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Transcript
Physiology Unit 14
except chapters 78 & 79
Endocrinology Learning Objectives
Chapters 74-76
1.
2.

What are two hormones that utilize enzyme-linked receptors? Hint: JAK-STAT and MAPKs?
Leptin and insulin,
also prolactin, IGF-I, and GH

What hormones are not stored in their producing gland?
Steroid hormones cannot be stored, they cannot be contained!
diet skin liver kidney
3.


4.
5.
6.
What are the factors that influence ADH production (2)? What is the primary ADH effect?
Increased extracellular osmolarity (brain) and low blood pressure (atria)
ADH concentrates urine

Which hormones are produced by the anterior pituitary?
GH, ACTH, TSH, FSH, LH, Prolactin






What factors besides GHRH increase GH levels? What’s a cool effect of GH that you overlooked? What are its metabolic effects?
Ghrelin, trauma, hypoglycemia/starvation, excitement, first 2 hours of sleep, and exercise
Enlargement of the internal organs
Increased protein synthesis,
reduced protein breakdown,
use of fatty acids for energy (causes ketosis in acromegaly),
and “insulin resistance:” decreased use of glucose, elevations in insulin, and increased glycolysis (increased free glucose with compensatory insulin increase)

Which anterior hypothalamic-released hormone is under negative secretory control?
Prolactin’s main “stimulus” is the absence of dopamine
Chapter 76
7.

What hormone levels are increased in Graves Disease?
Only T3 and T4 plasma levels increase; their stimulator does not


How does a radioimmunoassay work? What does a comparatively low amount of bound radioactive hormone mean?
Antibody is mixed with fluid containing hormone to be measured, and at the same time a standard amount of radioactively tagged hormone is added
So low radioactive hormone means there is a high level of hormone in the organism


What causes exopthalmos?
TSIs (Immunoglobins) produced in Graves disease cause exopthalmos
Hormonal changes (over forms of hyperthyroidism) do not cause exopthalmos



What do thiocyanate, propylthiouracil, and high dose iodide do?
Thiocyanate: decreases iodine trapping, increases thyroglobulin production, goitrogen
Propylthiouracil: blocks peroxidase, goitrogen
High dose iodide: shrinks thyroid gland, decreases all thyroid activity phases for a few weeks
8.
9.
10.
Chapter 77
11.


12.
13.
What is the rate-limiting step of steroid synthesis? What hormone stimulates it?
Cholesterol desmolase: cholesterol => pregnenalone
Stimulated by ACTH

How do blood volume and sodium concentration change in hyperaldosteronism? Other substances that are altered? How is hypoaldosteronism different?
The change is transient, and is quickly countered by pressure natriuresis and pressure diuresis; “aldosterone escape”
Blood pressure increases, metabolic alkalosis occurs, and hypokalemia ensues…
i.
but not changes in blood volume or sodium concentration!
NOTE: 0 aldosteronism is not compensated for=> hypovolemia & hyperkalemia





How does cortisol prevent and reduce inflammation (5)?
Stabilizes lysozomal membranes of damaged cells
Decreases permeability of capillaries
Decreases migration of leukocytes and decreases phagocytosis (less prostaglandins)
Suppresses immune system
Reduces IL-1 (reduces fever)

Where is 11β-hydroxysteroid dehydrogenase type 2 expressed?
Renal tubular cells; it converts cortisol to corticosterone


Where are prohormone convertase 1 and 2 expressed?
PC1 is expressed in the pituitary; results in cleavage of POMC to ACTH and β-lipotophin
PC2 is expressed in the hypothalamus; further cleaves products to MSH and β-endorphin


