feel upset or trigger a panic attack.” What psychological defense is she describing?

A

Isolation of affect

10
Q

Kate is a 40-year-old woman who presents to clinic for a routine physical. You take a thorough history and find that overall she has been healthy, except for a year-long depressive episode when she was 25. She has never been suicidal. Her family history is significant for her mother’s struggles with anxiety and depression. She does not currently feel depressed, and has no concerns with her mental or physical health today. Kate wants to know what kind of risk she has for future episodes of depression. How do you answer her?

A

Risk factors for depression include F>M, family history (somewhat heritable), history of stressful life events including childhood abuse, comorbidities with alcohol use, substance use, personality disorders, anxiety disorders, and previous episodes. While baseline risk for depressive episodes is about 16%, having had one previous episode increases the chance of recurrence to 50%, which continues to increase with more previous episodes. Other medical conditions may also lead to depressive symptoms.

In Kate’s case, her risk of recurrence is about 50%, given that she has had a previous episode of depression. She also has a family history of depression, which does contribute to that risk.

11
Q

A 65-year-old man presents to the ED and appears to be unresponsive to verbal stimuli. He has no known history of trauma. You immediately begin an exam, including a full neuro exam. You find that his left pupil is slightly dilated and sluggish in response to light, and he has a positive Babinski sign in response to the plantar reflex test on his right foot. He displays appropriate motor responses to noxious stimuli. His breathing is eupneic. You decide to order an emergent CT scan to check for structural abnormalities. What are you checking for, and what do you suspect is going on?

A

Checking for structural abnormalities that could be causing an uncal herniation, specifically a temporal mass or a bleed near the temporal lobe that could cause it to herniate through the tentorial notch. That would compress cranial nerve III, leading to some of the symptoms seen. As the uncal herniation progresses, it may cause cerebral peduncle compression, which could lead to contralateral hemiparesis, decreasing level of consciousness, and potentially death.

12
Q

A 45-year-old woman presents to the ED after a motor vehicle accident. She is stabilized in the ED, has surgery to fix her broken femur, and is admitted to your internal medicine service. She wakes up from surgery without complications, although complains of a headache over the next day or two. About 3 days after being admitted to your service, she begins to experience visual hallucinations and appears agitated. Her body temperature is 40 degrees, her pulse is 130, and her respiratory rate is 28. Her blood pressure is elevated as well. She is diaphoretic and flushed. Blood cultures, urine cultures, and a lumbar puncture rule out infection, and you detect no illicit substances in her blood and urine. What may be going on, and how would you treat it?

A

This is a classic presentation of delirium tremens in alcohol withdrawal. Delirium tremens can be lethal if untreated. Its symptoms are clouding of the sensorium, hallucinations, agitation, and increased autonomic activity. It tends to occur 2-14 days after the last drink. It is often seen in patients who are admitted to the hospital and have no access to alcohol, and therefore go into alcohol withdrawal. It is treated with benzodiazepines, which ramp up GABA-A receptor activation, causing inhibition that calms down the symptoms.

13
Q

A 22-year-old man is dropped off at the ED by his friends, who say that he seems to be “out of control.” In the ED, he is oriented to person and place but not to time, and he is very agitated. He has a grand mal seizure while he is being triaged. His vitals are all elevated. His friends tell you that he was at a concert, and had “several drinks, probably at least 5 shots,” but they cannot account for anything else he was doing over the course of the night. What are you concerned might be going on?

A

Cocaine intoxication - vitals will be up, altered mentation, agitation, seizures. In contrast, cocaine withdrawal presents with decreased mood and fatigue. This scenario rules out alcohol withdrawal because he has had multiple alcoholic drinks very recently. However, if he has an alcohol use disorder, he might be at risk of alcohol withdrawal if he is admitted.

14
Q

A 32-year-old woman is dropped at the front door of the ED in a state of altered level of consciousness. She is oriented to person but not place or time, and is very sleepy. In order to get any information from her, you have to continually wake her up. Her respiratory rate is 10. There are track marks on her arms. You find in her chart that she has a history of repeated visits to this ED for chronic knee pain. What drugs should you be considering, and how might you treat this patient?

