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Physiology > Endo 3 > Flashcards

Endo 3 Flashcards

1
Q

what is Ca2+ important for?

A
  • membrane stability
  • neuronal transmission (depolarization threshold)
  • bone structure/ muscle function
  • blood coagulation
  • hormone secretion
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2
Q

what is phosphate important for?

A
  • cellular energy (ATP)
  • nucleic acid backbone
  • intracellular signaling pathways (activation/deactivation of enzymes)
  • bone structure
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3
Q

what is worse- hypocalcemia or hypophosphatemia?

A

hypocalcemia- muscle tetany- depolarization threshold is lowered, becomes easier to depolarize membrane with less calcium in extracellular space

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4
Q

what often causes hyperphosphatemia?

A

a “crush” injury of soft tissue which releases phosphate (10x more phosphate than Ca2+ in soft tissue)

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5
Q

describe the Ca2+ and Pi in plasma

A

Ca2+ - 10 mg/dl- 50% ionized, 45% albumin-bound, 5% complexed (albumin levels can give idea of Ca2+)
Pi- 4 mg/dl- 84% ionized, 10% bound

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6
Q

2 main regulators of Ca2+ and what they target

A
  1. Parathyroid hormone (PTH)- bone, kidney

2. Vitamin D - bone, kidney, gut

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7
Q

where is most of Ca2+ stored in body?

A

99% in bone- is exchangeable pool

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8
Q

how many parathyroid glands and where do you have them? main cell and what do they do? second type of cell?

A

4, on top of the thyroid gland

  • chief cell- synthesize PTH (parathyroid hormone)
  • oxyphil cell
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9
Q

what is PTHrP ?

A

Parathyroid related peptide ; mimics action of PTH in bone and kidney (binds receptor just as well, despite dissimilar structure) ; has no role at all for Ca2+ regulation under normal conditions; produced by a lot of tumors

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10
Q

which part of PTH is active? what has the longest half life?

A

N-terminal; C-terminal (not indicative of real PTH In blood)

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11
Q

what are the two parathyroid receptors?

A

PTH 1R- bone and kidney- GPCR (what also binds PTHrP, un-cleaved peptide)

PTH 2R- doesn’t bind PTHrP, binds active form

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12
Q

net effect of PTH

A

increase plasma Ca2+ levels, decrease phosphorus

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13
Q

key characteristics of osteoblasts

A
  • have PTH receptors
  • important for mineralization of bone; will extrude Ca2+/Pi from interior of bone (stored in hydroxyapeptite crystals vesicles inside osteoblasts); promote mineralization (hardening of bone)
  • derived from mesenchymal stem cells
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14
Q

osteoclasts

A
  • derived from HSCs, make precursors, not mature/active until mononucleated cells come together to form a multi-nucleated cell
  • do NOT express PTH receptors AT ALL
  • all PTH actions are happening indirectly through osteoblasts
  • important for breaking down bone
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15
Q

osteocytes

A
  • bone matrix
  • terminally differentiated from osteoblasts
  • communicate with osteoblasts to shuttle ca2+ back and forth
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16
Q

steps of PTH action

A

1) PTH stimulates osteoblasts to release M-CSF
2) M-CSF acts on its two targets- HSCs to make more osteoclast precursors, and stimulates osteoblasts to secrete RANK-L
3) RANK-L binds to RANK on osteoclast precursors, activating them to mature status
4) mature osteoclasts secrete hydrolytic enzymes which dissolves bone mineral and hydrolyzes bone matrix - releasing Ca2+ and Pi to systemic circulation
5) osteoblasts export Ca2+ and Pi into the extracellular space for bone mineralization - important for plasma homeostasis

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17
Q

what binds up RANK-L to keep it from activating RANK on osteoclast precursors? what inhibits/activates it?

A

OPG
inhibited by cortisol
activated by estrogen

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18
Q

what are the actions of PTH on the thick ascending limb of the kidney?

A

1) stimulates CYP1alpha to encode 1 alpha hydroxylase which converts 25-OH-vit D to its active from (1,25-(OH)2-vit D
2) stimulates Ca2+ channel insertion into apical membrane of distal tubule

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19
Q

what is the relationship between serum calcium and serum PTH?

A

low Ca2+, high PTH

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20
Q

three places that have the calcium sensing receptor

A

1) chief cells of parathyroid gland
2) kidney tubules
3) C-cells that secrete calcitonin in thyroid

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21
Q

what two actions does ca2+ on CaSr in the parathyroid gland have?

A

1) inhibits transcription of PTH

2) breaks down PTH already made

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22
Q

what two actions does Vit D in the parathyroid gland have?

