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Neuro > Peripheral Nerve Disorders II - Exam 4 > Flashcards

Peripheral Nerve Disorders II - Exam 4 Flashcards

1
Q

What is the etiology of muscular dystrophy? How does a pt get muscular dystrophy?

A

Complex set of INHERITED myopathic disorders.

inherited: X linked recessive!!

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2
Q

Muscular dystrophy presents as ________ WITHOUT _______ often ______. What lab value will be elevated?

A

muscle weakness and wasting

WITHOUT sensory loss

progressive

elevated CK

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3
Q

What are the 2 types of MD that we learned about in lecture? Which one is worse? What percentage of all MD?

A

Duchenne MD** worse: 23%

Becker MD: 10%

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4
Q

What groups of muscles are commonly affected in both Duchenne and Becker MD?

A

shoulders, forearms and thighs

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5
Q

How does Duchenne MD compare to Becker MD? include protein _____

A

Duchenne is more severe s/s
-dystrophin (protein) is markedly reduced or absent

Becker: similar to DMD but later onset and milder course
-dystrophin levels are normal, but protein is qualitatively altered (misshapen)

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6
Q

In MD the genetic defect is located on the _______. What is it? What does it code for?

A

short arm of X chromosome

dystrophin: (protein): helps anchor the outside of the muscle cell to the inside of the muscle cell. plays a huge role in strength of muscle

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7
Q

Can DMD be recognized in early pregnancy?

A

YES! can be recognized in early pregnancy in about 95% of women

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8
Q

What is the trend with regards to MD as a pts ages?

A

older the pt gets the higher likely they are to die, survival rates into adulthood is not great

58% of males 20-24

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9
Q

How does Duchenne MD typically present?

A

weakness usually around 2-3 years old

starts proximal and moves distal, weakness is progressive

Gower’s sign

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10
Q

What is Gower’s sign? What disease is it commonly seen with?

A

using hands to push up to stand, shows progressive muscle weakness

MD

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11
Q

Besides weakness, name additional s/s of Duchenne MD.

A
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12
Q

What are the 4 typical comorbidities associated with Duchenne MD?

A

primary dilated cardiomyopathy: MITRAL regurg. can lead to heart failure and arrhythmias in later stages

fractures

progressive scoliosis

impaired pulmonary function due to respiratory muscle weakness

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13
Q

______ is the clinical distinction between Becker and Duchanne MD. How long can they remain _______? ______ is usually worse when compared to Duchanne

A

retained strength

Usually ambulatory at least until age 15 and commonly into adult life

WORSE: cardiac dz in Becker due to retained ability to exercise

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14
Q

As a PCP, what 3 tests should you order if you suspect MD? Then what should you do?

A

serum CK

EKG

EMG

refer to neuromuscular specialist/ MD center

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15
Q

What will the serum CK show in a pt with MD? When is it at its peak? Is CK elevated or decreased in carriers?

A

elevated in DBMD patients prior to clinical signs of disease

Peaks ~age 2; usually 5-10x ULN or more; then falls by 25% per yr

CK increased up to 10x ULN in carriers - 50% DMD carriers, 30% BMD carriers

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16
Q

What will the EKG show in a pt with MD? What will the EMG show?

A

tall right precordial R waves, increased R/S ratio, deep Q waves in I, aVL, V5-6
DMD also associated with conduction disturbances leading to variety of arrhythmias

EMG: myopathic changes

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17
Q

_____ is the first line and confirms dx test in MD

A

Genetic analysis

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18
Q

What will a muscle bx show in a pt with MD? What about dystrophin specifically? Give DMD and BMD results

A

degeneration, regeneration, isolated “opaque” hypertrophic fibers, replacement of muscle by fat and connective tissue

DMD - most pts have total or near-total absence of dystrophin

BMD - ~85% with abnormal size and amount; ~15% with normal size, abnormal amount

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19
Q

______ is the mainstay of tx for MD. When is it recommended to start? What age? What are the dosing considerations?

A

Glucocorticoids (prednisone)

start before significant physical decline occurs

boys 4+ years old whose motor skills have plateaued or starting to decline

do NOT abruptly stop, need to taper and may need stress dosing

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20
Q

What are 3 good parameters to assess benefits of glucocorticoids in MD?

