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Exam 2 - GI and Liver > Eye & Neuro Exam > Flashcards

Eye & Neuro Exam Flashcards

1
Q

What does Zinc toxicity cause?

A

copper deficiency

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2
Q

Name (3) lower motor signs

A

atrophy, hypOrefleixia, and fasciculations

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3
Q

What does Tensilon test look for?

A

myasthenia gravis

Tension = Edrophonium

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4
Q

Tx of acute MS exacerbation?

A

steroids

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5
Q

Chronic MS treatment

A

Glatiramer and Interferon Beta

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6
Q

What happens on L and R lateral gaze in pt w/ lesion of LEFT MLF (INO)?

A

When they look left, everything is fine

When they look right (opposite), the Left eye is not able to (looks straight ahead) and the Right eye has nystagmus

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7
Q

DaT scan

A

looks at Dopamine in the substantial nigra - evaluating for Parkinson’s
(differentiate essential tremor from Parkinson’s tremor)

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8
Q

What is Hemiballismus? Most frequent cause?

A

a violent form of dyskinesia involving one side of the body, most marked in the upper limb.

stroke in the CONTRAlateral sub thalamic nucleus (thus, decreased activity of the sub thalamic nucleus of the basal ganglia)

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9
Q

What happens in Progressive Supranuclear Palsy? What is the characteristic presenting sx?

A

impaired downward gaze and postural instability

characteristic sx = Early falls

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10
Q

Narcolepsy treatment that is a wake-promoting agent

A

Modafinil

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11
Q

(4) clinical sx of Narcolepsy

A

short naps are REFRESHING
poor sleep at night
sleep paralysis
falling asleep (hypnogogic)/awake hallucinations

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12
Q

Pt is told a joke, feels weak and collapses to the floor. What dx is this characteristic for and what is the mechanism?

A

Narcolepsy. The pt is stimulated w/ laughter (cataplexy) and loses muscle tone.
Mechanism = REM is intruding on their wakefulness and they get atonia, specifically due to Orexin deficiency

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13
Q

MOA of Ethasuxamide

A

Calcium channel blocker. Tx for Absence seizures

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14
Q

(4) voltage-gated Na channel blockers

A

phenytoin, carbamazepine, lamotrigine, and oxycarbazepine

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15
Q

(2) main categories of drugs that increase GABA(a) action. What does this increased GABA action do?

A 
Benzodiazepines (Diazepam, Lorazepam, Clonazepam) and Barbiturates (Phenobarbital and Primidone)
Increased GABA(a) action DECREASES neuron firing

[barbiDURATes increase DURATion]

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16
Q

First line tx for status epilepticus

A

Benzodiazepines (Diazepam, Lorazepam, Clonazepam)

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17
Q

Ezogabine MOA and big adverse effect. What condition is it used for?

A

MOA = K+ channel opener; Turns people blue

An anti-convulsant used as adjunctive treatment for partial epilepsies

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18
Q

Which two N. meningitidis vaccines cover the B serotype? What type of vaccines are they?

A

Trunemba and Bexsero

Both Protein vaccines (recombinant FHBP)

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19
Q

What is the early stage of African sleeping sickness? Which (2) drugs specifically tx this stage? Which drug treats the late stage?

A

The early stage is the ‘blood-only’ stage before it has crossed the BBB. Tx = Pentamidine and Suramine.

Late stage is CNS penetrance. Tx = Melarsoprol

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20
Q

male with episodic (fluctuating) weakness and double vision (diplopia) = classic question stem for…

A

myasthenia gravis

v. Lambert-Eaton where extra ocular muscles are spared

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21
Q

Name (4) different areas of the brain most sensitive to ischemia or hypoxic/anoxic injury

A
  • CA1 region of hippocampus (Sommer sector)
  • cerebral cortex layers 3, 5, and 6
  • Purkinje cells of cerebellum
  • caudate and putamen
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22
Q

(3) high yield areas in brain for hypertensive hemorrhages

A

basal ganglia, thalamus, and the pons

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23
Q

Which type of brain hematoma may have a “lucid interval”?

