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Hematology > Neurology > Flashcards

Neurology Flashcards

1
Q

With all neuro BIT and MAT

A

BIT = CT

MAT = MRI

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2
Q

right sided weakness of face, arm, legs and Speech deficits. and a left homonymous hemianopsyia

which artery is occluded?

A

LEFT MCA occlusion

BIT = CT

MAT = MRI

Within first 3-4 hours do thrombolytics

Clear with catheter if within 6 hrs.

MCA SPARES the FOREHEAD!!!

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3
Q

For any stroke what is the next best steps taken?

A
  1. BIT = CT
  2. Thrombolytics within first 3-4 hrs
  3. Catheterization within first 6 hrs of presentation

If after 3-4 hours what do you give? Aspirin.

If already on aspirin switch to clopidogrel or add dipyramidol

Whats always contraindicated in stroke?
Heparin

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4
Q

Whats always contraindicated in stroke?

A

Heparin

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5
Q

Leg weakness more than upper extremity weakness + COGNITIVE and personality changes + Incontinence

which artery is this?

A

ANTERIOR

cerebral artery

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6
Q

what do you do if patient presents after 3-4 hours of stroke symptom onset?

A

Aspirin.

What if they are already on aspirin?

Switch to clopidogrel or add Dipyramidol

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7
Q

How do you know difference between stroke and facial palsy?

A

MCA Stroke will SPARE the forehead.

Facial palsy will include the forehead.. upper and lower face.

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8
Q

which muscle group is stronger.. extensors or flexors?

A

Extensors.

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9
Q

Storke and visual fields

A

Left MCA occlusion will cause a right homonymous hemianopsia (right half of visual field in BOTH eyes is gone).

Right MCA will cause left.

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10
Q

15% of strokes bleed - Hemmhoragic stroke.. what can we do for these patients?

A

nothing. we cant do anything for these patients.

surgical decompression is only done for epidural or subdural bleeds.. not hemhorragic strokes.

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11
Q

CT scan and stroke reads

A

three main kinds of strokes:

  1. hemhoragic
  2. embolic
  3. ischemic

CT scan will pick up hemhoragic strokes right away - blood.

Embolic and Ischemic take time.. CT scan becomes 95% sensitive to rule these out after 4-5 days of the event.

The MRI only needs 12-24 hours to become 95% sensitive for embolic / ischemic.. so if its not showing up on CT and you are suspecting stroke do a MRI.

MRA becomes 95% sensitive within 2-3 hours for embolic and ischemic

so the scans are helpful.. but you dont base therapy (TPA / Aspirin / Cath) on the results of the scan, but on the NEUROLOGIC SYMPTOMS

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12
Q

What dictates therapy in a stroke?

A

neurologic symptoms.

not the scans.

Still.. 1st thing we will always do for stroke symptoms is a CT. and MRI is still best test for Stroke. But start treatment based on symptoms and time of presentation.

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13
Q

adding clopidogrel

A

In the heart you ADD clopidogrel if patient is on aspirin already and patient has anginal symptoms.

In STROKE you NEVER add clopidogrel you SWITCH from aspirin to clopidogrel.
adding clopidogrel in storke will result in bleeding.

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14
Q

what if patient has stroke and MI and got a stent for the MI?

A

then you treat the most dangerous one - MI

In stents you MUST give both aspirin and clopidogrel

Meaning you give both aspirin and clopidogrel… even though the combo is contraindicated in stroke.. you have to give it.

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15
Q

stenting in stroke

A

NEVER stent a stroke - leads to rupture

MI you can stent no problem

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16
Q

Echo of the carotid

A

if patient comes in with stroke symptoms and on echo you find 70-99% occlusion then you do SURGERY –> carotid end arterectomy

If patient has NO symptoms but you find 70-99% occlusion of the carotid what do you do?
NOTHING.

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17
Q

If patient has NO symptoms but you find 70-99% occlusion of the carotid what do you do?

A

Nothing. –> carotid endarterectomy is a dangerous procedure.. it kills people. we avoid it if there is no symptoms.

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18
Q

what drug should everyone with a non-hemhoragic stroke get?

A

STATIN@!!!

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19
Q

someone under 50 getting a stroke what should you think about?

A

vasculitis / auto-immune disease

Check:

  1. ESR - inflammatory vasculitis
  2. ANA / VDRL –> hyper coag states in diseases like Lupus
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20
Q

where in the brain do you have to have a stroke to lose consciousness?

A

Brain stem

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21
Q

Dizzy / LOC + Dysarthria + Dysphagia + Diplopia (CN 3 & 6), + Bilateral findings

A

Posterior circulation stroke either in the:

  1. Vertebral artery
  2. Basilar artery

The only way to view a stroke in these is MRI!!!

there is no way to lose consciousness from a stroke in any location other than in the brain stem.. and these are the arteries that supply the brain stem.

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22
Q

what foods are migraines associated with?

A

cheese
chocolate
red wine
menstruating

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23
Q

Cluster headache

A

refers to a symptom pattern - meaning the headaches are short and multiple and recur (clusters).

Symptoms seen:

  1. teary red eye
  2. nasal stuffiness
  3. UNIlateral

Abortive therapy triptans and ergotamines.. in pregnancy / htn / cad use 100% oxygen!

Preventive therapy - Verapimil

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24
Q

Migraines

A

Visual disturbances
normal exam
normal MRI
normal CT etc.

abortive therapy - Triptans and Ergotamines (cause vasoconstriction)

We think that migraines are caused by vasoconstriction followed by vasodilation.. ant the pain comes when there is the vasodilation.. so the abortive treatments focus on causing constriction

In CAD / HTN / Prego.. use pain killers instead of triptans / ergotamines

Preventive therapy - if yo uhave more than 3-4 migraines per month use non-selective BBs PROPANOLOL! or Topiramate or TCAs or Divalproex sodium

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25
Q

When are triptans and ergotamines CONTRAINDICATED??

A
  1. CAD
  2. HTN
  3. Pregancy

the constrictive effects of triptans and ergotamines will make all of the above worse!!

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26
Q

trigeminal neuralgia pain

A

carbamazipine

seizure meds are always good for neuro pain

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27
Q

post herpetic neuralgia or peripheral neuropathy pain

A

gabapentin
pregabalin
TCAs

seizure meds are always good for neuro pain

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28
Q

62yo male comes in with

LOC
CT is negative
dizziness
weakness of right arm
ataxia left leg
sensory R leg
Echo is negative
holter is negative
Right carotid artery doppler shows 85% stenonsis what is the next step in management?
A

Thrombolytics (first 3-4 hrs)
aspirin after that

you will NOT do a carotid endarterectomy.

all of this patients findings are pointing to a posterior stroke. LOC / dizziness etc. bilateral findings! –> vertebral or basialr findings (posterior findings)

The findings of the carotid are incidental.. but the patient does not have any symptoms of Right carotid artery stroke.. thus its asymptomatic.. thus WE WILL NOT DO SURGERY for this patient.

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29
Q

stupor vs delirium?

A

Both are caused by the following:

  1. Increased or Decreased Na
  2. Hypoxia
  3. Hypoglycemia
  4. Hypercalcemia
  5. Liver or renal pathology (hepatic encephalopathy / Uremia).
  6. Drugs / toxins
  7. CNS issues.

If someone comes in with delirium / stupor or seizure.. all of the above have to be tested for and ruled out FIRST.

The difference between delirium and stupor is intensity and duration… otherwise they are the same spectrum of disease.

Seizure is the WORST manifestation of delirium and stupor. So if someone comes in with seizure.. make sure you rule out all of the above first.

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30
Q

what is the BIT of seizure?

A

best initial test of seizure is CT and ruling out all of the causes of delirium / stupor.

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31
Q

what is epilepsy

A

seizure disorder of unclear etiology.. meaning you check all the causes of stupor / delirium and found nothing.

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32
Q

Types of seizures

A

Generalized vs Partial

Generalized - whole body
Partial - specific area of body twitching.

Simple vs Complex:

Simple = awake

Complex = not awake (LOC)

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33
Q

what is the best anti-epileptic therapy for long term or for pregnancy?

A

we dont know.

this will not be on exam since we dont know.

we know the WORST ones in pregnancy:

  1. valproic acid
  2. phenytoin

both of these interfere with follate.. so dont give these..

but what is best.. we dont know

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34
Q

what is Best initial therapy for STATUS EPILEPTICUS?

A

This we know:

1. First line is always benzos
if they keep seizing
2. 2nd line is fosphenytoin.
if they keep seizing
3. Phenobarbital
if they keep seizing
4. General anesthesia (NM blockade)

Benzos:

Lorazepam or Benzodiazepam!

if that doesn’t work then use fosphenytoin.

Fosphenytoin = phenytoin.. except fosphenytoin does NOT cause AV block or decreased BP.

3rd agent added is Phenobarbital

4th agent added is Neuromuscular blocakde – this will stop muscular contractions.. but the patient is STILL SEIZING!! so the NM blockade is just allowing you to INTUBATE the patient and add midazolam and proofol

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35
Q

for patients after status epilepticus.. they will be put on an anti-seizure med.. what is the best one and when can you stop taking it?

A

We do NOT do long term treatment for first time seizures because the majority of them happen at home and go away by themselves.. we treat long term in the following circumstances:

  1. If the patient came to the hospital status epilepticus and we had to use drugs to break the seizure.
  2. cause of the seizure is uncorrectable - CNS diseases or tumors etc.
  3. strong family history of seizures.
  4. abnormal EEG

WE DO NOT KNOW THE BEST ONE.. wont ask that

We dont know when you can stop either.. but we keep patients on the meds for 2-3 years.. if they are seizure free… that whole time. then we can stop.