A

Timed muscle function tests
pulmonary function tests
age at loss of independent ambulation

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21
Q

________ : systemic glucocorticoid specifically for DMD. What is potential SE? More or less SE when compared to prednisone?

A

Deflazacort (Emflaza)

may stunt growth

LESS general SE when compared to prednisone

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22
Q

________ is the newest glucocorticoid option for MD but it is expensive

A

Vamorolone (Agamree)

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23
Q

________ binds to exon 51 of mRNA, causes skipping of exon 51 in translation of the DMD gene. What percent of DMD pts have this variant? What is the theoretical end result?

A

Eteplirsen (Exondys 51)

13% of DMD pts have exon-51 variants

increases dystrophin

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24
Q

______ and ________ Causes skipping of exon 53 in translation of the DMD gene. What percent of DMD pts have this variant?

A

Golodirsen (Vyondys 53) and Vitolarsen (Viltespo)

8% of DMD pts have exon-53 variants

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25
Q

________ Causes skipping of exon 45 in translation of the DMD gene. What percent of DMD pts have this variant?

A

Casimersen (Amondys 45)

8% of DMD pts have exon-45 variants

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26
Q

________ Adeno-associated virus capsid (AAVrh74) with a gene that encodes for ________. What is it designed to do?

A

Delandistrogene moxeparvovec (Elevidys)

microdystrophin

Designed to deliver to skeletal and cardiac muscle

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27
Q

How are the gene editing drugs given to pt? How is Delandistrogene moxeparvovec (Elevidys) given to pts?

A

gene editing: weekly infusions

Delandistrogene moxeparvovec (Elevidys): ONE IV infusion. that is it

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28
Q

_______ Promotes read-through of inappropriate nonsense (stop) codons, allowing bypass of nonsense codon and continuation of translation process to produce dystrophin

A

ataluren (PTC 124)

NOT YET APPROVED IN THE US

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29
Q

What are 2 additional emerging tx options for MD?

A

Myostatin inactivating antibodies: Myostatin is a protein that inhibits muscle growth

Cell Therapy

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30
Q

_______ Promotes muscle formation and reduces fibrosis, fatty replacement, and inflammation of muscles and IS NOT restricted to specific gene variants. What drug class?

A

Givinostat (Duvyzat)

histone deacetylase inhibitor

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31
Q

When is Givinostat (Duvyzat) commonly used? What do you need to monitor? When can you NOT give it?

A

adjuvant medication in MD on top of gene editing drugs and prednisone

monitor platelet count, triglycerides, and QTc interval

Do not give if baseline platelets <150,000

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32
Q

What the additional medications needed to tx cardiac comorbities? What testing?

A

steroids may reduce new-onset and progressive cardiomyopathy,

ACEi and/or ARB beginning at age 10

Echocardiogram yearly at onset

Cardiac MRI beginning around age 7 and then annually

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33
Q

What do you need to counsel pts on with regards managing/preventing orthopedic complications in MD?

A

Gentle aerobic exercise - swimming, cycling, assisted exercise

Physical therapy to help reduce contractures

nutrition: need calcium and Vit D

orthotics, braces, surgical release of contractures, tx fractures, standing wheelchairs

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34
Q

The DMD prognosis may see early improvement when the kid is ______. The median survival rate in DMD is ______.
The mean survival rate in BMD is ______.

A

3-6 years old but will have gradual deterioration

DMD: 35 years old

BMD: mid 40s

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35
Q

What is the MC cause of death in BMD?

A

heart failure from dilated cardiomyopathy

can consider heart transplant

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36
Q

Charcot- Marie- Tooth is a spectrum of disorders caused by a specific mutation in one of several ______. What does it result in?

