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Endocrine > Physiology Highlights > Flashcards

Physiology Highlights Flashcards

1
Q

What form of peptide hormone:
• Enters the ER
• Exits the ER
• Exits the Golgi

A

Enters ER as PreProHormone, Exits ER as ProHormone, and Exits the Golgi as the Hormone

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2
Q

Thyroid Hormone needs to act on a receptor in the nucleus but is hydrophilic, so how does it get there?

A

Na+ exchanger

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3
Q

What hormones work via the cAMP signaling pathway?

A

FLAT ChAMP + Calcitonin, GHRH, and Glucagon

FSH
LH
ACTH
TSH

CRH
hCG
ADH (V2 receptor)
MSH
PTH
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4
Q

What hormones work via the Gq pathway?

A

GOAT HAG

GnRH
Oxytocin
ADH (V1 receptor)
TRH

Histamine (H1 receptor)
Angiotensin II
Gastrin

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5
Q

What molecules signal through the growth hormone pathway?

A

Insulin and Growth Factors (IGF-1, FGF, Prolactin, PDGF, EGF)

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6
Q

What molecules signal through the JAK/STAT pathway?

A

PIGGET

Prolactin
Immunomodulators (IL's, Cytokines)
GH
G-CSF
Erythropoietin
Thrombopoietin
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7
Q

What side of a follicular cell faces the blood vessel?

A

Basal Side of Follicular Cells Faces the blood Vessel

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8
Q

What is the major product of the thyroid?

A

T4

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9
Q

How does thyroglobulin that has undergone internal rearrangement and endocytosed get cleaved to T3 and T4?

A

Fusion of the thyroglobulin containing lysosome with an endosome allows for this

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10
Q

T or F: Iodine entry into follicular cells is ATP dependent

A

True, it requires co-transport with sodium (Sodium gradient created by Na/K ATPase

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11
Q

What is the only endocrine organ requiring a trace element to operate?

A

Thryoid

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12
Q

What is the half life of T4?

• T3?

A

T4 half life is 8 days

T3 half life is 24 hours

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13
Q

Where are type I 5’/3’ monodeiodinases found?

A

Liver
Kidney
Thyroid

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14
Q

Where are type II 5’/3’ monodeiodinases found?

A

Brain
CNS
Placenta

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15
Q

Where are type I and III 5/3 monodeiodinases found?

A

All tissue

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16
Q

What is the only organ to express deiodinase during starvation?

A

Brain - always expressed

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17
Q

What happens to thyroid hormone in the gut?

A

Enterohepatic Cycling (due to glucoronidases of bacteria)

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18
Q

What conditions lead to an increase in thyroid binding globulin?

A

Pregnancy

Oral Contraceptives

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19
Q

What conditions lead to a decrease in thyroid binding globulin?

A

Hepatic Failure

Steriods

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20
Q

What are the 5 main actions of Thyroid hormone?

A
  1. Increased Metabolic Rate
  2. Heart Effects
  3. Catabolic Effects
  4. Bones
  5. CNS
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21
Q

How does thyroid hormone raise the basal metabolic rate?

A

Increased Na/K ATPase

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22
Q

How does thyroid hormones causes heart problems?

A

Increased O2 consumption by tissue - increased workload

Increased Ca2+ ATPase

Increased Beta1-receptors

Increased Myosin

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23
Q

What is the role of Thyroid Hormone in bone development?

A

Synergistic Effect with GH to Mature Bones

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24
Q

What type of neurons are in the Hypothalamic-Hypophyseal tract?

A

Magnocellular Neurons - large and unmyelinated

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25
Q

What molecules are provasopressin and prooxytocin cleaved into?

A

Provasopressin => Vasopressin + Neurophysin I

Prooxytocin => Oxytocin + Neurophysin II

**These are cleaved on release of the hormone from the posterior pituitary

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26
Q

What is the most important hormone for growth during puberty?

A

Growth hormone

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27
Q

What anterior pituitary cell type is most likely to get injured in a traumatic event?
• 2nd most likely?

A

Somatotrophs

Lactotrophs would be the 2nd most likely

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28
Q

What anterior pituitary hormone is regulated by ultrashort, short, and long loop feedback?

A

GH
Ultrashort => GHRH negative on hypothalamus
Short => GH negative on hypothalamus
Long => IGF-1 from liver onto hypothalamus

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29
Q

What are some non-TRH promoters of prolactin?

