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general nursing tingz!🧸🩺🌠 > alzheimer's is a b****🐟 > Flashcards

alzheimer's is a b****🐟 Flashcards

1
Q

hippocampus?

A

new memory center and spatial navigation.

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2
Q

entorhinal cortex?

A

gateway to the hippocampus, hub for recall of memory information and spatial navigation.

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3
Q

amygdala?

A

emotion hub.

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4
Q

cerebral cortex?

A

outer layer of the brain.

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5
Q

parietal lobe?

A

sensory processing.

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6
Q

temporal lobe?

A

hearing and memory.

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7
Q

occipital lobe?

A

vision.

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8
Q

frontal lobe?

A

thinking, planning, problem solving.

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9
Q

apraxia?

A

it’s a problem with making movements on purpose although muscles work fine.

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10
Q

aphasia?

A

this is a language issue. can’t understand or express their native tongue.

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11
Q

agnosia?

A

this is when the brain can’t recognize things even if the 5 senses work fine.

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12
Q

anomia?

A

this is a type of aphasia where people struggle to find the right names of things despite knowing what they want to say.

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13
Q

cognitive assessment test?

A

this is a test doctors use to check how well someone’s brain is working.

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14
Q

mri (magnetic resonance imaging)?

A

mri is a method doctors use to look inside the body. strong magnets and radio waves give detailed pictures.

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15
Q

ct (computed tomography)?

A

ct is an x-ray-based test that takes many pictures of the body from different angles. not as detailed as mri tho.

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16
Q

amyloid pet scan?

A

this scan looks for clumps of protein called amyloid in the brain.

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17
Q

what is a spinal tap (lumbar puncture) and how does it relate to alzheimer’s?

A

doctors take a sample of cerebrospinal fluid (CSF) from the spine.

in relation to alzheimer’s, they look for a bunch of signals in the fluid, like elevated levels of tau (which signals general neuron damage) or elevated levels phosphorylated-tau (p-tau is associated with tau tangles). or decreased levels of amyloid beta protein (cuz it’s clumping in plaques, not swimming in CSF, that’s why it’s decreased)

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18
Q

apolipoprotein e (ApoE)?

A

ApoE is a protein in the blood that helps move fats around that show a genetic based increased risk of alzheimer’s.

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19
Q

cholinesterase inhibitors?

A

these are medicines used to slow down the developement of alzheimer’s (remember there’s no cure as of 2025) by stopping the enzyme cholinesterase from breaking down acetylcholine.

acetylcholine helps with thinking in the brain. without it, the whole brain system works less efficiently, making confusion/memory loss worse.

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20
Q

nmda antagonists?

A

Drug name: memantine

memantine is a medication for moderate to severe alzheimer’s. blocks nmda receptors that can get overactive, causing brain damage (excitotoxicity). ultimately regulates glutamate.

In alzheimer’s, the brain is already under attack from things like amyloid plaques and tau tangles. overactive nmda receptors make the damage worse by killing even more brain cells.

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21
Q

donepezil brand name and function?

A

brand name: aricept

donepezil is a cholinesterase inhibitor used to treat mild to moderate alzheimer’s.

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22
Q

rivastigmine brand name and function?

A

brand name: exelon

rivastigmine is another cholinesterase inhibitor. comes in pill or patch.

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23
Q

galantamine brand name and function?

A

brand name: razadyne

galantamine is similar to rivastigmine but comes a quick-release or extended relase tablets. or oral solution. approved for mild to moderate alzheimer’s and can have mild affects on mood.

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24
Q

what is acetylcholinesterase?

A

this is an enzyme that breaks down acetylcholine into choline and acetate, ending its signaling activity at synapses.

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25
Q

glutamate?

A

brain’s “GO” neurotransmitter. it get excitatory. stimulates nerve cells to receive info.

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26
Q

acetylcholine?

A

neurotransmitter boss of the muscles’ contractions and glands’ productions. helps to think in general too.

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27
Q

neurofibrillary tangles?

A

tau protein gone rogue. hyperphosphorylated tau protein now due to hyperphosphorylation.

micro-tubules collapse. nutrient roadblock = dying neuron.

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28
Q

beta-amyloid protein plaque?

A

sticky gunk on the outside blocking communication. no neuron communication = no purpose = dying neuron.

also activates the immune system sending unnecessary inflammation to the brain.