14.
15.
Chapter 79, PTH and Calcitonin
16. What are the three major functions of calcitonin? [Exam Q]
 Inhibits Ca absorption by osteoclasts
 Inhibits osteoclastogenesis
 Inhibits Ca reabsorption in the kidney and intestines
17. What are three effects of D3?
 Increase in Ca and Pi absorption is caused by D3
i. Via gene expression modifications, stims 2 Ca pumps and calbindin
 Increase in osteoclast number and activity
 Decrease in PTH synthesis
18. What two effects (1 is indirect) does PTH always have, and what effect depends on dose?
 Calcium and phosphate absorption in the GI (indirect, via vitamin D activation)
 Calcium reabsorption and phosphate secretion in the kidney
 Bone catabolism/anabolism:
i. Osteoclast activity if PTH is constantly elevated
ii. Or osteoblast activity if PTH is only elevated 3-5 hours a day
19. What is really bad about rapid PTH increases?
 CaHPO4 deposition in the alveoli (kidneys can’t excrete the phosphate fast enough)
 Or osteitis fibrosa cystica (fucked bones) from PTH increases in general
Chapter 80, male reproduction
20.
What five hormones seem to be necessary for spermatogenesis?

T, LH, and FSH of course, but also GH and to a lesser extent E seem to be needed
21.
22.


What cell type produces T? When is this type plentiful (when stimulated)?
Leydig cells
2nd trimester (stimulated by hCG), in the newborn male for a few months, and after puberty

How does T modify blood composition (2)? What does it do to the skeleton?
Increases hematocrit, likely through increasing BMR


23.
Increases reabsorption of sodium in distal tubules
Promotes growth spurt, but early uniting of epiphyses

What hormone do Sertoli cells release in order to inhibit the ant. pituitary [and hypothalamus]?
inhibin

What is Frolich syndrome?
= adiposogenital syndrome = hypothalamic enuchism = insufficient GnRH and overating
24.
Chapter 81-83, pregnancy
25. Describe the menstrual cycle succinctly:
 Anterior pituitary secretes increasing FSH and LH
 FSH & LH stimulates follicles to secrete estrogen and inhibin
 Estrogen up-regulates LH (on thecal cells) and FSH (on granulosa cells) receptors
 Rapid increase in estrogen by follicle self-stim causes the pituitary to produce an LH surge
 LH ruptures the follicle (all but one became atretic)
 The corpus luteum produces E and later P for 14 days
[Super-succinct: pituitary stims follicle, stims pituitary, stims follicle to rupture]
26. What hormone is responsible for growth the endometrium?
 Estrogen
 Progesterone converts it to its glandular phase and helps maintain the endometrium
27. How does estrogen change the vaginal epithelium?
 Coverts epithelium from cuboidal to stratified—more resistant to infection and trauma
28. Which hypothalamic nuclei control female sexual activity?
 Arcuate
29. What does pregnanediol tell you?
 It’s a product of progesterone metabolism—check it to see if ovulation has occured
30. What features of fetal blood help it to obtain sufficient oxygen (3)?
 Fetal hemoglobin, greater hemoglobin concentration, and double Bohr effect (one in mother,
one in fetus)
31. When is the placenta able to produce sufficient quantities of P and E to permit removal of the
corpus luteum without losing the endometrium and causing abortion? What is necessary for its
maintenance during this period?
 7th week
 hCG
32. Why do pregnant women sometimes get hirsuitism?
 The fetal zone of the adrenal glands produces lots of DHEA and 16-hydroxy-DHEA, which is
converted to estrogen by the trophoblast cells in the placenta, which is metabolized to
testosterone in the mom
33. What are the effects of cervical stretching leading up to childbirth (2)? What else stimulates
uterine contractions?
 Uterine contractions and oxytocin release
 Increasing ratio of E to P after the 7th month (mostly more E)
34. How does arterial resistance change in fetal vasculature after birth? Why?
 Pulmonary resistance drops down, and systemic resistance goes way up


Inflation of the lungs decreases pulmonary vessel pressure
Loss of placental blood flow increases systemic pressure
35. What happens to babies born of diabetic mothers?
 Macrosomia, but more importantly ARDS occurs in conditions of hyperinsulinemia
i. Therefore, ARDS occurs only to children of type II diabetics
36. What can delay breathing of newborns?
 Prolonged hypoxia during delivery can cause depression of the respiratory center