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Human Disease and Therapeutics > Lecture 6 (Quiz 2) > Flashcards

Lecture 6 (Quiz 2) Flashcards

1
Q

What are the 8 mechanisms for CNS Degenerative Disorders?

A
  1. Hypoxia (decreased oxygen in tissues)
  2. Excitatory amino acids (Glutamate and Aspartate)
  3. Ion Fluxes (usually Ca)
  4. Free Radicals (Reactive O2, Reactive NO2/ROS,RNS)
  5. Immune responses (Autoimmune diseases)
  6. Infections (usually viral)
  7. Apoptosis (is programmed cell death, but can go wrong)
  8. Protein aggregation
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2
Q

What is the name of the cluster of proteins found in patients with Parkinson’s Disease? What are the three main clinical manifestations of Parkinson’s Disease? There are 4 other clinical manifestations of Parkinson’s Disease, including postural abnormalities, autonomic and neuroendocrine, late symptoms and oral status. Describe each of these.

A
  • Lewy bodies
  • Tremor, Rigidity & Bradykinesia (slowness of movement)
  • Postural abnormalities: Stooped posture, shuffling of feet.
    Autonomic and neuroendocrine: Salivate/Drool (due to dysphasia), Slurred speech, and Dysphasia/Chocking (inability to swallow very well).
    Late symptoms: Depression, Immobile, and Loss of bowel function.
    Oral status: High carries, and High number of root canals.
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3
Q

The Hoehn and Yahr scale depict the 5 stages of Parkinson’s Disease. What are the 5 stages?

A
  • Stage 1: Only one side of body is affected, with minimal to no fictional impairment.
  • Stage 2: Both sides of body are affected but posture and balance remain normal.
  • Stage 3 (Moderate Disease): Both sides of the body are affected, and there is mild imbalance when standing/walking, however, individual is still independent.
  • Stage 4 (Advanced Disease): Both sides of the body are affected, and there is disabling instability while standing/walking. Requires substantial help and cannot live alone.
  • Stage 5: Severe, fully developed disease is present. The person is often cachectic, restricted to a bed/wheelchair unless aided.
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4
Q

At the age of 80 ___% of individuals have Parkinson’s Disease. At 50-60?

A
  • 80: 50%
  • ## 50-60: 1%
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5
Q

What part of the brain is affected with Parkinson’s Disease? What is molecule is greatly decreased in these parts of the brain with Parkinson’s Disease? Once Parkinson’s reaches the Striatum, it interacts with two other neuronal systems, what are they? This causes what and ends up causing Parkinson’s Disease?

A
  • Caudate or Striatum
  • Dopamine
  • GABA and ACh
  • You lose the Nigrostriatal Dopamine Pathway which increases Cholinergic activity. (Increases Choline???)
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6
Q

Causes of Parkinson’s disease can be either environmental or genetic, what are 4 examples of environmental causes? What are 2 genes involved in Parkinson’s Disease?

A
  • Environmental:
    - Mg (in welders) and Hg (in dentists)
    - Pesticides (Quinones, found in farmers)
    - Trauma
    - Dopamine (creates radicals and Quinones)
  • Genetics:
    - Synuclein (Aids in trafficking of vesicles, causes Protein Aggregation)
    - Larkin
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7
Q

One basis of treatment for Parkinson’s Disease is Pharmacologically. What are the two major drugs involved in this form of treatment and how do they work? What drug can be used to improve the effectiveness of the Levodopa-Carbidopa drug use?

A
  • Levodopa (L-DOPA) and Carbidopa
  • Levodopa (L-DOPA) is used to produce more Dopamine in the brain, however, it is difficult to cross the Blood-Brain Barrier and is quickly metabolized. Carbidopa blocks the peripheral metabolism of L-DOPA to make it have a higher concentration in the brain where it is needed.
  • Entacapone
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8
Q

There are several drugs that can be used to treat Parkinson’s Disease, what drug:
- Is an Anticholinergic (inhibits ACh) medication that is useful for treating tremors.

A
  • Benztropine
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9
Q

There are several drugs that can be used to treat Parkinson’s Disease, what drug:
- Is a Dopamine precursor that is transformed into Dopamine in the Substantia Nigra after crossing the Blood Brain Barrier and aids with rigidity.

