WGU: D027: Advanced Pathopharmacological Foundations
2026 Latest Updated Questions With Answers Success
Guide.
1. What are some physical - Brain shrinks dramatically; nerve cell death and tissue loss
changes from Alzheimer's de- - Cardinal signs: plaques (abnormal clusters of protein frag-
mentia? ments) 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 in- - To treat symptoms related to memory, thinking, language,
hibitors prescribed for? judgment, and other processes
- Helps delay or slow the worsening of symptoms
4. What does cholinesterase in- - Prevent the breakdown of acetylcholine, a chemical messen-
hibitors do? ger that is important for learning and memory
- Supports communication among nerve cells by keeping the
acetylcholine high
5. What are some commonly - Donepezil (aricept)
prescribed cholinesterase in- - Galantamine (razadyne)
hibitors? - Rivastigmine (exeleon)
6. Which cholinesterase in- - Donepezil (aricept)
hibitor can be used for all
stages of Alzheimer's?
7. Which cholinesterase in- - Galantamine (razadyne)
hibitor can be used for - Rivastigmine (exeleon)
mild-to-moderate stages of
Alzheimer's?
8. Which cholinesterase in- - Rivastigmine (exeleon)
hibitor can be
, used for mild-to-moderate
Alzheimer's and Parkinson's?
9. What medication combina- - Memantine (namenda) and donepezil (aricept)
tion is used to treat moder-
ate-to-severe Alzheimer's?
10. What is memantine (namen- - Prescribed to improve memory, attention, reason, language,
da) used for? and the ability to perform simple tasks
- Can be used alone or with other Alzheimer's disease treat-
ments
11. How does memantine (na- - Regulates the activity of glutamate, a chemical involved in
menda) work? information processing, storage, and retrieval
- Improves mental functioning and ability to perform daily
activities for some people
12. What is the difference in MOA - Cholinesterase inhibitors prevent the breakdown of acetyl-
between cholinesterase in- choline, whereas memantine (namenda) regulates the activity
hibitors and memantine (na- of glutamate
menda)?
13. What is ataxia? - Also known as cerebellum attacks
- Degenerative disease of the nervous system
- Many symptoms mimic those of being drunk (i.e. slurred
speech, stumbling, falling, and incoordination)
14. What causes the symptoms of - The damage caused to the cerebellum, the part of the brain
ataxia? that is responsible for coordinating movements
- Can also be caused by damage to part of the spinal cord and
nerves
15.
, What is the treatment for - No treatment
ataxia? - In some cases, treating the underlying causes (i.e. stopping
medications that cause ataxia)
- In other cases, it is a result from chicken pox or other viral
infections (likely to resolve on its own)
- Genetic causes/predisposed disposition is usually chronic
16. What causes ataxia in the pe- - Genetic predisposition
diatric population? - Fragile X-Associated Tremor/Ataxia Syndrome (FXTAS)
- Prader-Willie Syndrome
17. What is Fragile X syndrome - A genetic condition inherited from parents which results in
(FXS)? various developmental problems
- Rare, but may be dangerous or life-threatening
- Present at birth and is a lifelong condition
- Rarely requires lab testing or imaging
- Often linked to autism (1/3 do have autism)
- X-linked disorder
18. Since Fragile X Syndrome - Often, females are carriers and males are attected
(FXS) is an X-linked disorder, - However, both males and females can be carriers, and both
does a specific gender have a can be attected by the condition
greater risk? - Usually milder in females
19. How did Fragile X Syndrome - The gene Fragile X (the FMR1 gene) is on the X syndrome
(FXS) get its name? - Mutation of the FMR1 gene
20. What is the difference be- - Both caused by mutations on the FMR1 gene, but they are
tween Fragile X-Associated caused by ditterent changes in this gene
Tremor/Ataxia Syndrome (FX- - FXS is caused by a full mutation
TAS) and Fragile X Syndrome - FXTAS is a premutation
(FXS)? - FXS is present at birth, but display these features in early life
- FXTAS develops in adulthood (usually after age 50) and the
, symptoms may appear slowly and develop over the years
- FXTAS individuals are usually healthy with normal cognitive
skills prior to the onset
21. How is Fragile X-Associated - Being a FMR1 premutation carrier
Tremor/Ataxia Syndrome (FX- - The appearance of neurological features such as ataxia (bal-
TAS) diagnosed? ance problems), tremors, and other symptoms
- MRI findings (changes in the brain)
22. What is Prader-Willie Syn- - Genetic disorder that attects many parts of the body and their
drome? growth
- Causes mental and behavioral problems
- Can be dangerous or life threatening if untreated
- Combination of contraceptives contraindicated in breast
feeding
- More common in females
- Confirmed from laboratory findings
23. What is the cause of Prad- - Depletion of chromosome 15 from father
er-Willi Syndrome? - Missing or non-working genes on chromosome 15
(15q11-q13)
- Most cases are not inherited and occur randomly
- Depletion of genes (genes from the region are missing)
- Uniparental disomy - both chromosomes are inherited from
the mother
- Imprinting mutation - genes on the paternal chromosome is
inactive
24. What does Prader-Willi Syn- - Caused the hypothalamus to malfunction (the area of the
drome do to the body? brain that attects hunger, thirst, sex and growth hormones)
- In infancy, an individual does not meet development mile-
stones suck as sitting up and walking
- Their eyes lack coordination
2026 Latest Updated Questions With Answers Success
Guide.