A

Suckling
Estrogen
Oxytocin
AVP

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30
Q

What are some non-dopamin inhibitors of prolactin?

A

Bromocriptine

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31
Q

T or F: somatostatin is a negative regulator of TSH release

A

True

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32
Q

Is there any long-loop regulation in the prolactin signaling system?

A

no - only short loop

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33
Q

Is there any short loop regulation in the thyroid signaling system?

A

no - only long loop

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34
Q

What cells in the male and female release inhibin B?

• what is the effect of this compound?

A

Sertoli Cell in men secrete Inhibin B

Granulosa Cells in women secrete Inhibin B

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35
Q

What are the negative regulators of GnRH release?

A
  • Testosterone and DHT = men
  • Androsteredion = females
  • PROLACTIN = BOTH
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36
Q

What are the Stimuli for Growth Hormone?

A
  • Hypoglycemia
  • Starvation
  • Decreased Fatty Acids
  • Arginine (amino acids in general)
  • Estrogen/Testosterone
  • STAGE III and IV sleep
  • ALPHA adrenergic agonists
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37
Q

What are some Inhibitory Factors for Growth Hormone Secretion?

A
  • Hyperglycemia
  • Hyperlipidemia
  • Obestity
  • Senescence
  • SOMATOSTATIN
  • Somatomedins (IGF-1)
  • GH
  • BETA adrenergic agonist
  • PREGNANCY
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38
Q

What is the effect of GH on all organs?

A

• Increased Amino Acid uptake and Protein Synthesis

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39
Q

What is the effect of GH on skeletal m and Adipose tissue?

A

DECREASED glucose uptake
INCREASED lipolysis

= DIABETICOGENIC EFFECT

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40
Q

During what times is prolactin release from pituitary not inhibited by Dopamine?

A

Pregnancy and Lactation

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41
Q

Where does dopamine that inhibits prolactin release come from?

A

Dopaminergic Neurons in the Hypothalamus

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42
Q

What are the primary 3 roles of prolactin in the body?

A

Breast Developement
Lactogenesis
Inhibition of Ovulation (via inhibition or GnRH)

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43
Q

What is required for the uterus to be responsive to the oxytocin released during delivery?

A

Estrogen is needed to upregulate oxytocin receptors on the uterus so that it can act to induce contraction

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44
Q

What are 3 factors that inhibit the release of ADH from the posterior pituitary?

A

EtOH
ANP
low Osm

45
Q

What is secreted by the F-cells in the pancreas?

A

Pancreatic Polypeptide

46
Q

What is secreted by the epsilon cells in the pancreas?

A

Ghrelin

47
Q

What is the arterial blood supply of the pancreas?

A

Splenic, Superior Mesenteric, and Pancreaticoduodenal

48
Q

What is the venous drainage of the pancreas?

• Why is this important?

A

Portal Vein is the final destination for the veins that drain the pancreas

Importance:
• 50% of secreted insulin is taken out of the blood on 1st pass in the liver

49
Q

What are the 3 methods of Cell-Cell communication in the pancreas?

A
  • Gap Junctions (alpha and beta cells)
  • Fenestrations
  • Innervation
50
Q

What is the half-life of insulin and C-peptide?

A

Insulin - 3 min

C-peptide - 19 min

51
Q

What is the release pattern of insulin like?

A

Biphasic with 10x increase in insulin following a meal (5min later) and another increase will take place after about 20 min if hyperglycemia is still uncorrected

5% of insulin is in vesicles ready to go, 95% is not; the 95% leads to potential for phase II secretion

52
Q

What type phase of insulin release do type II diabetics depend on?

A

T2DM uses phase II

53
Q

Amylin

• Function and Cell type

A

Amylin:
• Lowers Glucagon
• Decreases Gastric Emptying

Beta-cells secrete amylin

54
Q

Pancreatic Polypeptide

• Function and Cell Type

A

PP
• Increases Gastrin
• Decreases Motility

Cell Type
• F-cells

55
Q

What is the stimulus for Pancreatic Polypeptide secretion?

A

Meal
Excercise
Vagal Stimulation

56
Q

What are the stimuli for Somatostatin release?

