Pda 2 Exam 2 Endocrine

Front 1

Functions of endocrine system

Back 1

Maintain homeostasis
Promote development

Front 2

Peptide and protein hormones

Back 2

All anterior pituitary and hypothalamic releasing hormones

Front 3

Steroids (4)

Back 3

Cortisol
Testosterone
Aldosterone
Estradiol

Front 4

Trophic vs. non-trophic

Back 4

Trophic acts on endocrine tissue
Non-trophic acts on non-endocrine tissue (liver, heart, muscle)

Front 5

Receptors for peptides

Back 5

--On cell surface
--Peptides too big to get into cells
--Activate ion channels or linked to 2nd messengers

Front 6

Receptors for steroids

Back 6

--inside cell
--in cytoplasm or on nucleus
--Ligand-receptor complex binds to DNA, promotes transcription and translation

Front 7

Receptors for amines

Back 7

--inside cell or on cell surface
--may also be on mitochondria

Front 8

(+) hypothalamic releasing hormones

Back 8

TRH
LHRH (GnRH)
CRH
GRH

Front 9

(--) hypothalamic releasing hormones

Back 9

Dopamine (inhibits prolactin)
Somatostatin (inhibits GH. TRH)

Front 10

(+) Anterior pituitary hormones

Back 10

TSH
LH/FSH
ACTH
GH

Front 11

(--) Anterior pituitary hormones

Back 11

Prolactin
GH

Front 12

Endocrine target tissues and hormones

Back 12

1. Thyroid -- T3/T4
2. Ovaries/Testies -- estrogen/testosterone
3. Adrenal gland -- cortisol
4. Liver -- IGF-1

Front 13

boney encasement of pituitary

Back 13

sella tarcica

Front 14

connection between hypothalamus and pituitary

Back 14

infundibulum

Front 15

Posterior pituitary hormones

Back 15

Vasopressin
Oxytocin

Front 16

Neural vs portal systems

Back 16

Portal -- hypothalamus to posterior pituitary through bloodstream
Neural -- hypothalamus to posterior pituitary

Front 17

Physiological role of GHRH

Back 17

synthesis and secretion of GH from AP

Front 18

Sermorelin acetate

Back 18

--1st 29 AAs of GHRH
--No longer manufactured
--Used to test AP function or treat hypothalamic dysfunction

Front 19

Direct effects of GH

Back 19

--Increase IGF-1 (mainly in liver)
--Increase triglyceride hydrolysis
--Increase glucose production in the liver

Front 20

Indirect effects of GH (mediated by IGF-1)

Back 20

--Anabolic effects assoc. w/ GH
--Chondrogenesis
--Differentiation/development of myocytes

Front 21

Physiological control of GH

Back 21

Somatostatin inhibits
GH provides -- feedback
IGF-1 provides -- feedback
Ghrelin promotes GH release

Front 22

Environmental GH promoters

Back 22

hypoglycemia
exercise
stress
high protein meals

Front 23

Environmental GH inhibitors

Back 23

Hyperglycemia
Sleep deprivation
Poor nutritional status (chronic)

Front 24

Diagnosis of GH excess

Back 24

--Confirm w/ plasma GH and IGF-1 levels
--Glucose tolerence test (side 3)

Hint 24

hyperglycemia doesn't suppress GH release in those w/ acrogmegaly or gigantism

Front 25

Octreotide/Sandostatin LA

Back 25

Somatostatin analog
For Excesss GH
N/V/D in 50%
decrease TSH-hypothyroidism
No -- feedback to AP tumor?

Hint 25

Longer duration of action, more pituitary selectivity
Octreotide: SC injection 3x/d
Sandostatin LAR: IM q 4 wks

Front 26

Lanreotide/Somatuline Autogel

Back 26

Somatostatin analog
For excess GH
N/V/D in 50%
decrease TSH-hypothyroidism
No -- feedback to AP tumor?