1. What are some physical - Brain shrinks dramatically; nerve cell death and tissue loss
changes from Alzheimer's de- - Cardinal signs: plaques (abnormal clusters of protein frag-
mentia? ments) 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 in- - To treat symptoms related to memory, thinking, language,
hibitors prescribed for? judgment, and other processes
- Helps delay or slow the worsening of symptoms
4. What does cholinesterase in- - Prevent the breakdown of acetylcholine, a chemical messen-
hibitors do? ger that is important for learning and memory
- Supports communication among nerve cells by keeping the
acetylcholine high
5. What are some commonly - Donepezil (aricept)
prescribed cholinesterase in- - Galantamine (razadyne)
hibitors? - Rivastigmine (exeleon)
6. Which cholinesterase in- - Donepezil (aricept)
hibitor can be used for all
stages of Alzheimer's?
7. Which cholinesterase in- - Galantamine (razadyne)
hibitor can be used for - Rivastigmine (exeleon)
mild-to-moderate stages of
Alzheimer's?
8. Which cholinesterase in- - Rivastigmine (exeleon)
hibitor can be
, used for mild-to-moderate
Alzheimer's and Parkinson's?
9. What medication combina- - Memantine (namenda) and donepezil (aricept)
tion is used to treat moder-
ate-to-severe Alzheimer's?
10. What is memantine (namen- - Prescribed to improve memory, attention, reason, language,
da) used for? and the ability to perform simple tasks
- Can be used alone or with other Alzheimer's disease treat-
ments
11. How does memantine (na- - Regulates the activity of glutamate, a chemical involved in
menda) work? information processing, storage, and retrieval
- Improves mental functioning and ability to perform daily
activities for some people
12. What is the difference in MOA - Cholinesterase inhibitors prevent the breakdown of acetyl-
between cholinesterase in- choline, whereas memantine (namenda) regulates the activity
hibitors and memantine (na- of glutamate
menda)?
13. What is ataxia? - Also known as cerebellum attacks
- Degenerative disease of the nervous system
- Many symptoms mimic those of being drunk (i.e. slurred
speech, stumbling, falling, and incoordination)
14. What causes the symptoms of - The damage caused to the cerebellum, the part of the brain
ataxia? that is responsible for coordinating movements
- Can also be caused by damage to part of the spinal cord and
nerves
15.
, What is the treatment for - No treatment
ataxia? - In some cases, treating the underlying causes (i.e. stopping
medications that cause ataxia)
- In other cases, it is a result from chicken pox or other viral
infections (likely to resolve on its own)
- Genetic causes/predisposed disposition is usually chronic
16. What causes ataxia in the pe- - Genetic predisposition
diatric population? - Fragile X-Associated Tremor/Ataxia Syndrome (FXTAS)
- Prader-Willie Syndrome
17. What is Fragile X syndrome - A genetic condition inherited from parents which results in
(FXS)? various developmental problems
- Rare, but may be dangerous or life-threatening
- Present at birth and is a lifelong condition
- Rarely requires lab testing or imaging
- Often linked to autism (1/3 do have autism)
- X-linked disorder
18. Since Fragile X Syndrome - Often, females are carriers and males are attected
(FXS) is an X-linked disorder, - However, both males and females can be carriers, and both
does a specific gender have a can be attected by the condition
greater risk? - Usually milder in females
19. How did Fragile X Syndrome - The gene Fragile X (the FMR1 gene) is on the X syndrome
(FXS) get its name? - Mutation of the FMR1 gene
20. What is the difference be- - Both caused by mutations on the FMR1 gene, but they are
tween Fragile X-Associated caused by ditterent changes in this gene
Tremor/Ataxia Syndrome (FX- - FXS is caused by a full mutation
TAS) and Fragile X Syndrome - FXTAS is a premutation
(FXS)? - FXS is present at birth, but display these features in early life
- FXTAS develops in adulthood (usually after age 50) and the
, symptoms may appear slowly and develop over the years
- FXTAS individuals are usually healthy with normal cognitive
skills prior to the onset
21. How is Fragile X-Associated - Being a FMR1 premutation carrier
Tremor/Ataxia Syndrome (FX- - The appearance of neurological features such as ataxia (bal-
TAS) diagnosed? ance problems), tremors, and other symptoms
- MRI findings (changes in the brain)
22. What is Prader-Willie Syn- - Genetic disorder that attects many parts of the body and their
drome? growth
- Causes mental and behavioral problems
- Can be dangerous or life threatening if untreated
- Combination of contraceptives contraindicated in breast
feeding
- More common in females
- Confirmed from laboratory findings
23. What is the cause of Prad- - Depletion of chromosome 15 from father
er-Willi Syndrome? - Missing or non-working genes on chromosome 15
(15q11-q13)
- Most cases are not inherited and occur randomly
- Depletion of genes (genes from the region are missing)
- Uniparental disomy - both chromosomes are inherited from
the mother
- Imprinting mutation - genes on the paternal chromosome is
inactive
24. What does Prader-Willi Syn- - Caused the hypothalamus to malfunction (the area of the
drome do to the body? brain that attects hunger, thirst, sex and growth hormones)
- In infancy, an individual does not meet development mile-
stones suck as sitting up and walking
- Their eyes lack coordination
