4th Exam: CNS study Flashcards

1
Q

Blood brain barrier is most important in development of:

A

edema, vasogenic

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2
Q

Depleted in substantia nigra in Parkinson’s:

A

neuromelanin

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3
Q

Path/ causes of parkinson’s:

A

head trauma (i.e., boxing), prior encephalitis, toxins like cycad beans, mutation in the alpha-synuclein gene, exposure to MPTP, previous viral infection in brain

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4
Q

Primarily affected in degenerative diseases of the nervous system:

A

neurons: atrophy, gliosis, and unique change

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5
Q

Major finding in Parkinson’s:

A

tremor at rest

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6
Q

Causes of brain edema:

A

Head trauma, cerebral infarction, brain tumor, CNS infection, metabolic stroke, hemorrhage, abcess

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7
Q

Effect of Alzheimer’s on brain:

A

bilateral diffuse atrophy

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8
Q

Central and disease initiating event in Alzheimers:

A

deposition of B-amyloid

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9
Q

Rod cell in brain is most closely related to:

A

microglia (macs of brain)

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10
Q

Lewy bodies are assoc w:

A

Parkinson’s

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11
Q

Causes of enlarged or swollen brain:

A

Vasogenic edema, cytotoxic edema, mass lesion, inc intracranial pressre

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12
Q

Huntingon’s effect on the motor system:

A

involuntary moves

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13
Q

Tabes dorsalis is assoc w:

A

disturbance of sensory function

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14
Q

Alzheimers is assoc w:

A

dementia

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15
Q

Where is the signature lesion in Parkinson’s?

A

Substantia nigra

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16
Q

Where is the sginature lesion in Alsheimer’s?

A

cerebral cortex

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17
Q

Brain edema:

A

can result from head trauma, may cause intracranial herniations, may lead to death, fluid may be extracellular in the brain

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18
Q

Dementia has the most profound effects on:

A

Memory: judgement, reasoning, calculation, language

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19
Q

`Parkinson’s:

A

tremor at rest, describes as “pill rolling”, chronic, progressive, leads to disability, lewy bodies ibnt eh substantia nigra

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20
Q

Define gliosis in brain:

A

Reactive process analogous to fibrosis in other organs, like scarring

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21
Q

Abnormal accumulation of B-amyloid are found here in pts w dementia:

A

Cerebral cortex

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22
Q

Dementia:

A

involvement of cerebrum, bilateral involvement of brain, atrophy of brain, often irreversible when dx s made early in course

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23
Q

In a destructive process in the brain such as infarction, the microglial cells enters the damaged area and gives rise to:

A

Gitter cell or mac

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24
Q

Parkinsonism is aka:

A

Parkinson’s syndrome

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25
Q

Inc numbers of CAG trinucleotide repeats in the mutant gene located on chromosome 4p are assoc w:

A

huntington’s

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26
Q

Abnormality foundin all cases of Alzheimer’s:

A

progressive dementia

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27
Q

Where is the greratest damage to the brain in Huntington’s disease?

A

Caudate nucleus

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28
Q

TF? The weight of the brain is increased in edema.

A

T

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29
Q

Finding always present in all types of hydrocephalus:

A

dilation of ventricles

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30
Q

pts w dementia:

A

impaired judgement, inability to perform calculation such as making change, decline from a previous level of ability, cerebral cortical atrophy

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31
Q

Cytotoxic edema of brain mainly affects:

A

cell sytoplasm

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32
Q

Brain herniation is assoc w:

A

edema

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33
Q

Duret hemorrhages are assoc w:

A

edema

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34
Q

Giiosis is a reaction to:

A

injury

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35
Q

Alzheimer’s lesions are found in this part of brain;

A

cerebrum

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36
Q

Infection likely to be assoc w later development of a necrotizing arteritis called PAN:

A

Hep B

37
Q

Sex more affected by thyroid disease:

A

women, 10X more

38
Q

TF? It is ok to work in pt w low thyroid hormone.

A

F

39
Q

can’t make thyroid hormone wo:

A

iodine

40
Q

prohormone:

A

T4 (thyroxine)

41
Q

active hormone

A

T3 (triiodothyronine

42
Q

80% of thyroid hormone levels are:

A

thyroxine, prohormone, the other 20% is T3

43
Q

Most iodine is derived from:

A

peripheral conversion from t4—t3 by removing Iodine

44
Q

Why is T3 more active than T4?

A

binds receptor w 10X higher affinity

45
Q

TF? T4 can act as TF’s and regulate genes.

A

F. T3 can, active

46
Q

Thyroid hormone (TH) is involved in:

A

CNS, growth and development, effects of metabolism, responsible for disposing lipids/carbs, profound effects on the CV system

47
Q

Why does T3 react better w receptors?

A

one less iodine

48
Q

Thyroid gland develops from:

A

primitive pharynx, foramen cecum, tongue

49
Q

Primitive pharynx forms:

A

thyroglossal duct, descends, becomes thyroid gland

50
Q

Median alange:

A

Tongue base, migrates caudally ~7weeks, forms thyroid follicles

51
Q

Lateral anlage:

A

4th/5th branchial pouch (ultimobranchial body), forms C-cells

52
Q

Ectopic thyroid locations (fails to descend):

A

Tongue base, midline neck, mediastinum

53
Q

% of people w a pyramidal lobe:

A

20

54
Q

Thyroid Development Anomalies:

A

Hypoplasia, aplasia , abnormal descent, thyroglossal duct cysts, thyroid hormones are necessary for normal development

55
Q

hypoplasia, aplasia in abnormal thyroid development lead to:

A

cretinism

56
Q

Cretinism:

A

Lack of thyroid hormone, can development mental retardation or developmental defects, baby protected during pregnancy because it has enough from maternal circulation

57
Q

How are all babies tested for hypoplasia, aplasia?

