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Endocrine System > Liver and Pancreas > Flashcards

Liver and Pancreas Flashcards

1
Q

What is the main function of the liver?

A

to maintain plasma glucose levels

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2
Q

What four hormones are secreted from the liver?

A
  1. Angiotensinogen
  2. Erythropoietin
  3. Thrombopoietin
  4. Insulin-like Growth Factors 1&2 (IGF-1, IGF-2)
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3
Q

Do patients with hypertension exhibit high or low levels of angiotensinogen?

A

high

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4
Q

How is angiotensinogen activated to angiotensin II?

A
  1. at the juxtaglomerular cells of the afferent arteriole, low blood pressure and low renal perfusion are sensed.
  2. Also sensed at the JG cells are low sodium due to a low GFR and low adenosine secretion
  3. these two things stimulate the JGA to secrete renin
  4. renin converts angiotensinogen to angiotensin I
  5. at the lung ACE converts angiotensin I to angiotensin II.
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5
Q

What does angiotensin II do?

A
  1. increased vasoconstriction in systemic arterioles
  2. increase aldosterone secretion (uptake of Na and water, increased secretion of K)
  3. increased secretion of ADH
  4. Increased Na+ reabsorption at PCT
    * *all effects work to increase the system blood volume and sodium concentration
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6
Q

What stimulates an increased level of angiotensinogen in the plasma?

A
  1. presence of glucocorticoids (cortisol, aldosterone, corticosterone)
  2. thyroid hormones (T3 & T4)
  3. presence of estrogens (estrone, estradiole, and estriol)
  4. cytokines
  5. angiotensin II
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7
Q

What organs does aldosterone work on?

A

kidney, colon and ileum

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8
Q

What makes erythropoietin?

A

synthesized and secreted by the liver and kidney

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9
Q

What is EPO?

A

glycoprotein/cytokine that stimulates erythrocyte precursors in bone marrow to being maturing into RBCs (erythrocytes)

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10
Q

Where is the principle site of EPO synthesis in the fetal stages of development (up to 32 weeks)?

A

the perisinusoidal Ito cells of the liver

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11
Q

What is the principle site of EPO synthesis after fetal development?

A

in the interstitial fibroblasts in the kidney in close association with peritubular capillaries and tubular epithelial cells

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12
Q

Does the liver still contribute to EPO production in adulthood?

A

Yes the liver and the kidney contribute, however the kidney is the PRINCIPLE site.

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13
Q

What is HIF-1?

A

hypoxia-inducible factors that are transcription factors present on the EPO synthesizing cells in the liver and kidney. The amount of HIF-1 regulates how much EPO production takes place. HIF-1 is constitutively produced.

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14
Q

How is EPO production regulated?

A

On each EPO synthesizing cell in the liver and kidney there are HIF-1’s. In situations of hypoxia, there are more HIF-1’s present leading to increased rate of production of EPO and eventually more differentiation. In situations of normal O2 or hyperpoxia, less HIF-1 is produced leading to a decreased rate of EPO synthesis and decreased rate of differentiation.

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15
Q

Where does erythropoeitin bind and what does it stimulate?

A

EpoR on progenitor cells and activates JAK2 cascade. Binding stimulates erythrocyte differentiation.

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16
Q

Where is EpoR found?

A
  1. Bone marrow

2. peripheral/central nerve cells

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17
Q

What are some other biological functions of EPO?

A
  1. brain’s response to neuronal injury

2. wound healing

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18
Q

What is the main function of thrombopoietin?

A
  • regulation of the number of platelets in whole blood (normal platelet count is 300,000)
  • regulates proliferation and survival of megakaryocytes and differentiation of megakaryocytic into platelets.
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19
Q

What is thrombopoietin (TBO) and where is it made?

A
  • cytokine
  • made in the liver parenchymal and sinusoidal endothelial cells, bone marrow stromal cells
  • made in the kidney at the PCT
  • striated muscle cells
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20
Q

Up to 32 weeks gestation, where are the major sources of TBO?

A

kidney and the striated muscle

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21
Q

Post gestation, where are the major sites of TBO production?