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29
Q

microglia

A

the mothers surrounding the neurons. immune cells that patrol the brain and spinal cord, responding to damage and pathogens.

30
Q

dying neurons make a what kind of brain?

A

atrophied.

31
Q

is it chronic or acute?

A

chronic.

32
Q

the parts of a neuron?

A

dendrites.
neucleus + soma.
axon.
myelin sheaths.
nodes of ranvier.
axon terminals.
synapses.

33
Q

what does nmda mean and what are nmda receptors?

A

nmda stands for N-Methyl-D-Aspartate, which is a synthetic chemical that scientists use to study a specific type of receptor in the brain. nmda receptors are a kind of glutamate receptor, meaning they interact with the brain’s main excitatory neurotransmitter, glutamate.

the receptor got its name because nmda can specifically activate it, mimicking the effects of glutamate. this helps researchers study how the receptor works.

34
Q

what is an action potential?

A

an action potential is the electrical signal traveling along a neuron.

35
Q

what happens during the absolute refractory period?

A

sodium (na⁺) channels are inactivated and cannot reopen.

potassium (k⁺) channels are open, allowing k⁺ to flow out and repolarize the neuron.

the neuron cannot fire another action potential, ensuring the signal moves forward only.

36
Q

does hyperpolarization always happen during the refractory period?

A

yes, hyperpolarization usually occurs during the relative refractory period.

potassium channels stay open slightly longer than necessary, causing the membrane potential to dip below the resting state (e.g., -80 mv).

37
Q

what happens during the relative refractory period?

A

sodium channels start resetting but require a stronger-than-usual stimulus to reopen.

potassium channels still be open, causing hyperpolarization (extra negative charge inside the neuron).

this prevents the signal from going backward but allows the neuron to prepare for the next signal.

38
Q

does hyperpolarization always happen during the refractory period?

A

yes, hyperpolarization usually occurs during the relative refractory period.

potassium channels stay open slightly longer than necessary, causing the membrane potential to dip below the resting state (e.g., -80 mv).

39
Q

how does the sodium-potassium pump restore the resting state?

A

the pump actively moves ions to their original positions using ATP. electrochemical gradient does not matter.:

3 na⁺ out and 2 k⁺ in, using atp.

this restores the resting membrane potential of about -70 mv.

40
Q

why can’t the signal travel backward during saltatory conduction?

A

sodium channels are inactivated in the absolute refractory period, so no depolarization can occur in the previous node.

the positive charge from
depolarization is attracted to the negative charge ahead (next node).

the refractory period ensures a one-way flow of the signal.

41
Q

what is the sequence of events in saltatory conduction for a node ?

A

(saltatory conduction refers to only what’s happening with the ion channels)

depolarization: sodium channels open at node a, and na⁺ floods in, creating a positive charge.

repolarization: at node a, potassium channels open, and k⁺ flows out, restoring negativity.

hyperpolarization: potassium channels stay open too long, making node a extra negative.

resting state restored: sodium-potassium pump resets ion concentrations at node a.

42
Q

what roles do potassium channels play during the refractory period?

A

during absolute refractory, k⁺ channels open to repolarize the membrane.

during relative refractory, k⁺ channels stay open, causing hyperpolarization.

43
Q

how do depolarization, repolarization, and the refractory period overlap?

A

depolarization (na⁺ in): happens before the refractory period.

repolarization (k⁺ out): happens during the absolute refractory period.

hyperpolarization (extra k⁺ out): happens during the relative refractory period.

44
Q

what is the electrochemical gradient?

A

the electrochemical gradient is the combined effect of two forces that influence the movement of ions:

concentration gradient – ions move from areas of high concentration to areas of low concentration.

electrical gradient – ions move toward areas of opposite charge

45
Q

what is atp?

A

atp (adenosine triphosphate) is a molecule that stores and transfers energy within cells. it consists of adenine (a nitrogenous base), ribose (a sugar), and three phosphate groups.

46
Q

how does atp generate energy?

A

by breaking the high-energy bond between the second and third phosphate groups, releasing energy that powers cellular functions.

47
Q

what happens when atp is broken down?

A

when atp is broken down, it loses a phosphate group, becoming adp (adenosine diphosphate) and releasing energy for the cell to use.

48
Q

what is phosphorylation?

