Exam 3 (week 1) Flashcards
how do endocrine glands transport secretions?
via capillaries, not glands
difference between growth and tropic hormone targets
growth hormones target non-endocrine tissue. tropic targets endocrine tissue
components of adenohypoph
- pars distalis
- tuberalis
- intermedia
components of neurohypoph
- pars nervosa
2. infundibulum (median eminence superiorly, infundibular process)
definition of pituitary stalk
pars tuberalis wrapped around infundibular process
staining of pituitary
pars distalis = heavily stained (secretory granules)
pars nervosa = pale (neurons)
embryonal origin of adenohypoph
ectoderm - rapthke’s pouch, groups up
embryonal origin of neurohypophysis
neuronal - infundibulum from floor of diencephalon - slides down posterior to adenohypophesis
embryological origin of pars intermedia
rathke’s pouch
embryological cell developmental issue with pituitary development
some remnants of rathke’s pouch of ectoderm origin of adenohypoph can remain and divide, becoming CRANIOPHARYNGOMA (benign tumor that compresses pituitary gland causing compression of optic chiasma)
connection between hypothalamus and neurophyophysis
DIRECT - via infundibulum (hypothalamoneurohypophysial tract)
connection between hypothalaus and adenohypophysis
pituitary portal vessles - arcuate makes releasing/inhibiting factors to work on adenohypophysis)
supra optic makes what hormone
vasopressin (ADH)
PVN makes what hormone
oxytocin
blood supply to pituitary gland (and what do they supply)
- superior hypophysial artery (supplies adenohypophysis)
- inferior hypophysial artery (supplies neurophypophysis)
- trabecular artery (connects superior and inferior)
blood route in adenohypophysis (5)
1) superior hypophysial to
2) primary capillary plexus (collects tropic hormones from hypothalamus)
3) portal veins carry hormones down to
4) secondary capillary plexus to stimulate endocrine cells is pars distalis
5) those hormones leave via phypophysial vein to system
blood route in neurohypophysis (3)
- blood from trabecular and inferior hypophysial artery flow into
- capillary plexus, at which point picks up hormones from PVN and supraoptic
- those then leave via the hypophysial vein
cells under histo in pars distalis (4)
- chromophils, which include:
- acidophils (more numerous)
- basophils
- chromophobes (unstained cytoplasm - most likely undifferentiated cells)
types of acidophils (and what do they produce)
- somatotrophs (GH)
2. mammotrophs (PRL)
types of basophils (and what do they produce)
- thyrotrophs (TSH)
- gonadotrophs (FSH & LH)
- corticotrophs (ACTH)
Which are more numerous - acidophils or basohils
acidophils
on mallory stain, what color are acidophils
orange
where in pars distalis are somatotrophs located
on the sides of pars distalis
where in pars distalis are thyrotrophs and corticotrophs located
median portion of pars distalis
where are mammotrophs and gonadotrophs located in pars distalis
scattered
what percentage of cell population in adenohypophysis is somatotrophs
40-50%
when in the day are peak levels of GH released
before awakening
pathway of GH effects
- GHRH released by hypothalamus triggers release of GH.
- GH in liver stimulates release of IGF-1
- ## IGF-1 binds to receptors on chondrocytes on long boneswhen levels of IGF-1 reach threshold, negative feedback to somatotrophs and to hypothalamus which releases somatostatin inhibit further activation of somatotrophs
how to inhibit somatotrophs (3)
- negative feedback due to high level sof IGF-1
- somatostatin from hypothalamus
- high levels of glucose
excess of GH in adults leads to
acromegaly (prominent jaw, big feet, big hands)
what percentage of cell population in adenohypophysis is mammotrophs
15-20% normally, higher and bigger in pregnant women
pathway of mammotroph activity
- (minor) prolactin-releasing factor and thyrotropin-releasing factor stimulate mammotrophs to release prolactin
- (major) stimulation of mammotrophs by suckling (decreases dopamine)
- prolactin acts of mammory gland
inhibited by dopamine release in hypothalamus
what is role of prolactin
- mammogenesis
- lactogenesis
- galactopoesis
FSH pathway
- gonadotropin releasing hormone from hypothalamus releases FSH from gonatotroph
- in women, FSH triggers proliferation of granuloma cells prodcuing estradiol
- in men, sertoli cells are triggred to make androgen binding proteins
what percentage of cell population in adenohypophysis is gonadotrophs
10%
LH pathway
- gonadotropin releasing hormone from hypothalamus stimulates gonadotroph to release LH
- in women, LH stimulates corpus luteum to make progesterone
- In men, Leydig cell is stimulated to make testosterone
what percentage of cell population in adenohypophysis is thyrotrophs
5%
TSH pathway
- thyrotrophic releasing hormone released from hypothalamus to trigger thyrotrop to release TSH
- ## TSH travels to thryroid gland to make T4 and T3 (only active component)Levels of T3 feedback inhibition to hypothalamus ONLY (not pituitary)
levels of THS, T4 and T3 in pituitary cause of hypothyroidism
TSH down
T4 down
T3 down
levels of THS, T4 and T3 in thyroid cause of hypothyroidism
TSH up
T4 down
T3 down
levels of THS, T4 and T3 in pituitary cause of hyperthyroidism
TSH up
T4 up
T3 up
levels of THS, T4 and T3 in thyroid cause of hyperthyroidism
TSH down
T4 up
T3 up
what percentage of cell population in adenohypophysis is corticotrophs
20%
ACTH pathway
- corticotropin releasing hormone from hypothalamus activates corticotrophs to release ACTH from pituitary
- ACTH travels to adrenal gland to release cortisol (mostly)
- cortisol travels to liver to be processed
- when cortisol levels are too high feedback to hypothalamus and pituitary
high levels of stress and ACTH levels
high levels of stress stimulate ACTH - make lots of cortisol, and then you crash because you shut down corticotrophs
why can’t you stop glucocorticoids quickly
don’t want patient to crash - taper slowly to allow corticotrophs to pick up slack and make ACTH to retain endogenous cortisol levels
what do you see in histo for pars intermedia
cysts filled with colloid
what cell type do you see in pars tuberalis
gonadotrops mostly (not physiologically significant)
are axons myelinated or unmyleinated in neurohypophesis
unmyelinated
cell types/structures in neurohypophysis on histo (3)
- unmyelniated axons
- pituicytes (glial cells) supporting axons
- venestrated cappilaries
role of oxytocin systemically (2)
- causes contraction of myometrium in uterus during labor
2. contraction of myopeithelial cells of lactating mammary alveoli (propulsion of milk)
role of ADH systemically (2)
- tunica media of arterioles - increase blood pressure (not significant)
- collecting tubule in kidney - increase water permeability
how to distinguish hypothalamic diabetes insipidus from nephrogenic diabetes insipidus?