A

liver and bone marrow, but some production still takes place in the kidney and the striated muscle

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22
Q

What increases the production of TBO in the liver and bone marrow?

A

the presence of interleukin 6 (IL-6)

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23
Q

Describe the feedback of TBO?

A

TBO plasma concentrations is controlled by platelets. In the platelets plasma membrane there is a receptor called the mol receptor (CD110. Once TBO binds this receptor, it is catabolized, thus lowering the plasma concentrations of TBO. ONLY FREE TBO STIMULATES MEGAKARYOCYTES. So, if lots of platelets, don’t need anymore differentiation. TBO gets catabolized by platelets at a higher rate meaning less megakaryocytic stimulation and thus less platelet production. The opposite occurs when there are low platelet counts, leading to an increase in megakaryocyte stimulation.

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24
Q

What are the stages of platelet differentiation?

A
  1. Megakaryoblast
  2. promegakaryocyte
  3. megakaryocyte
    - serial mitotic divisions without cell division
    - cytoplasm maturation (increased granules and channels)
  4. megakaryocyte sheds platelets into the sinusoids of bone marrow
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25
Q

What is Insulin-Like Growth Factors (1&2)?

A

are endocrines and target tissues in a paracrine/autocrine fashion
IGF-1: main juvenile and growth promoting factor following gestation
IGF-2: main growth promoting factor during gestation

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26
Q

Where is IGF synthesized?

A

liver

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27
Q

What stimulates IGF synthesis?

A

Presence of GH. (hypothalamus releases GHRH, which causes anterior pituitary to release GH which stimulates the liver to produce IGF-1 and 2)

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28
Q

What inhibits IGF synthesis?

A
  1. poor nutrition
  2. GH insensitivity or lack of GH receptors
  3. failures in the downstream pathway after GH
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29
Q

What does IGF-1 bound to?

A

IGF-BP (binding proteins). There are 6 different types and approximately 98% of IGF-1 is bound to an IGF-BP.

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30
Q

What is IGF-BP-3?

A

the most abundant protein and accounts for 80% of all IGF binding. It binds IGF-1 in a 1:1 ratio.

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31
Q

How does IGF-1 act on its target tissues?

A
  1. on target tissues there is a receptor called IGF1R (tyrosine kinase) and IGF-1 binds to this receptor
  2. binding activates a signaling cascade for AKT signaling pathway (stimulator of cell growth and proliferation as well as inhibitor of apoptosis)
  3. tyrosine kinases can activate many pathways, a common one being the PI3K and mTOR pathway (phosphatidylinositol-3 kinase and rapamycin)
    * *similar pathway is followed by IGF-2
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32
Q

What are the systemic effects of IGF-1 and IGF-2?

A
  • causes body growth and maintenence in the skeletal muscle, cartilage, bone, liver, kidney, nerves, skin, hematopoietic cells and lungs
  • can also regulate nerve cell growth and development, regulate neural cellular DNA synthesis
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33
Q

What are the symptoms if there is a deficiency of HGH or IGF-1?

A

short stature

34
Q

How can you treat GH deficiency?

A

give patients recombinant HGH and you will see an increase in size

35
Q

What is Laron’s Syndrome and how do you treat it?

A
  • deficiency in IGF-1 and patients are smaller but everything is formed correctly. (different from being a midget).
  • can treat with recombinant IGF-1 but they must receive the treatment before onset of puberty
  • most common in Ecuador
36
Q

Where are estrogens modified?

A

In the liver

37
Q

How are estrogens modified?

A

In the liver, 50% of the estrogens (3 of them, estradiole estrone and estriol) are conjugated into water soluble compounds. They are conjugated with glucuronides, sulfates and thioether. These conjugated compounds are then secreted from the liver in the GI tract via bile and feces, or can be secreted into the plasma when they go to the kidney and get excreted.

38
Q

What happens to thyroid hormone in the liver?

A

T4 is converted to T3

39
Q

What happens to Vit. D in the liver?

A

D2 and D3 are converted to precursor for calcitriol (25-dihydrozycholecalciferol)

40
Q

What are the endocrine and exocrine portions of the pancreas?