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36
Q

for patients who have seizures what can you do in terms of them driving?

A

cant take away their cars.. cant report to DMV.

You can ONLY ask them to not drive.

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37
Q

subarachnoid hemhorage

A

looks a lot like meningitis:

  1. stiff neck
  2. photophobia
  3. Headache
  4. Kernig and burzinski sign
  5. papilledema

SAH can be differentiated because it will have the following in addition to the above:

  1. SUDDEN onset
  2. 50% will have Loss of consciousness.
  3. CT scan will show blood for 95% of patients… IF it does not.. THEN and only then.. you do the LP.

Why do you have the LOC? because the sudden increase in ICP causes loss of consciousness.

Treatment :

  1. Nimodipine
  2. Angiogram to embolize using platinum
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38
Q

Pseudotumor Cerebri

A
  1. papilledema
  2. increased ICP
  3. 6th CN palsy (abducens)

treat with weight loss and acetazolamide.

Can use VP shunt and drain fluid if acetazolamide doesn’t work.

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39
Q

Dorsal columns

A

position and vibration sense.

In B12 deficiency when you get subacute combined degeneration you ONLY lose position and vibration sense.

in neurospyhilis you ONLY lose position and vibration sense

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40
Q

spinothalamic tract

A

pain and temp.

crosses at spinal cord so the deficit will always be on the OPPOSITE side of lesion!!!

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41
Q

Spinal trauma

A

lose everything below level of trauma

weakness, incontinence, pain temp etc.. everything

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42
Q

Syringomyelia

A

A bubble in the spinal cord after trauma.. this will cause everything around the spinal cord.

The tracts closest to the spinal cord are pain and temp.. SO now you will get BILATERAL (since its all around spinal cord) loss of pain and temp.. hits tracks on both sides of spinal cord

Cape like distribution.

Diagnose with MRI

Treat with surgery

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43
Q

ipsilateral position and vibration sense lost + CONTRAlateral pain and temp lost.. what happened?

A

Hemi section of spine = Brown Sequard.

Caused by being knifed in the back or bayontted in the back. Can also be caused by a cancer compressing half of the spinal cord

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44
Q

anterior spinal cord lesion

A

everything is lost EXCEPT position and vibration sense (posterior spinal cord).

In Subacute combined degeneration or neurosyphilis you only LOSE position and vibratory sense.

In Anterior spinal cord lesion you only RETAIN position and vibratory and lose all other things (motor / pain / temp / sensation)

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45
Q

patient comes in with fever + headache + focal signs +/- seizures –> what do you do next?

A

CT / MRI

If CT shows ring enhancing lesions then you have to consider two things. Is the patient HIV + of not?

  1. HIV + –> its either Toxoplamosis or Lymphoma.
  2. Not HIV + –> then it can be any cancer or infection.

If they are HIV+ treat the patient with Pyrimethamine and Sulfadiazine (if alergic to sulfa then use CLINDAMYCIN. After this do CT again in 2 weeks and if its smaller then its Toxoplasmosis. If it doesnt get better.. NOW you have to biopsy the patient and see whats in the abscess and treat accordingly.

What do you do for the HIV negative people?

BIOPSY is the first step. Dont try any drugs just biopsy.

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46
Q

Tuberous Sclerosis vs Neurofibromatosis vs Sturge webber

A

Tuberous Sclerosis:
1. skin adenomas
2. shagreens patches –> leathery skin patches
3. Ash leaf spots –> hypopigmented spots
4. Mental retardation
5. seizures
6. intracrainal calcifications
No Treatment for disease.. treat the seizures as they come.

NeuroFibromatosis:
1. Deafness --> CN 8 injury
2. Meningioma
3. seizures
No treatment.. treat issues as they arise
Sturge Webber:
1. Port Wine stain
2. Intracranial calcification's
3. Eye problems
4. Hemiparesis
No treatment.. treat issues as they arise
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47
Q

Parkinsonism

A

1 issues with parkinsons:

  1. Slowed gait
  2. Orthostasis!!!

secondary:

  1. resting tremor (goes away with intention)
  2. progressive supranuclear palsy –> cant look up or down very well.. patients keep tripping.

No tests for parkinsons. CLINICAL diagnosis.

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48
Q

how do you differentiate essential tremor from parkinson?

A

essential tremor is there MOSTLY with intention.
Improves with propanolol or alcohol.

Parkinsons is purely resting.. goes away with intention.

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49
Q

Parkinsons treatment

A 
Pharmacologic
Sinemet (levodopa, carbidopa) best for bradykinesia but may cause dizziness, headache, and hallucinations

Bromocriptine and pergolide directly activate dopamine receptors in the basal ganglia

Anticholinergics (benztropine/trihexyphenidyl) for tremor

Amantadine effective in increasing dopamine in mild disease

Selegiline inhibits one of the two major enzymes that breaks down dopamine in the brain

COMT inhibitors - TOlcapone, Entacapone –> increase the life span of dopamine.. are not used by themselves.. always added on to other drugs.

Surgical - pallidotomy for refractory cases

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50
Q

40% of patients being treated for parkinsons end up getting pscyhotic symptoms.. What do you do when patients on parkinsons treatment get psychotic symptoms?

A

add an antipsychotic.

The best antipscyhotic to use in these patients is QUETIAPINE.. because it has the lowest incidence of extrapyramidal effects

The WRONG answer is stopping the parkinsons drugs.

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51
Q

Huntingtons

A
  1. Emotional Lability (the highs are too high.. and the lows are too low)
  2. Choreiform movement disorders (dance like movement)
  3. Dementia

Caused by CAG repeats

Treatment:
for the movement the treatment is Tetrabenazine

no cure or treatment for the actual disease itself

Seen in 40-50 year olds

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52
Q

what if you have huntingtions and give a child up for adoption?

A

The adoption seal can be broken and the adopted child should be notified

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53
Q

Tourettes syndrome

A

tics, grunts, coprollalia

treatment = antipsychotics

  1. haloperidol
  2. ziprasidone
  3. risperidone
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54
Q

what do you give for spastic bladder causing urge incontincence

A

Anticholinergics:

  1. Oxybutinin
  2. Tolterodine
  3. Trospium
  4. Solifenacin
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55
Q

what do you give for an a-tonic bladder –> leading to urinary retention?

A

give cholinergics

Bethanechol

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56
Q

what is intranuclear opthalmoplegia?

A

Disease of the MLF.

Presentation:
lets say you are trying to look to the right. one eye will not be able to cross the midline. the 2nd eye will have horizontal nystagmus (going back and forth).

very commonly seen in multiple sclerosis

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57
Q

multiple sclerosis.

A

Symptoms:

  1. spasticity - pain
  2. loss of motor or sensory in diff parts of the body at diff times.
  3. overactive bladder or urinary retention.
  4. intranuclear opthalmoplegia

BIT and MAT = MRI!! of brain AND spinal cord

2-3% of patients will not have findings on MRI.. for these patients do a spinal tap. On CSF you will see oligo clonal bands = IgG

Treatment:
For individual symptoms the treatment is clear:

for acute exacerbations = High dose corticosteroids

for pain from spasticity = baclofen or tizanidine

For fatigue use amantadine (we dont know why it works but it does)

For flu like symptoms = beta interferon

fingolimod is the ONLY MS drug that is oral.. all the others are injection.

*symptoms can get worse in hot temperatures.. patients who move to hot areas will have exacerbation of symptoms

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58
Q

ALS

A

LMN findings = weakness &
wasting of muscle, fasiculations.

Has Upper motor neuron findings as well - this is what distinguishes it from charcot marie tooth

NO SENSORY DISTURBANCE

Hyper reflexia - elevated DTRs

spasticity –> causes the pain in ALS

what stays intact in ALS?
EVERYTHING except for motor function.

treatment = Riluzole.. prevents progression of ALS.

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59
Q

Charcot Marie Tooth

A

LMN findngs = weakness &
wasting of muscle, tremor (not fasiculations).

Effects mostly the Lower extremities.

How is it diff from ALS? ALS also has upper motor neuron findings.. Charcot Marie tooth does NOT.
Also charcot marie tooth has sensory disturbance. ALS does NOT
Hyporeflexia - Decreased DTRs

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60
Q

mononeuritis multiplex vs peripheral neuropathy

A

peripheral neuropathy is caused by things like:
vincrsitine, b12 deficency, alcohol and it affects nerves that are so small they dont have names.. treated with:
Pregablin / gabapentin / TCAs or 2nd line = antiseizure meds (phenytoin / valproic acid).

Mononeuritis multiplex is on large nerves that do have names (Radial / ulnar, tarsal, peroneal).. usually caused by trauma or vasculitis.. in vasculitis.. the vaso nervosrum is inflammed (the blood vessels surrounding nerves) this leads to the nerves being squeezed by the vessels.

For these diseases NEVER DO and MRI (USMLE question).. it doesnt help.

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61
Q

carpal tunnel

A 
causes:
hypothyroid
pregnancy
acromegally
amyloidosis

Treatment:
1st line - splint
if that doesnt work steroids
if that doesnt work surgery

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62
Q

radial nerve and peroneal nerve injury

A

radial nerve injury - foot drop
peroneal nerve injury - foot drop

Tarsal tunnel - same thing as carpal tunnel.. but this one is the tarsal nerve and in the foot.

carpal tunnel is the median nerve in the hand.