A

1: opioids, given her history and the track marks. Treatment should be naloxone, given multiple times if needed to end her opioid intoxication.

15
Q

A patient who has been in the hospital for 2 days is given IV fluids that include glucose. The patient rapidly develops ataxia, ophthalmoplegia, and confusion. The patient has no history of neurological disorders. What is this syndrome, and what is a potential cause?

A

This is Wernicke’s encephalopathy, caused by giving glucose without thiamine in a patient in alcohol withdrawal. It occurs because thiamine is a cofactor in glucose metabolism, and the moment glucose is given, all the thiamine is essentially sucked out of the system. This is a problem because thiamine is needed in nerves as well. Giving thiamine before giving glucose can prevent this from occurring.

16
Q

A patient presents to the ED with facial numbness on the left side. At this moment, the patient is hemodynamically stable. You immediately do a neuro exam. You find that the patient has reduced sensation to the skin of the face on the left forehead and upper cheek, ptosis, asymmetric pupils, and decreased extraocular movements on the left side. What do you expect might have caused this?

A

A lesion - aneurysm, stroke, tumor, etc. in the left cavernous sinus could cause these symptoms, as CN III, IV, V1, V2, and VI all appear to be affected in this patient.

17
Q

A 75-year-old patient presents to the ED. The patient is hemodynamically unstable, with a blood pressure of 80/50. The patient’s wife tells you that the patient was fine until an hour ago, then got a severe headache and started to become less and less responsive. There is no history of trauma. On CT you see a lentiform-shaped area of brightness. What is going on in this patient?

A

Epidural hemorrhage, usually due to rupture of a meningeal artery, typically the middle meningeal. Blood will not cross the sutures of skull bones. This is a very fast bleed and needs to be treated immediately.

18
Q

A 36-year-old woman presents to your primary care clinic today for a follow-up after a surgery for carpal tunnel release. You have seen her before for management of depression and anxiety, and for follow-up after a suicide attempt 2 years prior. Today she seems very upset, and says, “My surgeon was the absolute worst! She wouldn’t listen to me at all, and I honestly don’t think she did a very good job. I’m in so much pain after the surgery, and it’s making me really anxious! That’s why I came to see you - you’re the only doctor I can trust to really understand my needs.” The surgical site appears to be healing nicely, and you tell her this, which makes her very happy. She thanks you profusely. You send her home, but she calls your clinic three times over the next week to ask questions about her surgery, and leaves four messages on MyChart asking for your advice as well. This is not unusual in comparison to previous encounters with this patient. What might be an underlying issue in this patient?

A

Borderline Personality Disorder! Characterized by interpersonal problems, affective instability, behavioral difficulties, and cognitive problems. It may lead to frequent suicide attempts, and has a lot of psych comorbidities. 5 factors are frequently present in the etiology - early separation or loss, disturbed parental involvement, verbal or emotional abuse, sexual abuse, neglect. Psychotherapy, especially DBT and psychodynamic psychotherapy, are the treatments of choice. It’s best to deal with present emotions and relationships rather than past ones. Meds are not a good choice for managing these patients.

19
Q

A 23-year-old man presents to your primary care clinic complaining of excessive sleepiness. While he is doing well at work, he finds himself dozing off at his desk on occasion. He frequently falls asleep while watching movies, and will even find himself falling asleep while doing social activities with other people. He’s felt this way for years - in college, for example, he frequently dozed off in the library or in class - but he’s asking about it now because his girlfriend is concerned about how tired he is. He has also noticed that he sometimes wakes up at night feeling like he can’t move, and when he laughs really hard his knees buckle. What might be going on? What kind of workup will you do, and what kind of treatment will you recommend?

A

Narcolepsy with cataplexy. This is an autoimmune disorder caused by loss of hypocretin/orexin-containing neurons in the lateral hypothalamus. It is associated with HLA-DQB1 0602. The essential symptom is excessive sleepiness. Other symptoms might include sleep paralysis, hypnagogic/hypnopompic imagery, and automatic behaviors. Workup includes a polysomnograph/overnight sleep test, and a multiple sleep latency test to see if he falls asleep quickly after less than 8 minutes (entering into REM sleep, which is abnormal for a nap). Treatment is to avoid sleep deprivation, take scheduled naps, use stimulants to help with sleepiness, and use antidepressants or sodium oxybate to treat the cataplexy.