A

Exocrine: digestive enzymes (98-99% of mass)
Endocrine: Islets of Langerhans (1-2% of mass)

41
Q

How much blood flow do the islets receive?

A

10-15% of total pancreatic flow

42
Q

What are the 8 main types of endocrine cells of the pancreas?

A
  1. alpha cells (20% of islet cells)
  2. beta cells (65%)
  3. D (delta) cells (10%)
  4. F (PP) cells (5%)
  5. Epsilon cells (1%)
  6. D1 cells
  7. EC cells
  8. G cells
43
Q

What do alpha cells of the pancreas secrete?

A

glucagon

44
Q

What do beta cells of the pancreas secrete?

A

insulin

45
Q

What do D cells of the pancreas secrete?

A

somatostatin

46
Q

What do F (PP) cells of the pancreas secrete?

A

pancreatic polypeptide (PP)

47
Q

What do epsilon cells of the pancreas secrete?

A

ghrelin

48
Q

What do EC cells of the pancreas secrete?

A

serotonin, secretin, motilin, substance P

49
Q

What do G cells of the pancreas secrete?

A

gastrin-but usually only found in fetal islets.

50
Q

What do D1 cells of the pancreas secrete?

A

vasoactive intestinal peptide. Found in the parenchyma as well as the islets

51
Q

What is Z-E syndrome?

A

presence of G cells in the pancreas secreting gastrin. Leads to uncontrolled gastrin secretion. Also called gastrinema

52
Q

How does blood and hormones travel?

A

Secreted from cells in the pancreas and then flows from the innermost cells to the outermost cells and drains into hepatic portal circulation so the liver gets all the hormones first. Cells are connected by gap junctions

53
Q

What is the structure of insulin and how is it made?

A

Made in the Beta cells and is two chains linked by disulfide bridges.

  1. Insulin is synthesized as a large molecule that gets proteolysed to preproinsulin then proinsulin and then insulin+ c peptide.
  2. insulin and c-peptide are both active
54
Q

What is the function of c-peptide?

A

makes e-NOS, endothelial nitric oxide synthase

55
Q

What is the main function of insulin?

A
  • stimulates the liver hepatocytes to store glucose as glycogen.
  • acts on carbs, proteins and fats
  • Insulin reaches the liver first where it undergoes endocytosis. The receptor and insulin are then degraded by IDE (insulin degrading enzyme)
56
Q

How are beta cells stimulated leading to the release of insulin?

A
  1. Some glucose enters the beta cells via GLUT 2 transporters
  2. catabolism of glucose leads to K+ channels to close
  3. beta cell depolarizes
  4. Ca channels are opened triggering insulin release via exocytosis
57
Q

What stimulates insulin release?

A
  1. high plasma glucose
  2. FFA (16-18 chain length)
  3. Amino Acids (esp arginine)
  4. GI hormones (gastrin, secretin, CCK, incretins GIP and GLP)
  5. acetylcholine and sulfonylurea
58
Q

What inhibits insulin release?

A
  1. catecholamines (NE and E via alpha receptors)

2. somatostatin

59
Q

What are the target tissues of insulin?

A
  1. Liver
  2. skeletal muscle
  3. adipose tissue
60
Q

How does insulin stimulate cells of target tissues?

A
  1. insulin binds to beta subunits of tyrosine kinases
  2. binding activates the tyrosine kinase
  3. activates insulin receptor substrate (IRS) and cascades
  4. leads to DNA and RNA expression and synths of more GLUT1-GLUT4 transporters in the plasma membrane
61
Q

How does insulin act on carbohydrates?

A
  1. plasma glucose increases leading to greater insulin release
  2. insulin enters the blood and interacts with target organs
  3. preformed glucose carriers are inserted into the plasma membrane of target tissue
  4. causes a decrease in plasma glucose and an increase in glycogen storage in the liver, increased skeletal muscle glycogen storage, and increased glycolysis to use glucose up and make energy, thus also lower blood glucose levels.
62
Q

What are the effects of increased insulin on glucose metabolism?

A
  1. increased glycogen synthesis and storage
  2. activation of glycogen synthase, glucokinase and phophofructosekinase
  3. inactivation of glycogen phosphorylase and glucose 6 phosphate
63
Q

How can you test if someone is diabetic?