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63
Q

7th CN palsy

A

upper and lower face palsy.

why do you get corneal ulcerations in 7th CN palsy?

because the 3rd CN opens the eye.. but the 7th closes it. In facial nerve palsy (7th CN) you cant close the eye.. it stays open and ulcerates.

they will also here soft noises very loudly. The stapedius which is the shock absorbed for the ear drum is controlled by the 7th CN.. when this is paralyzed.. soft noises become very loud.

treatment = steroids

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64
Q

Gullian Barre

A

caused by DEMYELINATION of PERIPHERAL nerve fibers. Motor nerves are most commonly affected but SENSORY and AUTONOMIC nerves may also be involved.

two things:

  1. ascending weakness
  2. loss of reflexes

the only other disease on earth that does this is - Polio.. eradicated in most of the world.

what is the MAT?
nerve conduction studies

Treatment:
IVIG / plasmapheresis

NEVER GIVE STEROIDS HERE!!!

what is the most important test to do on someone coming in with GBS syptoms: check respiratory function with one of the 3 tests:

  1. PFTs
  2. FVC
  3. Peak INSPIRATORY pressure.
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65
Q

Myasthenia Gravis

A

double vision and decreased ability to chew.

BIT = AcH receptor antibodies

if AcH receptor antibodies are absent then do the Anti-MusK –> this is also specific to Myasthenia gravis

MAT = single fiber electromyography

Best treatment:
Pyrdiostigmine and Neostigmine –> these are both achesterase inhibitors –increases available AcH.

If youre under 70:
Thymectomy results in 70% improvement (not making antibodies anymore).

If youre above 70.. youre too old for thymectomy so we will give these patients anti-immune drugs:
1. myclophenelate
cyclosporine
azathrioprine

Durring myasthenic crisis use EITHER:
IVIG or plasmapheresis NOT BOTH.

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66
Q

if someone comes in with myasthenic symptoms what are the 2 things you want to screen for?

A
  1. Aminoglycosides –> these are the only drugs in the world that can mimic myasthenic symptoms.
  2. Thymoma –> cancer.. of thymus do CHEST CT!!
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67
Q

what is the side effects of achesterase inhibitors?

A

too much ach = fluids everywhere

salivation / lacrimation / diarrhea

Glycopyrolate –> this drug specifically will block muscuranic receptors in the mouth to prevent salivation. this is given to counteract some of the adverse effects of pyridostigmine / neostigmine.

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68
Q

alzheimers

A

Treat by increasing Ach:

  1. Donepzil
  2. Rivastigmine
  3. Galantamine

Memantine - preserves cell

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69
Q

Crutzfelt Jacob Disease

A

suspect in patients 50-70 who present with Rapidly progressive dementia and MYOCLONIC Jerks.. Patients eventually lose the ability to move and speak and become comatose.

Negative MRI
Negative LP (no infection)

must have 2 out of 4 clinical features:

  1. Myoclonus
  2. Akinetic mutism
  3. Cerebellar or visual disturbance
  4. Pyramidal / extra-pyramidal dysfunction (hypokinesia)
  5. Periodic sharp wave complexes on EEG and / or positive 14-3-3- CSF assay.

Definitive diagnosis is with above features + brain biopsy (gold standard) or demonstrated PRNP gene mutations.

Brain biopsy = MAT

14-3-3- protein will be found in CSF on LP.. this will spare you from having to do a brain biopsy.

There is no treatment.

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70
Q

Lewy Body dementia

A

vivid hallucinations (very detailed random hallucination) + Parkinson symptoms

at autopsy you will see “eosinophilic intracytoplasmic inclusions” representing accumulations of ALPHA SYNUCLEIN PROTEIN - may be seen in neurons of the SUBSTANTIA NIGRA.

Treatment for LEWY BODY DEMENTIA =

Carbidopa - levodopa for parkinsonism and CHOLINESTERASE inhibitors for cognitive impairment

If psychotic symptoms persist then add a SECOND gen antipsychotic (not first gen because, first gen will cause more neuroleptic symptoms)

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71
Q

Normal pressure hydrocephalus

A

wet
wacky
wobbly

Will show up on CT scan

Shunt these patients.

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72
Q

huntingtons

A

emotional lability
choreiform movements

Treat movement disorder with TETRABENZINE!!

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73
Q

which drugs can potentiate the effects of warfarin thus possibly leading to intracranial bleeds?

A

Normal INR for healthy people 1.1.

Normal INR for pepople being treated for a-fib etc. = 2-3.

INRs above this are supratheraputic and can lead to bleeds

Acetaminophen and phenylephrine both potentiate the anticoagulation effects of warfarn and can lead to bleeding.

Patients with warfarin associated intracerebral hemorrhage must have their anticoagulation reversed IMMEDIATLEY:

  1. Initial therapy is IV Vitamin K which has sustained response but takes 12-24 hurs to be effective (promotes clotting factor synthesis in liver).
  2. Prothrombin complex concentrate (PCC) should also be provided as it contains vitamin k dependent clotting factors 2,7,9,10 - which offeres rapid (within minutes) reversal of warfarin .. but only lasts for hours.. so need to make sure you give vita K also.

If PCC is not available you can use fresh frozen plasma.

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74
Q

syringiomyelia

A

disruption of csf drainage from the central canal of spinal cord leading to fluid filled caivty that compresses surrounding neural tissue.

Most common cause is usually a MVA. SYmptoms normally develop months to years later!

Damage most often is seen in spinothalamic (pain and temp) tract and upper extremity motor fibers, due to their medial locations around the central canal.

Will see upper extremity weakness and loss of pain and temp (cape like distribution).

will have preserved dorsal column function (light touch, vibration, position)

definitive diagnosis - MRI

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75
Q

botulism

A

descending progression of weakness

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76
Q

Fetal Alcohol syndrome

A

Leading cause of preventable birth defects.

Facial Dysmorphisms in FAS:

  1. Small palpebral fissures
  2. Smooth philtrum (vertical groove above upper lip)
  3. Thin vermilion border

height / weight / growth is compromised usaully below 10th% for age and sex.

microcephaly often present

cognitive and behavioral disorders:

  1. intellectual disability
  2. adhd
  3. social withdrawl
  4. delays in motor and language
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77
Q

Down syndrome

A 
MCC gentic cause of developmental delay
face:
1. flat facial profile
2. slanted palpebral fissures
3. small low set ears

Body:

  1. excessive skin at nape of neck
  2. Single transverse palmar crease
  3. clinodactyly
  4. large space between the first 2 toes
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78
Q

fragile x syndrome

A

most common x-linked inherited cause of intellectual disablity

CGG trinucleotide repeat expansion in FMR1 gene

face:

  1. long narrow face
  2. prominent forehead and chin
  3. large ears
  4. macrocephaly

Body:
1. macroorchidism

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79
Q

CMV

A

MCC congential viral infection and can cause developmental delay but also causes:

  1. sensorineural deafness
  2. blindness
  3. jaundice
  4. hepatosplenomegaly
  5. petechiae
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80
Q

hypoplastic fingers / nails and cleft palate are classic physical findings seen where?

A

fetal hydantoin syndrome - moms on phenytoin

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81
Q

congenital rubella

A

developmental delay +

  1. sensorineural deafness
  2. cataracts
  3. hepatosplenomegaly
  4. purpura
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82
Q

what is the largest risk factor for stroke?

A

HYPERTENSION!!

patients with HTN have 4x risk of stroke compared with normotensive patients.

hypertension increases the risk of stroke more than any other risk factor including hypercholestrolemia, diabetes, smoking, family history and sedentary lifestyle.

mild or moderate alochol consumption (1-2 drinks daily) reduces the risk of stroke

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83
Q

Single brain abscess

A

A single brain abscess in a non - HIV patient is usually the result of direct extension from an adjacent tissue infection (otits media, sinusitis, dental infection).

The 2 most commonly isolated organisms are:

  1. Staph Aureus
  2. Strep viridans

Brain imaging is first step –> CT scan or MRI. Initially will be normal but 1-2 weeks later the infection consolidates to a RING ENHANCING LESION with central NECROSIS.

Diagnosis requires BIOPSY (CT guided).

Empiric antibiotics with MEtro, Ceftriaxone and Vanc).

Also can be a neoplasm (lymphoma / blioblastoma) - These also present as a SINGLE RING ENHANCING lesion

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84
Q

Herpes encephalitis

A

acute symptoms of AMS, focal deficits and / or focal seizures. CT scan of the brain reveals HYPODENSE lesions in the temporal lobe. Ring enhancement is very uncommon.

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85
Q

HIV pt with ring enhancing lesion on CT

A

Nocardia - seen with CD4 <100

Toxoplasma - seen with CD4 <100

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86
Q

Absence seizures vs Inattentive staring spells

A

Absence seizures:

these are generalized seizures and are characterized by sudden impairment of consciousness in children 4-10 y/o.

  1. Occur during all activities
  2. relatively short .. less than 20 seconds.
  3. lack of response to vocal or tactile stimulation
  4. presence of automatisms (eye lid fluttering, lip smacking)
  5. NO loss of postural tone.

Absence seizures can be provoked by HYPERVENTILATION and are diagnosed via EEG –> characteristic 3-hz spike-wave discharge pattern during episodes.

First line treatment - Ethosuximide.

Inattentive Staring Spells:

  1. occurrence mainly during boring activities.
  2. variable length, often more than 1 min.
  3. respond to vocal or tactile stimulation
  4. lack of automatism
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87
Q

Babinksi sign

A

upward deviation of the great toe when the sole of the foot is stroked –> evidence of hyperreflexia and suggests Upper motor neuron lesion.

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88
Q

Alcoholic cerebellar degeneration

A
  1. progressive gait dysfunction
  2. turncal ataxia
  3. nystagmus
  4. intention tremor or dysmetria (tremor when attempting to touch a target)
  5. impaired rapid alternating movements (dysdidadochokinesia)
  6. may have muscle hypotonia leading to a pendular knee reflex (swinging more than 4 times is abnormal)
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89
Q
  1. Encephalopathy
  2. Ocular Dysfunction
  3. Gait ataxia
A

wernicke encephalopathy

Always give Thiamine first, before glucose!