A

myelin genes

defects in myelin structure, maintenance, and formation

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37
Q

**______ is the MC type of hereditary neuropathy. How is it inherited? MC in males or females?

A

Charcot-Marie-Tooth (CMT)

autosomal dominant

3x more common in males

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38
Q

When does CMT usually present? What is the presenting symptom? How does it progress?

A

1st-3rd decade of life

distal leg weakness (e.g., foot drop): usually foot deformities or gait disturbances in the childhood or early adult life

slow progression moves distal to proximal, eventually involves UE and LE

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39
Q

What will the MSK exam of the lower extremities reveal in pt with CMT?

A

Foot Drop - reduced or absent dorsiflexion

Pes cavus - high arch and hammertoes

Atrophy of muscles below knee - “inverted champagne bottle” legs or “stork legs”

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40
Q

What will the MSK exam of the upper extremities reveal in CMT?

A

Claw hand - due to atrophy of muscles in hand

Hand weakness - poor finger control, poor handwriting, difficulty with zippers and buttons, and clumsiness with manipulating small objects

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41
Q

What will the neuro exam reveal in a pt with CMT?

A
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42
Q

What 2 types of sensation will be diminished in CMT?

A

diminished proprioception and vibration (due to LARGE fiber neuropathy)

pt will not complain of sensory loss because they never had the sensation to begin with

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43
Q

What will the EMG and NCS of a pt with CMT show? Why is it important to correctly dx CMT early?

A

Confirms evidence of neuropathy
If negative, consider a different diagnosis

need to start interventions ASAP especially PT

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44
Q

______ confirms diagnosis of CMT. Why?

A

genetic testing

also helps to rule out other genetic sources of neuropathy

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45
Q

What is the tx for CMT?

A

SUPPORTIVE CARE!!! no specific dz modifying therapy

PT: daily stretching

ankle foot orthotics/foot sx if needed

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46
Q

**What 2 medications need to be avoided in CMT? What type of medications are they?

A

vincristine and paclitaxel

both chemo drugs

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47
Q

What is the prognosis of a pt with CMT?

A

slow progressing dz and pts often live a full life span but have an impaired quality of life

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48
Q

What do you need to monitor for in CMT?

A

Screen periodically for conditions that can exacerbate neuropathy:

Diabetes mellitus
Vitamin deficiencies
Immune-mediated neuropathies

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49
Q

What is Guillain-Barré Syndrome (GBS)? **What 3 things does it result in?

A

acute, IMMUNE-MEDIATED (not genetic) polyradiculoneuropathy that results in
weakness, paralysis, and diminished reflexes

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50
Q

What is the usual trigger for GBS? **specifically _______. What does it lead to?

A

Inflammatory/immune-associated trigger (usually a recent infection)

-> specifically Campylobacter jejuni

leads to production of ANTIBODIES that cause myelin destruction or axon damage in peripheral nerves

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51
Q

risk of GBS increases as you _____, MC in males or females?

A

more common as a pt ages

slightly more common in males

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52
Q

What is the MC form of GBS?

A

Acute inflammatory demyelinating polyneuropathy (AIDP)

53
Q

How does GBS present? When do s/s usually progress? What will pts commonly complain of? When is the nadir (lowpoint) of the dz?

A

new acute neuro symptoms that present as SYMMETRICAL muscle weakness that usually begins the legs and ascends

“rubbery legs” and weakness tends to progress

Symptoms usually progress over a period of 2 weeks

nadir: by 4 weeks

54
Q

____ of GBS occurs a few weeks after acute infectious process usually ____ or _____ in nature

A

66%

GI or respiratory in nature

with campylobacter jejuni the MC etiology

55
Q

rare, but possible to see GBS after ??????

