Neurology PPT Pt. 1 (hypoglycemia, pain, muscular dystrophy, myasthenia gravis)

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79 Terms

1
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what are the 3 energy sources for our neurons?

glucose, glycogen, and ketones

2
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do neurons store glucose?

NO, so it has to be readily available

3
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where is neural energy stored?

as glycogen in the glial cells

4
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why does diabetes have a large impact on the brain?

thing SUGAR — because neurons can’t store glycogen and depend SOLELY on available glucose

5
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how can a pt experience insulin shock & what is this ultimately causing?

when an overdose of insulin is administered — hypoglycemia

6
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what does hypoglycemia cause (and is thus why it’s VERY serious)?

neurological deficits

7
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what is the normal serum glucose range?

60-120

8
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what does a serum glucose range that’s between 60 & 120 tell you?

that it’s normal

9
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what does a glucose range less than 60 mean?

that they are hypoglycemic

10
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how would you diagnose someone with hypoglycemia?

by assessing a change in mental status via the Glasgow and AAOx4 assessment

11
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what would someone’s score be on the Glasgow coma scale if they were in a coma?

LESS than 8

12
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a pt walks in with a headache, is diaphoretic, tachycardic, and has a change in mental status. what would you identify is going on?

they are hypoglycemic

13
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what is the chain of events that lead to hypoglycemia (other than insulin shock, illness, or strenous exercise)?

lack of oxygen to the brain causes hypoxia(this is that mental change) and a lack of glucose

14
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what are the criteria for a change in mental status? (LKST MENTALLY- you’ve got this)

  • clouding of consciousness (altered mental status)

  • confusion (disoriented, difficulty following commands)

  • lethargy (drowsy)

  • obtunded (slow response to stimuli)

  • stupor

  • coma (unarousable)

  • death

15
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what is the glasgow coma scale? (IMPORTANT)

what is the glasgow coma scale? (IMPORTANT)

16
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what are the interventions (the things you need to think about when treating) for hypoglycemia?

perfusion, ventilation, oxygen, hydration

17
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what is the first thing you should administer to treat hypoglycemia?

GLUCOSE — oral or IV (aka ENERGY)

18
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what form of glucose should you consume to PREVENT rebound hypoglycemia?

complex carbs (like crackers)

19
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why would you consume complex carbs when treating hypoglycemia?

to prevent rebound hypoglycemia

20
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what type of pain is being described:

aching pain that originates in deep body structures with stimulus from pressure, ischemia, or tissue damage (ex: bone pain)

deep somatic

21
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what type of pain is being described:

intermittent pain for a short duration that indicated tissue damage or impending tissue damage (ex: chest pain)

acute pain

22
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what are the typical causes of neuropathic/bone pain?

nerve compression & nerve entrapment

23
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what type of nerve damage is associated with neuropathic pain?

peripheral nerve damage

24
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what do the following put a pt at an increased risk for:

DB, hypothyroidism, renal insufficiency, ETOH abuse

nerve pain

25
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a pt presents with persistent and/or intermittent pain (with regards to timing — it comes ang goes), and notes that it’s stabbing, jabbing, burning, and shooting pain. what would you identify is going on?

they’re experiencing neuropathic pain OR bone pain (this would be from a fracture, osteomyelitis, osteoporosis, or metastatic cancer)

26
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what is the tx for neuropathic pain that’s caused by DB?

glycemic control

27
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what are the interventions (for all types) for neuropathic pain?

  • tricyclic antidepressant agents

  • glucocorticoids

  • opioids

28
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when would you use tricyclic antidepressant agents when treating neuropathy?

when treating peripheral nerve pain

29
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when would you glucocorticoids use when treating neuropathy?

when treating bone pain

30
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when would you use opioids when treating neuropathy?

as a LAST RESORT

31
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what is neuralgia?

severe brief repetitive attacks of lightning-like throbbing pain that occurs along the spinal/cranial nerves — nerve pain

32
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what is the cause of neuralgia?

it’s idiopathic, but maybe neuromuscular compression

33
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what do the following out you at an increased risk for:

MS, tumors, herpes zoster, shingles, & varicella

neuralgia

34
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what do the different manifestations of neuralgia depend on?

the nerve affected (ex: CN V or shingles)

35
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a pt presents with sudden onset of sharp stabbing pain, NO numbness, & facial tics/spasms. what would you identify they’re experiencing and is going on?

they’re experiencing neuralgia, specifically Cranial Nerve V (Trigeminal)

36
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how would you treat cranial nerve V (trigeminal) neuralgia?

  • avoid the eye irritant

  • carbamazepine (Tegretol)

37
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what is required for someone to experience postherpetic/shingles?

having chickenpox & being older than 60 years old

38
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what causes the activation of shingles?

decreased immunity and thus increased viral replication

39
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how do you treat shingles?

getting the attenuated herpes zoster vaccine & antiviral agents

40
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what are the s/s of herpes?

throbbing, burning pain (a type of neuralgia)

41
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what is required for somone to experience phantom pain?

an amputation

42
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a pt complains of a tingling and squeezing pain that’s followed by burning, cramping, and shooting pain. the pain subsides occasionally, but has persisted for years. what type of neuralgia is this describing?

phantom pain (requires an amputation)

43
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what are the theorized causes of phantom pain (currently it’s idiopathic)?

  • regenerating nerves

  • spinal cord neurons

  • the brain

44
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what is the tx for phantom pain?