20
Q

Lizzie is an 18-year-old who presents to your clinic for her annual physical. You are a family practice physician who has cared for Lizzie throughout her life so far. Her upbringing has been fairly typical, with caring parents and a safe, supportive home environment. She has had no significant medical challenges. As a child, Lizzie was very shy, and you remember that when you would bring a medical student into the room who Lizzie had not met, Lizzie would freeze and stop talking. She seemed to have grown out of that. Today, Lizzie comes in and is concerned about college applications and dating, and both topics appear to be very stressful for her to discuss. What condition should you consider evaluating her for, and why might you suspect that condition to be present?

A

While her current symptoms aren’t directly indicative of any psychological disorder, Lizzie appears to have had an anxious temperament as a child, which is a strong indicator of increased risk for developing an anxiety disorder as an adult. Other risk factors for anxiety include SERT allele changes, chronic stress, family history of anxiety and depression, parental stress, etc. It would be worth asking Lizzie more questions about the stress and anxiety that she has been experiencing, in order to determine whether you should be concerned about a diagnosis of Generalized Anxiety Disorder or another anxiety disorder.

21
Q

A 37-year-old male patient presents to clinic for a follow-up visit with his wife and 5-year-old son. At his last visit, he had complained of symptoms of abnormal, exaggerated movements in his arms that he couldn’t control. He was adopted as an infant, and does not know his family history, so you ordered genetic testing. The results came back showing an abnormal number of CAG repeats on the short arm of chromosome 4. While you called him to tell him the diagnosis, today you are discussing next steps. Your patient has a few questions for you. He wants to know about his prognosis and potential treatments, and about whether he should get genetic testing for his son as well. His wife has no known genetic disorders and no family history of any Mendelian disorders. What do you do?

A

This patient has Huntington’s Disease. Huntington’s is an autosomal dominant disorder caused by extra CAG repeats on the short arm of chromosome 4, leading to an abnormal huntingtin protein, with no cure and no treatment that can slow disease progression. It is due to degeneration of the caudate nucleus leading to issues with the indirect basal ganglia pathway.

This patient’s prognosis is not great - this is a neurodegenerative disease that will eventually be fatal. It has a slow onset, though, and a gradual progression. The patient, in addition to abnormal movements, will likely develop cognitive changes and emotional difficulties.

There are no cures or disease-modifying treatments. Chorea symptoms may be reduced by dopamine receptor blockers like atypical antipsychotics, or by monoaminergic terminal deplete rs, or by GABA agonists like benzodiazepines.

The question of whether to test his son is an ethical dilemma. You and the family will want to discuss the fact that the son has a 50% chance of having the abnormal huntingtin protein and therefore developing the disease; however, he most likely won’t develop the disease until his 30s-50s. As there is no cure/treatment, it is unclear what benefit testing would have. However, the family may also want the peace of mind of knowing.

22
Q

A 34-year-old woman presents to clinic with a chief complaint of difficulty moving her eyes. Lab tests demonstrate that she has antibodies against nicotinic acetylcholine receptors. What is her diagnosis, its pathophysiology, and its treatment?

A

Myasthenia gravis - an autoimmune channelopathy with antibodies against nAChRs. Degradation of the receptors leads to decreased production of muscle APs. Specific receptor subtypes that are susceptible are common in eye muscles. This leads to eye muscle fatigue, as well as fatigue of other muscles. The disorder can be treated in part with anticholinesterases like pyridostigmine, which increase ACh in the cleft to counteract the loss of receptors. It can also be treated with immunosuppression.

23
Q

A young father brings his 18-month-old daughter to the ED with the chief complaint that “she has a high fever and seems really upset, and we can’t calm her down.” The child has a temperature of 102.7 and appears irritable and lethargic. You flex her neck forward and notice that her legs spontaneously flex at the hips and knees. On lumbar puncture, she has elevated PMNs, low glucose, and elevated protein. You send the sample for additional testing. What do you expect to find.

