Review Session "Must Knows" Flashcards
1
Q
TH functions like
A
steroid hormone
2
Q
Steroid hormones act via
A
transcriptional effects
3
Q
GHRH produced in what nuclei?
A
Arcuate nucleus
4
Q
GnRH produced in what nuclei?
A
POA
5
Q
CRH produced in what nuclei?
A
PVN (parvocellular division)
6
Q
TRH produced in what nuclei?
A
PVN
7
Q
Somatostatin produced in what nuclei?
A
PeVN
8
Q
Name 2 hypothalamic releasing hormones manufactured in the PVN
A
CRH and TRH
9
Q
Does prolactin have a hypothalamic releasing factor?
A
No. It’s under tonic inhibitory control of dopamine.
10
Q
Under pathological conditions, excessive TRH can stimulate
A
Prolactin
11
Q
Prolactin is a potent inhibitor of
A
GnRH
12
Q
SS inhibits GH release at the
A
anterior pituitary
13
Q
SS inhibits GHRH pulsatility at the
A
hypothalamus
14
Q
Name 2 hormones produced by acidophiles
A
Prolactin, Growth Hormone
15
Q
Name 4 hormones produced by basophiles
A
FSH
LH
ACTH
TSH
16
Q
AVP-secreting magnocellular neurons are derived from what brain nuclei?
A
SON and PVN
17
Q
AVP-secreting parvocellular neurons are derived from what brain nucleus?
A
PVN
18
Q
What are the two divisions of the PVN?
A
Magnocellular and parvocellular
19
Q
AVP-secreting magnocellular neurons regulate
A
Water balance
20
Q
AVP-secreting parvocellular neurons regulate
A
stress
21
Q
What happens to the zona fasciulata under exogenous corticosteroid treatment (long-term)
A
atrophy
22
Q
What’s the precursor gene for ACTH and alpha-MSH
A
POMC
23
Q
Small cell lung carcinomas can secrete
A
excess ACTH
24
Q
Kd refers to hormone affinity or specificity to receptor?
A
Affinity
25
Receptor kinases versus receptor linked kinases
Receptor kinases have intrinsic kinase activity; linked don't.
26
Name hormones that bind receptor-linked kinases (3)
GH
Prolactin
EPO
27
Name hormones that bind regular receptor kinases (3)
Insulin
IGF-1
ANP
28
Recite the melatonin synthesis pathway
Tryptophan to 5-HTP via tryptophan hydroxylase (RLS). 5-HTP to 5HT. 5HT to melatonin through N-acetyltransferase (RLS for melatonin, in PINEAL gland).
29
Recite the dopamine synthesis pathway
1. Tyrosine
...tyrosine hydroxylase (RLS)....
2. X-Dopa (L-Dopa is active)
3. Dopamine
...dopamine B-hydroxylase (ACTH promotes)...
4. Norepinephrine
...PMNT (cortisol promotes)...
5. Epinephrine
30
Where is melatonin synthesized
pineal gland
31
PRIMARY lesion in thyroid gland will show up as...
High basal TSH, since no T3/4 to negatively feedback on a. pit
Responsive to TRH challenge
32
SECONDARY lesion in pituitary gland will show up as what, on the TRH test?
Low baseline TSH, unresponsive to TRH challenge
33
High GnRH pulse releases
LH at ant. pit
34
Low GnRH pulse releases
FSH at ant. pit
35
Where is the hypophyseal portal system? Whats the blood supply?
Ant. pit, superior hypophysial artery.
36
Kallman's
GnRH can't migrate
37
Lesion to adenohypophysis. What kind of hormones impaired?
FLAT (basophile 10%) PiG (acidophile 40%)
38
2 main causes of central diabetes insipidus?
Etiology: 2 main causes
1. Decreased AVP release – most common defect
Hypothalamic or pituitary defect due to trauma, cancer, or infectious disease.
2. Decreased renal responsiveness to AVP
Genetic: X-linked mutation in AVP type-2 receptor – 90% males Acquired: lithium treatment, hypokalemia AVP levels are normal in these cases.
39
The secretion of which hormones is suppressed by somatostatin?
GH and TSH!
Note: TH promotes GH release. They're connected.
40
SS14 is made where?
Brain. This is the one that suppresses GH and TSH.
41
SS28 is made where?
Intestines.
42
What are burin, PC1, PC2?
The endopeptidases Furin, PC1, and PC2 aid in processing of the mature SS28 and SS14.
