462 Final 12/8 Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

A mass of cells whose growth is uncontrolled and serves no useful function. These cells are neurons and can not be divided of reproduced.

A

Tumors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

A cancerous tumor is

A

Malignant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

A noncancerous tumor is

A

Benign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

The distinct border between the mass of the tumor cells and the surrounding tissue

A

Encapsulated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

No clear-cut border between the tumor and normal tissue, this also removes healthy tissue.

A

Infiltration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

A tumor sheds cells that travel through the bloodstream and create new growth of new tumors.

A

Metastases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How do tumors damage brain tissue?

A

Compression and infiltration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What moves healthy tissue and creates lesions in the brain? This can destroy brain tissue directly, or it can indirectly by blocking the flow of cerebrospinal fluids that creates hydrocephalus (brain swelling)

A

Compression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Tumors do not arise from neurons, because mature neurons are not capable of dividing. [T/F]

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a cancerous brain tumor composed of several types of glial cells? It is also very malignant, fast-growing, and has a low rate of living.

A

Glioma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

An encapsulated, bengin brain tumor composed of cells that constitute the meninges. It is also not cancerous and has a high rate of living.

A

Meningioma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

This disorder causes cell death due to the excitation of firing neurons that create an excessive amount of calcium (excitotoxicity). These neurons are unable to get to resting potential.

A

Seizure disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

The distinction between ________ and ________ seizures relates to whether these spread from a definite focus within the brain.

A

Partial;Generalized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

An alcoholic who abruptly stops drinking may experience a seizure because

A

of a sudden release from the inhibiting effects of the drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Obstructive strokes can be caused by

A

Thrombi or emboli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which of the following will produce a hemorrhagic stroke?

A

Bleeding within the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

A definite focus or source of irritation. The scarred region is caused by an old injury or a developmental abnormality, it also won’t spread.

A

Partial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Widespread and involves the majority of the brain. This is the most common type of stroke that involves muscle spasms, and loss of consciousness, and is dramatic in its appearance.

A

Generalized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Cause changes in consciousness but does not allow the individual to lose consciousness as they are able to remember but unable to respond.

A

Simple partial seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

This leads to loss of consciousness

A

Complex partial seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

This is the most severe form of seizure and is sometimes referred to as grand mal seizure. It is also a type of generalized seizure.

A

Tonic-Clonic Seizure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Excitation of the neurons surrounding a seizure. Acts as a warning/feeling before having a tonic-clonic. It also tells us where the seizure starts/originates.

A

Aura

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

The beginning of a tonic-clonic where all muscles contract forcefully.

A

Tonic phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Muscles begin to tremble, then start to jerk convulsively, eyes roll, violent grimaces, and tongue may be bitten.

A

Clonic phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Children have these types of seizures as they will stop what they are doing and stare off into the distance for a few seconds, often blinking their eyes repeatedly. They become unresponsive and do not notice their attacks as they can have up to a hundred times a day.

A

Absent Seizure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

A patient undergoing a series of seizures without regaining consciousness is

A

Status epileptics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Evidence of hippocampus damage is correlated with the number and severity of seizures. [T/F]

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Severe hippocampus damage caused by excessive release of what NT?

A

Excessive glutamate binds to AMPA and NMDA, allowing a calcium influx to disrupt the mitochondria which over-excites and controls the opening/closing of ion channels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Causes of seizures:

A
  • Scarring from injury
  • High fever from drugs or infections
  • Withdrawal from alcohol or barbituates….Why? Overcompensation
  • Genetics…. Deficits in the control of ion channels; Many instances are idiopathic ( unknown cause)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Treatments for seizures?

A

Anticonvulsant drugs, which increase the effectiveness of inhibitory synapses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is a ketogenic diet?

A

A seizure treatment that consists of calories from fats with moderate protein and low amounts of carbohydrates. This leads to the production of ketones which are produced by the liver through the breakdown of fats when the blood level of glucose is low. It is believed that proper glucose metabolism will prevent seizures and a single meal rich in carbs will increase the risk of a seizure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

No symptoms occur before this stroke and alcohol and smoking drastically increase the risk of having this.

A

Hemorrhagic stroek

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Is a blood clot that forms in blood vessels. Anticoagulant drugs can make the blood less likely to clot.

A

Thromus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

A piece of material that forms in one part of the vascular system, breaks off and is carried throughout the bloodstream until it reaches a small artery. Antibiotics can suppress the infection.

