4th Exam: CNS study Flashcards Preview

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Flashcards in 4th Exam: CNS study Deck (88)
1

Blood brain barrier is most important in development of:

edema, vasogenic

2

Depleted in substantia nigra in Parkinson's:

neuromelanin

3

Path/ causes of parkinson's:

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

4

Primarily affected in degenerative diseases of the nervous system:

neurons: atrophy, gliosis, and unique change

5

Major finding in Parkinson's:

tremor at rest

6

Causes of brain edema:

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

7

Effect of Alzheimer's on brain:

bilateral diffuse atrophy

8

Central and disease initiating event in Alzheimers:

deposition of B-amyloid

9

Rod cell in brain is most closely related to:

microglia (macs of brain)

10

Lewy bodies are assoc w:

Parkinson's

11

Causes of enlarged or swollen brain:

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

12

Huntingon's effect on the motor system:

involuntary moves

13

Tabes dorsalis is assoc w:

disturbance of sensory function

14

Alzheimers is assoc w:

dementia

15

Where is the signature lesion in Parkinson's?

Substantia nigra

16

Where is the sginature lesion in Alsheimer's?

cerebral cortex

17

Brain edema:

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

18

Dementia has the most profound effects on:

Memory: judgement, reasoning, calculation, language

19

`Parkinson's:

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

20

Define gliosis in brain:

Reactive process analogous to fibrosis in other organs, like scarring

21

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

Cerebral cortex

22

Dementia:

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

23

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

Gitter cell or mac

24

Parkinsonism is aka:

Parkinson's syndrome

25

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

huntington's

26

Abnormality foundin all cases of Alzheimer's:

progressive dementia

27

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

Caudate nucleus

28

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

T

29

Finding always present in all types of hydrocephalus:

dilation of ventricles

30

pts w dementia:

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

31

Cytotoxic edema of brain mainly affects:

cell sytoplasm

32

Brain herniation is assoc w:

edema

33

Duret hemorrhages are assoc w:

edema

34

Giiosis is a reaction to:

injury

35

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

cerebrum

36

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

Hep B

37

Sex more affected by thyroid disease:

women, 10X more

38

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

F

39

can’t make thyroid hormone wo:

iodine

40

prohormone:

T4 (thyroxine)

41

active hormone

T3 (triiodothyronine

42

80% of thyroid hormone levels are:

thyroxine, prohormone, the other 20% is T3

43

Most iodine is derived from:

peripheral conversion from t4—t3 by removing Iodine

44

Why is T3 more active than T4?

binds receptor w 10X higher affinity

45

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

F. T3 can, active

46

Thyroid hormone (TH) is involved in:

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

47

Why does T3 react better w receptors?

one less iodine

48

Thyroid gland develops from:

primitive pharynx, foramen cecum, tongue

49

Primitive pharynx forms:

thyroglossal duct, descends, becomes thyroid gland

50

Median alange:

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

51

Lateral anlage:

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

52

Ectopic thyroid locations (fails to descend):

Tongue base, midline neck, mediastinum

53

% of people w a pyramidal lobe:

20

54

Thyroid Development Anomalies:

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

55

hypoplasia, aplasia in abnormal thyroid development lead to:

cretinism

56

Cretinism:

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

57

How are all babies tested for hypoplasia, aplasia?

thyroid hormones from blood sample from the heel

58

A baby will develop cretinism if this is not recognized:

hypoplasia, aplasia

59

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

non

60

Most common locations for abnormal descent:

tongue, thorax

61

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

when blocking swalloiwing

62

Possible problems if thyroglossal duct cysts do not disappear

can become inflamed/ secondarily infected

63

Experiment showing that thyroid hormones are necessary for normal dev:

Kclo4 experiment w tadpoles

64

What develops abnormally in the frg wo thyroid hormone?

the body

65

Cretinism

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

66

Lingual thyroid

Lump in neck, with persistent thyroid tissue

67

Normal Thyroid Gland:

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

68

Cell types in normal thyroid gland:

Follicular cells, C Cells

69

C Cells:

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

Thyroid Follicle

- 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

What happens if thyroid follicle is damaged, inflamed?

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

72

TSH stimulates:

thyroid hormone synthesis at the basal side of the cell

73

Where does thyroid hormone synthesis occurs?

apical side of cell,

74

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

TSH

75

Movement of iodine in relation to the gradient;

against graidient by ATPase, provided by Na/K pup

76

How is iodine attached to tyrosine?

by TPO

77

Parts of the feedback loop:

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

78

Hyperplastic Thyroid:

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

79

Thyroid Atrophy

o Due to low TSH levels
o High circulating thyroid hormone (in tumor)

80

- Measure TSH

o Low levels TSH usually means not enough thyroid hormone
o Used to determine hypo/hyperthyroidism

81

Thyroid Hormone Action:

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

TF? There is one TH receptor.

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

83

How are TH involved in normal gowthe and development?

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

mitochondrial oxygen consumption increase due to TH:

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

85

What happens if you give a person thyroid hormone?

→ 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

Increased contractility and heart rate leads to


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

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

More substrates for TCA cycle

88

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

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