43
GH acts on effectors cells through what pathway?
JAK-STAT
44
Name 4 inhibitors of GH release
SS28, IGF1, Free fatty acids, Glucose
45
Name 4 promoters of GH release
```
GHRH
Hypoglycemia
Catecholamines (exercise)
Amino acids
Thyroid hormone
```
46
GH effect on adipose?
Via Jak/STAT:
| Decrease glucose uptake (keeps GLUT4 intracellular), increase lipolysis
47
GH effect on muscle cells?
Via Jak/STAT:
Decrease glucose uptake (keeps GLUT4 intracellular)
48
GH effect on liver?
Via JAK/STAT:
```
Increase RNA synthesis
Increase protein synthesis
Increase gluconeogenesis
Increase IGF BP
Increase IGF
```
49
IGF-1 effect on bone, heart, lung, chondrocytes?
Increase protein synthesis
Increase RNA/DNA synthesis
Increase cell size/number
GROWTH
50
IGF-1 effect on muscle? ****
Increase amino acid uptake
Increase protein synthesis
(it acts like insulin at muscle)....but it is INSULIN DEPENDENT...glut 4...need energy to power the growth of muscle!
51
Diabetes type 1 eats a steak. What will happen?
GH is released (free AA's) but no insulin, so no IGF-1. So starvation amidst plenty.
52
What is the rate limiting step of steroid hormone synthesis? What hormone regulates this step?
Steroidogenic regulatory protein (StAR), which transfers the free cholesterol from the outer to the inner mitochondria. This is RLS. This is promoted by ACTH.
53
What does does p450cc catalyze?
p450cc is desmolase.
| Free cholesterol to pregnenalone.
54
Prednisone
More potent GC effect, than MR effect.
55
Why does prednisone not increase blood pressure?
Because it acts on GC receptors not MR.
56
Cortisol: MR or GR potency?
1:1
Equal potency for both! That's why we need 11-Beta-HSD2 to convert it to cortisone, lest it activates the MR receptor!
57
Which has a stronger GR activity: prednisone or methylprednisone?
Methylprednisone
58
What drug has zero MR relative potency?
Dexamethasone
59
What drug has more MR potency than GC potency?
Fludrocortisone
60
Fludrocortisone. 1st thought?
MR>>>>>>GR
61
Dexamethasone. 1st thought?
No MR potency! All MR!
62
Prednisone and methylprednisone. 1st thought?
GR>>>>MR. Methylprednisone is stronger than regular prednisone.
63
```
Which of the following will raise your BP the most?
A. Cortisol
B. Prednisone
C. Methylprednisone
D. Dexamethasone
E. Flurdocortisone
```
E
64
11BHSD2 is blocked by carbenoxolone. Or too much licorice. Effect?
Excess MR activation. High BP, high Na and H20 retention.
65
Local cortisol production by what enzyme?
11-beta-HSD1
| Novel DMT2 target
66
Blood from capsular artery sees steroid hormones in what order?
Mineralocorticoids, glucocorticoids, androgens, catecholamines (not a steroid hormone)
67
What are the direct and indirect ways that cortisol suppresses inflammation?
Direct: cortisol-GR directly sequesters NFK-B so it can't transcribe TNF-alpha
Indirect: Cortisol-GR increases transcription of IkB, which then sequesters NFK-B so it can't enter nucleus
68
Cortisol increases transcription of proteolysis via what factors?
E3 ubiquitin ligase
| MuRF-1
69
How do BOTH hypo and hyperthyroidism lead to goiter?
Hypothyroidism: low T3/T4 due to lack of iodine, or TPO defect, or hashimotos. Results in lack of negative feedback on TSH secretion from basophils in ant. pituitary, thus lots of TSH.
Hyperthyroidism: high T3/T4 due to too much stimulation by TSH or autoantibodies to TSH-R (grave's disease).
70
Why don't you want to use aspirin for thyroid storm?
Aspirin suppresses thyroid binding globulin, increasing T3/4 levels
71
2 types of parathyroid cells
Chief cells - make PTH
| Oxyphil cells - unknown function
72
Hashimoto's
Auto-antibodies destructive to thyroid tissue
73
KEY OBESITY STATISTICS
BMI>30 (at least 20% of population)
Waist:hip > 0.95 in men
Waist:hip > 0.85 in women
74
Metabolic syndrome X statistics
4 requirements
1. Dyslipidemia (TG>150mg/dl, HDL135/80)
3. Visceral obesity
(waist>40in in men, >35in women)
4. Insulin resistance (fasting glucose > 100mg/dl)
75
PPAR-gamma agonists
TZD - used for insulin resistance and T2DM
(aka avandia)
Induces differentiation of adipocytes, increase fat storage, and weight gain side effect.