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90
Q

Slurred speech, ataxia, HYPOtension, depressed mental status.

A

Benzo Overdose

Flumazenil is a competitive antagonist of the GABA / Benzo receptor.

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91
Q

Alzheimers disease

Starts with MEMORY symptoms before anything else (anterograde memory loss - forming new memories, immediate recall).. distant memories are preserved.

Later findings include:

  1. personality and behavioral changes (apathy, agitation).
  2. neruopsych changes (delusions, paranoia)
  3. neuro manifestations (myoclonus, seizures)
  4. Apraxia (difficulty with motor tasks)
  5. Urinary incontinence.
A

Alzheimers disease’

This is the most common cause of dementia in the U.S.

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92
Q

Dementia with Lewy Bodies

A

In addition to the presence of dementia, the diagnosis requires 2 or more of the following clinical features:

  1. Parkinsonism
  2. Fluctuating cognition
  3. visual hallucinations
  4. REM sleep behavior disorder
93
Q

Frontotemporal Dementia

A

Begins with PERSONALITY and BEHAVIORAL changes and then later with memory deficits.

Occurs around age 60.. much earlier than alzheimers or anything.

94
Q

Normal Pressure Hydrocephalus

A
  1. abnormal gait - broad based and shuffling
  2. cognitive impairment
  3. urinary incontinence

Gait impairment is the most prominent feature and is the first presenting symptom!

vetricular enlargement on CT

95
Q

vascular dementia

A

Deficits in executive function are much more severe than memory deficits early in the course of the disease.

96
Q

how is stroke categorized

A

Stroke is either Ischemic or Hemohragic.

Hemorrhagic is further broken down into Subarachnoid hemorrhage or Intracerebral Hemorrhage.

Intracerebral Hemorrhage is characterized by:
1. ACUTE focal neurologic deficits that gradually worsen over minutes to hours.
2. as the hemorrhage expands symptoms of elevated ICP (headache, vomiting, AMS) may develop.
HTN is the most important risk factor for developing this.

Subarachnoid Hemorrhage - presents with the sudden onset of SEVERE headache that may be associated with brief loss of consciousness, nausea/ vomiting, and meningismus.

Patients with Ischemic stroke: Have an abrupt onset of FOCAL NEURO deficits, but lack headache and impaired consciousness. A previous history of TIA is characteristic of ischemic stroke.

97
Q

BIT for any suspected stroke?

A

CT w/o Contrast.

MRI is more sensitive.. but its more expensive, slower and not available everywhere.. so its not first line.

CT angiogram can be done but only after a noncontrast CT

98
Q

essential tremor

A

Action Tremor –> worse when trying to do goal-directed actions (buttoning shirt, drinking from a glass)

Strong family history link

Usually bilateral

affects hands > arms > head > legs

Treatment:

  1. BB –> first line
  2. anticonvulsants – primidone
  3. small amounts of alcohol
  4. Benzos – clonzaepam

Parkinson has a RESTING tremor not action.

99
Q

falling with something in mouth

A

cervical INTERNAL carotid artery dissection.

Diagnosis = CT or MRA

Dissection –> thunderclap headache, symptoms of an ischemic stroke (hemiparesis, facial droop, aphasia).

100
Q

homocystinuria

Lens dislocation
intellectual disability
marfanoid features
Increased risk of arterial and venous thrombi

A

homocystinuria

101
Q

NFI vs NF2

A

NF1:
Autosomal Dominant –> mutation in NF1 gene.
cognitive deficits, seizures.

  1. cafe au-lait macules
  2. AXILLARY AND INGUANL FRECKLING (not seen in NF2)
  3. Lisch Nodules (iris hamartomas)
  4. Neurofibromas (optic pathway glioma)

Must get yearly opthalmologic exams.

NF2:
Acoustic neuromas (vestibular schwannomas) usually bilateral.
DO NOT have cafe-au-lait macules or axillary / inguinal freckling.

102
Q 
ash leaf spots
angiofibromas
shagreen patches
bengin tumors in multiple organs
intracardiac rhabdomyomas
A

Tuberous Sclerosis

103
Q

what finding on neuroimaging is the hall mark of a prolonged seizure

A

Cortical laminar necrosis

hall mark of prolonged seizures. More than 5 minutes of seizing can cause cortical laminar necrosis.

Pathophys - excitatory cytotoxicity leads to brain dying.

104
Q

vincristine side effect?

A

peripheral neuropathy.

will also cause loss of ankle jerk reflexes. Occasionally there can be motor nephropathy resulting in weakness and BILATERAL FOOT DROP!

105
Q

pseudotumor cerebri what is the pathophys?

A

obese female with dull headache.

Normal neuroimaging but elevated CSF pressure.

Pathophys –> impaired absorption of CSF by the arcachnoid villi.

Treatment –> weight loss is first line.. 2nd line is acetazolamide.

if both of these fail next step is shunting or optic never sheath fenestration to prevent blindness.

106
Q

diffuse axonal injury

A

the most significant cause of morbidity in patients with traumatic brain injuries.

Frequently due to traumatic deceleration injury and results in a vegetative state.

CT scan - Numerous minute punctuate hemorrhages with blurring of the gray-white interface.

MRI is more sensitive than CT for diagnosing

107
Q

Epidural vs subdural vs subarachnoid

A

epidural - biconvex collection on CT

Subdrual - Crescentic collection on CT

Subarachnoid hemorrhage - acute severe headache and CT will show presence of blood within subarachnoid space

108
Q

Myasthenia gravis

A

NMJ disorder caused by autoantibodeis against Ach receptors in the motor end plate

109
Q

Alzheimers disease treatment

A

cholinesterase inhibitors:

  1. donepezil
  2. rivastigmine
  3. galantamine
110
Q

Multiple sclerosis acute attack treatments

A

for acute attacks use IV glucocorticoids first.

IF that doesn’t work do plasma exchange.

111
Q

Solitary and periventricular, weakly ring enhancing mass on MRI.

A

CNS Lymphoma

Presence of EBV DNA in the CSF is specific for this condition.

112
Q

heat storke vs heat exhaustion

A

same disease except heat stroke ALSO has CNS dysfunction (confusion, irritablity, seizures).

treatment - Rapid cooling – ice water immersion preffered, if dont have that then do evaporative cooling

make sure to give fluids and correct electrolytes

antipyretics make no difference here.

113
Q

what is the primary risk factor for intraventricular hemorrhage?

A

Prematurity

114
Q

RLS

A

first line treatment:
Dopamine agonists –> Pramipexole!

2nd line –> Alpha-2-delta calcium channel ligands (gabapentin enacarbil)

115
Q

angle closure glaucoma

A

Headache and decreased vision.

Occurs in people above 60 y/o.

On examination:

  1. Conjunctival Erythema
  2. Mid-dilated pupil that is poorly reactive to light
116
Q

why do patients get ipsilateral dialtion of the pupil from a epidural hematoma?

A

Trauma –> middle meningieal artery rupture –> epidural hematoma

If an epidural hematoma is left untreated it will cause worsening intracranial HTN which will result in UNCAL HERNIATION.

On exam patients with
uncal herniation will have dilation of the pupil on the ipsilateral side of the lesion due to Oculomotor nerve compression, along with ipsilateral hemiparesis due to contralateral crus cerebri compression.

Emergent craniotomy should be performed in patients with focal neuro deficits to prevent brain herniation and death.

117
Q

seizure vs syncope

A

Seizure = sudden LOC + loss of postural tone + DELAYED retrun to baseline mental status.

Syncope = transient LOC + loss of postural tone + IMMEDIATE spontaneous return to baseline neurological function.

118
Q

acetaminophen toxicity

A

very predictable:

  1. nausea / vomiting
  2. RUQ pain
  3. Elevated LFTs
  4. Potential liver failure / death

NO SEIZURES

119
Q

Bacterial Meningitis in children > 1 month

A

Fever, Increased ICP (headache, vomiting , AMS), Meningial irritatoin (nuchal rigidity)

Tx : IV Vanc & Ceftriaxone or Cefotaxime

If HIB –> add Dexamethasone

Complications –> up to 50% of kids with BACTERIAL meningitis will have long term consequences including:

  1. Intellectual / behavioral disabilities
  2. hearing loss (sensorineural due to infection / inflammation of the 8th CN, the cochlea or the labyrinth)
  3. seizures
  4. cerebral palsy

All patients who have had bacterial meningits must undergo audiologic testing to identify any hearing deficits.

120
Q

Todd paralysis

A

self limited, focal weakness or paralysis after a focal or generalized seizure.

Presents in the postictal period with hemiparesis or complete hemiplegia involving extremities on one side of the body.

typicaly resolves within 36 hours.. treatment is supportive.

121
Q

The presence of an extra-axial well circumscribed or round homogenously enhancing dural-based mass on MRI is strongly suggestive of what?

A

Meningioma

Meningiomas undergo calcification and can appear hypredense on non-contrast head CT.

Meningiomas are benign but can cause mass effect and thus cause symptoms. The treatment of choice is COMPLETE RESECTION.

122
Q

how do brain metastis present on imaging?

A

Brain Mets is much more common than primary brain tumors.

Present as multiple - ring-enhancing lesions at the grey-white junction (intra-axial).

