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2025|26 WGU D027 PATHOPHARMACOLOGICAL ADVANCED FOUNDATIONS EXAM | 400+ ACTUAL QUESTIONS & DETAILED SOLUTION | A’ GUIDE| NEW!!!

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2025|26 WGU D027 PATHOPHARMACOLOGICAL ADVANCED FOUNDATIONS EXAM | 400+ ACTUAL QUESTIONS & DETAILED SOLUTION | A’ GUIDE| NEW!!! 1. What are some physical changes from Alzheimer's dementia?: - Brain shrinks dramatically; nerve cell death and tissue loss - Cardinal signs: plaques (abnormal clusters of protein fragments) and tangles (twisted strands of another protein) 2. How is Alzheimer's treated?: - There is no cure, but there are pharmacological and non-pharmacological treatments - Cholinesterase inhibitors - Memantine (namenda) 3. What are cholinesterase inhibitors prescribed for?: - To treat symptoms relat- ed to memory, thinking, language, judgment, and other processes - Helps delay or slow the worsening of symptoms 4. What does cholinesterase inhibitors do?: - Prevent the breakdown of acetyl- choline, a chemical messenger that is important for learning and memory - Supports communication among nerve cells by keeping the acetylcholine high 5. What are some commonly prescribed cholinesterase inhibitors?: - Donepezil (aricept) - Galantamine (razadyne) - Rivastigmine (exeleon) 6. Which cholinesterase inhibitor can be used for all stages of Alzheimer's?: - Donepezil (aricept) 7. Which cholinesterase inhibitor can be used for mild-to-moderate stages of Alzheimer's?: - Galantamine (razadyne) - Rivastigmine (exeleon) 8. Which cholinesterase inhibitor can be used for mild-to-moderate Alzheimer's and Parkinson's?: - Rivastigmine (exeleon) 9. What medication combination is used to treat moderate-to-severe Alzheimer's?: - Memantine (namenda) and donepezil (aricept) 10. What is memantine (namenda) used for?: - Prescribed to improve memory, attention, reason, language, and the ability to perform simple tasks

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WGU D027 PATHOPHARMACOLOGICAL.
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WGU D027 PATHOPHARMACOLOGICAL.

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1. What are some physical changes from Alzheimer's dementia?: - Brain
shrinks dramatically; nerve cell death and tissue loss
- Cardinal signs: plaques (abnormal clusters of protein fragments) and
tangles (twisted strands of another protein)
2. How is Alzheimer's treated?: - There is no cure, but there are
pharmacological and non-pharmacological treatments
- Cholinesterase inhibitors
- Memantine (namenda)
3. What are cholinesterase inhibitors prescribed for?: - To treat symptoms
relat- ed to memory, thinking, language, judgment, and other processes
- Helps delay or slow the worsening of symptoms
4. What does cholinesterase inhibitors do?: - Prevent the breakdown of
acetyl- choline, a chemical messenger that is important for learning and memory
- Supports communication among nerve cells by keeping the acetylcholine high
5. What are some commonly prescribed cholinesterase inhibitors?:
- Donepezil (aricept)
- Galantamine (razadyne)
- Rivastigmine (exeleon)
6. Which cholinesterase inhibitor can be used for all stages of Alzheimer's?:
- Donepezil (aricept)
7. Which cholinesterase inhibitor can be used for mild-to-moderate stages
of Alzheimer's?: - Galantamine (razadyne)
- Rivastigmine (exeleon)
8. Which cholinesterase inhibitor can be used for mild-to-
moderate Alzheimer's and Parkinson's?: - Rivastigmine (exeleon)
9. What medication combination is used to treat moderate-to-
severe Alzheimer's?: - Memantine (namenda) and donepezil (aricept)
10. What is memantine (namenda) used for?: - Prescribed to improve
memory, attention, reason, language, and the ability to perform simple tasks
1 n/ n52

,- Can be used alone or with other Alzheimer's disease treatments
11. How does memantine (namenda) work?: - Regulates the activity of
glutamate, a chemical involved in information processing, storage, and retrieval
- Improves mental functioning and ability to perform daily activities for some people
12. What is the difference in MOA between cholinesterase inhibitors
and memantine (namenda)?: - Cholinesterase inhibitors prevent the
breakdown of acetylcholine, whereas memantine (namenda) regulates the
activity of glutamate
13. What is ataxia?: - Also known as cerebellum attacks
Degenerative disease of the nervous system




2 n/ n52

, - Many symptoms mimic those of being drunk (i.e. slurred speech, stumbling, falling,
n n n n n n n n n n n


n and incoordination)
n


14. What causes the symptoms of ataxia?: - The damage caused to the
n n n n n n n n n n n


n cerebel- lum, the part of the brain that is responsible for coordinating movements
n n n n n n n n n n n n


- Can also be caused by damage to part of the spinal cord and nerves
n n n n n n n n n n n n n