A 
epidural hematoma (blood on top of dura and underneath skull)
(ex. Liam Neeson's wife died in skiing accident; had lucid interval)
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24
Q

(3) high yield diseases to associate with berry aneurysms

A

Marfans, Ehrlos, and ADPKD

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25
Q

Which vessel may be compressed in a subfalcine (cingulate gyrus) herniation?

A

ACA

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26
Q

Cowdry A inclusions seen with which 2 viruses? What does a Cowdry A inclusion look like and where in the cell is it?

A

herpes simplex virus and CMV

intra-NUCLEAR: looks like the nucleus has been smudged out and replaced by a red blob with a halo around it

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27
Q

Which area of the spinal cord is affected by polio? What does it cause?

A

anterior horn cells, causing flaccid paralysis with muscle wasting and hypOreflexia

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28
Q

Named inclusions in rabies and where are they found?

A

Negri bodies

in hippocampus and Purkinje cells of the cerebellum

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29
Q

2 viruses that can cause Poliomyelitis

A

Poliovirus and EV-71

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30
Q

3 viruses that can cause Meningitis/Encephalitis

A

Coxsackie A, B, and Echovirus

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31
Q

Two diseases that only Coxsackie B causes

A

Myocarditis/Pericarditis and

Pleurodynia (pain in pleural cavity)

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32
Q

2 viruses that cause Hand Foot and Mouth Disease

A

Coxsackievirus A and EV-71

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33
Q

What 2 diseases can EV-71 cause?

A

poliomyelitis and hand foot and mouth disease

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34
Q

which virus causes herpangina?

A

Coxsackie A

herpangina = mouth blisters

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35
Q

Which enterovirus (EV) causes respiratory infections?

A

EV-68

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36
Q

2 viruses that cause acute hemorrhagic conjunctivitis

A

EV-70 and Coxsackie A

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37
Q

Which 2 picornaviruses cause generalized infection of newborns?

A

Echovirus and Coxsackie B

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38
Q

Which enterovirus (EV) is associated with a more severe brain stem encephalitis?

A

EV-A71

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39
Q

What’s the transmission of N. meningitidis? How does this play into abx prophylaxis for people around infected pt?

A

exchanging secretions (ex. kissing or sharing lip gloss)

Thus, Rifampin only needs to be given to CLOSE contacts of the infected pt

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40
Q

gram stain and morphology of Haemophilus influenza. Name (4) other bacteria in this category

A

gram (-) coccobacilli

Bordetella pertussis, Pasteurella, Brucella, and Franciscella

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41
Q

(2) reasons why a previously healthy child may get H. influenza

A

1) previously undiagnosed immune deficit

2) non-vaccinated child

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42
Q

pathognomonic for HSV1

A

temporal lobe encephalitis with a fever (will see temporal lobe enhancement on MRI)

hemorrhaging and necrosis would be late MRI findings

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43
Q

what is the traumatic injury association with epidural hematoma?

A

skull fracture

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44
Q

Arteriorvenous malformations typically cause what type of bleed? What is the typical onset?

A

subarachnoid hemorrhage b/c blood is in leptomeninges

presents typically with sudden, thunder-clap onset

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45
Q

apple green birefringence in blood vessel indicates…

A

amyloid deposition

w/ Alzheimer’s pt, think amyloid angiopathy b/c see beta-amyloid in neuritic plaques of AD patients

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46
Q

contrecoup contusion - what is it and could it cause?

A

hitting the head while moving, will cause hemorrhage on the opposite side of the place where hit

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47
Q

patients presenting with bacterial meningitis and decreasing level of consciousness makes you worried for…

A 
cerebral edema 
(if tap their spine, their brain can herniate through = major concern. So do imaging FIRST)
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48
Q

(4) patient circumstances that require getting imaging BEFORE doing a lumbar puncture

A

patients who present with:
-a deceased level of consciousness (make sure they don’t have cerebral edema)
-a specific neuro abnormality
-have a hx of cancer
or are immunosuppressed (b/c they may not be able to manifest a full inflammatory rxn)

All other patients can go straight to LP w/out imaging

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49
Q

(3) meds given to presumed bacterial meningitis

A
  • Vancomycin: covers multi-drug-resistant Strep pneumo
  • Ceftriaxone: covers (3) = Neisseria meningitidis, regular (non-drug-resistant) Strep, pneumo, and E. Coli
  • Dexamethasone: decreases risk of sensorineural deafness (most common complication after infection)
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50
Q

CSF appearance in bacterial meningitis

A

cloudy (normal CSF is clear)

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51
Q

What is Pseudotumor Cerebri? What is dx in pt w/ Pseudotumor Cerebri?

