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107 Cards in this Set

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Origin of posterior pituitary?
Floor of 3rd venticle, neuro-ectoderm
Origin of anterior pituitary?
Rathke's pouch
What 2 nuclei produce the nonapeptides of the posterior pituitary?
Supraoptic --> vasopressin (ADH)

Paraventricular --> oxytocin
# of amino acids and size of posterior pituitary hormones.
ADH/vasopressin
oxytocin
9
1.1 kD
What makes up a pre-prohormone?
SP (signal peptide)
the nonapeptide
neurophysin
GP (glycoprotein)
In which part of the cell is the signal peptide of the preprohormone removed?
ER
Functions of oxytocin - what secretes this?
Milk-let-down reflex- contraction of the myoepithelial cells in alveoli storing milk (via neutral control)

Smooth muscle of myometrium of uterus (parturition) -- a positive feedback loop; responds to neural signals and vagina stretch.

Oxytocin + G protein coupled receptor --> phospholipase C cascaid --> increased [Ca] and smooth muscle contraction.
Functions of ADH - what secretes this?
Increase permeabilityto water in colecting duct and distal tubule; increase blood pressure and decrease blood flow in the vasa recta, regulate osmotic pressure and volume of ECF. Also increases permeability of distal nephron to urea - UT1.
How does ADH work?
Binds V2 receptors on basolateral membrane of distal nephron cells. The receptors are coupled to G proteins that activate the adenylyl cyclase cascade and result in phosphorylation of aquaporin 2 (AQP 2) water channel and their insertion into the membrane. ADH also stimulates transcription of the AQP2 gene.
What would stimulate the supraoptic nucleus?
Increase in osmotic pressure in the ECF and a decrease in volume of ECF. Baroreceptors and "volume receptors". Also decreased BP.
Stress, pain.
Opiates and barbiturates.
Diabetes insipidus (pituitary)
Lack of secretion/production of ADH, degenerative pathology of supraoptic nucleus- neurosecretory cells can't produce ADH.

Increased H2O excretion, polyuria (hypotonic urine), ECF volume decreases, increased osmotic pressure and hypotension, increased fluid inteake to compensat.

Treatment: administration of ADH.
Nephrogenic diabetes insipidus
Inability of the KIDNEY to respond to ADH.

ADH RECEPTOR DEFECTS (V2 receptors).
Primary polydipsia
Compulsive water drinking - a psychiatric problem. Causes diabetes insipidus.
How do you distinguish between diabetes insipidus, nephorgenic diabetes, and polydipsia?
Determine urine osmolality after dehydration and ADH administration.
SIADH
Syndrome of Inappropriate ADH Secretion. Hypersecretion of ADH.

Ectopic production of ADH-like substances, some carcinomas may secrete ADH, blood loss/surgery/anaesthesia may stimulate.

Overhydration, hyponatremia (low sodium levels in blood), hypoosmolarity.
Another word for posterior pituitary.
Neurohypophysis.
Another word for anterior pituitary.
Adenohypophysis.
What kind of cell population makes up the anterior pituitary?
glandular (secretory)
What connects the anterior pituitary to the hypothalamus?
Hypothalamic-hypophyseal portal system.
What are the releasing hormones?
GnRH (gonadotropin releasing hormone), GHRH (GHreleasing hormone), GHIH, TRH (thyrotropin RH), PIH, CRH (corticotropin RH)

