Lecture 4 - Part 2 Flashcards

(39 cards)

1
Q

What is the ethology of epilepsy and seizures?

A

Head trauma, CNS infection, drug and alcohol abuse, CNS tumors, cerebrovascular disease

Majority have no known precipitating event

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2
Q

What is the pathophysiology of epilepsy and seizures?

A
  • Few seconds to several minutes
  • Generalized and partial
  • Single seizure vs. epilepsy
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3
Q

How do you go from diagnosis of seizures to epilepsy?

A

2 or more seizures is diagnosed as epilepsy

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4
Q

What is the treatment for epilepsy and seizures?

A

• Anti-epileptic Drugs (AEDs)
-Phenytoin (Dilantin): inhibits vit D and folate metabolism and thiamine absorption (enteral feeds held)
• Major issue in hospitalized patients
- Valproic acid, Carbamazepine (Tegretol), Gabapentin : weight gain
-Zonisamide & Topiramate: weight loss

• Surgical Treatments

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5
Q

How can we treat epilepsy and seizure with the diet?

A

Ketogenic diet for intractable epilepsy
- High-fat, low-carbohydrate diet
- Mechanisms poorly understood but effective
- Current variations of ketogenic diet
• Medium-chain triglyceride (MCT) diet; low-glycemic-index treatment (LGIT); and modified Atkins diet (MAD)

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6
Q

What is the traditional veto diet?

A
  • Ratio of 3-4g fat/ 1 g PRO + CHO
  • About 90% kcal from fat
  • Mostly fatty foods like butter/cream,  starchy foods
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7
Q

What are the nutrition implications of epilepsy and seizures?

A
  • Inadequate nutrient intake
  • Ensure adequate protein and energy to promote growth of child
  • Limited food choices
  • Drug-nutrient interactions (Vit D, Ca, folate, thiamine)
  • Potential weight gain or loss
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8
Q

how can we monitor and evaluate epilepsy and seizures?

A

• Β-hydroxybutyrate in addition to standard labs
• Vitamin/mineral deficiencies, nutritional status, proper growth
Monitoring and Evaluation
• Seizure frequency records

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9
Q

What is a stroke?

A

Disruption of brain function due to blockage or

interruption of blood flow

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10
Q

What is an aneurysm?

A

Occurs when part of an artery wall weakens, allowing it to balloon out or widen abnormally

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11
Q

What are the non-modifiable risks of stroke and aneurysm?

A
  • Age, gender, ethnicity, genetics

* Previous stroke

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12
Q

What are the modifiable risks of stroke and aneurysm?

A
  • Management of HTN, CVD, DM, hyperlipidemia

* Cigarette smoking, alcohol use, illicit drug use, diet, oral contraceptive use, exercise

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13
Q

What is the nutritional implications of stroke and aneurysm?

A
  • Impairment of ability to chew, swallow, self-feed
  • Dysphagia
  • Individualize nutrition support
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14
Q

What are typical diagnoses when dealing with stroke and aneurysm?

A

Inadequate energy intake, inadequate oral intake, inadequate fluid intake, inadequate protein-energy intake,
swallowing difficulty,
self-feeding difficulty

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15
Q

How would you intervene nutritionally if you have a stroke/aneurysm?

A
  • Modify consistency of food or liquids, positioning of patient, swallow exercises
  • Manage dysphagia
  • Manage modifiable risk factors
  • Enteral nutrition support
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16
Q

What is TBI?

A

Traumatic brain injury

Penetrating brain injuries or closed head injuries due to accidents, falls, violence, firearms, sports
• Falls most common
• Shaken baby syndrome

17
Q

Who is more likely to get a TBI?

A

60% males

More common than breast cancer, spinal injury and HIV/AIDS

18
Q

What is the nutriton implications for TBI?

A
  • Hypermetabolism
  • Hyperglycemia
  • Insulin resistance
  • Increased gluconeogenesis
  • Lipolysis
  • Catabolism as evidenced by nitrogen excretion
19
Q

What is a SCI?

A

Spinal cord Injury

  • Injury to the spinal cord involving fracture or compression of the vertebrae with consequent damage to nerve cells
  • Paraplegia
  • Quadriplegia
20
Q

What are the nutritional implications of SCI?

A

Nutritional needs similar to TBI

Obesity and CVD

In begining needs are going to be very high, need the extra nutrition and protein but over time those needs will decrease
• If in wheelchair need to manage wt gain

21
Q

What are neurodegenerative disorders?