76
Hypothalamic appetite modulators
Stimulators: Neuropeptide Y, AGRP
Inhibitors: aMSH, CART
77
Best measure for diabetes
HbA1C (glycosylated RBC)
78
In the follicular phase, what two hormones are inhibiting anterior pituitary release of FSH/LH?
Inhibin and estrogen from ovary
79
In the ovulatory phase, something special happens with estrogen
Surpasses threshold amount and switches from negative to positive feedback to ant. pituitary, promoting LH/FSH surge.
80
In the Luteal phase, the follicle reorganizes into the corpus luteum, which begins making...
E2 and progesterone. Strong negative feedback to anterior pituitary (LH/FSH) and hypothalamus (GnRH)
81
What marks the beginning of a new menstrual cycle?
absent hCG, and LH, E2, and progesterone, promotes sloughing of endometrium (bleeding/menses)
82
Theca cells (female) come from same progenitor as their male counterpart....
Leydig cells (spermeogenesis support)
Theca cells don't have aromatase...they help granulosa cells make estrogen.
83
Granulosa cells (female) come from the same progenitor as their male counterpart...
Sertoli cells
Granulosa cells make the estradiol because they have aromatase.
84
Female phenotype, no uterus
XXY klinefelters.
MIF from sertoli cells degraded mullein ducts.
85
Give an example of male pseudohermaphroditism
Phenotypically female, with testes.
86
If T too low in development
excess gonoadotropic signalling promotes scar tissue formation on testes
87
Larynx enlargement is due to action of
Testosterone
88
Where does in the seminiferous tubule does spermatogenesis occur, anatomically?
BASAL COMPARTMENT of seminiferous tubule --> blood testes barrier --> inner seminiferous tubule --> lumen of tubules
89
Are spermatogonia inside or outside the blood-testes barrier?
Outside! Once the first meiotic division starts, the spermatogonium turns into a "primary spermatocyte" that crosses the blood-testes barrier!
90
Leading cause of female infertility
Female infertility quadruples between 20 and 40 years old. Also:
PCOS (polycystic ovarian syndrome). Root cause of PCOS is insulin resistance and androgen production (causing infertility)...and increased conversion to estrogens (weight gain)....sleep apnea, hirsuitism...
91
Leading cause of male infertility
androgen deficiency: inadequate production or action of T, promotes poor spermatogenesis. Or defects in seminal tract. Idiopathic oligospermia.
Note: infertility doesn't mean impotence (erectile dysfunction)
92
What is the role of CRH during parturition?
CRH potentiates contracture response to prostaglandins and oxytocin.
93
Decrease in Progesterone/E2 ratio
promotes contractions
94
Increase in E2/Progesterone ratio
promotes contractions
95
Increase in Progesterone/E2 ratio
promotes quiescence
96
Decrease in E2/progesterone ratio
promotes quiescence
97
Inhibin B
secreted by follicular cells. negative regulation of LH/FSH
98
Inhibin A
secreted by corpus luteum. negative regulation of LH/FSH
99
Paracrine effect of inhibin, on theca cells
PROMOTES androgen production in inhibin cells. remember that inhibin lacks aromatase, which is why it makes androgens (androstenedione) for later aromatization at the granulosa cell
100
What is TCF72?
most highly associated genetic polymorphism...T2DM
101
what does insulin do to serum K and Pi levels?
Decreases K and Pi (increases uptake into the cell; indirect stimulation of Na/K pump)
102
Effect of insulin on HCO3- and pH?
increases HCO3-
| Increases pH
103
Effect of insulin on lipolysis and ketone bodies
Stops lipolysis, so no more substrates for ketone body synthesis, so no ketoacidosis and thus no left shift in equilibrium towards CO2,
104
AVP potentiates the effect of
CRH (think AVP pertains to stress)
105
Insulin counter-regulatory hormones
GH
Cortisol
Glucagon
Catecholamines
106
PCB
competes with thyroid hormone binding to TBG. Increases TH production
107
DES
Non-steroidal estrogen
| DES daughter tragedy