A

Embolus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Neurons starve to death because of the lost of their supply of

A

Glucose and oxygen to metablolize

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

One approach to minimizing the amount of brain damage caused by strokes is

A

Administration of a clot-dissolving drug called tPA (tissue plasminogen activator) after the onset of a stroke has clear benefits, but only if given within three hours. Beyond these three hours, it will cause damage to the BBB and tPA goes into the brain to create issues.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

The risk factors of strokes are

A
  • High blood pressure
  • Smoking
  • Diabetes
  • High cholesterol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

The linings of arteries develop a layer of plaque, deposits of cholesterol, fats, calcium, and cellular waste products.

A

Atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Atherosclerosis is not a precursor to heart attacks and ischemic stroke. [T/F]

A

False

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Atherosclerotic plaques often form in the

A

Internal carotid artery

41
Q

The internal carotid artery does what?

A

Supplies most of the blood flow to cerebral hemispheres. Plaques can cause severe narrowing of the interior of the artery, greatly increasing the risk of a massive stroke. Unblocking can cause an increase of blood flow but too much can cause brain damage.

42
Q

Caused by degeneration of the nigrostriatal system, the dopamine-secreting neurons of substantial nigra send axons to basal ganglia.

A

Parkinson’s Diease

43
Q

A mutation on chromosome 4 results in a protein called

A

Alpha-Synuclein

44
Q

Alpha-Synuclein becomes _________ and forms _________, especially in dopaminergic neurons.

A

Misfolds;Aggregates

45
Q

Disrupts the permeability membrane, in other words, it disrupts ions that enter or exit. There is an argument over whether this creates cell dysfunction or a sign of cell dysfunction. It is also referred to as scar tissue.

A

Aggregate

46
Q

What is a Lewy body?

A

An aggregate unique for Parkinson’s.

47
Q

What is a toxic-gain of function?

A

Production of a protein that produces a toxic effect (it adds something)

48
Q

The longer the protein, the more misfolds. [T/F]

A

True

49
Q

What is Parkin?

A

A gene mutation on chromosome 6 is also a loss of function. This mutation permits high levels of defective protein to accumulate in dopaminergic neurons. It is also responsible for the ubiquitination process.

50
Q

The movement of defective proteins to the proteasomes by tagging them with ubiquitin (directing the movement of important proteins in the cell). It also gets rid of misfolded proteins and breaks them down into their constituent amino acids.

A

Ubiquitination

51
Q

What does defective Parkin do?

A

It fails to ubiquitinate the abnormal proteins and accumulates them which eventually kills the cell. This mutation is a loss of function as it takes away from normal functioning. Dopaminergic neurons are sensitive to this accumulation.

52
Q

An organelle that is responsible for destroying defective or degraded proteins within the cell.

A

Proteasome

53
Q

A protein that attaches itself to faulty or misfolded proteins and targets them to be destroyed by the proteasome.

A

Ubiquitin

54
Q

What is one therapeutic procedure for Parksinson’s?

A

The destruction of the internal division of the globus pallidus (Gpi)

55
Q

The output of the GPi which is directed through the thalamus to the motor cortex is

A

Inhibitory

56
Q

Decreased release of dopamine in the caudate nucleus and putamen that is seen in Parkinson’s patients causes an _________ in the activity of the Gpi

A

increase

57
Q

Damage to the GPi might be expected to

A

Relieve Parkson’s symptoms

58
Q

What did Kaplitt et al. (2007) introduce?

A
  • Genetically modified virus into subthalamic nucleus of Parkinson’s patients.
  • Virus-delivered gene for GAD, an enzyme responsible for the biosynthesis of the major inhibitory neurotransmitter GABA. Changes neurotransmitters from glutamate to GABA.
59
Q

Huntington’s is a genetic disorder that produces motor, cognitive, and psychiatric impairments. It is an unstable expansion of CAG (DNA sequence) and it is also the degeneration of the

A

Striatum and cortex

60
Q

Fluid movement that is overexaggerated

A

Chorea

61
Q

The lack of ability to initiate movement

A

Akinesa

62
Q

Slowness in execution of movement

A

Bradykinesia

63
Q

Abnormal posture

A

Dystonia

64
Q

Htt is expressed throughout the entire brain and has a role in ____________

A

Intracellular functions
- Protein trafficking
- Vesicle transport
- Endocytosis
- Postsynaptic signaling
- Anti-apoptotic function

65
Q

Is responsible for Huntington’s and disrupts intracellular functions

A

mHtt

66
Q

Activation of proteases

A

N-Terminal fragments, an amino acid that develops aggregates faster. Fragments enter the nucleus.