small peptides, act through cAMP, origin: median eminence
What hormones are controlled by releasing hormones?
gonadotrophs - LH - gonads
FSH - gonads
somatotrophs - GH - muscle, liver
thyrotrophs - TSH - thyroid
Luteophophs-Prolactin - breats
Corticotrophs - ACTH - adrenal cortex
Major prolactin-inhibiting hormone?
dopamine
Another word for GHIH
somatostatin
General characteristics of GH
191 amino acids
2 disulfide bridges
acts on ALL SOMATIC CELLS
growth of cells in both number and size.
GH has direct effect on what?
Protein synthesis (anabolism)
Lipolysis-mobilization of fats, increase in ketone bodies
decrease in RQ
HYPERGLYCEMIC EFFECT (increase in blood glucose), increase glycogen storage.
GH has indirect effect on what?
somatomedins and IGF's (insulin-like growth factors) --> skeletal grwoth, protein synthesis, cell proliferation
Describe GH secretion.
Episodic/in pulses.
Increases at night.
Stimulated by plasma glucose and certain a.a.
Goes up during strenuous excecise and during sleep.
Hypopituitarism
Hypothyroidism
Decreased adrenal cortex function (Addison's)
Hypogonadism.
Increase insulin sensitivity, negative nitrogen balance, hypoglycemia.
Dwarfism (prior to adolescence).
Laron Dwarfism
Laron Dwarfism
IGF receptor defect
Hyperpituitarism
hyperthyroidism
Increase ACTH - Cushing's
Hyperprolactinemia - amenorrhea
Hypergonadism.
Hyperglycemia/diabetes mellitus, positive nitrogen balance, increase in GH.

Giantism (PRIOR to closure of epiphyseal plate)

Acromegaly (AFTER CLOSURE)-bone thickness increases
Diagnosis for acromegaly
Glucose suppression test.
What are the 2 types of cells in the thyroid gland?
Parafollicular (C cells) - involved in calcium regulation.

Follicular cells - T3 and T4
What is required for thyroid hormones.
1 mg iodine per week.

Follicular cells can trap iodine against a conc. gradient of 25-50:1.
Half life of T3 and T4
T4: 6-8 days
T3: 1-3 days
THyroid hormones are bound to what in the blood?
Glycoprotein
TBF: thyroid binding globulin
albumin
small amt- thyroid binding prealbumin.
Synthesis of the binding proteins by the liver for thyroid hormones is increased when?
pregnancy
oral contraceptives
What is the OVERALL effect of the thyroid gland?
CALORIGENIC AGENT.
Stimulate cellular metabolism -- increased O2 consumption and inreased heat production.

Measure BMR.
Metabolic effects of T4
Increased protein synthsis
Increase lipolysis
Increased breakdown of cholesteral.
Increased glycogenolysis
Increase gluconeogenesis
Hyperglycemic effect
Increase Krebs cycel enzymes and oxidation.
Good incoupling agent of oxidative phosphorylation.
Stimulates Na/K atpase
Graves Disease
Hyperthyroidism. PRIMARY. autoimmune disease.

ANtibodies to antigens in the thyroid result in the formation of thyroid stimulating immunoglobulin (TSI) or long acting thyroid stimulator (LATS).
Most common cause of hypothyroidism.
Hashimoto's thyroiditis (adult)
What would cause primary, secondary, and tertiary hypothyroidism?
primary - thyroid failure
secondary - pituitary TSH deficit
tertiary - hypothalamic deficiency of TSH
Cretinism
Hypothyroidism in newborn and child.
Poor skeletal growth, puffiness, poor nervous system development with mental retardation.
Myxedema
clinical picture of hypothyroidism in adult. Deposition of glycoasminoglycans in intracelluar spaces in skin and muscle, puffy face, puffy eyes, apathetic appearance.
Endemic goiter.
Dietary deficiency in iodide. We use iodized salt.
Goiter
enlarged thyroid.
associated with either hypo or hyperthyroidism.
always due to TSH or TSH-like stimulation of thyroid.
Cause of juvenile form of diabetes.
Depletion of insulin production by B-cells. Burned out.
Cause of adult form of diabetes.
Lack of responsiveness of target cells to insulin; increased refractory form.
Hallmark of diabetes.
hyperglycemia (increased blood glucose)
Tests for insulin levels.
R1A
Glucose Tolerance Testing (fasting).
measure glucose in urine.
Measure plasma and urinary ketone bodies.
Cells of the pancreas.
Double gland.
Acinar cells - GI secretion.
Islet cells - endocrine secretion.