A

surgery, trauma, bone marrow transplantation, or systemic diseases like SLE and Hodgkin lymphoma

56
Q

In GBS _____ symptoms often precede ____ symptoms. _____ is often present in shoulders, back, thighs and buttocks

A

Sensory symptoms often precede motor symptoms

deep, aching muscular pain

57
Q

10% of GBS patients will present with ______ initially. 10-30% of GBS pts will develop ______ requiring _______

A

arm or facial muscle weakness

respiratory weakness

ventilation

58
Q

What are 3 other neuro symptoms commonly seen in GBS?

A

reduced or absent DTR in 90% of pts

CN or bulbar palsies: Bells Palsy, oropharyngeal weakness, oculomotor weakness

dysautonomia: think reduced gut motility (ileus) urinary retention, HTN or hypotension, Tachy or bradycardia, fever

59
Q

What will the brain/spine MRI with gadolinium contrast show in a pt with GBS?

A

May show thickening and enhancement of cranial and spinal nerve roots and cauda equina

sensitive but not specific for GBS

60
Q

What will NCS/EMG show in a pt with GBS? What is important to note?

A

Confirms polyneuropathy; differentiates between axonal and demyelinating subtypes

Normal study early on does not rule-out GBS aka can also be normal and still have GBS

61
Q

**What does LP with CSF analysis show in a pt with GBS? **What is important to note? Who should it be done on?

A

**elevated CSF protein with a normal CSF WBC

**CSF can also be NORMAL

ALL pts that are suspected to have GBS

62
Q

What is the management for GBS? _____ needs to be completed beside every 4 hours. ______ to avoid contractures

A

-hospitalization!! due to risk of respiratory failure
- PM: NSAIDs, gabapentin or carbamazepine or amitryptyline. careful with opioids due to risk of ileus
-LMWH for DVT prophylaxis
-tx HTN (esmolol or nitroprusside) or hypotension (IV fluids or pressors PRN)
- Tx tachy/bradycardia

Serial bedside PFTs - every 4 hours assessing pulmonary muscle strength

daily ROM exercises to avoid contractures

63
Q

What is the GBS SPECIFIC tx options? Which one is preferred? When does it need to be administered?

A

Plasmapheresis or IVIG** preferred

within 4 weeks of symptom onset

64
Q

_____ removes autoantibodies, immune complexes, cytotoxic constituents. What is the tx schedule?

A

Plasmapheresis

4-6 treatments over 8-10 days

65
Q

______ derived from donated plasma; supplements the pts immune response. What is the tx schedule?

A

IVIG

requires less time - one tx daily x 5 d

66
Q

What is the timeline associated with GBS? What is the average time to recovery? _____ is a very common reported continued symptom

A

s/s progression for up to 2 weeks

nadir around 4 weeks

plateau of unchanging symptoms for 2-4 weeks

then gradual improvement of symptoms

200 days

fatigue

67
Q

What are poor prognostic factors for GBS?

A

older than 60

rapid onset of weakness

severe weakness at time of admission

respiratory weakness/vent support

severe NCS/EMG abnormalities

preceding diarrheal illness

68
Q

Motor neuron action potential releases _____ into the synaptic cleft. What is presynaptic rundown?

A

acetylcholine (ACh)

temporary depletion of presynaptic ACh

69
Q

_____attaches to the ACh receptor (AChR) on the ______ of the muscle cell
ACh-AChR binding results in ______

A

Acetylcholine

postsynaptic fold

muscle contraction

70
Q

______ breaks down Ach and prevents excessively prolonged _______

A

Acetylcholinesterase

muscle contraction

71
Q

What is the etiology of myasthenia gravis?

A

neuromuscular disease - weakness and fatigability of skeletal muscles as a result of autoimmune attack that causes a decrease in acetylcholine receptors (AChRs) at NMJs and loss of postsynaptic folds

72
Q

In myasthenia gravis, what happens as a result of the decrease in acetylcholine receptors (AChRs) at NMJs and loss of postsynaptic folds?

