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med phys: cranial nerves and endocrine
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Biology
12th
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174 Terms
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1
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thyroid gland has two types of cells
follicular and parafollicular
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follicular cells of the thyroid
secrete thyroxine (T4)
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parafollicular cells of the thyroid
secrete calcitonin, c-cells from last brachial pouch
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T4 (thyroxine)
prohormone, 4 iodine atoms, more common
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T3 (triiodothyronine)
active form by removing an iodine, more effective
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as an embryo the thyroid had a duct to
the tongue (thyroglossal duct)
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parathyroid
glands behind thyroid, secrete PTH
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thyroxine-binding globulin (TBG)
transport T3 and T4 in the blood, protein
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thyroid peroxidase (TPO)
attaches iodine to benzene rings of tyrosine
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iodination
adding iodine
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T3/4 raise basal metabolic rate
stimulate catabolism and anabolism (create and use glucose, proteins, and fatty acids)
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protein synthesis and proteolysis
net result in muscle breakdown
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thermogenesis
heat generation from thyroid stimulated metabolic activity
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thyrotropin (TSH)
regulating hormone for thyroid from pituitary
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coupling
cross-link iodinated tyrosines into thyroxine
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follicular cell structure
ring of epithelial storing thyroxine because iodine is a scarce resource
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reverse T3
deactivated T3 due to it being able to freely move into cells
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hormone categories
modified amino acids, polypeptides, steroids
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modified amino acids
small, usually modified tyrosine, one or two benzene rings
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polypeptides
most hormones, oxytocin, ACTH
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steroids
lipids, 4 ring structure, end in -one, estrogen/aldosterone
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hyperthyroidism
high T3/4
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hypothyroidism
low T3/4, high TSH
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free vs total thyroxine
free: not attached to carrier proteins, small smount
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nuclear medicine scan
functional image tracking radiotracers
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isthmus
bridge connecting two thyroid lobes
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beta particles
high energy electrons that are harmful to tissue
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gamma rays
less harmful, used for diagnostic imaging
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I-123
emits gamma rays, used for thyroid imaging
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I-131
destroys thyroid as treatment for hyperthyroidism
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salivary glands and kidneys show up on iodine scan
both excrete iodine from the bloodstream
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ddx of hypothyroidism
iodine deficiency, missing thyroid (high TSH), pituitary failure (low TSH)
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hashimoto’s disease, autoimmune thyroiditis
high ant-TPO levels, high TSH, low T3/4
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hashimoto’s initially appears hyperthyroid
inflammation from anti-TPO causes thyroid to release all T3/4
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thyroid is very faint on nuclear scan
hypothyroidism
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ddx of hyperthyroidism
pituitary overstimulation (high TSH) or autonomous thyroid (low TSH)
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grave’s disease
autoimmune, anti-TSH-R stimulate thyroid to be enlarged and overactive
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bulging eyes
grave’s disease can enlarge the extraocular muscles
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thyrotoxicosis
excess T3/4 can damage the heart and case arrhythmias
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thyroid is large and dark on nuclear scan
hyperthyroidism
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hot nodule
autonomous, unregulated, portion of thyroid when generally hypothyroid
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multiple hot nodules
can become hyperthyroid and thyrotoxicosis
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goiter
enlarged thyroid
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cold nodule
non functioning section of thyroid, cyst or tumor
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hypothalamus
drives physiological needs, change behavior (hunger, sleep, sex)
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hypothalamus and optic chiasm
next to each other, know day/night cycle
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anterior pituitary structure
epithelial tissue from embryotic mouth
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posterior pituitary
neurons and glia from hypothalamus
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hormones vs neurotransmitters
very similar molecules but cell to cell vs bloodstream communication
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posterior pituitary hormones
neurocrine, oxytocin and vasopressin
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vasopressin