A

someone w/ raised intracranial pressure, but no mass or lesion raising it.
Idiopathic Intracranial Hypertension (IIH) has been diagnosed by LP with CSF pressure > 250 mm

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52
Q

(4) most common sx of IIH/Pseudotumor cerebri patients

A
  • headache
  • blurry vision
  • tinnitus or “wooshing noise” in ear
  • pain behind the eye
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53
Q

Tension-type headaches - (4) characteristic sx. How are they subcategorized?

A

Sx = dull, bifrontal, pressing, tightening pain

Tention-type HAs can be chronic or episodic. Episodic divided into frequent or infrequent.

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54
Q

For what condition are Triptan meds contraindicated? What alternate medications might be considered?

A

hypertension

consider using beta blocker or calcium channel blocker

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55
Q

“sense of restlessness” is a big tip off for what category of headache?

A

cluster

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56
Q

What is the tx for acute attacks of cluster headaches? What about for prevention of cluster headaches?

A 
Acute = 100% oxygen via facemask
Prevention = Verapamil (Ca channel blocker)
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57
Q

What medication can be used to induce remission of cyclical cluster headaches?

A

Prednisone (anti-inflamm steroid)

If pt has, for ex, cycle of 6 weeks on HAs and 6 weeks off, Prednisone can be used to induce the off cycle

58
Q

If concerned for Temporal arteritis (Giant cell arteritis), what (3) tests should be considered?

A

CRP and ESR, followed by temporal artery biopsy

59
Q

(2) major complications from untreated Temporal (Giant Cell) Arteritis

A

blindness and stroke

60
Q

characteristic of typical Giant Cell Arteritis patient and presentation

A

new onset HA in elderly male

61
Q

Mechanism of Temporal (Giant Cell) Arteritis

A

Autoimmune
infiltration in intima and media by mononuclear cells
skip lesions; therefore biopsy needs to be 2.5 cm

62
Q

What medication can be used to tx pseudotumor cerebri? How does it work?

A

Acetazolamide
It’s a carbonic anhydrase (CA) inhibitor. And CA is an enzyme involved in production of spinal fluid. [side note: caffeine actually increases production of spinal fluid!]

63
Q

definition of aura v. premonitory sx

A

aura: specific neurological sx like visual, speech, or sensory issues associated with the headache

premonitory sx: ex = thirst or yawning

64
Q

what is the cerebral blood flow course during aura? How does this explain the aura?

A

-first a wave of hyPOperfursion, then
-a wave of hyPERperfusion, then
-normalization of cerebral bloodflow
due to these changes, have associated dysfunction of the cortex, e.g. visual or speech disturbances with the migraine

65
Q

(3) anti-emetics used in acute tx of migraine

A

promethazine, metoclopramide, and prochlorperazine

66
Q

What tx is contraindicated in pseudotumor cerebri patients?

A

corticosteroidems!

67
Q

(3) steps in evaluating a stroke patient (in order!)

A
  1. localize the lesion - L or R? Then is it in cortex, brainstem, NMJxn, etc
  2. etiology (ex. is it an emboli coming from the heart?)
  3. secondary stroke prevention (e.g. statins, BP control)
68
Q

Localize the lesion of someone presenting with language abnormalities (aphasia)

A

L cerebral hemIisphere

69
Q

Stroke v. TIA

A

both present w/ onset of neuro impairment due to a vascular insult. BUT, stroke results in a permanent cerebral infarction, whereas TIA does NOT. TIA resolves and results in no damage to the brain.

70
Q

metaphor of workers on strike related to stroke area and the penumbra

A

some workers have already dipped = the necrotic core

but some workers on strike will start working again if increase pay (bloodflow), and those are the neurons ini the penumbra

71
Q

What is the FDA-approved window to give TPA for stroke?