in HDI, ADH levels are down (inability to reuptake water) - can treat with exogenous ADH
in NDI - see loss of function of ADH V2 or AQP-2 genes (inability to reuptake water) - refractive to exogenous ADH
how do hormones travel down axon in neurohypophysis and how is release regulated
with neurophysin transporter (1 = oxytocin, 2 = vasopressin)
pituicytes at axon ending allow connection with capillaries after neural cue
path between light and pineal gland (5)
- light into eye
- suprachiasmatic nucleus
- hypothalamospinal tract
- superior cervical ganglion
- pineal gland - decrease melatonin
embryologic origin of pineal gland
roof of posterior diencephalon
histo of pineal gland parenchyma (3)
- pinealocytes (95%) - oval poorly stained loose chromatin
- glial interstitial cells (5%) dense chromatin, elongated nuclei
- BRAND SAND - black calcified concretions (increases with age)
how and when does basal ganglia suppress or promote movement (resting, purposeful, repeated)
in resting state, basal ganglia suppress all movements
when we choose to move a certain way, basal ganglia select appropriate movements and suppress all others
repeated and sequential movements become habits (freeing up cerebral cortex to think about other things)
what neurotramsiter is involved in reward or punishment reinforcement of behavior
dopamine
how is OCD related to basal ganglia
basal ganglia are crucial for initiation, selection, “one at a time” actions
parkinson’s - hyper or hypokinesia
hypo - has trouble initiating movement
protein deposition related to parkinsons
alpha synuclein
4 major functions of basal ganglia
- voluntary motor activities
- regulatory
- procedural learning
- routine behaviors (habits)
tail of caudate is continuous with what
amygdala
which is more medial, globus pallidus or putamen?
globus pallidus - tucked under/within putamen
what do you also see in section where you can see subthalamic nuclei
mamillary bodies
what is corpus striatum/striatum?
caudate plus putamen
what neurotransmitter is responsible for pathways between cortex and striatum
glutamate (excitatory)
what neurotransmitter is responsible for pathways between susbtantia nigra and striatum
dopamine fibers onto GABA neurons (modulating)
projection from globus pallidus to thalamus (is it inhibitory or excitatory?)
inhibitory
what percentage of substantia nigra dopamine neurons for symptoms to begin?
80%
movement symptoms in parkinsons (3)
- resting pill rolling tremor
- bradykinesia
- hypokinesia
muscle symptoms of parkinsons (3)
- increased muscle tone
- lead-pipe rigidity
- cog-wheel rigidity
neuron type death in huntingtons
GABA neurons die from prefrontal to caudate
movement symptoms of Huntington’s
- chorea (continuous rapid movements)
2. athetosis (writhing)
hemiballismus cause and symptoms
stroke in subthalamic nucleus
periods of violent flailing movements
direct pathway purpose
to initiate movement
connection/interaction between VA/VL and cortex
VA/VL is directly/recipricolay connected to primary motor cortex, at a default is inhibited by internal globus pallidus
interaction between globus pallidus and thalamus for motor control
internal globus pallidus produces GABA inhibition of VA/VL cells to suppress all movements
interaction between putamen and globus pallidus for motor control
putamen usually is quiet, but when action is initiated, putamen fires GABA-ergic potential to the interal globu pallidus to allow VA/VL to send info to primary motor cortex
what makes putamen cells fire (inputs)
1) cerebral cortex (premotor, motor and somatosensory)
excitatory glutamatergic input
2) association cortex
3) limbic lobe
direct pathway purpose
for movement selection
what is VSED
voluntary stopping eating and drinking
what is the cell often targeted in neurodegenerative diseases
neurons (functional groups of neurons)
genetics of Huntingtons
AD, extra DNA in chromosome 4 (repeating CAG trinucleotide unit)
Huntington’s has over 36 repeats (normal is less than 34)
what areas of brain is affected in Huntingtons
both deep (caudate, putamen, thalamus) and superficial (cerebral cortex)
Friedreich’s ataxia genetics
AR extra DNA in chromosome 9 (extra repeat in GAA in frataxin gene)
Friedreich’s ataxia affects what part of brain
causes spinocerebellar degeneration
Peroneal muscular atrophy/charcot-marie-tooth genetics
AD extra DNA in chromosome 17, repeat in PMP22 gene for myelin structural protein
what part of CNS does peroneal muscular atrophy affect and what symptoms occur
myelin damage and axonal loss in peripheral nerves - distal leg weakness and muscle atrophy
duchenne muscular dystrophy genetics
X linked recessive loss of dystrophin gene in X chromosome
duchenne affects what cells/structures, and what symptoms occur
structural protein in skeletal muscle - slow progressive wasting, loss of function, respiratory paralysis