123
Q

Benign Tumors and Malignant tumors

A

Benign Tumors:

  1. Pituitary adenoma (most common)
  2. Craniopharyngioma –> occurs commonly in kids.. but 50% occur in adults
  3. Meningioma
  4. Pituicytoma (low grade glioma)

Malignant tumors:

  1. Primary (Germ cell tumors, choroma, lymphoma)
  2. Metastatic (breast, lung etc)
124
Q

Craniopharyngiomas

A

benign tumors arising from rathkes pouch. Press on pituitary gland –> bitemopral hemianopia.. endocrine abnormalities.

Diagnosis confirmed with MRI or CT

Treatment = surgery and /or radiotherapy.

125
Q

Neuroimaging findings for

NPH
Fronto-temporal dementia
Alzheimers

A

Alzheimers - Temporal and Parietal lobe atrophy

Fronto-temporal dementia - Frontal and Temporal lobe atrophy

NPH - Enlarged ventricles and NO cortical atrophy

126
Q

Hemi-Neglect syndrome

A

characterized by ignoring the left side of a space – Involves the right (non-dominant) parietal lobe

127
Q

what is the # 1 abortive therapy for cluster headaches?

A

100% oxygen

sub cuteaneous Sumatriptan can be used also as long as there are not contraindications (ischemic heart disease, prego)

128
Q

tetanus MOA

A

C. Tetani secretes toxin that binds to the peripheral nerve terminals –> using retrograde axonal transport it arrives at the CNS synapse –> here it blocks the release of inhibitory neurotransmitters Glycine and GABA across the synaptic cleft.

this process takes long.. so symptoms occur a few days to several weeks following inoculation and can include sweating , dysphagia, tachy, labile BP, Trismus /lockjaw, painful muscle spasms, muscle stiffness!

129
Q

Intraventricular Hemorrhage

A

Premature babies are at increased risk due to less developed vasculature. Acute changes in cerebral perfusion (hypotension, hypoxia, hypo or hyper ventilation) are all risk factors.

Majority of infants with IVH are asymptomatic!

Sympomatic infants will present with the following:

  1. lethargy
  2. Hypotonia
  3. Apnea
  4. Seizures
  5. Bulging fontanelle
  6. Increased Head circumference.

Diagnosis is made by Cranial Ultrasound!

130
Q

what is the best test to confirm parkinsons disease?

A

PHYSICAL EXAM!!!

Caused by accumulation of alpha-synuclein within the neurons of the substantia nigra pars compacta, which ultimately leads to the death of these neurons.

3 cardinal signs on PE:

  1. Resting Tremor
  2. Rigidity
  3. Bradykinesia

2 of these 3 suggest parkinsons which can be CONFIRMED by PE

131
Q

How do you diagnose brain death?

A

its a clinical diagnosis.. and differs from country to country.

The characteristic findings are absent cortical and brain stem functions:

  1. pupillary light reaction
  2. oculovestibular reaction
  3. heart acceleration after atropine injection
  4. Spontaneous respiration at pco2 =60

DTRs will be preserved because that is a spinal cord function.

132
Q

Optic Neuritis

A

Primarily in young women

associated with MS

Immune mediated demyelinaiotion.

Symptoms:

  1. Acute in onset.. peaks at 2 weeks.
  2. Monocular vision loss
  3. Eye pain WITH MOVEMENT
  4. WASHED OUT COLOR VISION
  5. AFFerent pupillary defect
  6. central scotoma

Normal fundoscopy

Diagnosis - mri of the orbits and brain.

Treatment - IV Corticosteroids!!

35% recur

133
Q

Acute anterior uveitis

A

PAINFUL + RED eye + Blurry vision and photophobia.

134
Q

Central Retinal Artery Occlusion

A

elderly patients almost exclussively.

ACUTE, SEVERE, painLESS monocular vision loss

Fundoscopy abnormalities - Retinal whitening, CHERRY RED SPOT –> always present.

135
Q

Macular Degeneration

A

painLESS, progressive loss of CENTRAL VISION, usually in older patients.

BOTH eyes are affected usually

Fundoscopid abnormalities –> DRUSEN (yellow deposits)

136
Q

Open angle glaucoma

A

gradual PAINLESS peripheral vision loss.

Fundoscopy - optic disc enlargement with an increased CUP:DISK ratio.

137
Q

Retinal Detachment

A

FLoaters or Flashes of light and lose peripheral vision FIRST

138
Q

dix hallpike test

A

used to diagnose BPPV
benign paroxysmal positional vertigo -

characterized by short episodes of vertigo with or without nausea/ vomiting due to specific head movements (rolling over in bed, looking up).

139
Q

Carotid sinus massage

A

used to diagnose / treat tacharrhytmias (PSVT).

140
Q

dementia with lewy bodies vs frontotemporal dementia vs prion disease

A

Dementia with lewy bodies:

  1. Visual HALLUCINATIONS
  2. spontaneous PARKINSONISM
  3. Fluctuating cognition

Frontotemporal Dementia:

  1. EARLY PERSONALITY CHANGES
  2. apathy, disinhibition and compulsive behavior
  3. Frontotemporal ATROPHY on neuroimaging

Prion Disease:

  1. Behavioral changes
  2. RAPID PROGRESSION
  3. MYOCLONUS and / or seizures

Vascular Dementia:

  1. STEPWISE decline
  2. early executive dysfuntion
  3. CEREBRAL INFARCTION and or deep white matter changes on neuroimaging.
141
Q

Trihexyphenidyl

A

used to treat the TREMOR in parkinsons.

tremor is usually the first symptom.. trihexyphenidyl should be perscribed to patients with just a tremor.

142
Q

wernicke encephalopathy

A

Seen in:

  1. alcoholics
  2. malnutrition - anorexia
  3. hyperemesis gravidarum

Patho phys – thiamine deficency.

Clinical features:

  1. ENCEPHALOPATHY - confusion
  2. OCULOMOTOR DYSFUNCTION (horizontal nystagmus)
  3. Postural and GAIT dysfunction - broad based wide gait

Treatment - IV Thiamine followed by glucose infusion

143
Q

epidrual hematoma

A

trauma to sphenoid - rupture of middle meningieal

BICONVEX (lens shaped) hyperdensity does NOT cross suture lines

Brief LOC followed by LUCID interval

Hematoma expansion leads to:
1. Increased ICP –> impaired consciousness, headache, nausea, vomiting

  1. Uncal herniation –> ipsilateral CN3 palsy + Hemiparesis

Treatment = URGENT surgical evacuation for symptomatic patients

144
Q

Pronator Drift Test

A

A physical exam finding that is relatively sensitive and SPECIFIC for Upper Motor Neuron or Pyramidal / Corticospinal Tract disease!

Useful in patients with subtle deficits as it can accentuate pyramidal motor weakness.

Performed by having the patient OUTSTRETCH the ARMS with the PALMS UP, and EYES CLOSED (so that only propioception is used to maintain arm position). Upper Motor Neuron Lesions cause more weakness in the supinator muscles compared to the pronator muscles of the upper limb. As a result, the affected arm drifts downard and the palm turns (Pronates) towards the floor)

Pyramidal tract signs - pronator drift, focal weakness, spasticity, hyperreflexia, and babinski sign

145
Q

cerebellar dysfunciton signs

A

ataxia
intention tremor
impaired rapid alternating movements

146
Q

Basal ganglia dysfunction signs

A

extrapyramidal signs such as - resting tremor, rigidity, bradykinesia, and choreiform movements.

147
Q

Subdural Hematoma

A

Rupture of bridging veins

Subdural bleeding can manifest as the following in children:

  1. Seizures
  2. Increased head circumference,
  3. Bulging / tense anterior fontanelle
  4. Papilledema
  5. AMS

Shaking will cause vitreoretinal traction and retinal hemorrhages –> pathagnomonic for ABUSIVE head trauma

When suspecting abuse do the following:
1. Non contrast head CT for evaluation of intracranial injury
2. Skeletal Survey - to identify occult fractures
MUST hospitalize and contact CPS

Elderly patients on the other hand can get chronic Subdural Hematomas also due to traumatic head injury.. in chronic SDH there is a slow bleed into subdural space.. still from the ruptured bridging veins. This leads to symptoms that can develop and present weeks after the fall / injury –> headache, somnolence and confusion are very common symptoms. May also have focal neuro deficits due to compression of the underlying cerebral cortex.

Diag
.

148
Q

Tabes Dorsalis Features

A

Syphilis has increased incidence in gays and HIV infected patients.

HIV+ pts develop neurosyphilis more rapidly

T. Pallidum spirochetes directly damage the dorsal sensory roots. Causing secondary degeneration of the dorsal columns.

Clinical findings:

  1. Difficulty walking / imbalance / many falls due to imbalance. – impaired knee and anckle reflexes, impaired vibratory and position sensation bilaterally. Broad based gait..
  2. Lancinating Pains - transient, shrap, stabbing pains in random parts (back, lower limbs, arms)
  3. Neurogenic urinary incontinence - Involuntary dribbling of urine
  4. Argyl Robertson Pupil - Bilateral small, irregular pupils that will POORLY constrict to light but will constrict normally when looking at something close to the nose (ACCOMMODATION)
149
Q

subacute combined degeneratoin

A

affects 3 tracts:

  1. Dorsal Columns - loss of position and vibration sense, Positive romberg sign
  2. Lateral Corticospinal Tracts - Spastic Paresis, Hyperreflexia
  3. Spinocerebellar tracts - Ataxia

Treatment = B12

150
Q

Acute Angle-Closure Glaucoma (ACG)

A

due to sudden narrowing or closure of the Anterior Chamber Angle.

This causes the lens to move foreward and rest against the Iris –> this partially covers teh anterior chamber angle and prevents nomral flow of aqueous humor (through the pupil and into the anterior chamber), therby INCREASING INTRAOCULAR PRESSURE.

