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Phys3 Hypothalamus
Phys3 Hypothalamus & Pituitary I & II
Question | Answer |
---|---|
Adenohypophisis | Anterior Pituitary (Glandular cells): 1.Pars Distalis. 2.Pars intermedia (not very active in humans). 3.Pars tuberalis (surrounds infundibular stalk). |
Neurohypophysis | Postierior Pituitary (Down growth of 3rd ventricle, contains neuronal tissue): 1.Pars Nervosa. 2.Median Eminence. 3.Infundibular stalk. |
What connects the Hypothalamus & the Anterior Pituitary? | Long portal vessels: 1.Axons in hypothalamus synapse onto capillary bed feeding long portal vessels. 2.Vessel travels down onto neurosecretory cells. 3.Activates a hormone secreting cell to release hormones into venous drainage. |
What connects the Hypothalamus & the Posterior Pituitary? | Nerve terminals of Hypothalamic (magnocellular) neurons are found in the Posterior Pituitary (direct axonal connection). **Terminals release hormone directly into venous drainage for bodily distribution. |
What 2 hormones do the magnocellular neurons release from their nerve terminals in the Posterior Pituitary? | 1.Oxytocin. 2.AVP (ADH). |
Main function of the Hypothalmic portal system | Carries hormones from hypothalamus to Ant pituitary to regulate hormone secretion from andenohypophysis. **Very limited vascular connection b/w lobes of pituitary. |
Difference b/w Magnicellular and Parvocellular Hypophyseotropic neurons? | 1.Magni: (long axon) Synapse onto capillary bed within the Posterior Pituitary (release oxytocin/AVP). 2.Parvo: (short axon) synapse onto portal capillary bed which then travels down to Anterior Pituitary (release stim/inhibit). |
Location of Magnicellular neuron nuclei | 1.SON. 2.PVH. |
Location of Pervocellular hypophyseotropic neuron nuclei | 1.PeVH. 2.PVH. 3.Arc. |
Which pituitary lobe is needed for propogation of species? | ANTERIOR. |
What Hormones does the Ant. Pituitary release? | 1.TSH. 2.FSH. 3.LH. 4.Prolactin. 5.GH. 6.ACTH. |
What Hormones does the Post. Pituitary release? | 1.Oxytocin. 2.AVP (ADH) |
In what form are Oxytocin & AVP synthesized? released? | 1.Synthesized: Pro-homones. 2.Released: Neurophysin I (AVP), Neurophysin II (Oxytocin). **Pro-homone is cleaved in secretory granules in the axon terminal. |
What Nuclei is AVP produced in | Supraoptic |
What Nuclei is Oxytocin produced in | Paraventricular. |
Primary Function of AVP/ADH? Mechanism of action? | Inc water uptake in kidney's collecting duct. 1.Inc synthesis & insertion of Aquaporin-2 H2O channels. **V2 receptor mediated: Gs-cAMP. |
Secondary actions of AVP/ADH? receptors? | 1.Arterial & venous constriction (V1a). 2.Stimulate ACTH release (V1b). 3.Stimulate spermaticord contraction (V1). 4.Skeletal muscle regeneration (V1a). |
What is the number 1 regulator of AVP/ADH? | Plasma Osmolality, they are directly related. **there is no osmolality level where there wont be some ADH release. |
4 things affecting the ADH/plasma osmolality relationship | 1.Rapid changes in osmolality. 2.Drinking. 3.Pregnancy (Dec threshold for ADH release). 4.Aging (Inc ADH response to osmolality changes, Inc plasma [ADH]). |
What [ADH] levels would you expect to see in a pregnant woman? | INCREASED [ADH] for a given osmolality. |
Stimulation of ADH is caused by | 1.Inc ECF osmolality. 2.Dec pressure in baroreceptors. 3.Ang II. 4.Inc in Na+ in CSF. 5.Hypoglycemic |
