Whaba notes 2 Flashcards

1
Q

Why can someone with MG p/w cholinergic crisis?

A

They’re on anti-AchEs

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2
Q

Presenting features of a cholinergic crisis in MG?

A
Increased salivation
Increased lacrimatin
Vomiting
Abdominal pain
Diarrhea
Sweating 
Pupillary constriction
Fasiculation
Worsening weakness (in extreme cases)
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3
Q

3 major features of Wernicke syndrome?

A
Acute global confusional state
Abnormal eye movements
Ataxic gait (mostly truncal)
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4
Q

Timeline of Wernicke synd?

A

Evolves over days-wks

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5
Q

5 major cognitive features of Wernicke syndrome?

A
Inattentiveness
Indifference
Decreased spontaneous speech
Impaired memory
Lethargy
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6
Q

Serious complication of wernicke synd?

A

Progression to coma

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7
Q

2 major ANS signs a/w Wernicke synd?

A

Tachycardia, orthostatic hypoTN

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8
Q

Loss of pupillary reactivity common or uncommon w/ Wernicke syndrome?

A

Uncommon

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9
Q

Describe the basics of Korsakoff syndrome

A

Chronic amnestic disorder, anterograde and retrograde

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10
Q

What are 3 important cognitive features preserved in Korsakoff?

A

Alertness
Attentiveness
Behavior

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11
Q

Which responds to tx- Wernicke or Korsakoff?

A

Wernicke

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12
Q

Underlying etiology of W-K syndrome?

A

Thiamine deficiency

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13
Q

Name 3 things other than alcoholism that can lead to W-K syndrome

A

Chronic hemodialysis
Drugs for obesity
HyperTH

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14
Q

3 features of tx of W-K synd?

A

Thiamine 50-100 mg daily
MVI
Bed rest (2/2 ANS sx)

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15
Q

In Wernicke-Korsakoff syndrome, you’ll see lesions in which 4 areas?

A

Medial thalamus
Hypothalamus
PAG of MB
Mammillary bodies

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16
Q

Describe the 5 features essential to Dx of botulism

A
  1. Hx ingestion home-canned foods or honey (infants)
  2. Rapid onset of ocular symptoms (diplopia, ptosis, blurry vision)
  3. Bulbar sx (dysarthria, dysphagia)
  4. Descending pattern of weakness
  5. Dilated pupils (no psNS)
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17
Q

Describe pathophys of botulism poisoning

A

Ingest toxin–> blood
Toxin irreversible binds to presynaptis nerve endings of PNS and CNS–> internalization of toxin–> blocks Ach release by cleaving polypeptides essential for docking of vesicles

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18
Q

In food borne botulism, what do you ingest that causes Sx?

A

Preformed toxin

19
Q

Describe Sx of food-borne botulism

A
N/V/D w/in 2-26 hr of ingestion
Constipation (once neuro sx present)
Early neuro: oculobulbar Sx
Respiratory weakness
Unreactive pupils
Areflexia
20
Q

Describe the oculobulbar Sx of botulism (6)

A
Dry mouth
Blurry vision
Diplopia
Dysarthria
Dysphagia
Dysphonia
21
Q

3 general (non-neuro) s/s of infantile botulism

A

Constipation (early in dz course)
Weak cry
Poor feeding

22
Q

As infantile botulism progresses, what Sx appear following constipation/weak cry/poor feeding? (5)

A
Progressive weakness
Poor suck
Loss of head control
Hypotonia
Decreased movement
23
Q

3 ANS features of infantile botulism?

A

HypoTN
Tachycardia
Dry mouth

24
Q

For diagnosis of botulism, what can you test for in blood? Stool?

A

Blood: Toxin
Stool: Toxin and C. botulinium

25
Q

What do you see on electrodiagnostic testing in botulism?

A

Small CMAP in response to supramaximal stimulus

26
Q

Botulism can present very similarly to MG. However, which one has much blurrier vision?

A

Botulism

27
Q

What may you need to do to control respiratory weakness in botulism?

A

Intubate

28
Q

Beside supportive care, what are 2 drugs you can give in botulism?

A

Trivalent botulinium antitoxin

Guanidine HCl

29
Q

Trivalent botulinium antitoxin: when should you give it, what are its benefits, and what’s its major ADE?

A

Must give early while toxin is still in blood
It decreases severity of disease and overall mortality
Anaphylaxis

30
Q

What is the role of anti-Ach drugs in botulism?

A

Controversial

31
Q

What is a literal paraphasia?

A

Substitution of one letter for another (wife vs wafe)

32
Q

What is a semantic paraphasia?

A

Substitution of one word for another (wife vs mom)

33
Q

What type of aphasia is caused by a lesion of the arcuate faciculus of the supramarginal gyrus?

A

Conduction aphasia

34
Q

Describe fluency, comprehension, and repetition in conduction aphasia

A

Fluent (w/ paraphesias)
Good comprehension
Loss of repetition

35
Q

Conduction aphasia: how are writing, naming, and reading? How common is hemiparesis?

A

Writing- poor
Naming and reading- variable
Hemiparesis- infrequent

36
Q

What sort of repetitions can you see in conduction aphasia?

A

Repetitions of substitutions

37
Q

For Wernicke’s aphasia, name the:

  • Broadmann’s area:
  • Location in the brain:
  • Arterial supply
A
  • BA 22
  • Posterior superior temporal lobe on dominant (left) side
  • Posterior division of MCA
38
Q

Wernicke’s aphasia: describe fluency, comprehension, naming, repetition, writing, reading, frequency of hemiparesis

A

Fluent, paraphesic
Poor: comprehension, naming, repetition, writing
Variable reading
Infrequent hemiparesis

39
Q

Do you see repetitions of substitutions in Wernickes or Broca’s aphasia?

A

Wernickes

40
Q

Broca’s aphasia, name the:

  • Broadmann’s area:
  • Location in the brain:
  • Arterial supply
A
  • BA 44
  • Inferior frontal gyrus
  • Anterior division of MCA on dominant (left) side
41
Q

Describe speech in Broca’s aphasia

A

Initially mute, then will start saying short sentences

42
Q

Under what circumstances can people with Broca’s aphasia read?

A

If they avoid the hemianopic part of their vision

43
Q

Broca’s aphasia: describe fluency, comprehension, naming, repetition, writing, reading, grammar, and frequency of hemiparesis

A
Nonfluent
Intact comprehension
Poor naming, repetition, writing
Variable reading
Disordered grammar
Hemiparesis common