raises blood pressure and fluid retention
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lack of vasopressin
diabetes insipidus, excess watery urine
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oxytocin
stimulates uterine contractions and milk letdown
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nonapeptides
posterior pituitary hormones, very small, only 9 amino acids
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hypothalamus hormones
releasing hormones (TRH, CRH, GnRH), stimulate other hormones
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pituitary hormones regulation
pos and neg feedback loops, create axes
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anterior pituitary hormones
tropins (TSH, ACTH, FSH, LH, GH), stimulate other endocrine glands
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thyrotropin (TSH)
stimulates thyroid
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corticotropin (ACTH)
stimulates adrenal cortex
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gonadotropins (FSH and LH)
stimulate gonads
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hypophyseal portal system
small veins connecting hypothalamus and anterior pituitary
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HPT axis
TRH (hypot), TSH (pit), thyroxine (thyroid)
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HPA axis
CRH (hypot), ACTH (pit), cortisol (adrenal cortex)
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HPG axis
GnRH (hypot), FSH/LH (pit), sex steroids (gonads)
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axes steps
hypothalamus energy conservation and amplification
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pars intermedia
secretes MSH for melanin production, very similar to ACTH
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adrenal gland has two parts
cortex and medulla
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phenylalanine
essential amino acids needed for adrenalin production
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catecholamines
versions of modified amino acids using tyrosine and has two -OH groups on a benzene ring
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catecholamine examples
dopamine, norepinephrine, and adrenalin
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epinephrine vs norepinephrine
Epi is methylated NE
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adrenal medulla
controlled by the spinal cord, part of sympathetic nervous system
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adrenal medulla hormones
secrete catecholamines for fight or flight
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corticosteroid regulation of adrenal medulla
veins from cortex to medulla synthesize NE to epi
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adrenal cortex hormones
steroids, aldosterone, cortisol, and DHEA
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steroid hormones features
carried by proteins in the blood, enter cells freely, receptors in nucleus
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aldosterone
regulates blood electrolytes, retains sodium
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DHEA
precursor to sex steroids, promotes growth and development
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cortisol
glucocorticoid, regulated by ACTH, catabolic steroid
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cortisol function
raises blood glucose through muscle breakdown (gluconeogenesis)
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cortisol surge
breakdown glycogen when sleeping for brain’s need of glucose
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glucocorticoids as immunosuppressants
used to treat asthma, autoimmune diseases, and other
common cause of hypercortisolism
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HPT axis regulation
pos feedback if thyroid is not working (high TSH levels)
neg feedback if thyroid is working
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symptoms of hyperthyroidism
weight loss, goiter, heat intolerance, high heart rate
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symptoms of hypothyroidism
weight gain, goiter, cold intolerance, slow pulse, swelling
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symptoms of hypercortisolism
truncal weight gain, muscle weakness, stretch marks, fractures, hypertension
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hypercortisolism labs
high cortisol and hyperglycemia
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cushing’s syndrome
usually iatrogenic from prescribed corticosteroids
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cushing’s disease
pituitary tumor with high ACTH
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hypoadrenalism
adrenal failure
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hypoaldosterone (Addison’s) symptoms
weight loss, dehydration, low blood pressure, skin pigmentation
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Addison’s labs
low cortisol, aldosterone, Na, glucose, blood pressure
high potassium, ACTH
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primary endocrine disorders
originate in gland (addison’s, hashimoto’s)
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secondary endocrine disorders
originate in the pituitary (cushing’s disease)
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secondary vs primary lab levels
high T3/4 with high TSH is not grave’s
low T3/4 with low TSH is not hashimoto’s
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pheochromocytoma
tumor of adrenal medulla, secretes excess adrenalin
usually in adrenal, but can be in spinal cord
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pheochromocytoma symptoms
heart palpitations, high blood pressure, abdominal pain, vomiting
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I-123 MIBG
uptake by sympathetic neurons
bind to NE transport
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adrenalin waste product
metanephrines (high levels if pheochromocytoma)
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adrenalin constricts and dilates blood vessels
alpha and beta adrenergic receptors
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