A

binds nuclear receptor (VDR) to

1) inhibit the synthesis of PTH
2) stimulate the transcription of CaSR

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23
Q

calciferol, cholecalciferol, calcidiol, calcitriol

A
  • calciferol- all types of vitamin D
  • cholechalciferol- vitamin D3- specifically from animal tissues/human skin; low affinity to receptors
  • calcidiol- 25-hydroxy-cholecalciferol (affinity for receptor is lower)
  • calcitriol- 1, 25-dihydroxy-vitamin D (activated by 1 alpha hydroxylase (activated by PTH))
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24
Q

3 targets of vitamin D

A

bone, gut, kidney

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25
Q

what does vit D do in bone

A

bone- osteoblasts and osteoclasts have VDRs; primary role is bone mineralization; VIT D breaking down old bone at expense of making new bone

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26
Q

what does vit D do in gut

A
  • increases transcellular Ca2+ absorption in duodenum by
    stimulating synthesis of Ca2+ channels and calbindin (controls free ionized Ca2+ levels inside cell)
  • stimulates Pi reabsorption from small intestine
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27
Q

what does vit D do in bone

A

bone- osteoblasts and osteoclasts have VDRs; primary role is bone mineralization (none= rickets); VIT D breaking down old bone at expense of making new bone

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28
Q

what is osteoporosis?

A
  • reduced bone density caused by glucocorticoid therapy, menopause, genetic, low Ca2+
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29
Q

what is hyperparathyroidism?

A
  • over activation of parathyroid gland due to hyperplasia/cancer/kidney failure (reduced vitamin D)
  • causes hyper-calcemia amd kidney stones
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30
Q

what does hypoparathyroidism cause?

A
  • hypocalcemic tetany

- Chvostek sign- twitching of facial muscles in response to tapping the facial nerve

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31
Q

what is rickets?

A

get unmineralized bone (soft bone) b/c you don’t have enough vitamin D, causes bowing of the legs (called osteomalacia in adults)
- get widened epiphyseal plates

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32
Q

what is pseudohypoparathyrodism?

A
  • defect in G-protein associated with PTHR
  • have low calcium, high PTH, high phosphate
  • also affects TSH, LH, FSH
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33
Q

parameters that change with PTH infusion

A

1) plasma Ca2+ rises
2) plasma Pi falls
3) tubular reabsorption of phosphate falls (TPR)
4) urinary hydroxyproline increases (enhanced bone resorption)

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34
Q

T/F Remove c-cells (calcitonin secreting cells in thyroid), you affect calcium levels in blood

A

false, but does inhibit osteoclast reabsorption

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35
Q

Is the pancreas a part of an endocrine axis? What makes up the endocrine pancreas?

A
  • NOT part of axis

- 3 major cell types clutered into groups- islets of langerhans- that don’t secrete into pancreatic duct

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36
Q

3 major cell types of endocrine pancreas

A

beta cells- 75%- synthesize and secrete insulin (“beta cell mass”)
alpha cells- 25%- synthesize and secrete glucagon
delta cells- 5%- synthesize and secrete somatostatin

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37
Q

major and minor pancreatic hormones

A

insulin- anabolic hormone
glucagon- catabolic hormone- get glucose back into blood

somatostatin
amylin (same vesicle as insulin)
pancreatic polypeptide
ghrelin

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38
Q

arrangement of alpha and beta cells in humans

A

alpha cells- glucagon- on outer edges, line capillaries

beta cells- insulin- in the middle (“the core”)

39
Q

describe how blood flow in pancreas alters hormone secretion

A
  • arteriole feeds center of islet where the beta cells out, blood flows out
  • beta cells making insulin which will directly impact glucagon on outside (glucagon has no direct action on beta cell to inhibit insulin)
40
Q

describe the insulin gene; which part is insulin?

A
  • signal- B chain- C chain- A chain*
  • insulin is A and B peptide folded together
  • without cleavage of C chain, insulin cannot bind receptor
  • C peptide secreted with insulin, is good indicator of pancreatic function (is pancreas able to secrete insulin?)
41
Q

Steps for insulin release from pancreatic beta cell

A

1) glucose outside beta cell transported in by GLUT2
2) glucose phosphorylated by glucokinase, g6p metabolism generates ATP
3) increased ATP closes K+ channels (SUR subunit), K+ stays in cell
4) cell depolarizes, opening voltage gated Ca2+ channel
5) vesicles exocytose

42
Q

What other pathways potentiate insulin release?

A

1) AAs & FAs can give more ATP to close K+ channel
2) GLP-1 receptor uses PKA pathway to potentiate Ca2+

3) catecholamines inhibit GLP pathway via alpha-adrenergic receptors

43
Q

how in what pattern is inulin released? how is impacted by type 2 diabetes?