Alpha - glucagon
Beta - insulin
Delta - somatostatin
Actions of insulin.
Hypoglycemic agent- decrease blood levels of glucose. Stimulate glucose transport INTO CELLS.
Increase in lipis (increase lipogenesis.
Protein anabolism, amino acids.
Stimulates cellular uptake of K+.
Increase in glycogen.
What does glucagon do?
Hyperglycemia agent -- increase blood glucose. LIVER is major target-hepatic production of glucose.
Stimulates glycogenolysis.
Decrease in lipids.
Consequences of hypoinsulinism.
Hyperglycemia
Glucosuria
Osmotic diuresis
Dehydration/polydipsia, cellular dehydration
Circulation problems
Loss of intracellular K+ --> neuromuscular and cardiac filuare.
Increased lipolysis, decrease in proteins.
ACIDOSIS (ketoacidosis).
cOMA.
Consequence of hyperinsulinism.
Insulin shock.
CAn be treated by immediate administration of glucose.

INsulin shock differentiated from diabetic coma by ACETONE BREATH.
What are the regions of the CORTEX of teh adrenal gland?
Zona glomerulosa - aldosterone
Zona Fasciculata - cortisol and androgens
Zona Reticularis - cortisol and androgens.
3 classes of steroid hormones produced by adrenal cortex.
Glucocorticoids - cortisol.
Mineralcorticoids - aldosterone.
Adrenal sex hormones - predominantly androgenic but some estrogenic hormones.
Why are steroid hormones bound to plasma protin?
decrease excretion of hormone.
Decrease catabolism of hormone.
Increase specificity to target cells.
10% of cortical is FREE.40% of aldoesterone is FREE.
Effects of CORTISOL.
Increase blood flucose (liver), protein catabolism, lipolysis, increase plama free fatty acid (PFFA), decrease glucose utilization.

Hypocalcemic agent.
Anti-inflammatory agent.
Immunosuppressive agent.
What regulates cortisol levels?
Stress
Diurnal variation
Neural signals
Effects of ALDOSTERONE (zona glomerulosa).
Na + in plasma.
K+ in cell.
Cl- in plasma.
H+ in cell.
H2O in plasma.
What causes secretion of aldosterone.
NOT ACTH!!!!!
RENIN --> ANGIOTENSIN II
Excess secretion of aldosterone results in
Hypernatremia
Hypokalemia
Systemic alkalosis
Factors that increase renin secretion
low perfusion pressure in afferent arteriole.
beta-adrenergic stimulation (sympathetic stimulation) of JG cells.
Low Na+ levels in Macula densa region.
Addison's Disease
Hypoadrenalism - combo of hypoaldoesteronism and hypocortisolism.
Cushing's Syndrom
Hyperadrenalism.

Hyperglycemia, centripetal obesity, "moon" face, protein wasting
Normal range of Ca++ level
9-11 mg%
percentages of non-diffusable calcium, ionized calcium, and complexed to anion calcium.
nondiffusable: 41%
ionized: 50%
complexed 9%
2 forms of Pi
HPO4 2-
H2PO4-
Ca x Pi = constant = ?
40
Flat bones
Inner layer of spongy bone - diploe
Enclosed by layers of cortical bone called the inner and outer tables.
Basal vs. alveolar bone
Basal: not dependent on dentition

Alveolar: grows in response to dental eruption.
most abundant protein in human plasma.
human serum albumin. produced in LIVER.
reference range = 3-5 g/dl
T1/2 = 20 days
MW = 67 kDa
what amino acids make up 20% of albumin?
aspartic acid and glutamic acid. These bind Ca to albumin. very acidic side groups.
Alkalosis vs acidosis in terms of ionized calcium
Alkalosis - less ionized calcium, falls to 40%

acidosis - more ionized calcium, >50% = osteomalaica, rickets
Hyperventilation syndrom
Less ionized calcium --> neuromuscular irritability --> increase in numbeness and tingling sensation.
Hypocalcemia
nervous sytem more excitable --> increased neuronal permeability to Na+ --> more spontaneous action potentials --> tetany and seizures.
carpopedal spasms, epileptic seizres, positive chvostek sign.
Acute - tetany
chronic - rickets, osteomalacia, osteoporosis
Hypercalcemia
depression of nervous ssytem
cardiac abnormalitiesi (acute - cardiac arrest)
GI abnormalities
precipitation of CaPo4 crystals
chronic: depression, poor memory, weak/lethargy, kidney stones, ectopic calcification.
What regulates plasma calcium?
PTH
vitamin D
calcitonin
cells of parathyroid gland
dark chief cells
light chief cells
oxyphil cells
general characteristics of PTH
84 amino acids