A

Give them 75-100grams of glucose. If after 2 hours their glucose levels are still really high, then they don’t have effective insulin or the insulin just isn’t present (type I vs type II)

64
Q

What happens if plasma glucose levels fall too low?

A

below 50mg/dL then get CNS impairment resulting in seizures and possible death

65
Q

What prevents insulin from lowering the blood glucose to levels lower than 50mg/dL?

A

anti-insulin hormones such as GH, glucagon, T3, T4, epinephrine, cortisol, all work to increase glucose levels. this results in the normal sharp increase in glucose levels after a meal followed by a slight undershoot after the meal.

66
Q

How does insulin affect lipids?

A
  1. increased lipogenesis and inhibition of lipolysis.
  2. promotes storage vs usage since glucose is at a high
  3. increases TG synthesis from FFA, intermediates from increased glycolysis, and via acetyl Co-A carboxylase which makes TG de novo from excess glucose
  4. fatty acid synthase is stimulated
    hormone sensitive lipase inhibited
  5. decreased beta oxidation (don’t need more energy, blocks action of glucagon)
  6. increased lipoprotein lipase (adipose takes up FFA and stores them)
67
Q

How does insulin affect proteins?

A

increase protein anabolism and inhibited protein catabolism.

  • increased AA transport into cells
  • increased transcription and translation and synthesis of new ribosomes
  • decreased lysosome activity
68
Q

What are some other random effects of insulin?

A
  • increased K+, phosphate and Mg into cells leading to cardiac pathologies due to hypokalemia. Occurs because insulin increases NaKATPase activity especially in skeletal tissues, so K+ pumped into cells.
  • thermogenesis
  • decreased appetite due to less peptide Y formation
69
Q

What is the main function of glucagon?

A

to raise blood glucose when hypoglycemic. Act by increasing uptake of AA to feed into gluconeogenesis and factor protein catabolism to make more glucose. Also results in an increased urea formation as a byproduct of the AA catabolism

70
Q

What increases glucagon release?

A

increase AA (especially arginine)
increase ACh
Increase NE and E
normal insulin levels are necessary for alpha cell sensitivity to glucose

71
Q

What decreases glucagon release?

A

somatostatin, FFA, insulin

72
Q

How does glucagon influence fat metabolism?

A
  1. breaks down TG into FFA and glycerol via hormone sensitive lipase
  2. FFA used for beta oxidation in mt.
  3. increased lipolysis to make energy and increase in ketones in the blood?
73
Q

When is somatostatin secreted?

A

When glucagon is high and there is elevated plasma glucose levels.

74
Q

What inhibits somatostatin?

A

insulin

75
Q

What is the role of somatostatin?

A
  • acts as a paracrine to inhibit insulin AND glucagon

- decreases rate of digestion and absorption of nutrients

76
Q

What stimulates pancreatic polypeptide release from PP cells (F cells) of the pancreas?

A
  • high blood protein
  • fasting
  • exercise
  • acute hypoglycemia
77
Q

What does PP do?

A

inhibits exocrine pancreatic secretion, gall bladder contraction, bile secretion, ileal motility.
**anything that slows down digestion.
increases colonic motility

78
Q

What does VIP do?

A

vasoactive intestinal peptide:

  • inhibits release of gastrin and HCl
  • Stimulates secretion of water and electrolytes form the SI and LI
  • Increases chief cell secretion of pepsinogen
  • relaxes GI tract sphincters
  • slows intestinal transit time
  • increases plasma glucose
79
Q

What do EC cells secrete and what do each of the hormones do?

A

Secretin: increases HCO3- secretion in pancreas and pancreatic enzyme secretion
Motilin: increases gastric and intestinal motility
Substance P: increases pancreatic flow and bicarb and amylase secretion

80
Q

What does ghrelin stimulate?

A
  • causes hunger by stimulating the hypothalamic hunger centers.
  • increase appeal go high calorie foods
  • accumulation of lipids in visceral fatty tissue
  • GH release

Endocrine System (16 decks)

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