A

This is most likely meningitis of bacterial origin, due to the Brudzinski sign and the lumbar puncture findings. In this age group, bacterial meningitis would most likely be due to N.meningitidis or S.pneumo (she is no longer a neonate). Treatment would be vancomycin + a third generation cephalosporin.

24
Q

A 39-year-old woman presents to clinic comparing of a severe headache with some vision loss. She says she can hear her heartbeat in her ears. She denies sudden onset of headache, nausea, vomiting, worsening of the headache with coughing, jaw claudication, and positional exacerbation of the headache. On general inspection, she is an overweight but otherwise well-appearing woman. Her neuro exam is normal with the exception of papilledema on fundoscopic exam. You order a head CT, which comes back normal. What do you suspect is going on, what test should you order to make the diagnosis, and how would you treat it?

A

Pseudotumor cerebri - most common in overweight women of childbearing age, and potentially caused by outflow abnormalities or something else leading to increased ICP. Diagnosis is made by lumbar puncture in the side position, with pressure >25 cm H2O. Treatment is weight loss, acetazolamide/dicumox, furosemide, corticosteroids, repeated lumbar puncture, and optic nerve sheath fenestration as a last resort.

25
Q

A patient presents to the ED complaining of sudden onset of a very severe headache. After you perform a history and physical exam, you decide to order some additional tests. What is your plan of action for evaluating this patient/referring to other providers?

A

CT head -> if positive, send to neurosurgery for angiogram.
-> if negative, do lumbar puncture.

Lumbar puncture -> if there is blood in the LP, send to neurosurgery for angiogram.
-> if normal LP, send for MRI/vascular imaging.

26
Q

You are seeing a patient in clinic for her annual physical. She is a well-appearing 66-year-old woman with a history of hypertension and high cholesterol. When you ask her if she has had any changes in her health recently, she replies, “Well, I had the worst headache of my life about a week ago… It was so bad I couldn’t think at all. I thought about going in to the emergency room but it was snowing, so I didn’t go, and it resolved in an hour or so, but it was really awful.” What could have caused her headache?

A

This is a thunderclap headache presenting retroactively. It could be an intracranial or subarachnoid hemorrhage, but since she didn’t die and showed up a week later, that is most likely not the case. It is more likely an unproven case of Benign Reversible Cerebral Vasoconstriction Syndrome, or it could be idiopathic.

27
Q

A 78-year-old woman with a history of pain in her hips and shoulders presents to clinic with a headache localized to the temporal region, jaw claudication, and some vision loss. What should you do emergently, and what else should you order?

A

This is temporal arteritis. It needs to be treated with high-dose prednisone immediately, and a clinical impression is most important for getting to that conclusion. A temporal artery biopsy should be ordered. CRP and ESR are most likely elevated, but normal lab values do not rule out this condition.

28
Q

A patient presents to the ED with headache and eye pain. The patient reports seeing halos in her vision. On exam you note some redness of the conjunctiva, and the corneas look edema tours. What emergent step(s) do you need to do?

A

This could be acute angle closure glaucoma, which is an ophthalmic emergency. The patient needs an ophthalmology evaluation within one hour, and/or pressure-decreasing eye drops.

29
Q

A 27-year-old male presents to your internal medicine clinic one week after a motorcycle accident in which he hit a tree. He did not go to the ED at that time, noting no neurological symptoms, although he did splint his wrist, which he thought might be sprained. Today he complains of lower back pain and a headache. The headache goes away when he is lying down. What might you do to evaluate this patient, and what is a generally uncommon diagnosis that should be on your differential?

A

This could be intracranial hypotension due to a leak of CSF due to trauma, if his motorcycle accident had caused puncture of the meninges in the spinal cord. The low back pain suggests that this could be possible, even though it is normally an uncommon diagnosis except for post-lumbar puncture. You should order an MRI, and look for sagging cerebellar tonsils, sagging pre pontine area, and increased meningeal enhancement.

