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AMED > Lecture 3: Cranial Nerves > Flashcards

Lecture 3: Cranial Nerves Flashcards

1
Q

CN I

A

Olfactory

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2
Q

CN II

A

Optic

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3
Q

CN III

A

Oculomotor

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4
Q

CN IV

A

trochlear

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5
Q

CN V

A

Trigeminal

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6
Q

CN VI

A

Abducents

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7
Q

CN VII

A

Facial

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8
Q

CN VIII

A

vestibulocochlear

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9
Q

CN IX

A

Glossopharyngeal

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10
Q

CN X

A

Vagus

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11
Q

CN XI

A

Accessory

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12
Q

CN XII

A

Hypoglossal

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13
Q

Which cranial nerve is commonly affected by dental and oral procedures?

A

CN V: Trigeminal

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14
Q

True or false, CN V is affected if CN VII experiences trauma?

A

False

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15
Q

What motor control does CN V have?

A

controls muscles of mastication

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16
Q

What are the muscles of mastication?

A

temporalis, masseter, pterygoid

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17
Q

How do you test the muscles of mastication?

A

have patient clench and palpate for tone and muscle bulk bilaterally

18
Q

How do you test the strength of pterygoid?

A

have the patient try to remain open mouth while trying to resist closure by the clinician?

19
Q

What does CN VII Control?

A

Muscles of facial expression

20
Q

Which nerve innervates the pharynx and tongue?

A

CN IX

21
Q

What does CN XII innervate?

A

tongue

22
Q

How do you test CN XII?

A

Examine tongue for atrophy and asymmetry. See if the tongue deviates to one side.

23
Q

What CN runs alongside CN XII?

A

CN X

24
Q

What is acromegalsy?

A

endocrine issue in which there is excess growth hormone released by the pituitary gland

25
Q

What clinical findings of acromegaly?

A

enlarged hands/feet, multiple diastema, enlarged mandible, diabetes, HTN

26
Q

What can limit growth cause?

A

lack of growth hormone, indiction of a tumor, secondary to radiation therapy, and genetics

27
Q

What are the clinical presentations of those with limited growth?

A

elevated cholesterol, low bone density, jaundice, limited growth and stature, single central incisor

28
Q

What is the clinical presentation of hyperparathyroidisM/

A

ossifying fibroma in mandible or maxillofacial complex

29
Q

What causes rickets?

A

Lack of vitamin D, calcium, or phosphate

30
Q

What are the clinical presentations of rickets?

A
  • caries
  • enamel hypoplasia (due to lack of vitamin D)
  • Delayed eruption or formation of dentition
  • large pulp chambers, short roots in dentition
31
Q

What is type I DM?

A

it is autoimmune mediated

32
Q

What is type II DM?

A

Insulin resistance

33
Q

What tests should you run for a patient with DM/

A

A1C, ECG interpretation, anti-hyperglycemic medication

34
Q

When looking at fasting glucose, what does that indicate?

A

it is a snapshot of the serum glucose at the time of sample blood draw

35
Q

What are diabetics at risk for?

A

silent MI due to diabetic neuropathy (typically masks chest pain

36
Q

What consideration should you have if your patient has DM/

A

Ensure that they have pre-operative carbohydrate intake and starting glucose

37
Q

What is the purpose of an insulin pump?

A

maintains a basal rate to ensure blood glucose stays with 90-120mg/dl

38
Q

What should you consider if a patient has a long appointment and has an insulin pump/

A

modify the basal rate in the absence of regular carbohydrate intake

39
Q

What is the concern that you should be wary about when you are giving anesthetic to a diabetc?

A

poorly controlled chronic diabetics usually are unable to tolerate increases of BP or HR, which can precipitate further arrhythmias

40
Q

What are the complications of diabetes?

A

diabetic ketoacidosis and hyperglcemic hyperosmolar state

41
Q

what is diabetic keotacidosis?

A

when the body does not have insulin to provide blood sugar to cells for energy, the liver will begin to break down it’s fat, which produces acids called ketones. If there are too many ketones then, this can upset the chemical balance of blood, and can poison the body.

AMED (2 decks)

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