15. What is the treatment for ataxia?: - No treatment
n n n n n n n n


- In some cases, treating the underlying causes (i.e. stopping medications that cause
n n n n n n n n n n n


n ataxia)
- In other cases, it is a result from chicken pox or other viral infections (likely
n n n n n n n n n n n n n n


n to resolve on its own)
n n n n


- Genetic causes/predisposed disposition is usually chronic
n n n n n


16. What causes ataxia in the pediatric population?: - Genetic predisposition
n n n n n n n n n


- Fragile X-Associated Tremor/Ataxia Syndrome (FXTAS)
n n n n


- Prader-Willie Syndrome n


17. What is Fragile X syndrome (FXS)?: - A genetic condition inherited
n n n n n n n n n n


n from parents which results in various developmental problems
n n n n n n n


- Rare, but may be dangerous or life-threatening
n n n n n n


- Present at birth and is a lifelong condition
n n n n n n n


- Rarely requires lab testing or imaging
n n n n n


- Often linked to autism (1/3 do have autism)
n n n n n n n


- X-linked disorder n


18. Since Fragile X Syndrome (FXS) is an X-linked disorder, does a n n n n n n n n n n


n specific gender have a greater risk?: - Often, females are carriers and males
n n n n n n n n n n n n


n are affected
n


- However, both males and females can be carriers, and both can be affected by the
n n n n n n n n n n n n n n


n condition
- Usually milder in females n n n


19. How did Fragile X Syndrome (FXS) get its name?: - The gene Fragile X
n n n n n n n n n n n n n


n (the FMR1 gene) is on the X syndrome
n n n n n n n


- Mutation of the FMR1 gene n n n n


20. What is the difference between Fragile X-Associated Tremor/Ataxia
n n n n n n n


n Syn- drome (FXTAS) and Fragile X Syndrome (FXS)?: - Both caused by
n n n n n n n n n n n


n mutations on the FMR1 gene, but they are caused by different changes in this
n n n n n n n n n n n n n


n gene
- FXS is caused by a full mutation
n n n n n n


- FXTAS is a premutation n n n


- FXS is present at birth, but display these features in early life
n n n n n n n n n n n


- FXTAS develops in adulthood (usually after age 50) and the symptoms may appear
n n n n n n n n n n n n


n slowly and develop over the years
n n n n n


- FXTAS individuals are usually healthy with normal cognitive skills prior to the onset
n n n n n n n n n n n n

3 n/ n52

, 21. How is Fragile X-Associated Tremor/Ataxia Syndrome (FXTAS)
n n n n n n


diag- nosed?: - Being a FMR1 premutation carrier
n n n n n n n n


- The appearance of neurological features such as ataxia (balance
n n n n n n n n


problems), tremors, and other symptoms
n n n n n


- MRI findings (changes in the brain)
n n n n n


22. What is Prader-Willie Syndrome?: - Genetic disorder that affects many
n n n n n n n n n


parts of the body and their growth
n n n n n n n


- Causes mental and behavioral problems n n n n


- Can be dangerous or life threatening if untreated
n n n n n n n


- Combination of contraceptives contraindicated in breast feeding n n n n n n


- More common in females n n n


- Confirmed from laboratory findings n n n


23. What is the cause of Prader-Willi Syndrome?: - Depletion of chromosome
n n n n n n n n n n


15 from father
n n n


- Missing or non-working genes on chromosome 15 (15q11-q13)
n n n n n n n


- Most cases are not inherited and occur randomly
n n n n n n n


- Depletion of genes (genes from the region are missing)
n n n n n n n n


- Uniparental disomy - both chromosomes are inherited from the mother
n n n n n n n n n


- Imprinting mutation - genes on the paternal chromosome is inactive
n n n n n n n n n


24. What does Prader-Willi Syndrome do to the body?: - Caused then n n n n n n n n n


hypothala- mus to malfunction (the area of the brain that affects hunger, thirst, sex
n n n n n n n n n n n n n n


and growth hormones)
n n n


- In infancy, an individual does not meet development milestones suck as sitting
n n n n n n n n n n n


up and walking
n n n


- Their eyes lack coordination
n n n


25. What is a key feature of Prader-Willi Syndrome?: - A constantn n n n n n n n n n


sense of hunger that usually begins around 2 years of age
n n n n n n n n n n n


- People with Prader-Willi Syndrome want to eat constantly because they never feel
n n n n n n n n n n n


full n


26. What are some symptoms in infants with Prader-Willi Syndrome?: -
n n n n n n n n n


Hypo- tonia with floppy structure and poor muscle tone
n n n n n n n n n


- Distinct facial features affecting the shape and size of eyes, lips, forehead, etc.
n n n n n n n n n n n n


- Poor sucking ability making it difficult to feed
n n n n n n n


- Always lethargic and poor responsiveness n n n n


- Underdeveloped genitals n


27. What is celiac disease?: - Autoimmune disease
n n n n n n


- Damages to the small intestinal epithelium when there is ingestion of gluten
n n n n n n n n n n n


- Loss of mucosal surface and brush border enzymes leads to severe malabsorption
n n n n n n n n n n n


that is more pronounced in the duodenum and jejunum
n n n n n n n n n




4 n/ n52

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