30
Q

Sarah is a 49-year-old woman who presents to clinic complaining of repeated headaches for the past 4 months that come about 4-5 days/week. They are often intense headaches on her left side, and come with some photophobia and nausea. They typically last about 6 hours if she doesn’t treat them. Her history is significant for having episodes of these headaches in the past, although not as frequently, and for anxiety. She is otherwise healthy. What is your diagnosis, and what treatments might you recommend for prophylaxis and self-management?

A

This appears to be chronic migraine: >15 days/month for at last three months with migraine-like features at least 8 days/month. Recommendations for treatment include NSAIDS (especially ibuprofen, ASA, naproxen), use of triptans, DHE, and infrequent use of Ketorolac, with antiemetic S as needed. Prophylactic treatments could include beta blockers, TCAs (amitryptiline, nortryptiline), valproate, topiramate. Prophylaxis is shown to lead to a 50% decrease in symptoms expected after 2 weeks.

31
Q

Mike is a 28-year-old man who works as a consultant. He presents to the ED complaining of “a really bad headache.” Upon entering the room, you see him up and pacing around by the bed. He says that the pain localized to the area around his right eye. He reports no trauma. The headache started 45 minutes ago and feels like an 8/10 in severity. He has had headaches like these before, always around the same time of year. His history is significant for a 10 pack-year smoking history. On exam you notice some right eyelid droop and miosis. What is your diagnosis and management?

A

This looks like a cluster headache. It is much less common than migraine, but is most often found in young/middle-aged male smokers. It is characterized by very intense pain, often lasts 15-180 minutes, and may have autonomic features and hypothalamic nuclei involvement. To manage, give O2 and sumatriptan acutely. Verapamil and steroids can be used as prophylaxis.

32
Q

A 28-year-old female presents to the ED with a chief complaint of an intense, pounding unilateral headache that gets worse when she moves around. She feels nauseous. She finds bright lights and loud noises uncomfortable. She has had symptoms for about 6 hours. She has never experienced this before. She reports symptoms preceding the onset of the headache, specifically zig-zagging lines in her vision about 15 minutes before the headache started. She believes that her mother has experienced similar headaches. Her physical exam is normal. She wants to know what the diagnosis is, and specifically wants to know what caused the zig-zagging lines. What do you tell her?

A

This is most likely an episodic migraine preceded by aura. An aura is somatosensory symptoms preceding a migraine, with a duration of typically less than one hour. Aura symptoms may include visual (scintillating scotoma, the zig-zag lines described in the case) or somatosensory (tingling starting at fingertips). Aura seems to be due to a cortical spreading depression, which is a wave of depolarization across the cerebral cortex. Vasoactive neuro peptides (substance P, CGRP, and neurokinin A) seem to be involved in neurogenic inflammation associated with migraine, as does serotonin. Migraine does seem to have a genetic basis.

33
Q

You are on an ophthalmology rotation, and at the end of the day you have three patients to write up who all came in with the chief complaint of diplopia. Mr. Jones has diplopia with only his left eye open. Ms. Smith has diplopia that is worse at a distance. Mrs. Johnson has diplopia only with both eyes open, but it is worse with near vision. How do these clues lead you to the etiology of each patient’s diplopia?

A

Mr. Jones has diplopia due to an ophthalmology issue - something with his cornea, lens, or retina. Ms. Smith has diplopia due to a cranial nerve, brainstem, or eye muscle issue, so her eyes are not working together. Mrs. Johnson has diplopia due to a convergence problem, which is common with advancing age.

With only one eye open? Yes -> ophthalmology issue
No -> CN/brainstem/eye muscle issue
Worse at distance or near? Distance -> eyes not working together
Near - convergence problem

34
Q

A 60-year-old man presents to the ED with new-onset severe headache for the past hour. He has ptosis on the left side, and the left eye is limited in its upward, downward, and rightward movement. He has profound pupillary dilation on the left side. Overall, you characterize the pupillary involvement as significantly out of proportion to the minor ophthalmoplegia. The patient says the symptoms have gotten progressively worse over the past 60 minutes. What is the most likely diagnosis/pathology, and what is most important in management?