  • meds - sympathetic blocks

  • TENS (transcutaneous electrical nerve stimulation)

  • therapy/hypnosis (attempting to rewire the brain)

45
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what is the cause of muscular dystrophy?

x-linked recessive genetic disorder (asymptomatic at birth), wheelchair bound by 12 ; a mutation of the dystrophin gene

46
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what is going on with muscular dystrophy?

the muscle is replaced with the fat/connective tissue — the skeletal muscle fibers are degenerated

47
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is the NERVOUS system affected in muscular dystrophy?

NO

48
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are skeletal muscle fibers affected in muscular dystrophy?

YES

49
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what is the bladder situation in someone who has muscular dystrophy?

incontinence is uncommon

50
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when do the clinical manifestation of muscular dystrophy present?

at 2-3 years old

51
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a patient presents with abnormal posturing, dyspnea, cardiopulmonary failure, cardiomyopathy, tachycardia, ST depression, increased CK and/or troponin, & pseudo hypertrophy. what would you infer is going on?

muscular dystrophy

52
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what is pseudo hypertrophy & what is it associated with?

this is larger thighs/calves and looks like muscle growth, but it is just muscle that’s replaced w connective tissue

53
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what are pts with muscular dystrophy at a high risk of devloping?

pneumonia & cardiopulmonary failure

54
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what are the things you’d do and see to dx muscular dystrophy?

  • hx & assessment, cardio imaging, & muscle biopsy

  • tachycardia

  • ST depression

  • echocardiogram

  • CK & troponin levels

  • muscle biopsy

55
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what would the echocardiogram of a pt with muscualr dystrophy show?

ST depression — cardiac muscle contractility dysfunction aka cardiomyopathy

56
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what would the CK & troponin levels be in pts who have muscular dystrophy?

increased

57
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why would you take a muscle biopsy to dx muscular dystrophy & what would this show?

to examine the genetic components — this is a muscular disease — there’d be a mutation of the dystrophin gene

58
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what are the interventions for muscular dystrophy?

  • no cure

  • passive exercise / stretching (to help maintain muscle)

  • pulmonary toileting & coughing/deep breathing (to exercise lungs)

59
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what is going on with myasthenia gravis?

this is a neuromuscular junction disorder (BNJ) and antibodies (produced by the thymus) are directed/attack ACh receptors in the neuromuscular junction

60
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because myasthenia gravis is when the muscular junction is attacked, what does this mean for neurons?

their impulses aren’t transmitted as easily (specifically, the impulse transmission between motor neurons & innervated muscle cells are affected)

61
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who are affected more with myasthenia gravis?

WOMEN

62
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a pt presents with muscle weakness and fatigue as well as ptosis (eye drooping), diplopia (double vision), aphasia (total loss of speech), and dysphagia (partial loss of speech). the pt notes that they first noticed facial weakness in their eyebrows and now feel it in their mouth (muscle weakness migrating from top of face to bottom). what would you suspect is going on?

they are experiencing myasthenia gravis

63
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what would you rely on to diagnose someone with myasthenia gravis?

your med hx & assess.; nerve stimulation study; immunoassay test (this confirms short ACh response test)

64
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what are the 2 different types of acetyl choline receptors affected in myasthenia gravis?

muscarinic & nicotinic

65
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when the muscarinic acetyl choline receptors are affected, what will happen?

there will be an increase in wheezing & secretion because this directly affects the smooth muscle & exocrine glands

66
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when the nicotinic acetyl choline receptors are affected, what will happen?

the diaphragm will be effected — this directly affects skeletal muscle

67
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is there a cure for myasthenia gravis?

there isn’t one

68
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what are the different txs (interventions) for myasthenia gravis? (MENTAL ANSWER)

  • sustain medication schedule (to prevent crisis)

  • supportive care bc there’s no cure — oxygenation + ventilation + tissue perfusion

  • plasmapheresis (removes antibodies)

  • controversial: thymectomy with cortocosteroids

69
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what causes a myasthenia gravis crisis?

severe decrease in ACh, under medication of AChE (acetycholinesterase) inhibitors — physical or emotional distress

70
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a pt presents with with muscle weakness, a compromised diaphragm, tachycardia, & mydriasis (dilated pupils). what would you infer is going on?

myasthenia gravis crisis

71
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what is affected in a myasthenia gravis crisis?

the respiratory muscles — AIRWAY, BREATHING, & CIRCULATION

72
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what are the interventions for myasthenia gravis crisis?

adequate medication of acetylcholinesterase inhibitors (AChE) - MEDICATE THEM

73
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what causes a cholinergic crisis?

  • pesticide use (chemicals)

  • OVER MEDICATION (especially in AChE inhibitors)

74
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what happens to the acetylcholine levels in pts who are having a cholinergic crisis?

they increase

75
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what is the “SLUDGE” mnemonic used for?

cholinergic crises clinical manifestations

76
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what are the clinical manifestation for a cholinergic crisis?

S increased salivation

Lacrimation

Urinary frequency

Diarrhea

GI cramping

Emesis or vomiting

BRADYCARDIA

MIOSIS

77
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what happens to the eyes are heartrate in myasthenia gravis crisis?

they dilate (mydriasis) & they become tachycardic

78
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what happens to the eyes are heartrate in cholinergic crisis?

they constrict (mitosis) & they become bradycardic

79
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what are the interventions for a cholinergic crisis?

anticholinergics → ATROPINE