A
  • All Nutrients (fat, carbs, protein)
  • GI hormones
  • Glucagon
  • Beta-adrenergic agonists
57
Q

What is the inhibitor or somatostatin release?

A

Insulin

58
Q

When are incretins secreted?

A

When there is glucose in the small intestine

59
Q

What are the Stimuli for Glucagon Release?

A
  • HypOglycemia
  • Protein Rich Meals (arginine, alanine)
  • CCK
  • Epinephrine - Beta action
  • Vagal Stimulation
60
Q

What are the stimuli for CCK release?

A
  • Ingested Fat
  • Fasting
  • Intense Excercise
61
Q

What inhibits Glucagon Release?

A
  • Insulin
  • Hyperglycemia
  • Somatostatin
62
Q

T or F: Glucagon acts on skeletal m.

A

False, this wouldn’t make sense, the goal of glucagon is to get glucose to the muscles not to steal glucose from them

63
Q

What is the effect of insulin on fatty acids?

A
  • Increased Fatty acid synthesis
  • HIGH serum Triglycerides
  • Increased Cholesterol Synthesis in the liver
64
Q

What is the effect of insulin on amino acids?

A

Sequesters amino acids into the muscles

65
Q

What is the effect of insulin on potassium?

A

Up-regulated Na/K ATPase leading to increased K+ uptake into cells and DECREASED SERUM K+

*Remember insulin can also act on the hypothalamic satiety center

66
Q

What are some proteins/molecules that increase insulin secretion from Beta cells?

A

Glucagon
GLP-1
CCK
AcH

67
Q

What are some inhibitors of insulin secretion?

A

Somatostatins

Catecholamines

68
Q

How does insulin decrease fatty acid oxidation?

A
  • Increased Malonyl CoA synthesis
  • Malonyl CoA is an inhibitor of CPT
  • NO CPT = No entry to mitochondria for fatty acid oxidation
69
Q

What are the incretins and what is their effect?

A

GLP-1 and GIP are the increatins

Effect:
• Increased Insulin
• Decreased Glucagon
• Gastric Emptying Decreased

70
Q

What is the stimulus for incretin release?

A

Glucose in the bowel

71
Q

Where is GLUT-1 found?

A

Brain
RBCs
Cornea
Placenta

72
Q

Where is GLUT-2 found?

A

Beta Cells
Liver
Kidney
Small Intestine

73
Q

Where is GLUT-3 found?

A

Neurons and Placenta (allowed glucose to cross the BBB)

74
Q

Why do T1DM patients get hyperkalemic?

A

Low Na/K ATPase prevents sequestration of K+

75
Q

What percentage of Ca can be found in the bones, extracellular compartment, and intracellular compartment?
• what about Phosphate?

A

Ca:
• Extracellular - 0.1%
• Bone - 99%
• Intracellular - 1%

Phosphate
• Extracellular - 0.1%
• Bone - 85%
• Intracellular - 14%

76
Q

What Percentage of Extracellular Ca and Phosphate is Free, Anion Bound, and Protein bound?

A

Ca:
• 50% free
• 10% anion bound
• 40% protein bound

Phosphate:
• 55% free
• 35% cation bound
• 10% protein bound

**Phosphate being less protein bound makes it much more filterable by the kidney

77
Q

Where can the CaSR be found?

A
  • Parathyroid
  • Kidney
  • C cells of the Thyroid
  • Bone
78
Q

What is the most important hormone in calcium homeostasis?

A

• PTH

79
Q

What is the half-life of PTH?

• why is this important?

A

T1/2 of PTH = Very Short; so there are a lot of breakdown products but you want to measure IN TACT PTH

80
Q

What is the effect of the long term low-intermittent doses of PTH?

A
  • Increased Osteoblast Differentiation

* Decreased Apoptosis

81
Q

Wha the short term effect of PTH on osteoCLASTS?

• long term?

A
  • Increased Ca2+ permeability and Increased Ca2+ pump activity on the membrane
  • Lowers the Ca-P product by decreasing phosphate reabsportion long term to increase bone mineralization?
82
Q

What hormones act in the distal tubule to increase Calcium Reabsorption?

A

PTH and Calcitriol

83
Q

What hormones act in the Proximal Tubule to decrease phosphate reabsorption?
• which increase phosphate reabsorption?