A

Compression of CN III by aneurysm of posterior communicating artery. This is an emergency, and requires immediate management by neurosurgery. This has 20% mortality. The abnormal pupil findings are most important for recognition of this condition in the context of acute-onset severe headache.

35
Q

A 2-year-old patient presents to clinic for her well-child visit. Her mother has noticed that for the past year or so, she has tended to tilt her head to the left, and you observe this as well in the office. Otherwise, the child has been well. You notice that the child has right hypertropia that is most pronounced when she looks to the left or tilts her head to the right. What is causing this finding, and is it a cause for concern?

A

This is a case of a trochlear nerve palsy, affecting the superior oblique muscle of the right eye (head tilt in the direction opposite, to compensate). Some cases, including this one, are congenital, appearing early in life and remaining stable. In an adult, a history of trauma or microvascular disease might point to a different etiology - traumatic damage to CN IV or microvascular mononeuropathy (especially in a diabetic patient). Those cases would present with head tilt and new-onset diplopia.

36
Q

A patient presents to the ED after having a stroke. The patient is in critical condition. You notice that the patient’s pupils are asymmetric, and the left pupil does not dilate when the patient is brought into the dimly lit CT suite for imaging, while the right pupil dilates normally. There is some slight ptosis as well, but it is not very noticeable. What pathway is affected by the stroke, and what are these clinical findings called?

A

This is Horner syndrome, a set of characteristic pupillary findings caused by a lesion to the oculosympathetic pathway, which is responsible for dilating the pupils. The oculosympathetic chain consists of three neurons. It starts in the superior cervical ganglion, and passes the ICA, CN VI, CN V3, etc. Any lesions along that path could lead to an inability of the affected pupil to dilate. A stroke in the lateral medulla could cause this finding, as could a tumor in the apex of the lung or a dissection of the internal carotid.

37
Q

A patient in the ED has a pupillary defect - neither pupil constricts when the right eye is presented with bright light. What is this called, and where is the location of the causative lesion?

A

This is a Marcus Gunn pupil sign, and it indicates a defect in the afferent limb of the pupillary light reflex pathway. This means that the lesion causing this defect is affecting CN II coming from the right side - a tumor, demyelination, optic neuritis, etc.

38
Q

A patient with a history of a stroke 1 month ago is seen in your ophthalmology clinic for evaluation of ongoing eye problems following the stroke. On exam you note that when you have the patient gaze to the right, the right eye demonstrates nystagmus and the left eye moves slowly. What is this phenomenon called, and what is the pathophysiology behind it?

A

Internuclear ophthalmoplegia - a lesion in the pathway required to synchronize eye movements, specifically a lesion between the two nuclei. It’s probably a problem with the paramedian pontine reticular formation, which normally moves both eyes to the same side smoothly.

39
Q

A 31-year-old woman presents to your family medicine practice with new-onset vertigo. She has a five-year history of relapsing-remitting multiple sclerosis. She denies feeling light-headed or having any palpitations, and says she has not fainted at all. On exam she has some nystagmus. She has no history of trauma. A Dix-Hallpike maneuver and a head impulse test fail to trigger the nystagmus. Her vitals are stable and she seems otherwise well. What do you suspect is going on, how would you diagnose it, and what kind of vertigo is this?

A

This is most likely central vertigo caused by a multiple sclerosis lesion somewhere in the vestibular system. Given her history and exam, this is a possible cause. Stroke is unlikely given her stable condition. The diagnosis can be confirmed via MRI to look for evidence of the multiple sclerosis demyelinating plaque in an associated location.

40
Q

Your patient is a 65-year-old woman who is concerned because she has recently become dizzy whenever she makes a sudden movement. Sitting up in bed makes her dizzy, and turning her head to the left side suddenly makes her dizzy. The dizziness does not occur at rest. Sitting on the exam table, she has no nystagmus. Her neuro exam is normal. She has had no recent illnesses. When you turn her head to the right and lower her down to a supine position on the exam table, though, that provokes upbeat, torsional nystagmus. What is your diagnosis, and how can you treat it?