A

Over-release of ACh from axon terminals to try to create an adequate response which results in presynaptic rundown and loss of acetylcholine receptors (AChRs) which results in progressively reduced muscle strength with repeated use

73
Q

What are the 2 types of autoantibodies that are associated with myasthenia gravis? Which one is more common?

A

anti-AChR - 80-90% of MG patients

anti-MuSK - muscle-specific tyrosine kinase

74
Q

Which MG autoantibody are associated with an underlying thymus disorder?

A

anti-AChR

75
Q

also possible to have the ______ form of MG. What will the test show?

A

Seronegative MG

neither antibody but still have clinical dx

76
Q

What is the bimodal peak of MG? What is the cause if it is seen in infants? MC in males or females?

A

females age 20s-30s, males age 50s-60s

Infantile - transient neonatal MG occurring in infants of myasthenic mother

slightly MC in women

77
Q

What are the risk factors for MG?

A

infections
hormonal changes
thymic abnormalities
medications: abx, BB, statins, anticholinergics, botox

78
Q

**What are the 2 cardinal features of MG?

A

weakness and fatigability

weakness increases as the day progresses (using the muscles) and IMPROVE with sleep

aka muscles get tired of doing normal activities that would not be an issue for a normal person (chewing, speaking, swallowing, holding the neck up, holding eyelids open)

79
Q

______ is the initial symptom in over 50% of patients. ____ is NOT affected

A

ocular (ptosis, diplopia, weak EOM)

pupils are NOT affected

80
Q

_____ and ____ are often asymmetric in myasthenia gravis. What 4 things are usually normal?

A

ocular palsies and ptosis

Normal pupillary responses, sensation, coordination, DTRs

81
Q

What is a myasthenic crisis? What usually precedes the crisis? Can it be triggered?

A

life-threatening exacerbation involving respiratory system. Weakness of diaphragm and intercostal muscles → hypoventilation, respiratory failure. NEED TO BE IN ICU!!

increased generalized weakness: pt needs to seek care immediately!!

yes! sx, childbirth, infection, tapering of immunosuppressive medications or can be spontaneous

82
Q

What is the ice pack test? What is the expected result if the pt has myasthenia gravis?

A

Ice Pack Test - for patients with ptosis

Ice pack on closed eyelid for 2 minutes.
Cold improves neuromuscular transmission

Positive (suggestive of MG) if ptosis improves

83
Q

_______ is positive in 85% of all MG pts, 50% of ocular MG. Does a negative test exclude MG?

A

Anti-AChR antibodies

negative does NOT exclude

84
Q

______ will be positive in 35-50% of MG pts who are anti-AChR negative

A

Anti-MuSK antibodies

85
Q

_________ will be positive in 30% of MG pts, 80% of thymoma pts

A

Anti-striated muscle (anti-SM) antibody

86
Q

_______ is the MC electrodiagnostic test for MG. What is another name for it? What will it show if the pt has MG? Normal?

A

Repetitive Nerve Stimulation

modified NCS

action potentials in MG pts drop rapidly by 10-15% for each show

action potentials stay normal in healthy pts

87
Q

________ also known as ______ is used only if other tests are inconclusive. Most sensitive test; (+) if increased interval between action potentials

A

Single-fiber electromyography

modified EMG

88
Q

What imaging would you want to order when working a pt up for myasthenia gravis?

A

chest CT to look at thymus

enlargement of the thymus is a pt over 40 is highly suspicious for MG

89
Q

What are the 4 major tx options for MG?

A
90
Q

What is the tx for mild/moderate MG?

A

Start with symptomatic tx

Add chronic immunomodulating tx if still uncontrolled

91
Q

What is the tx for severe generalized MG or rapidly progressive MG?

A

Start with rapid immunomodulating therapy

PLUS chronic immunomodulating therapy

PLUS symptomatic therapy

92
Q

What is the tx for refractory MG disease?

A

Pts who fail to respond to symptomatic and chronic immunomodulating therapy - monthly IVIG

93
Q

What is the tx for myasthenic crisis?