Sudden angle closure typically occurs as a respone to pupilary dilation from medications or other stimuli (dim light):

  1. Anticholinergics (tolterodine)
  2. Sympathomimetics
  3. Decongestants

Symptoms:

  1. Rapid onset of eye pain - may see halos around lights
  2. Injected eye, and the PUPIL will be DILATED and POORLY responsive to light.
  3. Tearing / headache / nausea and vomiting as the IOP increases.

Untreated ACG can lead to severe and permanent vision loss within 2-5 hours of symptoms – rapid treatment is mandatory

151
Q 
Myasthenia Gravis 
vs
Lambert Eaton syndrome
vs
Dermatomyositis / polymyositis
A 
Myasthenia Gravis: POST synapitc Ach Receptors
Fluctuating muscle weakness:
1. Ocular - Ptosis, Diplopia
2. Bulbar - Dysphagia, Dysarthria
3. Facial, neck, limb muscles
NO LOSS OF REFLEXES

Lambert-Eaton syndrome: Presynaptic Ca Channels:

  1. Initial symptoms- Symmetric Proximal Muscle Weakness (standing from a chair, combing hair, putting dishes overhead)
  2. Autonomic dysfunction (dry mouth, Erectile dysfuntion. etc.)
  3. CN involvement (ptosis)
  4. DIMINISHED or ABSENT DTRs

Dermatomyositis / Polymyositis: Muscle Fiber Inflammation / injury:
1. Symmetrical and More PROXIMAL muscle weakness
2. Interstital Lung DISEASE, esophageal dysmotility, Raynaud Phenomenon
3. Polyarthritis
4. Esophageal Dysmotility
5. SKIN FINDINGS (Gottorn Papules, Heliotrope rash) in dermatomyositis
NO LOSS OF REFLEXES

152
Q

What is the MCC of Lumbar SPnial Stenosis?

A

Lumbar Spinal Stenosis is a common cause of pain in the low back and legs - may result from ANY condtion that narrows the spinal canal and compresses never roots.

The MCC of lumbar spinal stenosis is Degenerative JOINT DISEASE

In DJD - disc herniation and facet osteophytes impinge on the spinal cord.

Flexion of spinal cord = widening = improved symptoms = walking up hill, sitting.

Extension = narrowing = worse symptoms = standing, walking downhill

only 10% of patients have a positive straight leg test. Neuro exam may also be completly noirmal.

Diagnosis is confimred radiologically - MRI demonstrates bony anatomy, neural structures, and soft tissue = Best test for suspected lumbar spinal stenosis.

153
Q

IVDU with known bacterial endocarditis gets a stroke.. how do you treat?

A

Patients with bacterial endo are at high risk for complications - including TIA or stroke due to septic emoli. This is commonly seen in the distribution of the MCA.

Treatment for a septic emboli causing stroke is IV antibiotics. NOT anti-platelets, heparin or warfarin.

154
Q

Botulism

A

Clostridium Botulinum toxin - inhibits PRESYNAPTIC ach release at NMJ.

Sources - Canned foods (fruits, veggies), Aged seafood (cured fish).

Clinical features:

  1. acute onset within 36 hrs of ingestion
  2. Bilateral cranial neuropathies (blurred vision, diplopia (fixed dilated pupil), facial weakness, dysarthria, dysphagia).
  3. Symmetric DESCENDING muscle weakness
  4. Diaphragmatic weakness with resp failure!

Diagnosis - Serum analysis for TOXIN

Treatment = EQuINE serum Heptavalent BOTULINUM ANTITOXIN.

155
Q

Organophosphate posioning

A

leads to too much AcH:

  1. Bradycardia
  2. Miosis
  3. Bronchospasm
  4. Vomiting / diarrhea

Atropine blocks the peripheral effects of Ach at muscuranic receptors, whereas PRALIDOXIME reactivates ACHesterase.

156
Q

Benign Paroxysmal Positoinal Vertigo (BPPV)

A

Due to Calcium Crystals within the SEMICIRCULAR CANALS (canaliths).

Brief and recurrent episodes described as a feeling of the room spinning when turning the head to one direction or looking up.

Will often have nystagmus and nausea (rarely vomit), without signigifcant ear pain, tinnitus or hearing loss.

157
Q

Diabetic autonomic dysfunction vs BPPV

A

in diabetic autonomic dysfunction - Postural HYPOtension with DIZZINess while standing.

158
Q

Meniere disease

A

Caused by excess endolymphatic fluid pressure in the inner ear that presents with the triad of:

  1. EPisodic Dizziness
  2. Low frequency Hearing Loss
  3. Tinnitus

Patients can develop vertigo that lasts for days and is associated with nausea, vomiting, and horizontal torsional nystagmus during the episode

159
Q

Vertebrobasilar Insufficiency

A

Reduced Blood Flow in the Posterior circulatoin of the brain, typically as a result of Emboli, Thrombi, or Arterial Dissection.

Symptoms:

  1. Vertigo (most common symptom)
  2. Dysarthria
  3. Diploplia
  4. Numbness
160
Q

Amyloid Angiopathy

A

Most Common Cause of Spontaneous LOBAR Hemorrhage –> particularly in adults > 60.

Occurs as a consequence of Beta Amyloid deposition in the walls of small to medium sized cerebral arteries –> resulting in vessel wall weakening and predisposition to rupture.

Not associated with systemic amyloidoses, rather, the amyloidogenic proteins are usually the same as those seen in ALZHEIMERS Dementia.

Hemorrhage usually occurs during routine activity and most often involves the OCCIPITAL and PARIETAL lobes.

Parietal Hemorrhages:

  1. Contralateral hemisensory loss (due to primary somatosensory cortex injury)
  2. Contralateral Hemineglect

Hematoma expansion = elevated ICP –> impaired consciousness, confusion, headahe, and nausea / vomiting

161
Q

MCC of INtracrainal hemorrhage in children?

A

AVM Rupture

162
Q

Cardioembolic STROKE

A

occurs commonly in the setting of a-fib.

Patients will have:

  1. Sudden onset neuro deficits that follow a Stuttering course
  2. Neuroimaging will CLASSICALLY show MULTIPLE ISCHEMIC infarcts at the GREY-WHITE matter junction
163
Q

Bilateral Acoustic Neuromas (vestibular schwannomas) are diagnositc of what disease?

A

NF2

The vestibular schwannomas can cause sensorineural hearing loss and are diagnostic of NF2.

Audiometry is the best initial screening test for the diagnosis of acousitc neuromas.

NF2 DO NOT have Cafe-au-lait spots or axillary / inguinal freckling.. thats ONLY in NF1

164
Q

Mallory Hylaine on liver biopsy is seen where?

A

Seen in alcoholic liver injury most commonly.

only other place seen in Wilsons Disease!@

165
Q

Wilsons disease diagnosis

A

Low serum ceruloplasmin + 1 of the below:

  1. Increased urinary copper excretion
  2. Kayser-Fleischer rings (slit lamp exam)
166
Q

PAS + and Diastase-resistant granules seen on liver biopsy indicate what?

A

Alpha-1 Antitrypsin deficiency

167
Q

Is the increased CSF pressure in NPH due to increased CSF production or decreased CSF absorption?

A

DECREASED CSF ABSORPTION!!!

CSF production usually increases at night in normal people.. There are NO diseases in which there is increased CSF production.

168
Q

How can you tell if someone with MS is having a TIA?

A

Neurological deficits related to an acute demyelinating plaque of MS usually last for DAYS to WEEKs

In contrast

TIA symptoms last for less than 24hrs.

Patients with MS and NEW neuro deficits should not always be assumed to have and MS exacerbation.. look at risk factors for stroke and TIA and rule those out first!

169
Q

Preventing recurrent TIA after the first one.

A

Look at risk factors:

  1. Discontinue tobacco use
  2. Start aspirin
  3. Start statin for hyperlipidemia
  4. Reduce BP
170
Q

what are features of Bulbar Dysfunction?

A

3 things:

  1. Dysarthria - weakness in muscles used for speech - slurring words
  2. Dysphagia - difficulty swallowing
  3. Fatigable Chewing
171
Q

An opening pressure above what mm H2O is considered high in Pseudotumor Cerebri?

A

> 250.

Pseudotumor cerebri: Young obese woman, with holocranial headache, vision changes (blurry vision and diplopia), pulsatile tinnitus (whooshing sound in ears).

Meds associated with pseudotumor cerebri:

  1. Isotretinoin
  2. Tetracyclines
  3. Growth Hormone
  4. Excessive Vitamin A

Evaluation of Pseudotumor Cerebri:

  1. complete ocular exam and neuroimaging to exclude secondary causes if increased ICP (mass, hemorrhage, cerebral vein thrombosis).
  2. LP to document opening pressure.

LP should be done with patient in lateral decubitus position and legs extended. Pressure above 250mm H2O = abnormal.

Empty sella in about 70% of patients

172
Q

Brain changes in neurodegenerative diseases:

Huntingtons
Alzheimers
Wilsons
Picks disease

A
  1. Huntingtons - atrophy of caudate nucleus
  2. Alzheimers - Diffuse atrophy of the cerebral cortex
  3. Wilsons disease - Atrophy of the lenticular nucleus
  4. Picks disease - atrophy of the temporal and frontal lobes.
173
Q

Glioblastoma multiforme apperance on CT?

A

Classic BUTTERFLY apperance with CENTRAL necrosis

174
Q

Sturge Weber Syndrome

A

Mutation in GNAQ gene –> causes capillary malformations including a leptomeningeal capillary-venous malformation affecting the brain and eye

Clinical features:

  1. Port wine stain (trigeminal nerve distribution)
  2. Leptomeningeal capillary-venous malformation
  3. Seizures +/- Hemiparesis
  4. Intellectual disability
  5. Visual Field Defects
  6. Glaucoma

Diagnosis:
MRI of brain WITH contrast –> detects intracranial vascular malformations and is diagnositc

Treatment:

  1. Laser THerapy
  2. Antiepileptic drugs
  3. Intraocular pressure reduction
175
Q

how does hyperventilation lower ICP?