A

BPPV - the most common cause of vertigo. It’s idiopathic, and is caused by calcium debris from the utricle entering the posterior canal. It is diagnosed by noting latency followed by upbeat, torsional nystagmus on the Dix-Hallpike maneuver. It can be treated by the Epley maneuver.

41
Q

A 54-year-old patient presents to your family medicine clinic with progressive hearing loss and vertigo for the past two months. He says his hearing is worse on his left side. You perform an audiogram in the clinic. He has high frequency hearing loss in both ears, but on the left side, he also has low-frequency hearing loss. What is your likely diagnosis/pathophysiology, is there anything you need to rule out, and how can you treat it?

A

Meniere’s disease, caused by endolymphatic hydrops (swelling of the labyrinth of the inner ear). To rule out a Schwannoma, a MRI should be performed. If this is in fact Meniere’s disease, it may be treated with intratympanic gentamycin. It may rarely need surgery.

42
Q

A 72-year-old man presents to clinic with a chief complaint of dizziness for the past two weeks. His history is significant for an URI a few weeks prior. The dizziness has a rapid onset, and comes with nausea and difficulty balancing. On exam, you have the patient look forward, and you move his head from side to side faster and faster. On rapid movement, you notice horizontal rotary nystagmus beating towards the right, with catch-up saccades beating in the direction of head rotation. What is your diagnosis, and which side’s vestibular nerve is affected?

A

Vestibular neuritis of the left side, because the nystagmus will beat towards the unaffected side. The diagnostic test performed is the head impulse test.

43
Q

A 21-year-old football player presents to the ED after a shoulder injury sustained in a tackle. His hand and wrist are supinated, and his hand is in a claw position. He is unable to abduct and adduct the fingers on his left hand. Other movements of the hand and wrist are difficult as well. He also has numbness in the left hand and some numbness in the left wrist. Based on this presentation, where is the nerve injury most likely located?

A

The presentation suggests an injury to C8 and T1 at the level of the nerve roots, which provide sensory innervation to the hand. C7 and C8 provide sensory innervation to the wrist. C8 and T1 would also innervate intrinsic muscles of the hand, such as the interossei and lumbricals, as well as the thenar and hypothenar muscles, and also innervate (in part) flexor carpi ulnaris and flexor digitorum profundus.

44
Q

The muscle biopsy of a 6-year-old boy with hip girdle weakness reveals that many of the muscle fibers have been replaced by fat, and the muscle fibers are rounded instead of polygonal with a lot of excess connective tissue. He has a family history of this disorder. What protein is most likely to be altered in this child?

A

Dystrophin - this is most likely Duchenne Muscular Dystrophy. Other muscular dystrophies include Becker MD, limb girdle MD (sarcoglycan proteins), and myotonic MD.

45
Q

An eighteen-month-old child is brought into clinic with generalized weakness. You notice limited eye movements and limited ability to smile and make distinctive facial movements. Her CK is slightly elevated. What do you expect to find on muscle biopsy?

A

This is a congenital myopathy. Characteristic histopathologic findings include rods, cores, or central nuclei in the muscle fibers. Those findings (which divide them into three types) are necessary for diagnosis and categorization. Treatment is PT/OT, orthotics/bracing, and BiPAP if respiratory muscles are involved.

46
Q

A 60-year-old man presents with a two-month history of shoulder and hip weakness. On exam you notice an erythematous rash on his upper chest and hands, as well as purple-red discoloration around his eyes. What do you expect to find on muscle biopsy?

A

Perivascular/perifascicular pattern of inflammatory infiltrate, with perifascicular atrophy, meaning that muscle fibers at the edge of the fascicles are atrophied. This is characteristic of dermatomyositis.

47
Q

A 57-year-old woman presents to clinic with a two-month history of shoulder and hip weakness. On exam her skin is clear of any rash, but on history she reveals that she was recently diagnosed with interstitial lung disease. What would you expect to find on muscle biopsy?

A

This is polymyositis. You will find inflammation, T cells predominating, around the muscle fibers, with T cels invading the non-necrotic muscle fibers.