4th Exam: CNS study Flashcards
Blood brain barrier is most important in development of:
edema, vasogenic
Depleted in substantia nigra in Parkinson’s:
neuromelanin
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
Primarily affected in degenerative diseases of the nervous system:
neurons: atrophy, gliosis, and unique change
Major finding in Parkinson’s:
tremor at rest
Causes of brain edema:
Head trauma, cerebral infarction, brain tumor, CNS infection, metabolic stroke, hemorrhage, abcess
Effect of Alzheimer’s on brain:
bilateral diffuse atrophy
Central and disease initiating event in Alzheimers:
deposition of B-amyloid
Rod cell in brain is most closely related to:
microglia (macs of brain)
Lewy bodies are assoc w:
Parkinson’s
Causes of enlarged or swollen brain:
Vasogenic edema, cytotoxic edema, mass lesion, inc intracranial pressre
Huntingon’s effect on the motor system:
involuntary moves
Tabes dorsalis is assoc w:
disturbance of sensory function
Alzheimers is assoc w:
dementia
Where is the signature lesion in Parkinson’s?
Substantia nigra
Where is the sginature lesion in Alsheimer’s?
cerebral cortex
Brain edema:
can result from head trauma, may cause intracranial herniations, may lead to death, fluid may be extracellular in the brain
Dementia has the most profound effects on:
Memory: judgement, reasoning, calculation, language
`Parkinson’s:
tremor at rest, describes as “pill rolling”, chronic, progressive, leads to disability, lewy bodies ibnt eh substantia nigra
Define gliosis in brain:
Reactive process analogous to fibrosis in other organs, like scarring
Abnormal accumulation of B-amyloid are found here in pts w dementia:
Cerebral cortex
Dementia:
involvement of cerebrum, bilateral involvement of brain, atrophy of brain, often irreversible when dx s made early in course
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
Parkinsonism is aka:
Parkinson’s syndrome
Inc numbers of CAG trinucleotide repeats in the mutant gene located on chromosome 4p are assoc w:
huntington’s
Abnormality foundin all cases of Alzheimer’s:
progressive dementia
Where is the greratest damage to the brain in Huntington’s disease?
Caudate nucleus
TF? The weight of the brain is increased in edema.
T
Finding always present in all types of hydrocephalus:
dilation of ventricles
pts w dementia:
impaired judgement, inability to perform calculation such as making change, decline from a previous level of ability, cerebral cortical atrophy
Cytotoxic edema of brain mainly affects:
cell sytoplasm
Brain herniation is assoc w:
edema
Duret hemorrhages are assoc w:
edema
Giiosis is a reaction to:
injury
Alzheimer’s lesions are found in this part of brain;
cerebrum
Infection likely to be assoc w later development of a necrotizing arteritis called PAN:
Hep B
Sex more affected by thyroid disease:
women, 10X more
TF? It is ok to work in pt w low thyroid hormone.
F
can’t make thyroid hormone wo:
iodine
prohormone:
T4 (thyroxine)
active hormone
T3 (triiodothyronine
80% of thyroid hormone levels are:
thyroxine, prohormone, the other 20% is T3
Most iodine is derived from:
peripheral conversion from t4—t3 by removing Iodine
Why is T3 more active than T4?
binds receptor w 10X higher affinity
TF? T4 can act as TF’s and regulate genes.
F. T3 can, active
Thyroid hormone (TH) is involved in:
CNS, growth and development, effects of metabolism, responsible for disposing lipids/carbs, profound effects on the CV system
Why does T3 react better w receptors?
one less iodine
Thyroid gland develops from:
primitive pharynx, foramen cecum, tongue
Primitive pharynx forms:
thyroglossal duct, descends, becomes thyroid gland
Median alange:
Tongue base, migrates caudally ~7weeks, forms thyroid follicles
Lateral anlage:
4th/5th branchial pouch (ultimobranchial body), forms C-cells
Ectopic thyroid locations (fails to descend):
Tongue base, midline neck, mediastinum
% of people w a pyramidal lobe:
20
Thyroid Development Anomalies:
Hypoplasia, aplasia , abnormal descent, thyroglossal duct cysts, thyroid hormones are necessary for normal development
hypoplasia, aplasia in abnormal thyroid development lead to:
cretinism
Cretinism:
Lack of thyroid hormone, can development mental retardation or developmental defects, baby protected during pregnancy because it has enough from maternal circulation
How are all babies tested for hypoplasia, aplasia?
thyroid hormones from blood sample from the heel
A baby will develop cretinism if this is not recognized:
hypoplasia, aplasia
If abnormal descent occurs, are these generally functional or non?
non
Most common locations for abnormal descent:
tongue, thorax
When would you have o remove the abnormally descended thyroid precursor?
when blocking swalloiwing
Possible problems if thyroglossal duct cysts do not disappear
can become inflamed/ secondarily infected
Experiment showing that thyroid hormones are necessary for normal dev:
Kclo4 experiment w tadpoles
What develops abnormally in the frg wo thyroid hormone?
the body
Cretinism
Puffy face due to buildup of mucopolysaccharides / ECM (Accumulation of fluid/glycosaminoglycans), Protruding tongue, Hypometabolic state, From not having thyroid hormone during development
Lingual thyroid
Lump in neck, with persistent thyroid tissue
Normal Thyroid Gland:
2 lobes, 20% of people have 3rd pyramidal lobe (2 lobes separated by isthmus), thyroid hormone stored in colloid, cuboidal epithelium
Cell types in normal thyroid gland:
Follicular cells, C Cells
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
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
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
TSH stimulates:
thyroid hormone synthesis at the basal side of the cell
Where does thyroid hormone synthesis occurs?
apical side of cell,
Every aspect of synthesis in the thyroid follicle is regulated by:
TSH
Movement of iodine in relation to the gradient;
against graidient by ATPase, provided by Na/K pup
How is iodine attached to tyrosine?
by TPO
Parts of the feedback loop:
paraventricular nucleus, TRH, pituitary, TSh, thyroid gland, thyroid hormone,
Hyperplastic Thyroid:
Due to increased TSH levels, low thyroid hormone, large increase in size
Thyroid Atrophy
o Due to low TSH levels
o High circulating thyroid hormone (in tumor)
- Measure TSH
o Low levels TSH usually means not enough thyroid hormone
o Used to determine hypo/hyperthyroidism
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
TF? There is one TH receptor.
F. several isoforms (TR-a, TR-B)
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
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
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
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
Increased expression of Na/K ATPase and turnover of lipid will lead to:
More substrates for TCA cycle
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