A

cerebral vasoconstriction (less CO2 results in vasoconstricion.. more CO2 results in vasodilation)

176
Q

Interventions for lowering ICP and mechanism

A

Head elevation - Increased venous outflow from brain

Sedation - Decreased metabolic demand and control of HTN

IV Mannitol - extraction of free water from brain tissue –> osmotic diuresis

Hyperventilation –> CO2 washout –> vasoconstriction

Removal of CSF –> reduction of CSF volume / pressure

177
Q

What is the first imaging study that should be done in Myasthenia gravis patients in whom the diagnosis is confirmed?

A

Chest MRI or CT –> look for thymoma

178
Q

Tension headache

A

Onset during stress

Band like pattern around the head (bilateral) mainly around temporal and occipital regions

Dull, tight and persistent (not throbbing or pulsatile like migraine)
NO Nausea or vomiting or Visual symptoms (photophobia)

can last anywhere from 30 mins to one week!!!

179
Q

what is the treatment for ALS?

A

Riluzole

Wont cure disease but can slow progression.

Its a glutamate inhibitor

Side effects - Dizziness, nausea, weight loss, elevated liver enzymes and Skeletal Weakness

180
Q

Homocystinuria

A

Marfanoid body habitus +

  1. intellectual disabilities
  2. THROMBOSIS
  3. autosomal recessive
  4. downward lens dislocation
  5. megaloblastic anemia
  6. fair complexion

Deficiency in systathionine synthase causes errors in METHIONINE metabolism resulting in ELEVATED homocystine and METHIONINE levels.

Treatment: Vitamin B6 and Vtiamin B12 to lower homocysteine levels. and make sure to give ANTICOAG or antiplatelets to prevent stroke, coronary heart disease, or venous thromboemoli

181
Q

Ehlers Danlos

A

A collagen disorder characterized by SCOLIOSIS, Joint LAXITY, and skin HYPER-ELASTICITY.

These patients DO NOT have tall stature, lens dislocation or hypercoagulability

182
Q

Marfans vs HOMOcystinuria

A

Both will also have the marfanoid body habitus:

  1. pectus deformity (chest pointing down)
  2. Tall stature long limbs
  3. Arachnodactyly
  4. Joint hyperlaxity
  5. Skin Hyperelasticity
  6. Scoliosis

HOwever Homocystinuria will also have fair complexion, developmental delay, and thromboembolic events.. MARFANS WILL NOt

183
Q

Crainopharyngiomas

A

Arrise in the sella turcica (SUPRATENTORIAL) right where the pituitary gland is.

They appear as cystic structures with calcification on imaging.

Symptoms include visual field defects and hormonal deficiencies (eg. growth hormone) due to compression of surrounding structures (optic chiasm, pituitary stalk)

184
Q

Ependymomas

A

Glial cell tumors that arrise from the EPENDYMAL cell lining of the ventricles and spinal cord.

In children the most common site is the 4th ventricle in the POSTERIOR FOSSA, where tumor expansion leads to obstruction of CSF and increased ICP.

Dont get a lot of weakness and seizures with these

185
Q

Glioblastomas

A

SUPRATENTORIAL - high-grade astrocytic tumors that typically arise in the cerebral hemispheres and present with seizures and signs of increased ICP. These are MUCH LESS common than low-grade astrocytomas in children

186
Q

Medulloblastoma

A

2nd most common tumor of the posterior fossa in children.

These tumors are INFRATENTORIAL tumors and typically arise from teh CEREBELLAR VERMIS and present with VOMITING, HEADACHES, and ATAXIA

187
Q

Neuroblastomas

A

Tumors that arise from SYMPATHETIC GANGLION CELLS and usually present with an abdominal mass. Mets can occur to the bone and liver.

Primary CNS tumors are much more common in pedicatric patients than are mets to the CNS

188
Q

What is the most common CNS tumor in peds?

A

Low grade ASTROCYTOMAS (specifically, PILOCYTIC ASTROCYTOMA) is the most common peds CNS Tumor.

In peds.. CNS tumors are the most common solid tumors and the 2nd most common malignancies after lukemias.

These tumors cause symptoms due to local pressure on adjacent structures and DO NOT undergo malignant transformation

189
Q

Supratentorial tumors vs posterior fossa tumors

A

Supratentorial tumor symptoms:

  1. Seizure
  2. Weakness
  3. Sensory Changes

Posterior Fossa Tumor:
1. cerebellar dysfunction (ataxia, dysmetria)

Signs of increased ICP (early morning headaches, vomiting, pailledema) can occur as the tumor enlarges REGARDLESS of location.

190
Q

During Transtentorial (uncal) herniation what nerve is most likely to be injured?

A

Oculomotor

191
Q

Internal capsule stroke presentation

A

patients will have a contralateral either PURE motor or sensory and motor deficits

192
Q

post stroke patient feels pain.. and its classically exacerbated by light touch.. where was the stroke and what is this called?

A

Stroke was in the Thalamus

This is called Thalamic Pain Syndrome (Dejerine-Roussy Syndrome)

193
Q

Ascending paralysis from a tick vs ascending paralysis from GBS

A

In a tick - the paralysis is usually quick onset.. over hours to days.

In GBS - the paralysis happens over days to weeks.

both present similarly..

differences:
GBS is symmetrical and has AUTONOMIC PROBLEMS associated with it

Tick - symmetrical.. bu tmore pronounced in one limb vs the other.. and NO autonomic problems

194
Q

Encephalitis symptoms

A

Herpes encephalitis is the most common cause of fatal sporadic encepahlitis in the U.S and is caused usually by HSV1

Presents with acute onset (less than 1 week duration) of FOCAL NEURO findings including:

  1. Altered mentation
  2. Focal Crainal nerve deficits
  3. Ataxia
  4. Hyperreflexia

Fever in 90% of patients
BEHAVIORAL CHANGES!

CSF examination:

  1. Increased lymphocytes
  2. Increased erythrocytes (hemmhoragic destruction of temporal lobes)
  3. Elevated protein levels

Specific to heprpes enchephalits:
Imaging: Temporal lobe lesions
MRI is better.. CT can be normal in up to 50% of patients

EEG = Prominent intermittent high amplitude slow waves (seen in 70-80% of patients)

PCR analysis of HSV DNA in CSF = GOLD STANDARD for diagnosis.

IV Acyclovir = treatment of choice

195
Q

Cryptococcal meningitis

A

Seen almost exclusively in IMMUNOCOMPOROMISED patients.. very uncommon in immunocompetent patients.

CSF findings:

  1. Low leukocytes.. with mononuclear predominance
  2. slightly elevated proteins
  3. low glucose
  4. elevated opening pressure

Use India Ink to detect organisms

196
Q

Conductive vs Sensorineural hearing loss

A

Conductive = any cause that limits sound from gaining access to the inner ear:

  1. Otits Externa or Media
  2. Cholesteatoma
  3. Trauma
  4. Cerumen
  5. Tympanic membrane perforation

Sensorineural = Disorder involving inner ear, cochlea, or auditory nerve

  1. Presbycusis
  2. Meniere disease
  3. Barotrauma
  4. Acoustic Neuroma
  5. Cerebrovascualr Ischemia
197
Q

Presbycusis (age related hearing loss) is characterized by what?

A

Progressive BILATERAL and SYMMETRIC, predominantly HIGH-FREQUENCY (sensorineural) hearing loss that occurs over many years.

Caused by DEGENERATIVE CHANGES of the inner ear or cochlear portion of the 8th crainal nerve.

They can hear well in 1 on 1 convos in a quiet room.. but when there is competing noise they cant hear anymore.

Bilateral TINNITUS can develop as the disease progresses

Unilateral or pulsatile tinnitus (seen in vascular malformations or pseudotumor cerebri) should prompt exploration of other diagnosis.

198
Q

Acoustic neuroma etiology and symptoms

A

arris from SCHWANN CELLS covering the VESTIBULAR BRANCH of the 8th CN.

as it grows it can cause symptoms such as VERTIGO, UNILATERAL TInNITUS, and SENSORINEURAL HEARING LOSS

199
Q

Cholesteatoma

A

Erosive and Expansile growth consisting of KERATINIZING SQUAMOUS EPITHELIUM. –> causes destruction of the bones of the MIDDLE EAR (ossicles), and sensorineural structures of the inner ear.

Otoscopic exam - WHITE PLAQUE on teh TM with or without perforation or retraction

200
Q

Otosclerosis

A

sclerotic changes within ossicles of the MIDDLE ear –> conductive hearing loss and normal otoscopic exam.

201
Q

what is the treatment of choice for agitation in the elderly?

A

low dose haloperidol

atypicals can also be used, but prolonged use can increase mortality in the elderly

Benzos are used for agitation in young patients.. but generally contraindicated in elderly.

202
Q

what is the most common form of hereditatry Ataxia?

A

Friedreich Ataxia.

Autosomal recessive disease - classically presents with progressive ataxia in adolescence.

Caused by excessive number of trinucleotide repeats (GAA) is most common in the FRATAXIN gene.

LOSS of POSITION and VIBRATORY SENSES due to deterioration of DORSAL SPINAL COLUMN.

dysarthria, limb weakness, loss of DTRs, progressive gait and limb ataxia.

KYPHOSCOLIOSIS and ARCHED FEET.

sequale:
most patients get HOCM, with an increased risk of arrhythmia and heart failure usually causing death by 40.