A
  • biphasic release
  • first phase- an immediate spike (insulin docked and ready to go)
  • second phase- glucose still being elevated as you digest food (stored & synthesized)

type 2 diabetes - bunted first phase, no second phase

44
Q

whats special about insulin receptors?

A
  • are tyrosine kinases, have intrinsic catalytic activity
  • insulin binds to alpha subunit
  • beta subunit is autophosphorylated & recruits IRSs (insulin receptor substrates)
45
Q

two responses of muscle cells to insulin

A

1) PI3K pathway (PIP/PKB/small G protein)- inserts glut4 into membrane, mediates insulins metabolic effects
2) MAPK pathway mediates mitogenic (growth) effects

46
Q

what is the only GLUT that is insulin dependent and which tissues is it found in?

A

GLUT4

muscle/fat

47
Q

which GLUT is important for regulating insulin release? where else is it found?

A

GLUT 2

pancreatic beta cells, liver, intestines, kidney

48
Q

what is the only GLUT that is insulin dependent and which tissues is it found in?

A

GLUT4
muscle/fat
where most of glucose goes/what causes hyperglycemia

49
Q

which GLUT is important for regulating insulin release? where else is it found?

A

GLUT 2

pancreatic beta cells, liver, intestines, kidney

50
Q

net outcome of insulin on three targets

A
  1. liver- promotes synthesis of TAGs and glycogen
  2. muscle- promotes synthesis of TAGs, glycogen and proteins (inhibits protein breakdown, increases AA/GH uptake)
  3. adipose tissue- promotes TAG production, glycolysis release FFAs from chylomicrons, inhibits lipolysis
51
Q

products from glucagon gene

A
  • tissue specific enzymatic activity
  • cleaved in pancreas- glucagon
  • cleaved in intestines- incretins (GLP1 & 2) (high carbs & fat); GRPP inactivates glucagon
52
Q

what stimulate glucagon?

A

catecholamines, amino acids - both act directly in alpha cells

53
Q

main targets of glucagon

A

mobilizes energy in liver and adipose tissue

54
Q

T/F Insulin promotes ketogenesis

A

FALSE- Insulin INHIBITS ketogenesis

* ketoacidosis is rare in type 2 diabetics

55
Q

T/F Glucagon directly inhibits beta cells and insulin directly inhibits alpha cells

A

FALSE- Catecholamines inhibit beta cells, insulin inhibits alpha cells

56
Q

T/F Insulin and glucagon target the same enzymes

A

true- by phosphorylating phosphatase or kinase domains

57
Q

what is somatostatin made by and stimulated by? inhibited by? what does it inhibit?

A
  • delta cells of pancreas; stimulated by high fat/high carb

- inhibited by insulin (blood flow) BUT also inhibits insulin release (w/ TUMOR)

58
Q

what does amylin do?

A
  • released with insulin, synergistic role

- makes amyloid deposits (vessels, heart, pancreas)

59
Q

what does ghrelin do?

A
  • made in stomach, responds to mechanical stimulus of lack of food (says you’re hungry); low ghrelin, high obesity
  • made in epsilon cells
  • inhibits insulin release by opening K+ channels
60
Q

counter-regulatory hormones of insulin

A
  • immediate: glucagon, catecholamines

- delayed response: growth hormone, cortisol

61
Q

where is renin produced and what does it do?

A
  • produced in JG cells of afferent arterioles

- cleaves angiotensinogen to angiotensin I

62
Q

where is erythropoietin produced and what does it do?

A

EPO made in kidney; stimulates proerythroblasts and differentiation of RBCs (increases number of red blood cells)

63
Q

major side effect of raising hematocrit too quickly

A

hypertension, leading to encephalopathy & seizures

64
Q

where are ANP and BNP released from and in response to? what do they do generally?

A

ANP- atrial myocytes- blood volume
BNP- ventricular myocytes- mechanical stretch

  • both are potent vasodilators, increase excretion of sodium/water; lower blood pressure
65
Q

out of ANP and BNP, which is the more useful diagnostic tool? what can it rule out?

A

BNP- longer half life, normal levels rule out heart failure

66
Q

what are 3 more specific actions of ANP and BNP? what are the 4 target organs?

A
  1. decrease vascular smooth muscle tone
  2. decrease PVR
  3. increase capillary permeability, increasing hematocrit
  • target organs:
    kidney, adrenal cortex, blood vessels, heart
67
Q

4 pathways targeted by decreased ECV

A
  1. JGA secretes renin
  2. sympathetic division of ANS
  3. posterior pituitary secretes ADH
  4. atrial myocytes secrete ANP
68
Q

what is an endocrine disrupter?