A

• Nutrition needs and status affected by progression
of disease
• Ethical decisions regarding nutrition support
• Nutrition therapy similar among progressive disorders

22
Q

What are the clinical manifestations of dementia?

A
  • Affect mental cognitive tasks: memory, reasoning, language, visual perception
  • Cause disorientation, abstract thinking, personality disorders, loss of purposeful action
  • Alzheimer’s disease most common
23
Q

What is the most important risk factor for dementia?

A

Age

Other risk factors include gender, cardiovascular disease, stroke, diabetes, free radical oxidative damage, Down syndrome, and a history of previous head injury

24
Q

What is Alzheimers disease?

A

Build-up of β amyloid plaque & neurofibrillary tangles in the brain associated with damage and loss of neurons & brain shrinkage

Progressive neurodegenerative disorder of the CNS

Malnutrition occurs as disease progresses Dysphagia

25
What is type 3 diabetes?
``` Growing evidence Alzheimer’s may be metabolic disease • Impaired • Brain insulin responsiveness • Glucose utilization • Energy metabolism • inflammation ``` Inflammation in brain (common in wt gain, an co morbidities of DM) can leads to decrease insulin responsiveness and lead to dementia
26
What is the nutrition diagnosis for dementia?
Related to inadequate intakes, underweight and malnutrition, impaired ability
27
How can we manage nutrition for dementia?
* Progressive loss of memory affecting shopping, food preparation, memory of eating * Eventual need for assistance * Manage dysphagia and prevent aspiration pneumonia * Prevent excessive weight loss * Prevent excessive loss of lean tissue & malnutrition
28
What is ALS?
``` Lou Gehrigs (motor neuron degenerative disorder) Amyotrophic Lateral Sclerosis ``` No cure Loss of motor neurons in the spinal cord and brain resulting in loss of voluntary movement Lose of the ability to walk, talk, eat, swallow, and eventually breathe Dysphagia, loss of motor control (e.g. problem self-feeding), hypermetabolism
29
What is the nutrition goal for ALS?
Prevent Mal nutrition Most common EN or PEG (percutaneous endoscopic tube directly into stomach)
30
What is GBS?
Guillain-Barre syndrome progressive paralysis, demyelination, sensory loss Acute onset often occurring 3-4 hrs following a GI or upper respiratory tract infection (autoimmune response) Recovery rate high
31
What are the nutrition implications/management of someone with GBS?
Chewing and swallowing difficulties and GI motility dysfunction cab lead to compromised oral intake Preservation of lean tissue is critical Aggressive nutrition support needed due to hypermetabolism and hypercatabolism • May require >40-45 kcal/kg and >2g pro/kg Respiratory muscle atrophy leads to poor outcomes Hypermetabolism, increase protein requirements, dysphagia
32
What is the pathophysiology of MS?
* Demyelination, damage to axons | * Communication between neurons is lost
33
What is the clinical manifestation of MS?
Symptoms vary depending on nerve affected • Numbness, tingling, ataxia, weakness, visual problems, dysphagia, constipation, bladder dysfunction.... Some types of MS are fast or slow progressing, or can enter into remission
34
What are the nutrition therapies for MS?
Fatigue weakness Dysphagia Wt gain As disease progresses dietary intervention for dysphagia may be warranted
35
In MS what could lead to the declining nutritional status?
* Side effects from drugs * Stage of disease progression * Role of PUFA’s, antioxidants, vitamin B12 and vitamin D still being investigated
36
What is PD?
Parkinsons Disease Neuromuscular, neurodegenerative disease caused by loss of dopamine-producing cells In addition to bradykinesia (slow movement ), mask-like facial features, shuffling while walking, depression, anxiety, pain, cognitive dysfunctio
37
What is TRAP and what is it used for?
For Parkinsons * “T”tremors * “R”rigidity * “A”akinesia (loss of voluntary movement) * “P” postural instability
38
What is the nutrition intervention for PD?
• High protein may interfere with L-dopa levels * Limit supplement levels of B6 * Pyridoxine enhances extra-cerebral metabolism of Levodopa –prevents therapeutic effects * Closely monitor weight status * Manage GI symptoms; swallowing impairment and gastroparesis
39
What is MG?
Myasthenia Gravis Autoimmune reaction destroys cellular receptors for acetylcholine Muscles tire easily, muscle weakness with physical activity Compromised chewing & swallowing • Bolus formation difficulties • Lip spill from weak jaw, tongue, lips