A

ICU admission with ventilation assistance

Rapid immunotherapy bridging with chronic immunotherapy

high dose glucocorticoids preferred if no CI due to short onset of clinical effect

94
Q

_______ is the Anticholinesterase Inhibitor that is first line in MG

A

pyridostigmine (Mestinon)

95
Q

______ MOA Stops degradation of ACh by enzymes in the neuromuscular junction.
More improvement with non-ocular weakness

A

pyridostigmine (Mestinon)

96
Q

What are the pt education dosing instructions for pyridostigmine (Mestinon)?

A

tid-qid: Typically just before eating or other activities that cause muscle fatigue

97
Q

______ is the first line therapy for chronic immunomodulating therapy in MG. When are high doses used?

A

Glucocorticoids - Prednisone

only used in hospitalized patients undergoing rapid immunomodulating therapy

98
Q

What are the immunomodulators used in chronic immunomodulating MG therapy? When are they used?

A

2nd line: Azathioprine, mycophenolate mofetil (CellCept), and cyclosporine

CIs to corticosteroids, or if symptoms are not controlled with adequate doses of prednisone

99
Q

What are the rapid immunomodulating therapies options in MG? When are they indicated?

A

plasmapheresis and IVIG

-Myasthenic crisis
-Pre-op treatment in MG - helps to prevent post-op “crisis”
-Bridging to slower acting immunotherapy
-Assist in maintaining remission in MG patients who are not controlled on other tx

100
Q

_____ may result in improvement or remission of MG and should be offered to any pt with ______

A

Thymectomy

thymoma on imaging

101
Q

What is the criteria to offer thymectomy to a MG pt who does NOT have thymoma present on imaging?

A

-Young (<50 y/o)

-Have generalized MG or disabling ocular MG

-Best results if AChR positive but can still offer to AChR-negative pts

102
Q

What is the tx for just ocular MG?

A

Symptomatic and chronic immunologic pharmacotherapy

Thymectomy if indicated

tx ptosis and diplopia: crutches, eyelid adhesive strips, artificial tears, eye patch, eyeglass lens occlusion, sx intervention if needed

103
Q

What is the clinical course associated with MG? progression usually peaks in first ____ of illness. What is the order of affected parts of the body?

A

slow progressive course of relapses and remissions

3 years

eyes/face → neck → UE → hands → LE

104
Q

What are some MG pt education points? What is the prognosis?

A

less than 5% mortality rate and most patients live a normal life-span

105
Q

chronic alcohol abuse puts a pt at high risk for ____ deficiency. _______ is when the CNS involvement occurs

A

Thiamine (B1) Deficiency

Wernicke-Korsakoff Syndrome

106
Q

What are the best sources of Thiamine (B1)?

A

fortified grains, pork, seeds, nuts

107
Q

What is dry beriberi? What is the predominant symptom?

A

ymmetric peripheral sensorimotor neuropathy with loss of DTRs
Mild sensory loss and/or burning dysesthesias in the toes and feet

Aching and cramping in the LE - PAIN may be the predominant symptom

108
Q

______ nystagmus→ ophthalmoplegia, ataxia, confusion. What deficiency?

A

Wernicke encephalopathy

thiamine (b1)

109
Q

_______ amnesia, confabulation, impaired learning ability. What deficiency?

A

Korsakoff psychosis

thiamine (B1)

110
Q

______ is the test to dx thiamine deficiency. Need to order _______ before and after thiamine dose. What is considered a postive result?

A

Thiamine or Thiamine pyrophosphate (TPP)

Erythrocyte transketolase activity (ETKA) test

positive result is a 10-25% increase in ETKA; test is lengthy and not readily available

111
Q

What does inadequate absorption or poor intake of B12 (cobalamin) lead to? **What is the MC cause? What are 3 additional causes mentioned in lecture?