67
Q

Protein misfolding

A

Hsp-40 and Hsp-70 are heat shock proteins that are chaperone proteins, they attempt to fix refolding of misfolded proteins. If it does not fix refolding then ubiquitin is tagged to these proteins and they get destroyed —> aggregate

67
Q

Inhibition of protein degradation

A

Ubiquitin is sequestered —> Cell death

68
Q

What is Rhes?

A

It plays a role in dopaminergic signaling and behavior. It is only expressed in the striatum and had Htt expression, but it may interact with mHtt. It is also a determinant of sumoylation.

69
Q

Deleting Rhes out of mice with HD made them less vulnerable to _____

A

motor and neuropathological symptoms

70
Q

RHES-KO stands for

A

Rhes knockout

71
Q

Clasping

A

Limbs come inward; as the disease progresses they clasp more / by 6 months they’re clasping in all limbs

72
Q

What was found in the study?

A

That there was about a 2-month delay in symptoms between HD/Rhes WT (normal Rhes expression) and HD/Rhes KO mice. Also removing Rhes created a decrease in brain size; when Rhes is removed you’re getting a slight delay in brain degeneration

73
Q

A modification process that regulates the stability of a protein and keeps that protein alive.

A

Sumoylation

74
Q

Competes with ubiquitin to attach to a protein and alters protein-protein interactions.

A

SUMO

75
Q

What enzymes are responsible for activating SUMO protein?

A

E1,E2, and E3

76
Q

The activation of SUMO

A

E1

77
Q

The conjugation of SUMO, binds it to the target protein.

A

E2

78
Q

Aids transfer of SUMO and is responsible for target specificity (coordinates which protein SUMO binds to and this is what Rhes is)

A

E3

79
Q

Sumoylation (keeps misfolded proteins alive) is inside the striatum and ubiquitination is outside the neuron. [T/F]

A

True

80
Q

Subramaniam et al. (2009,1010)

A
  • Looked at the presence of sumoylated proteins
  • Greatly reduced sumoylation in Rhes KO mice
  • Also looked at sumoylation in the cerebellum
81
Q

Produces severe degeneration of the hippocampus, entorhinal cortex, neocortex, nucleus basalis, locus coeruleus, and raphe nuclei.

A

Alzheimer’s Diease

82
Q
  • Extracellular deposit containing a dense core of B-amyloid protein.
  • We all have this but people with Alzheimer’s have an excessive amount
  • Surrounded by degenerating axons and dendrites and activated microglia and reactive astrocytes
  • Phagocytic glial cells destroy the axons and dendrites (cannot receive communication or encode it)
A

Amyloid Plaque

83
Q

Dying neurons contain intracellular accumulations of twisted protein filaments that severed as the cell’s internal skeleton.

A

Neurofibrillary Tangle

84
Q

The twisted proteins are _______ that normally severe as a component of microtubules (brings nutrients NT, and etc to be relayed; Railroad tracks)

A

Tau Proteins

85
Q

The formation of amyloid plaques is a result of the production of a defective form of

A

AB(beta)

86
Q

A gene encodes the production of the B-amyloid precursor protein (APP) and is cut apart in two places by enzymes called ______ to produce 40 or 42 amino acid AB.

A

Secretases

87
Q

Cuts the tail off

A

B-Secretases

88
Q

Cuts the head off

A

V-Secretases

89
Q

____ amino acid AB produces the short form in normal brains

A

40

90
Q

____ amino acid AB produces long form in AD patients.

A

41

91
Q

Gene on chromosomes 1 and 14 determines where secretase cut APP

A

Presenilin

92
Q

Apolipoprotein E (ApoE)

A
  • All of us have this gene and you produce one of these: if you produce E4 it interferes with our ability to get rid of misfolded proteins (ubiquitination)
  • E2 allele is found to protect against A disease by getting rid of misfolded proteins
  • This gene is on chromosome 21
93
Q

Risk factors for AD are

A

Obesity, hypertension, high cholesterol, diabetes, traumatic brain injury , and level of education

94
Q

Current treatments for AD:

A
  • Acetylcholinesterase inhibitors (movement and learning)
  • NMDA receptor antagonists (preventing excitotoxicity from the disease-preventing the amount of calcium coming in)
  • These drugs have no effect on the process of neural degeneration
95
Q

2 genetic links for Parkinson’s are
toxic gain on chromosome __
toxic loss on chromosome ___

A

4 (gain) and 6 (loss)

96
Q

______ process is the cutting of misfolded proteins and allows them to reform properly ____ is the scissors

A

ubiquitin
protease

97
Q

The death of neurons following a stroke is caused by

A

Over-stimulation of nerve cells by abnormally high levels of glutamate