A

thyroid hormones from blood sample from the heel

58
Q

A baby will develop cretinism if this is not recognized:

A

hypoplasia, aplasia

59
Q

If abnormal descent occurs, are these generally functional or non?

A

non

60
Q

Most common locations for abnormal descent:

A

tongue, thorax

61
Q

When would you have o remove the abnormally descended thyroid precursor?

A

when blocking swalloiwing

62
Q

Possible problems if thyroglossal duct cysts do not disappear

A

can become inflamed/ secondarily infected

63
Q

Experiment showing that thyroid hormones are necessary for normal dev:

A

Kclo4 experiment w tadpoles

64
Q

What develops abnormally in the frg wo thyroid hormone?

A

the body

65
Q

Cretinism

A

Puffy face due to buildup of mucopolysaccharides / ECM (Accumulation of fluid/glycosaminoglycans), Protruding tongue, Hypometabolic state, From not having thyroid hormone during development

66
Q

Lingual thyroid

A

Lump in neck, with persistent thyroid tissue

67
Q

Normal Thyroid Gland:

A

2 lobes, 20% of people have 3rd pyramidal lobe (2 lobes separated by isthmus), thyroid hormone stored in colloid, cuboidal epithelium

68
Q

Cell types in normal thyroid gland:

A

Follicular cells, C Cells

69
Q

C Cells:

A

Scarce, responsible for specific tumor types, produce calcitonin (unknown effect) (Calcium lowering hormone), Wo thyroid, no effect on body calcium, major calcium regulator is really PTH*, (Also located in the back of thyroid gland (parathyroid gland)), Responsible for medullary carcinoma of the thyroid

70
Q

Thyroid Follicle

A
  • Large reservoir of thyroid hormone (3 month supply!)
  • Surrounded by follicular cells, blood vessels, lymphatic vessels, basement membrane, C cells
  • Filled with thyroglobulin (TGB)
  • Thyroid hormone stays bound to TGB
  • 2-3 months supply in a follicle, - Regulated by TSH, - Iodine movement
71
Q

What happens if thyroid follicle is damaged, inflamed?

A

major inc in blood levels of thyroid hormone, Hyperthyroidism until the problem is resolved, wlll shut down other pw’s if not resolved

72
Q

TSH stimulates:

A

thyroid hormone synthesis at the basal side of the cell

73
Q

Where does thyroid hormone synthesis occurs?

A

apical side of cell,

74
Q

Every aspect of synthesis in the thyroid follicle is regulated by:

A

TSH

75
Q

Movement of iodine in relation to the gradient;

A

against graidient by ATPase, provided by Na/K pup

76
Q

How is iodine attached to tyrosine?

A

by TPO

77
Q

Parts of the feedback loop:

A

paraventricular nucleus, TRH, pituitary, TSh, thyroid gland, thyroid hormone,

78
Q

Hyperplastic Thyroid:

A

Due to increased TSH levels, low thyroid hormone, large increase in size

79
Q

Thyroid Atrophy

A

o Due to low TSH levels

o High circulating thyroid hormone (in tumor)

80
Q
  • Measure TSH
A

o Low levels TSH usually means not enough thyroid hormone

o Used to determine hypo/hyperthyroidism

81
Q

Thyroid Hormone Action:

A

bind intracellular receptors that complex with TH response elements to bind nuclear DNA and influence gene transcription, non genomic actions, - TH’s also interact with the mitochondrial genome
- TH’s essential for normal growth and development, Increase mitochondrial oxygen consumption (BMR), - Increased expression of Na/K ATPase and turnover of lipid, - Increased contractility and heart rate

82
Q

TF? There is one TH receptor.

A

F. several isoforms (TR-a, TR-B)

83
Q

How are TH involved in normal gowthe and development?

A

o Necessary for nervous tissue development
o Promotes Growth Hormone synthesis in pituitary
o Increased mitochondrial function necessary for metabolism and tissue differentiation
o Required for male and female fertility

84
Q

mitochondrial oxygen consumption increase due to TH:

A

Increase ATP synthesis and consumption, Increased dissipation of heat, Oxidative phosphorylation becomes more inefficient, possible increase in mitochondrial membrane permeability to protons

85
Q

What happens if you give a person thyroid hormone?

A

→ oxygen consumption in most tissues will increase
• Why? Increase activity of variety of enzymes/increases output of fuels through the mitochondria (transport)
• Oxidation of fuels → more heat produced

86
Q

Increased contractility and heart rate leads to

A

o Increased adrenergic receptor in heart
• Ex. Epinephrine increase → increase rate of heart contraction , (Permissive effects), Increases myosin and calcium ATPase (increases contractile proteins), Increase O2 delivery, No thyroid hormones: weak cardiovascular system

87
Q

Increased expression of Na/K ATPase and turnover of lipid will lead to:

A

More substrates for TCA cycle

88
Q

Effects of inc contractility and HR as a result of TH:

A

o Increased adrenergic receptor in heart
• Ex. Epinephrine increase → increase rate of heart contraction
• Permissive effects
o Increases myosin and calcium ATPase (increases contractile proteins)
o Increase O2 delivery
o No thyroid hormones: weak cardiovascular system