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Endocrine > Things I don't know: Phys > Flashcards

Things I don't know: Phys Flashcards

1
Q

superior hypophysial arteries

A

supply pars tuberalis, median eminence, infundibulum

arise from internal carotid and posterior communicating artery of circle of Willis

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2
Q

inferior hypophysial artieries

A

supply pars nervosa

arise from internal carotid

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3
Q

primary capillary plexus

A

drain into hypophysial portal veins
arise from superior hypophysial arteries
give rise to secondary capillary plexus

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4
Q

11B-hydroxysteroid dehydrogenase 2

A
  1. converts cortisol to cortisone in cells where aldosterone is active
    kidney, colon, salivary gland
    cortisone does NOT bind aldosterone receptor
  2. local neg. feedback on cortisol, CRH and ACTH
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5
Q

permissive effects

A

TH/GC increase response of fat cells to Epi/NE ability to do lipolysis

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6
Q

second messengers

A

amplify and disperse signal of hormone once hormone binds the receptor

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7
Q

Factors that alter TBG levels

  1. increase
  2. decrease
A
  1. hepatitis, heroin, pregnancy

2. steroids (depends on type)

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8
Q

5’/3’ vs 5/3 monodeoiodinase

A

5’/3’: active T3 (outer iodine chopped off)

5/3: rT3 (inner iodine chopped off)

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9
Q

What can decrease uptake of I- into the follicular cell?

A

ClO-, TcO-, SCN

hypocholorite, technetium (oxidized), thiocynate

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10
Q

How does TSH (thyrotropin) increase TH secretion?

A
  1. increase Na/I symporter activity
  2. stimulates iodination of thyroglobulin
  3. stimuates conjugation of iodinated tyrosine to generate T4, T3
  4. increases endocytosis of iodinated thyroglobulin into follicular cells
  5. stimulates proteolysis of iodinated thyroglobulin in lysoendosomes
  6. increase T4, T3 into circulation
  7. exerts growth factor effects on thyroid cells (hypertrophy, hyperplasia)
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11
Q

glycogen synthase

A

glycogenesis
add activated UDP glucose (made from glucose to G1P) to glycogen
increased by: G6P
phosphorylation: inactive

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12
Q

glycogen phosphorylase

A 
glycogenolysis
releases G1P that can be dephosphorylated to glucose
activated by: stress (increase in AMP)
inhibited by: G6P
phosphorylation: active
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13
Q

gluconeogenesis

A

liver

glucose made from amino acids, lactate, FA oxidation products

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14
Q

rate limiting enzymes in gluconeogenesis

A
  1. phophoenolpyruvate carboxykinase (PEPCK)
  2. fructose-1,6-bisphosphatase (FBPase)
  3. glucose-6-phosphatase (G6Pase)
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15
Q

Order that we use energy stores (fed)

A
  1. circulating glucose
  2. glycogen breakdown
  3. gluconeogenesis
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16
Q

insulin receptor cascade

A
  1. receptor TK
  2. transautophaosphorlate itself
  3. PI3K binds
  4. PIP3 (second messenger) is generated
  5. recruit PDK1 (kinase)
  6. PDK1 and mTORC2 phosphorylate and activate Akt
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17
Q

Akt

A

INSULIN

  1. MOST important protein kinase in mediating insulin function
  2. phosphorylates and inactivates FOXO (decreases gluconeogenesis)
  3. activate mTORC1: protein synthesis
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18
Q

AS160 and RGC 1/2

A 
Akt activates (via insulin)
proteins that regulate activity of small GTPases involved in GLUT4 translocation
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19
Q

AMPK and GSK-3

A

phosphorylate glycogen synthase and inactivate it

inactivated by: INSULIN

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20
Q

phosphorylation of glycogen synthase and glycogen phosphorylase

A

glycogenolysis

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21
Q

dephosphorylation of glycogen synthase and glycogen phosphorylase

A

glycogenesis

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22
Q

protein phosphatase

A

removes phosphate from glycogen synthase

activated by: INSULIN

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23
Q

fructose-2,6-bisphosphate

A

increases in glycolysis

inhibits FBPase

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24
Q

FOXO

A

transcription factor forG6Pase and PEPCK

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25
Q

glucagon receptor cascade

A
  1. Gs
  2. AC
  3. cAMP
  4. PKA
    INCREASE blood glucose
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26
Q