inhibition of ADH is caused by | 1.Dec in ECF osmolality. 2.Inc vol & stretch in low pressure baroreceptors. 3.ANP. 4.Dec temp. 5.Alpha Agonists. 6.thyroid hormone. 7.Lithium. |
3 types of Diabetes Insipidus (DI)? (DI is not enough ADH) | 1.Hypothalamic DI: Deficiency in ADH (problem with magnicellular neurons). 2.Nephrogenic DI: Renal resistance to ADH (renal disease). 3.Dipsogenic DI: excessive water drinking. |
What is the most common cause of Euvolemic hyposmolality? | Syndrome of inappropriate anti-duresis (SIAD). **4 different types A-D. |
Causes of SIAD | 1.Neoplastic disease. 2.CNS disorders. 3.Pulmonary disease. 4.Drugs. |
Two important steps before diagnosing SIAD? | 1.Always compare plasma [ADH] levels to osmolality levles. 2.rule out all other causes of euvolemic hyposmolality (Hypothyroidism & Glucorticoid deficiency). |
Primary functions of oxytocin | SMOOTH MUSCLE CONTRACTION 1.Milk ejection. 2.Uterine contraction. **also ovulation & ejaculation |
What causes oxytocin stimulation? | 1.Suckling. 2.Estradiol (Progesterone withdraw). 3.Fergusson reflex. |
What inhibits oxytocin release? | 1.Catecholamines. 2.Opiods. |
What receptor does oxytocin use? | Gq |
Can the linkage precursors generate multiple types of offspring cells (ones that release different hormones)? | YES. **some cells of the anterior pituitary gland share a common lineage, so error at a point during the developmental process may impact one or more cell types. |
3 hypothalamus hormones influencing Prolactin release from Ant Pituitary? | INHIBITORY: 1.Dopamine (Lactotrophs-Gi). 2.Somatostatin. STIMULATE: 1.Tyrotropin releasing h. |
3 hypothalamus hormones influencing TSH release from Ant Pituitary? | STIMULATORY: 1.Thyrotropin releasing h. (thyrotrophs-Gq). INHIBITORY: 1.Somatostatin. 2.Dopamine |
3 hypothalamus hormones influencing GH release from the Ant pituitary. | INHIBITORY: 1.Somatostatin (somatotrophs-Gi). STIMULATORY: 1.Growth hormone releasing h (somatotrophs-Gs). 2.Thyrotropin releasing h. |
Hypothalamus hormone influencing LH and FSH release from the Ant pituitary | Gonadotropin releasing H (Gonadotrophs-Gq/Gs) |
Hypothalamus hormone infulencing ACTH release from the Ant Pituitary | Corticotropin releasing h (Corticotrophs-Gs). |
Prolactin | 1.Protein hormone. 2.Lactotrophs. 3.Primarily circulates as MONOmer. 4.Receptors: breast & pituitary. 5.Activates JAK/STAT pathway. 6.Primary fnc: production of milk. **Inhibits reproduction via inhibiting GnRH secretion. |
Galacteria | HYPERsecretion of prolactin. milky discharge in men & women. |
What stimulates release of prolactin | 1.Estrogen. 2.Serotonin. 3.TRH. 4.breast manipulation. 5.Sleep. |
What Inhibits release of prolactin | 1.Dopamine. 2.PRL. 3.Somatostatin. |
GH | 1.Protein hormone. 2.Somatotrophs. 3.2 splice variants (growth promoting, diabetogenic effects). 4.receptors on liver, adipose, skeletal muscle. 5.Activates JAK/STAT. |
HYPOsecretion of GH | Dwarfism |
HYPERsecretion of GH | 1.Pre-occification of epiphyseal plates: Gigantism. 2.Post-occification of epiphyseal plates: Acromegaly. |
IGF-I & IGF-II | Somatomedians that are insulin-like growth factors. **IGF-I is released from liver when it is stimulated by GH targeting muscle and bone growth. |
what stimulates release of GH | 1.ACh. 2.fasting. 3.TRH. 4.stress. 5.Hypoglycemia. 6.GHRh. 7.Alpha-adrenergic |
What suppresses release of GH | 1.Somatostatin. 2.GH. 3.gluccocorticoids. 4.Hyperglycemia. 5.Hypothyroidism. 6.IGF-I (somatomediates) |