Diagnosis is confirmed with GENETIC TESTING

203
Q

a deficiency in what vitamin is associated with an increased risk of developing MS?

A

Vitamin D.

Yes.. lack of vitamin D is affiliated iwth getting MS…

204
Q

90% of patients with REM sleep behavior disorder will go on to develop what?

A

Parkinsons disease or dementia with lewy bodies.

205
Q

Lesh-Nyhan Syndrome

A

X-linked recessive

Deficency of HGPRT –> results in Hypoxanthine and URIC acid accumulation in tissues.

Symptoms:

  1. Delayed milesstones and HYPOTONIA in infancy
  2. intellectual disability
  3. SELF MUTILIATION
  4. By AGe 3 they develop - EPS - Dystonia, chorea, and SPASTICITY

Gouty arthritis in late, untreated disease

206
Q

Rett Syndrome

A

A neurodevelopmental disorder in girls. - Characterized by normal development until 6 months, followed by REGRESSION of SPEECH and MOTOR function and development of sterotypical hand movements HAND WRINGING

207
Q

Conus Medullaris vs Cauda Equina Syndrome

A

Cauda Equina Syndrome:

  1. Usually BILATERAL, severe RADICULAR pain (pain along a dermatome)
  2. Saddle hypo/anesthesia
  3. ASYMMETRIC motor weakness
  4. HYPOreflexia / areflexia (loss of reflexes)
  5. Late-onset Bowel and bladder dysfunction

Cauda Equina causes LOWER MOTOR NEURON signs at SPINAL NERVE roots, because the spinal nerve roots are part of the peripheral nervous system.

Conus Medullaris:

  1. Sudden onste severe back pain
  2. PERianal Hypo/anesthesia
  3. SYMMETRIC motor weakness (big diff vs. cauda equina)
  4. HYPERREFLEXIA (another big diff)
  5. Early onset bowel and bladder dysfunction

COnus Medularis causes UPPER and lower motor neuron symptoms as CONUS is part of the SPINAL CORD (CNS).

Management of BOTH = EMERGENCY MRI + IV glucocorticoids + Neurosurgical EVAL.

208
Q

Can diabetic neuropathy cause spasticity?

A

NO!

Diabetic neuropathy is STRICTLy a disease of LMN.. it does not affect UMN.

Spasticity, and + babinski signs are UMN lesions.

209
Q

CHild with otitis media develops morning headaches and vomiting whats the next best step?

A

you are suspecting that the otits media and mastoiditis has spread and caused bacterial infection reusling in a temporal brain abscess..
The vomiting and headahces are what suggest the intracrainal pathology.

Before you do LP or anything you MUST do a CT with contrast or MRI.

It will demonstrate a ring enhancing lesion with surrounding edema if the abscess is present.

210
Q

Malignant hyperthermia

A

halothane and succinylcholine

211
Q

heat stroke

A

Acute COnfusion, Hyperthermia, Tachycardia, Persistent Epistaxis. Heat stroke is DEFINED by core tem >104 F (40C)

Complications:

  1. Rhabdo –> renal failure
  2. ARDS
  3. DIC –> bleeding.. Epistaxis
212
Q

alcoholic cerebellar degeneration vs vitamin B12 deficency

A

Alcoholic Cerebellar Degeneration:
Caused by 10 years or more of heavy alcohol use –> caused by degeneration of PURKINGE CELls in the CEREBELLAR VERMIS –> these neurons are largely responsible for TRUNCAL coordination –> damagre results in WIDE-BASED GAIT and POSTURAL INSTABILITY.

Symptoms:

  1. WIDE BASED GAIT
  2. INCOORDINATION in legs
  3. Cognition is INTACT
Diagnosis is CLINICAL:
1. IMPAIRED TAndem walking (heel-knee-shin)
2. PRESERVED finger-nose testing
CT/MRI - CEREBELLAR atrophy
NO loss of vibration and proprioception
Treatment = alcohol cessation

B12 deficency may cause SPINAL CORD DEGENERATION - and cause Ataxia, symmetric paresthesia, and LOSS of VIBRATION and PROPRIOCEPTION sensation.

213
Q

PKU

A

Deficency of phenalalnine hydroxylase –> results in inablity to metabolize Penylalanine into tyrosine… which in turn causes build up of Phenylalalnine and its neurotoxic byproducts.

Untreated patients will have intellecutal disability, seizures, fair complexion and musty odor.
Hypopigmentation includes eyes, brain nuceli, hair and skin

Diagnosis -
Quantitative Amino Acid analysis (will show elevated phenylalanine levels)

Newborn screening can be done via Tandem Mass SPectrometry

Treatmet = dietary restriction of phenylalanine (no high protien foods).

If detected early and treated early.. they will have a normal mental development and life span.

214
Q

Aldolase B deficiency

A

causes hereditary FRUCTOSE intolerance.

Introduction of fruits and veggies is followed by Accumulation of FRUCTOSe-1-PHOSPHATE.

Affected infants - vomiting, poor feeding, lethargy.

Seizures and encephlaopathy follow if fructose is not removed from the diet

215
Q

Jaundice + Hepatomegaly + failure to thrive a few days after birth.. after consumption of breast milk or regular infant formula is indicative of what deficency?

A

Deficency of glactose-1-phosphate uridyl transferase in RBCs

This disease is called GALACTOSEMIA

216
Q

what is the most common cause of deep intracerebral hemorrhage?

A

example: Basal ganglia hemorrhage

MCC is Hypertensive vasculopathy involving the SMALL PENETRATING BRANCHES of the major cerebral arteries

217
Q

what is the MCC of intraparenchymal brain hemorrhage in children?

A

AVMs

218
Q

what is the most common cause of spontaneous lobar / cortical hemorrhage in the elderly?

A

Cerebral Amyloid Angiopathy

219
Q

Amaurois Fugax

A

Curtain over eye

Rapid PAINLESS, transient monocular vision loss.

Caused by ATHEROSCLEROTIC EMBOLI originating from the same side CAROTID ARTERY.

TO diagnose do a DUPLEX ULTRASOUND OF THE NECK.

Fundoscopic exam is usually normal.. but may show embolic plaques and retinal whitening

220
Q

Myasthenic crisis treatment

A

First INTUBATE!

Then (temporarily) STOP pyridostigmine –> cholinergics cause excess secretions.. and this can block airways

Then give IVIG or Plasmapheresis (preferred) + corticosteroids

221
Q

what parkinsonian drugs can cause percipitation of acute angle closure glaucoma?

A

Anticholinergics (used to treat tremors in parkinson)

Trihexyphenidyl.

Anticholinergics cause MYDRIASIS which can precipiate acute ACG.

Untreated ACG will damage the optic nerve and result in permanent vision loss within 2-5 hours of symptom onset.

222
Q

what is the most common cause of CN3 palsy in adults?

A

Ischemic neuropathy caused by POORLY controlled DIABETES

THey will have a down and out gaze, but PRESERVED pulillary response.

223
Q

what are functions of the femoral nerve?

A

Leg flexion at the hip

Leg extension at the knee

224
Q

what are functionso f the tibial nerve?

A

FLEXION

of the knee, and toes and plantar flexion

225
Q

How does Spinal Epidural Abscess present?

A

Classic Triad:

  1. Fever (50%)
  2. Focal / severe BACK PAIN
  3. NEURO findings - motor/sensory, bowel/bladder, paralysis

MCC = S. Aureus (65% of cases)

HOw do you get it? Innoculating sources:
1. Distant infection - cellulitis, joint/bone
2. Spinal procedures (epidural cath)
3 IVDU

Diagnosis:

  1. Elevated ESR
  2. MRI of SPINE!!
  3. Blood and aspirate cultures

Tx:
Broad spectrum ABX - van + cef

May require aspiratoin / surgical decompression

226
Q

Differential diagnosis of myopathies

A

Glucocorticoid induced = normal ESR and CK:
Proximal muscle WEAKNESS and atrophy NO pain.

Polymyalgia Rheumatica = Normal CK and elevated ESR:
muscle PAIN and STIFFNESS in shoulder and pelvic girdle. Tenderness and decreased ROM in shoulder, neck and hip
Responds RAPIDLY to GLUCOCORTICOIDS.

Inflammatory Myopathies = Elevated Ck and ESR:
Pain and Tenderness + Skin RASH and inflammatory ARTHRITIS.

Statin-induced Myopathy = Normal ESR and Elevated CK:
Prominent muscle PAIN and TENDERNESS usually without weakness.
Rare Rhabdo.

Hypothyroid Myopathy = Normal ESR and ELEVATED CK (just like statin ):
Muscle pain and cramps and weakness, Delayed DTRs and Myxedema.
Features of HYPOTHYROIDISM

227
Q

Infant botulism vs Foodborne botulism

A

Infant botulsim - caused by ingestion of C. Botulinum SPORES from environmental dust.
Treatment = Human derived botulism immune globulin

Foodborne botulism (can occur in anyone.. even if infant got honey) = ingestion of PREFORMED C. Botulinum TOXIN
Treatment = EQUINE-derived botulism ANTITOXIN

Remember - botulism causes DESCENDING paralysis

228
Q

what 3 factors are known to decrease SIDS incidence?

A
  1. limiting prenatal and postnatal smoke exposure
  2. Pacifier use during sleep
  3. Room sharing (without bed sharing) with care taker
229
Q

Metastatic brain cancer

A

most commonly comes from LUNG first, breast 2nd, melanoma, colon etc.

Primary solitary brain mets seen in:

  1. Breast
  2. Colon
  3. Renal cell carcinoma

Multiple Brain MEts seen in:

  1. Lung
  2. Malignant Melanoma

Hematology (13 decks)

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