A

3 hours

72
Q

What does ‘modifiable risk factor’ mean? Name (6) modifiable risk factors for stroke

A

modifiable = something we can change via lifestyle or meds. Include:
-HTN, DM, HLD, CAD, A-fib, and smoking/drugs/alcohol

73
Q

Name (5) non-modifiable stroke risk factors

A

age, gender, race, genetics, and family/past medical hx

74
Q

Explain the NIHSS stroke scale and name (3) examples of sx it assesses

A

Divided into 11 categories of fxn assessed on neuro exam. Scoring goes from 0 to 42. 0 = completely normal neuro exam. 42 = dead person. So higher the score, worse the outcome for the pt.

Ex. #1 assess level of consciousness, orientation to questions, and response to commands

75
Q

All right-handed people and most left-handed people are dominant in which hemisphere?

A

LEFT

meaning their language function is located in the L hemisphere

76
Q

(3) key sx of a Left MCA/ACA stroke

A

Aphasia + Right-sided weakness

may also have gaze deviation to the LEFT - b/c right side is now unopposed and pushing gaze to the weak side

77
Q

sx of a Right MCA/ACA stroke

A

left-sided neglect - if bad enough, may not even realize the left side isn’t working

78
Q

What is the purpose of a non-contrast head CT of a stroke pt?

A

to rule out hemorrhage (hemorrhage shows up on CT right away, whereas ischemia won’t show up on CT for 8 hrs)

79
Q

What will the MRI tell you in a pt with stroke sx?

A

verify whether or not they had a stroke

80
Q

What is an ASPECTS score and what is it used for?

A

Used only for MCA strokes. Evaluate head CT on points system (total 10 points) to look for perfusion = “poor man’s perfusion scan.”

Score of 6 or higher = eligible for mechanical thrombectomy

81
Q

What is RAPID imaging and what is it used for?

A

It compares cerebral blood flow v. perfusion. difference between the 2 will show the penumbra area (the penumbra is included on the MR perfusion)

82
Q

What tx can you do for stroke pt that is not eligible for TPA (>3 hrs) or mechanical thrombectomy?

A

permissive HTN: where lay head of bed flat and let BP go way up to 150 - thus, increasing blood flow and pressure to the brain. Point is to save the penumbra!

83
Q

What does TPA do for strokes?

A

dissolves clots and inhibits fibrinogen

84
Q

Name (4) exclusion criteria where TPA can NOT be given to a patient between the 3-4.5 hour window

A
  • Age > 80 yo
  • h/o DM and Stroke
  • coumadin (any oral anti-coagulants)
  • NIHSS score > 25
85
Q

T/F: tPA works on all stroke subtypes

A

true

86
Q

What is ELVO and what is the standard of care tx?

A

Emergent Large Vessel Occlusion

If pt has ELVO, you activate Cath lab (mechanical thrombectomy). Trials showed NNT = 4-7, which is really good!

87
Q

(5) diff vessels included in ELVO

A

Occlusion of:

ACA, PCA, Basilar artery, ICA, and M1/proximal M2

88
Q

What % of infants with congenital toxoplasmosis are asymptomatic?

A

70-90%

BUT they may develop sx months to years later

89
Q

Classic triad of congenital Toxoplasmosis

A

Chorioretinitis
Hydrocephalus
Intracranial calcifications

90
Q

Of the asymptomatic infants who were infected congenitally w/ Toxo, what is the most common late finding?

A

chorioretinitis, which can result in vision loss

91
Q

what type of calcifications are seen on head CT of congenital CMV infection?

A

linear PERIVENTRICULAR calcifications

92
Q

What is the most common congenital infection in the developed world?

A

CMV (Cytomegalovirus)

93
Q

What is the most common sequela of congenital CMV infection?

A

sensorineural hearing loss (usually progressive and leads to profound hearing loss in affected ear)

94
Q

What is the tx for life-threatening congenital CMV? Tx for mild CMV sx?

A

Ganciclovir for life-threatening
oral Valganciclovir for mild sx
6 month tx course. Help reduce hearing loss

95
Q

(3) major findings for congenital Rubella

A

bilateral cataracts
purpuric rash
pigmentary retinopathy (‘salt-and-pepper retina’)

96
Q

When is the biggest risk of congenital rubella defects from maternal infection?