PKA

A

GLUCAGON and ADRENALINE

  1. activates glycogen phosphorylase kinase to phosphorylate glycogen phosphorylase
  2. directly phosphorylates glycogen synthase
  3. inactivates PFK-2
  4. phosphorylates CREB
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27
Q

phosphofructokinase-2 (PFK-2)

A

generates fructose-2,6-bisphosphate (increases glycolysis, inhibits gluconeogenesis)
inactivated by PKA

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28
Q

CREB

A

transcription factor
activates transcription of PEPCK, FPBase, G6Pase (gluconeogenesis)
activated by PKA

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29
Q

glucagon works where

A

liver: gluconeogenesis, glycogenolysis

does NOT do glycolysis, muscle glucose oxidation

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30
Q

adrenaline works where/how

A

short term, rapid: glucose to blood for muscle
liver: gluconeogenesis, glycogenolysis
fat: lipolysis
muscle: glucose oxidation
activated by: direct sympathetic innervation, high levels of phenylethanolamine-N-methyltransferase

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31
Q

hormone sensitive lipase (HSL)
adipocyte triglyceride lipase (ATGL)
perilipin

A 
lipolysis
activated by (phosphorylated): adrenaline
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32
Q

long term glucose control during fasting

A

GH and cortisol

increase blood glucose during prolonged fast to get blood to brain

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33
Q

incretins (GLP-1 and GIP1)

A

gut

enhance insulin release

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34
Q

DDP-4

A

degrade incretins

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35
Q

order that we use energy stores (fasting)

A
  1. creatine phosphate
  2. glycolysis
  3. glycogenolysis
  4. gluconeogenesis
  5. fat oxidation
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36
Q

autonomic effects on insulin and glucagon

A

sympathetic: increase glucagon, less insulin
parasympathetic: increase insulin, less glucagon

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37
Q

How is the synthesis of steroid hormones regulated?

A

GPCR signaling

Gs (cAMP/PKA) or Gq (IP3)

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38
Q

What happens when aldosterone binds the mineralocorticoid receptor?

A

transcription

  1. Na/K pump: Na in, K out of body
  2. ENac: Na in
  3. SGK1: protein kinase that activates several transporters by post translation modification
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39
Q

renin

A

converts angiotensinogen to angiotensin I

increase: JG decrease stretch, increase sympathetic tone, decrease BP/BV

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40
Q

JG cells

A

secrete renin

when: decreased stretch, decreased glomerular flow, increased sympathetic activity

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41
Q

angiotensin converting enzyme

A

angiotensin I to II

42
Q

angiotensin II

A
  1. increased sm. muscle constriction
  2. increased salt reputake directly
  3. increase aldosterone
43
Q

cortisol

A

maintain blood glucose in times of fasting/stress for brain, resp. system, CV system
transcription of: PEPCK, pyruvate carboxylase, G6Pase
gluconeogenesis, glycogenolysis, lipolysis, muscle proteolysis
insulin resistance
increase B receptors: sensitizes tissue to EPINEPHRINE
TRANSCRIPTIONAL control ONLY
decrease: growth, immune, reproductive

44
Q

NE

A

low circulating levels (lower than needed for adrenergic response): utilized synaptically where local concentrations are high
only two times it can circulate in high enough concentrations to activate adrenergic receptors: HEAVY EXERCISE, PHEOCHROMOCYTOMA

45
Q

epi receptors

A

alpha1: Gq (IP3/Ca): vasoconstriction
alpha2: Gi (inhibits cAMP)
beta: Gs (cAMP/PKA): cardiac output, blood to muscle, glycogenolysis, gluconeogenesis, glycolysis, lipolysis

46
Q

night shift

A

increased cortisol, altered circadian

higher risk: DM, CV, sleep probs

47
Q

MC2R

A

Gs

receptor for ACTH

48
Q

AGTR1

A

Gq

angiotensin II receptor

49
Q

CRHR1/2 and ACTHR

A

CRH receptor and ACTH receptor
Gs
released by: stress
decreased by: cortisol, receptor desensitization, 11BHSD2