A

phosphorylation is the process of adding a phosphate group (po₄³⁻) to a molecule, usually a protein, which can alter its function, activity, or location within the cell.

49
Q

how does phosphorylation affect a protein’s function?

A

phosphorylation can change a protein’s shape, activity, or ability to bind to other molecules, thereby activating or deactivating its function.

50
Q

what enzyme is responsible for adding phosphate groups during phosphorylation?

A

kinases are enzymes that add phosphate groups to molecules, typically proteins, during phosphorylation.

51
Q

what do axon terminals contain?

A

axon terminals contain synaptic vesicles, which are filled with neurotransmitters (chemical messengers).

52
Q

what is the role of axon terminals in neurotransmission?

A

axon terminals release neurotransmitters into the synaptic cleft, allowing communication between neurons or between neurons and other cells (like muscle cells).

53
Q

what triggers the release of neurotransmitters from axon terminals?

A

the arrival of an action potential at the axon terminal opens voltage-gated calcium channels, allowing calcium ions (Ca²⁺) to enter, which triggers neurotransmitter release.

54
Q

what is the synaptic cleft?

A

the synaptic cleft is the small gap between the axon terminal and the postsynaptic cell where neurotransmitters are released and transmit the signal.

55
Q

what role do calcium ions play in axon terminals?

A

calcium ions (Ca²⁺) enter the axon terminal when the action potential arrives, causing the synaptic vesicles to fuse with the presynaptic membrane and release neurotransmitters.

56
Q

how are beta-amyloid plaques formed?

A

beta-amyloid plaques form when enzymes called beta-secretase and gamma-secretase abnormally cleave the amyloid precursor protein (app), producing sticky beta-amyloid peptides that clump together.

57
Q

what is the role of amyloid precursor protein (app) in beta-amyloid plaque formation?

A

app is a normal protein in cell membranes that, when abnormally cleaved, produces beta-amyloid peptides that form plaques in the brain.

58
Q

how are neurofibrillary tangles formed?

A

neurofibrillary tangles form when tau protein becomes hyperphosphorylated, detaches from microtubules, and clumps together inside neurons.

59
Q

what role do beta-secretase and gamma-secretase play in beta-amyloid plaque formation?

A

beta-secretase and gamma-secretase abnormally cleave amyloid precursor protein (app), producing beta-amyloid peptides (especially the sticky Aβ42 peptide, which is prone to clumping) that form plaques.

60
Q

what are the three main stages of alzheimer’s disease?

A

early (mild), middle (moderate), and late (severe).

61
Q

what is the primary symptom in the early stage of alzheimer’s?

A

mild memory loss, such as forgetting recent events or names.

62
Q

how does the middle stage of alzheimer’s differ from the early stage?

A

memory loss worsens, confusion increases, and individuals may need help with daily tasks.

63
Q

what behavioral changes are common in the middle stage?

A

mood swings, agitation, and possible wandering.

64
Q

what happens in the late stage of alzheimer’s?

A

individuals lose the ability to communicate, require full-time care, and have severe physical decline.

65
Q

what is a hallmark sign of alzheimer’s progression across all stages?

A

a gradual and persistent decline in memory and cognitive abilities.

66
Q

when does difficulty with recognizing loved ones typically occur?

A

during the middle and late stages of the disease.

67
Q

what stage involves a significant loss of independence?

A

the middle stage.

68
Q

can early-stage alzheimer’s symptoms mimic normal aging?

A

yes, symptoms like mild forgetfulness can resemble typical aging, making early diagnosis difficult.

69
Q

what are some physical symptoms in the late stage of alzheimer’s?

A

difficulty swallowing, immobility, and increased vulnerability to infections.

70
Q

what are the seven “m’s” for the nurses role in alzheimer’s?

A

memory
movement
mental health
maintain safety
maximize communication
medical needs

71
Q

what is aducunamab and what are its side effects?

A

IV infusion given every 4 weeks to decrease beta-amyloid plaques.

side effects include brain bleeding/swelling.

72
Q

why does hyperphosphorylation happen?

A

dysregulation of kinases (enzymes that add phosphates) and phosphatases (enzymes that remove phosphates) due to genetic mutations, oxidative stress, or other cellular dysfunctions.

general nursing tingz!🧸🩺🌠 (8 decks)

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