A 
1st trimester
(80-85% incidence of defects - e.g. hearing loss - if mother infected w/ rubella in 1st trimester)
97
Q

What are the typical defects to the fetus when mom gets rubella < 8 weeks of pregnancy?

A

cardiac = PDA or pulmonary artery stenosis
and
eye = cataracts and pigmentary retinopathy (salt-and-pepper)

98
Q

Name nerve root pairs associated with: biceps, brachioradialis, and triceps DTRs

A

Biceps AND Brachioradialis = C5/6

Triceps = C6/7

99
Q

Which deep tendon reflexes test nerves roots C5/6

A

both biceps and brachioradialis

100
Q

Name nerve root pairs associated with the patellar and ankle deep tendon reflexes

A

patellar = L3/4

ankle = S1

101
Q

Which deep tendon reflex tests nerve roots L3/4?

A

patellar DTR

102
Q

Which deep tendon reflex tests nerve root S1?

A

ankle DTR

103
Q

definition of neuropathy

A

things that affect the nerves, either sensory or motor = neuropathies. If affects a single nerve = mononeuropathy. Multiple nerves = polyneuropathy

104
Q

polyradiculoneuropathy

A

multiple nerve roots AND peripheral nerves are affected

105
Q

(2) examples of a mononeuropathy

A

carpal tunnel syndrome (median nerve at the wrist)

peroneal mononeuropathy: compressed peroneal nerve, often at fibular head. Can cause foot drop on that side, as well as numbness in perineal nerve territory.

106
Q

definition of Radiculopathy and (3) sx it can cause

A

a lesion of a particular nerve root. this may cause:

  1. ‘radicular’ (shooting or shock-like) pains radiating down the extremity in that dermatome
  2. weakness of muscles in that nerve root (myotome)
  3. depressed reflexes involving that root
107
Q

(3) sx of a C6 radiculopathy

A
  1. pain or numbness radiating down arm to to thumb
  2. weak biceps, deltoids, and forearm pronator (C6 myotome)
  3. diminished reflexes of biceps and brachioradialis
108
Q

What receptor on muscles are activated via motor nerves?

A

Nicotinic cholinergic receptors

109
Q

Does botulism/botox work on the pre or post-synaptic neuromuscular jxn?

A

PRE-synaptic junction by cleaving SNARE proteins, which help vesicles full of Ach attach and fuse with the membrane. So botulism/botox keeps Ach from being released into synapse.

110
Q

Differences in sx between a pre- and post-synaptic neuromuscular junction disorder

A

Pre-synaptic = dry mouth, hot (can’t sweat), blind (can’t produce tears). Since issue is releasing Ach and Ach is used in many other systems besides muscles, have more sx besides weakness with pre-synaptic disorder!

Post-synaptic will mostly just have weakness

111
Q

Definition of myopathy and (3) general characteristics of myopathies

A

myopathy = muscle disorder. In general, they are:

  • symmetric
  • proximal weakness (ex. weakness of shoulder or hip girdles)
  • myalgias/cramping (but NO sensory complaints like numbness or tingling. Those should make you think of a nerve disorder)
112
Q

Which type of nerves are measured by nerve conduction studies?

A

the thickest, fastest fibers

113
Q

What are orphaned muscle fibers on nerve conduction studies (NCS) and how are they detected?

A

they are muscle fibers that have been de-innervated. On NCS they make a noise called a fibrillation or a positive sharp wave.
[*Note: sharply positive wave on EMG is pointing sharply DOWN]

114
Q

Define “neuropathic” motor units. How do they appear on nerve conduction studies?

A

the surviving motor units (after some have degenerated) that are now responsible for innervating more muscle fibers.
Motor unit waves have higher amplitude (taller), longer duration (wider), and are polyphasic (complex waveform). Sign of RE-innervation!

115
Q

Which cells mediate problem in Myasthenia Gravis?

A

B-cell mediated - they make the Abs against Ach receptors

But T-cells are also involved (i.e. thymus)!