50
Q

How does chronic stress prepare the body for acute stress

A

increases B adrenergic receptors so that they are more sensitive to epinephrine

51
Q

Hormones needed at

  1. prenatal
  2. infantile
  3. juvenile (1-12 yrs)
  4. adolescent (F 10-14, M 12-16)
  5. adult
A

1 and 2: insulin

  1. GH, Insulin, T3, Vit. D
  2. add sex steroids to number 3
  3. limited growth
52
Q

GHRH receptor

A

Gs (PKA)

53
Q

somatostatin receptor

A

Gi

54
Q

Why does GH decrease with age?

A

decrease in GHRH secretion

55
Q

IGF-1 receptor

A

receptor TK

mTORC1: mediates muscle growth

56
Q

GH receptor

A

JAK/STAT

produce mRNA by binding DNA promoters

57
Q

GH

A

gluconeogenesis, lipolysis
protein synthesis
IGF-1 release

58
Q

IGF-1

A

muscle and bone growth

glucose uptake in muscle: promote glycogen and lipid storage

59
Q

hormones that enhance/decrease GH signaling

A
  1. insulin: fetal growth, IGF-1 secretion, protein synthesis
  2. TH: GH production, CNS development
  3. Testosterone/Estrogen: GH secretion at puberty, close epiphyseal plate, protein synthesis (T only)
  4. cortisol: inhibits GH release, protein catabolism
60
Q

TH and GH

A

REGQUIRED for GH synthesis

61
Q

Distribution of Ca
in body?
in plasma?
excretion?

A

body: 99% in bone
blood: 50% free, 40% protein bound, 10% anion bound
excretion: most in feces, little in kidney

62
Q

normal total serum Ca range

A

8.5-10.5 mg/dL

63
Q

Ca uses

A 
bone, tooth 
muscle contraction
AP
second messenger
cofactor
excitation-secretion (exocytosis)
64
Q

Pi uses

A 
energy (ATP, etc.)
second messenger
DNA/RNA, membranes
bone, tooth
phosphorylation of enzymes
intracellular anion
65
Q

Pi distribution
body?
plasma?
excretion?

A

body: 85% bone, 14% intracellular, 1% extracellular
plasma: 55% free, 10% protein bound, 35% cation bound
excretion: most urinary, feces also significant

66
Q

normal total serum phosphorus range

A

3-4.5 mg/dL

children: 4.5-6.5 mg/dL (active bone growth)

67
Q

How do you know whether Pi and Ca will be mineralized into bone or bone resorption?

A

bone deposition: Ca x PO4 greater than solubility product
bone resorption: Ca x PO4 less than solubility product
high plasma Ca and P: calcification in bone and soft tissue
low plasma Ca and P: bone resorption

68
Q

Why is it important to know concentration of intact PTH?

A

PTH is rapidly cleared from circulation

69
Q

What activates Vit D from 25 to 1,25

A

PTH

70
Q

osteoprotegerin

A

osteoblast
prevents RANKL from binding RANK
stimulated by: estrogen
inhibited by: PTH

71
Q

intermittent low dose PTH

A

increase bone formation

enhance proliferation and differentiation of osteoblasts

72
Q

What is the best indicator of Vit. D status?

A 
serum 25 (OH)D
calcifediol, calcidiol
73
Q

calciferol

A

vit. D

74
Q

cholecalciferol

A

vit. D3

75
Q

ergocalciferol

A

vit. D2

76
Q

calcitriol

A

active Vit. D
1, 25
increases: calbindin, epithelial Ca channels, Na/PO4 transporter
activates 24 alpha hydroxylase

77
Q

24, 25 dihydroxyvitamin D

A

inactive Vit. D

78
Q

calcifediol

A

25 Vit. D

79
Q

calcidiol

A

25 Vit D

80
Q

25 alpha hydroxylase

A

liver

vit. D3 or D2 to 25 (OH) Vit. D3

81
Q

1 alpha hydroxylase

A

kidney
25 to 1,25 Vit D.
inhibited by: Ca, FGF23
stimulated by: PTH

82
Q

24 alpha hydroxylase

A

kidney
25 to 24,25 Vit. D
stimulated by: Ca, FGF23, calcitriol

83
Q

FGF23

A

decrease: 1 alpha hydroxylase (decrease active Vit. D), Na/PO4 cotransporters in kidney (Npt2a/c), PTH
stimulates: 24 hydroxylase,
inactivates Vit. D
increased by: phosphate, calcitriol, PTH
causes: HYPOPHOSPHOTEMIA

84
Q

UV light role in vit. D

A

provitamin D (7-dehyrdocholesterol) to cholecalciferol

85
Q

how does Vit. D promote intestinal Ca and PO4 absorption?