A
  • Levodopa (L-Dopa)
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10
Q

There are several drugs that can be used to treat Parkinson’s Disease, what drug:
- Inhibits the conversion of systemic dopamine to aid in the concentration of DA in the brain and decreases systemic effects of Levodopa.

A
  • Carbidopa (used with Levodopa)
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11
Q

There are several drugs that can be used to treat Parkinson’s Disease, what drug:
- Aids in reducing the absorption of Levodopa and Carbidopa.

A
  • Entacapone (usually used with Levodopa, and Carbidopa)
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12
Q

There are several drugs that can be used to treat Parkinson’s Disease, what drug:
- Is a Dopamine agonist that aids in providing a longer lasting direct stimulation of Dopamine receptors.

A
  • Pramipexole
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13
Q

There are several drugs that can be used to treat Parkinson’s Disease, what drug:
- Blocks Monoamine Oxidase from metabolizing Dopamine from being metabolized in the brain.

A
  • Selegiline
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14
Q

You can also treat Parkinson’s Syndrome by using surgical techniques. What method is used to do this? What doe it do? When is it mostly effective?

A
  • Deep Brain Stimulation (DBS)
  • Aids by enhancing Dopamine release which helps with physical tremors, but not necessarily the cognitive portion.
  • Most effective at early onset.
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15
Q

What Parkinson’s Disease drugs have been associated with Glossitis (increased tongue size)? Which one causes gingivitis as well? Bruxism?

A

Glossitis:

  • L-Dopa with Carbidopa.
  • L-Dopa with Carbidopa and Entacapone.
  • Ropinirole

Gingivitis:
- Ropinirole

Bruxism:

  • L-Dopa
  • Selegiline
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16
Q

When should major dental intervention be accomplished with Parkinson’s Disease? How long should appointments with these patients be? When should their PD medication be taken? When taking Levodopa and/or Entacapone, what should you be aware of?

A
  • Early in the course of PD.
  • Short (less than 45 min).
  • 90 minutes before treatment. (Start appointment 90 minutes after taking meds).
  • Patients should be limited to 3 cartages of lidocaine / other anesthetics.
17
Q

What are tips for Parkinson’s Disease that should be given to both the patient and the caregiver for dental health?

A
  • Electric toothbrush
  • Use ‘one-handed’ strategies
  • Apply fluoride gel treatments
  • Use non-alcoholic based mouthwashes (chlorhexidine/baking soda)
  • Dental visits should be scheduled for the mornings.
  • Take meds 90 min. before appointment.
  • If necessary, plan several short visits instead of long ones.
18
Q

In seeing patients with Parkinson’s Disease, many will have Xerostomia, Sialorrhea, Medication effects, Tremor and bradykinesia, and Poor lip closure. How do you solve these problems?

A
  • Xerostomia: Frequent sips of water, avoid alcohol or smoking.
  • Sialorrhea: Use of anticholinergic medications.
  • Medication effects: NA
  • Tremor and Bradykinesia: Use an electric tooth brush, using a straw will assist with rinsing.
  • Poor lip closure: Send to a speech pathologist.
19
Q

What are the 2 major clinical manifestations of Huntington’s Disease (Chorea) and some info about each?

A
  • Abnormal moves (jerking, grimacing, debilitating)

- Progressive intellectual dysfunction

20
Q

In Huntington’s Disease (Chorea), what are it’s features in the brain to distinguish it (pathophysiology)? What causes these feature changes? How do you diagnose it?

A
  • Enlarged ventricles of the brain due to loss of Caudate neurons due to high levels of Dopamine causing a deterioration of the cell bodies in the Striatum.
  • The genetic trait of the Huntington’s Gene is thought to be related to the increase of activity of Glutamate and the NMDA receptors which causes a loss of GABA levels.
  • Genetic Screen
21
Q

How do you treat for Huntington’s Disease? *(Meds become less effective as time continues)

A
  • Haloperidol (D-2 Antagonist/Neuroleptic)
  • Citalopram (Antidepressant)
  • Baclofen (Beta-Agonist, helps with rigidity)
22
Q

What are the three basic stages of Alzheimer’s?