Hint 26

Lanreotide: IM q 10-14 days
Somatuline Autogel: IM q 4 wks

Front 27

Pegvisomant

Back 27

GH receptor antagonist
For excess GH

Hint 27

--Binds to GH receptor, doesn't activate JAK-STAT pathway
--concern: no GH receptor activation may increase tumor size

Front 28

Irradiation for GH excess

Back 28

Not selective for tumor cells
All AP cells must be replaced

Front 29

Surgery for excess GH

Back 29

Option if tumor is large and seen by PET/MRI
Trans-sphenodal surgery

Front 30

Somatropin

Back 30

Identical to human GH
Use until child reaches 18

Hint 30

SC injections daily

Front 31

Laron dwarfism

Back 31

People can make and release GH, but have defect in GH receptor in liver; can't make IGF-1

Hint 31

Looks the same as pituitary/hypothalamic dwarfism

Somatropin doesn't help Laron dwarfism

Front 32

Increlex

Back 32

--recombinant IGF-1
--used for Laron dwarfism
--helpful for other types of dwarfism too

Front 33

Role of prolactin (women)

Back 33

--develops breast tissue w/ E & P during pregnancy
--causes milk production after birth

Front 34

Control of prolactin release

Back 34

Dopamine inhibits PRL release; take away DA to cause PRL release

Hint 34

TRH increases PRL release only if abnormally high; not a physiological releasing factor

Front 35

causes of hyperprolactinemia (3)

Back 35

--Pituitary adenoma
--Dopamine antagonist (treatment for schizophrenia or emesis
--Primary hypothyroidism (no -- feedback to TRH)

Front 36

Consequences of high PRL

Back 36

Infertility
Galactorrhea

Front 37

Bromocriptine

Back 37

--Somewhat selective D2 antagonist
--For hyperprolactinemia
--Supresses PRL release and reduces adenoma size over time

Hint 37

Dosing 2-3 x/day
Headache
N/V
First dose phenomenon

Front 38

Carbergoline

Back 38

Selective D2 antagonist
For hyperprolactinemia
Suppresses PRL release and reduces adenoma size over time

Hint 38

Better tolerated than bromocriptine
Less N/V
Can produce heart valve problems w/chronic use
Dosing 1-2 x/week

Front 39

Oxytocin in uterine contractions

Back 39

Stimulus for release: dilation of cervix
Stretch receptors are activated, relay back to hypothalamus through a neuron to cause oxytocin release
Prostaglandins and oxytocin both imp. in labor and delivery

Front 40

Oxytocin in milk letdown

Back 40

Oxytocin does not influence milk production
Letdown=movement of milk to appropriate reservoirs

Hint 40

release of oxytocin to promote letdown is controlled by higher centers

Front 41

Clinical uses of oxytocin

Back 41

1. Induce or augment labor in last trimester
2. Promote milk letdown
3. Reduce or prevent postpartum hemorrhage

Front 42

Physiological roles of vasopressin

Back 42

Adjust plasma osmolality -- osmo receptors in hypothalamus detect osmolality and cause synthesis and release of VP when activated

Hint 42

Maintain plasma volume -- stretch receptors in the atria detect the amount of stretch upon filling with blood. a decrease in stretch (and therefore volume) sends signals to the hypothalamus to release VP. 15-20% blood loss needed

Front 43

VP at collecting ducts

Back 43

More water passes from urine to plasma
Mediated by V2 receptors

Front 44

VP as a vasoconstrictor

Back 44

Acts as a vasoconstrictor at high concentrations to maintain BP during hemorrhage
Mediated by V1 receptors

Front 45

V2 pathway

Back 45

1. VP binds to V2 receptors
2. Gs-adenylyl cyclase-cAMP-PKA pathway is activated
3. aquaporin transport shifts toward apical membrane

Front 46

Central vs nephrogenic DI

Back 46

Central DI: from decreased VP release from posterior pituitary

Hint 46

Nephrongenic: V2 receptors are defective: VP is released, but no site of action

To determine whether central or nephrogenic, give VP

Front 47

Causes of central DI

Back 47

damage/injury or tumor of hypothalamus or posterior pituitary

Front 48

Causes of nephrogenic DI

Back 48

1. Congenital/genetic
2. Drug-induced (Lithium or demeclocycline

Front 49

Syndrome of Inappropriate Antidiuretic Hormone

Back 49

Patient secretes lots of VP, even when Posm<285

Hint 49

Urine is concentrated and blood is hypo-osmolar

Front 50

Treatment of SIADH

Back 50

Short term: water restriction
Long term: lithium or demeclocycline

Front 51

Desmopressin (dDAVP)

Back 51

Vasopressin agonist
Central DI
Nocturnal enuresis
3000x more potent for V2 over V1

Hint 51

Arginine Vasopressin
--deaminated at 1-Cys
--substituting D-arginine for L-arginine

Front 52

Tolvaptan

Back 52

--Selective V2 antagonist
--SIADH
--Congestive heart failure to decrease plasma volume

Front 53

Conivpatan

Back 53

--V1/V2 antagonist
--SIADH
--Congestive heart failure to decrease plasma volume