A
  1. Ca enters cell through epithelial channels
  2. Ca binds calbindin: diffusion to basolateral membrane
  3. Ca-ATPasw and Na/Ca exchanger to move across basolateral membrane

increase Na/PO4 transporter

86
Q

How does HIGH vit. D effect bone resorption?

A

increase bone resorption

inhibits PTH

87
Q

Which bone cell has gap junctions for communication?

A

osteoblast

88
Q

Cbfa1

A

causes precursor to become osteoblast

89
Q

PHEX

A

secreted by osteoblasts

regulates amount of PO4 excreted by kidney

90
Q

osteocyte

A

comes from osteoblast
long cellular processes in canaliculi for communication: sense strain, repair
secrete GF to activate osteoblasts

91
Q

lining cells

A

former osteoblast
surface of bones
responsible for immediate release of Ca if blood Ca low
protect bone from chemicals
receptors for hormones, factors that induce bone remodeling

92
Q

which cells come from bone marrow derived

  1. mesenchymal progenitors
  2. hematopoietic progenitors
A
  1. osteoblast, osteocyte, lining cells

2. osteoclast (monocyte/macrophage)

93
Q

reserve cells

A

long bones
source of chondrocytes
slow proliferation

94
Q

flat chondrocytes

A

long bones
proliferate rapidly
secrete chondrocyte collagen and matrix to form cartilage

95
Q

hypertrophied chondrocytes

A

long bones

undergo apoptosis

96
Q

indian hedgehog

A

long bones
secreted by hypertrophied chondrocytes
cause secretion of PTHrp from round chondrocytes

97
Q

PTHrp

A

long bones

keeps flat chondrocytes in proliferating phase and delays hypertrophied stage

98
Q

sclerostin

A

bone remodeling
secreted by osteocytes
inhibits Wnt signaling in cells near surface

99
Q

What happens when a bone crack forms?

A
  1. osteocytes near crack undergo apoptosis
  2. osteocytes detect strain: secrete GFs, PGs, NO
  3. canopy forms: release stromal cells from sclerotin (inhibition factor)
  4. stromal cells generate pre-osteoblasts and M-CSF to help generate osteoclasts
  5. pre-osteoblasts: proliferate, Wnt signaling, ILs, bone morphogenic proteins, express RANKL
  6. formation of osteoclast: acid, cathepsin K
  7. IGF, TGF-B released
  8. osteoclast apoptosis
  9. pre-osteoblast into osteoblast that stop making RANKL and secrete OPG to block pre-osteoclast
  10. osteoblasts secrete osteoid and then mineralize it (months) then become lining cells, osteocytes, or apoptose
  11. accumulate minerals for years
100
Q

BMU (basic multicellular unit)

A

many spreading over bone in many places

forming and resorbing bone

101
Q

pancreatic enzyme secretion

A
  1. synthesis on rough ER
  2. hydrophobic leader seq. so that it can pass through the cisterna (membrane) of RER
  3. budded off into transitional elements
  4. in golgi: incorporated into vacuoles that concentrate enzymes until mature zymogen granule
  5. zymogen granule moves to the apical membrane and waits for a stimulus
  6. Ca is 2nd messenger that causes release
    all steps are ongoing except 6
    steps 3-5 require ATP
102
Q

pancreatic secretion

  1. cephalic phase (sham feeding)
  2. intestinal
A
  1. increase in enzymes but not much aqueous secretion
  2. major phase
    decrease in pH: secretin: release bicarb
    digestion products (FA and AA): I cells: CCK: vagovagal: enzyme secretion and bicarb secretion

Endocrine (7 decks)

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