What inhibits GH/IGF | 1.undernutrition. 2.Acute/chronic illness. 3.GH/IGF-I receptor deficiency. |
Negative feedback loops for GH | 1.IGF-I inhibits both somatotroph formation & hypothalamus release of GHRh. 2.GH inhibits hypothalamus release of GHRh. |
Positive feedback loops for GH | Both GH & IGF-I stimulate hypothalamus release of SRIF(somatostatin) which inhibits somatotrophin formation. |
Key functions of GH | 1.Inc lipolysis. 2.Stimulation of protein synthesis. 3.Antagonism of insulin action. 4.Stimulates Linear growth. |
Somatostatin | Protein hormone released from hypothalamus, Inhibits release of: 1.Pituitary: GH, Prolactin, TSH, ACTH. 2.Pancreas: Insulin & Glucagon. 3.Enteroendocrine in GI system: secretions. **5 different receptors allow it to produce multiple effects. |
ACTH | 1.Protein hormone. 2.corticotrophs. 3.Maintains adrenal gland |
Hypersecretion of ACTH | Cushings disease. |
Hyposecretion of ACTH | 1.Metabolic disorders. 2.Reproduction problems. |
Negative feedback loops for ACTH (Primary regulator) | Glucocorticoids inhibits: 1.formation of corticotroph (which stimulates ACTH release from Ant pituitary). 2.Hypothalamus release of CRH (corticotroph releasing hormone) which stimulates corticotroph formation. |
What stimulates release of ACTH | 1.CRH. 2.Stress. 3.Sleep/wake transition. |
What inhibits release of ACTH | 1.Cortisol (glucocorticoids). 2.ACTH. 3.Somatostatin. |
TSH | 1.glycoprotein hormone (alpha & beta chain, Beta distinguishes TSH from LH & FSH). 2.Thyrotrophs. 3.TRH stimulates transcription of both alpha & beta chains. 4.Long half-life. **glycosalation problems will affect its fnc b/c its glycosalated. |
TSH Feedback loops | 1.Negative: Thyroid hormone inhibits the hypothalamus' release of TRH (forms thyrotroph) & formation of thyrotroph. 2.Positive: Stimulates hypothalamus' release of somatostatin which inhibits thyrotroph formation. |
What stimulates release of TSH? | 1.TRH. 2.cold weather. 3.Leptin. |
What inhibits release of TSH? | 1.Thyroid hormone (T3/T4). 2.fasting. 3.Somatostatin. 4.dopamine. 5.GH. 6.Cortisol. **Cross-talk |
Gonadotrophins (FSH & LH) | 1.Glycoprotein hormones (alpha & beta chain). 2.Gonadotrophs. 3.Stimulated by GnRh. 4.Receptors on gonads. 5.G-protein receptors (FSH:cAMP, LH:cAMP & PLC) |
Is it easier to detect HYPOsecretion of gonadotrophins in males or females? | FEMALES. |
Negative gonadotroph feedback loops | Both Testosterone (males) and Estrogen/progesterone (females) have an inhibitory effect on GnRh release from hypothalamus & LH/FSH release from pituitary. |
Anterior Pituitary Target cell of Hypothalamic release of Dopamine? what do these cells release? | Lactotrophs. They release (via Gi) Prolactin. |
Anterior Pituitary Target cell of Hypothalamic release of TRH? what do these cells release? | Thyrotrophs. they release (via Gq) TSH. |
Anterior Pituitary Target cell of Hypothalamic release of Corticotropin releasing hormone? what do these cells release? | Corticotrophs. They release (via Gs) ACTH. |
Anterior Pituitary Target cell of Hypothalamic release of Gonadotopin releasing hormone? what do these cells release? | Gonadotrophs. They release (via Gq/Gs) LH, FSH. |
Anterior Pituitary Target cell of Hypothalamic release of Growth hormone releasing hormone? what do these cells release? | Somatotrophs. They release (via Gs) GH. |