A

demyelination

pernicious anemia

vegan diets, GERD meds (H2 blockers, PPIs) and metformin

112
Q

What are s/s of B12 deficiency? What is the contradicting symptom mentioned in lecture?

A

paresthesias in hands, sensory changes, anemia, red swollen tongue, angular cheilitis, behavioral changes

hyperreflexia but ABSENT ACHILLES REFLEX

113
Q

What labs do you order to check B12 levels? order _____ or ______ if result is borderline. What will the results show?

A

Serum cobalamin (B12 levels)

MMA and homocysteine: will be elevated in the absence of B12

114
Q

In B12 deficiency, after treated with ______ at least 50% of patients exhibit _________

A

IM cyanocobalamin must be IM/IV

one or more permanent neurologic deficits

115
Q

_________ associated with rapid, significant weight loss and recurrent, protracted vomiting. How does it present? What is the tx?

A

Polyneuropathy may occur after gastric surgery for ulcer, cancer, wt loss

numbness and paresthesias in the feet

parenteral vitamins because cannot do anything that involves the GI tract because problem is GI related

116
Q

_______ is the MC DM complication. Morphologic abnormalities of the ______ present early in the disease course

A

diabetic neuropathy

vasa nervorum

117
Q

_______ is the MC form of diabetic peripheral neuropathy. Pts lose sensation in a ________. _____ symptoms appear first

A

Distal symmetric polyneuropathy

stocking-glove pattern

sensory: dulled perception of vibration, pain, temperature, light touch

118
Q

in distal symmetric polyneuropathy, _______ occur early in course and ______ occur in high pressure areas

A

Diminished ankle DTR

Calluses and ulcerations

119
Q

_______ is the MC diabetic mononeuropathy

A

median mononeuropathy at the wrist

120
Q

______ is the MC diabetic polyradiculopathy. How does it present?

A

Diabetic amyotrophy

Severe pain in anterior thigh followed in a few days-weeks by weakness and quadriceps wasting with improvement in pain

121
Q

What is the tx for painful DM neuropathies?

A

strict glycemic control

antidepressants: duloxetine (Cymbalta) or venlafaxine (Effexor)

TCAs: amitriptyline (Elavil)

anticonvulsants: gabapentin (Neurontin) or pregabalin (Lyrica)

adjunct: +/- topical therapies: capsaicin and lidocaine gel

122
Q

What are 6 types of autonomic diabetic neuropathies? What is the generic tx of each?

A

Gastroparesis: d/c GLP-1, then try metoclopramide, small frequent meals

diarrhea: hydration and supportive care

constipation: increased fiber and fluids

bladder dysfunction

orthostasis

erectile dysfunction

123
Q

What are the serious SE of metoclopramide?

A

Tardive dyskinesia and extrapyramidal SE - especially > 3 mo use, FDA cautioned against using for long term use

124
Q

alcoholic neuropathy is a gradually progressive ______ caused by neurotoxicity of _______. Can affect ______, _____ and _______

A

axonal polyneuropathy

acetaldehyde (metabolite of ethanol)

sensory, motor and autonomic functions

125
Q

What is alcoholic neuropathy complicated by?

A

demyelination when co-existing nutritional deficiency present (especially B vitamin deficiencies)

126
Q

alcoholic neuropathy is commonly seen more in the ______. These patients are more susceptible to ______. ______ is seen later in disease process when disease is more severe

A

legs: paresthesias of feet/toes

compression of peripheral nerves

autonomic disease

127
Q

_______ is alcoholic neuropathy that also presents with CNS symptoms

A

Wernicke-Korsakoff

128
Q

What is the tx for alcoholic neuropathy? What is the prognosis?

A

Thiamine supplementation

Improved nutrition and cessation of drinking!!

Low doses of TCAs, gabapentin, or mexiletine (antiarrhythmic rx) may help with burning dysesthesia

varies with compliance with treatment but
complete recovery from severe neuropathy is uncommon

129
Q
A

Neuro (13 decks)

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