116
Q

during nerve AP, which step is like a fire alarm telling vesicles full of Ach to head for the exits?

A

The influx of extracellular Ca+ into the nerve via the voltage-gated Ca channels

117
Q

What is a common finding in 2/3rds of Lambert-Eaton Myasthenia patients

A

paraneoplasm - usually small cell lung carcinoma

but LEMS may PREcede tumor dx by 3-4 years

118
Q

what is affected in polyneuropathy?

A

axons of sensory AND motor nerves. Can be either axonal problem (more common) or demyelinating problem.

119
Q

(3) different forms of polyneuropathy

A
  1. Toxic (hyperglycemia/uncontrolled DM, EtOH, heavy metals)
  2. Nutritional (low B12 or high B6)
  3. Autoimmune (guillain-barre syndrome)
120
Q

another name for Guillain-Barre syndrome

A

AIDP = Acute Inflammatory Demyelinating Polyradiculoneuropathy

121
Q

typical progression of ALS (Amyotrophic Lateral Sclerosis)

A

tends to start in one extremity and then spread to contralateral extremity. Then tends to move either rostrally or caudally - e.g. going from arms to legs or from arms to brainstem, causing slurred speech, dysphagia, affecting breathing

122
Q

what is polymyositis and how does it commonly present?

A

symmetric proimal weakness = issues w/ stairs, chairs, and combing hairs.
progresses over weeks or months with dysphagia and dysphonia

123
Q

what is the pathology of Dermatomyositis?

A

perifascicular muscle fiber degeneration

dermatomyositis is an inflammatory myopathy with a rash

124
Q

classic presentation of inclusion body myositis

A

pt with weakness of knee extensors (quads) and forearm flexors (trouble gripping things b/c forearm flexors do PIP joints)

125
Q

Muscle bx of Inclusion body myositis

A

eosinophilic cytoplasmic inclusions and muscle fibers with one or more “rimmed vacuoles” lined with granular material

126
Q

What does the CSF show in Guillain-Barre syndrome?

A

Albumunocytologic dissociation = elevated protein WITHOUT elevated WBCs.

127
Q

Common antecedent to Guillain-barre syndrome

A

URI or GI infection, most frequently identified organism = Campylobacter jejuni

128
Q

Tx for Guillain-Barre

A

IVIG or plasmapheresis

129
Q

(2) main ways to prevent cataracts

A

UV protection and stop smoking

130
Q

What is the tx for cataracts?

A

surgery: Intraocular Lens Implant

131
Q

What (3) groups are most at risk for glaucoma?

A
  • elderly
  • African Americans
  • those with family hx of glaucoma
132
Q

Who is most at risk for angle-closure glaucoma?

A

China and India

133
Q

What happens to vision in glaucoma?

A

First, get scotoma in middle of vision and then periphery closes in more and more until eye goes blind

134
Q

What is the general idea of vision loss in glaucoma?

A

slow process of losing the connection between the eye and the brain. Since it is slow, brain fills it in at first. Not aware of visual field loss until later in disease.

135
Q

Normal intraocular pressure range

A

12-20 mm Hg

avg = 16 mm Hg

136
Q

What is the tx goal with glaucoma? What specific treatments are used?

A

to halt progression of optic nerve damage by lowering the IOP. Do this w/ medicine, laser tx, and glaucoma or filtering surgery (i.e. placing a drainage implant)

137
Q

Early v. Late sx of Age-related Macular Degeneration (AMD)

A

Early: difficulty reading or driving; straight lines may be crooked

Advanced: central blind spot with peripheral vision intact

138
Q

T/F: You can eventually go completely blind with Age-related macular degeneration (AMD)

A

False. You get loss of central vision with AMD, but the peripheral vision always remains. Versus Glaucoma that can cause total blindness

139
Q

(5) medical treatments for AMD

A

High dose of Vitamins A, C, and E

+ Zinc and Copper

140
Q

Pathology of Age-related Macular Degeneration. Treatment for this?

A

growth of new, abnormal blood vessels in the retina that leak fluid and blood. Leads to loss of vision

Tx = VEGF Ab/antagonists: stop new blood vessels from growing

Exam 2 - GI and Liver (4 decks)

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