A

PTH and FGF23 prevent reabsorption of Phosphate

Calcitriol increases Phosphate reabsorption

84
Q

What are alternative names for Vitamins D3 and D2?

A

D3 - Cholecalciferol

D2 - Ergocalciferol

85
Q

What is the best indicator of Vitamin D status?

A

Calcidiol

86
Q

What factors increase the action of 24 alpha hydroxylase?

• what is the purpose of this?

A

Only Positive Regulation via:
• Calcitriol
• Ca2+
• FGF23

87
Q

What factors increase the action of 1 alpha hydroxylase?

• which decrease the action of 1 alpha hydroxylase?

A

Increased Action:
• PTH

Decreased Action:
• Calcium
•FGF23

88
Q

What is the action of vitamin D on PTH synthesis?

A

Vit D decreased PTH synthesis in chief cells

89
Q

What cells release Calcitonin and what is its action?

A

Parafollicular C cells produce calcitonin which leads to:
• Decreased Osteoclast activity
• Decreased Renal reabsorption of Ca2+
• Decreased Phosphate Reabsorption

90
Q

What is the main physiologic role of calcitonin?

A

• Protects against calcium loss in periods of Ca2+ mobilization like pregnancy and Lactation

Overall plays a pretty small role in calclium regulation in adults

91
Q

What feedback relationship of Vitamin D and FGF23?

A

• Vitamin D increases FGF23 synthesis both directly and through its action of increasing serum phosphate

92
Q

What is the feedback relationship of PTH and FGF23?

A
  • PTH does negative feedback on FGF23 indirectly by decreasing serum phosphate
  • FGF23 has a direct inhibitory effect on PTH synthesis in cheif cells of the parathyroid
93
Q

What is the difference in venous drainage of the right and left adrenals?

A

Right Adrenals drain directly into the IVC via the Right Suprarenal vein

Left Adrenals drain into the Left Renal Vein via the Left Suprarenal vein before draining into the IVC

94
Q

What vessel shunts oxygenated blood from the zona glomerulosa to the medulla?

A

Medullary Arteriole

95
Q

What are the linear vessels that run through the zona fasiculata?

A

Cortical Sinuses

96
Q

What layer of the Adrenal Cortex has cells with large Smooth ERs?

A

Granulosa

97
Q

In what layer of the adrenal cortex are you likely to see lipid droplets?

A

Fasiculata

98
Q

What is the main controller of catacholamine release from the adrenal medulla?

A

Sympathetic NS

99
Q

When is cortisol released in the highest amounts?

A

Just before waking

100
Q

What receptor for ACTH is found on the adrenal medulla?

A

Melanocyte Type 2 Receptor (MC2R) - this is a Gs receptor using cAMP by defn

101
Q

What are the 2 controllers of aldosterone release from the cortex?

A

K+ (via direct effects on Ca2+ channels on cell membrane) and Angiotensin II (via Gq path)

102
Q

What is the effect of Aldosterone?

A
  • Increased K+ excretion
  • Increased Na+ retention
  • Decreased H+ in plasma
103
Q

What enzyme does licorice act on?

A

• 11 beta hydroxysteroid dehydrogenase 2

104
Q

What is the half-life of aldosterone?

• glucocorticoids (cortisol)?

A

Aldosterone - 15-20 min

Glucocorticoids - 60-70 min

105
Q

What does aldosterone get metabolized to in the LIVER?

A

• Tetrahydrogluconoride

106
Q

What are the 6 major effects of Glucocorticoids?

A
  1. CNS alterations
  2. Increased Gluconeogenesis
  3. Anti-inflammatory/Immunosuppressive Effects
  4. Increased Vascular Response to Catecholamines
  5. Decreased Bone
  6. Increased GFR
107
Q

What CNS effects do glucocorticoids have?

A
  • Decreased REM
  • Increased Slow Wave Sleep
  • Increased Wake Time
108
Q

What processes take place so that glucocorticoids can increase gluconeogenesis?

A

Anti-Insulin Effects:
• Increased Lipolysis (increased ketone bodies) => via permissive effects with GH
• Increased Muscle Breakdown
• Decreased Peripheral Glucose Use

109
Q

What is the importance of Glucocorticoids in the vascular response to catecholamines?

A

PERMISSIVE EFFECTS with catecholamines from increased alpha-1 receptors

Endocrine (4 decks)

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