A

chemicals that may interfere with the body’s endocrine system and produce adverse developmental, reproductive, neurological, and immune effects in both humans and wildlife

69
Q

two examples of endocrine disruptors?

A
  1. PCB- competes with thyroid hormone binding globulin, results in goiters
  2. DES/BPA- synthetic estrogen, increases cervical and vaginal cancers
70
Q

what happens during early starvation?

A

80% energy from released fatty acids, breakdown of liver glycogens, and break down of proteins (300g/day)

71
Q

describe the metabolic switch

A
  • after a prolonged fast, brain starts using ketone bodies instead of glucose
  • free AAs from the breakdown of protein activate GH, which is trying to conserve lean body mass, get less protein breakdown (20 g/day)
  • only occurs with no intake at all, is very important
72
Q

4 criteria for metabolic syndrome (syndrome x)

A
  1. visceral obesity (waist size)
  2. insulin resistance (fasting glucose)
  3. dyslipidemia (high TAGs/HDL)
  4. hypertension
73
Q

primary hormone produced by adipose tissue; what does it do?

A

leptin
(increased fat cells, increased leptin)
- inhibits appetite and food intake during the fed state

74
Q

what transcription factor is important for TAG synthesis? what is it activated by?

A

Sterol- regulatory binding protein 1C (SREBP-1C)

  • promotes TAG synthesis
  • activated by lipids & insulin
75
Q

what is a nuclear steroid receptor that regulates TAG storage and adipocyte differentiation? what is its clinical use?

A

PPARgamma

  • regulates TAG storage
  • was targeted by TZD to treat insulin resistant type II diabetes by making more fat cells
76
Q

what are the hypothalamic hormone regulators of appetite, regulated by leptin?
(leptin stimulation= decreased food intake)

A

stimulators (inhibited by leptin): neuropeptide Y, AGRP

inhibitors (activated by leptin)- alphaMSH (from POMC), CART

77
Q

what happens with leptin deficiency?

A

leptin normally decreases food intake, by removing it, mice eat themselves to death

78
Q

what is insulin resistance and what does it cause?

A

insulin not efficiently transported into cells; have high plasma glucose and high circulating insulin, which down regulates insulin receptors; over time, pancreas reduces insulin output; beta cells can get depleted and cause switch from type 2 to type 1 diabetes

79
Q

in obesity, what responses are exaggerated following an increase in plasma glucose?

A

increased insulin, increased c-peptide

80
Q

what three measures are used to diagnose diabetes mellitus type 2?

A
  • elevated HbA1C > 6.5% (glucose increases glycosylated RBCs, measures average over long period of time)
  • fasting blood glucose > 126 mg/dl
  • oral glucose tolerance test > 200 mg/dl
81
Q

3 key symptoms of diabetes mellitus type 2

A
  • polyphagia- excessive hunger
  • polyuria- excess glucose in urine (causing H20 and sodium loss) increases plasma osmolarity
  • polydipsia- excessive thirst
82
Q

what does metformin do?

A
  • inhabits hepatic gluconeogenesis

- increases insulin receptor activity (makes more sensitive to insulin)

83
Q

what characterizes type 1 diabetes?

A

autoimmune destruction of beta cells, development of ketoacidosis (no insulin)

84
Q

describe diabetic ketoacidosis

A
  • no insulin + increased counterregulatory hormones
  • increased FFA release
  • metabolism of ketones increases blood acidity
  • dehydration + acidosis results in diabetic coma
85
Q

what are some counterregulatory hormones to insulin?

A

GH, cortisol, glucagon, catecholamines

86
Q

3 things diabetes metabolism causes

A

decreased cellular glucose uptake
increased protein catabolism
increased lipolysis

87
Q

what causes diabetic coma?

A

dehydration, increased plasma osmolarity

88
Q

3 important genes for islet cell development

A
  1. PDX1- islet neogenesis/beta cell proliferation
  2. TCF72- beta cell proliferation
  3. neurogenin 3- all endocrine cell development
89
Q

type 2 diabetes risk factors

A
  1. impaired beta cell proliferation during childhood (malnutrition, mother)
  2. propensity for insulin resistance (high calories, low exercise)
90
Q

describe insulin secretion & beta cell mass during T2DM progression

A
  • initially both increase during the impaired fasting glucose stage, then decrease during early stages of T2DM
91
Q

what does an incretin mimetic do?

A

e.g. GLP1 agnoist

restores the 1st phase of insulin secretion and improves the second

92
Q

T/F beta cell replication continues through adulthood

A

false- occurs during embryonic development, continues through adolescence, then stops

93
Q

most genes identified in the GWAS studies affect

A

beta cells (development, proliferation, survival, function)

Physiology (22 decks)

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