A
  • Early: Person can still function and work. Recent memory begins to fade.
  • Moderate: Difficulty functioning. Everyday tasks become difficult due to a loss of memory. Difficult for them to live by themselves.
  • Late: Don’t remember anything or anybody mostly (may be able to recall very old memories). Motor functions deteriorate. No judgement. Stop eating.
23
Q

What three major areas of the brain are affected by Alzheimer’s disease and what do they affect?

A
  • Hippocampus: Main area that affects memory.
  • Frontal Cortex: Cognitive degeneration.
  • Nucleus Basalis: Connects to Hippocampus.
24
Q

There are two Histological effects that lead to Alzheimer’s, what are they and what are they made of? What causes Alzheimer’s disease? Genetically what has caused Alzheimer’s disease?

A
  • Senile Plaques (Beta Amyloid Proteins that aggregate together))
  • Neurofibrillary Tangles (Tau Proteins that aggregate together)
  • Decrease in ACh, and Beta Amyloid from Amyloid Precursor Proteins (APP) and Tau Proteins.
  • The gene that clips Amyloid Precursor Proteins (APP) Proteins has been altered (could be associated with chromosome 21, Downs Syndrome). Eventually this will cause protein aggregation and inflammation that will disrupt and kill cells.
25
Q

How do you diagnose Alzheimer’s? What drugs are used to treat Alzheimer’s disease?

A
  • Can’t usually until after death (Post-Mortem)
    Drugs used:
  • Donepezil (Cholinesterase Inhibitor, aids with cognitive and fictional decline) **(All other drugs just aid with symptoms from Alzheimer’s, but don’t treat the cause).
  • Antipsychotics, Neuroleptic (Haloperidol), and Antidepressants.
26
Q

What 4 techniques should the dentist suggest to help these patients?

A
  • Short simple instructions
  • Use ‘watch me’ technique
  • Monitor daily oral care
  • Keep up regular dental visits as long as possible
27
Q

What are some clinical manifestations of Multiple Sclerosis? Multiple Sclerosis is a disease where Scandinavians seems to be more frequent, but low in Asian/Japanese, is a Genetic based disorder and effects Older adolescence/young adults. In which gender is it more common? What causes Multiple Sclerosis?

A
  • Decreased or loss of sensitivity with: Optic, Hearing, Sensory, Smell, Taste, Depression, Autonomics, Cognition, Fatigue (General/Specific) Heat worsens this fatigue and a variable/episodic depression (rollercoaster).
  • 2:1 more common in females.
  • A virus triggers an autoimmune response that destroys the myelin sheath of axons, causing a decreased or destroyed signal.
28
Q

There are 4 levels of classification in Multiple Sclerosis patients (Benign, Relapsing Remission, Relapsing Progressive, Chronic Progression). What makes them different?

A
  • Benign: Not many symptoms, slight and unprogressive. Many won’t know that anything is wrong.
  • Relapsing Remission: On/Off: Times where things are good and then others where they may be tired, vision/sensory problems and difficulty in daily activities. Can feel completely normal at times. (May think they are sick, but not necessarily have MS.)
  • Relapsing Progressive: MS does not turn off.
  • Chronic Progression: No remission/improvement and will eventually die.
29
Q

What is the diagnosis for Multiple Sclerosis?

A
  • Take a MRI: White areas on MRI can mean early stages of MS. More than 2 lesions to be considered MS.
30
Q

What is the main drug used to treat Multiple Sclerosis and what does it do? (two drugs that can be used in extreme circumstances). There are several drugs that treat the side effects of MS such as: Tamsulosin, Metamucil, Prozac, Modafinil, Gabapentin, and Clonazepam. What do these help with?

A
  • Prednisone: Steroids for anti-inflammatory, aids to manage relapses. (In extreme situations can also use Interferon and Methyltrexate.)
    -Tamsulosin: Bladder dysfunctions
    Metamucil: Bowel dysfunction
    Prozac: Depression
    Modafinil: Fatigue
    Gabapentin: Pain
    Clonazepam: Tremors

Human Disease and Therapeutics (27 decks)

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