HYPERCALCEMIC

PHOSPHATURIC AGENT
Effects of PTH
mobilization from bone (increase osteoclast activity), renal conservation of Ca2+ (reabsorption), Ca2+ absorption from gut.
PTH, calcitonin ,and vitamin D effects on Pi
PTH --> increase excretion
CT --> increase excretion
Vit D --> decrease excretion
calcium absorption at gut requires what?
Vitamin D. Ca2+ permeability is low so the gut requires a transport mechanism whch results from vitamin D action.
Actions of calcitonin
Produced by parfollicular cells.

HYPOCALCEMIC AGENT = no calcium mobilization. Bone is major target organ. Stimulates bone formation by icnreasing osteoblastic activity.
High plasma Ca2+ levels --> what happens?
calcitonin secretion.
low plasma Ca2+ levels --> what happens?
PTH secretion
PRIMARY hyperparathyroidism vs. SECONDARY hyperparathyroidism.
Primary: chief cell hyperplasia

Secondary: vitamin D deficiency or renal failure
How does the parathyroid gland sense [Ca2+]?
CaSR = calcium sensing receptor.
PTH gene expression.
High calcium decreases PTH mRNA.

Low calcium increases PTH mRNA.
Structure of CaSR
member of G protein-couple dreceptor family.
7 hydrophobic helices that anchor it in the plasma membrane.
large extracellular domain (600 a.a.)
large cytosolic tail (200 a.a.)
INACTIVATING MUTATION in CaSR
causes FHH: familial hypercalcemic hypocalciuria. Higher levels of plasma Ca2+ needed to reduce PTH secretion. Level of circulating PTH stays the same - higher levels of plasma Ca2+ persist --> PERSISTENT HYPERCALCEMIA.
Activation of CaSR
activation of phospholipase C (PLC) --> 2nd messengers of DAG and IP3.

INhibition of adenylate cyclase, which suprresses intracellular concentration of CAMP.
ACTIVATING MUTATION in CaSR
PTgland is tricked to thinking serum calcium level is elevated when it's really not!

decrease in serum calcium and decrease in PTH.
calcimimetic drug vs. calcilytic drug.
calcimimetic: decrease in PTH secretion (ex: SENSIPAR)

calcilytic: block CaSR --> increase PTH secretion
PTHrP
parathyroid hormone-related protein.

Placental transfer of Ca2+
endochondral bone formation.
a secretory product of human tumors associated with HHM = humoral hypercalcemia of malignancy.
Types of Rickets
Type I; defect in conversion to active vitamin D.

Type II: non-functional vitamin D receptor.
Paracrine vs autocrine factors
paracrine: cells that are not part of the classic endocrine system secrete factors into the interstitial space where they signal neighboring cells.

autocrine: release factors in the interstitial space that act on the secreting cell itself.
classes of hormones
amino acid derivatives - catecholamines, thyroid hormone

peptides

steroids
steroid hormones are synthesized where?
in mitochondria from CHOLESTEROL.

rate of synthesis = rate of secretion so not stored in the cell..
primary male sex organ
testes (gonads)
secondary male sex organs
accessory

vasa efferentia, paired epididymides, vas deferens, seminal vesicles, ejaculatory ducts, Cowper's glands, prostate gland, urethra, penis.
2 compartments of testis
1) seminiferous tubules
2) interstitial tissue
Seminiferous tubules
exocrine function: production of gametes, aka spermatogenesis

2 cells types:
germ cells --> spermatazoa
Sertoli cells
Interstitial tissue of Testis
Endocrine function: secretes testosterone

Interstitial/Leydig cells
2 main circulating androgens
testosterons, androstenedione (A)

3 keto, oxidation of the A ring, 17 oxygen.
testosterone production
GnRH from hypothalamus --> LH secretion from pituitary
EUNUCHOIDISM
deficiency of testosterone (hypogonadism) before puberty.